We used cryo-electron microscopy to obtain three-dimensional images of our tool-molecule, DT-061, bound to PP2A, says study co-senior author Derek Taylor, Ph.D., an associate professor of pharmacology and biochemistry at Case Western Reserve University and member of the Case Comprehensive Cancer Center. This allowed us to see for the first time precisely how different parts of the protein were brought together and stabilized by the compound. We can now use that information to start developing compounds that could achieve the desired profile, specificity and potency to potentially translate to the clinic.

The researchers propose calling this class of molecules SMAPs for small molecule activators of PP2A.

Along with cancer, PP2A is also dysregulated in a number of other diseases including cardiovascular and neurodegenerative diseases. And the researchers are optimistic the findings could also open opportunities to develop new medicines against diseases like heart failure and Alzheimers as well.

The research required a marriage of scientific disciplines and areas of expertise, notes co-senior author Goutham Narla, M.D., Ph.D., chief of the division of genetic medicine in the department of internal medicine at the U-M Medical School.

Its an illustration of how collaboration and team science can solve some of the questions like this that scientists have been asking for many years, Narla says. Solving the structure without the biological knowledge of how best to apply it against cancer, would only be half of the story. And if we were just activating PP2A, killing cancer cells and slowing the growth of cancer without the structural data that would be a really nice half-story as well. But working together, we now have a story about being able to drug this previously undruggable tumor suppressor.

The study was led by first authors Daniel Leonard, an M.D. and Ph.D. student and member of Narlas lab when the research was at Case Western Reserve and the Case Comprehensive Cancer Center, and research scientist Wei Huang, Ph.D., of the Taylor lab.

There has been a lot of activity and excitement in recent years around the development of kinase inhibitors small molecule compounds that go after the protein kinases whose dysfunction is involved in the explosive growth and proliferation of cancer cells. That is, turning off cancers on switch, Leonard explains.

The new research attacks cancer from the opposite side of the equation, turning on cancers off switch by stabilizing protein phosphatases whose malfunction removes a key brake on cancer growth.

In the paper, the researchers speculate how a combination of both approaches simultaneously might offer an even more powerful one-two punch potentially helping to overcome cancers ability to evolve to thwart a singular approach.

The binding pocket we identified provides a launch pad for optimizing the next generation of SMAPs toward use in the clinic in cancer, and potentially other diseases, Huang adds.

Additional authors include Danica D. Wiredja, Yinghua Chen, Daniela M. Schlatzer, Janna Kiselar, Nikhil Vasireddi and Abbey L. Perl of Case Western Reserve University; Sudeh Izadmehr, Nilesh Zaware and Matthew D. Galsky of the Icahn School of Medicine at Mount Sinai; Caitlin M. OConnor of the University of Michigan; Zhizhi Wang and Wenqing Xu of the University of Washington; David L. Brautigan of the University of Virginia; and Stefan Schchner and Egon Ogris of the Medical University of Vienna.

The research was supported by grants from the National Institutes of Health (R01 CA240993, R01 GM133841, R01 CA181654, F30 TRN216393, T32 GM007250), and an American Heart Association Postdoctoral Fellowship (17POST33650070).

DT-061 was developed at the Icahn School of Medicine at Mount Sinai, which has filed for patent protection on the tool compound. Narla, Ogris and Taylor have ownership interest in RAPPTA Therapeutics, which has licensed the cryo-EM coordinates for the clinical and commercial development of novel series of small molecule PP2A activators from the University of Michigan and Case Western Reserve; the authors and institutions stand to benefit financially. The Medical University of Vienna has filed a patent on a monoclonal antibody used in the study.

Paper cited: Selective PP2A Enhancement Through Biased Heterotrimer Stabilization, Cell. DOI: 10.1016/j.cell.2020.03.038

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Turning On the 'Off Switch' in Cancer Cells - Michigan Medicine

Scientists are trying to tackle the lack of diversity seen in genomics research, but even ambitious efforts, like the NIHs All of Us program, often fall short, especially when it comes to the inclusion of Indigenous communities. This is one of the reasons why the Decolonize DNA Day conference is taking place on April 24th, one day before the National DNA Day.

Traditionally, National DNA Day is an annual celebration of the discovery of DNA's double helix structure (1953) and the completion of the Human Genome Project (2003).

I was having conversations with colleagues on what would it mean to decolonize DNA, says Krystal Tsosie, an Indigenous (Din/Navajo) PhD student at Vanderbilt University. As an Indigenous academic, we always talk about what it means to Indigenize and re-Indigenize different disciplines of academia that have been historically more white-centred or white-dominated... and what it would mean to remove the colonial lens.

In collaboration with Latrice Landry and Jerome de Groot, Tsosie co-organized the Decolonize DNA Day Twitter conference to help re-frame narratives around DNA. Each speaker will have an hour to tweet out their "talk" and lead conversations on various topics, including how DNA ancestry testing fuels anti-Indigeneity and how to utilize emerging technologies to decolonize precision medicine.

