New Vegan Cheese Wedges

Nicole Axworthy wrote . . . . . . . . .

In late June, artisanal cheese brand Cheeze & Thank you will launch at nine locations of Whole Foods Markets in Chicago, IL. The cheeses will be available at Edgewater, Gold Coast, Hyde Park, South Loop, Halsted, Streeterville, Lincoln Park, Lakeview, and West Loop locations in flavors such as Dill Havarti, Herbed Feta, Black Garlic Truffle Fontina, Mustard Seed Smoked Gouda, Giardinera Jack, and Mozzarella Capri. Cheeze & Thank you offers cheese options that are soy-based, nut-based, and seed-based.

The woman-run brand was created by Megan Schmitt when she began transitioning from vegetarian to vegan. At the time, she wasn’t satisfied with the vegan cheese options on the market, so she began making her own. “I come from a family of entrepreneurs, and initially I thought about starting a vegan restaurant when I lived in St. Louis, MO” Schmitt told VegNews. “It wasn’t until I moved to Chicago that Cheeze & Thank You really started. I didn’t have many friends here so to occupy my time, I started getting back into cheese-making.” One of Schmitt’s vegan friends told her she should start selling her cheese and put her in touch with local collective Chicago Vegan Test Kitchen. “That’s where I started actually selling my product and it all just kind of took off from there,” she said.

With the debut of Cheeze & Thank you at Whole Foods, Schmitt plans to expand to smaller local shops in Chicago and St. Louis, MO. “I’d love Cheeze and Thank You to be available at all major grocery stores as well as independently owned shops,” Schmitt said. “I just need to figure out logistics from a distribution side.”

Source: Veg News

Music Might Help Soothe Ailing Hearts

Music influences people’s heart rates, and one piece of music will affect individuals’ hearts differently, a new, small study shows.

The findings could lead to novel, drug-free treatments for such conditions as high blood pressure and heart rhythm disorders, or to help people relax or stay alert, the researchers said.

Previous studies that examined physical responses to music measured changes in heart rate after participants listened to recordings simply categorized as sad, happy, calm or violent.

This new study of three patients with mild heart failure requiring a pacemaker took a more targeted approach.

During a live, classical piano concert, researchers used the patients’ pacemaker leads to measure the electrical activity of their hearts during significant changes in tempo, volume or rhythm.

“We used precise methods to record the heart’s response to music and found that what is calming for one person can be arousing for another,” said Elaine Chew, a senior researcher at the French National Center for Scientific Research in Paris.

“Even though two people might have statistically significant changes across the same musical transition, their responses could go in opposite directions. So for one person the musical transition is relaxing, while for another it is arousing or stress-inducing,” Chew said.

For example, someone who doesn’t expect a transition from soft to loud music could find it stressful, while another person might find it relaxing.

The small study was presented recently at the European Society of Cardiology virtual meeting. Research presented at meetings is typically considered preliminary until published in a peer-reviewed journal.

“By understanding how an individual’s heart reacts to musical changes, we plan to design tailored music interventions to elicit the desired response,” Chew said in a society news release.

Pier Lambiase, a professor of cardiology at University College London in the U.K., was the study’s medical leader.

He said tailored interventions could be used to reduce blood pressure or lower the risk of heart rhythm disorders without the side effects of medication.

The researchers are now conducting tests with eight patients to further confirm their findings.

Source: HealthDay

Antibody Designed to Recognize Pathogens of Alzheimer’s Disease

Researchers have found a way to design an antibody that can identify the toxic particles that destroy healthy brain cells – a potential advance in the fight against Alzheimer’s disease.

Their method is able to recognise these toxic particles, known as amyloid-beta oligomers, which are the hallmark of the disease, leading to hope that new diagnostic methods can be developed for Alzheimer’s disease and other forms of dementia.

The team, from the University of Cambridge, University College London and Lund University, designed an antibody which is highly accurate at detecting toxic oligomers and quantifying their numbers. Their results are reported in the Proceedings of the National Academy of Sciences (PNAS).

