tag:blogger.com,1999:blog-38861186582760143552024-03-13T10:17:18.384-07:00HEALTH FROM TRUSTED SOURCESOnly good, independent and reliable information about health from experts.Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comBlogger4959125tag:blogger.com,1999:blog-3886118658276014355.post-27870203047075435612021-03-29T03:28:00.000-07:002021-03-29T03:28:02.215-07:00COVID-19 Linked to Potentially Dangerous Eye Abnormalities<p><a href="https://press.rsna.org/timssnet/media/pressreleases/14_pr_target.cfm?ID=2249" target="_blank">Radiological Society of North America</a> :Researchers have found significant abnormalities in the eyes of some people with severe COVID-19.Of 129 COVID-19 patients in the study, nine had nodules in the
macular region, the area in the back of the eye responsible for our
central vision, with eight of them having nodules in both eyes.This is the first time these findings have been described using MRI.</p><p>Researchers using MRI have found significant abnormalities in the
eyes of some people with severe COVID-19, according to a study
published in the journal <em>Radiology</em>. The study results support
the need for eye screening in these patients to provide appropriate
treatment and management of potentially severe ophthalmological
manifestations of COVID-19.<span></span></p><a name='more'></a>
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<img alt="Augustin Lecler, M.D., Ph.D." class="headshot-image" src="https://press.rsna.org/pressrelease/2021_resources/2249/lecler_hs-sm.jpg" />
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<p class="headshot-caption">Augustin Lecler, M.D., Ph.D.</p>
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<p>The COVID-19 pandemic has affected more than 100 million people
since it began early in 2020. While the virus primarily attacks the
lungs, it has been linked with eye abnormalities like conjunctivitis,
also known as pink eye, and retinopathy, a disease of the retina that
can result in a loss of vision. Eye abnormalities visible on MRI exams
have been reported but there is limited research on the nature and
frequency of these abnormalities.</p>
<p>To find out more, the French Society of Neuroradiology (SFNR)
initiated a study of 129 patients with severe COVID-19 who underwent
brain MRI. </p>
<p>Of the 129 patients, nine (7%) had abnormal MRI findings of the
globe, or eyeball. The MRI scans showed one or more nodules in the back
part, or posterior pole, of the eyeball. Eight of the nine patients
had spent time in the intensive care unit (ICU) for COVID-19.</p>
<p>“We showed that a few patients with severe COVID-19 from the French
COVID-19 cohort had one or several nodules of the posterior pole of the
globe,” said study lead author Augustin Lecler, M.D., Ph.D., associate
professor at the University of Paris and neuroradiologist from the
Department of Neuroradiology at the Foundation Adolphe de Rothschild
Hospital in Paris. “This is the first time these findings have been
described using MRI.”</p>
<p>All nine patients had nodules in the macular region, the area in the
back of the eye responsible for our central vision. Eight had nodules
in both eyes.</p>
<p>The results suggest that screening should be considered in all
patients with severe COVID-19 to detect these nodules. In clinical
practice, this screening could include dedicated exploration of the
eyes with high-resolution MRI, the researchers said. Additional
recommended exams include fundoscopy, which uses a magnifying lens and a
light to check the back of the inside of the eye, and optical coherence
tomography, a noninvasive test that provides a 3D picture of the
structure of the eye.</p>
<p>Dr. Lecler noted that severe eye problems might largely go unnoticed
in the clinic, as COVID-19 patients hospitalized in the ICU are often
being treated for much more severe, life-threatening conditions. </p>
<p>“Our study advocates for screening of all patients hospitalized in
the ICU for severe COVID-19,” Dr. Lecler said. “We believe those
patients should receive specific eye-protective treatments.”</p>
<p>The mechanism behind nodule formation remains unknown, the
researchers said, although it could be related to inflammation
triggered by the virus. Inadequate drainage of the veins of the eyes, a
problem found in patients who spend time in the ICU in the prone
position or intubated, may also be a factor. Seven of the nine patients
with eye abnormalities in the study had been placed in a prone position
in the ICU for an extended time. </p>
<p>The researchers are performing follow-up clinical and MRI
examinations in the survivors to monitor the nodules and see if they
carry any clinical consequences such as vision loss or visual field
impairment. </p>
<p>They are also performing MRI examinations in new patients with
severe COVID-19 from the second and third waves of the pandemic, using
more comprehensive ophthalmological tests to correlate with the MRI
results. </p>
<p>The effects on patients with moderate COVID-19 are currently under investigation. </p>
<p>“We have launched a prospective study with dedicated high-resolution
MR images for exploring the eye and orbit in patients with light to
moderate COVID,” Dr. Lecler said. “Therefore, we will be able to know
whether our findings were specific to severe COVID patients or not.”</p>
<p>The findings support previous research that showed COVID-19 exacts a
greater toll in people with existing health problems. Of the nine
patients with eye nodules, two had diabetes, six were obese and two had
hypertension.</p>
<div id="footnotes">
<p>“Ocular MRI Findings in Patients with Severe COVID-19: A
Retrospective Multicenter Observational Study.” Collaborating with Dr.
Lecler were François Cotton, M.D., Ph.D., François Lersy, M.D.,
Stéphane Kremer, M.D., Ph.D., and Françoise Héran, M.D., on behalf of
the SFNR’s COVID study group. </p>
<p><em>Radiology</em> is edited by David A. Bluemke, M.D., Ph.D.,
University of Wisconsin School of Medicine and Public Health, Madison,
Wisconsin, and owned and published by the Radiological Society of North
America, Inc. (<a href="https://pubs.rsna.org/journal/radiology" target="_blank">https://pubs.rsna.org/journal/radiology</a>)</p>
<p>RSNA is an association of radiologists, radiation oncologists,
medical physicists and related scientists promoting excellence in
patient care and health care delivery through education, research and
technologic innovation. The Society is based in Oak Brook, Illinois. (<a href="https://www.rsna.org/">RSNA.org</a>)</p>
<p>For patient-friendly information on MRI, visit <a href="https://www.radiologyinfo.org/" target="_blank"><em>RadiologyInfo.org</em></a>.</p>
</div>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-61896077798059508052021-03-29T03:22:00.000-07:002021-03-29T03:22:06.483-07:00Study Shows Flu Vaccine Lessens COVID-19 Symptoms in Children<p></p><div class="separator" style="clear: both; text-align: center;"><a href="https://medicine.missouri.edu/sites/default/files/2021-02/shot-young-boy-iStock-477562584-800x450.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" data-original-height="450" data-original-width="800" height="113" src="https://medicine.missouri.edu/sites/default/files/2021-02/shot-young-boy-iStock-477562584-800x450.jpg" width="200" /></a></div><a href="https://medicine.missouri.edu/news/study-shows-flu-vaccine-lessens-covid-19-symptoms-children" target="_blank">University of Missouri</a> :Researchers from the University of Missouri School of Medicine have discovered that children who receive a seasonal flu shot are less likely to suffer symptoms from a COVID-19 infection. The finding comes from a review of more than 900 children diagnosed with COVID-19 in 2020.<br /><p></p><p>“It is known that the growth of one virus can be inhibited by a previous viral infection,” said <a class="external" href="https://www.muhealth.org/doctors/anjali-patwardhan-md" target="_blank">Anjali Patwardhan, MD</a>,
professor of pediatric rheumatology and child health. “This phenomenon
is called virus interference, and it can occur even when the first virus
invader is an inactivated virus, such as the case with the flu
vaccine.”<span></span></p><a name='more'></a><p></p>
<p>Patwardhan reviewed records from 905 pediatric patients diagnosed
with COVID-19 between February and August 2020 to determine each
patient’s influenza vaccination history. She discovered the COVID-19
positive children who received the influenza vaccine in the current flu
season had lower odds of experiencing symptoms, respiratory problems or
severe disease. She also found that children with COVID-19 who received
the pneumococcal vaccine also had lower odds of experiencing symptomatic
disease.</p>
<p>“Research on the pediatric population is critical because children
play a significant role in influencing viral transmission,” Patwardhan
said. “Understanding the relationship and co-existence of other viruses
alongside COVID-19 and knowing the vaccination status of the pediatric
patient may help in deploying the right strategies to get the best
outcomes.”</p>
<p>Patwardhan said it will also be important to explore the connection
between vaccinations and COVID-19 symptoms in a larger
geographical-multiracial study.</p>
<p>“Based on these findings, we hypothesize that the higher incidence of
COVID-19 in minority populations may also reflect their low vaccination
rate apart from other health inequalities,” Patwardhan said.</p>
<p>Patwardhan’s co-author is MU School of Medicine colleague <a href="https://medicine.missouri.edu/faculty/adrienne-ohler-phd">Adrienne Ohler, PhD,</a> associate research professor. Their study, “<a class="external" href="https://www.cureus.com/articles/49162-the-flu-vaccination-may-have-a-protective-effect-on-the-course-of-covid-19-in-the-pediatric-population-when-does-severe-acute-respiratory-syndrome-coronavirus-2-sars-cov-2-meet-influenza" target="_blank">The
Flu Vaccination May Have a Protective Effect on The Course of COVID-19
in the Pediatric Population: When Does Severe Acute Respiratory Syndrome
Coronavirus 2 (SARS-Cov-2) Meet Influenza</a>,” was recently published in the journal Cureus. <br /></p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-73590015032985458942021-03-29T03:17:00.000-07:002021-03-29T03:17:09.347-07:00Study reveals frequency and characteristics of stroke in COVID-19 patients<div style="text-align: left;"><h3 style="text-align: left;"><small><span style="font-weight: normal;"><a href="https://medicine.missouri.edu/news/study-reveals-frequency-and-characteristics-stroke-covid-19-patients" target="_blank">University of Missouri</a> :A study conducted by researchers from the University of Missouri
School of Medicine and MU Health Care shows coronavirus patients with
stroke face increased need for long-term care.</span></small></h3></div><div><p class="lead">A review of nearly 28,000 emergency department
records shows less than 2% of patients diagnosed with COVID-19 suffered
an ischemic stroke but those who did had an increased risk of requiring
long-term care after hospital discharge. Those are the findings from a
study conducted by researchers from the <a href="https://medicine.missouri.edu/" target="_blank">University of Missouri School of Medicine</a> and <a class="external" href="https://www.muhealth.org/" target="_blank">MU Health Care</a>.<span></span></p><a name='more'></a><p></p>
<p>The researchers teamed up with the MU Institute for Data Science and
Informatics and the Tiger Institute for Health Innovation to review data
from 54 health care facilities. They found 103 patients (1.3%)
developed ischemic stroke among 8,163 patients with COVID-19.
Comparatively, 199 patients (1.0%) developed stroke among 19,513
patients who didn’t have COVID-19.</p>
<figure class="align-left" role="group"><img alt="Adnan I. Qureshi, MD" data-entity-type="file" data-entity-uuid="8ccfb19e-7a34-4e1f-8210-c114c703b2e1" src="https://medicine.missouri.edu/sites/default/files/inline-images/Qureshi_Adnan-21-250x300_0.jpg" /><figcaption>Adnan I. Qureshi, MD</figcaption></figure><p>“Patients
with COVID-19 who developed acute ischemic stroke were older, more
likely to be black and had a higher frequency of cardiovascular risk
factors,” said lead researcher <a class="external" href="https://www.muhealth.org/doctors/adnan-qureshi-md" target="_blank">Adnan I. Qureshi, MD</a>, a professor of clinical neurology at the MU School of Medicine.</p>
<p>The mean age of COVID-19 patients with stroke was 68.8 compared with
54.4 for those without stroke. Among those with COVID-19 and stroke, 45%
were Black, 36% were white and 6% were Hispanic. They tended to have
hypertension (84%), high fat content in the blood (75%) and diabetes
(56%).</p>
<p>“We also found that COVID-19 patients with stroke had a significantly
higher rate of discharge to a destination other than home compared to
stroke patients without COVID-19,” Qureshi said. “Patients with COVID-19
tend to have multisystem involvement and elevated markers of
inflammation, which have been shown to increase the rate of death or
disability.”</p>
<p>Qureshi said his findings are somewhat different from earlier studies
that suggested patients with COVID-19 who developed stroke were younger
and without preexisting cardiovascular risk factors.</p>
<p>“Even if COVID-19 was a predisposing factor, the risk was mainly seen
in those who were already at risk for stroke due to other
cardiovascular risk factors,” Qureshi said.</p>
<p>In addition to Qureshi, the study authors include fellow MU School of Medicine collaborators <a class="external" href="https://www.muhealth.org/doctors/camilo-gomez-md" target="_blank">Camilo R. Gomez, MD</a>, professor of clinical neurology; <a class="external" href="https://www.muhealth.org/doctors/brandi-french-md" target="_blank">Brandi French, MD</a>, associate professor of vascular and clinical neurology; <a class="external" href="https://www.muhealth.org/doctors/farhan-siddiq-md" target="_blank">Farhan Siddiq, MD</a>, assistant professor of neurological surgery; Iryna Lobanova, MD, research specialist in the Department of Neurology; <a class="external" href="https://www.muhealth.org/doctors/syed-naqvi-md" target="_blank">S. Hasan Naqvi, MD</a>,
associate professor of clinical medicine; William Baskett, graduate
student; Wei Huang, graduate student; Daniel Shyu, medical student;
Danny Myers, PhD, senior development project manager; Murugesan Raju,
PhD, post-doctoral fellow; and Chi-Ren Shyu, PhD, director, MO
Informatics Institute. </p>
<p>Their study, “<a class="external" href="https://www.ahajournals.org/doi/pdf/10.1161/STROKEAHA.120.031786" target="_blank">Acute Ischemic Stroke and COVID-19</a>,”
was recently published in the journal Stroke. Part of the support for
this study was provided by the National Institutes of Health. The
authors of the study declare that they have no conflicts of interest
related to this study and the content does not necessarily represent the
official views of the National Institutes of Health.</p>
</div><div style="left: -99999px; position: absolute;">A study conducted by
researchers from the University of Missouri School of Medicine and MU
Health Care shows coronavirus patients with stroke face increased need
for long-term care.</div>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-60622117266963333802021-03-29T03:10:00.007-07:002021-03-29T03:10:46.759-07:00Targeted RNA Nanoparticle Shows Early Promise as Treatment for Liver Cancer<p><a href="https://cancer.osu.edu/news/targeted-rna-nanoparticle-shows-early-promise-as-treatment-for-liver-cancer" target="_blank"></a></p><div class="separator" style="clear: both; text-align: center;"><a href="https://cancer.osu.edu/-/media/images/shared/media-room/cancer/press-releases/2020/september/rna-nanoparticle-illustration.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" data-original-height="601" data-original-width="800" height="150" src="https://cancer.osu.edu/-/media/images/shared/media-room/cancer/press-releases/2020/september/rna-nanoparticle-illustration.jpg" width="200" /></a></div>Ohio University : A new targeted RNA nanoparticle designed to carry a chemotherapy drug
along with a therapeutic oligonucleotide against chemical efflux gene
might provide an effective treatment for liver cancer, according to a
new study led by researchers at The Ohio State University Comprehensive
Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove
Research Institute (OSUCCC – James). <span><a name='more'></a></span>
<p></p><p>The study, published in the <em>Journal of Controlled Release</em>, shows that the RNA nanoparticles efficiently target hepatocellular carcinoma (HCC, one kind of <a href="https://cancer.osu.edu/for-patients-and-caregivers/learn-about-cancers-and-treatments/cancers-conditions-and-treatment/cancer-types/liver-cancer">liver cancer</a>)
cells and are stable, safe and effective both in laboratory and animal
studies. The findings suggest that the nanoparticles could offer an
effective new treatment for HCC.</p>
<p>The RNA nanoparticles carry a chemotherapeutic drug, Paclitaxel, and
display molecules that target HCC cells. They also contain a microRNA
that inactivates a chemical efflux pump called p-glycoprotein, which
usually pumps out chemotherapeutic drugs from the liver cells, making
cancer untreatable.</p>
<p>The liver can be regarded as the body’s checkpoint for blocking and
removing toxins from the body. In the body, for most chemicals or drugs,
no matter if they were intravenously injected or absorbed through
intestines, their first step station is the liver. </p>
<p>“Liver cells express drug exporter pumps that are used to remove
chemotherapeutic drugs and detoxify the body. This renders the treatment
with chemical drugs ineffective and contributes to drug resistance,”
says study leader and corresponding author <a href="https://cancer.osu.edu/find-a-researcher/search-researcher-directory/peixuan-guo">Peixuan Guo, PhD</a>, professor at Ohio State’s <a href="https://pharmacy.osu.edu/" target="_blank">College of Pharmacy</a> and the Sylvan G. Frank Endowed Chair in Pharmaceutics and Drug Delivery. Guo also is a member of the OSUCCC – James <a href="https://cancer.osu.edu/for-cancer-researchers/research/research-programs/translational-therapeutics">Translational Therapeutics Program</a>. “This could be why liver cancer responds poorly to chemotherapy treatment.”</p>
