Publisher Health

In one of many scoops for The Times, he revealed how the tobacco industry had kept secret its own research showing that nicotine was harmful and addictive.Philip J. Hilts, who as a science reporter for The New York Times in 1994 exposed a tobacco company’s decades-long cover-up of its own research showing that tobacco was harmful and nicotine was addictive, died on April 23 in Lebanon, N.H. He was 74. The cause was complications of liver disease, his son Ben said.Mr. Hilts was a longtime journalist, writing for The Times, The Washington Post and other publications, and was the author of six nonfiction books on scientific, medical and social topics.His work on tobacco made headlines not only in The Times but also across the country. In 1994, he obtained internal documents showing that executives of the Brown & Williamson Tobacco Corporation were struggling with whether to disclose to the surgeon general what they knew in 1963 about the hazards of smoking; their own research showed that cigarettes were addictive and caused lung cancer or predisposed people to it.The Brown & Williamson executives, Mr. Hilts wrote, “chose to remain silent, to keep their research results secret, to stop work on a safer cigarette and to pursue a legal and public relations strategy of admitting nothing.”Mr. Hilts’s article, on the front page of The Times, appeared a month after top executives of the seven biggest American tobacco companies testified before Congress that nicotine was not addictive. Two years later, they were all under federal investigation for potentially lying under oath and were no longer leading their companies.The Justice Department eventually dropped its criminal investigation into whether the executives had perjured themselves. But in 1998, four tobacco companies and 46 states reached what was the largest civil litigation settlement in American history, with the companies agreeing to pay the states $206 billion over 25 years. Millions of internal company documents of the sort that Mr. Hilts and other news organizations had relied on were made public in the process.Mr. Hilts also broke major stories about breast implants, contraceptives and deceit in the cosmetic device industry. He was among the first reporters to cover the AIDS epidemic.An adventurous type — he was a scuba diver and world traveler — he wrote a dispatch from an active volcano a mile below the Pacific Ocean. He covered the confessions of a healer in Zambia who claimed to be “curing” AIDS. And he examined a law-enforcement practice of using hypnosis to “refresh” the memories of witnesses; his findings of problems with hypnosis led to the release of four men from prison.Most recently, he served as director of the Knight Science Journalism Program at the Massachusetts Institute of Technology, from 2008 to 2014.His books include “Smokescreen: The Truth Behind the Tobacco Industry Cover-Up” (1996), which examined the industry’s 40-year disinformation campaign on cigarette smoking; “Protecting America’s Health: The FDA, Business and One Hundred Years of Regulation” (2003), a history of the Food and Drug Administration; and “Rx for Survival: Why We Must Rise to the Global Health Challenge” (2005), in which he described how wealthy nations can help fight the threat of new and resurgent outbreaks of disease around the world.Mr. Hilts was the author of six hard-hitting nonfiction books on scientific, medical and social topics.Philip James Hilts was born on May 10, 1947, in Chicago. His father, Edward, was a nonfiction writer who also wrote historical fiction for children. His mother, Katherine (Bonn) Hilts, worked at a Sears store in several departments, including as a switchboard operator.Philip was one of seven children and grew up mainly in Hinsdale, Ill., a suburb west of Chicago.After high school, he served briefly in the merchant marine before attending Georgetown University in Washington, from 1965 to 1967. He then dropped out and hitchhiked to San Francisco to participate in the “Summer of Love,” when the hippie and counterculture movements were in full bloom.He returned to Georgetown in 1969 but never graduated, deciding instead to take up journalism. He undertook short stints as a reporter and photographer at small suburban newspapers and at The Washington Daily News in Washington, D.C., and The Rocky Mountain News in Denver before becoming a freelance magazine writer.He joined The Washington Post as a staff writer in the 1980s, taking time out for a Nieman fellowship at Harvard from 1984-85. He moved over to The Times’s Washington bureau in 1989 as a staff writer until 1996, when he became a contract writer until 2002.Mr. Hilts received several journalism fellowships, including one that sent him to Botswana, where he taught journalism. Most of his fellowships were devoted to science writing.He married Mary Donna McKeown, a fellow reporter at The Washington Daily News, in 1974; she died in 1987. In 1993, he married Carisa Cunningham, who at the time worked for nonprofit AIDS organizations; they divorced in 2011. He married Una MacDowell, who was a researcher in math and science education, in 2013. They lived in Cambridge, Mass., and Rochester, Vt. He died in a hospital.In addition to his wife and his son Ben, he is survived by another son, Sean; two daughters, Alexis and Kate Hilts; a grandson; four brothers, Edward, Paul, Michael and Mark; two sisters, Jeanne Young and Elizabeth Hilts; and two children from his wife’s first marriage, William and Nora MacDowell Coon.At his death, Mr. Hilts was finishing a book about Lynn Margulis, a biologist whose research into the origin of cells helped transform the study of evolution, and who was married for a time to the astronomer Carl Sagan.

