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Study shows asthma drug salbutamol’s potential as Alzheimer’s treatment

A new study reveals that the common asthma drug salbutamol may offer potential as a treatment for Alzheimer’s disease.

Alzheimer’s disease is the most common form of dementia, affecting 47 million people worldwide and its prevalence is expected to triple to more than 130 million cases by 2050.

No effective treatments that cure the disease or slow down its progression have been discovered. However, this new early-stage study has revealed that repurposing an existing drug, salbutamol, offers significant potential as a low cost and rapid response option.

Extensive analytical in-vitro experiments conducted by the research team show that salbutamol is effective at reducing the accumulation of insoluble fibers of the tau protein—which is found in the brains of people with Alzheimer’s disease. These microscopic fibers accumulate into neurofibrillary tangles and can cause neuron destabilization, brain cell death, and are a key characteristic of the disease’s progression.

Much Alzheimer’s disease research has focused on the build-up of amyloid plaques, caused by misfolding of the amyloid-β protein. However, because of disappointing results from numerous therapies targeting Aβ aggregation, more attention is shifting towards tau.

This study, led by researchers at Lancaster University, used a new automated ‘high throughput’ screening approach to study the structure of the misfolding tau protein with a special analytical technique called ‘Synchrotron Radiation Circular Dichroism’ (SRCD) at Diamond Light Source, the UK national synchrotron light source in Oxfordshire. With this powerful technique they were able to look at a selection of more than 80 existing compounds and drugs simultaneously to determine their effectiveness at preventing the formation of tau fibrils.

This method confirmed the compound epinephrine, more commonly known as adrenaline, was effective at stabilizing the tau proteins and preventing the formation of tau tangles. However, our bodies do not easily absorb epinephrine and it rapidly gets metabolized, so the scientists then looked at a range of readily available compounds with similar chemical structures. This search revealed four current drugs as possible candidates—etamivan, fenoterol, dobutamine and salbutamol.

Etaminvan and fenoterol were found to have little effect on the assembly of tau tangles. Dobutamine, which is used for the rapid treatment of heart attacks and heart failure, was found to have some benefit. However, because its effects are very short-lived, and because it needs to be administered intravenously, it is not ideal as a basis for treatment of Alzheimer’s disease.

Further tests using a range of analytical techniques all revealed salbutamol could inhibit tau aggregation in vitro. Tests where salbutamol was added to solutions containing tau resulted in drastically reduced density of fibrous tau structures responsible for the tau neurofibrillary tangles.

The researchers believe that salbutamol interacts with an early stage of tau fibril formation, reducing their ability to form an initial nucleus which drives the aggregation process.

Because it is easily ingested, absorbed into the brain, and remains in the body for several hours, salbutamol has attractive properties as a research avenue for potential new treatment for Alzheimer’s.

Dr. David Townsend, of Lancaster University and lead author of the research, said: “Our work highlights the potential impact of repurposing drugs for secondary medical uses, by discovering a novel therapeutic strategy that impedes the molecular pathology of Alzheimer’s disease, and which may have otherwise gone unstudied.

“Salbutamol has already undergone extensive human safety reviews, and if follow up research reveals an ability to impede Alzheimer’s disease progression in cellular and animal models, this drug could offer a step forward, whilst drastically reducing the cost and time associated with typical drug development.”

Professor David Middleton, co-author of the research, said: “This work is in the very early stages and we are some way from knowing whether or not salbutamol will be effective at treating Alzheimer’s disease in human patients. However, our results justify further testing of salbutamol, and similar drugs, in animal models of the disease and eventually, if successful, in clinical trials.”

Dr. Rohanah Hussain, of Diamond Light Source, Senior Beamline Scientist and co-author said: “Diamond B23 beamline unique micro-collimated beam has made high throughput CD possible allowing the screening of many compounds through structural activity correlation crucial in drug discovery.”