<p>Earlier work by Guo and his team showed that RNA nanoparticles have
rubbery or amoeba-like properties that enable them to stretch, shrink
and then return to their normal shape.</p>
<p>“We believe that this amoeba and rubber-like property enables RNA
nanoparticles to slip through the poorly formed walls of tumor blood
vessels and enter the tumor mass,” said Guo, who directs Ohio State’s
Center for RNA Nanobiotechnology and Nanomedicine.</p>
<p>“This same rubbery property could allow the kidneys to filter RNA
nanoparticles from the blood and excrete them in the urine, thereby
eliminating them from the body swiftly,” said Guo. “This, in turn, could
reduce retention of anticancer RNA nanoparticles in vital organs,
lowering the drug’s toxicity. </p>
<p>For this study, Guo and his colleagues constructed the RNA
nanoparticles using six RNA strands that self-assembled into a globular
structure. The nanoparticle served as a cargo system to deliver both
Paclitaxel and microRNA (miR122) along with HCC targeting ligands. They
conjugated 24 molecules of Paclitaxel, along with HCC targeting
molecules (a derivative of galactosamine) and one microRNA to the
multivalent RNA nanoparticle. The sequence for the microRNA extends from
one of the RNA strands. The final structure is about 18 nanometers in
size.</p>
<p>The study’s key findings include:</p>
<ul><li>RNA nanoparticles selectively bind and deliver therapeutic agents into liver cancer cells efficiently.<br />
<br />
</li><li>The attached miR122 effectively inhibits the liver drug-efflux pump.<br />
<br />
</li><li>RNA nanoparticles carrying both Paclitaxel and miR122 more
effectively inhibited tumor growth compared to Paclitaxel or miR122
alone; nanoparticles without treatment groups showed no cancer-cell
inhibition effects.<br />
<br />
</li><li>Animal studies showed that the RNA nanoparticle formulation
targeted tumor cells effectively and strongly inhibited tumor growth due
to the synergistic effect of Paclitaxel and miR122, without affecting
healthy organs. </li></ul>
<p>“Overall,” said Guo, “our findings suggest that the rubber-like
multivalent RNA nanoparticles could offer an effective treatment for
liver cancer — currently an incurable, deadly disease.”</p>
<p>This research was funded by the National Institutes of Health (CA151648).</p>
<p>Collaborators in this study are: Hongzhi Wang, Satheesh Ellipilli,
Xin Li and Mario Vieweger of The Ohio State University; and Wen-Jui Lee
and Yuan-Soon Ho, Taipei Medical University, Taiwan.</p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-42256200024289761262021-03-29T03:08:00.002-07:002021-03-29T03:08:16.934-07:00In a COVID-19 World, Speech Disturbance May Be the Most Important Stroke Sign to Look Out For<p> </p><p style="margin-bottom: 12pt;"><span><a href="https://www.pennmedicine.org/news/news-blog/2021/february/in-a-covid19-world-speech-disturbance-may-be-the-most-important-stroke-sign-to-look-out-for" target="_blank">University of Pennsylvania</a> :With an increase in remote work, virtual meetings</span><span>,</span><span>
and video chats, many of us may not realize we are now on the front
lines of stroke detection via the speakers on our computers, phones and
other devices. </span></p>
<p><span>Across<strong> </strong>the world, fewer people are going to the hospital to be treated for stroke, but that’s not because fewer people are having them.<strong> </strong>In July,<strong> Renyu Liu, MD</strong></span><span>,
a professor of Anesthesiology and Critical Care in the Perelman School
of Medicine at the University of Pennsylvania published a </span><a href="https://onlinelibrary.wiley.com/doi/10.1111/cns.13442"><span>study</span></a><span>
in CNS Neuroscience & Therapeutics that found that since the start
of the COVID-19 pandemic the global average for stroke hospitalizations
decreased by about 42 percent, statistics spurred by people </span><a href="https://www.aarp.org/health/conditions-treatments/info-2020/er-care-during-covid-19.html"><span>afraid to seek emergency medical care for fear of catching COVID-19</span></a><span>. In a recently </span><a href="https://onlinelibrary.wiley.com/doi/10.1111/cns.13608" target="_blank"><span>published editorial</span></a><span>
in the same journal, Liu suggests that that the pandemic, with its
social distancing and mask wearing, may be also be contributing to a
decline in people recognizing the common warning signs of stroke.<span></span></span></p><a name='more'></a><p></p>
<p><span>Traditionally, </span><span>FAST (Face, Arms, Speech, Time) has
been the acronym used to educate the public about stroke symptoms. Liu
points out that this acronym puts its greatest emphasis on symptoms that
are harder to notice during the pandemic: </span><span>F</span><span>acial
drooping is one of the common signs of stroke, but you might not notice
it on someone who is wearing a mask, or standing far away. When we’re
all spending less time apart, and socially distanced when we are around
others, arm weakness may also fly under the radar. With a major shift to
more video chats as a main means of communication, speech disturbance
may be the only sign of stroke people might readily be able to pick up
on. For example, in October during a virtual learning session, a </span><a href="https://www.cnn.com/2020/10/17/us/teacher-saves-grandma-life-stroke-trnd/index.html"><span>Michigan teacher</span></a><span>
noticed the slurred speech of the grandparent of one of her students,
quickly arranging for 911 to be called to the home, potentially saving
the grandmother’s life. </span></p>
<p><span>All of this is why Liu and his collaborators suggest an
alternative to the FAST acronym, which places facial drooping and arm
weakness ahead of speech disturbance. Liu proposes the adoption of </span><a href="https://onlinelibrary.wiley.com/doi/10.1111/cns.13608"><span>Stroke 9-1-1 (S911), a novel program</span></a><span>,
where “S” represents “Stroke” and “Speech Disturbance” while urging
people to immediately call 911. The 9 also stands as a reminder to get
people to spell n-i-n-e to verify slurred speech, the 1 stands for one
weak arm, and the second 1 stands for 1 uneven face, crooked mouth.</span></p>
<p><span>Liu also argues that FAST relies heavily on people’s understanding of the English language, and that S911 is easier to remember.</span></p>
<p><span>“Some 13.5 percent of the U.S. population — 44 million people —
is foreign born, the highest level ever, and many are not proficient in
English. A report from the Migration Policy Institute found that 22
percent of the U.S. population does </span><span>not speak English at home,” he said. </span></p>
<p><span>He hopes that Stroke 911 can be used as a practical alternative
tool to promote the stroke awareness with an emphasis on the speech
disturbance. And it’s not the first time he has proposed a change like
this. In 2017 Liu, who grew up and practiced medicine in China before
coming to the U.S., noticed that FAST was not the best acronym for a
population that didn’t speak English as a first language. </span><a href="https://www.pennmedicine.org/news/internal-newsletters/system-news/2017/february/it-s-as-easy-as-1-2-0"><span>He
collaborated with Jing Zhao, MD, PhD, a neurologist at Minhang
hospital, Fudan University, China, to create a new system without a
language barrier.</span></a><span> They used Stroke 120, because 120 is China’s emergency number and it caught on quickly.</span></p>
<p><span>Liu hopes that more people in the U.S. can learn about the
importance of recognizing speech disturbances as a stroke symptom,
hopefully leading to quicker hospital referrals and better outcomes for
patients overall. Even as COVID keeps us apart, he says everyone can
play a role in saving a life – even via video chat.</span></p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-90998837808645259332021-03-29T03:04:00.000-07:002021-03-29T03:04:05.266-07:00Text Message Program Shows 60 Percent of Opioid Tablets Unused After Common Procedures<p> </p><div class="h2-main" id="prnewsmaincontent_0_hTagline" style="text-align: left;"><span class="h2-main__title"><a href="https://www.pennmedicine.org/news/news-releases/2021/march/text-message-program-shows-60-percent-of-opioid-tablets-unused-after-common-procedures" target="_blank"></a><div class="separator" style="clear: both; text-align: center;"><a href="https://www.pennmedicine.org/news/news-releases/2021/march/text-message-program-shows-60-percent-of-opioid-tablets-unused-after-common-procedures" target="_blank"></a><a href="https://www.pennmedicine.org/news/-/media/images/pr%20news/news/2021/march/opioid.ashx?la=en" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" data-original-height="526" data-original-width="800" height="132" src="https://www.pennmedicine.org/news/-/media/images/pr%20news/news/2021/march/opioid.ashx?la=en" width="200" /></a></div>University of Pennsylvania :A
Penn Medicine new study of how text messaging could inform opioid
prescribing practices showed that 60 percent of opioids are left over
after orthopaedic and urologic procedures.</span>More than half of the opioid tablets prescribed for patients who
underwent orthopaedic or urologic procedures went unused in a new study
by researchers at the Perelman School of Medicine at the University of
Pennsylvania. Using an automated text messaging system that regularly
checked in with patients on their pain and opioid use, the study also
showed that most opioids are taken within the first few days following a
procedure and may not be necessary to manage pain even just a week
following a procedure. The study was published today in <em>JAMA Network Open</em>.
<span><a name='more'></a></span><p>“Through simple text messaging we highlight a method which gives
clinicians the information they need to reduce prescribing and manage
pain,” said co-lead author <a href="https://centerfordigitalhealth.upenn.edu/anish-agarwal"><strong>Anish Agarwal, MD,</strong></a>
a clinical innovation manager in the Penn Medicine Center for Digital
Health and an assistant professor of Emergency Medicine. “We found that
more than 60 percent of the opioid tablets prescribed went unused, which
tracks with the team’s <a href="https://www.pennmedicine.org/news/news-releases/2021/february/high-patient-uptake-for-text-message-system-monitoring-opioid-use-in-real-time">preliminary studies.</a>
We can begin to use these data in multiple ways: One approach would be
to look at trends in patient-reported use and tailor future prescribing
to meet the anticipated pain for the majority of patients undergoing a
specific procedure.”</p>
<p>In response to the opioid crisis, using text messaging to keep track
of how many prescriptions patients actually take after a procedure – and
to potentially right-size the amount prescribed – is relatively new but
growing in popularity. The traditional ways that clinicians track their
patients’ opioid use could use a boost.</p>
<p>“Right now, care teams rely heavily on patient recall, which they may
not be able to remember in detail; phone calls, which require a lot of
effort in making calls; or tracking from the health system ordering,
which does not provide information from the patients themselves about
how much they are using, and how much pain they are in,” explained
co-lead author <a href="https://www.pennmedicine.org/providers/profile/daniel-lee"><strong>Daniel Lee, MD,</strong></a>
an assistant professor of Urology. “So with these older methods, either
the data we are getting could be inaccurate, or the way we get the data
is not scalable for an entire health system.”</p>
<div style="float: right; margin: 10px; width: 400px;"><img alt="opioid infographic" height="200" src="https://www.pennmedicine.org/news/-/media/images/pr news/news/2021/march/opioid text infographic.ashx?la=en" width="400" />
</div>
<p>Using automated text messaging systems, then, provides the
opportunity for large-scale, near-real-time polling of patients. But as
an emerging method, it requires study.</p>
<p>With that in mind, Agarwal, Lee, co-author <a href="https://www.pennmedicine.org/providers/profile/eric-hume"><strong>Eric Hume, MD,</strong></a> director of Quality and Safety and an associate professor of Orthopaedic Surgery, and senior author <a href="https://www.med.upenn.edu/apps/faculty/index.php/g275/p8644305"><strong>M. Kit Delgado, MD,</strong></a>
an assistant professor of Emergency Medicine and Epidemiology, and
their team set out to test the text messaging system. Over a span of
several months in 2019, they enrolled patients who’d had common
orthopaedic and urologic procedures, ranging from knee arthroscopy to
hand fracture fixes and vasectomies to prostatectomies.</p>
<p>A little more than 900 patients – approximately 45 percent of those
eligible – participated in the study. About 80 percent were orthopaedic
patients and just under 20 percent had urological procedures.
Participants were asked to rate their pain (on a scale of zero to 10),
as well as if they felt able to manage that pain on the fourth day
following their procedure. Subsequent texts went out on days seven, 14
and 21 to measure the change over time. Each of these texts also
inquired about opioid tablet use which was matched to their initial
prescription.</p>
<p>As time went on, the text messages showed that the average pain
scores fell among patients of both classifications of procedures. At the
same time, the ability to manage pain climbed, according to patients.
However, this all seemed to be accomplished with fewer and fewer opioid
pills, the study showed, and certainly far fewer than were prescribed.
By day seven, most patients had actually stopped taking tablets (the
average patient in the study took zero tablets by day seven).</p>
<p>The average Orthopaedic Surgery patient took six tablets across the
entire study period, but had been prescribed 20. Among Urology patients,
one tablet was the average amount used, compared to seven prescribed.
The study showed that, across the board, 64 percent of patients didn’t
even use half of their prescription, and only 21 percent of Orthopaedic
Surgery patients and 11 percent of Urology patients needed a refill a
month out from their procedure.</p>
<p>“Having data on our prescription of opioids and the amount that was
unused is eye-opening,” said Hume. “This is so much more powerful and
engaging than a generic message to reduce prescribing without an eye
toward patient needs.”</p>
<p>The team believes that knowing the difference between prescription
rates and use, along with finding this reliable way to measure that
difference, will be a game-changer in pain management for surgical
procedures.</p>
<p>“The potential to translate these findings to tailor post-operative
prescribing to patient needs and change national practice is high,” said
Delgado, who also serves as Co-Chair of the Penn Medicine Opioid Task
Force. “This study has national implications, as it shows that patients
only take a fraction of the amounts that we know are prescribed on
average across the country. Previously we showed the median amount of
opioid pills prescribed to be <a href="https://www.pennmedicine.org/news/news-releases/2020/august/opioid-prescription-rates-for-knee-surgery-patients-vary-but-higher-strength-dosage-common">40 tablets for knee arthroscopy</a> and <a href="https://www.auajournals.org/doi/full/10.1097/JU.0000000000000343">20 tablets for prostate or bladder resections</a>.
We are in the process of rolling this automated text messaging platform
to additional surgical groups within the health system and will
continue to share our learnings to guide practice on a broader scale.”</p>
<p>This study was partly funded by the United States Food and Drug Administration (FDA, grant number HHSF223201810209C).</p>
<p>Other authors include Brian Sennett, Zarina Ali, Ruiying Xiong,
Jessica Hemmons, Evan Spencer, Dina Abdel-Rahman, Rachel Kleinman,
Hannah Lacko, Annamarie Horan, Mary Dooley, and Sami Mehta.</p></div>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-29401007709133205352021-03-29T02:57:00.005-07:002021-03-29T02:57:20.236-07:00Cancer Immunotherapy May Also Treat Certain Autoimmune Diseases <p></p><div class="separator" style="clear: both; text-align: center;"><a href="https://labblog.uofmhealth.org/sites/lab/files/2021-03/T-cell_attaching_to_cancer_cell.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" data-original-height="450" data-original-width="800" height="112" src="https://labblog.uofmhealth.org/sites/lab/files/2021-03/T-cell_attaching_to_cancer_cell.jpg" width="200" /></a></div><p><a href="https://labblog.uofmhealth.org/lab-report/cancer-immunotherapy-may-also-treat-certain-autoimmune-diseases" target="_blank">University of Michigan</a> :The new approach blocks the interaction between cancer cells and immune receptors, showing promise in mice.<span><span><span><span> <br />A
team of researchers has found disrupting the interaction between cancer
cells and certain immune cells is more effective at killing cancer
cells than current immunotherapy treatments.</span></span></span></span></p><div><div class="paragraph paragraph--type--text paragraph--view-mode--default"><div class="clearfix text-formatted field field--name-field-text field--type-text-long field--label-hidden field__item">
<p><span><span><span><span>The findings, which include studies in cell lines and animal models, appeared in <em>JCI Insight</em> and focus on </span><a href="https://doi.org/10.1172/jci.insight.145662" target="_blank"><span>a protein called CD6 as a target for a new approach to immunotherapy</span></a><span>.<span></span></span></span></span></span></p><a name='more'></a><p></p>
<p><span><span><span><span><span>Over the past two decades, new
approaches to cancer treatment have been developed that block immune
checkpoints, which are receptors on the surface of certain immune cells,
like natural killer T cells. Cancer exploits these immune cells and
render them dormant. </span></span></span></span></span></p>
<p><span><span><span><span>This treatment, called checkpoint inhibitor
immunotherapy, gives these immune cells a chance to fight back.