Scientists at Scripps Research have invented a way to image, across different tissues and with higher precision than ever before, where drugs bind to their targets in the body. The new method could become a routine tool in drug development.
Described in a paper in Cell on April 27, 2022, the new method, called CATCH, attaches fluorescent tags to drug molecules and uses chemical techniques to improve the fluorescent signal. The researchers demonstrated the method with several different experimental drugs, revealing where — even within individual cells — the drug molecules hit their targets.
“This method ultimately should allow us, for the first time, to see relatively easily why one drug is more potent than another, or why one has a particular side effect while another one doesn’t,” says study senior author Li Ye, PhD, assistant professor of neuroscience at Scripps Research and The Abide-Vividion Chair in Chemistry and Chemical Biology.
The study’s first author, Zhengyuan Pang, is a graduate student in the Ye lab. The study also was a close collaboration with the laboratory of Ben Cravatt, PhD, Gilula Chair of Chemical Biology at Scripps Research.
“The unique environment at Scripps Research, where biologists routinely work together with chemists, is what made the development of this technique possible,” Ye says.
Understanding where drug molecules bind their targets to exert their therapeutic effects — and side effects — is a basic part of drug development. However, drug-target interaction studies traditionally have involved relatively imprecise methods, such as bulk analyses of drug-molecule concentration in entire organs.

Though purging is often a condition associated with bulimia nervosa, new research at Ohio University suggests that a different kind of eating disorder could also be responsible.
The study, published in the International Journal of Eating Disorders, sought to differentiate the little understood “purging disorder” from the more well-documented bulimia nervosa, with which it is often confused. The research was led by K. Jean Forney, an assistant professor of psychology in the College of Arts and Sciences at Ohio University who specializes in eating disorders.
Both purging disorder and bulimia nervosa are eating disorders characterized by self-induced vomiting and other types of purging. However, a central characteristic of bulimia is large, out-of-control eating episodes, whereas purging disorder isn’t defined by binge eating. Moreover, purging is an essential attribute of purging disorder, whereas bulimia nervosa may include non-purging behaviors like fasting or excessive exercise.
“In both conditions, people are going to extreme lengths to control their weight,” Forney said.
Because bulimia nervosa is well understood, it is easily diagnosed in the Diagnostic and Statistical Manual of Mental Disorders (DSM), which is used to diagnose mental health disorders. Purging disorder, however, hasn’t been well researched, and thus falls into the more ambiguous “residual” categories of the DSM.
“People tend to think conditions in the residual category are less dangerous, but that isn’t true,” Forney said. “There is plenty of cross-sectional data that suggest that the purging disorder is just as serious as bulimia nervosa.”
Because of its relative obscurity in the psychiatric world, until it is better understood, people suffering from purging disorder do not have psychiatric or psychological treatments that have been tested for their specific symptom presentation. Forney hopes that that the current study can provide a starting point for future intervention-related research.