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Pfizer's coronavirus shot shows promise by triggering immune response

Experimental coronavirus vaccine from Pfizer triggered levels of antibodies up to THREE TIMES greater than those seen in recovered patients, early data shows

  • Researchers randomly gave 45 healthy volunteers either a low dose, a medium dose or a high dose of a coronavirus vaccine, or a placebo
  • Those who received the vaccine were given two shots, except the high dose group after half developed fever
  • The vaccine generated levels of neutralizing antibodies between 1.8 and 2.8 times greater than those seen in recovered patients 
  • No life-threatening side effects were seen and Pfizer hopes to start a large-scale human trial later this summer 

An experimental coronavirus vaccine being tested by Pfizer Inc and its German partner BioNTech showed encouraging early results, the companies announced on Wednesday.

The trial recruited 45 people, who received either a low, medium or high dose of the vaccine in two shots or a placebo.    

Volunteers given either the low or medium dose had immune responses in the range expected to be protective, when compared to COVID-19 survivors, according to the preliminary findings.

The results, which were published on pre-print site medRxiv.org, have been submitted for publication in a scientific journal, but have not yet been peer-reviewed.    

Researchers randomly gave 45 healthy volunteers either a low dose, a medium dose or a high dose of a coronavirus vaccine, or a placebo. Pictured: The first patient enrolled in Pfizer’s COVID-19 vaccine clinical trial at the University of Maryland School of Medicine in Baltimore receives an injection, May 4

Those who received either two shots of the low or medium dose of the vaccine generated levels of neutralizing antibodies between 1.8 and 2.8 times greater than those seen in recovered patients (above)

‘We still have a ways to go and we’re testing other candidates as well,’ Philip Dormitzer, chief scientific officer for viral vaccines at Pfizer’s research laboratories, told STAT News. 

‘However, what we can say at this point is there is a viable candidate based on immunogenicity and early tolerability safety data.’ 

The vaccine candidate from Pfizer and Biotech uses part of the pathogen’s genetic code to get the body to recognize the coronavirus and attack it if a person becomes infected. 

For the study, three groups of 12 received either a 10-microgram dose, a 30-microgram dose or a 100-microgram dose. Nine were given a placebo.

The highest dose shot caused fevers in about half of the group, so a second shot wasn’t given.

Three weeks later, participants were given a second dose. Following that, 8.3 percent of the 10-microgram group and 75 percent of the 30-microgram reported fevers.  

However, these side effects did not result in hospitalization, nor were considered life-threatening, and resolved after about one day.  

The immunization generated not just antibodies against the virus but specifically neutralizing antibodies, meaning they stop the virus from infecting human cells.

Results showed the levels of neutralizing antibodies were between 1.8 and 2.8 times greater than those seen in recovered patients. 

Volunteers who received one 100-microgram dose had lower levels of antibodies than those who were given two shots of the low or medium dose. 

Following news of the preliminary results, shares of Pfizer rose by four percent on Wednesday.

The US pharmaceutical giant hopes to begin a large-scale trial this summer, but did not specify which jab it would be testing. 

Around 200 vaccines are being developed around  the world with more than 15 currently in later-stage human trials such as AztraZeneca in partnership with Oxford University, Inovio and Moderna.

A number of pharmaceutical companies are expected to begin human trials later this summer including Johnson & Johnson, Merck and Sanofi.  

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Designing anew: Radical COVID-19 drug development approach shows promise

Nearly every drug that is, or has ever been, used was derived from nature—harnessing compounds created by organisms over eons to fight diseases. But decades ago, biochemists postulated that it might be possible to design a new drug from scratch by linking up amino acids in precise ways.

The tricky part, as it turned out, was predicting in advance how the amino acids in a protein would fold. The folded form determines the three-dimensional shape of the protein, as well as its electrostatic potential, and hydrophobicity (the degree to which a molecule is repelled from a mass of water)—factors that are critical when it comes to designing an effective drug.

David Baker, professor of Biochemistry at the University of Washington and head of the Institute for Protein Design there, pioneered methods for using computers to predict how proteins fold. Based on that knowledge, he and his team have designed new, never-before-seen proteins for use as drugs, sensors, or even biological logic gates.

