Publisher Health

Several U.S. cities have instituted taxes on drinks with added sugar in order to reduce consumption, but new research suggests these policies currently have one fatal flaw.
The study found that sugary drink taxes only reduce purchasing if price tags at stores mention that consumers are paying that tax when they buy the drink.
“If cities want these policies to be effective, they need to regulate how these sugary drinks are labeled at the stores where they are sold — and they currently don’t do that,” said Grant Donnelly, lead author of the study and assistant professor of marketing at The Ohio State University’s Fisher College of Business.
The findings suggest that price tags should mention the tax, but not the amount, because consumers tend to overestimate how much the tax is, Donnelly said. If they know the true size of the tax, they are more willing to pay it.
Among the cities that currently have a tax on sugary drinks are Philadelphia, San Francisco, Seattle, and Boulder.
The study was published online recently in the journal Psychological Science.

We all know the scene from countless courtroom dramas: A witness points at the defendant and confidently declares to judge and jury: “That’s the one, that’s who did it!” But is it? Perhaps. If that same witness was also confident the very first time their memory was tested — write a team of psychological scientists and criminologists led by memory expert John Wixted of the University of California San Diego. Otherwise, there’s too high a chance that a contaminated memory will convict an innocent person.
As most of us also know, people have been convicted of crimes they didn’t commit on the basis of eyewitness memory. Some of these wrongful convictions have later been overturned by DNA or other physical evidence. But that type of evidence doesn’t always exist. To reduce the likelihood of injustice, the researchers suggest a simple, no-cost reform to our system of jurisprudence. “Test a witness’s memory of a suspect only once,” the researchers urge in a paper published by Psychological Science in the Public Interest, a journal of the Association for Psychological Science.
“The first test is the most reliable test,” says Wixted, a professor of psychology at UC San Diego, who has been working on memory for more than 30 years and eyewitness memory specifically for the past decade. “The first test probes the witness’s memory but also unavoidably contaminates the witness’s memory. All tests beyond that very first one only serve to test contaminated memory and to contaminate it further. And once a memory is contaminated, there is no way to decontaminate it.”
In their paper, Wixted and his co-authors — Gary Wells of Iowa State University, Elizabeth Loftus of UC Irvine and Brandon Garrett of the Duke University School of Law — explain how many wrongful convictions of innocent prisoners in which a witness conclusively identified the defendant in court began with something other than a conclusive initial eyewitness identification.
It’s not that witnesses are vindictive or malicious, or that anyone else in the process is either. Nor is it the case that eyewitness memory is so hopelessly faulty that it shouldn’t be admitted as evidence at all. But our system of jurisprudence ignores the confidence with which first identifications are made and relies too often on subsequent identifications, usually the very last one made in the courtroom. At that point, at trial, perhaps a year or more after the crime has been committed, witnesses have usually become so familiar with a suspect’s face that they are certain they’re remembering the face. And in fact, they are remembering — but very possibly not from the time the crime was committed. Rather, they’re remembering having seen the person in a line-up (sometimes multiple times) or even on news or social media.
“Memory is malleable,” Wixted says. “And because it’s malleable, we must avoid repeated identification procedures with the same witness and suspect. This recommendation applies not only to additional tests conducted by police investigators butalso to the final test conducted in the courtroom.”
In their paper, the researchers describe the latest science on eyewitness memory, including findings based on signal detection theory, elaborative processing and source misattribution. To make a decision about a face in a lineup (signal detection theory), the witness has to compare that face to their memory of the perpetrator (elaborative processing). Doing so automatically creates a memory of that face. Even if the initial decision is “no, that is not him,” the face will seem more familiar on any later test. Often, the witness loses sight of the fact that the face is familiar because of the previous lineup test and comes to believe that the face is familiar because it is in fact the face of the perpetrator (source misattribution).