Unfortunately, though, patients that become cancer-free are often left
with autoimmune conditions that, in some patients, can eventually be
fatal. </span></span></span></span></p>
<p><span><span><span><span>Only approximately one third of patients with cancer ultimately benefit from currently available immune checkpoint inhibitors. </span></span></span></span></p>
<p><span><span><span><span>“I’m interested in how cancer cells interact
with certain immune cells to control the immune response to cancer, and
how the immune system interacts with organs and tissues to cause
autoimmune diseases,” says study senior author </span><a href="https://www.uofmhealth.org/profile/729/david-alan-fox-md" target="_blank"><span>David Fox, M.D.</span></a><span>, a rheumatologist and cancer researcher at the </span><a href="https://www.rogelcancercenter.org/" target="_blank"><span>University of Michigan Rogel Cancer Center</span></a><span>. “How can researchers intervene to alter these interactions and simultaneously destroy cancers while preventing autoimmunity?” </span></span></span></span></p></div>
</div>
</div>
<div>
<div class="quote-container">
<div class="quote-image"><a href="https://www.uofmhealth.org/profile/729/david-alan-fox-md" target="_blank">
<div class="field field--name-field-quote-image field--type-image field--label-hidden field__items">
<div class="field__item"> <img alt="David Fox, M.D. photo" height="104" src="https://labblog.uofmhealth.org/sites/lab/files/2021-03/Fox_729%20%281%29.jpg" width="74" />
</div>
</div>
</a></div>
<div class="quote">
<div class="field--name-field-quote">"Until now, we haven’t
been able to get immune cells to kill cancer cells without triggering an
immune response that can be harmful to patients."</div>
<a href="https://www.uofmhealth.org/profile/729/david-alan-fox-md" target="_blank">
<div class="field field--name-field-title field--type-string field--label-hidden field__item">David Fox, M.D.</div>
</a>
</div>
</div>
</div>
<p><span><span><span><span>Fox’s
lab and collaborators at the Cleveland Clinic Research Foundation have
been studying the roles of CD6 and receptors it interacts with as it
related to autoimmunity for many years. Previously, the research team
was able to create man-made CD6 and CD318, a receptor that CD6 interacts
with, to </span><a href="https://www.cancer.org/treatment/treatments-and-side-effects/treatment-types/immunotherapy/monoclonal-antibodies.html" target="_blank"><span>act like human antibodies in the immune system and fight off cancer cells</span></a><span>.</span></span></span></span></p>
<p><span><span><span><span>This new study proved successful in
combatting human breast cancer, lung cancer and prostate cancer in cell
lines, indicating that the anti-CD6 antibody, known as UMCD6, could be
useful in treating a wide range of cancer types. </span></span></span></span></p>
<p><span><span><span><span>They also grafted human breast cancer cells
into immunocompromised mice, and followed up with transferring human
immune cells into the mice. When given an injection of UMCD6, the tumors
almost completely disappeared in just one week, compared to mice
treated without UMCD6. </span></span></span></span></p>
<p><span><span><span><strong><em><span><span><span><span><span>Like Podcasts? Add the </span></span></span></span></span></em></strong><a href="https://www.amazon.com/Michigan-Medicine-News-Break/dp/B07CS5B9LY/?sa-no-redirect=1&pldnSite=1" target="_blank"><em><strong><span><span><span><span><span><span>Michigan Medicine News Break</span></span></span></span></span></span></strong></em></a><em><strong><span><span><span><span> on</span></span></span></span></strong></em><em> </em><a href="https://itunes.apple.com/us/podcast/michigan-medicine-news-break/id1390241260?mt=2" target="_blank"><em><strong><span><span><span><span><span><span>iTunes</span></span></span></span></span></span></strong></em></a><em><strong><span><span><span><span> or anywhere you listen to podcasts.</span></span></span></span></strong></em></span></span></span></p>
<p><span><span><span><span>The findings have implications beyond this
first description of a potential new approach to against cancer. The
ability of UMCD6 to prevent and treat autoimmune diseases makes the
potential implications for cancer immunotherapy especially intriguing,
the researchers say. </span></span></span></span></p>
<p><span><span><span><span>It’s been known that CD6 has to play a role
in autoimmunity, since mice that don’t have CD6 on their immune cells
have major suppression of autoimmune diseases. </span></span></span></span></p>
<p><span><span><span><span>Prior research has shown that an antibody
that binds to CD6 and pulls it from the cell surface to the inside of
the cell can effectively treat autoimmune mouse models of three
different human diseases: rheumatoid arthritis, </span><a href="https://www.uofmhealth.org/conditions-treatments/cmc/arthritis/rheumatoid" target="_blank"><span>an inflammatory disease that causes the immune system to inflame the membrane that lines the joints</span></a><span>, multiple sclerosis, </span><a href="https://www.uofmhealth.org/conditions-treatments/brain-neurological-conditions/multiple-sclerosis-ms" target="_blank"><span>a disease that affects the central nervous system, brain and spinal cord</span></a><span>, and uveitis, </span><a href="https://www.uofmhealth.org/conditions-treatments/uveitis-iritis" target="_blank"><span>an eye disease that can cause blindness</span></a><span>.</span></span></span></span></p>
<p><span><span><span><span>Now, when treated with UMCD6, Fox saw the
mice show striking reductions in disease activity, autoimmunity and
organ damage in mice.</span></span></span></span></p>
<p><span><span><span><span>“When UMCD6 binds to CD6 on these specific
immune cells, it creates a CD6 cluster that dives into the interior of
the cell, allowing no CD6 to remain on the cell surface” says Fox. “This
causes the killer T cells to seek out and destroy the cancer cells much
more aggressively. At the same time, removing CD6 from the surface of
CD4 cells, with the same UMCD6 antibody, controls and limits the
activity of the CD4 cells, which are the cells that instigate autoimmune
diseases.”</span></span></span></span></p>
<p><span><span><span><span>“Until now, we haven’t been able to get
immune cells to kill cancer cells without triggering an immune response
that can be harmful to patients,” he adds. “What we’ve created here
completely challenges prevailing concepts.”</span></span></span></span></p>
<p><span><span><span><span>So how close are researchers to studying UMCD6 in humans?</span></span></span></span></p>
<p><span><span><span><span>There are ongoing studies of anti-CD6
antibodies in India, where an anti-CD6 antibody has been approved for
the treatment of psoriasis. However, in the United States, substantial
research remains to be done to translate the discovery from laboratory
models to human clinical trials.</span></span></span></span></p>
<p><span><span><span><span>“If UMCD6 is proven to successfully treat
cancer and prevent recurrences, this could overcome the major current
limitations to checkpoint inhibition success in human cancer
immunotherapy,” says Fox. “I look forward to seeing what lies ahead in
this field of research.”</span></span></span></span></p>
<p><span><span><span><em><span>Disclosure: Fox is a member of JCI Insight’s editorial board.</span></em></span></span></span></p>
<p><span><span><span><em><span>This study was supported by funds from
the NIH Autoimmunity Center of Excellence and NIH Training Grant
T32AR007080, with additional funds acquired from the University of
Michigan Rogel Cancer Center, the Michigan Translational Research &
Commercialization program, and the Frederick G.L. Huetwell and William
D. Robinson Professorship in Rheumatology at the University of Michigan.</span></em></span></span></span></p>
<p><span><span><span><strong><span>Paper cited: </span></strong><span>“CD6 is a target for cancer immunotherapy,” <em>JCI Insight</em>. </span><a href="https://doi.org/10.1172/jci.insight.145662" target="_blank"><span>DOI: 10.1172/jci.insight.145662</span></a></span></span></span></p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-77286706886819658182021-03-29T02:54:00.002-07:002021-03-29T02:54:10.564-07:00Vaping Marijuana Associated with More Symptoms of Lung Damage than Vaping or Smoking Nicotine <p><a href="https://labblog.uofmhealth.org/rounds/vaping-marijuana-associated-more-symptoms-of-lung-damage-than-vaping-or-smoking-nicotine" target="_blank">University of Michigan</a> :Adolescents who vape cannabis are at greater risk for respiratory symptoms indicative of lung injury than teens who smoke cigarettes or marijuana, or vape nicotine, a new University of Michigan study suggests.<span><span><br />Adolescents
who vape cannabis are at greater risk for respiratory symptoms
indicative of lung injury than teens who smoke cigarettes or marijuana,
or vape nicotine, a new University of Michigan study suggests.<span></span></span></span></p><a name='more'></a><p></p><div><div class="paragraph paragraph--type--text paragraph--view-mode--default"><div class="clearfix text-formatted field field--name-field-text field--type-text-long field--label-hidden field__item">
<p><span><span>The result challenges conventional wisdom about vaping nicotine, says the study's principal investigator, <a href="https://nursing.umich.edu/faculty-staff/faculty/carol-j-boyd" target="_blank">Carol Boyd, Ph.D.</a>, the Deborah J. Oakley Collegiate Professor Emerita at the University of Michigan School of Nursing.</span></span></p>
<p><span><span>"I thought that e-cigarettes (vaping nicotine) would be
the nicotine product most strongly associated with worrisome respiratory
symptoms," she says. "Our data challenges the assumption that smoking
cigarettes or vaping nicotine is the most harmful to the lungs. If we
control for vaping cannabis in our analyses, we find there is a weaker
relationship between e-cigarette or cigarette use and respiratory
symptoms when compared to vaping cannabis." </span></span></p>
<p><strong><em><span><span><span><span><span>Like Podcasts? Add the </span></span></span></span></span></em></strong><span><span><span><a href="https://www.amazon.com/Michigan-Medicine-News-Break/dp/B07CS5B9LY/?sa-no-redirect=1&pldnSite=1" target="_blank"><em><strong><span><span><span><span><span><span>Michigan Medicine News Break</span></span></span></span></span></span></strong></em></a></span></span></span><em><strong><span><span><span><span> on</span></span></span></span></strong> </em><span><span><span><a href="https://itunes.apple.com/us/podcast/michigan-medicine-news-break/id1390241260?mt=2" target="_blank"><em><strong><span><span><span><span><span><span>iTunes</span></span></span></span></span></span></strong></em></a></span></span></span><em><strong><span><span><span><span> or anywhere you listen to podcasts.</span></span></span></span></strong></em></p>
<p><span><span>Boyd, who also co-directs U-M's Center for Drugs,
Alcohol, Smoking and Health, stressed that the findings do not mean that
vaping nicotine or smoking cigarettes or marijuana are not bad for you.
These products also produce symptoms of lung injury, but not to the
same degree as vaping marijuana, she explains.</span></span></p>
<p><span><span>"In short, it is all bad, but if you also vape cannabis
you have a greater number of unhealthy respiratory symptoms than if you
just smoke cigarettes or marijuana, or vape e-cigarettes," Boyd says.
"Without a doubt, cigarettes and e-cigarettes are unhealthy and not good
for lungs. However, vaping marijuana appears even worse." </span></span></p>
<p><span><span>Boyd and colleague <a href="https://nursing.umich.edu/faculty-staff/faculty/philip-veliz" target="_blank">Philip Veliz, Ph.D.</a>,
U-M research assistant professor of nursing, wanted to explore the
association of unhealthy respiratory symptoms among U.S. adolescents
currently using cigarettes, e-cigarettes or cannabis and who had vaped
cannabis within their lifetime. </span></span></p>
<p><span><span><span><a href="https://labblog.uofmhealth.org/newsletter" target="_blank"><em><strong><span><span><span><span>MORE FROM THE LAB: Subscribe to our weekly newsletter</span></span></span></span></strong></em></a></span></span></span></p>
<p><span><span>Adolescents who reported vaping marijuana were roughly
twice as likely to report "wheezing and whistling" in the chest than
those who did not. Current use of cigarettes, e-cigarettes and cannabis
were associated with some respiratory symptoms, such as dry cough, but
most associations were not significant after controlling for vaping
cannabis. </span></span></p>
<p><span><span>The researchers also found that an asthma diagnosis was
most strongly associated with symptoms of future lung injury than
cigarettes, e-cigarettes, cannabis use and vaping cannabis. </span></span></p>
<p><span><span>One study limitation is that the researchers did not look
at co-use of vaping cannabis and the use of cigarettes or e-cigarettes.</span></span></p>
<p><span><span>"Future studies need to assess if it is the combination
of vaping both nicotine and cannabis that is creating so many
respiratory issues," Veliz says. "It may be the combination of vaping
cannabis along with smoking cigarettes is what leads to the high rates
of respiratory symptoms among youthful marijuana vapers."</span></span></p>
<p><span><span>Boyd and Feliz looked at self-reported symptoms from a
sample of adolescents ages 12-17 years, from the 2016-2018 Wave of the
Population Assessment of Tobacco and Health Study. Symptoms were:
wheezing and whistling in the chest; sleep disturbed or speech limited
due to wheezing; sounded wheezy during or after exercise; and dry cough
at night not associated with chest illness or infection. </span></span></p>
<p><span><span><strong>Paper cited:</strong> "</span></span><span><span>Cannabis, Vaping, and Respiratory Symptoms in a Probability Sample of U.S. Youth," <em>Journal of Adolescent Health</em>. <a href="https://doi.org/10.1016/j.jadohealth.2021.01.019" target="_blank">DOI: </a></span></span><a href="https://doi.org/10.1016/j.jadohealth.2021.01.019" target="_blank"><span><span>10.1016/j.jadohealth.2021.01.019</span></span></a></p></div>
</div>
</div>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-77700232462387318232021-03-29T02:50:00.005-07:002021-03-29T02:50:50.349-07:00Research Group Identifies Potential Therapeutic Target for Lupus<p><a href="https://labblog.uofmhealth.org/lab-report/research-group-identifies-potential-therapeutic-target-for-lupus" target="_blank">University of Michigan</a> :<span><span>Inhibiting IRE1α, a molecule activated by the endoplasmic reticulum in neutrophils, counters disease progression in lupus mice.</span></span><span><span><span><br />A recent study published in <em>JCI </em>found that </span><a href="https://doi.org/10.1172/JCI137866" target="_blank"><span>a
neutrophil’s endoplasmic reticulum, the organelle that normally makes
proteins in the cell, becomes stressed in the autoimmune disorder lupus.
This stress activates a molecule called IRE1α, which appears to play a
critical role in lupus pathogenesis</span></a><span><span><span> in mice</span></span></span><span>.<span></span></span></span></span></p><a name='more'></a><p></p><div><div class="paragraph paragraph--type--text paragraph--view-mode--default"><div class="clearfix text-formatted field field--name-field-text field--type-text-long field--label-hidden field__item">
<p><span><span><span>A multidisciplinary research group at the
University of Michigan, spanning microbiology, dermatology and
rheumatology, discovered that IRE1α orchestrates the release of
neutrophil extracellular traps, or NETs, from lupus neutrophils. NETs
are sticky, spider web-like structures that cause inflammation when
released at the wrong time or in the wrong place. </span></span></span></p>
<p><span><span><span>NETs play an important role in the pathogenesis of
lupus and other autoimmune diseases, where they trigger autoantibody
formation and contribute to blood vessel clotting and damage.</span></span></span></p>
<p><span><span><span>Thanks to the previous work of study authors </span><a href="https://medicine.umich.edu/dept/microbiology-immunology/basel-abuaita-phd" target="_blank"><span>Basel Abuaita, Ph.D.</span></a><span> and </span><a href="https://medicine.umich.edu/dept/microbiology-immunology/mary-oriordan-phd" target="_blank"><span>Mary X. O’Riordan, Ph.D.</span></a><span>,
microbiologists and immunologists at Michigan Medicine, the research
group knew that the IRE1α pathway was important for neutrophil
activation in models of another potentially deadly disease,
Staphylococcus aureus infection.</span></span></span></p>
<p><span><span><span>“Given that neutrophils are over-activated in
lupus, we hypothesized that the IRE1α pathway might be part of the story
in this disease, too,” says Gautam Sule, Ph.D., a postdoctoral fellow
in rheumatology at Michigan Medicine. “It’s what prompted this
collaboration, and the result was the discovery of an abnormally
activated IRE1α pathway in lupus patient neutrophils, which tracks
closely with disease severity.” </span></span></span></p>
<p><span><span><a href="https://labblog.uofmhealth.org/newsletter" target="_blank"><em><strong><span><span><span><span><span><span>MORE FROM THE LAB: Subscribe to our weekly newsletter</span></span></span></span></span></span></strong></em></a></span></span></p>
<p><span><span><span>However, this new study posed unique challenges, because according to </span></span></span><span><span><span>study author </span><a href="http://michmed.org/knight-lab" target="_blank"><span>Jason S. Knight, M.D., Ph.D.</span></a><span>, a rheumatologist at Michigan Medicine, neutrophils aren’t easy to study.</span></span></span></p></div>
</div>
</div>
<div>
<div class="quote-container">
<div class="quote-image"><a href="https://www.uofmhealth.org/profile/2925/jason-scott-knight-md" target="_blank">
<div class="field field--name-field-quote-image field--type-image field--label-hidden field__items">
<div class="field__item"> <img alt="Knight jason photo" height="104" src="https://labblog.uofmhealth.org/sites/lab/files/2021-03/Knight_jason_photo.jpg" width="73" />
</div>
</div>
</a></div>
<div class="quote">
<div class="field--name-field-quote">"This project wouldn’t have been possible if either one of our groups had tried to go at it alone."</div>
<a href="https://www.uofmhealth.org/profile/2925/jason-scott-knight-md" target="_blank">
<div class="field field--name-field-title field--type-string field--label-hidden field__item">Jason S. Knight, M.D., Ph.D.</div>
</a>
</div>
</div>
</div>
<div> <div class="paragraph paragraph--type--text paragraph--view-mode--default">
<div class="clearfix text-formatted field field--name-field-text field--type-text-long field--label-hidden field__item"><p><span><span><span>“Although
neutrophils are the most common white blood cells in circulation,
they’re hard to work with in the laboratory because they don’t live long
and there isn’t a good cell line system to replicate their functions,”
he says. </span></span></span></p>
<p><span><span><span>This meant the research team had to purify
neutrophils from human blood on a daily basis for their experiments but,
luckily, the work paid off. </span></span></span></p>
<p><span><span><span>While the team now understands more about
neutrophil biology in lupus, they say there’s still more digging to do
and the next steps will include an analysis of a larger group of
patients with lupus, and likely other related diseases such as
antiphospholipid syndrome. </span></span></span></p>
<p><span><span><span>“This was a great partnership of basic cell
biologists and translational scientists. This project wouldn’t have been
possible if either one of our groups had tried to go at it alone,” says
Knight. “We’re lucky to be at a place like U-M where these partnerships
are not only possible but actively encouraged.”</span></span></span></p>
<p><span><span><strong><span><span><span><span>Like Podcasts? Add the </span></span></span></span></strong><a href="https://www.amazon.com/Michigan-Medicine-News-Break/dp/B07CS5B9LY/?sa-no-redirect=1&pldnSite=1" target="_blank"><em><strong><span><span><span><span><span><span>Michigan Medicine News Break</span></span></span></span></span></span></strong></em></a><em><strong><span><span><span><span> on</span></span></span></span></strong></em><em><strong> </strong></em><a href="https://itunes.apple.com/us/podcast/michigan-medicine-news-break/id1390241260?mt=2" target="_blank"><em><strong><span><span><span><span><span><span>iTunes</span></span></span></span></span></span></strong></em></a><em><strong><span><span><span><span>, </span></span></span></span></strong></em><a href="https://podcasts.google.com/search/michigan%20medicine%20news%20break" target="_blank"><strong><em><span><span><span>Google Podcast</span></span></span></em></strong></a><em><strong><span><span><span><span> or anywhere you listen to podcasts.</span></span></span></span></strong></em></span></span></p>
<p><span><span><span><span><span>Additional study authors include Paul
A. Steffes, M.D., Andrew T. Fernandes, Shanea K. Estes, M.L.I., Craig J.
Dobry, Ph.D., Deepika Pandian, Johann E. Gudjonsson, M.D., Ph.D., and
J. Michelle Kahlenberg, M.D., Ph.D.</span></span></span></span></span></p>
<p><span><span><span>The work was supported by the Burroughs Wellcome
Fund, the National Center for Advancing Translational Sciences of the
National Institutes of Health, the Taubman Medical Research Institute
Innovation Program, the Lupus Research Alliance and the Postdoctoral
Translational Scholars Program Fellowship Award. Grant numbers include
NIH R21AI135403, NIH R01HL134846, 2UL1TR000433, NIH-P30AR075043, NIH
R01AR071384 and NIH R01AI130025.</span></span></span></p>
<p><span><span><strong><span>Paper cited: </span></strong><span>“Endoplasmic reticulum stress sensor IRE1α propels neutrophil hyperactivity in lupus,” <em>JCI</em>. </span><a href="https://doi.org/10.1172/JCI137866" target="_blank"><span>DOI: 10.1172/JCI137866</span></a><span>.</span></span></span></p></div>
</div>
</div>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-73879663571223697092021-03-21T01:21:00.001-07:002021-03-21T01:21:20.701-07:00Melanoma patients respond to immunotherapy after changes to gut microbiome<p><a href="https://today.oregonstate.edu/news/melanoma-patients-respond-immunotherapy-after-changes-gut-microbiome" target="_blank">Oregon State University</a> : Statistical modeling developed by Oregon State University researchers
has confirmed that changes to melanoma patients’ gut microbiome led
them to respond to a type of treatment capable of providing long-term
benefit.
</p><p>
<a href="https://science.sciencemag.org/content/371/6529/595">Findings</a> were published in Science.</p>
<p>
The modeling technique invented by Andrey Morgun of the OSU College of
Pharmacy and Natalia Shulzenko of Oregon State’s Carlson College of
Veterinary Medicine is known as transkingdom network analysis.<span></span></p><a name='more'></a><p></p>
<p>
The human gut microbiome is a community of more than 10 trillion
microbial cells from about 1,000 different bacterial species, and
transkingdom network analysis integrates multiple types of “omics” data –
metagenomic, metabolomic, lipidomic, proteomic, etc. – in determining
how interactions among specific types of gut microbes help or hinder
biological functions in the host. </p>
<p>
In this case, the <a href="https://www.eurekalert.org/pub_releases/2021-02/uop-ftt012921.php">microbial interactions</a>
involved how well the body responds to a type of cancer treatment known
as anti-programmed cell death protein therapy, abbreviated to anti-PD-1
therapy. It allows immune cells to react more strongly to cancer.</p>
<p>
“It was pretty dramatic,” said Morgan, associate professor of
pharmaceutical sciences. “We found altering the gut microbiome can take a
patient with advanced melanoma who has never responded to
immunotherapy, which fails about 60% of the time with this kind of
cancer, and convert the patient into one who responds to it.”</p>
<p>
Morgun and former OSU postdoctoral researcher Richard Rodrigues, now at
the National Cancer Institute, were part of a collaboration led by
immunologists Giorgio Trinchieri and Amiran Dzutsev from NCI and medical
oncologists Hassane Zarour and Diwakar Davar of the University of
Pittsburgh that tested fecal microbiota transplants’ ability to help
melanoma patients benefit from anti-PD-1 immunotherapy.</p>
<p>
The scientists collected fecal samples from patients who responded
particularly well to the therapy and in a clinical trial gave the
samples, via colonoscopy, to advanced melanoma patients who had never
before responded to immunotherapy.</p>
<p>
The patients then received the anti-PD-1 drug pembrolizumab, and this
time it had the desired effect, turning non-responders into responders.
