Publisher Health

Researchers from The University of Texas at Dallas Center for Vital Longevity (CVL) have discovered that brain correlates of age-related memory decline are more complicated than previously believed, a finding that could affect efforts to preserve cognitive health in older people.
Dr. Michael Rugg, CVL director and professor of psychology in the School of Behavioral and Brain Sciences, is the senior author of a study, published online Nov. 30 and in the Jan. 24 print edition of The Journal of Neuroscience, that found that age-related neural dedifferentiation, marked by a decline in the functional specialization of different brain regions, is driven by multiple mechanisms.
As people age — even in good health — the brain becomes less precise in how different classes of visual information are represented in the visual cortex. This reduction in neural selectivity, or dedifferentiation, is linked to worsening memory performance.
Using functional MRI (fMRI), the researchers examined the brain activity patterns of participants as they viewed images that belonged to broad categories of panoramic scenes and objects. Some of the images were repeated, thus allowing measurement of the brain’s activity patterns elicited by image categories, as well as by individual stimulus items. The participants included groups of healthy young and older adults — 24 men and women with an average age of 22 years, and 24 with an average age of 69 years.
“At the category level, as we expected, we found that the older group showed reduced selectivity for scenes compared to the younger group, but not for objects,” Rugg said. “But when we looked at individual items, selectivity for both scenes and objects were reduced in the older group. This implies that the mechanisms driving dedifferentiation at the single item level are not the same as those at the category level. We had, to this point, assumed they were one and the same mechanism.”
The implication, Rugg said, is that knowing how selective an individual’s brain is for categories does not predict how selective the brain will be for individual items.
“There isn’t a one-size-fits-all theory of age-related neural dedifferentiation,” said Rugg, who is also the Distinguished Chair in Behavioral and Brain Sciences. “This has important implications for how we understand and investigate age differences in neural selectivity, some measures of which are predictive of memory performance. Moving forward, we’re going to have to be more cautious in how we generalize from category-level findings to what’s happening more broadly in the brain as people grow older.”
Corresponding author Sabina Srokova PhD’22, a former student of Rugg’s who is now a research associate at the University of Arizona, said the findings suggest at least two independent factors drive the reduction in selectivity in older adults.

“We know that the neural mechanisms underlying category-level selectivity are robustly related to memory success across the adult lifespan,” Srokova said. “However, the factors that contribute to the relationship between neural selectivity, age and memory abilities remain unknown.
“Now that we believe different neural mechanisms are at work in these two contexts, it’s crucial that we continue to study them separately.”
Researchers will next examine the mechanisms that contribute to age-related declines in category-level selectivity using simultaneous recording of eye movements during fMRI scanning.
Additional study authors include Dr. Joshua D. Koen, a former postdoctoral fellow in Rugg’s functional Neuroimaging of Memory laboratory, and lab research assistant Ayse Aktas.
The work was funded by the National Institute on Aging, a component of the National Institutes of Health (R56AG068149 and RF1AG039103), and by the nonprofit organization BvB Dallas.

Fatty liver, which can lead to liver damage and disease, can occur from both overeating and starvation. Now, new research shows how naturally starvation-resistant cavefish, unlike other animals, are able to protect their liver and remain healthy. The findings have implications for understanding and potentially addressing liver conditions in humans.
Researchers from the Stowers Institute for Medical Research in collaboration with Universite Libre de Bruxelles in Belgium and Iowa State University compared cavefish to other animals more susceptible to starvation, and identified a gene responsible for the development of starvation-induced fatty liver. The study, published in Life Science Alliance on March 11, 2024, led by co-first authors Ansa Cobham, Ph.D., in the lab of Associate Investigator Nicolas Rohner, Ph.D., and Macarena Pozo-Morales, Ph.D., in the lab of Assistant Professor Sumeet Pal Singh, Ph.D., also showed that this evolutionarily conserved gene can be targeted by an existing drug candidate to protect against liver damage.
“This same approach can be applied to what we see in overconsumption,” Rohner said. “In Western societies where, often, too many calories and not enough exercise is a problem, this new understanding may lead to prevention or potential treatment of fatty liver disease.”
“We have discovered for the first time an organism — cavefish — that can avoid fatty liver under starvation conditions,” said Cobham. “Fatty liver can result in complications like liver cirrhosis and liver failure. This study helps us understand more about the biology underlying these diseases in humans.”
Cavefish are cousins of the Mexican tetra river fish that flooded into underground caves over 100,000 years ago. The researchers show that in the absence of food, cavefish at early developmental stages not only survive much longer than their river fish counterparts, but also do not accumulate liver fat.
“This was the first time we clearly showed that the mechanism for this resistance is accomplished by not accumulating excess fat in the liver,” said Rohner.
The accumulation of fat in liver cells leads to organ damage and atrophy or wasting away. The researchers compared gene expression levels between cavefish, river fish, zebrafish, and even fruit flies, identifying a gene that is activated during prolonged periods of starvation in all but cavefish.