The Food and Drug Administration on Friday laid out a tentative timetable for deciding whether to authorize a coronavirus vaccine for America’s youngest children, announcing that June 8 is the earliest date that it will present data to its outside advisers for a recommendation.The nation’s 18 million children under 5 are the only group not yet eligible for vaccination against the coronavirus.The agency said it understood the urgency of protecting that group and that it would act quickly “if the data support a clear path forward following our evaluation.”The F.D.A. laid out a packed June schedule, setting aside three days for its outside advisory committee to consider the pediatric vaccine applications from Moderna and Pfizer-BioNTech, and another day to debate and presumably vote on proposals to update existing vaccines so they work better against a range of coronavirus variants. The dates are tentative, the agency said, because the companies have not yet completed their applications for emergency authorization.The agency’s release of a schedule came after some critics raised concerns that it was delaying action on Moderna’s application in order to compare it with data from Pfizer, which is not expected in full until June. The F.D.A. commissioner, Robert Califf, said that was not the case in interviews on Thursday and Friday. “Categorically, there is no reason for the F.D.A. to wait,” he told Andy Slavitt on the podcast “In the Bubble.”Moderna said Thursday that it had asked the F.D.A. to authorize its vaccine for children six months to 6 years old, saying its clinical trial showed the vaccine was safe and produced an antibody response comparable to that of adults ages 18 to 25. That met the trial’s criterion for success. It said the vaccine appeared to be 51 percent effective against symptomatic infection among those younger than 2, and 37 percent effective among those 2 to 5.Those efficacy rates are far below those of earlier clinical trials conducted by both Moderna and Pfizer before the highly transmissible Omicron variant emerged. Omicron and its subvariants have proven far more adept at evading protection from antibodies that constitute the immune system’s first line of defense against infection.Because there were no cases of serious illness or hospitalization among any of the trial participants, it was not possible to judge how well the vaccine protects against Covid’s worst outcomes.Moderna said it would finish submitting its data to the F.D.A. by May 9. Pfizer and BioNTech are expected to complete their application to vaccinate children under 5 in June. The vaccine regimens are different: Moderna is proposing two doses, using one-fourth the strength of an adult dose. Pfizer and BioNTech are working on a three-dose regimen, at one-tenth the strength of the adult dose.Pfizer’s vaccine is already authorized for everyone 5 years and older, while Moderna’s shots are limited to adults. Moderna has previously requested authorization of its vaccine for children between the ages of 6 and 17. The company said it plans to submit data supporting and updating those requests in about two weeks.The F.D.A. appears to want to consider Moderna’s applications to vaccinate several age groups at the same time. Dr. Peter Marks, who oversees vaccine regulation, testified at a Senate hearing this week that it takes more time to review applications that cover a broader swath of the population.If so, that stance could trigger criticism. “That would certainly make the messaging somewhat easier: ‘Here’s this vaccine. It’s now available for all kids,’” Dr. Jesse L. Goodman, a former chief scientist with the F.D.A., said in an interview Thursday.But, he added: “The Pfizer vaccine is available for the older children. This younger group right now is the major unmet need. I don’t think there would be something wrong with authorizing the vaccine for the younger ones first, if they were ready.”The agency set June 28 for the advisory committee to consider the issue of how best to update the existing vaccines. Researchers working for the National Institutes of Health and vaccine manufacturers have been racing to try to redesign the vaccines so they are more effective against newer virus variants. Federal health officials have said they need to choose one or more revised versions by June in order to manufacture doses by the fall, when they expect the coronavirus to resurge.The agency also said that it plans to present vaccine data on June 7 from Novavax, which has developed a vaccine using a more conventional approach than the Pfizer-BioNTech and Moderna shots that have now been used to inoculate hundreds of millions of Americans.Those vaccines are based on newer messenger RNA technology, while Novavax’s vaccine is protein-based. Protein-based vaccines have been used for decades and generally have a strong track record of safety and mild side effects.If authorized, it is not clear what role Novavax vaccine would play in the nation’s vaccination program. But some experts suggest that people who are hesitant to take the Moderna or Pfizer-BioNTech shots might be more willing to accept the more conventional Novavax doses. It is also possible that a protein-based vaccine might work well as a booster to Pfizer or Moderna shots.

