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About 7.5 million Americans suffer from psoriasis, an autoimmune disease that shows up as patches of red, inflamed skin and painful, scaly rashes. Although there are effective treatments for psoriasis, not everyone responds to these therapies — and for many, the relief is temporary.
“These therapies don’t reduce disease by 100 percent, and they don’t cure the disease” says La Jolla Institute for Immunology (LJI) Professor Michael Croft, Ph.D. “And if you take patients off those drugs, the disease almost always comes back.”
Now Croft and his team in LJI’s Center for Autoimmunity and Inflammation have discovered how a key protein called TWEAK damages skin cells in psoriasis patients. Their findings, in mice and with human skin cells, suggest targeting TWEAK may help control the disease
“We think TWEAK might be considered a potential target for the treatment of psoriasis,” says Rinkesh Gupta, Ph.D., a postdoctoral fellow at LJI and first author of the new Science Immunology study. “It’s good to have this chance to develop a new therapeutic option.”
The findings build on the Croft Lab’s previous work showing that TWEAK can interact with the most common type of skin cell, called a keratinocyte. By investigating TWEAK-deficient mice, the researchers found that TWEAK is a driver of inflammation in a model of psoriasis.
The new study shows that TWEAK does not work alone. By studying human keratinocytes, the researchers discovered that TWEAK teams up with two other proteins, called tumor necrosis factor (TNF) and interleukin-17 (IL-17), to trigger inflammation. This trio appears to control the production of inflammatory molecules and the expression of additional inflammation-associated proteins in patients with psoriasis.

The inherited progressive disorder cystic fibrosis (CF) causes severe damage to the lungs, and other tissues in the body by affecting the cells that produce mucus, sweat, and digestive juices. In individuals carrying mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which encodes an ion channel controlling the flow of ions and water in and out of cells, the mucus in airways and other passageways, which normally is thin and slippery, becomes sticky and thick — thus instead of acting as a lubricant, it becomes a congestant.
Advances in patient screenings and breakthrough therapies allow CF patients now to live into their mid- to late 30s or 40s, sometimes even longer. However, even the ~90% of patients (dependent on continent) with the most common CFTR mutation, called ?F508, who can be treated with available drugs, are still plagued by bacteria settling in their mucus, which causes inflammation in their lungs. The repeated bouts of infection and inflammation, as well as a chronic lower-grade inflammation between infections, gradually weakens and scars patients’ airways, which eventually causes their respiratory systems to fail. For the remaining ~10% of patients with various other CFTR mutations, no targeted treatments even exist yet. A major barrier to developing new and urgently needed treatments is the lack of human in vitro models that recapitulate the CF disease’s pathology.
Now, a multidisciplinary research team at Harvard’s Wyss Institute for Biologically Inspired Engineering led by Wyss Founding Director Donald Ingber, M.D., Ph.D. and supported by a grant from the Cystic Fibrosis Foundation, have developed a microfluidic Organ Chip device the size of a USB memory stick that recapitulates key pathological hallmarks from CF patients more accurately than other in vitro systems have so far. The model replicates CF-specific changes in multiple hallmarks of the disease, including in the airway’s mucus layer, beating of mucus-transporting cilia, pathogen growth, inflammatory molecules, and the recruitment of white blood cells, providing a comprehensive preclinical human model in which to investigate new CF therapies. The findings are published in the Journal of Cystic Fibrosis.
“Now that we are able to accurately model CF pathology, including microbiome and inflammatory responses, in human Airway Chips, we have a way to attack challenges that are important to CF patients,” said Ingber. “The bundled capabilities of this advanced in vitro model can help accelerate the search for drugs that may dampen the exaggerated immune response in patients, treat them with more personalized therapies and, help solve problems that CF patients face every day which cannot be addressed by existing treatments.” Ingber also is faculty lead of the Wyss’ Bioinspired Therapeutics & Diagnostics Platform, as well as the Judah Folkman Professor of Vascular Biology at Harvard Medical School and Boston Children’s Hospital, and Professor of Bioengineering at the Harvard John A. Paulson School of Engineering and Applied Sciences.