“Expression levels of this gene are reduced in cavefish, which is a good indicator that if we are able to target this gene in humans, we may be able to treat or manage human metabolic diseases such as Type 2 diabetes and obesity,” said Cobham.
The team’s findings indicate that the starvation-induced gene not only regulates fatty liver disease, but its mechanism has also been conserved from fruit flies to fish to humans, or approximately 400 million years of animal evolution.
Inhibiting this gene’s protein in zebrafish and river fish larvae and deleting the gene in fruit flies resulted in less liver fat and larger livers indicating this protects the liver from damage and atrophy.
“The collaboration between Dr. Sumeet Singh’s team in Belgium, our team at Stowers, and scientists from Iowa State University combined our collective expertise in zebrafish, cavefish, and fruit flies to uncover the mechanism for starvation-induced fatty liver,” said Rohner.

A new analysis led by researchers at the Johns Hopkins Bloomberg School of Public Health estimates that 68 percent of Chicago children under age six live in households with tap water containing detectable levels of lead.
For their analysis, the researchers used machine learning, an artificial intelligence technique, to gauge likely levels of lead in tap water in households across Chicago, based on an existing dataset that includes results from 38,385 tap water tests taken from 2016 to 2023. The tests were from households that had registered for a free self-administered testing service for lead exposure.
The threshold the researchers used was the lowest detectable level of lead in the water tests, one part per billion — roughly the equivalent of a half teaspoon of water in an Olympic-size swimming pool. More than two-thirds — 69 percent — of the tests exceeded this level. From this, the machine learning model predicted lead-contaminated water in 75 percent of residential city blocks, covering 68 percent of Chicago children under 6. The Environmental Protection Agency’s current “action” level for lead in drinking water — the point at which a municipality must take additional steps — is 15 ppb. The analysis found that 9 percent of tests had lead levels over 15 ppb. The analysis also found racial inequities in exposure levels and testing rates.
The findings were published online March 18 in JAMA Pediatrics.
Lead is considered a serious environmental toxin, especially for children, with no “safe” exposure level. Lead pipes were used and often required before they were banned in the U.S. in 1986. Many cities still use lead water pipes that were installed prior to their ban. Chicago has more than any other U.S. city, an estimated 400,000 lead pipes that supply water to as many as 2.7 million people. Across the U.S., more than 9.2 million households get water through lead pipes and service lines, according to the Environmental Protection Agency.
The EPA has proposed that U.S. cities replace all lead water service lines within 10 years. Under the proposal, Chicago would get 40 years to comply, given the disproportionate burden its water infrastructure poses.
“The extent of lead contamination of tap water in Chicago is disheartening — it’s not something we should be seeing in 2024,” says study lead author Benjamin Huynh, PhD, an assistant professor in the Bloomberg School’s Department of Environmental Health and Engineering.