The health of residents living alongside a bus route in Gothenburg, Sweden, became considerably better when hybrid buses were replaced by buses fully powered by electricity. Along with the noise levels there was a reduction of fatigue, day time sleepiness and low mood, a study at the University of Gothenburg shows.
In the fall of 2019, all-electric buses were introduced on bus route 60 in Gothenburg. The implementation was linked to the ElectriCity project, with its participants from industry, research, and public agencies working for sustainable travel in an urban setting.
In places, the roads along this bus route in question are highly uneven. Noise levels from the preceding system of bus transportation had been perceived as disturbing, especially on the uphill stretches. Previous noise-level measurements had indicated that disturbance from low-frequency noise in indoor environments was present in the residential area.
How much the electric bus transportation would affect the noise levels was not clear, and the same applied to how people’s health would be influenced. The low-frequency noise was particularly important, since it has a high disturbance potential and it is further less well attenuated by façades or noise barriers.
Low-frequency noise hard to block
“We can be disturbed by different noises, but the issue with low-frequency noise is that it’s attenuated less well by facades or windows and therefore intrudes into people’s homes more easily. Even small increases in its level are perceived as very noticeable,” says Kerstin Persson Waye, Professor of Environmental Medicine at Sahlgrenska Academy, University of Gothenburg, who heads the Sound Environment and Health group that conducted the research.

As communities continue a shift toward normalcy in the wake of the Covid-19 pandemic, researchers at the Georgia Institute of Technology have helped quantify the effectiveness of one of the most commonly-debated mitigation measures taken across the country.
A new study published in BMC Public Health shows that hybrid learning utilizing alternating school days for children offers a significant reduction in community disease spread. Total closure in favor of remote learning, however, offers little additional advantage over that hybrid option.
This research will help decision-makers in the event of another Covid-19 outbreak or one from a similar infectious disease.
“Early in the pandemic when school closures were becoming the norm, many debated the pros and cons of this measure,” said Pinar Keskinocak, the William W. George Chair and Professor in ISyE and the principal investigator on the study. “Do we get enough benefit to offset the social costs and impacts on education? This research shows that there is a benefit in infection reduction, especially in the absence of effective pharmaceutical interventions, and most of the benefits can be attained with a hybrid approach.”
This study is particularly relevant for the early days of an infectious disease outbreak when policymakers face the difficult decision of enacting school closures in their respective districts. Using an agent-based simulation model of Covid-19 spread, researchers projected the impact of various school reopening strategies: complete closure, alternating school days where one cohort attended in person twice a week and another cohort on the opposite days, younger children only, and regular (i.e. all students return to in-person learning).
Results showed that compared to schools reopening with regular attendance, the percentage of the population infected reduced by 13, 11, 9, and 6 percent with each respective strategy. The conclusions were that some level of closure — younger children only, alternating days, and completely remote — offers significant reduction in community-wide infections. The benefit of complete closure over a hybrid approach, however, was minimal.
The assumption in all cases was that individuals who contracted the virus would remain at home.
“The additional benefit of complete school closure compared to hybrid was relatively small,” Kestinocak said. “The implementation of an alternating day model can be challenging but could have public health benefits early in the pandemic or during a new wave, providing social and learning benefits as well.”
Other challenges remain that were not investigated in this particular research — costs on families in the event of school closures, learning tradeoffs, properly equipping students for virtual learning, and others. This is just one element of many for policymakers to consider, Keskinocak said.
Story Source:
Materials provided by Georgia Institute of Technology. Note: Content may be edited for style and length.

A study recently completed at the University of Helsinki revealed that the fungal microbiota in the gut is more abundant and diverse in children treated with antibiotics compared with the control group even six weeks following the start of the antibiotic course. In light of the findings, a reduction in the number of gut bacteria as a result of antibiotic therapy reduces competition for space and leaves more room for fungi to multiply.
“The results of our research strongly indicate that bacteria in the gut regulate the fungal microbiota and keep it under control. When bacteria are disrupted by antibiotics, fungi, Candida in particular, have the chance to reproduce,” says PhD student Rebecka Ventin-Holmberg from the University of Helsinki.
A new key finding in the study was that the changes in the fungal gut microbiota, together with the bacterial microbiota, be part of the cause of the long-term adverse effects of antibiotics on human health.
Long-term changes in infant gut microbiota
Antibiotics are the most commonly prescribed drugs for infants. They cause changes in the gut microbiota at its most important developmental stage. These changes have also been found to be more long-term compared with those of adults.
“Antibiotics can have adverse effects on both the bacterial and the fungal microbiota, which can result in, for example, antibiotic-associated diarrhea,” Ventin-Holmberg says.