Transkingdom network analyses confirmed the microbiome’s role.</p>
<p>
“Putting everything together, we showed that the fecal microbiota
transplants and anti-PD-1 drug can change the gut microbiome and
effectively reprogram a tumor’s microenvironment so anti-PD-1 resistance
is overcome,” Morgun said.</p>
<p>
Of 15 patients with advanced melanoma – an aggressive form of skin
cancer – who received the combined treatment, six of them showed either
tumor reduction or disease stabilization that lasted for more than a
year.</p>
<p>
“The promising findings clearly warrant more investigation in bigger
clinical trials,” Morgun said. “That way we can better identify
microbial, bloodstream and intratumor biomarkers to select melanoma
patients most likely to benefit from microbiome-based therapy. We really
expect that eventually we’ll identify a collection of bacteria with a
high success percentage for converting immunotherapy non-responders into
responders.”</p>
<p>
Merck and the National Institute of Health supported this research.</p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-52473172292573459162021-03-21T01:18:00.001-07:002021-03-21T01:18:06.175-07:00Cells burn more calories after just one bout of moderate aerobic exercise, OSU study finds <p><a href="https://today.oregonstate.edu/news/cells-burn-more-calories-after-just-one-bout-moderate-aerobic-exercise-osu-study-finds" target="_blank">Oregon State University</a> : In a recent study testing the effects of exercise on overall
metabolism, researchers at Oregon State University found that even a
single session of moderate aerobic exercise makes a difference in the
cells of otherwise sedentary people.
</p><p>
Mitochondria are the part of the cell responsible for the biological
process of respiration, which turns fuels such as sugars and fats into
energy, so the researchers focused only on mitochondria function.<span></span></p><a name='more'></a><p></p>
<p>
“What we found is that, regardless of what fuel the mitochondria were
using, there were mild increases in the ability to burn off the fuels,”
said Matt Robinson, lead author on the <a href="https://journals.lww.com/acsm-msse/Abstract/9000/Substrate_specific_Respiration_of_Isolated.96110.aspx">study</a> and an assistant professor in the <a href="https://health.oregonstate.edu/">College of Public Health and Human Sciences</a>.</p>
<p>
OSU researchers recruited participants who do not follow a regular
exercise routine and had them ride a stationary bike for an hour at a
moderate intensity. They biopsied their muscles 15 minutes later to test
how efficient the mitochondria were after the exercise was completed
and compared those results with a resting day.</p>
<p>
Post-exercise, study participants’ mitochondria burned 12-13% more
fat-based fuel and 14-17% more sugar-based fuel. While the effects were
not drastic, they were consistent, Robinson said.</p>
<p>
“It’s pretty remarkable that even after just one hour of exercise,
these people were able to burn off a little more fuel,” he said.</p>
<p>
Previous research in the field has long established that regular
exercise creates lasting change in people’s metabolism, making their
bodies burn more energy even when they’re not working out.</p>
<p>
Prior studies have looked at highly trained or athletic people, but
Robinson’s team wanted to look specifically at singular bouts of
exercise in people who were generally active and disease-free but who
did not have structured exercise regimes. These people were on the lower
end of fitness, which is associated with low mitochondrial abundance
and energy production. Participants were monitored while working out at
approximately 65% of their maximal effort, where they could keep up the
cycling pace for an hour or more and still comfortably carry on a
conversation.</p>
<p>
Robinson said they’re hoping these results help break down the mental
barrier of people thinking they need to be elite athletes for exercise
to make an impact on their health.</p>
<p>
“From a big picture health perspective, it’s very encouraging for
people to realize that you can get health benefits from a single session
of exercise,” Robinson said. “We’re trying to encourage people, ‘You
did one, why don’t you try to do two? Let’s do three.’</p>
<p>
“We know that exercise is good for you, in general. But those benefits
of that single bout of exercise seem to fade away after a day or two.
You get the long-term benefits when you do that exercise again and again
and you make it a regular habit.”</p>
<p>
In this study, Robinson’s research team focused narrowly on
mitochondria to find out how big a role mitochondria play in the overall
function of muscle metabolism. Other studies are looking at changes in
blood flow to the muscle and how the muscle metabolizes fats versus
sugars.</p>
<p>
From a disease perspective, Robinson said it’s clear that obesity and
diabetes involve impairments in metabolism. Physiologically, when the
body undergoes exercise, sugars tend to be burned off first while fats
are stored, but in cases of diabetes and obesity, there is some
dysregulation in metabolism that causes the body to not be able to
switch between the two types of fuel.</p>
<p>
Exercise can help reset that system, he said.</p>
<p>
“Since those get burned off in the mitochondria, our hope is that with
exercise, we could increase the mitochondria and then improve how the
body burns off fats and sugars,” he said.</p>
<p>
Other recent and ongoing studies at OSU are investigating whether high
intensity interval training (HIIT) sessions might alter a specific
pathway by which fats are burned off in the mitochondria, and how
certain proteins in the muscle shuttle fat around to either be stored or
burned.</p>
<p>
The study was completed in collaboration with <a href="https://www.samhealth.org/find-a-location/s/samaritan-athletic-medicine-center">Samaritan Athletic Medical Center</a> through Samaritan Health Services, with several physicians working on campus with OSU researchers in the <a href="https://health.oregonstate.edu/labs/tmrl">Translational Metabolism Research Laboratory</a>. Co-authors were Sean Newsom, Harrison Stierwalt and Sarah Ehrlicher.</p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-82005899517118384822021-03-20T00:00:00.001-07:002021-03-20T00:00:11.869-07:00Deep Learning Outperforms Standard Machine Learning in Biomedical Research Applications, Research Shows<p></p><div class="separator" style="clear: both; text-align: center;"><a href="https://news.gsu.edu/files/2021/01/Deep-learning-neural-network.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" data-original-height="422" data-original-width="800" height="105" src="https://news.gsu.edu/files/2021/01/Deep-learning-neural-network.jpg" width="200" /></a></div><a href="https://news.gsu.edu/2021/01/13/deep-learning-outperforms-standard-machine-learning-in-biomedical-research-applications-research-shows/" target="_blank">Geordia State University</a> : Compared to standard machine learning models, deep learning models
are largely superior at discerning patterns and discriminative features
in brain imaging, despite being more complex in their architecture,
according to a <a href="https://www.nature.com/articles/s41467-020-20655-6">new study</a> in <em>Nature Communications</em> led by Georgia State University.
<p></p><p>Advanced biomedical technologies such as structural and functional
magnetic resonance imaging (MRI and fMRI) or genomic sequencing have
produced an enormous volume of data about the human body. By extracting
patterns from this information, scientists can glean new insights into
health and disease. This is a challenging task, however, given the
complexity of the data and the fact that the relationships among types
of data are poorly understood.<br /><span></span></p><a name='more'></a><p></p>
<p>Deep learning, built on advanced neural networks, can characterize
these relationships by combining and analyzing data from many sources.
At the <a href="https://trendscenter.org/">Center for Translational Research in Neuroimaging and Data Science (TReNDS)</a>, Georgia State researchers are using deep learning to learn more about how mental illness and other disorders affect the brain.</p>
<p>Although deep learning models have been used to solve problems and
answer questions in a number of different fields, some experts remain
skeptical. Recent critical commentaries have unfavorably compared deep
learning with standard machine learning approaches for analyzing brain
imaging data.</p>
<p>However, as demonstrated in the study, these conclusions are often
based on pre-processed input that deprive deep learning of its main
advantage—the ability to learn from the data with little to no
preprocessing. <a href="https://trendscenter.org/anees-abrol/" rel="noopener" target="_blank">Anees Abrol</a>,
research scientist at TReNDS and the lead author on the paper, compared
representative models from classical machine learning and deep
learning, and found that if trained properly, the deep-learning methods
have the potential to offer substantially better results, generating
superior representations for characterizing the human brain.</p>
<p>“We compared these models side-by-side, observing statistical
protocols so everything is apples to apples. And we show that deep
learning models perform better, as expected,” said co-author <a href="https://www.cs.gsu.edu/profile/sergey-plis/">Sergey Plis</a>, director of machine learning at TReNDS and associate professor of computer science.</p>
<p>Plis said there are some cases where standard machine learning can
outperform deep learning. For example, diagnostic algorithms that plug
in single-number measurements such as a patient’s body temperature or
whether the patient smokes cigarettes would work better using classical
machine learning approaches.</p>
<p>“If your application involves analyzing images or if it involves a
large array of data that can’t really be distilled into a simple
measurement without losing information, deep learning can help,” Plis
said.. “These models are made for really complex problems that require
bringing in a lot of experience and intuition.”</p>
<p>The downside of deep learning models is they are “data hungry” at the
outset and must be trained on lots of information. But once these
models are trained, said co-author <a href="https://cas.gsu.edu/profile/vince-calhoun/">Vince Calhoun</a>,
director of TReNDS and Distinguished University Professor of
Psychology, they are just as effective at analyzing reams of complex
data as they are at answering simple questions.</p>
<p>“Interestingly, in our study we looked at sample sizes from 100 to
10,000 and in all cases the deep learning approaches were doing better,”
he said.</p>
<p>Another advantage is that scientists can reverse analyze
deep-learning models to understand how they are reaching conclusions
about the data. As the published study shows, the trained deep learning
models learn to identify meaningful brain biomarkers.</p>
<p>“These models are learning on their own, so we can uncover the
defining characteristics that they’re looking into that allows them to
be accurate,” Abrol said. “We can check the data points a model is
analyzing and then compare it to the literature to see what the model
has found outside of where we told it to look.”</p>
<p>The researchers envision that deep learning models are capable of
extracting explanations and representations not already known to the
field and act as an aid in growing our knowledge of how the human brain
functions. They conclude that although more research is needed to find
and address weaknesses of deep-learning models, from a mathematical
point of view, it’s clear these models outperform standard machine
learning models in many settings.</p>
<p>“Deep learning’s promise perhaps still outweighs its current
usefulness to neuroimaging, but we are seeing a lot of real potential
for these techniques,” Plis said.</p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-46957466900017366152021-03-19T23:56:00.005-07:002021-03-19T23:57:49.785-07:00Stereotypes Can Harm Performance Of Older Adults On Cognitive And Physical Tasks<p><a href="https://news.gsu.edu/2021/02/18/stereotypes-can-harm-performance-of-older-adults-on-cognitive-and-physical-tasks/" target="_blank">Georgia State University</a>: When older adults are viewed as cognitively or physically impaired,
they perform below their abilities on tasks, according to a recent
review article by <a href="https://psychology.gsu.edu/profile/sarah-barber/">Sarah Barber</a>, a psychology and gerontology researcher at Georgia State University. Groups who are stigmatized—whether due to race, socioeconomic status
or age—perform more poorly when they are faced with negative
stereotypes, Barber said. She found expectations of others can play a
powerful role in how well older adults perform on cognitive tasks and
motor skills such as driving.<span></span></p><a name='more'></a><p></p>
<p>The phenomenon is known as “stereotype threat,” according to Barber. Her review article, published in the <a href="https://www.sciencedirect.com/science/article/abs/pii/S2211368120300358?via%3Dihub">Journal of Applied Research in Memory and Cognition</a>, looks at recent studies as well as those dating back to the mid 1990s, all of which show the power of this phenomenon.</p>
<p>“The concept was originally formulated to look at stereotypes around
race,” Barber said, but the effect turned out to be much broader. She
said it can affect older adults by affecting their memory, physical
performance, driving abilities and even job satisfaction.</p>
<p>Older adults frequently encounter the challenge of stereotype threat
at their physician’s office, where they routinely go for checkups,
Barber said, and where they may sometimes be given cognitive tests as
well. Research shows about 17 percent of individuals aged 50 and older
experience stereotype threat at the doctor’s office, and about 8 percent
worry their physician is negatively evaluating them because of their
age. This can lead older people to underperform on the cognitive tests
they are given and can lead to greater distrust of physicians, greater
dissatisfaction with healthcare services, poorer self-reported mental
and physical health, and even higher rates of hypertension.</p>
<p>Just as important in stereotypes about age, Barber said, is negative self-evaluation, which she reviewed <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5731480/">in a 2017 paper</a>.</p>
<p>“People worry that there is truth to the negatives,” she said. “When
they forget, they may worry they are on a slippery slope towards
dementia and decline.”</p>
<p>That can be detrimental and actually lead to more forgetting. When
conducting her own research on this topic, Barber said “I was struck by
the negative things older adults would say about themselves, and I’d
wonder how much better they might be performing if they weren’t so
worried.”</p>
<p>These stereotype threat effects can also affect physical performance.</p>
<p>“Older adults are often stereotyped as being slow, weak, feeble and frail,” Barber said.</p>
<p>In lab studies, she said, stereotype threat can also lead to slower walking and weaker grip strength for older adults.</p>
<p>“We need to make people feel confident in their own abilities,” she
said, “and feel that they will be respected no matter how they perform.”</p>
<p>Barber said older adults would also benefit from looking at their own attitudes about aging.</p>
<p>“Your own attitude about aging is highly predictive of your aging
outcomes,” she said. “Those who have positive attitudes about aging live
longer, have better memory function and recover more easily from
illnesses.”</p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-619120491174013732021-03-19T23:51:00.000-07:002021-03-19T23:51:03.794-07:00Strategies to accelerate diagnosis and treatment of rare cardiovascular diseases<p></p><div class="separator" style="clear: both; text-align: center;"><a href="https://ysm-res.cloudinary.com/image/upload/w_1026/h_576,c_scale,e_unsharp_mask:70/c_scale,e_blur:1700,u_v1:yms:prod:1fe56dec-90ef-49ad-ab76-fd378353e9ec,w_1026,h_576/v1/yms/prod/1fe56dec-90ef-49ad-ab76-fd378353e9ec" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" data-original-height="449" data-original-width="800" height="112" src="https://ysm-res.cloudinary.com/image/upload/w_1026/h_576,c_scale,e_unsharp_mask:70/c_scale,e_blur:1700,u_v1:yms:prod:1fe56dec-90ef-49ad-ab76-fd378353e9ec,w_1026,h_576/v1/yms/prod/1fe56dec-90ef-49ad-ab76-fd378353e9ec" width="200" /></a></div><a href="https://medicine.yale.edu/intmed/cardio/news-article/30663/" target="_blank">Yale</a> :The
current landscape for patients with rare cardiovascular disease has
shifted. Using genome sequencing Yale physician-scientists have begun to
elucidate the pathophysiology of genetic disorders and develop
treatment guidelines and recommendations. With these advanced diagnostic
tools, our team of international experts can offer clinical diagnosis,
genetic testing, and risk assessment for patients.<span><a name='more'></a></span><p></p><h2>Underlying cause of rare diseases</h2><p>In
2017, the Yale Cardiovascular Genetics Program was one of the first
clinical centers to use whole exome sequence analysis to detect novel
disease genes. After conducting whole exome sequencing with a group of
200 patients, the research team identified specific mutations that
resulted in a more accurate diagnosis of inherited cardiovascular
disease. The results were published in <span class="MsoHyperlink"><em><a href="https://www.ahajournals.org/doi/10.1161/CIRCGENETICS.116.001573?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed">Circulation: Genomic and Precision Medicine</a></em></span>.
According to the authors, “The use of whole exome sequencing has the
potential to revolutionize the way we practice medicine by generating
large-scale personalized genetic information.”</p><p><a href="https://medicine.yale.edu/profile/arya_mani/">Arya Mani, MD</a>,
director of the cardiovascular genetics program, and his colleagues
have identified several genetic mutations linked to rare disorders; more
recently CELA2A, a gene responsible for regulating calcium-dependent
insulin secretion and sensitivity, has been identified as a promising
target for novel therapies. In <span class="MsoHyperlink"><em><a href="https://www.nature.com/articles/s41588-019-0470-3">Nature Genetics</a></em>,</span> the authors concluded that CELA2A could have a “physiologic role in cellular glucose metabolism.”
</p><hr /><h2>Hypertrophic Cardiomyopathy </h2><p><a href="https://www.yalemedicine.org/conditions/cardiomyopathies">Hypertrophic cardiomyopathy</a>
(HCM) affects an estimated one in 500 adults. Yale’s well-established
program offers comprehensive diagnostic, treatment, education, and
research for hypertrophic, dilated, arrhythmogenic, and restrictive
cardiomyopathies. Yale is the only program in the state of Connecticut
to be listed as a Center of Excellence by <a href="https://www.4hcm.org/">the Hypertrophic Cardiomyopathy Association</a>. With the addition of <a href="about:blank">John Stendahl, MD, PhD</a>, a graduate of Yale’s advanced fellowship training, the program is expanding to support patients with hereditary disorders.</p><p>With
FDA approval pending, mavacamten is poised to become the first
disease-specific therapy for obstructive hypertrophic cardiomyopathy. As
<a href="about:blank">Daniel Jacoby, MD</a>, director of comprehensive heart failure and cardiomyopathy program, reported on September 12 in <span class="MsoHyperlink"><em><a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31792-X/fulltext">The Lancet</a></em></span>,
the EXPLORER-HCM trial indicated an improvement in exercise capacity
and a reduction in left ventricular outflow tract obstruction. Further
analysis may also reveal a reduction in left ventricular mass and
hypertrophy.
</p><p>The American College of Cardiology released <a href="https://www.ahajournals.org/doi/10.1161/CIR.0000000000000937">updated guidelines</a>
in 2020 which emphasized personalized approaches regarding decisions
around implantable cardioverter-defibrillator placement and exercise
guidelines. Two additional clinical trials —<a href="https://clinicaltrials.gov/ct2/show/NCT03723655">MAVA-LTE</a> and <a href="https://clinicaltrials.gov/ct2/show/NCT04349072">VALOR-HCM</a> — are now ongoing to determine the long-term safety and efficacy of this novel treatment.