To model and compare the microstructure and function of vascularized CF airways, the authors grew lung airway cells obtained from human CF patients or healthy individuals in one of two parallel running hollow channels of a microfluidic device under air, recapitulating the lung’s air-transporting environment. In the second channel, which is separated from the first one by a porous membrane, they recreated a human blood vessel from human lung microvascular cells that was perfused with a blood substitute medium.
“This first microphysiological model of a CF airway closely mimics what we know from airways in CF patients. Maintaining the typical composition of all relevant cell types, it developed a thicker mucus layer, and its ciliated cells exhibit higher densities of cilia that beat at a higher frequency compared to Airway Chips created with airway cells from healthy individuals,” said co-first author and former Postdoctoral Fellow on Ingber’s team Ratnakar Potla, M.B.B.S., Ph.D. “Importantly, these pathological changes were accompanied by an enhanced inflammatory response in the modeled CF bronchial epithelium that is much like the one observed in CF patients.” Potla is now Senior Scientist of complex in vitrosystems at Genentech-Roche.
After culturing the Airway Chips for two weeks, the researchers measured the levels of pro- and anti-inflammatory factors flowing out of the Airway Chip’s vascular channel that are known to be involved in the inflammatory response in the lungs of CF patients. Among other changes, the level of the pro-inflammatory cytokine IL-8 was increased in CF chips compared to those in control Airway Chips. Interestingly, IL-8 is known for its ability to attract the type of white blood cells know as neutrophils that also drive inflammation in the lungs of CF patients.
When the researchers then actually flowed human neutrophils through the vascular channel of the CF Airway Chips, they observed that more of the immune cells spontaneously adhered to the surface of vascular cells, squeezed themselves through the vascular cell layer and porous membrane, and accumulated in the airway epithelial cell layer of the air channel — recapitulating a process known as “transmigration.”
But the CF-mimicking airway tissue not only stimulated immune cell recruitment, it also supported the growth of the bacterium, Pseudomonas aeruginosa, which is present in the microbiome of normal lung but can grow out of control and cause lung infections in human CF patients. Twenty-four hours after they introduced a fluorescently labeled version of P. aeruginosa into the airway channel of chips created with bronchial epithelial cells from CF patients, the team detected higher numbers of the pathogen in CF-specific mucus than in mucus in healthy Airway Chips. As a consequence, the levels of pro-inflammatory cytokines were further increased, thus replicating the infection-inflammation cycle seen in CF patients.
As next steps, the team will further personalize their CF Lung Airway Chip by generating versions in which bronchial epithelial, vascular endothelial, and immune cells all are obtained from the same patient. “For this proof-of-concept study, we have only used CF-specific bronchial airway cells from patients carrying the frequent ?F508 CFTR mutation. But different CFTR mutations may also affect the function of endothelial and immune cells and differ in their effects,” said co-first author Roberto Plebani, Ph.D. “By developing a panel of patient-specific Airway Chips using cells from patients with different mutations, and also by directly measuring the activity of differently compromised CFTR ion channels on-chip, drug responses and efficacies could be investigated in a highly personalized manner.” Plebani worked in Ingber’s lab as a visiting professor from the “G. d’Annnunzio” University of Chieti-Pescara in Italy, and spearheaded the project in Ingber’s group with Potla.
Other authors on the study were former and present members of Ingber’s team, including Mercy Soong, Haiqing Bai, Ph.D., Zohreh Izadifar, Ph.D., Amanda Jiang, Renee Travis, Chaitra Belgur, Alexandre Dinis, Mark Cartwright, Ph.D., Rachelle Prantil-Baun, Ph.D., Pawan Jolly, Ph.D., and Sarah Gilpin, Ph.D.; and Mario Romano, Ph.D. and Professor at the “G. d’Annnunzio” University of Chieti-Pescara in Italy. The study was funded by the Cystic Fibrosis Foundation, Harvard’s Wyss Institute for Biologically Inspired Engineering, and the Programme Operativo Nazionale Ricerca e Innovazione.