For their study, Huynh and colleagues set out to quantify the exposure faced by Chicago children under six.
The researchers began with a publicly available dataset from the Chicago Department of Water Management that contained 38,385 tap water test results for lead that participating Chicago households had taken from January 2016 to September 2023. The results covered about 36 percent of residential blocks in the city.
The researchers then combined these data with U.S. Census and other official data on block-by-block demographics and used machine learning techniques to extrapolate — from the partial coverage of the tap water test results — the likely block-by-block risk of having lead-contaminated water.
The analysis also used the city’s self-reported household survey data to estimate that 19 percent of exposed children — about 129,000 across the city — used unfiltered tap water for drinking. Using modeling, the researchers estimate that exposed children have approximately twice the amount of lead in their blood as unexposed children do.
The analysis suggested there are racial disparities in lead exposure in Chicago. For example, a 10 percentage-point increase in the Hispanic population was associated with an 11.2 percent increase in the chance of lead contamination. The analysis also suggests that Hispanic residents of the city were the least likely to drink unfiltered tap water, with 12 percent responding that they did. By contrast, 32 percent of white residents reported using unfiltered tap water as their primary drinking water source.
As for testing rates, Black and Hispanic populations were less likely to be tested for lead exposure, suggesting gaps in outreach. Ten percentage-point increases in Black and Hispanic populations were associated with 3- and 6-percent decreases respectively in chances of being tested for lead.
The authors note that the study has several limitations. The data on lead testing were anonymized at the block level, so the researchers were not able use household-specific data. The researchers did not have access to city-wide pediatric health records, and so had to model the health impacts of lead exposure instead of directly estimating them from data.

Although prevention and treatment strategies are available for influenza, they are not sufficient for vulnerable populations such as young children and newborns. In a new study, published in Virology, a multidisciplinary team of researchers have studied newborn piglets to better understand the progression of influenza infections.
The influenza A virus can infect a variety of birds and mammals, including humans and pigs, due to which it is a threat to public health and food security. While it causes mild to moderate infections in healthy individuals, susceptible human populations are at a higher risk. Even though vaccines and therapeutics are available, they are either less effective or they cannot be used in newborns and infants.
“Previous studies have looked at mice models, but compared to mice, pigs are a better model especially for studying immunity,” said Ying Fang (CGD/MMG), a professor of veterinary medicine. “This study is an extension of what we did in the past, where we looked at the effect of maternal immunity on piglets. It is the first study to use neonatal piglet models to elucidate the interactions between the host microbiota and the influenza virus.”
The respiratory tract in mammals is home to millions of microorganisms — collectively known as the microbiota. Other research groups have found that the microbiota can dictate an individual’s susceptibility to respiratory infections, either by improving immunity or making the infections worse.
To understand the interactions between the virus and the microbiota, the researchers used four types of viruses that differed based on their ability to cause disease. They introduced these virus suspensions drop-by-drop into each nostril of the piglets and monitored them for 5 days to see whether they displayed any symptoms, including changes in body temperature. The researchers also used nasal swabs to sample the microorganisms that were present at the beginning of the infection and after 5 days.
The team found that certain bacterial species, including Staphylococcus, were associated with the presence of lung lesions, higher rectal temperature, and viral loads, while others, such as Lactobacillus and Megasphaera, had the opposite effect. These results are in agreement with other studies that have shown that Staphylococcus is linked to inflammation and infection in other influenza and COVID-19 models.
“It is possible that microbes are mediating the impact of the virus on the host,” said Christopher Gaulke (MME), an assistant professor of pathobiology. “This means that we could potentially prevent some of the damaging impacts of these infections by providing animals or even humans with probiotic microbes that could be protective.”
They also found that regardless of what microbes were present on the first day, the infection disrupted the numbers and types of bacteria that were present in the nasal passages.

“These results suggest that by looking at the microbiota, we can predict whether a pig is infected regardless of the infecting virus strain. Although it might not be the best diagnostic tool at the moment, because it is relatively expensive, falling costs and improvements in statistical approaches could soon lead to low-cost microbiome-based diagnostics of swine health. It also highlights the possibility that we could use microbiome-based therapeutics to mitigate the impacts of influenza,” Gaulke said.
The researchers are now interested in lengthening the duration of the study to observe the long-term changes in the microbial composition.
“In this study, we focused on the acute phase of infection, so we don’t know the long-term impact: how long they take to recover the original levels of the microorganisms and whether they recover completely and resemble the uninfected pigs,” Fang said.
“We will also need to test whether these results hold in swine farms and whether they can implement anything that we come up with in our experimental barns,” Gaulke said. “Down the road, it would be interesting to see if these sorts of changes occur in human infants that are infected with influenza virus.”