This approach is known as de novo protein design. There are currently only a few drugs in trial that have used this approach, but it holds incredible potential—and at no time has such an approach been more critical than now.

The platform that the Institute for Protein Design developed allows for the rapid design of protein binders to target proteins of interest. Computer (in silico) simulations generate a library of candidate protein sequences that are then tested at their in-house testing facility. Promising candidates are evolved both in silico and in the wet lab until a final binding protein is created.

Starting in January, researchers in the Baker Lab began have been using their methodology to design a drug or vaccine to treat COVID-19. Their studies involve calculating the three-dimensional shape of millions of possible proteins, and then computationally testing how such proteins would fit into, and dock with, parts of the SARS-CoV-2 virus.

To assist in this effort, they are using the Stampede2 supercomputer at the Texas Advanced Computing Center (TACC)—one of the fastest in the world—as well as the network of volunteer computers known as [email protected] (Rosetta is the name of the software developed in the Baker Lab to predict protein folding and to design new proteins.)

“In just a two-month span, our team has been able to computationally design millions of protein therapeutics that target the seven major proteins related to COVID-19,” Baker reported in March.

To date, 733,000 proteins have been ordered, 323,000 of these protein therapeutics have been tested in the laboratory, and more than 2,000 have shown binding signals to their respective targets.

From Scaffolds to Protein Structures

The team began by testing its collection of 20,000 scaffold proteins that form the starting point for future drugs or vaccines. Each can be docked in over 1,000 orientations; and each dock is subsampled 1,000 times with slight perturbations—leading to 20 billion potential interactions to compute.

“In the scaffold phase, we’re looking for signs these are going to be atomically accurate,” said Brian Coventry, a Ph.D. student in the group working on the project. “If we’re off by 0.1 nanometers, there’s no way it will work. These things have to be perfect.”

The top 1 million of these docks then move forward to sequence design where each position on the scaffold backbone must be assigned an amino acid. With 20 amino acid choices at each position, and a variety of conformations for each, the computer must solve the combinatorial explosion to assign the best combination of amino acids to each scaffold.

From the 1 million designed proteins, they determine the most promising subset—roughly 100,000 proteins. The team sends a text file containing DNA sequences for these candidates to Agilent, a company that can create synthetic DNA molecules on demand. Agilent returns test tubes with physical DNA, which is then inserted into yeast genomes in such a way that the various synthetic proteins are made and displayed on tethers from the cell membrane of yeast, allowing them to be tested against the virus.

Based on the initial computational and experimental results, the team then engages in site saturation mutagenesis, where each individual amino acid on the chain is mutated at every location and re-tested to see how it behaves.

“We get data back and look at what made a given protein better or worse. And we ask the question: ‘Does this protein look like it’s working for the right reasons?'” Coventry said.

Based on the results and insights from the mutagenesis, they go one step further and develop a combo library that includes degenerate codons, where alternate nucleotides replace the typical ones in a given amino acid.

The best combination of mutations and replacements undergo further experimental testing including bacterial expression and thermodynamic analysis. Using this method, they derived 50 highly promising leads for the spike protein binder from an initial screening of 100,000 proteins.

“The spike protein binder is the most likely to result in a drug because of its mechanism of action,” Coventry said.

But the ability to create designer proteins is not the lab’s only innovation, nor is a single binder their final goal. They are also pioneering a new approach to drugs called mini-protein binders that combine the specificity of antibodies with the high stability and manufacturability of small molecule drugs.

Mini-protein binders have been shown to have much greater stability at elevated temperatures and better neutralization than comparable antibodies and natural protein derivatives. They are also approximately 1/30th of the molecular weight of typical proteins, and can be synthesized chemically, which enables the introduction of a wide variety of functionalities. Probably as a result of their small size and very high stability, they elicit little immune response.

“We aim to connect four to six of the most potent neutralizers in a single chain by flexible linkers to achieve highly avid binding with little potential for escape,” Baker said in a presentation to the Defense Advanced Research Projects Agency (DARPA), one of the funders of the research.