</p><hr /><h2>Cardiac Amyloidosis</h2><p>Yale serves as the premier institution across southern New England for the evaluation and treatment of <a href="https://www.yalemedicine.org/search?q=Cardiac+Amyloidosis">cardiac amyloidosis</a>,
which is caused when deposits of an abnormal protein called amyloid
affect heart function. Cardiac amyloidosis disproportionately affects
Caribbean and African-American communities and is a leading cause of
heart failure. </p><p>Advances in cardiac imaging and the <a href="https://medicine.yale.edu/news-article/21622/">development of targeted therapies</a><span class="MsoHyperlink"> including patisiran, inotersen, and tafamidis</span>
for transthyretin amyloidosis (ATTR) has led to progress for patients
with cardiomyopathy and inherited cardiovascular disease. <a href="https://medicine.yale.edu/profile/edward_miller/?tab=bio">Edward Miller, MD PhD</a>, director of the clinical nuclear cardiology laboratory, co-authored a <a href="https://link.springer.com/article/10.1007/s11886-020-01284-3">review</a> last year with <a href="https://medicine.yale.edu/profile/cesia_gallegoskattan/">Cesia Gallegos Kattan, MD</a>, which examined the benefits of positron emission tomography (PET) radiotracers to detect cardiac amyloidosis. </p><p>“There
is unmet and critical need to develop tracers to distinguish between
amyloid types and quantify response to treatment,” the authors wrote. To
help address this, Jacoby, Miller, and Gallegos Kattan have partnered
with <a href="https://medicine.yale.edu/genetics/profile/oyere_onuma/">Oyere Onuma, MD, MSc</a>, cardiovascular disease prevention specialist, <a href="https://medicine.yale.edu/profile/matthew_burg/">Matthew Burg, PhD</a>, a clinical psychologist, and <a href="https://medicine.yale.edu/profile/kristie_harris/">Kristie Harris, PhD</a>, a postdoctoral associate in cardiovascular medicine, as well as <a href="https://medicine.yale.edu/profile/curt_scharfe/">Curt Scharfe MD, PhD, FACMG</a>, and <a href="https://medicine.yale.edu/profile/michael_murray/">Michael F. Murray MD, FACMG, FACP</a>, from the Department of Genetics. </p><p>Ongoing clinical research at Yale can also contribute to future discoveries. The V142I <span class="MsoHyperlink">mutation in the ATTR</span>
gene is thought to be associated with an increased risk of cardiac
amyloidosis. The Yale Cardiovascular Amyloid group has an ongoing
partnership with Ernest C. Madu, MD, FACC, from the Heart Institute of
the Caribbean in Kingston, Jamaica, to develop methods to screen
high-risk patients for amyloidosis as well as a novel community
partnership being developed with the <a href="https://medicine.yale.edu/ycci/clinicaltrials/trial/9344/">Yale Center for Clinical Investigation</a> and the New Haven community to better understand the impact of V142I ATTR locally.</p><p>Two additional studies <a href="https://medicine.yale.edu/ycci/clinicaltrials/trial/270/">THAOS</a>,
a global, multi-center, longitudinal observational survey open to all
patients with transthyretin-associated amyloidoses (ATTR), and <a href="https://medicine.yale.edu/ycci/clinicaltrials/find/6631.trial">ATTRIBUTE-CM</a>,
a phase 3 randomized clinical trial of AG10 in patients with
symptomatic transthyretin amyloid cardiomyopathy, will help develop the
next generation of therapeutics.</p><p>To learn more about clinical research within the Section of Cardiovascular Medicine, visit <a href="https://medicine.yale.edu/intmed/cardio/">Cardiovascular Medicine</a>.
</p><div class="news-content__item"><div class="news-submitter"><span>Submitted by Elisabeth Reitman on February 26, 2021</span></div></div>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-10682072657511625192021-03-19T23:44:00.003-07:002021-03-19T23:45:15.946-07:00Double duty: Gut’s immune system helps regulate food processing, too<p> </p><div class="feature-media"><figure class="caption-wrapper full-width" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="Illustration, man looking at digestive system with magnifying glass." height="116" src="https://news.yale.edu/sites/default/files/styles/featured_media/public/ynews-381842949.jpg?itok=FKN-6Urh&c=a75e254fe1da31f2732f6b0d7bce1413" width="200" /><figcaption class="caption">(© stock.adobe.com)</figcaption></figure></div>
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<p><a href="https://news.yale.edu/2021/03/18/double-duty-guts-immune-system-helps-regulate-food-processing-too" target="_blank">Yale</a> : The small intestine is ground zero for survival of animals. It is
responsible for absorbing the nutrients crucial to life and it wards off
toxic chemicals and life-threatening bacteria.In a new study published March 18 in the journal Science, Yale
researchers report the critical role played by the gut’s immune system
in these key processes. The immune system, they found, not only defends
against pathogens but regulates which nutrients are taken in.
<span></span></p><a name='more'></a><p></p><p>The findings may provide insights into origins of metabolic disease
and malnutrition that is common in some undeveloped regions of the
world.</p>
<p><span class="dquo">“</span>We were surprised that the immune system
was so involved in nutrition,” said first author Zuri Sullivan, a former
graduate student in the immunology department at Yale and now a Howard
Hughes Medical Institute Hanna H. Gray postdoctoral fellow at Harvard.
“And the study lays the groundwork for understanding how this reciprocal
interaction works.”</p>
<p>Working in the lab of senior author Ruslan Medzhitov, Yale’s Sterling
Professor of Immunobiology and an investigator at the Howard Hughes
Medical Institute, Sullivan became interested in how the diets of humans
and other animals can dramatically change the organization of their
digestive tracts. For instance, the digestive systems of carnivores and
herbivores are organized differently to accommodate their specialized
diets. Omnivores have the most complex system, which must adapt to a
diverse diet of proteins, fats, and carbohydrates depending upon what’s
available in the environment.</p>
<p>Sullivan, Medzhitov, and a group of colleagues decided to study how
the large numbers of immune cells present inside intestinal tracts might
influence nutrition. For instance, a specific immune system signaling
molecule, known as interleukin-22 (IL-22), plays a key role in
combatting bacterial pathogens such as those that cause food poisoning.
The presence of IL-22 also seems to prevent the uptake of certain
nutrients in the digestive system when pathogens are present.</p>
<p>In a series of experiments, the researchers discovered that a
specific group of immune system cells — gamma delta T cells — can
suppress expression of interleukin-22 in mice and allow the cells on the
intestinal wall to activate digestive enzymes and nutrient
transporters.</p>
<p>In addition to providing insights into malnutrition in some parts of
the world — where bacterial infections lead to chronic expression of
IL-22 and suppress the uptake of nutrients. The findings might also
eventually help researchers develop ways to combat high rates of
metabolic diseases, such as Type 2 diabetes and obesity in the developed
world, Sullivan said.</p>
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</div><div class="media-contact"><p class="eyebrow">Media Contact</p><p class="contact">Bess Connolly: <a href="mailto:elizabeth.connolly@yale.edu">elizabeth.connolly@yale.edu</a>, 203-432-1324</p></div></div></div> </div>
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Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-63084075278016681882021-03-19T23:40:00.007-07:002021-03-19T23:40:46.699-07:00Babies pay attention with down payment from immature brain region<p></p><div class="separator" style="clear: both; text-align: center;"><a href="https://news.yale.edu/sites/default/files/styles/featured_media/public/ynews-67614689.jpg?itok=K6weh53d&c=a75e254fe1da31f2732f6b0d7bce1413" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" data-original-height="465" data-original-width="800" height="116" src="https://news.yale.edu/sites/default/files/styles/featured_media/public/ynews-67614689.jpg?itok=K6weh53d&c=a75e254fe1da31f2732f6b0d7bce1413" width="200" /></a></div><a href="https://news.yale.edu/2021/03/16/babies-pay-attention-down-payment-immature-brain-region" target="_blank">Yale</a> :Anyone who has watched an infant’s eyes follow a dangling trinket
dancing in front of them knows that babies are capable of paying
attention with laser focus.
<p></p><div class="story clearfix"><p>But with large areas of their young brains still underdeveloped, how do they manage to do so?<span></span></p><a name='more'></a><p></p>
<p>Using an approach pioneered at Yale that employs fMRI (or functional
magnetic resonance imaging) to scan the brains of awake babies, a team
of university psychologists shows that, when focusing their attention,
infants under a year of age recruit areas of their frontal cortex, a
section of the brain involved in more advanced functions that was
previously thought to be immature in babies. The findings were
published <a class="extlink" href="https://www.pnas.org/content/118/12/e2021474118" target="_blank">March 16 in the Proceedings of the National Academy of Sciences</a>.</p>
<p><span class="dquo">“</span>Attention is the gateway to what infants perceive and learn,” said <a class="extlink" href="https://medicine.yale.edu/profile/nicholas_turk-browne/" target="_blank">Nick Turk-Browne</a>,
professor of psychology at Yale and senior author of the paper.
“Attention is the bouncer at the door, determining what information gets
into the brain, which eventually creates memories, language, and
thought.”</p>
<p>Most previous research related to attention in babies has depended
upon tracking their gaze while they are presented with visual stimuli, a
process that theoretically offers insights into what is going on in
their minds. Left unanswered are questions about which sections of the
brain are involved in these responses, and how and why they allocate
attention in the ways they do. </p>
<p>Attention in babies could depend upon on sensory areas of the brain,
which process stimuli such as touch and visual stimuli and helps them
react to the external world. These brain regions develop earlier in
infancy than regions of the frontal cortex, which are usually associated
with internal functions such as control, planning, and reasoning.</p>
<p>The ability to use brain imaging with infants allowed “us to look
behind the mirror,” for the neural origins of attention, Turk-Browne
said.</p>
<p>For the study, they used the new fMRI technology to track the neural
activity of 20 babies aged from 3 to 12 months, tracking which regions
of their brains became activated as they focused their attention in
response to a series of images.</p>
<p>In a series of tests, the babies were shown a screen on which a
target would appear on either the left or right side. In each case,
these appearances were preceded by one of three visual cues signaling
where the target would appear: on the same side that the target would
appear, on both sides of the screen (thus uninformative), or on the
opposite side. Researchers monitored the babies’ eye movements as they
completed these tasks. <a class="extlink" href="https://www.youtube.com/watch?v=iQjCuZwkuLA" target="_blank">See a video of the experiment</a>. </p>
<p>As expected, the babies were much quicker to move their eyes to the
target when first presented the correct cue, confirming that the cues
had focused their attention. Simultaneously, the researchers used brain
imaging technology to see which areas of the brain were recruited during
these tasks. In addition to sensory areas of the brain, they found that
activity also increased in two areas of the frontal cortex, the
anterior cingulate cortex, and the middle frontal gyrus, areas of the
brain that when fully developed are involved in controlling adult
attention.</p>
<p><span class="dquo">“</span>This doesn’t mean these regions play the
same role in babies as in adults, but it does show that infants use them
to explore their visual world,” said Cameron Ellis, a Ph.D. candidate
in psychology at Yale and first author of the paper.</p>
<p>Studying how the brain is enlisted during development “will help
researchers uncover the foundations of human learning, which could one
day help improve early-childhood education and reveal the roots of
neurodevelopmental disorders,” Ellis said.</p>
<p>Other authors on the study are Yale graduate students Lena Skalaban and Tristan Yates.</p>
</div>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-5612124658484696482021-03-17T12:22:00.001-07:002021-03-17T12:22:16.405-07:00Increasing Pollen Rates Affect COVID Infection Rates<p><a href="https://www.publichealth.columbia.edu/public-health-now/news/increasing-pollen-rates-affect-covid-infection-rates" target="_blank">Columbia</a> :A new study found that pollen-which is also being affected by climate
change---can help explain additional COVID infection rates during the
Spring when tree allergies become dominant. How much of an impact?
Based on these data, an increase of pollen abundance by 100 grains per
cubic meter of air resulted in an average increase in infection rates of
4 percent. The results are published in <em>PNAS</em> titled "<a href="https://www.pnas.org/content/118/12/e2019034118" target="_blank">Higher Airborne Pollen Concentrations Correlated with Increased SARS-CoV-2 Infection Rates.</a>"<span></span></p><a name='more'></a><br />
“We tested for relationships between SARS-CoV-2 infection rates and
pollen concentrations, along with humidity, temperature, population
density,” said <a href="https://www.publichealth.columbia.edu/people/our-faculty/lhz2103">Lewis Ziska</a>, PhD, professor of <a href="https://www.publichealth.columbia.edu/academics/departments/environmental-health-sciences-ehs">Environmental Health Sciences </a>at <a href="https://www.publichealth.columbia.edu/">Columbia Mailman School of Public Health </a>and
a co-author. “We found that spring pollen, sometimes in synergy with
humidity and temperature, explained, on average, 44 percent of the
infection rate variability. Without lockdown, an increase of pollen
abundance resulted in a 4 percent average increase of infection rates. A
strict lockdown cut the increase by half.”<br />
<br />
In the spring of 2020, the outbreak of the coronavirus pandemic
appeared to coincide with the tree pollen season in the northern
hemisphere. These observations prompted an international team of headed
by researchers at the Technical University of Munich (TUM) and the to
conduct an extensive investigation. The team collected data on airborne
pollen concentrations, weather conditions and SARS-CoV-2 infections –
taking into consideration the variation of infection rates from one day
to another and the total number of positive tests. In their
calculations, the team also included data on population density and the
effects of lockdown measures. The researchers analyzed pollen data from
130 stations in 31 countries on five continents.<br />
<br />
The team showed that in some German cities, concentrations of up to 500
pollen grains per cubic meter per day were recorded during the study –
which led to an overall increase in infection rates of more than 20
percent. In regions where lockdown rules were in effect, however, the
infection numbers were on average only half as high at comparable pollen
concentrations.<br />
<br />
High pollen concentrations lead to a weaker immune response in airways
to viruses that can cause coughs and colds. When a virus enters the
body, infected cells usually send out messenger proteins. This is also
the case with SARS-CoV-2. These proteins, known as antiviral
interferons, signal nearby cells to escalate their antiviral defenses to
keep the invaders at bay. Additionally, an appropriate inflammation
response is activated to fight the viruses.<br />
<br />
But as the researchers explained, if airborne pollen concentrations are
high, and pollen grains are inhaled with the virus particles, fewer
antiviral interferons are generated. The beneficial inflammatory
response itself is also affected. Therefore, on days with a high
concentration of pollen, it can lead to an increase in the number of
respiratory illnesses. This also holds true for COVID-19. Whether
individuals are allergic to the different pollen types is irrelevant.<br />
<br />
The author caution that people in high-risk groups should, therefore,
be informed that high levels of airborne pollen concentrations lead to
an increased susceptibility to viral respiratory tract infections. They
can protect themselves by watching pollen forecasts and by wearing dust
filter masks. They further emphasize that when studying the spread of
SARS-CoV-2, environmental factors such as pollen must be taken into
account. Increased awareness of these effects are an important step in
preventing and mitigating the impact of COVID-19.
<p></p><span><!--more--></span><span><!--more--></span><p>
Co-authors are Athanasios Damialis, <span style="font-size: 18px;">Stefanie Gilles, Franziska Kolek, Daniela Bayr, Maria Plaza, Sigrid Kaschuba, Vivien Leier-Wirtz, and Claudia Traidl-Hoffmann, </span>Technical University of Munich; Mikhail Sofiev, <span style="font-size: 18px;">Viktoria Sofieva, </span>Finnish Meteorological Institute, Helsinki; Leonard Bielory,
Rutgers University; László Makra, University of Szeged, Hungary; and <span style="font-size: 18px;">Maria del Mar Trigo, </span>University of Malaga, Spain. <br /></p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-29087707433995610202021-03-17T12:20:00.001-07:002021-03-17T12:20:06.587-07:00Led Study Shows Fear and Anxiety Share Same Bases in Brain<p><a href="https://www.umdrightnow.umd.edu/news/umd-led-study-shows-fear-and-anxiety-share-same-bases-brain" target="_blank">University of Maryland</a> :Anxiety, the most common family of mental illnesses in the
U.S., has been pushed to epic new heights by the COVID-19 pandemic, with
the Centers for Disease Control and Prevention estimating that nearly 1
in 3 U.S. adults and a staggering 41% of people ages 18-29 experienced
clinically significant anxiety symptoms in late August. Now, the
findings of a recent<a href="https://www.jneurosci.org/lookup/doi/10.1523/JNEUROSCI.0704-20.2020" target="_blank"> UMD-led study</a> indicate that some long-accepted thinking about the basic neuroscience of anxiety is wrong.<span></span></p><a name='more'></a>
<p></p><p>The report by an international team of researchers led by Alexander
Shackman, an associate professor of psychology at UMD, and Juyoen Hur,
an assistant professor of psychology at Yonsei University in Seoul,
South Korea, provides new evidence that fear and anxiety reflect
overlapping brain circuits. The findings run counter to popular
scientific accounts, highlighting the need for a major theoretical
reckoning. The study was published last week in the Journal of
Neuroscience.</p>
<p>“The conceptual distinction between ‘fear’ and ‘anxiety’ dates back
to the time of Freud, if not the Greek philosophers of antiquity,” said
Shackman, a core faculty member of UMD’s Neuroscience and Cognitive
Science Program, and 2018 recipient of a seed grant award from UMD’s <a href="http://www.bbi.umd.edu/news/news_story.php?id=13273">Brain and Behavior Initiative</a>,
“In recent years, brain imagers and clinicians have extended this
distinction, arguing that fear and anxiety are orchestrated by distinct
neural networks. </p>
<p>However, Shackman says their new study adds to a rapidly growing
body of new evidence suggesting that this old mode is wrong. “If
anything, fear and anxiety seem to be constructed in the brain using a
massively overlapping set of neural building blocks,” he said. </p>
<p>Prevailing scientific theory holds that fear and anxiety are
distinct, with different triggers and strictly segregated brain
circuits. Fear—a fleeting reaction to certain danger—is thought to be
controlled by the amygdala, a small almond-shaped region buried beneath
the wrinkled convolutions of the cerebral cortex. By contrast, anxiety—a
persistent state of heightened apprehension and arousal elicited when
threat is uncertain—is thought to be orchestrated by the neighboring bed
nucleus of the stria terminalis (BNST). But new evidence from Shackman
and his colleagues suggests that both of these brain regions are equally
sensitive to certain and uncertain kinds of threats.</p>
<p>Leveraging cutting-edge neuroimaging techniques available at the
Maryland Neuroimaging Center, their research team used fMRI to quantify
neural activity while participants anticipated receiving a painful shock
paired with an unpleasant image and sound—a new task that the
researchers dubbed the “Maryland Threat Countdown”. </p>
<p>The timing of this “threat” was signaled either by a conventional
countdown timer—i.e. “3, 2, 1…”—or by a random string of numbers—e.g.