After weight loss, people with overweight and obesity express more of the protein Kallistatin* in subcutaneous white adipose tissue. This was demonstrated by researchers from the DZD in a recent study. In addition, Kallistatin improves metabolism and could open up new therapeutic options for people with obesity and type 2 diabetes in future. The results have now been published in Molecular Metabolism.
An increasing number of people are developing type 2 diabetes and obesity. These are highly complex and multifaceted diseases. In order to treat them sustainably, new approaches to therapy are needed. Clinical studies on humans have shown that heavily overweight individuals produce less Kallistatin. Kallistatin is a protein that has various effects in the body. Among other things, it is involved in counteracting inflammation and healing wounds. The role that Kallistatin plays in glucose metabolism and its potential suitability as a therapeutic target are currently being investigated by researchers from the German Center for Diabetes Research (DZD), the Institute for Diabetes Research and Metabolic Diseases (IDM) of Helmholtz Munich at the Eberhard-Karls-University of Tübingen, and the Department of Diabetology, Endocrinology and Nephrology at the University Hospital Tübingen.
Kallistatin Expression Increases After Weight Loss
To this end, they measured Kallistatin expression in subcutaneous white adipose tissue in 47 individuals with overweight to obesity before and after weight loss. The result: Kallistatin expression increases after weight loss.
Kallistatin Improves Hepatic Insulin Sensitivity
Additionally, the researchers examined the effect of the protein in an animal model. In the process, they observed that human Kallistatin improves hepatic insulin sensitivity in diet-induced obese mice.
“Our results suggest that Kallistatin may be an interesting, yet challenging, therapeutic target for people with obesity and insulin resistance,” says lead author Leontine Sandforth. “Because Kallistatin has insulin-sensitizing effects in the liver, it should be investigated as a potential liver-specific target for emulating the beneficial effects of weight loss and potentially treating type 2 diabetes and obesity,” adds last author Prof. Andreas Birkenfeld.

Coronary heart disease is a major global health problem, especially among people with type 2 diabetes. Researchers at the German Center for Diabetes Research (DZD), Helmholtz Munich, and Ludwig-Maximilians-University Munich (LMU) have identified novel protein biomarkers that are associated with the development of CHD in people with and without diabetes. The results have been published in Cardiovascular Diabetology.
Coronary heart disease (CHD) is one of the most common causes of death worldwide — especially in Europe: Here, it is responsible for nearly half of all deaths. Among middle-aged adults, individuals with type 2 diabetes (T2D) have a two to four times higher risk of developing CHD than people without T2D. The research team investigated the predictive performance of protein biomarkers on incident CHD in individuals with and without T2D.
For their study, the researchers used data from Cooperative Health Research in the Region of Augsburg (KORA). The validation cohort included 888 participants from the KORA-Age1 study with 70 incident cases of CHD (19 vs. 51 cases in the group with T2D and without T2D, respectively) during 6.9 years of follow-up. They tested blood samples of the subjects for 233 plasma proteins related to cardiovascular disease and inflammation.
The researchers thus identified two proteins associated with incident CHD in individuals with diabetes and 29 proteins in those without baseline T2D. Six of these proteins are novel candidates for incident CHD.
The results of this study contribute significantly to a better understanding of the pathophysiology of CHD in T2D patients and offer potential new approaches to the prevention and treatment of this serious complication. They underscore the importance of further research in this area and the role of the German Center for Diabetes Research in resolving pressing issues related to diabetes and its complications.

A new study of camera-trap images complicates the idea that all wildlife thrived during the Covid lockdowns.In the early months of the Covid pandemic, when every bit of news seemed bleak, there was one heartwarming narrative that took hold: With humans stuck in their homes, the world was safe again for wild animals, which could now wander freely through cities, parking lots or fields that once might have been crowded with people.But a new global study, which used wildlife cameras to track human and animal activity during the Covid lockdowns, suggests that the story was not that simple.“We went in with a somewhat simplistic notion,” said Cole Burton, a wildlife ecologist and conservation biologist at the University of British Columbia, who led the research. “You know, humans stop, animals are going to breathe a sigh of relief and move around more naturally. And what we saw was quite different.”Although humans disappeared from some places during the lockdowns, they surged into others, like parks that remained open when little else was, the researchers found. And there was enormous variability in how wild mammals responded to changes in human behavior. Carnivores and animals living in remote, rural places, for instance, were more active when people faded from the landscape, while the opposite was generally true for large herbivores and urban animals.The study, which was published in Nature Ecology & Evolution on Monday, deepens and complicates scientists’ understanding of what has been called the “anthropause,” when pandemic lockdowns radically altered human behavior. It also highlights the nuanced ways in which humans affect the lives of wild animals, as well as the need for varied and multifaceted conservation efforts, the authors said.“There’s no ‘one size fits all’ solution when it comes to mitigating the impacts of human activity on wildlife,” said Kaitlyn Gaynor, a wildlife ecologist and conservation biologist at the University of British Columbia. “Because we see that not all species are responding similarly to people.”We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