“We try to get many binders and connect them with linkers,” Coventry explained further. “The idea is that you get an avidity effect”—the accumulated strength of multiple affinities. “At least one of those proteins will be binding at any given time and the virus particle won’t be able to escape the chain. Since the binders block the viral binding epitope, the virus will not be able to enter our cells.”

Building on Collaborations

TACC is currently supporting more than 40 COVID-19 research projects. The one from the Baker Lab has been among the largest users of compute time on Stampede2 since it began in March.

“TACC has a lot of computing power and that has been really helpful for us,” Coventry said. “Everything we do is purely parallel. We’re able to rapidly test 20 million different designs and the calculations don’t need to talk to each other.” This type of approach, known as high-throughput screening, is a good fit for Stampede2’s architecture.

Baker and his team were able to ramp up quickly on TACC resources in part because of their involvement in an ongoing DARPA-funded program known as the Synergistic Discovery and Design (SD2), a multi-institution collaboration whose goal is to develop data-driven methods to accelerate scientific discovery.

Since 2017, the SD2 program has been developing pipelines to “design-test-learn” faster, using a combination of high-performance computing, advanced data management practices, automated laboratory testing, and machine learning. The collaboration between the Baker Lab and TACC is emblematic of that methodology and is helping to accelerate their research from idea to reality.

According to Dr. Matthew Vaughn, Director of Life Sciences Computing at TACC, the protein design project appears poised to yield powerful new therapeutic molecules for the fight against COVID-19 due in part to the remarkable synergy between computational simulation and experimentation.

“The rapid pace at which the Baker lab has been able to onboard and become productive on a leadership-class resource like Stampede 2 reinforces just how critical our national investments in advanced computing capability and methodology have been and will continue to be in the future,” Vaughn said.

The team’s next milestone will be to develop multiple inhibitors that can reduce the response by half and that can be linked those together into a big molecule, or construct, that is well behaved.

Further testing to establish whether the mini-binder provokes an immune response would follow, and then the construct would be tested for efficacy in a petri dish, then in animals and humans.

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Anti-inflammatory coatings might reduce complications after implant surgery, study shows

New coatings on implants could help make them more tissue compatible. Researchers at the Martin Luther University Halle-Wittenberg (MLU) have developed a new method of applying anti-inflammatory substances to implants in order to inhibit undesirable inflammatory reactions in the body. Their study was recently published in the International Journal of Molecular Sciences.

Implants, such as pacemakers or insulin pumps, are a regular part of modern medicine. However, it is not uncommon for complications to arise after implantation. The immune system identifies the implant as a foreign body and attempts to remove it. “This is actually a completely natural and useful reaction by the immune system,” says Professor Thomas Groth, a biophysicist at MLU. It helps to heal wounds and kills harmful pathogens. If this reaction does not subside on its own after a few weeks, it can lead to chronic inflammation and more serious complications.

“The immune system attracts various cells that try to isolate or remove the foreign entity. These include macrophages, a type of phagocyte, and other types of white blood cells and connective tissue cells,” explains Groth. Implants can become encapsulated by connective tissue, which can be very painful for those affected. In addition, the implant is no longer able to function properly. Drugs that suppress the immune response in a systemic manner are often used to treat chronic inflammation, but may have undesired side effects.

Thomas Groth’s team was looking for a simple way to modify the immune system’s response to an implant in advance. “This is kind of tricky, because we obviously do not want to completely turn off the immune system as its processes are vital for healing wounds and killing pathogens. So, in fact we only wanted to modulate it,” says the researcher. To do this, his team developed a new coating for implants that contains anti-inflammatory substances. For their new study, the team used two substances that are already known to have an anti-inflammatory effect: heparin and hyaluronic acid.