Understanding the molecular mechanisms that specify and maintain the identities of more than 200 cell types of the human body is arguably one of the most fundamental problems in molecular and cellular biology, with critical implications for the treatment of human diseases. Central to the cell fate decision process are stem cells residing within each tissue of the body.
When stem cells divide, they have the remarkable ability to choose to self-renew — that is, make a copy of themselves — or mature into defined lineages. How a specific lineage identity is maintained every time a stem cell divides can now be better understood thanks to the work of a team led by biochemists at the University of California, Riverside.
The study led by Sihem Cheloufi and Jernej Murn, both assistant professors in the Department of Biochemistry, shows how a protein complex, called chromatin assembly factor-1, or CAF-1, controls genome organization to maintain lineage fidelity. The report appears today in Nature Communications.
Each time a cell divides, it has to create a replica of its genome — not only its DNA sequence but also how the DNA is packaged with proteins into chromatin. Chromatin is organized into genomic sites that are either open and easily accessible or more densely packed and less accessible (or closed).
“Identities of different cells rely heavily on the genome sites that are more open because only genes located in those regions can potentially become expressed and turned into proteins,” Cheloufi explained.
She added that to maintain cell identity during cell division, the locations of open and closed chromatin, or “chromatin organization,” must be faithfully passed onto the new replica of the genome, a task largely entrusted to CAF-1.

Researchers from the University of Copenhagen and Aalborg University presents a new study demonstrating that a small molecule in brain cells affects the level of hypocretin, which is responsible for making us feel awake during the day and tired at night. People with a genetic variation of this molecule have a higher risk of suffering from daytime sleepiness.
When brain scientist Birgitte Kornum from the Department of Neuroscience recently arrived in Rome for one of the largest sleep conferences in the world, she was completely taken aback. There were pharmaceutical companies everywhere — with stands, information material and campaigns.
They all wanted to treat daytime sleepiness or to turn off the brain at night. And a lot of them focussed on hypocretin, which is a protein found in brain cells and which has recently attracted a lot of attention within sleep research.
This is because hypocretin is suspected to play a role in both insomnia, which is a decreased ability to fall asleep at night, and in narcolepsy, which is a decreased ability to stay awake during the day. People suffering from insomnia may have too much hypocretin in the brain, while people suffering from narcolepsy have too little. Researchers also suspect hypocretin to play a role in depression, ADHD and other mental disorders.
A lot is already known about the hypocretin system in the brain. There is even a new drug for insomnia countering the effect of hypocretin, latest introduced in Canada in 2018. According to Birgitte Kornum, though, the problem is that we know very little about how hypocretin is regulated inside the cells.
Therefore, Associate Professor Birgitte Kornum and her colleagues set out to shed light on the issue in a new study, which has recently been published in the reputed journal PNAS. The study combines tests on mice, zebrafish and human cells, and the researchers cooperated with their neighbours at the University of Copenhagen’s Department of Cellular and Molecular Medicine, among others.

Scientists have taken the first step to creating the next generation of wearable health monitors.
Most research on measuring human biomarkers, which are measures of a body’s health, rely on electrical signals to sense the chemicals excreted in sweat. But sensors that rely on perspiration often require huge amounts of it just to get a reading.
A new study suggests that a wearable sensor may be able to monitor the body’s health by detecting the gases released from a person’s skin.
“It is completely non-invasive, and completely passive on the behalf of the user,” said Anthony Annerino, lead author of the study and a graduate student in materials science and engineering at The Ohio State University.
Some wearable devices, like smartwatches or fitness trackers, are already capable of measuring pulse rates or temperatures, but this team’s method would allow the technology to sense biomarkers related to metabolic disorders, like heart disease or diabetes.
Their research is published in the journal PLOS One.