The findings from the National Institutes of Health are at odds with previous research that looked into the mysterious health incidents experienced by U.S. diplomats and spies.New studies by the National Institutes of Health failed to find evidence of brain injury in scans or blood markers of the diplomats and spies who suffered symptoms of Havana syndrome, bolstering the conclusions of U.S. intelligence agencies about the strange health incidents.Spy agencies have concluded that the debilitating symptoms associated with Havana syndrome, including dizziness and migraines, are not the work of a hostile foreign power. They have not identified a weapon or device that caused the injuries, and intelligence analysts now believe the symptoms are most likely explained by environmental factors, existing medical conditions or stress.The lead scientist on one of the two new studies said that while the study was not designed to find a cause, the findings were consistent with those determinations.The authors said the studies are at odds with findings from researchers at the University of Pennsylvania, who found differences in brain scans of people with Havana syndrome symptoms and a control groupDr. David Relman, a prominent scientist who has had access to the classified files involving the cases and representatives of people suffering from Havana syndrome, said the new studies were flawed. Many brain injuries are difficult to detect with scans or blood markers, he said. He added that the findings do not dispute that an external force, like a directed energy device, could have injured the current and former government workers.The studies were published in The Journal of the American Medical Association on Monday alongside an editorial by Dr. Relman that was critical of the findings.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Published3 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, Michelle BatesBy Antonia MatthewsBBC News The wait to be diagnosed with endometriosis has increased to almost ten years, a “devastating” milestone say women with the condition.It now takes almost a year more than before 2020 to be diagnosed, according to research published by Endometriosis UK, which is setting up new volunteer-led support groups in Wales.The wait in Wales is also the longest in the UK, the research found.The Welsh government said it knew there was “room for improvement”.”Nobody listened to me, and to feel like women are still going through that 20 years after my diagnosis is horrific,” said Michelle Bates.The 48-year old from Cardiff was diagnosed aged 25 after suffering with “harrowing” pain from age 13 onwards – a 12-year wait.NHS Wales: Plan to cut waiting lists to a year by 2025Specialist endometriosis nurses appointedCall for menstrual wellbeing lessons in school”I went back and forth to the GP with my mum, who was the only one who believed in my pain,” she said. Ms Bates said she “knew there was something wrong” but explained her diagnosis was “accidental”.”I remember passing out at work one day. I was in so much pain,” recalled Ms Bates, who works in finance.An ultrasound for suspected appendicitis revealed three very large cysts, including one hanging from her ovary that was 12cm (4.7 inch) in diameter.She had just got married, and was told by her surgeon she had the worst case of endometriosis they had ever seen.In her early 30s and going through IVF, another doctor told her she was menopausal.”My chances of having a child were dashed,” Ms Bates said.What is endometriosis?The disease causes tissue similar to the lining of the womb to build up in other organs, such as the ovaries or fallopian tubes.Tissue builds up every month, and then breaks down and bleeds. Unlike cells in the womb that leave the body as a period, this blood can’t escape and can result in inflammation and scar tissue.It can cause severe, chronic pain and fatigue and can make it difficult to get pregnant.Some of the main hormone-based treatments for endometriosis include oral contraceptive pills and the intrauterine system (IUS), or coil.Other treatment options include surgically removing endometriosis tissue.There is no cure.Source: NHS/Endometriosis UK’Massively gaslighted’The study by Endometriosis UK, which is based on a survey of 4,371 people who received a diagnosis of endometriosis, showed almost half of all respondents (47%) had visited their GP 10 or more times with symptoms prior to receiving a diagnosis, and 70% had visited five times or more.It also found 78% of people who later went on to receive a diagnosis of endometriosis – up from 69% in 2020 – were told by doctors