“16, 21, 8.” In both conditions, threat anticipation recruited a
remarkably similar network of brain regions, including the amygdala and
the BNST. Across a range of head-to-head comparisons, the two showed
statistically indistinguishable responses.</p>
<p>The team examined the neural circuits engaged while waiting for
certain and uncertain threat (i.e. “fear” and “anxiety”). Results
demonstrated that both kinds of threat anticipation recruited a common
network of core brain regions, including the amygdala and BNST. </p>
<p>These observations raise important questions about the <a href="https://www.nimh.nih.gov/research/research-funded-by-nimh/rdoc/index.shtml" target="_blank">Research Domain Criteria</a>
(RDoC) framework that currently guides the U.S. National Institute of
Mental Health’s quest to discover the brain circuitry underlying anxiety
disorders, depression, and other common mental illnesses. “As it is
currently written, RDoC embodies the idea that certain and uncertain
threat are processed by circuits centered on the amygdala and BNST,
respectively. It’s very black-and-white thinking,” Shackman noted,
emphasizing that RDoC’s “strict-segregation” model is based on data
collected at the turn of the century.</p>
<p> “It’s time to update the RDoC so that it reflects the actual state
of the science. It’s not just our study; in fact, a whole slew of
mechanistic studies in rodents and monkeys, and new meta-analyses of the
published human imaging literature are all coalescing around the same
fundamental scientific lesson: certain and uncertain threat are
processed by a shared network of brain regions, a common core,” he
said. </p>
<p>As the crown jewel of NIMH’s strategic plan for psychiatric research
in the U.S., the RDoC framework influences a wide range of biomedical
stakeholders, from researchers and drug companies to private
philanthropic foundations and foreign funding agencies. Shackman noted
that the RDoC has an outsized impact on how fear and anxiety research is
designed, interpreted, peer reviewed, and funded here in the U.S. and
abroad.</p>
<p>“Anxiety disorders impose a substantial and growing burden on global
public health and the economy,” Shackman said, “While we have made
tremendous scientific progress, existing treatments are far from
curative for many patients. Our hope is that research like this study
can help set the stage for better models of emotion and, ultimately,
hasten the development of more effective intervention strategies for the
many millions of children and adults around the world who struggle with
debilitating anxiety and depression.”</p>
<p>This work was supported by the National Institute of Mental Health and the University of Maryland, College Park.</p>
<p dir="ltr">The research team also included Allegra S. Anderson,
Vanderbilt University; Jinyi Kuang, University of Pennsylvania; Manuel
Kuhn, Harvard Medical School; Andrew S. Fox, University of California,
Davis; and Jason F. Smith, Rachael M. Tillman, Hyung Cho Kim, and
Kathryn A. DeYoung, all from the University of Maryland, College Park.</p>
<p> </p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-59700335243037630542021-03-17T12:12:00.006-07:002021-03-17T12:24:18.841-07:00Tobacco companies hook kids on sugary drinks <p> </p><p><img align="left" alt="Punchy Mascot" height="148" src="http://sugarscience.ucsf.edu/assets/images/media_gallery/punchy-img.png" width="147" /><a href="http://sugarscience.ucsf.edu/soft-drink-companies-copy-tobacco-playbook-to-lure-young-users.html" target="_blank">UCSF</a> :Tobacco conglomerates that used colors, flavors and marketing
techniques to entice children as future smokers transferred these same
strategies to sweetened beverages when they bought food and drinks
companies <a href="https://www.bmj.com/content/bmj/364/bmj.l736/F1.large.jpg">starting in 1963</a>, according to a study by researchers at UC San Francisco.<br />The study, which draws from a cache of previously secret documents from the tobacco industry that is part of the <a href="https://www.industrydocumentslibrary.ucsf.edu/tobacco/">UCSF Industry Documents Library</a>
tracked the acquisition and subsequent marketing campaigns of sweetened
drink brands by two leading tobacco companies: R.J. Reynolds and Philip
Morris. It found that as tobacco was facing increased scrutiny from
health authorities, its executives transferred the same products and
tactics to peddle soft drinks. <a href="https://www.bmj.com/content/364/bmj.l736">The study was published</a> in the March 2019 issue of <i>BMJ</i>.<span></span></p><a name='more'></a><br /><br />“Executives in the two largest U.S.-based tobacco companies had developed colors <img align="right" alt="Kool-Aid Package" height="286" src="http://sugarscience.ucsf.edu/assets/images/media_gallery/kool_aidadhirez.jpeg" width="285" />and
flavors as additives for cigarettes and used them to build major
children’s beverage product lines, including Hawaiian Punch, Kool-Aid,
Tang and Capri Sun,” said senior author <b><a href="https://profiles.ucsf.edu/laura.schmidt">Laura Schmidt</a></b>, PhD, MSW, MPH, of the <b><a href="https://healthpolicy.ucsf.edu/philip-r-lee-institute-health-policy-studies">UCSF Philip R. Lee Institute for Health Policy Studies</a></b>.
“Even after the tobacco companies sold these brands to food and
beverage corporations, many of the product lines and marketing
techniques designed to attract kids are still in use today.”<br /><br /><b><a class="glossary_term" data-id="glossary_25" href="http://sugarscience.ucsf.edu/glossary_fruit_juice">Fruit Juice</a>, Sports Drinks Linked to Obesity, Metabolic Disease</b><p></p>
<p>American youth currently consume an average of 143 calories a day in
sugary beverages, according to the Centers for Disease Control and
Prevention. These calorie-dense drinks do not provide the satiety of
foods and are associated with obesity and <a class="glossary_term" data-id="glossary_19" href="http://sugarscience.ucsf.edu/glossary_metabolic_syndrome">metabolic syndrome</a>, a cluster of conditions that increase the risk for <a class="glossary_term" data-id="glossary_12" href="http://sugarscience.ucsf.edu/glossary_heart_disease">heart disease</a>, <a class="glossary_term" data-id="glossary_43" href="http://sugarscience.ucsf.edu/glossary_stroke">stroke</a> and <a class="glossary_term" data-id="glossary_6" href="http://sugarscience.ucsf.edu/glossary_type_2_diabetes">Type 2 diabetes</a>.</p>
<p>Sugary beverages include most fruit juices, sports and energy drinks, soda and other beverages sweetened with added <a class="glossary_term" data-id="glossary_40" href="http://sugarscience.ucsf.edu/glossary_sugars">sugars</a>, including honey, <a class="glossary_term" data-id="glossary_49" href="http://sugarscience.ucsf.edu/glossary_fructose">fructose</a>, <a class="glossary_term" data-id="glossary_41" href="http://sugarscience.ucsf.edu/glossary_glucose">glucose</a>, <a class="glossary_term" data-id="glossary_33" href="http://sugarscience.ucsf.edu/glossary_sucrose">sucrose</a>, dextrose, corn sweetener, malt syrup, corn syrup, brown sugar and raw sugar.</p>
<p>The new papers, which are available in the UCSF Truth Tobacco
Industry Documents Library, a subset of the UCSF Industry Documents
Library, reveal connections between the tobacco and food industries.</p>
<p>Tobacco giant R.J. Reynolds led the transition to sweetened beverages
in 1963 when it purchased Hawaiian Punch from Pacific Hawaiian Products
Company, according to the documents. The beverage previously had been
promoted to adults as a cocktail mixer, but R.J. Reynolds sought to beef
up the drink’s “Punchy” mascot – a counterpart to the “Joe Camel”
cartoon character the company used to promote cigarettes – and featured
it on toys, schoolbook covers, comics, tumblers, clothing and TV
commercials. Punchy became the “best salesman the beverage ever had,”
according to tobacco industry documents.</p>
<p>In the ’60s and ’70s, the company conducted taste tests with children
and mothers to evaluate sweetness, colors and flavors for Hawaiian
Punch product line extensions. The children’s preferences were
prioritized, the authors noted.</p>
<p>By 1983, R.J. Reynolds introduced the nation’s first juice box,
marketed as a “handy little carton that comes with its very own straw.”
This innovation was largely responsible for a 34 percent jump in sales,
according to industry documents </p>
<p><b>Kool-Aid Joins Marlboro</b></p>
<p>Meanwhile, tobacco competitor Philip Morris had acquired Kool-Aid,
via General Foods, in 1985. The company flipped its marketing audience
from families to children, created its “Kool-Aid Man” mascot, and
launched collaborations with branded toys, including Barbie and Hot
Wheels. It also developed a children’s Kool-Aid loyalty program
described as “our version of the Marlboro Country Store,” a cigarette
incentives program.</p>
<p>“The Wacky Wild Kool-Aid style campaign had tremendous reach and impact,” said first author <a href="https://directory.ucsf.edu/people/search/id/25792"><b>Kim Nguyen, ScD, MPH</b></a>,
who is also with the UCSF Philip R. Lee Institute for Health Policy
Studies. “Lots of kids in the ’80s dreamed of getting swag from the
Wacky Warehouse. What is really ‘wacky’ is that the Kool-Aid kid program
was modeled after a tobacco marketing strategy designed to build
allegiance with smokers.”</p>
<p><a href="http://sugarscience.ucsf.edu/soft-drink-companies-copy-tobacco-playbook-to-lure-young-users.html" target="_blank">UCSF</a> : By 2004, Philip Morris had developed at least 36 child-tested flavors
to its Kool-Aid line, of which some – like “Great Bluedini” –
integrated colors with cartoon characters. The tobacco giant also
acquired Capri Sun and Tang, and used similar child-focused integrated
marketing strategies to drive those sales.<span></span></p><!--more--><p></p>
<p>Most sweetened beverage manufacturers claim to limit marketing to
children of unhealthy foods and drinks. The industry launched both the
Children’s Advertising Review Unit, to promote responsible advertising
to children through industry self-policing, and the Children’s Food and
Beverage Advertising Initiative, which states that it devotes 100
percent of “child-directed advertising to better-for-you foods.”</p>
<p>“The industry claims that these tobacco-inspired marketing strategies
are not actually targeting children and should be excluded from these
industry-led agreements” said Schmidt. “But the evidence cited in our
research shows that these product lines and marketing techniques were
specifically designed for and tested on children.”</p>
<p>The authors conclude that, given the current high rates of childhood
obesity, there is a clear need to replace current industry-led voluntary
standards with well-enforced government regulations on marketing sugary
beverages to children.</p>
<p>“Parents do play a significant role in what their kids eat and
drink,” Nguyen said. “However, we cannot underestimate the influence of
these beverage corporations and their marketing. They intentionally
develop marketing campaigns that appeal to kids by making the drinks fun
and exciting.”</p>
<p>The <b><a href="https://www.industrydocumentslibrary.ucsf.edu">UCSF Industry Documents Library</a></b>
was launched in 2002 as a digital portal for tobacco documents. Today,
the library includes close to 15 million internal tobacco, drug,
chemical and food industry documents used by scientists, policymakers,
journalists and community members in their efforts to improve and
protect the health of the public.</p>
<p><b>Co-Authors, <a href="https://profiles.ucsf.edu/stanton.glantz">Stanton Glantz, PhD,</a> </b>from the <b><a href="https://tobacco.ucsf.edu/">UCSF Center for Tobacco Control Research and Education</a></b>; <b><a href="https://directory.ucsf.edu/people/search/id/123609">Casey Palmer, MS, RN</a></b>, from the UCSF Philip R. Lee Institute for Health Policy Studies contributed to this study.</p>
<p><b>Funding:</b> Laura and John Arnold Foundation, CrossFit Foundation, the National <a class="glossary_term" data-id="glossary_39" href="http://sugarscience.ucsf.edu/glossary_cancer">Cancer</a> Institute.</p>
<p><b>Disclosures:</b> No <a class="glossary_term" data-id="glossary_3" href="http://sugarscience.ucsf.edu/glossary_conflicts_of_interest">conflicts of interest</a>.</p>
<p><b>Read more:</b> <a href="https://www.bmj.com/content/364/bmj.l736">https://www.bmj.com/content/364/bmj.l736<br /></a><b>Press coverage:</b> <a href="https://www.nytimes.com/2019/03/14/health/big-tobacco-kool-aid-sugar-obesity.html">https://www.nytimes.com/2019/03/14/health/big-tobacco-kool-aid-sugar-obesity.html<br /></a><span class="s1"><b>Video:</b><a href="https://www.youtube.com/watch?v=18C11XIa0t0&list=PLPdSQGGMt89f6fA3n_owvD9A3Puq7_omB"> Unveiling UCSF's Food Industry Documents Archive</a> </span></p>
<p class="p3"> </p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-86791643052959189872021-03-17T05:34:00.003-07:002021-03-17T05:34:17.233-07:00How COVID-19 Causes Loss of Smell<p><span style="font-weight: normal;"><span style="font-size: small;"><a href="https://hms.harvard.edu/news/how-covid-19-causes-loss-smell" target="_blank">Harvard</a> :Olfactory support cells, not neurons, are vulnerable to novel coronavirus infection.</span></span> Temporary loss of smell, or anosmia, is the main neurological symptom
and one of the earliest and most commonly reported indicators of
COVID-19. Studies suggest it <a href="https://elifesciences.org/articles/58227">better predicts</a>
the disease than other well-known symptoms such as fever and cough, but
the underlying mechanisms for loss of smell in patients with COVID-19
have been unclear.<span></span></p><a name='more'></a><p></p>
<p>Now, an international team of researchers led by neuroscientists at
Harvard Medical School has identified the olfactory cell types <span>in the upper nasal cavity </span>most vulnerable to infection by SARS-CoV-2, the virus that causes COVID-19.</p>
<p>Surprisingly, sensory neurons that detect and transmit the sense of smell to the brain are not among the vulnerable cell types.</p>
<p><a href="https://hms.harvard.edu/news-events/sign-email-communications">Get more HMS news here</a></p>
<p>Reporting in <a href="https://advances.sciencemag.org/content/early/2020/07/24/sciadv.abc5801"><em>Science Advances</em></a>
on July 24, the research team found that olfactory sensory neurons do
not express the gene that encodes the ACE2 receptor protein, which
SARS-CoV-2 uses to enter human cells. Instead, ACE2 is expressed in
cells that provide metabolic and structural support to olfactory sensory
neurons, as well as certain populations of stem cells and blood vessel
cells.</p>
<p>The findings suggest that infection of nonneuronal cell types may be
responsible for anosmia in COVID-19 patients and help inform efforts to
better understand the progression of the disease.</p>
<p>“Our findings indicate that the novel coronavirus changes the sense
of smell in patients not by directly infecting neurons but by affecting
the function of supporting cells,” said senior study author <a href="https://connects.catalyst.harvard.edu/Profiles/display/Person/37334">Sandeep Robert Datta</a>, associate professor of neurobiology in the Blavatnik Institute at HMS.</p>
<p>This implies that in most cases, SARS-CoV-2 infection is unlikely to
permanently damage olfactory neural circuits and lead to persistent
anosmia, Datta added, a condition that is associated with a variety of
mental and social health issues, particularly depression and anxiety.</p>
<p>“I think it’s good news, because once the infection clears, olfactory
neurons don’t appear to need to be replaced or rebuilt from scratch,”
he said. “But we need more data and a better understanding of the
underlying mechanisms to confirm this conclusion.”</p>
<p>A <a href="https://jamanetwork.com/journals/jamaotolaryngology/article-abstract/2767781">majority</a> of COVID-19 patients experience some level of anosmia, most often temporary. Analyses of <a href="https://elifesciences.org/articles/58227">electronic health records</a>
indicate that COVID-19 patients are 27 times more likely to have smell
loss but are only around 2.2 to 2.6 times more likely to have fever,
cough or respiratory difficulty, compared to patients without COVID-19.</p>
<p>Some studies have hinted that anosmia in COVID-19 differs from
anosmia caused by other viral infections, including by other
coronaviruses.</p>
<p>For example, COVID-19 patients typically recover their sense of smell
over the course of weeks—much faster than the months it can take to
recover from anosmia caused by a subset of viral infections known to
directly damage olfactory sensory neurons. In addition, many viruses
cause temporary loss of smell by triggering upper respiratory issues
such as stuffy nose. Some COVID-19 patients, however, experience anosmia
<a href="https://jamanetwork.com/journals/jamaotolaryngology/fullarticle/2764417">without</a> any nasal obstruction.</p>
<h6><strong>Pinpointing vulnerability</strong></h6>
<p>In the current study, Datta and colleagues set out to better
understand how sense of smell is altered in COVID-19 patients by
pinpointing cell types most vulnerable to SARS-CoV-2 infection.</p>
<p>They began by analyzing existing single-cell sequencing datasets that
in total catalogued the genes expressed by hundreds of thousands of
individual cells in the upper nasal cavities of humans, mice and
nonhuman primates.</p>
<figure class="align-left" role="group"><img alt="ace2" data-entity-type="" data-entity-uuid="" src="https://media.giphy.com/media/WUy2HBh53WI1GcI422/giphy.gif" /><figcaption><em>Animation: Rick Groleau</em></figcaption></figure><p>The team focused on the gene <em>ACE2</em>,
widely found in cells of the human respiratory tract, which encodes the
main receptor protein that SARS-CoV-2 targets to gain entry into human
cells. They also looked at another gene, <em>TMPRSS2</em>, which encodes an enzyme thought to be important for SARS-CoV-2 entry into the cell.</p>
<p>The analyses revealed that both <em>ACE2</em> and <em>TMPRSS2</em>
are expressed by cells in the olfactory epithelium—a specialized tissue
in the roof of the nasal cavity responsible for odor detection that
houses olfactory sensory neurons and a variety of supporting cells.</p>
<p>Neither gene, however, was expressed by olfactory sensory neurons. By
contrast, these neurons did express genes associated with the ability
of other coronaviruses to enter cells.</p>
<p>The researchers found that two specific cell types in the olfactory epithelium expressed <em>ACE2</em>
at similar levels to what has been observed in cells of the lower
respiratory tract, the most common targets of SARS-CoV-2, suggesting a
vulnerability to infection.</p>
<p>These included sustentacular cells, which wrap around sensory neurons
and are thought to provide structural and metabolic support, and basal
cells, which act as stem cells that regenerate the olfactory epithelium
after damage. The presence of proteins encoded by both genes in these
cells was confirmed by immunostaining.</p>
<p>In additional experiments, the researchers found that olfactory
epithelium stem cells expressed ACE2 protein at higher levels after
artificially induced damage, compared with resting stem cells. This may
suggest additional SARS-CoV-2 vulnerability, but it remains unclear
whether or how this is important to the clinical course of anosmia in
patients with COVID-19, the authors said.</p>
<figure class="align-right" role="group"><img alt="notes" data-entity-type="" data-entity-uuid="" src="https://hms.harvard.edu/sites/default/files/assets/News/500-nose.png" /><figcaption><em>A
cartoon of the olfactory bulb and epithelium. Cells of note - Top
right: A pericyte (light orange) wraps around a blood vessel (red).