The vote was months in the making for the roughly $2 trillion measure, one of the most consequential bills in decades. Now it faces a difficult path in the Senate.WASHINGTON — The House on Friday narrowly passed the centerpiece of President Biden’s domestic agenda, approving $2 trillion in spending over the next decade to battle climate change, expand health care and reweave the nation’s social safety net, over the unanimous opposition of Republicans.The bill’s passage, 220 to 213, came after weeks of cajoling, arm-twisting and legislative legerdemain by Democrats. It was capped off by an exhausting, circuitous and record-breaking speech of more than eight hours by the House Republican leader, Representative Kevin McCarthy of California, that pushed a planned Thursday vote past midnight, then delayed it to Friday morning — but did nothing to dent Democratic unity.Groggy lawmakers reassembled at 8 a.m., three hours after Mr. McCarthy finally abandoned the floor, to begin the final series of votes to send one of the most consequential pieces of legislation in half a century to the Senate.Speaker Nancy Pelosi opened the final push with what she called “a courtesy to” her colleagues: “I will be brief.” She then put the House’s actions in lofty terms.“Under this dome, for centuries, members of Congress have stood exactly where we stand to pass legislation of extraordinary consequence in our nation’s history and for our nation’s future,” she said, adding, the act “will be the pillar of health and financial security in America.”The bill still has a long and difficult road ahead. Democratic leaders must coax it through the 50-50 Senate and navigate a tortuous budget process that is almost certain to reshape the measure and force it back to the House — if it passes at all.But even pared back from the $3.5 trillion plan that Mr. Biden originally sought, the legislation could prove as transformative as any since the Great Society and War on Poverty in the 1960s, especially for young families and older Americans. The Congressional Budget Office published an official cost estimate on Thursday afternoon that found the package would increase the federal budget deficit by $160 billion over 10 years.Representative Kevin McCarthy pushed a planned Thursday vote past midnight.Sarahbeth Maney/The New York TimesThe assessment indicated that the package overall would cost slightly more than Mr. Biden’s latest proposal — $2.1 trillion rather than $1.85 trillion. It offers universal prekindergarten, generous subsidies for child care that extend well into the middle class, expanded financial aid for college, hundreds of billions of dollars in housing support, home and community care for older Americans, a new hearing benefit for Medicare and price controls for prescription drugs.More than half a trillion dollars would go toward shifting the U.S. economy away from fossil fuels to renewable energy and electric cars, the largest investment ever to slow the warming of the planet. The package would largely be paid for with tax increases on high earners and corporations, estimated to bring in nearly $1.5 trillion over 10 years.Savings in government spending on prescription drugs were projected to bring in another $260 billion, though a scaled-back measure to allow Medicare to negotiate drug prices for some medications was estimated to save only $79 billion, far less than the Democrats’ original $456 billion proposal would have.“This bill will be transformational, and it will be measured in the deeper sense of hope that Americans will have when they see their economy working for them instead of holding them back,” Representative Steny H. Hoyer of Maryland, the House majority leader, said Thursday during what was supposed to the closing debate.The fact that the bill could slightly add to the federal deficit did not dissuade House Democrats from proceeding to vote for it, in part because the analysis boiled down to a dispute over a single line item: how much the I.R.S. would collect by cracking down on people and companies that dodge large tax bills.The budget office predicted that beefing up the I.R.S. with an additional $80 billion of funding would bring in just $127 billion over 10 years on net. That is far less than the $400 billion the White House estimates it would bring in over a decade, both through enforcement actions and by essentially scaring tax cheats into paying what they owe.The legislation is moving through Congress under special rules known as reconciliation that shield it from a filibuster, allowing Democrats to push it through over unified Republican opposition in the Senate.Even pared back from the $3.5 trillion plan President Biden originally sought, the House measure could prove as transformative as any legislative effort since the 1960s.Doug Mills/The New York TimesIt is a key piece of Mr. Biden’s domestic policy agenda, paired with a $1 trillion infrastructure package that the president signed into law this week. Its path to Friday’s vote was arduous, from midsummer to deep autumn, with negotiations pitting liberal lawmakers against centrists and House Democrats against senators.Democrats in the Senate and House had