There is a divide between people who are doing the science or the academic work, and the people who we want to inform, says Tsosie. Twitter is a great way to bridge that divide.

The Decolonize DNA Day conference is simply one effort to Indigenize genomics. Tsosie is also a co-founder of the Native BioData Consortium, a non-profit organization consisting of researchers and Indigenous members of tribal communities, focused on increasing the understanding of Native American genomic issues.

We dont really see a heavy amount of Indigenous engagement in genetic studies, which then means that as precision medicine advances as a whole [] those innovations are not going to be applied to Indigenous people, says Tsosie. How do we get more Indigenous people engaged?

Some of the answers can be found in a recent Nature Reviews Genetics perspective, penned by Indigenous scientists and communities, including those from the Native BioData Consortium. The piece highlights the actions that genomics researchers can take to address issues of trust, accountability, and equity. Recommended actions include the need for early consultations, developing benefit-sharing agreements, and appropriately crediting community support in any academic publications.

By switching power dynamics, were hoping to get genomic researchers to work with us, instead of against us, says Tsosie.

Excerpt from:

On National DNA Day, scientists are trying to take the colonialism out of genetics - Massive Science

The Covid-19 pandemic is teaching me that the world can change almost overnight when it faces a big problem.

When President Trump declared a national emergency, my medical practice shifted almost instantly from in-person appointments to telehealth visits. The Drug Enforcement Administration allowed doctors like me to prescribe buprenorphine, a controlled substance used to combat opioid addiction, after a telephone consult, a move experts have been seeking for years. The Department of Health and Human Services waived privacy constraints for telehealth visits, which have long tied up this type of medicine, allowing doctors to use commonly available platforms like FaceTime, Facebook Messenger, Skype, and Zoom to provide medical care.

And Congress quickly passed the CARES Act, a $2 trillion aid package to fight Covid-19 that included sending $1,200 checks to individuals and families who were most vulnerable to job loss and other financial stressors.

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As a psychiatrist who treats opioid addiction and works at a minority-serving hospital, I am delighted by these long-sought changes. But I am also frustrated that they have happened so quickly. Frustrated because the U.S. has been facing an equally large and equally deadly problem racism for years and has done little to address it.

Black people are dying at alarming and disproportionate rates from Covid-19. In cities, the statistics are nothing short of tragic. In Chicago, for example, 70% of coronavirus deaths are among Black people, who make up only 30% of the citys population. A similar pattern is seen in other cities and counties across the country.

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Black and brown people have been seeking reparations to address the systemic injustices they have faced for decades. Yet there has never been an economic stimulus to address the impact of racism on health, quality of life, and advancement.

The countrys response to the new coronavirus does, however, suggest that we are taking steps toward addressing the damaging threat of racism.

First, though, we have to name it. Policy leaders across the country urged Trump to declare a national emergency because they understood the power of naming a crisis. In the same way, we need to declare that racism is a national emergency. It is a virus in the truest sense: a corrupting influence that spreads through communities and across the nation. Systemic racism has harmed and killed millions of Americans through its corruption of health care, criminal justice, and the economic marketplace.

Dr. Deborah Birx, who serves as the coronavirus response coordinator for the White House coronavirus task force, recently suggested that Black people are dying of Covid-19 at higher rates due to underlying medical conditions. She is right if she means that the underlying condition is racism, not its manifestations like high blood pressure and diabetes. Racism has created inequality in access to health care, housing, wealth, education, and employment, all of which undermine health. It is time to name racism as the crisis it is.

Second, we must shift policy to address the circumstances of those affected by the crisis. For Covid-19, that means finding unique ways to care for patients. To address racism, we must do that and go even further. We must not only come up with new ways to reach patients who have been disadvantaged but must also address the dire circumstances that racism has created.

The first time I ever used telehealth was after Covid-19 had emerged as a nationwide threat. My patient, who was homeless, had been sitting in a park all day, waiting for my call. He knew if we didnt connect, he would not be able to get the medication he needed to help him stay free from using heroin. He adjusted his life to meet health cares demands. Thats not the way health care should be it should meet patients where they are and address the circumstances they are in.

During that call, I didnt stick to my usual script: Any problems filling your prescription? Any medication side effects? Any cravings or heroin use since the last visit? Instead, I talked with him about the challenges he was facing at the shelter. He asked about how to manage his day since he couldnt stay inside. I also let him know where he could find a hot meal on a daily basis.

I wish our health care system would take a similar approach and see value in working on problems like housing and food insecurity. Some are calling this concept structurally competent care; it needs to become our new normal.

Third, we must deal with the economic consequences of the crisis. For Covid-19, thats the thrust of the CARES Act. In Boston, where I completed my medical training, the median net worth of white families was more than $200,000. The median net worth of black families was $8. Undoing racism means passing something like the CARES Act to provide funds for those disadvantaged by racism.

I respect Dr. Anthony Fauci, a key member of the White House coronavirus task force, who acknowledged the role of health disparities in Covid-19. He has said that we must deal with these issues once we get beyond the pandemic.