“There is an urgent unmet need for quantitative methods to recognise oligomers – which play a major role in Alzheimer’s disease, but are too elusive for standard antibody discovery strategies,” said Professor Michele Vendruscolo from Cambridge’s Centre for Misfolding Diseases, who led the research. “Through our innovative design strategy, we have now discovered antibodies to recognise these toxic particles.”

Dementia is one of the leading causes of death in the UK and costs more than £26 billion each year, a figure which is expected to more than double in the next 25 years. Estimates put the current cost to the global economy at nearly £1 trillion per year.

Alzheimer’s disease, the most prevalent form of dementia, leads to the death of nerve cells and tissue loss throughout the brain, resulting in memory failure, personality changes and problems carrying out daily activities.

Abnormal clumps of proteins called oligomers have been identified by scientists as the most likely cause of dementia. Although proteins are normally responsible for important cell processes, according to the amyloid hypothesis, when people have Alzheimer’s disease these proteins -including specifically amyloid-beta proteins – become rogue and kill healthy nerve cells.

Proteins need to be closely regulated to function properly. When this quality control process fails, the proteins misfold, starting a chain reaction that leads to the death of brain cells. Misfolded proteins form abnormal clusters called plaques which build up between brain cells, stopping them from signalling properly. Dying brain cells also contain tangles, twisted strands of proteins that destroy a vital cell transport system, meaning nutrients and other essential supplies can no longer move through the cells.

There have been over 400 clinical trials for Alzheimer’s disease, but no drug that can modify the course of the disease has been approved. In the UK, dementia is the only condition in the top 10 causes of death without a treatment to prevent, stop, or slow its progression.

“While the amyloid hypothesis is a prevalent view, it has not been fully validated in part because amyloid-beta oligomers are so difficult to detect, so there are differing opinions on what causes Alzheimer’s disease,” said Vendruscolo. “The discovery of an antibody to accurately target oligomers is, therefore, an important step to monitor the progression of the disease, identify its cause, and eventually keep it under control.”

The lack of methods to detect oligomers has been a major obstacle in the progress of Alzheimer’s research. This has hampered the development of effective diagnostic and therapeutic interventions and led to uncertainty about the amyloid hypothesis.

“Oligomers are difficult to detect, isolate, and study,” said Dr Francesco Aprile, the study’s first author. “Our method allows the generation of antibody molecules able to target oligomers despite their heterogeneity, and we hope it could be a significant step towards new diagnostic approaches.”

The method is based on an approach for antibody discovery developed over the last ten years at the Centre for Misfolding Diseases. Based on the computational assembly of antibody-antigen assemblies, the method enables the design of antibodies for antigens that are highly challenging, such as those that live only for a very short time.

By using a rational design strategy that enables to target specific regions, or epitopes, of the oligomers, and a wide range of in vitro and in vivo experiments, the researchers have designed an antibody with at least three orders of magnitude greater affinity for the oligomers over other forms of amyloid-beta. This difference is the key feature that enables the antibody to specifically quantify oligomers in both in vitro and in vivo samples.

The team hopes that this tool will enable the discovery of better drug candidates and the design of better clinical trials for people affected by the debilitating disease. They also co-founded Wren Therapeutics, a spin-out biotechnology company based at the Chemistry of Health Incubator, in the recently opened Chemistry of Health building, whose mission it is to take the ideas developed at the University of Cambridge and translate them into finding new drugs to treat Alzheimer’s disease and other protein misfolding disorders.

The antibody has been patented by Cambridge Enterprise, the University’s commercialisation arm.

Source: EurekAlert!


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Thousands of Dutch COVID-19 Patients Have Permanent Lung Damage

Janene Pieters wrote . . . . . . . . .

Thousands of Netherlands residents who recovered from Covid-19, the respiratory disease caused by the novel coronavirus, may be left with permanent damage to their lungs, resulting in decreased capacity and more difficulty absorbing oxygen, Leon van den Toorn, pulmonologist chairman of the Dutch association of physicians for pulmonary disease and tuberculosis NVALT, said to newspaper AD.