Bottom right: Olfactory sensory neurons (light red, orange) surrounded
by sustentacular cells (tan) and basal cells (yellow and light orange).
Image: Brann et. al., 2020.</em></figcaption></figure><p>Datta and
colleagues also analyzed gene expression in nearly 50,000 individual
cells in the mouse olfactory bulb, the structure in the forebrain that
receives signals from olfactory sensory neurons and is responsible for
initial odor processing.</p>
<p>Neurons in the olfactory bulb did not express <em>ACE2</em>. The gene
and associated protein were present only in blood vessel cells,
particularly pericytes, which are involved in blood pressure regulation,
blood-brain barrier maintenance and inflammatory responses. No cell
types in the olfactory bulb expressed the <em>TMPRSS2</em> gene.</p>
<h6><strong>Smell loss clue</strong></h6>
<p>Together, these data suggest that COVID-19-related anosmia may arise
from a temporary loss of function of supporting cells in the olfactory
epithelium, which indirectly causes changes to olfactory sensory
neurons, the authors said.</p>
<p>“We don’t fully understand what those changes are yet, however,”
Datta said. “Sustentacular cells have largely been ignored, and it looks
like we need to pay attention to them, similar to how we have a growing
appreciation of the critical role that glial cells play in the brain.”</p><p><span style="font-weight: normal;"><span style="font-size: small;"> </span></span></p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-82374482409899220192021-03-17T05:31:00.005-07:002021-03-17T05:31:36.950-07:00Noninvasive occipital and trigeminal neuromodulation technology cleared by FDA for the acute treatment of migraine<p><span style="font-size: small;"><a href="https://americanheadachesociety.org/news/neurolief-relivion-announcement" target="_blank">American Headache Society</a> :<span style="font-weight: normal;">Device worn as headset delivers stimulation to six branches of the occipital and trigeminal nerves</span>On Ma<span style="font-weight: normal;">rch 2, Neurolief announced that it has received Food and Drug Administration (FDA) clearance for its Relivion<sup>®</sup>
system, a non-invasive, multi-channel neuromodulation system for at
home, acute treatment of migraine attacks. The device is worn as a
headset and stimulates occipital and trigeminal nerves according to the
company’s March 2 press release.
<span></span></span></span></p><a name='more'></a><p></p><p><b>Clinical trial</b></p>
<p>According to the company’s release, FDA marketing clearance is based
on the results of a multicenter, prospective, randomized, double-blind,
placebo-controlled clinical study. 46% of the patients in the active
group reached complete pain freedom compared to only 11.8% of patients
in the control group. No serious adverse events were reported, the
statement adds. The study was conducted at clinical centers in the
United States and Israel and evaluated the safety and efficacy of the
device with 131 patients who met the International Classification of
Headache Disorders (ICHD-3) criteria of migraine with or without aura.</p>
<p>This study has not yet been published in a peer reviewed journal. See
the company’s press release including additional information about the
clinical trial <a href="https://www.businesswire.com/news/home/20210302005356/en/Relivion%C2%AE-Wearable-Brain-Neuromodulation-Technology-Cleared-by-FDA-for-the-Treatment-of-Migraine" rel="noopener noreferrer" target="_blank">here</a>.</p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-86205533366242042662021-03-17T05:28:00.004-07:002021-03-17T05:28:20.924-07:00Socioeconomic Factors Account for Variability in Language Skills in Preschoolers with Autism Spectrum Disorders<p><a href="https://journals.lww.com/jrnldbp/Abstract/2021/02000/Socioeconomic_Factors_Account_for_Variability_in.3.aspx?context=FeaturedArticles&collectionId=3" target="_blank">Developmental Behavioural Pediatrics</a> :Although no longer required for a diagnosis, language delays are
extremely common in children diagnosed with autism spectrum disorders
(ASD). Factors associated with socioeconomic status (SES) have
broad-reaching impact on <span class="ej-keyword" data-value="language development">language development</span> in early childhood. Despite recent advances in characterizing autism in early childhood, the relationship between SES and <span class="ej-keyword" data-value="language development">language development</span> in ASD has not received much attention.<span></span></p><a name='more'></a><p></p>
<h3>The objective of this study was </h3>
<p>to examine whether toddlers and preschoolers with ASD from
low-resource families are more likely to experience language delays
above and beyond those associated with autism itself.</p>
<h3>Methods: </h3>
<p>Developmental and diagnostic assessments including the Mullen
Scales of Early Learning, the Autism Diagnostic Observation Schedule,
Second Edition, and the Vineland Adaptive Behavior Scales were obtained
from 62 young children with ASD and 45 typically developing children
aged 15 to 64 months. Sociodemographic information including household
income, maternal education, and racial/ethnic identity was obtained from
caregivers. Multiple regression models were used to test for
associations between socioeconomic indices and language scores.</p>
<h3>Results: </h3>
<p>Maternal education accounted for variability in expressive
language (EL) and receptive language (RL), with lower SES indices
associated with lower language skills, and more so in children with ASD.</p>
<h3>Conclusion: </h3>
<p>These results demonstrate that variability in EL and RL
skills in young children with autism can be accounted for by
socioeconomic variables. These findings highlight the necessity for
targeted intervention and effective implementation strategies for
children with ASD from low-resource households and communities and for
policies designed to improve learning opportunities and access to
services for these young children and their families.</p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-65942764147966530022021-03-17T05:25:00.003-07:002021-03-17T05:25:27.892-07:00How do you treat coronavirus? Here are physicians’ best strategies<p><a href="https://www.sciencemag.org/news/2021/03/how-do-you-treat-coronavirus-here-are-physicians-best-strategies" target="_blank">Science</a> :Ready or not, the patients were coming. This time last year,
physicians around the world prepared, most for the first time in their
careers, to treat a new disease—over and over and over again.</p>
<p>“There was a terrible sense of foreboding, like in a movie when the
minor key music starts playing,” says Robert Arntfield, a critical care
physician at Western University in London, Canada.</p>
<p>In Wuhan, China, the doctors who first encountered the pandemic
coronavirus raced to share surprising symptoms and possible treatments
with far-flung colleagues.<span></span></p><a name='more'></a><p></p>
<p>In Tokyo, ill cruise ship patrons from the <em>Diamond Princess</em>
were wheeled into the hospital of the National Center for Global Health
and Medicine. Infectious disease physician Norio Ohmagari dusted off the
best treatment plan he had: one for the related coronavirus that causes
Middle East respiratory syndrome. “Honestly,” he says, “we were not
quite sure what we could do.”</p>
<p>In the United Kingdom’s Cynon Valley, a man arrived at a clinic for
routine bloodwork, then announced he had a high fever and cough. Shouts
went out for a doctor. As primary care physician Chris Butler prepared
to assess the patient, “I was dropping my gloves,” he says. “I was
pretty nervous.”</p>
<p>Over the harrowing year that followed, clinical evidence on how to
treat the pandemic coronavirus poured in—a muddy torrent of hundreds of
thousands of papers, preprints, and press releases. Many physicians were
torn between waiting for results from large clinical trials, the gold
standard of evidence, and offering something, anything, to the gravely
ill patients in front of them. “These are smart physicians who are
watching people get very sick, watching people die, feeling helpless,
and wanting to do whatever they can,” says Lisa Moores, a pulmonary and
critical care physician at the Uniformed Services University of the
Health Sciences in Bethesda, Maryland.</p>
<p>Unproven drugs became first-line treatments. “Tens or hundreds of
thousands of patients got ineffective or harmful therapies,” says
Matthew Semler, a critical care physician at Vanderbilt University,
citing widespread use of the antimalarial drug hydroxychloroquine, now
known to prevent neither disease nor death.</p>
<p>Physicians memorized treatment guidelines one day only to learn
they’d changed the next. “When you have the whole world working on
something at the same time … the evidence evolves fast,” says Meghan
Lane-Fall, a critical care physician who studies health care delivery at
the University of Pennsylvania (UPenn). “Every time I take care of a
COVID patient … I have to sit down and go, ‘OK, what are we doing now?’”
Even today, she says, “There is no single standard of care.”</p>
<div class="entity entity-paragraphs-item paragraphs-item-image">
<figure class="figure">
<div class="figure__head">
<img src="https://www.sciencemag.org/sites/default/files/styles/inline__450w__no_aspect/public/cs_0319N_SoC_Charts.jpg?itok=KXeQUO0b" /> </div>
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<p><span data-sheets-userformat="{"2":4769,"3":{"1":0},"8":{"1":[{"1":2,"2":0,"5":{"1":0}},{"1":0,"2":0,"3":3},{"1":1,"2":0,"4":1}]},"10":2,"12":0,"15":"Arial"}" data-sheets-value="{"1":2,"2":"In Milan, a team of intensive care unit doctors and nurses gathers information to coordinate care for COVID-19 patients."}">In Milan, a team of intensive care unit doctors and nurses gathers information to coordinate care for COVID-19 patients.</span></p>
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Daniele Frediani/Archivio Daniele Frediani/Mondadori Portfolio/Getty Images
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<p>Yet 12 months after the World Health Organization (WHO)
declared a pandemic, physicians have gleaned a rough understanding of
COVID-19’s pathology and an aspirational strategy for treating it: Early
in the illness, the goal is to stave off severe disease by stopping the
virus from replicating. As infection progresses, the primary enemy
becomes a hyperactive immune response that <a href="https://www.sciencemag.org/news/2020/04/how-does-coronavirus-kill-clinicians-trace-ferocious-rampage-through-body-brain-toes">wreaks havoc on the body’s organs</a>.</p>
<p>A few therapies—mostly repurposed drugs—have risen to the top.
Dexamethasone, a cheap and common steroid, surprised doctors by slicing
mortality in the sickest patients in a randomized trial; another
anti-inflammatory, tocilizumab, also helped patients survive. The
antiviral drug remdesivir, which appeared to speed recovery in some
studies but not in others, is widely used in hospitalized patients.
Monoclonal antibodies, meanwhile, are playing catch-up: Given early,
they may help avert severe disease, but they can be tough to deliver to
outpatients, and some appear less potent against new viral variants.
Beyond drugs, physicians have honed their intensive care unit (ICU)
practices to support patients’ failing organs.</p>
<p>COVID-19 remains enigmatic—and deadly—but shifts in care appear to
have helped. An analysis published this month of nearly 200,000 patients
in 555 U.S. hospitals found <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2777028?utm_source=For_The_Media&utm_medium=referral&utm_campaign=ftm_links&utm_term=030521">mortality rates dropped from 22.1% in March 2020 to 6.5% in August</a>,
although factors beyond new treatments, such as reduced crowding in
hospitals, may have also played a role. After a traumatic year, doctors
describe scientific progress they couldn’t have imagined—and a crisis
that brought into stark relief the challenges of applying research to
the art of medicine.</p>
<p><span class="section-break-style">“I’m sorry to say</span> that your COVID test came back positive.”</p>
<p>More than 120 million people have heard some version of those words,
setting them on an uncertain path. About 10% to 15% will veer into
serious illness, and others will face enduring, sometimes disabling
symptoms. Gamely pumping the brakes are primary care doctors, trained to
handle everything from warts to stomach bugs. “My patients are my
family,” says Ada Stewart, a physician in South Carolina and president
of the American Academy of Family Physicians (AAFP), who is haunted by
the loss of about 10 of her patients to the virus.</p>
<div class="entity entity-paragraphs-item paragraphs-item-image align-right">
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<p><span data-sheets-userformat="{"2":5025,"3":{"1":0},"8":{"1":[{"1":2,"2":0,"5":{"1":0}},{"1":0,"2":0,"3":3},{"1":1,"2":0,"4":1}]},"10":2,"11":0,"12":0,"15":"Arial"}" data-sheets-value="{"1":2,"2":"Family physician Ada Stewart watches her COVID-19 outpatients for signs of worsening disease."}">Family physician Ada Stewart watches her COVID-19 outpatients for signs of worsening disease.</span></p>
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<span class="credit">
AAFP
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</figcaption>
</figure>
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<p>Newly diagnosed patients “come into the clinic asking, ‘What
can you give me right now that can prevent me from going down this
pathway … [of becoming] very, very sick?’” says Jacqueline Chu, a
physician in primary care and infectious disease who serves a
working-class population in Chelsea, Massachusetts, that has been hit
hard by COVID-19; her clinic is affiliated with nearby Massachusetts
General Hospital.</p>
<p>Outpatient care is often basic, and Chu offers the same advice she
does for riding out any virus at home: fluids, rest, and acetaminophen
for pain and fever. But doctors now know <a href="https://jamanetwork.com/journals/jama/fullarticle/2765184">which patients are more likely to develop serious disease</a>; they keep closer tabs on the <a href="https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2763184">elderly</a> and those with heart disease, diabetes, or <a href="https://onlinelibrary.wiley.com/doi/10.1111/obr.13128">obesity</a>.
When scientists at the Cleveland Clinic crunched data on everyone
receiving a positive COVID-19 test through their health system, they
identified another risk factor for severe illness: <a href="https://journals.plos.org/plosone/article/authors?id=10.1371/journal.pone.0237419">living in some of the poorest ZIP codes</a>. Those patients now get 2 weeks of daily check-ins to spot symptoms quickly.</p>
<p>Doctors also know that even robust young people who appear to be
recovering one day can deteriorate the next. To spot falling blood
oxygen levels, pulse oximeters have become the new thermometers, widely
recommended for home use.</p>
<p>Testing experimental treatments for newly diagnosed people has proved
difficult. Some clinical trials struggle to find participants because
community clinics are disconnected from trial infrastructure, says
Butler, who runs <a href="https://www.principletrial.org/">the PRINCIPLE trial</a>,
among the largest studying high-risk people with COVID-19 at home, out
of the University of Oxford’s Nuffield Department of Primary Care Health
Sciences.</p>
<p>PRINCIPLE’s chief successes thus far have been in identifying what doesn’t work: In late January, <a href="https://www.nihr.ac.uk/news/principle-trial-finds-no-benefit-from-antibiotics-azithromycin-and-doxycycline-for-covid-19-patients/26680">it announced that the antibiotics azithromycin and doxycycline</a>—tried
because they have some anti-inflammatory and antiviral properties and
because bacterial infections may set in after the virus takes hold—<a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)00461-X/fulltext">failed to speed recovery in outpatients</a>.</p>
<p>Other trials have racked up failures, too. After months of urging
COVID-19 survivors to donate antibody-rich plasma for infusion into
infected people, the U.S. National Institutes of Health (NIH) this
month <a href="https://www.nih.gov/news-events/news-releases/nih-halts-trial-covid-19-convalescent-plasma-emergency-department-patients-mild-symptoms">halted a trial of convalescent plasma</a> in patients with mild and moderate illness, finding it wasn’t improving outcomes. Last week, a preprint on a large U.K. trial <a href="https://www.medrxiv.org/content/10.1101/2021.03.09.21252736v1">reported no survival benefit in hospitalized patients</a>, either. Trials in outpatients are ongoing.</p>
<p>Such failures can guide care and help doctors dissuade patients from
embracing dubious treatments. “I had patients buying COVID ‘treatment
packs’ from Mexico” that claimed to include antibiotics, steroids, and
vitamins, says Andrew Carroll, a family physician in Chandler, Arizona.
“None of this has any basis in research.”</p>
<p>Sarah Coles, who practices family medicine in nearby Phoenix, chairs
the AAFP commission that issues treatment guidelines to its 136,000
members. These days she’s tracking data on a promising therapy:
monoclonal antibodies. These labmade proteins mimic the body’s own
immune response and are designed to block the virus from attaching to
cells. In November 2020, after <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2035002">interim trial data</a> suggested they could <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2029849">cut the risk of hospitalization by two-thirds</a> and
prevent deaths, the U.S. Food and Drug Administration (FDA) gave
emergency use authorization to monoclonal antibodies made by the drug
companies Regeneron and Eli Lilly and Co.</p>
<figure class="graphic entity entity-paragraphs-item paragraphs-item-figure">
<h2 class="figure__hed">Cornerstones of care</h2>
<figcaption class="figure__dek"><p class="p1">Doctors have few
treatments for the early stages of COVID-19, but have developed a small
arsenal of therapies to employ as symptoms become more severe. Research
continues on how and when to administer drugs, oxygen, and other
treatments.</p>
</figcaption>
<figure class="figure">
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<figure class="svg-object" data-src="/sites/default/files/svgimg/210309NF_COVID-care_drupal.svg.png" style="padding-bottom: 48.586%;">
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</image>
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Fluids, rest,acetaminophen
Monoclonal antibodies appear to reduce risk of hospitalization in outpatients at high risk of severe disease— provided patients can access them.
The antiviralremdesivir is widely used in hospitalized patients, but evidence is mixed on its ability to shorten hospital stays; it hasn't been shown to improve survival.
Oxygen, delivered through nasal prongs, a mask, or an inva-sive breathing tube, is crucial to COVID-19 care. But how it’s administered varies among hospitals.
Anticoagulants can prevent blood clots that are common in COVID-19 patients, but physicians must weigh the risk of bleeding when deciding the right dose.
The immunosuppressant drugs dexamethasone and tocilizumab have both reduced mortality in large clinical trials of hospitalized patients, showing that it's possible to tame the potentially deadly inflammation that characterizes severe disease.