But I disagree with him on that. We must deal with them now.

Morgan Medlock, M.D., is an assistant professor of psychiatry at Howard University College of Medicine in Washington D.C. and the editor of Racism and Psychiatry: Contemporary Issues and Interventions (Springer, 2019)

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Covid-19 will pass. What about the racism it has illuminated? - STAT

TBTAK has invested TL 2.3 billion ($ 300 million) for the development of 16 vaccine and other medicine projects over the past five years in Turkey, the president of the Scientific and Technological Research Council of Turkey (TBTAK) said Saturday.

A platform consisting of 41 Turkish institutions has mobilized to develop medicines and vaccines against COVID-19 pandemic, professor Hasan Mandal noted, adding that efforts to develop anti-coronavirus drugs and vaccines were launched late December in coordination with the Ministry of Industry and Technology and proposals to be carried out within a 9 to 12 month period were taken into account and evaluated.

There are 16 projects working in synergy both in medicine and vaccine groups thanks to the COVID-19 Turkey Platform, which includes 225 researchers from 25 universities, eight public research bodies and eight private firms, Mandal added.

For medicine in pre-clinical phases, we'll be in the production phase this summer, probably much earlier. For vaccine, pre-clinical phase will be completed within a nine-month period, Mandal said. He added that it is now time for institutions cooperating with the science body to prove their valor.

The modeling of molecules in the medicine group began with the identification of over 10,026 molecules that could provide a solution for this virus, Mandal explained, adding synthesis works regarding this and its production are now underway.

In order to fight with a virus that you recently came across, you have to know it and define it correctly. All proceeding phases are tied to this. For that, it should be isolated from all external conditions and genetic characterization of the virus should be carried out. We will have genetic characterization of this virus determined next week. This situation shows the competence of this country. We now know this virus and this will be among the most important indicators how we will fight it both on the medicine side and vaccine side, Mandal said.

Link:

Turkey's top scientific body invests TL 2.3 billion on 16 vaccine projects over 5 years | Daily Sabah - Daily Sabah

In an article published inCancer Immunology Research, researchers suggested that immune suppression and increased infection could occur during the precancerous period.1

However, cancer can occur through a lifespan, therefore the authors indicated that further research is necessary to clarify these precancer trends.

"Cancer can develop in an inflammatory environment caused by infections, immunity disruption, exposure to chemical carcinogens, or chronic or genetic conditions,"co-author of the study Shinako Inaida, PhD, a visiting researcher at the Graduate School of Medicine at Kyoto University in Japan, said in a press release.2"An individual's immunity is thought to be a factor in the development of cancer, but additional research is needed to understand the relationship among precancerous immunity, infections, and cancer development.

In this 7-year case-control study of people 30 years of age, researchers looked to determine the prevalence of influenza, gastroenteritis, hepatitis, and pneumonia infections to indirectly assess whether infections correlated to the formation of malignant cancer. Using data extracted from a large medical claims database of a Japanese social health insurance system, researchers identified 2,354 people with their first cancer diagnosis occurring in the seventh year of the study for the case group and 48,395 people with no cancer diagnosis by the seventh year of the study for the control group.

The most common cancers diagnosed in the case group were digestive and gastrointestinal, head and neck, and stomach cancers. Other cancer types diagnosed in the case group included cancers within the following categories:

The yearly prevalence rates of influenza, gastroenteritis, hepatitis, and pneumonia infections were found to increase throughout the study period, with the case group experiencing higher rates of infection compared to the control group. Moreover, age-adjusted odds ratios (OR) and 95% confidence intervals (CI) in cases 1 year before cancer detection were significantly higher. During this year, the infection prevalence rates for the case group were higher than the control group by 18% for influenza (OR, 1.29; 95% CI, 1.14-1.46), 46.1% for gastroenteritis (OR. 1.60; 95% CI, 1.41-1.82), 232.1% for hepatitis (OR, 3.38; 95% CI, 2.12-5.37), and 135.9% for pneumonia (OR, 2.36; 95% CI, 1.79-3.13).

In patients with influenza infections, significant ORs were found only in the second and sixth years before cancer diagnosis. Further, for each cancer site, an increased rate of infection prior to cancer diagnosis was observed.

The researchers also found that certain infections appeared to have a greater correlation with specific cancer types. For example, the odds of influenza infection just before cancer detection were highest for those who developed male germ cell cancers. Additionally, the odds of pneumonia were found to be highest in those who later developed stomach cancer and the odds of hepatitis infection were highest in those who developed hematologic, blood, bone, or bone marrow cancers.

"Interestingly, we found that infection afflicting a specific organ did not necessarily correlate with increased risk of cancer in the same organ," Inaida explained.

Notably, the researchers only extracted the first cancer diagnosis for each patient and given that the observation period was limited to 8 years, further cancer diagnoses may have been missed. The data also did not include information such as the grade or stage of tumors, which may have been important to estimating each precancerous period.