The researchers also detail three real-life cases to underscore the theoretical and experimental points: The cases of John Jerome White and Steven Gary Titus,both of whom were convicted of rape on the basis of witness memories and whose convictions were later overturned, and the case of Charles Don Flores.
The Flores case is especially instructive, Wixted says. It inspired him to assemble the research team for this paper — outlining the latest scientific understanding of eyewitness memory and calling for reform.
On January 29, 1998, in a suburb of Dallas, two men entered the home of Elizabeth Black, who was later found shot dead. A neighbor saw the men enter Black’s home shortly before the murder, and she became a key witness. When the police captured suspected triggerman Richard Childs, the witness immediately identified Childs from a photo lineup as one of the two men she saw that morning. Childs also confessed to the murder and was sentenced to 35 years in prison. The police suspected Flores as the accomplice because he was engaged in a drug deal with Childs only hours before the murder, and at his 1999 trial, the same witness confidently identified Flores as the other man she saw enter her neighbor’s house. However, on the day of the crime in January of 1998, the witness told police that the accomplice was a white male with shoulder-length hair. After being hypnotized to calm her nerves, she helped to make a composite sketch of the perpetrator with a police artist. Consistent with her initial description, the sketch was that of a white male with shoulder-length hair. The police then showed her a photo lineup containing Flores — a Hispanic male with a crew cut — along with five similar-looking Hispanic males. She rejected the lineup, presumably because none of the faces even remotely matched her memory of the accomplice. Yet, Wixted says, while examining the faces on that first and only uncontaminated test of her memory for Flores, she became unavoidably familiarized with his face. By the time of the trial, she no longer had any doubt that he was the man she saw that morning.
The witness’s initial description of the accomplice and her rejection of the lineup mean that the eyewitness evidence in this case, properly understood, Wixted says, points in the direction of innocence. Instead, her confident courtroom testimony was interpreted as evidence of guilt and helped persuade the jury to convict Flores. He has been on death row ever since, and a governor’s clemency now seems to be his last hope.

Researchers at Baylor College of Medicine have uncovered a more detailed picture of how the intestinal epithelium — the lining of the intestines — heals itself after infection with rotavirus. A meticulous single-cell analytical approach to study the repair process in an animal model revealed that the damaged epithelium contains a variety of cell types involved in repairing it through broad coordinated responses that ultimately heal the damaged tissue.
The researchers also unexpectedly discovered that, in addition to enterocytes, which are the cell type typically infected by rotavirus, tuft cells, another cell type in the intestinal epithelium, also are infected and may contribute to the repair response of the epithelium following damage. The findings, published in the Proceedings of the National Academy of Sciences, not only provide a better understanding of the healing process following rotavirus infection, but also may contribute new clues about how the virus causes disease.
“Diseases of the digestive tract affect about 60 million Americans each year. These conditions often are associated with damage to the epithelium, which compromises its functions, including digestion of food and absorption of nutrients, and affects overall health,” said co-corresponding author Dr. Sarah Blutt, associate professor of molecular virology and microbiology at Baylor.
The researchers’ goal on this project was to contribute a better understanding of the repair process following damage to the intestinal epithelium caused by rotavirus in a mouse model. This virus causes approximately 179 million cases of acute gastroenteritis and about 128,000 deaths annually, particularly in children. Getting into the details of the cellular response to the damage resulting from the infection can lead to improved therapies.
Intestinal healing requires teamwork
The internal surface of the intestines is lined with a layer of epithelial cells that folds multiple times, forming many thin, finger-like projections called villi, with crypts between them. Rotavirus infects and kills enterocyte cells residing at the tips of the villi.

The process of purifying biopharmaceutical drugs remains a costly and time-consuming challenge. A deeper understanding of how unwanted elements within biomanufactured proteins bind to the molecules developed to remove them could help researchers make purity processes more efficient, more complex, and increasingly scalable.
In research published in Langmuir, a team led by Steven Cramer, an endowed chair professor of chemical and biological engineering at Rensselaer Polytechnic Institute, explored the fundamentals of how different molecules interact with various surfaces during the purification process.