In the laboratory, the scientists treated a surface with the two substances by applying a layer that was only a few nanometres thick. “The layer is so thin that it does not affect how the implant functions. However, it must contain enough active substance to control the reaction of the immune system until the inflammatory reaction has subsided,” adds Groth. In cell experiments, the researchers observed how the two substances were absorbed by the macrophages, thereby reducing inflammation in the cell cultures. The untreated cells showed clear signs of a pronounced inflammatory reaction. This is because the active substances inside the macrophages interfere with a specific signaling pathway that is crucial for the immune response and cell death. “Both heparin and hyaluronic acid prevent the release of certain pro-inflammatory messenger substances. Heparin is even more effective because it can be absorbed by macrophage cells,” Groth concludes.

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Trouble paying medical bills can lead to longer episodes of homelessness, new study shows

Even before the pandemic left COVID-19 patients with staggering hospital bills, many people, especially those who are uninsured, were often overwhelmed with medical bills

Research shows that medical debt burdens millions of Americans: Depending on how “medical debt” is defined, studies from nonprofits and academic institutions generally show from 16% to 28% of adults carry that burden.

And medical debt and housing instability often go hand in hand. In a new University of Washington study of people experiencing homelessness in King County, unpaid medical bills were their primary source of debt, and that debt extended their period of homelessness by an average of two years.

“So many people have lost their jobs, and then they lose their health insurance. They may not be able to pay even small medical bills or co-pays and still have rent or mortgage payments. If they get sick with coronavirus, or some other medical condition, this can be the perfect storm that puts people out on the street and increases the time they spend there,” said Jessica Bielenberg, who conducted the study for her master’s thesis from the UW School of Public Health.

The study was published June 8 in the journal Inquiry: The Journal of Health Care Organization, Provision, and Financing.

Little research has been done linking medical debt and homelessness, Bielenberg pointed out. While her study did not find a direct causal relationship between the two, it did determine that among those experiencing homelessness, the inability to pay off medical bills, even a few hundred dollars, was associated with considerably more time spent unhoused.

Bielenberg and her co-authors worked with two Seattle organizations supporting shelters and encampments for the homeless: SHARE and Nickelsville. The team surveyed 60 adult residents about their health and financial situation, including other debts and past periods of homelessness. Two-thirds of participants were white; 15% were Black, and 7% were Native American.

Participants whose medical bills had been sent to collections had experienced homelessness for an average of 22 months longer than those who hadn’t had such trouble paying bills; Black, Indigenous and people of color who were unable to pay their medical bills reported being homeless a year longer than white participants with the same financial challenge.

“If Black lives really mattered, we wouldn’t systematically exclude those folks from good jobs—and a good job in America is a job with health insurance,” said co-author Marvin Futrell, a clinical instructor in the UW Department of Health Services and an organizer with SHARE and Nickelsville.

In all, more than 80% of participants reported having debt of some kind, such as doctor bills, student loans, credit cards or payday loans. Of those participants, 68% reported medical debt, the majority of which had been sent to collections.

In about one-third of cases, the amount of medical debt was relatively small—less than $300. That underscores what, for many people, can be a domino effect, Bielenberg said: One lost job, or lack of health insurance, can saddle a person with debts they have to prioritize, if they can pay them at all.

Medical debt is a different kind of debt than, say, outstanding credit card bills or student loan payments, which can be protective against homelessness in the short term, Bielenberg explained. Someone making student loan payments has an education, which can enhance their earning power, while credit cards and payday loans can cover basic necessities, even though they come with high interest rates. Medical debt, by its nature, stems from an illness or injury and may accompany job loss or lack of health coverage.

But what might be perceived as a safety net—health insurance—wasn’t always that, Bielenberg found. Two-thirds of participants were enrolled in Washington’s Medicaid program, Apple Health, while others received coverage from Medicare, the Indian Health Service or the Veterans Health Administration. Some 16% reported having no insurance coverage.

Insurance doesn’t always cover everything, Bielenberg said, and even the comfortably insured may lose track of costs that are their responsibility.

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Those with IDD living in group homes more likely to die from COVID-19, study shows

A new study published recently in Disability and Health Journal by researchers from Syracuse University and SUNY Upstate Medical University shows that people with intellectual and developmental disabilities (IDD) living in residential group homes are more likely to be diagnosed with COVID-19 and die from the virus than those without IDD.