Immuno- suppressants
Ventilator
Dialysis
Monoclonal antibodies
Oxygen
Hospitalization
Recovery
Discharge
Death
Fever
Hypoxia
Blood clots
Viral replication
Viral replication
Immune overreaction
Respiratory failure
Kidney failure
Possible lingering symptoms
Cough
Loss of smell
Anticoagulants
Treatments
Disease course
Remdesivir
O
2
<figure class="graphic entity entity-paragraphs-item paragraphs-item-figure"><figure class="figure"><div class="figure__head"><figure class="svg-object" data-src="/sites/default/files/svgimg/210309NF_COVID-care_drupal.svg.png" style="padding-bottom: 48.586%;"><svg id="Layer_1" style="enable-background: new 0 0 700 340.1;" viewbox="0 0 700 340.1" x="0px" xml:space="preserve" xmlns="http://www.w3.org/2000/svg" y="0px">
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<text class="st9 st8" transform="matrix(1 0 0 1 68.2969 205.5952)">1 to 2 weeks</text>
</g>
<g>
<text class="st9 st8" transform="matrix(1 0 0 1 252.5122 205.5952)">1 to 2 weeks or more</text>
</g>
</svg>
</figure> </div>
<figcaption>
<div class="caption">
<span class="credit">
N. Desai/<cite>Science</cite>
</span>
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</figcaption>
</figure>
</figure>
<p>But the antibodies have to be infused at a hospital or
specialized site within days of the first symptoms—a logistical
challenge. “We have not created the on-ramps” to ease access, says David
Wohl, an infectious disease doctor at the University of North Carolina
(UNC), Chapel Hill, who’s working to widen the entry points. The 1800
doses administered at UNC are a fraction of what patients needed, he
suspects. And in South Carolina, Stewart has rural patients without
transportation for whom the therapy is literally out of reach.
Meanwhile, supplies of the drugs have fluctuated, and <a href="https://www.nature.com/articles/s41586-021-03398-2">at least some monoclonals seem to falter when facing new viral variants</a>.</p>
<p>What’s more, official guidance is equivocal on antibodies. With clinical trials ongoing, NIH treatment guidelines say <a href="https://www.covid19treatmentguidelines.nih.gov/anti-sars-cov-2-antibody-products/anti-sars-cov-2-monoclonal-antibodies/">there are “currently insufficient data to recommend either for or against” most monoclonal antibodies</a>, although on 2 March the agency suggested <a href="https://www.covid19treatmentguidelines.nih.gov/statement-on-bamlanivimab-plus-etesevimab-eua/">an Eli Lilly cocktail be offered to those at high risk of severe disease</a> days
after symptoms appear. The guidelines strike some physicians as too
conservative. But Coles wants to see outcomes from more trial
participants before fully embracing monoclonals. “We’ve been burned
before,” she says.</p>
<p>With a meager arsenal, physicians like Coles and Stewart listen
carefully, coach patients on symptoms to watch for, and make judgment
calls. One day not long ago, a patient of Stewart’s 1 week out from
diagnosis described intense fatigue and chest pain. Stewart felt her own
worries rising. “Get to the hospital,” she advised. Once there, the
patient turned out to have blood clots in both lungs and was quickly
admitted—passing into the hands of a new medical team trying to shield
her from the worst.</p>
<p><span class="section-break-style">COVID-19 patients</span> who arrive
at the hospital doors have reached a precarious point. Most have
endured at least a week of fever, coughing, and fatigue as viral
particles multiplied throughout their bodies. Now, they’re on the cusp
of a more perilous stage, in which a misfiring immune system can wreak
havoc on their organs.</p>
<p>Elevated levels of immune signaling molecules in the blood are a
marker of danger. But one of the clearest signs of trouble is a blood
oxygen level below 94%, says Varidhi Nauriyal, an infectious disease
specialist at the University of Pittsburgh. So the first treatment for
people hospitalized with COVID-19 is oxygen, typically delivered through
a mask or nasal prongs.</p>
<p>Most patients also get remdesivir, the lone COVID-19 treatment that’s
been formally approved by FDA. The antiviral caught researchers’
attention early last year for its ability to inhibit SARS-CoV-2 in a lab
dish. In April, an international NIH-sponsored trial reported that the
drug shortened hospital stays by several days. But in October, WHO’s
much larger trial, Solidarity, found <a href="https://www.sciencemag.org/news/2020/10/very-very-bad-look-remdesivir-first-fda-approved-covid-19-drug">no improvement in recovery time or mortality</a>. NIH’s treatment guidelines recommend remdesivir, but WHO’s do not.</p>
<div class="entity entity-paragraphs-item paragraphs-item-image">
<figure class="figure">
<div class="figure__head">
<img src="https://www.sciencemag.org/sites/default/files/styles/inline__450w__no_aspect/public/173A8878_1280x720.jpg?itok=s9dslMd8" /> </div>
<figcaption>
<div class="caption">
<div class="caption__text">
<p><span data-sheets-userformat="{"2":4769,"3":{"1":0},"8":{"1":[{"1":2,"2":0,"5":{"1":0}},{"1":0,"2":0,"3":3},{"1":1,"2":0,"4":1}]},"10":2,"12":0,"15":"Arial"}" data-sheets-value="{"1":2,"2":"Nurses arrange medications for a COVID-19 patient in [London, ]Ontario, Canada"}">A nurse arranges medications for COVID-19 patients in </span><span>Canada’s Ontario province.</span></p>
</div>
<span class="credit">
Robert Arntfield
</span>
</div>
</figcaption>
</figure>
</div>
<p>“It doesn’t seem to be the miracle drug that we would like it
to be,” says Mangala Narasimhan, a pulmonary and critical care physician
at New York’s Northwell Health system. But because remdesivir has few
side effects and became entrenched in many treatment plans early in the
pandemic, it remains standard therapy in most hospital wards and some
ICUs, says Leora Horwitz, a hospitalist and health care systems
researcher at New York University’s Langone Health. “I don’t think it’s
going to do people any harm, I just don’t think it’s going to do them
very much good,” she says.</p>
<p>Patients are also routinely treated for a common complication of COVID-19: blood clots, which develop in the veins of <a href="https://journal.chestnet.org/article/S0012-3692(20)35146-1/fulltext">an estimated 17% of hospitalized patients</a> and <a href="https://www.thrombosisresearch.com/article/S0049-3848(20)30120-1/pdf">nearly 30% of ICU patients</a>.
Those clots can travel to the lungs, cutting off blood flow to the
heart, or to the brain, where they can cause a stroke. Many guidelines
call for giving most people a low, prophylactic dose of anticoagulants
on admission.</p>
<p>But as patients worsen, physicians struggle over whether to up the
anticoagulant dose, which boosts the risk of gastrointestinal and
intracranial bleeding. Three trials—the United Kingdom’s REMAP-CAP, the
NIH-led ACTIV-4, and Canada’s ATTACC—are rushing to clarify the risks
and benefits.</p>
<p>In December 2020, all three trials stopped enrolling ICU patients,
citing concerns about bleeding; preliminary results posted in a preprint
this month found <a href="https://www.medrxiv.org/content/10.1101/2021.03.10.21252749v1">no survival benefit in the ICU</a>.
But in January, interim results from more than 1000 non-ICU patients
looked promising: Compared with a prophylactic dose, full-dose blood
thinners <a href="https://www.nih.gov/news-events/news-releases/full-dose-blood-thinners-decreased-need-life-support-improved-outcome-hospitalized-covid-19-patients">reduce the need for organ support</a> and may also reduce mortality, NIH announced.</p>
<p>If those data hold up, they are “pretty profound,” says Todd Hecht, a
hospitalist and director of the anticoagulation management program at
the Hospital of the University of Pennsylvania (HUP). Perhaps ICU
patients were simply so sick that high-dose anticoagulants had no
effect, he says.</p>
<figure class="graphic entity entity-paragraphs-item paragraphs-item-related-articles align-right">
<h3 class="figure__hed">Related</h3>
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</figure>
<p>Large, randomized trials are the best way to disentangle the
complex realities of COVID-19 care. But doctors sometimes sought faster
ways to help the patients in front of them. At Henry Ford Hospital in
Detroit, the flood of deteriorating patients in March 2020 prompted
doctors to consider a then-unproven therapy: corticosteroids, drugs used
for decades to reduce inflammation in conditions from asthma to
allergies. Infectious disease specialist Mayur Ramesh and his team
reviewed emerging evidence from China and decided to run what they
called a “quasiexperiment.” Starting in late March, they gave all
COVID-19 patients on oxygen a 3-day course of the corticosteroid
methylprednisolone and compared their outcomes with those of patients
admitted earlier.</p>
<p>The team debated doing a full clinical trial, says Nauriyal, who was
then helping supervise Henry Ford’s ICU. But many had high hopes for the
therapy and didn’t want to withhold it from a control group.</p>
<p>By early April, they saw a signal in their data: Of 81 patients
admitted before steroids were added to treatment, 44% moved to the ICU
and 26% died; for 132 patients admitted later, <a href="https://academic.oup.com/cid/article/71/16/2114/5840526">those numbers were 27% and 14%</a>.
Convinced the treatment was saving lives, Ramesh called colleagues at
dozens of other institutions to spread the word. But without the rigor
of a randomized trial or peer-reviewed data, few hospitals were willing
to change their practice.</p>
<p>The Henry Ford team continued to dose patients with steroids, other
medications, and oxygen, and many got better. But as everywhere, some
patients deteriorated. As their lungs or other organs failed, they were
transferred to a new space full of hissing and beeping equipment: the
ICU.</p>
<p><span class="section-break-style">“They’re all the same.”</span> That
was the impression Lane-Fall had when the first seven COVID-19 patients
arrived in her ICU at HUP in March 2020. “And they’re all super-sick.”</p>
<p>U.S. records suggest nearly 30% of COVID-19 patients admitted to the
hospital move to the ICU. Those critically ill patients face an
inflammatory assault on their lungs and other organs. Many have multiple
blood clots, and some require dialysis to support faltering kidneys.</p>
<p>When patients with lung failure began to fill ICUs 1 year ago, many
physicians fell back on years of experience with acute respiratory
distress syndrome (ARDS), a life-threatening buildup of fluid in lungs
damaged by trauma or infection. “If someone had told me, ‘You’re going
to be hearing a lot of stuff, but this is ARDS. Treat ARDS,’ that would
have gone a huge way” toward reassuring physicians, says UPenn critical
care physician George Anesi. In COVID-19 treatment, “Some of the
foundational principles of critical care medicine really emerged [as]
true,” he says. Those include proning—periodically flipping patients
onto their stomachs to make full use of their lungs—and management of
mechanical ventilators.</p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-59252804140343697362021-03-16T01:10:00.005-07:002021-03-16T01:10:45.540-07:00Simple Skin Swab Could Diagnose Parkinson’s Disease<p> </p><p><a href="https://www.clinicalomics.com/topics/patient-care/neurological-disorders/simple-skin-swab-could-diagnose-parkinsons-disease/" target="_blank">Clinicalomics</a> :Researchers at the University of Manchester have developed a test
that can diagnose Parkinson’s disease from sebum collected by swabbing
the skin.</p>
<p>The test uses mass spectrometry and was able to identify 10 chemicals
in the sebum skin swabs from Parkinson’s patients that differed from
those without the neurodegenerative condition. According to a press
statement, it was able to diagnose the disease with 85% accuracy.<span></span></p><a name='more'></a><p></p>
<p>“Not only is the test quick, simple and painless but it should also
be extremely cost-effective because it uses existing technology that is
already widely available,” said Perdita Barran, Ph.D., a professor at
the University of Manchester who led the research.</p>
<p>“We are now looking to take our findings forwards to refine the test to improve accuracy even further.”</p>
<p>There is currently no conclusive preclinical test for Parkinson’s
disease, which affects around 6 million people across the globe. It is
normally diagnosed based on physiological changes and observations by
physicians meaning that by the time a formal diagnosis is confirmed,
much damage has already occurred to the brain’s dopaminergic neurons.</p>
<p>While there is not currently a cure for Parkinson’s, like many
degenerative diseases, early diagnosis can help slow down progression.
Treatments like levodopa or carbidopa are more effective if given early
and other non-drug treatments like increased exercise can also help slow
progression. An early stage, non-invasive test could therefore be very
beneficial for those impacted by this disease.</p>
<p>A common non-motor symptom of Parkinson’s disease is seborrheic
dermatitis, present in around 60% of those affected, where the skin
produces abnormally high levels of oily sebum. To assess if sebum from
Parkinson’s patients was different from healthy individuals Barran and
colleagues carried out a mass spectrometry study.</p>
<p>“Studies of sebum are commonplace in dermatological conditions such
as acne, however sebum as a biofluid has rarely been used in disease
diagnostics,” write the researchers in the journal <em><a href="https://www.nature.com/articles/s41467-021-21669-4#Sec2">Nature Communications</a></em>.</p>
<p>Sebum samples were taken from 80 Parkinson’s patients who had yet to
start drug treatment, 138 medicated Parkinson’s patients and 56 healthy
controls matched for factors like age and gender.</p>
<p>Overall, 10 chemical compounds were found to be present in
significantly different amounts in Parkinson’s versus control
participants. Except for one compound, the changes in the chemicals were
very similar in treated and non-treated Parkinson’s patients versus
controls.</p>
<p>These compounds are largely linked to lipid metabolism — the changes
observed were in chemicals linked to the carnitine shuttle, sphingolipid
metabolism, arachidonic acid metabolism and fatty acid biosynthesis.</p>
<p>Further work would be needed to confirm this, but the team believes
the test they developed could also show disease changes over time and
perhaps give an indication of prognosis. They are planning to create a
spin-out company to commercialize and develop the test further.</p>
Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.comtag:blogger.com,1999:blog-3886118658276014355.post-16691553495323717052021-03-16T01:01:00.007-07:002021-03-16T01:01:51.840-07:00The Risks and Benefits of Running Barefoot or in Minimalist Shoes<p> </p><p><a href="http://www.runresearchjunkie.com/the-risks-and-benefits-of-running-barefoot-or-in-minimalist-shoes/" target="_blank">RunningResearch</a> :Nine formal systematic reviews of the evidence have so far been
published looking at the evidence on barefoot or minimalist running
having systematic benefits or not. Every single one of them concluded
the same thing (reviewed <a href="http://www.runresearchjunkie.com/what-evidence-is-there-that-barefoot-running-is-better-to-reduce-inury-risk/">here</a> and <a href="http://www.runresearchjunkie.com/barefoot-running-current-state-of-the-play/">here</a> and <a href="http://www.runresearchjunkie.com/evidence-that-barefoot-running-is-better-part-deux/">here</a>).
Despite those conclusions, all by people from different backgrounds and
published in a variety of different journals, you still see claims that
the evidence is that there are systematic benefits. I can’t figure that
out. Now we have yet another systematic review of the evidence:<span></span></p><a name='more'></a><p></p>
<blockquote><p><strong>The Risks and Benefits of Running Barefoot or in Minimalist Shoes; A Systematic Review</strong><br />
Kyle P. Perkins, William J. Hanney, PhD, PT, DPT, ATC and Carey E. Rothschild, PT, DPT, OCS, SCS, CSCS<br />
<a href="http://sph.sagepub.com/content/6/6/475.abstract">Sports Health: A Multidisciplinary Approach November/December 2014 vol. 6 no. 6 475-480</a><br />
Context: The popularity of running barefoot or in minimalist shoes has
recently increased because of claims of injury prevention, enhanced
running efficiency, and improved performance compared with running in
shoes. Potential risks and benefits of running barefoot or in minimalist
shoes have yet to be clearly defined.<br />
Objective: To determine the methodological quality and level of evidence
pertaining to the risks and benefits of running barefoot or in
minimalist shoes.<br />
Data Sources: In September 2013, a comprehensive search of the Ovid
MEDLINE, SPORTDiscus, and CINAHL databases was performed by 2
independent reviewers.<br />
Study Selection: Included articles were obtained from peer-reviewed
journals in the English language with no limit for year of publication.
Final inclusion criteria required at least 1 of the following outcome
variables: pain, injury rate, running economy, joint forces, running
velocity, electromyography, muscle performance, or edema.<br />
Study Design: Systematic review.<br />
Level of Evidence: Level 3.<br />
Data Extraction: Two reviewers appraised each article using the Downs
and Black checklist and appraised each for level of evidence.<br />
Results: Twenty-three articles met the criteria for this review. Of 27
possible points on the Downs and Black checklist, articles scored
between 13 and 19 points, indicating a range of evidence from very
limited to moderate. Moderate evidence supports the following
biomechanical differences when running barefoot versus in shoes: overall
less maximum vertical ground reaction forces, less extension moment and
power absorption at the knee, less foot and ankle dorsiflexion at
ground contact, less ground contact time, shorter stride length,
increased stride frequency, and increased knee flexion at ground
contact.<br />
Conclusion: Because of lack of high-quality evidence, no definitive
conclusions can be drawn regarding specific risks or benefits to running
barefoot, shod, or in minimalist shoes.</p></blockquote>
<p>Like all the other reviews, they concluded the same thing: there is no evidence for the claimed benefits!</p>
<p>They did find some strength of evidence that for this</p>
<blockquote><p>overall less maximum vertical ground reaction forces,
less extension moment and power absorption at the knee, less foot and
ankle dorsiflexion at ground contact, less ground contact time, shorter
stride length, increased stride frequency, and increased knee flexion at
ground contact</p></blockquote>
<p>Which is evidence that barefoot/minimalism is different to shod. None
of that says its better, it just says its different. For some runners
that may help and for other runners that may hurt – ie its subject
specific.</p>
<p>As always, <strong>I go where the evidence takes me until convinced otherwise</strong>….and this is what ALL the evidence is saying … nuff said.</p>
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</p>
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</p>
<p><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Sports+Health%3A+A+Multidisciplinary+Approach&rft_id=info%3Adoi%2F10.1177%2F1941738114546846&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+Risks+and+Benefits+of+Running+Barefoot+or+in+Minimalist+Shoes%3A+A+Systematic+Review&rft.issn=1941-7381&rft.date=2014&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=http%3A%2F%2Fsph.sagepub.com%2Flookup%2Fdoi%2F10.1177%2F1941738114546846&rft.au=Perkins%2C+K.&rft.au=Hanney%2C+W.&rft.au=Rothschild%2C+C.&rfe_dat=bpr3.included=1;bpr3.tags=Medicine">Perkins,
K., Hanney, W., & Rothschild, C. (2014). The Risks and Benefits of
Running Barefoot or in Minimalist Shoes: A Systematic Review <span style="font-style: italic;">Sports Health: A Multidisciplinary Approach</span> DOI: <a href="http://dx.doi.org/10.1177/1941738114546846" rev="review">10.1177/1941738114546846</a></span></p>
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</p>
<p class="updated left" id="authorsure-last-updated" itemid="http://www.runresearchjunkie.com/the-risks-and-benefits-of-running-barefoot-or-in-minimalist-shoes/" itemscope="itemscope" itemtype="http://schema.org/WebPage">Last updated by <span class="author vcard" style="float: none;"><span class="fn"><a class="authorsure-author-link" href="http://www.runresearchjunkie.com/author/Craig/" rel="author">Craig Payne</a></span></span>.</p>Dr Guichard MDhttp://www.blogger.com/profile/10992056106602355877noreply@blogger.com