Many people underestimate the consequences of the coronavirus Van den Toorn said to the newspaper. The virus and the body’s response to it can cause permanent damage to the lungs, he said. “In severe cases, a kind of scar formation occurs, we call this lung fibrosis. The lungs shrink and the lung tissue becomes stiffer, making it harder to get enough oxygen.”

Van den Toorn expects that “there may be thousands of people in the Netherlands who suffered permanent injury to the lungs from corona”. Of the 1,200 Covid-19 patients who so far recovered after admission to intensive care, “almost 100 percent went home with residual damage”, he said to AD. And about half of the 6 thousand people who were hospitalized, but did not need intensive care, will have symptoms for years to come.

So far 45,500 people in the Netherlands tested positive for the coronavirus. Many did not get sick enough to need hospital care. In this group, Van den Toorn expects that permanent problems will be less serious, but still possible.

According to Van den Toorn, recovered coronavirus patients who continue to suffer from shortness of breath after a few weeks, or who have a severely reduced exercise capacity, should go see a lung doctor. “There may be a low oxygen level in the blood, which is harmful to the body.”

Van de Toorn said the NVALT wants to avoid making the same mistakes with coronavirus that were made with Q fever, an infectious disease that broke out in 2007 and lasted until 2011. Hundreds of people still suffer from serious health problems as a result of Q fever. Prime Minister mark Rutte apologized to them on behalf of the Dutch government in 2017.

“People with a history of corona infection should be monitored closely to see if recovery is complete,” Van de Toorn warned. The Dutch Lung Fund is setting up a platform to do just that.

Source: NLTimes

New Model Predicts the Peaks of the COVID-19 Pandemic

As of late May, COVID-19 has killed more than 325,000 people around the world. Even though the worst seems to be over for countries like China and South Korea, public health experts warn that cases and fatalities will continue to surge in many parts of the world. Understanding how the disease evolves can help these countries prepare for an expected uptick in cases.

This week in the journal Frontiers, researchers describe a single function that accurately describes all existing available data on active cases and deaths–and predicts forthcoming peaks. The tool uses q-statistics, a set of functions and probability distributions developed by Constantino Tsallis, a physicist and member of the Santa Fe Institute’s external faculty. Tsallis worked on the new model together with Ugur Tirnakli, a physicist at Ege University, in Turkey.

“The formula works in all the countries in which we have tested,” says Tsallis.

Neither physicist ever set out to model a global pandemic. But Tsallis says that when he saw the shape of published graphs representing China’s daily active cases, he recognized shapes he’d seen before–namely, in graphs he’d helped produce almost two decades ago to describe the behavior of the stock market.

“The shape was exactly the same,” he says. For the financial data, the function described probabilities of stock exchanges; for COVID-19, it described daily the number of active cases–and fatalities–as a function of time.

Modeling financial data and tracking a global pandemic may seem unrelated, but Tsallis says they have one important thing in common. “They’re both complex systems,” he says, “and in complex systems, this happens all the time.” Disparate systems from a variety of fields–biology, network theory, computer science, mathematics–often reveal patterns that follow the same basic shapes and evolution.

The financial graph appeared in a 2004 volume co-edited by Tsallis and the late Nobelist Murray Gell-Mann. Tsallis developed q-statitics, also known as “Tsallis statistics,” in the late 1980s as a generalization of Boltzmann-Gibbs statistics to complex systems.

In the new paper, Tsallis and Tirnakli used data from China, where the active case rate is thought to have peaked, to set the main parameters for the formula. Then, they applied it to other countries including France, Brazil, and the United Kingdom, and found that it matched the evolution of the active cases and fatality rates over time.

The model, says Tsallis, could be used to create useful tools like an app that updates in real-time with new available data, and can adjust its predictions accordingly. In addition, he thinks that it could be fine-tuned to fit future outbreaks as well.

“The functional form seems to be universal,” he says, “Not just for this virus, but for the next one that might appear as well.”

Source: EurekAlert!


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