they were making a “fuss about nothing”, or comments to that effect.”We are massively gaslighted and invalidated by healthcare professionals,” said Charl Davies from Blaenavon, Torfaen.Image source, Charl DaviesThe 31-year-old was told the pain she was experiencing from the age of 10 onwards, when her periods started, was “just normal period pain” and “a normal part of being a woman”.”I was blacking out and fainting,” Ms Davies, a tattoo artist, said. “We’re taught to believe agonising period pain is normal pain.”She said receiving her diagnosis was a “very bittersweet feeling”, adding she was sick of hearing she had “a low pain threshold”.Lowri Shepstone, from Brecon, Powys, had to wait 17 years for a diagnosis and said she was also told her symptoms were not abnormal.Image source, Lowri Shepstone”Have a hot water bottle, and we’ll put you on the pill,” was her GP’s response when she was a teenager, she said.”The day I actually got a diagnosis, I nearly burst into tears.”The realisation something was seriously wrong was almost a relief, the 38-year-old said.’Real suffering'”There’s real suffering behind endometriosis,” Ms Bates said. “You kind of look OK but it robs you of enjoyment.” She said colleagues showed little understanding and she was left feeling isolated and low. “When you are having intercourse, you find yourself crying afterwards and thinking: ‘this is not normal’,” she said.Ms Shepstone also pointed out women suffering from endometriosis suffer from “endo belly”, caused by bloating.”You can look eight months pregnant but not be pregnant and potentially not be able to have children,” she said.”It’s like a cruel trick.”Ms Davies is due to undergo a third laparoscopy next month to remove tissue – a procedure she says she has waited 70 weeks for.She said daily pain made every day a struggle, even leaving her feeling suicidal.”I’ve got a body clock that is ticking. I can’t start a family until I’ve had the surgery and then there is a small window of opportunity,” she said.”As a woman, it makes you feel completely inadequate.”Three new Endometriosis UK volunteer groups will offer help for people with the condition in the Swansea area, in west Wales and in and around Wrexham.’Woefully inadequate’Female health charity Fair Treatment for the Women of Wales said patients who had access to an endometriosis nurse had “nothing but praise and gratitude for the care they offer”.”However, one endometriosis nurse per health board is woefully inadequate,” said Debbie Shaffer, policy and research director at the charity.”Some of the endometriosis nurses have told us that they have a patient list of over 1,000 at any one time.”The Welsh government said it had funded dedicated endometriosis nurses within each health board across NHS Wales.”Patient feedback suggests they feel supported, listened to, and have a better understanding of their condition,” the spokesman said.”But we know there is room for improvement, and we are working with the endometriosis nurses to identify areas for improvement.”More on this story’My debilitating condition has cost me £20K’Published8 March 2023Specialist endometriosis nurses appointedPublished8 March 2022Waits ‘too long’ for endometriosis helpPublished7 March 2018

Federal law requires states to go after the assets, usually homes, of people who died after receiving benefits for long-term care.The letter came from the state department of human services in July 2021. It expressed condolences for the loss of the recipient’s mother, who had died a few weeks earlier at 88.Then it explained that the deceased had incurred a Medicaid debt of more than $77,000 and provided instructions on how to repay the money. “I was stunned,” said the woman’s 62-year-old daughter.At first, she thought the letter might be some sort of scam. It wasn’t.She asked not to be identified, because the case is unresolved and she doesn’t want to jeopardize her chances of getting the bill reduced. The New York Times has reviewed documentation substantiating her account.The daughter moved into the family’s Midwestern home years earlier, when her widowed mother, who had vascular dementia, began to need assistance.Her mother was well insured, with Medicare, a private supplemental “Medigap” policy and long-term care insurance. The only reason she enrolled in Medicaid was that she had signed up for a state program that allowed her daughter to receive modest payments for caregiving.But that triggered additional monthly charges through a Medicaid managed care organization, and now the state wants that money back.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.