Cramer is a leading expert in chromatographic bioprocessing, a separation technique used in biopharmaceutical purification to selectively choose which components of a protein mixture should be kept and which components should be removed. Ions or molecules, known as ligands, are developed to bind to specific components that should either be saved or discarded during this process.
“This is part of a very big effort to understand the fundamentals of how these molecules interact with surfaces,” said Cramer, a member of the Rensselaer Center for Biotechnology and Interdisciplinary Studies (CBIS), where the work was performed. “Our group is trying to ramp up the intellectual level of this kind of analysis in a variety of ways.”
This new paper builds upon research by the Cramer Lab recently published in Biotechnology and Bioengineering. In that work, researchers used nuclear magnetic resonance (NMR) spectroscopy and complex computer simulations to examine the fundamentals of how different molecules interact with various surfaces and ligands, including how and where binding happens, and if certain molecular interactions affect the binding process.
Working with Merck Pharmaceuticals and Bio-Rad Laboratories and using the NMR core facility in CBIS run by co-author Scott McCallum, the team looked at the Fc part of an IgG1 antibody and how ligands interact with that section of the antibody protein in particular. (If you were to picture an antibody looking like the letter “Y,” the Fc part would be the tail.) IgG1 antibodies are used in a large majority of biopharmaceutical drugs, meaning a deeper understanding of how their components interact with various molecules and ligands could have widespread implications.
In the Langmuir paper, the team took its exploration even deeper by adding nanoparticles to the surface of various proteins in order to see exactly where the ligands were binding.
“With this approach, we can then also look at some of the subtle interactions that are happening,” Cramer said. “Sometimes these ligands come together and form these clusters of ligands, and these clusters actually drastically change the behavior.”
This work, Cramer said, could lead to the development of new and improved materials and ligands. It also could help researchers develop more nuanced and specific ways of separating out unwanted molecules that are very similar to another type of molecule that needs to remain. All of these advancements could improve the drug purification process, making it more efficient and effective.
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Multiple studies in humans and mouse models indicate that sleep disruptions raise the risk of Alzheimer’s disease (AD) by increasing the accumulation of disease-relevant proteins such as amyloid-beta (A-beta) in the brain. In the current study, a team led by researchers at Baylor College of Medicine discovered that, in an animal model of Alzheimer’s disease, restoring normal sleep by returning to normal the activity of the thalamic reticular nucleus (TRN), a brain region involved in maintaining stable sleep, reduced the accumulation of A-beta plaques in the brain.
Published in the journal Science Translational Medicine, the study suggests that TRN not only may play a previously unsuspected driving role in symptoms associated with Alzheimer’s, but also that restoring its normal activity could be a potential therapeutic approach for this severe condition.
The TRN is quiet in AD
“Our interest in studying the TRN in the context of Alzheimer’s disease began when we observed in an animal model that TRN activity was generally reduced when compared to the TRN activity of animals without the condition,” said corresponding author Dr. Jeannie Chin, associate professor of neuroscience at Baylor.
When we sleep, the TRN is in general more active than when we are awake, Chin explained. This increased TRN activity reduces the perception of peripheral sensory information. Consequently, when we sleep, we typically are not aware of sounds, lights and other sensations, which helps us get a good night sleep.
“Observing that the TRN in our animal model was less active than in animals without the condition, we investigated the possibility that a quiet TRN could be a reason for the sleep interruptions that are common in people with Alzheimer’s disease,” said first author Dr. Rohan Jagirdar, an instructor in the Chin lab.

Copper has been clinically improving the lives of people since about 1500 BCE, when an Egyptian physician first recorded its use as a treatment for inflammation. Some 35 centuries later, researchers at Johns Hopkins Medicine and Italy’s Catholic University of the Sacred Heart medical school have provided solid evidence that the first metal used medicinally may now have a new role — helping save children from a devastating central nervous system cancer known as medulloblastoma.