Another limitation highlighted by the researchers was that patients with infection who did not visit the hospital may have been overlooked. Moreover, influenza vaccination status may prevent infection, although a patient's influenza vaccination record was not available in for this dataset.

Patients who feel unwell, potentially because of cancerous status, tend to see doctors more often, the authors wrote. Although our study considered four major infections, analysis of other infections and the timing of infection before malignant cancer detection, which can potentially be a factor for later cancer development, remains to be studied.

References:

1. Inaida S, Matsuno S. Previous Infection Positively Correlates to the Tumor Incidence Rate of Patients with Cancer.Cancer Immunology Research.doi:10.1158/2326-6066.CIR-19.0510.

2. Increased rate of infections may indicate a future cancer diagnosis [news release]. American Association for Cancer Research. Published April 17, 2020. eurekalert.org/pub_releases/2020-04/aafc-iro041520.php. Accessed April 17, 2020.

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Infection Rate May Indicate a Future Diagnosis of Cancer - Cancer Network

Social media posts attribute a list of points about the novel coronavirus to Johns Hopkins, a leading source of information on the virus. But the US universitys medical program said it is not the source of the claims, and while some are accurate, experts say others contain false or misleading information.

EYE-OPENING KNOWLEDGE FROM John Hopkins University, says one of the posts, variations of which have circulated on Facebook since at least March 23, 2020.

Others attribute the claims to Irene Ken, a physician whose daughter is an Asst. Prof in Infectious Disease at Johns Hopkins University, or to a Prof in infectious diseases at Johns Hopkins University, or to John Hopkins Hospital.

The points also appear on Reddit here and here, while versions have been posted on Instagram here, here and here.

Johns Hopkins is tracking the spread of COVID-19 -- the disease caused by the novel coronavirus -- providing statistics on deaths and infections as well as other information for both policymakers and the public, meaning its name lends authority to those who cite it.

But Johns Hopkins Medicine said it is not affiliated with the points circulating online, posting on its Facebook page that rumors and misinformation like this can easily circulate in communities during a crisis.

The rumors that we have seen in greater volumes are those citing a Johns Hopkins immunologist and infectious disease expert. We do not know the origin of these rumors and they lack credibility, it said.

And "we have no information" on whether Irene Ken or her daughter exist, a spokesperson for Johns Hopkins Medicine said.

Some of the points themselves are also problematic. AFP Fact Check breaks them down below.

Claim: The virus is not a living organism, but a protein molecule (DNA) covered by a protective layer of lipid (fat), which, when absorbed by the cells of the ocular, nasal or buccal mucosa, changes their genetic code. (mutation) and convert them into aggressor and multiplier cells.

Several parts of this description are false, experts say.

The coronavirus arrives as an RNA molecule that comes wrapped in lipid and protein -- the first point is complete nonsense as written, Dr. Benjamin Neuman, an expert in coronaviruses who chairs the Biological Sciences department at Texas A&M University-Texarkana, told AFP by email.

There are no aggressor or multiplier cells -- not sure what that might even be referring to, he said.

Dr. Julian Leibowitz, an expert in coronaviruses who is a professor of microbial pathogenesis and immunology at Texas A&M's College of Medicine, agreed.

This is not true on many levels. The virus is an RNA virus, it contains no DNA, and its RNA genome is encased in a protein and is then enveloped by a lipid bilayer that contains several viral proteins, he said by email.

When the virus infects cells the virus RNA expresses its genes, it does NOT mutate the genes of the host to convert them into aggressor and multiplier cells, Leibowitz said.

Claim: Since the virus is not a living organism but a protein molecule, it is not killed, but decays on its own. The disintegration time depends on the temperature, humidity and type of material where it lies.

This point is accurate, according to Dr. Wendy Keitel, professor of molecular virology and microbiology at Baylor College of Medicine.

As mentioned, the decay or loss of the viruses ability to infect does depend on temperature, humidity and the type of material where it lies, she said by email.

Claim: The virus is very fragile; the only thing that protects it is a thin outer layer of fat. That is why any soap or detergent is the best remedy, because the foam CUTS the FAT (that is why you have to rub so much: for 20 seconds or more, to make a lot of foam). By dissolving the fat layer, the protein molecule disperses and breaks down on its own.

Some viruses are very fragile; others are not fragile at all, said Keitel, with coronaviruses being significantly less stable than smallpox, for example.

Soap or detergent is a very effective way to help remove viruses from hands, she said, but while the detergent is important for removing soil and may have some effect on inactivation of the virus, the major effects are friction (rubbing the surfaces) and rinsing off the viruses.

Claim: HEAT melts fat; this is why it is so good to use water above 77 degrees Fahrenheit for washing hands, clothes and everything. In addition, hot water makes more foam and that makes it even more useful.

This point is misleading; while the virus is sensitive to heat, Keitel said that it is likely that a temperature high enough to inactivate coronavirus would be too hot for handwashing.

Hands can be washed in warm or cold water as long as the use of soap and the duration of cleansing is at least 20 seconds, she said.