According to the researchers, the disparity is likely related to a higher prevalence of comorbid diseases among those with IDD, and/or a higher percentage of people with IDD living in congregate residential settings.

Their study, “COVID-19 Outcomes among People with Intellectual and Developmental Disability Living in Residential Group Homes in New York State,” was published in the Disability and Health Journal. Utilizing data from the New York Disability Advocates (NYDA) and the New York State Department of Health COVID-19 Tracker, the study compared COVID-19 outcomes between 20,431 people with IDD who live in residential group homes in the state of New York to the overall outcomes for New York State.

“The rates of COVID-19 diagnosis and death were substantially higher for people with IDD living in residential group homes,” said researcher Scott Landes, an associate professor of Sociology at Syracuse University’s Maxwell School of Citizenship and Public Affairs and a research affiliate for the Lerner Center for Public Health Promotion. “This may partly be due to many individuals in this population having pre-existing health conditions that are associated with more severe COVID-19 outcomes.

“However, we are concerned that these severe outcomes may be more related to the current design of the IDD service system in the United States, in which states rely heavily on providing care in congregate settings with limited support and resources,” Landes said. “This is proving deadly during the current pandemic.”

The study was conducted by: Landes; two researchers from SUNY Upstate Medical Center in Syracuse, N.Y., Dr. Margaret Turk, SUNY Distinguished Service Professor of Physical Medicine & Rehabilitation, and Dr. Margaret Formica, associate professor of Public Health & Preventative Medicine and associate professor of urology; Katherine McDonald, professor and Chair of the Department of Public Health in the David B. Falk College of Sport and Human Dynamics at Syracuse University; and Dalton Stevens, a sociology Ph.D. candidate at Syracuse University. Here is a more detailed look at their findings:

People with IDD living in residential group homes in New York State were at greater risk of severe COVID-19 outcomes:

Case rates (a measure of the number of people diagnosed with COVID-19):

  • 7,841 per 100,000 for people with IDD.
  • 1,910 per 100,000 for New York State.

Case-fatality (a measure of the proportion of death among those who contract the disease indicating disease severity):

  • 15 percent for people with IDD.
  • 7.9 percent for New York State.

Mortality rate (a measure of the rate of death from a disease among a total population indicating burden of deaths due to a specific disease):

  • 1,175 per 100,000 for people with IDD.
  • 151 per 100,000 for New York State.

The study also examined each of these COVID-19 outcomes across regions of New York State. The differences in cases and mortality rate were confirmed across all regions of the state. However, case-fatality rate was only higher for people with IDD in and around the New York City region.

“The results of this present study reinforce our initial study that showed higher case-fatality rates among people with IDD using the TriNetX COVID-19 Research Network platform,” researcher Dr. Margaret Turk said. “People with IDD are a poorly recognized and vulnerable group that does not often receive adequate attention within society in general, and within our healthcare system in particular. Further research is needed to determine the possible effects that access to—or quality of—medical care has on COVID-19 outcomes for this group.”

Although U.S. states have been collecting data on COVID-19 outcomes among people with IDD served by the residential group home system, very few have publicly shared any of this data, and those that have shared data have done so sparingly.

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Research shows patients and clinicians rated telemedicine care positively during COVID-19 pandemic

After surveying almost 800 gastroenterology and hepatology patients and their physicians at Penn Medicine, 67% of both viewed their video and telephone appointments held during the peak of the COVID-19 pandemic as positive and acceptable substitutes to in-person appointments. One caveat the researchers uncovered, however, was that patients 60-years-old and older as well as black patients of any age viewed these appointments as slightly less positive compared to younger patients and those of other ethnic backgrounds. The survey shows the strength of Penn Medicine’s telemedicine program, points to patient groups who could benefit from enhanced engagement strategies, and suggests that telemedicine in general can be a suitable replacement for many types of in-person visits. The findings were published in the latest issue of Gastroenterology.