The prospective therapy — in which copper ions are combined with a drug once heralded as treatment for alcoholism — is described in a study published today in the journal PLOS ONE.
According to the National Cancer Institute, a medulloblastoma is a fast-growing, cancerous tumor originating in the brain or spinal cord. Predominantly seen in children younger than 10, medulloblastoma is the most common pediatric brain malignancy, with between 250 and 500 new cases diagnosed annually.
Overall, the survival rate for children with medulloblastoma that has not spread is about 70%, but this can drop to as low as 40% depending on the patient’s age, the molecular subtype of the tumor (there are four), the extent of any surgical removal of previous tumors, and whether there has been metastasis (spread to other parts of the body). Treatment for pediatric medulloblastoma has traditionally been surgery, radiation and chemotherapy, individually or in combination.
The recent Johns Hopkins Medicine-led study looked at an alternative therapy.
“Disulfiram [DSF], a medication that’s been used for nearly 70 years to treat chronic alcoholism, has great promise being ‘repurposed’ as an anticancer agent, especially when it is complexed with metal ions such as copper [Cu++],” says study senior author Betty Tyler, associate professor of neurosurgery at the Johns Hopkins University School of Medicine. “Since the combination [DSF- Cu++] hasn’t previously been evaluated for potential pediatric use, we wanted to assess its safety and effectiveness against the two pediatric medulloblastoma subtypes with the worst five-year survival rates.”
“Our goal is to pave the way toward a successful treatment that could be used for children, either alone or teamed with conventional radiation and chemotherapy,” says study co-author Henry Brem, M.D., director of the Department of Neurosurgery at the Johns Hopkins University School of Medicine. “Characterizing how DSF-Cu++ works at the molecular level was critical for future exploration of its clinical use against pediatric medulloblastoma.”

As women age, their risk of cardiovascular disease (CVD) exceeds men’s largely because of decreased levels of estrogen that regulate vascular function. As a result, much research is focused on various risk factors. A new study suggests that eating alone may contribute to an increased risk of heart disease in older women. Study results are published online today in Menopause, the journal of The North American Menopause Society (NAMS).
As part of the overall effort to reduce the incidence of CVD, there has been a growing awareness of healthy eating habits; however, the importance of having an eating companion has been largely overlooked in previous studies. Recent changes in society have meant that more people than ever are eating alone. Some of the primary reasons include a rise in the number of single-person households. Social distancing protocols introduced in response to the COVID19 pandemic have further restricted eating meals with others. Additionally, mobile platforms for food delivery services have become more popular, further motivating people to eat alone.
With more people eating alone, health concerns have been raised. A previous study reported that a higher frequency of eating alone is associated with a higher risk of abdominal obesity and elevated blood pressure. When eating alone, people tend to eat faster, which often leads to increases in body mass index, waist circumference, blood pressure, and blood lipid levels, all of which can increase the risk of metabolic syndrome and CVD.
Eating alone also can affect mental health and has been reported as a risk factor for depression, which is also linked with an increased risk of CVD. Although these findings suggest that eating alone is a risk factor for CVD in older women, few studies have investigated the relationship between eating alone and the prevalence of CVD. Researchers in this study involving nearly 600 menopausal women aged older than 65 years sought to compare health behaviors and nutritional status between older women eating alone and those eating with others and to investigate the relationship between eating alone and the prevalence of CVD and its risk factors in older women.
On the basis of the results of this study, researchers concluded that older women who ate alone had poorer nutritional knowledge and intake. More specifically, it was found that older women who ate alone had lower intakes of energy, carbohydrates, dietary fiber, sodium, and potassium that those who ate with others. In addition, older women eating alone were 2.58 times more likely to have angina, a type of chest pain caused by reduced blood flow to the heart and a symptom of coronary artery disease. These results suggest the value of nutrition education and CVD screening for older women who mainly eat alone.