Neumen said that there are proteins in the coronavirus that do indeed denature with heat, but the virus is used to growing in human lungs and intestines, and it is stable up to temperatures a little above 100 degrees F.

He also highlighted issues with the points information about heat melting fat.

There are fats that melt at different temperatures -- for example, bacteria that live in methane ice and bacteria that live on the rims of... deep ocean volcanoes both have membranes made of lipid molecules (what this person is calling fat), but they have very different melting points, Neuman said.

Claim: Alcohol or any mixture with alcohol over 65% DISSOLVES ANY FAT, especially the external lipid layer of the virus.

This is not too far off from reality, Neuman said.

Keitel agreed: Alcohol is believed to destroy the essential viral proteins and may disrupt the lipid (fatty) layer that is part of the coat.

Claim: Any mix with 1 part bleach and 5 parts water directly dissolves the protein, breaks it down from the inside.

This is true, but excessive, according to Neuman.

A standard store-bought hypochlorite bleach will indeed kill the virus, but it works at half the specified concentration, he said.

Claim: Oxygenated water helps long after soap, alcohol and chlorine, because peroxide dissolves the virus protein, but you have to use it pure and it hurts your skin.

This is false.

The amount of oxygen dissolved in water would have very little effect on the virus. This suggests some kind of sham medical product to oxygenate water for health benefits, Neuman said.

Leibowitz agreed: Oxygenated water does not generate hydrogen peroxide and alcohol kills the virus after one minute of exposure.

Claim: NO BACTERICIDE OR ANTIBIOTIC WORKS. The virus is not a living organism like bacteria; antibiotics cannot kill what is not alive.

This is true, unless it is a product also aimed at viruses.

Many products are both bactericidal and virucidal (destroying both, physically), but it is correct that a specific bactericide would not be effective, according to Neuman.

Antibiotics generally do not inactivate viruses; hence, treatment of a viral infection with a common antibiotic would not be expected to inactivate the virus, and it could cause harmful side effects, Keitel said, while also noting that a number of disinfecting chemicals have both antibacterial and antiviral activities.

Claim: NEVER shake used or unused clothing, sheets or cloth. While the virus is glued to a porous surface, it is very inert and disintegrates between 3 hours (fabric and porous), 4 hours (copper and wood), 24 hours (cardboard), 42 hours (metal) and 72 hours (plastic). But if you shake it or use a feather duster, the virus molecules float in the air for up to 3 hours, and can lodge in your nose.

The recommendation is accurateif the items in question are contaminated with the virus.

The current public health recommendations at this time are to avoid shaking contaminated materials due to the theoretical possibility that the contaminated surfaces could release infectious material, said Keitel.

If your feather duster is covered in large amounts of SARS-CoV-2, then I would agree -- don't shake it. Otherwise, it's fine to dust as usual, Neuman said, using the official name for the novel coronavirus.

And Leibowitz said that the numbers mentioned in this point are not quite right.

The virus can survive for at least 8 days on metal (steel) or hard plastic at room temperature but the relative survival on cardboard, paper, or fabric is relatively short and about 3 hours is the number I have seen, he said.

Claim: The virus molecules remain very stable in external cold, or artificial as air conditioners in houses and cars. It also needs moisture to stay stable, and especially darkness. Therefore, dehumidified, dry, warm and bright environments will degrade it faster.

Neuman said the virus does not do well in any of the environments mentioned.

It remains stable almost indefinitely in a specialized -80 degree Celsius freezer, but tends to fall apart eventually at any higher temperature including a regular -20 degree Celsius home freezer, he said.

And according to Leibowitz, the relationship between humidity and virus survival shows that it is less stable at both high and very low humidity but it was most stable at 20% humidity, which is actually pretty low. Cold increases survival time.

Claim: UV LIGHT on any object that may contain it and break down the virus protein. For example, to disinfect and reuse a mask is perfect. Be careful, it also breaks down collagen (which is protein) in the skin.

UV light can inactivate viruses, but Keitel said it is not recommended for the general public to use this method.

At this time it is not recommended for non-medical personnel to attempt to use UV light to inactivate viruses for the purpose of disinfection of face masks. Cloth masks should be washed frequently in hot soapy water and dried in a drier, Keitel said.

As for the effect of UV on the virus, Neuman said that it crosslinks nucleotides in the virus RNA -- it can damage protein as well, but that is the mechanism of inactivation.

Keitel said that UV light has multiple potential ways of inactivating viruses, including effects on the proteins and on the genetic material.

AFP Fact Check has addressed the topic of using UV light against the novel coronavirus here.

Claim: The virus CANNOT go through healthy skin.

This is true but the reasoning is off, according to Neuman. There aren't any cells with the viral receptor in skin, healthy or unhealthy, so it would not be able to infect.

Keitel said that at this time there is no evidence that this coronavirus can go through healthy skin, and that injury to the skin is required in order for many viruses to gain entry through the skin.

Claim: Vinegar is NOT useful because it does not break down the protective layer of fat.