“In one week, our gastroenterology and hepatology practice went from doing roughly 5% of our visits per week with telemedicine to 94%,” said the study’s corresponding author, Shivan Mehta, MD, MBA, MSHP, an assistant professor of Medicine at the Perelman School of Medicine at the University of Pennsylvania. “Given the speed at which our practice ramped up telemedicine use and the external stressors faced by both patients and clinicians during this pandemic, it’s notable that the implementation of remote visits was so well-received.”

From March 16 to April 10, 2020, 94% of gastroenterology and hepatology appointments at Penn Medicine were performed using telemedicine in order to mitigate risks of COVID-19 spread while continuing to advance care as patients self-isolated at home. A telemedicine visit meant either a video visit (similar to FaceTime or Skype) or one via phone in which clinicians largely performed routine and non-urgent care. After reporting back using a 5-point rating system, 67% of patients who did a video or phone visit during this time reported that the visits were “good/better” than regular in-person visits with 96% saying that they were “somewhat/very satisfied with medical care” they received. When asking clinicians, 88% thought the visits were “good/better” than in-person and just over 80% said they were “somewhat/very satisfied” with the medical care they were able to provide their patients.

While patient satisfaction was high overall and across groups of people based on age and ethnicity, older patients and patients who are black rated these telemedicine appointments a little lower than their peers. Specifically, 61% of the 60-plus group and 62% of black patients thought found the visits to be “good/better” than traditional visits.

“This shows we should investigate the reasons why these particular patients don’t feel telemedicine meets their needs to the same extent as their peers,” said the study’s first author, Marina Serper, MD, MS, an assistant professor of Medicine at Penn. “For older patients, it’s likely their unfamiliarity with video visits and some of the technology, but the reasons are less clear when looking at black patients.”

The Division of Gastroenterology and Hepatology as well as the other departments at Penn have been developing, implementing, and studying telemedicine practices for the last few years. Clinicians have gone through telemedicine training, processes have been designed and changed based on research and patient and doctor feedback, and prior to COVID-19, great care was taken in rolling out telemedicine in a deliberate way which allowed for different methods to be tested scientifically.

“It seems easy to jump right in with telemedicine, but the approach at Penn has been to implement it in a measured way where we can learn from the outcomes and bring the best care to patients,” said Mehta. “I think this tactic is part of the reason our patients found telemedicine so favorable. Nevertheless, I think we can deduce that telemedicine as a whole is going to be appreciated by patients.”

While the study counted both video and telephone visits as “telemedicine,” video visits were favored among participants. Researchers said it’s worth noting that not every patient has access or easy access to the technology needed to participate.

“Our research makes a case that the internet should really be considered a healthcare need,” said Serper.

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Alicia Silverstone Shows Off Son Bear’s Impressive Kitchen Skills

Chef in the making! Alicia Silverstone‘s son, Bear, is getting a head start on his cooking skills — and his mom couldn’t resist sharing his progress.

The Clueless star, 43, posted a video via Instagram on Tuesday, June 23, of her 9-year-old son cutting onions in the kitchen. Bear wore sunglasses on his face for protection as he diligently diced the vegetable. “Are these good enough?” he asked Silverstone, who can be heard laughing in the background.

“Bear takes his onion chopping very seriously…” she captioned the post.

The Kind Diet author told Us Weekly in August 2019 that she credits Bear’s vegan diet for him being a well-behaved child.

“I’ve never had to raise my voice to Bear,” she said at the time. “I can just say ‘no, thank you’ and we respect each other and listen to each other. So much of that is because he’s not … a lot of it is the parenting, but a lot of it is the food. When your kid feels good, they act well.”

She also revealed that her son — whom she shares with her ex-husband Christopher Jarecki — reaches for healthy options when he gets hungry. “I’m imagining that doesn’t count as a picky eater,” Silverstone said. “He eats kale pretty much almost every day. And he eats bok choy, and he eats cabbage and he has brown rice and quinoa.”