Study results are published in the article “Association between eating alone and cardiovascular diseases in elderly women: a cross-sectional study of KNHANES 2016 data.”
“This study shows that older women who eat alone are more likely to have symptomatic heart disease. They are also more likely to be widowed and to have lower incomes and poorer nutritional intake. These results are not surprising given that lower socioeconomic status and social isolation contribute to lower quality of life, greater rates of depression, and poorer health. Given that women live longer than men, finding ways for older women who are socially isolated to engage and create meaningful social ties may not only improve their nutrition but also their overall health while simultaneously reducing healthcare costs,” says Dr. Stephanie Faubion, NAMS medical director.
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As SARS-CoV-2 continues to spread and mutate, it’s important to identify new treatment options. Molnupiravir is an investigational oral antiviral being developed for the treatment of COVID-19, and has been submitted for review by the U.S. Food and Drug Administration. Researchers now report in ACS Central Science that they have engineered enzymes to help manufacture the pill, resulting in a much shorter and higher-yielding synthesis than current methods.
Originally developed to treat influenza, molnupiravir works by causing viruses to make errors when copying their own RNA, introducing mutations that inhibit replication. Recently, interim phase 3 clinical trial findings indicated that molnupiravir reduced the risk of hospitalization and death from COVID-19 for newly diagnosed, at-risk patients, and that it worked equally well against different SARS-CoV-2 variants. John McIntosh, Patrick Fier and colleagues at Merck and Codexis set out to develop a shorter, higher-yielding and sustainable way to synthesize the molecule.
The researchers developed a three-step synthesis of molnupiravir from a sugar molecule called ribose. They identified enzymes or chemical treatments to sequentially add the appropriate chemical groups to ribose to generate the molecule. For the second step of the synthesis, the team identified bacterial enzymes that weakly catalyzed the desired reactions. Using in vitro evolution, they greatly enhanced these enzymes’ activities. The new synthetic route, which also included a phosphate recycling strategy, was 70% shorter and had a seven-fold higher overall yield than the original route.
The authors acknowledge funding from Merck Sharp & Dohme Corp.
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A new machine learning model developed by Timothy Chan, MD, PhD, of Cleveland Clinic and colleagues accurately predicts whether immune checkpoint blockade (ICB), a growing class of immunotherapy drugs, will be effective in patients diagnosed with a wide variety of cancers.
The forecasting tool assesses multiple patient-specific biological and clinical factors to predict the degree of response to immune checkpoint inhibitors and survival outcomes. It markedly outperforms individual biomarkers or other combinations of variables developed so far, according to findings published in Nature Biotechnology.
With further validation, the tool may help oncologists better identify patients most likely to benefit from ICB. Discerning, prior to treatment, patients for whom ICB would be ineffective could reduce unnecessary expense and exposure to potential side effects. It could also indicate the need to pursue alternate treatment strategies, such as combination therapies.
“It’s important to know which treatment modalities patients are most suited for,” said Dr. Chan, director of Cleveland Clinic’s Center for Immunotherapy & Precision Immuno-Oncology. “Our model provides a more comprehensive understanding of the diversity of responses among patients to immune checkpoint blockade. It’s the first to assemble such a large-scale set of clinical and genomic variables that have predictive value for immunotherapy across numerous cancer types.”
These latest findings build on earlier work from Dr. Chan, who discovered that patients with high tumor mutation burden and DNA repair deficiencies respond well to immune checkpoint therapy. These findings have been validated by clinical trials and the FDA approved as the first tumor type-agnostic approvals for any cancer therapy.
Immune checkpoints are proteins on specific immune cells (T cells) that when activated, or “turned on,” prevent immune responses from being too strong and destroying healthy cells. Some cancer cells are able to hijack checkpoint signaling in order to disguise themselves and avoid being targeted by a patient’s immune system. Checkpoint inhibitors are a class of immunotherapy drugs that prevent cancer cells from activating these checkpoints.