It is accurate that vinegar is not recommended, but that this is because there is no data to support the claim that it works, and it can be harmful to surfaces, Keitel said.

Claim: NO SPIRITS, NOR VODKA, work. The strongest vodka is 40% alcohol, and you need 65%. Edit: there are a few alcohols more than 65%, and Vodka does come in 50%, but still not strong enough to kill the virus.

This is generally correct, but there is at least one vodka that is 96% ethanol, and would be OK, according to Neuman.

The use of spirits for disinfection is not recommended and has not been studied. Consumption of alcohol for this purpose is discouraged, Keitel said.

Claim: LISTERINE WORKS! It is 65% alcohol.

This is false: Listerine is only 27% ethanol, and would not work reliably, Neuman said.

First, it has not been tested against the coronavirus. Second, not all Listerine contains alcohol. Third, the alcohol content does not exceed about 20%, significantly lower than the recommended concentration for disinfection purposes, said Keitel.

And Listerine does not contact all surfaces where the virus may be located (e.g., nasal, lower respiratory tract), she said.

Claim: The more confined the space, the more concentration of the virus there can be. The more open or naturally ventilated, the less.

This is true, but distance between individuals is much more important. The virus spreads mostly by small droplets (about 10 microns diameter) generated from coughs and sneezes and they do not stay in the air very long and mostly settle out of the air after traveling less than 6 feet, said Leibowitz.

Neuman said: The size of the space doesn't matter so much -- it is a case of whether the virus is in it. Most buildings would have HEPA-filtered air, which is designed to catch coronavirus-sized particles and remove them from what we breathe.

Claim: You have to wash your hands before and after touching mucosa, food, locks, knobs, switches, remote control, cell phone, watches, computers, desks, TV, etc. And when using the bathroom.

This is a harmless and a reasonable idea, Neuman said, while Keitel said that it is recommended to do so after touching potentially contaminated surfaces.

Claim: You have to Moisturize dry hands from so much washing them, because the molecules can hide in the micro cracks. The thicker the moisturizer, the better.

According to Neuman, you most certainly do not have to moisturize, but if you find it more comfortable, you can. It has no bearing on the virus, and is certainly not protective in the way mentioned here.

And Leibowitz said that you may want to moisturize your hands from lots of hand washing but the virus doesnt hide in the cracks.

Claim: Also keep your NAILS SHORT so that the virus does not hide there.

This is not a game of peek-a-boo -- you are unlikely to get respiratory droplets under your fingernails, and even if you did, the virus is unlikely to go from under your fingernails onto your mucosal membranes, Neuman said.

Leibowitz agreed, saying: This virus is spread by the respiratory route and nail length has nothing to do with this.

AFP Fact Check has debunked more than 350 examples of false or misleading information about the novel coronavirus crisis. A complete list of our fact checks on the topic in English can be found here.

See the article here:

Misleading coronavirus information falsely attributed to Johns Hopkins - AFP Factcheck

Newswise Irvine, CA April 22, 2020 A new study explains how cocaine modifies functions in the brain revealing a potential target for therapies aimed at treating cocaine addiction. The study was published this week in Cell Reports.

Researchers from the University of California, Irvine have demonstrated that a key receptor for dopamine, called D2 (D2R), intervenes in the mechanism through which cocaine modifies functions in the striatum, a region of the brain responsible for the psychomotor and rewarding effects of drugs like cocaine, directly involved in the process of addiction.

In our study, we show that D2R signaling over cholinergic interneurons (ChIs) and acetylcholine (Ach) release exerts a major control in the striatum, which is required for the normal functioning of striatal circuits, said Emiliana Borrelli, PhD, a professor of microbiology and molecular genetics, pharmaceutical sciences, and member of the Center for Epigenetics and Metabolism at the UCI School of Medicine.

Cocaine use drastically elevates dopamine levels in the striatum, and causes the dopamine D2 receptor (D2R) to inhibit striatal acetylcholine signaling, resulting in cocaine-induced changes in behavior and the striatal genomic response, said Borrelli. By genetic ablation of D2R in cholinergic interneurons, we disrupt the dopamine-mediated inhibition of these neurons and reduce the addictive effects of drugs like cocaine.

The study indicates that D2R activation in cholinergic interneurons is indeed central to the control of striatal neuronal circuits and significantly affects the motor and cellular responses to cocaine.

Our study emphasizes the importance of the dopaminergic control on striatal responses to psychostimulants and may pave the way for future therapeutic strategies to treat substance use disorders, said Borrelli.

Cocaine is a psychomotor stimulant that when ingested stimulates the central nervous system increasing motor activity and producing euphoria, excitement, and a feeling of reward. Understanding how psychomotor stimulants modify striatal functions is critical to fighting addiction to this drug.

According to the American Addiction Centers, nearly a million American adults (over age 12) struggled with a cocaine use disorder in 2017. The Foundation for a Drug Free World, states cocaine is one of the most dangerous drugs known to man. Once a person begins taking the drug, it has proven almost impossible to become free of its grip physically and mentally. Physically it stimulates key receptors (at nerve endings that sense changes in the body) within the brain that, in turn, create a sense of well-being to which users quickly develop a tolerance. Only higher dosages and more frequent use can bring about the same effect.