The California native told Us and other reporters at the #BlogHer20 panel in May that Bear has “more energy” than most kids because he is vegan.

“I always laugh, like, ‘Oh, my poor vegan baby, he’s so weak,’ because he’s jumping all over the place and he’s so wild. But there’s a calmness to him and a centeredness,” the Diary of a Wimpy Kid star explained. “He’s not off the charts.”

Silverstone, who is also vegan, added that the diet is also beneficial for her as a parent. “If I don’t eat well, I don’t sleep well, and if I don’t sleep well, I’m a grumpy mama,” she said. “Whereas if I’ve eaten well and I sleep well, everything’s a joy … that’s all food.”

The Book Club actress made headlines in May when she shared that she and her son bond over more than just food. “My son and I take baths together, and when he’s not with me, I take a bath and that really feels nourishing and comforting,” she told The New York Times.

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Cancer study shows how chemicals cause complex cell mutations

Fresh insights into why some harmful substances are so efficient at causing cancer could aid the quest for better treatments.

New research reveals how chemicals can cause changes in cells to help them dodge the body’s immune system and build resistance to cancer drugs.

Scientists tracked the impact of a toxic substance—similar to compounds found in tobacco, exhaust and some plants—to better understand how chemicals cause mutations in our cells’ DNA.

The team found that damage caused by the substance lingered long enough to be inherited when a cell divides. The damage stops cells’ replication machinery reading DNA sequences correctly giving a high chance of a new mutation each time a new copy is made.

Each cell division with the damage produces a new combination of mutations. Because only certain combinations of mutations will turn healthy cells cancerous, the more combinations produced, the greater the chances of disease.

This rapid increase in new combinations of mutations means more throws of the genetic dice that are capable of producing cancer cells.

The greater genetic diversity introduced into cells as a result of these extra throws provides more opportunities for tumors to evade the body’s immune system and develop resistance to treatment.

The unique mutation patterns recognized by the team allowed them to trace back to the point where a turmour develops. This new found clarity will aid future research understand the mechanisms behind cancer development and DNA repair processes.

A group led by the Universities of Edinburgh and Cambridge and the German Cancer Research Center identified the specific combinations of mutations that will create cancer cells. The findings could help doctors prescribe the most appropriate course, and dosage, of chemotherapy for patients.

The team studied how cancer cells evolved in the livers of mice given the tumor-causing chemical, diethylynitrosamine. It causes lingering DNA damage like that triggered by a chemical called aristolochic acid, which is found in some plants and herbal medicine and linked to liver cancer.

The DNA damage is also similar to that caused by UV light and a wide a range of polycyclic aromatic hydrocarbons present in tobacco smoke, vehicle exhaust and some burnt food. Temozolomide and other drugs used in chemotherapy were also found to produce lingering DNA damage.

All of the mutations had a clear pattern that suggested damage took place on just one of the two DNA helix strands. This process, where most mutations stem from damage to a single strand, is now known as lesion segregation. Knowing segregation had occurred, helped the team pinpoint the cancer causing mutations.

Having identified mutation patterns in mice, the team used published data from human cells, to find evidence of lesion segregation in cancer patients that had been caused by chemicals and ultraviolet radiation.

The research is the result of collaboration between researchers from EMBL European Bioinformatics Institute near Cambridge and the Institute for Research in Biomedicine, Barcelona.

The study is published in Nature. It was funded by Cancer Research UK with support from the European Research Council, the Wellcome, the Helmholtz Society and the Medical Research Council.

Professor Martin Taylor, University of Edinburgh’s MRC Human Genetic Unit, said: “DNA lesions caused by cancer-causing agents are individual to each strand and can trigger several generations of mutations. It is important to be aware of this when tumors are being treated and new drugs are being developed.”

Dr. Duncan Odom, a director of research at the University of Cambridge’s Cancer Research UK Cambridge Institute, said: “The concept of lesion segregation helps us better understand how the surprising complexity of mutations in cancer cells can arise. It may help explain how cancer cells can react so flexibly and, in turn, shape cancer genome evolution.”

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