This research was supported by funds from the Institut de la Sant et de la Recherche Medicale (INSERM). First author, PhD student R.G. Lewis, received support from a UCI School of Medicine Deans Fellowship and the Dr. Lorna Carlin Scholar Award.

About the UCI School of Medicine

Each year, the UCI School of Medicine educates more than 400 medical students, and nearly 150 doctoral and masters students. More than 700 residents and fellows are trained at UCI Medical Center and affiliated institutions. The School of Medicine offers an MD; a dual MD/PhD medical scientist training program; and PhDs and masters degrees in anatomy and neurobiology, biomedical sciences, genetic counseling, epidemiology, environmental health sciences, pathology, pharmacology, physiology and biophysics, and translational sciences. Medical students also may pursue an MD/MBA, an MD/masters in public health, or an MD/masters degree through one of three mission-based programs: the Health Education to Advance Leaders in Integrative Medicine (HEAL-IM), the Leadership Education to Advance Diversity-African, Black and Caribbean (LEAD-ABC), and the Program in Medical Education for the Latino Community (PRIME-LC). The UCI School of Medicine is accredited by the Liaison Committee on Medical Accreditation and ranks among the top 50 nationwide for research. For more information, visit som.uci.edu.

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New study could lead to therapeutic interventions to treat cocaine addiction - Newswise

As many people yearn to return to some form of normalcy, states are beginning to consider what the reopening of nonessential businesses should look like. In his daily press briefing Gov. Andrew Cuomo (D-N.Y.) said a crucial first step for reopening is widespread COVID-19 testing which New York State currently lacks.

On that same day, Dr. Augustine M.K. Choi, Weill Cornell Dean, announced a new initiative to begin antibody testing employees of Weill Cornell.

Current testing efforts across the state are focused on detecting those with the SARS-CoV-2 virus, but in order to begin reopening businesses people must be tested for previous exposure to the virus.

The current diagnostic used to test patients suspected of having COVID-19 at WCM is a real time reverse transcription polymerase chain reaction, an effective and relatively fast method to detect genetic material. It can be used to detect the RNA present in the SARS-CoV-2 virus.

PCR is the gold standard because its such a highly sensitive and specific test and can deliver reliable and accurate diagnosis in as fast as 2-5 hours. Compared to other available platforms its much faster and more accurate, said Dr. Melissa Cushing, pathology, in Chois update.

However, as institutions begin to test for people who were exposed to the virus and recovered, another method is required antibody testing. Instead of testing for the genetic material of the virus itself, antibody tests search for the antibodies that the body creates in response to COVID-19. These antibodies are formed between three and 15 days after experiencing symptoms, according to Cushing.

As of April 17, testing was made available for New York Presbyterian staff that tested positive for COVID-19 or had a COVID-19-like illness and returned to work.

WCM plans to make more testing available to its staff, as it works to increase its testing capabilities. Cushing predicted that this public testing is at least several weeks away. Experiencing the brunt of statewide shortages of certain materials, WCM also requires access to reagents and more high output platforms to increase its testing capabilities.

We need to really scale up with the amount of reagents we have with our current tests. Then we are really looking to some of the commercial labs to provide the large, high frequency platforms that we already use in our labs so that the process can be much more automated, Cushing said. That is our goal to be testing as many people that need to be tested in our city.

In order to address the testing insufficiencies on a statewide level, the governor issued an executive order on April 17 that directs all public and private labs capable of conducting virology testing to coordinate with the State Department of Health to prioritize coronavirus testing.

The testing and tracing is the guideposts through this. As we are working our way through the next several months the testing, which is informing us as to who can go back to work helping us isolate people, its about testing, Cuomo said in his daily briefing on April 17. Testing is a totally new challenge. Nobody has done this and what we need to do on testing.

According to Cuomo, the lack of infrastructure to facilitate widespread testing mirrors the earlier lack of coordination between hospitals, which the Surge and Flex initiative addressed the initiative coordinated the distribution of scarce medical supplies between public and private hospitals across the state.

Besides the lack of infrastructure, another impasse to wide scale testing is the availability of the materials specifically chemical reagents necessary to run the tests.

Currently, this order will not affect the labs on Cornells Ithaca campus.

Cornell University is not offering any human testing for COVID-19 on campus at this point. We will always follow all state/federal government regulations as appropriate, John Carberry, a University spokesperson, wrote in a statement to The Sun.

Cornell is affiliated with two of the 301 laboratories and hospitals capable of performing viral testing the Allyn B Ley Clinical Laboratory housed in Cornell Health and the Hospital for Special Surgery Dept of Pathology and Laboratory Medicine in New York City.

Initially, 28 laboratories with clinical laboratory permits from the state health department and experience in molecular-based virology could conduct testing. However, this system is unable to meet the demand for the widespread testing needed to reopen New York State.

We dont have a testing system that can do this volume, or that can be ramped up to do this volume. We dont have a public health testing system, its de minimis if you look at what our government department of health have, Cuomo said.

The state has begun its efforts to perform antibody tests on 3,000 individuals to better understand what percentage of the population is currently immune to the virus. The plan is being supported financially by former New York City mayor Michael Bloomberg, who pledged more than $10 million to create a test and trace program.

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As Cuomo Issues New Executive Order, Weill Cornell Medicine Ramps Up COVID-19 Testing - Cornell University The Cornell Daily Sun

Administrative affairs | For UW employees | Honors and awards | News releases | UW and the community

April 23, 2020

Three University of Washington faculty members, including President Ana Mari Cauce, are among the 2020 fellows of the American Academy of Arts and Sciences, one of the nations oldest and most prestigious honorary societies. Trisha Davis, professor and chair of biochemistry at the UW School of Medicine, and Tatiana Toro, the Craig McKibben and Sarah Merner Professor of Mathematics, are also among the 276 artists, scholars, scientists, and leaders in the public, non-profit and private sectors who were announced as new fellows Thursday.

We congratulate these incoming members of the Academy for excelling in a broad array of fields; we want to celebrate them and learn from them, said Nancy C. Andrews, chair of the Board of Directors of the American Academy. When Academy members come together, bringing their expertise and insights to our work, they help develop new insights and potential solutions for some of the most complex challenges we face.

Cauce who was named to the Educational and Academic Leadership section of the Academys Public Affairs, Business and Administration class became the 33rd president of the UW on Oct. 13, 2015 after serving as interim president for seven months and having previously served as provost and executive vice president.

Throughout her career, Cauce has championed access to higher education, including through the Husky Promise, which provides full tuition to eligible Washington students who otherwise could not attend college. As part of her strong belief in ensuring access to higher education for all, just one month into her role as interim president she engaged students in an honest discussion about race and equity, launching an effort to create a more just and diverse community.

Cauce is a professor of Psychology and American Ethnic Studies, with secondary appointments in the Department of Gender, Women and Sexuality Studies and the College of Education. She maintains an active research program, focusing on adolescent development, with a special emphasis on at-risk youth. She is also a strong advocate for women and underrepresented minorities to pursue careers in science, technology, engineering and mathematics.

Davis was named to the Cellular and Developmental Biology (including Genetics), Microbiology and Immunology Section of the Biological Sciences Class of the Academy. Davis and her colleagues explore the dynamics of the chromosome capture that occurs in preparation for cell division.

Impressive molecular machinery tries to assure that each cell resulting from the split receives a proper set of chromosomes. Mistakes in sorting, separating and distributing the chromosomes could cause serious problems, such as cancer. Davis team looks at how the movement and segregation of chromosomes is orchestrated. This chromosome assembly is trial and error, but cells usually can find and fix mistakes. As chromosomes attach to the separation machinery, checkpoints tune into to the connection and the tension it produces. If this quality assurance detects that a chromosome is incorrectly captured, it is released for another try.

The Davis lab uses many ways of examining this and related controls. These include genetic analysis, proteomics, quantitative microscopy, computational modeling and biochemical assays.

Davis holds the Earl W. Davie/ZymoGenetics Chair in Biochemistry at UW Medicine. She also heads the UWs Yeast Resource Center, funded by the National Institutes of Health to develop technologies for exploring protein structure and function.

Toro was named to the Mathematics, Applied Mathematics and Statistics section of the Academys Mathematical and Physical Sciences class. Her research centers on the premise that objects, which may at first appear irregular or disordered, actually have regular features that are quantifiable. Toros work spans geometric measure theory, harmonic analysis and partial differential equations. Toro studies the mathematical questions that come up in systems where the known data are rough, as well as interfaces that arise in noisy minimization problems.

In addition to her research, Toro has also worked to increase diversity in mathematics. She helped launch Latinx in the Mathematical Sciences, including two conferences through the National Science Foundation highlighting the achievements of Latinx mathematicians.

Toro joined the UW faculty in 1996 and her career includes numerous honors and accolades. Last year, she received the UWs Marsha L. Landolt Distinguished Graduate Mentor Award. In 2017, she was elected as a Fellow of the American Mathematical Society. Toro has also been a Guggenheim Fellow, an Alfred P. Sloan Research Fellow and a Simons Foundation Fellow.

Founded in 1780, the American Academy of Arts and Sciences is one of the countrys oldest learned societies and independent policy research centers, convening leaders from the academic, business and government sectors to respond to the challenges facing the nation and the world.

The new members join the company of Academy members elected before them, including Benjamin Franklin and Alexander Hamilton in the eighteenth century; Ralph Waldo Emerson and Maria Mitchell in the nineteenth; and Robert Frost, Martha Graham, Margaret Mead, Milton Friedman, and Martin Luther King, Jr. in the twentieth.

Learn more about the Academys mission, members, and work on its website amacad.org.

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