hoped to reach agreement on a final bill before either chamber voted, but that plan was ditched weeks ago amid persistent infighting.And from the beginning, Republicans — who made it clear they could never support a package of the scope and ambition Mr. Biden had proposed — were cut out of the reconciliation talks. While some Republicans voted for the infrastructure measure, they unanimously opposed the expansive social safety net package, arguing that it would constitute a “socialist” encroachment of the federal government into every aspect of American life, and would exacerbate rising costs across the country.Mr. McCarthy, the minority leader, took advantage of the House’s so-called “magic minute” — a custom that allows leaders to speak without time constraints when they are granted their minute of floor time.He held the floor well into Friday morning, railing for more than eight hours against the bill and the Biden administration, breaking the record for the longest consecutive House speech set by Ms. Pelosi in 2018 before he concluded at 5:10 a.m. Some Democrats pointedly walked out before he began to speak, and at times interrupted his speech against the bill with boos, heckles and jeers.“Every page of all this new Washington spending shows just how irresponsible and out of touch the Democrats are to the challenges that America faces today,” Mr. McCarthy said during his diatribe, which appeared designed more to rally his Republican base behind a message for the midterm elections in a debate that had been scheduled to last just 20 minutes.But just hours later, Democrats filed into the chamber, joking about the lack of sleep. And if Democrats feared the political consequences, it was not evident from the final tally, which reflected support among those from the most competitive districts.The only Democrat who opposed the bill, Representative Jared Golden of Maine, did so after raising concerns this month about the inclusion of a provision that would generously increase the federal tax deduction for state and local taxes paid, from $10,000 a year to $80,000. Understand the U.S. Debt CeilingCard 1 of 6What is the debt ceiling?

After weeks of contradictory statements and confusing guidelines about which Americans need booster shots of coronavirus vaccines, federal health officials are poised to recommend them to everyone over 18.An advisory panel to the Centers for Disease Control and Prevention is scheduled to meet on Friday to weigh the pros and cons of recommending the boosters to all adults. But the discussion is not expected to turn up any surprises, and the final recommendations from the agency itself are likely to align with President Biden’s promise that all adults would be eligible for extra doses. The meeting is to begin at 12 p.m. Eastern time.Desperate to dampen even a dim echo of last winter’s horrors, the Biden administration is betting that booster shots will shore up what some have characterized as waning immunity among the fully vaccinated. The Food and Drug Administration authorized boosters of the Pfizer-BioNTech and Moderna vaccines for all adults on Friday.Research suggests that the shots may help forestall at least some infections, particularly in older adults and those with certain health conditions.After an all too brief respite, coronavirus infections are inching up again, particularly in parts of the country where cooler weather is hustling people indoors.The C.D.C.’s decision will land just as Americans are poised to travel, likely in record numbers, to spend the holidays with family and friends. Given the roughly 100 million Americans who have yet to receive a single dose of vaccine, holiday travel and get-togethers could send cases skyrocketing, as they did last year.Several European countries are also offering boosters to all adults in a bid to contain fresh waves of infections. France has gone so far as to mandate booster shots for those over age 65 who wish to get a health pass permitting access to public venues.“Look what other countries are doing now about adopting a booster campaign virtually for everybody,” Dr. Anthony S. Fauci, the Biden administration’s top Covid adviser, said at a conference on Tuesday. “I think if we do that, and we do it in earnest, I think by the spring we can have pretty good control of this.”But many experts, including some who advise federal agencies, are skeptical that boosters alone can turn the tide. While the extra shots can strengthen immunity in older adults, they are unlikely to offer much benefit to adults under 65, who remain protected from severe illness and hospitalization by the initial immunization, the experts said.It is also unclear whether booster shots can significantly slow the spread of the virus. The limited evidence available suggests that vaccines can blunt transmission, but only to a limited extent and for a limited period..css-1xzcza9{list-style-type:disc;padding-inline-start:1em;}.css-3btd0c{font-family:nyt-franklin,helvetica,arial,sans-serif;font-size:1rem;line-height:1.375rem;color:#333;margin-bottom:0.78125rem;}@media (min-width:740px){.css-3btd0c{font-size:1.0625rem;line-height:1.5rem;margin-bottom:0.9375rem;}}.css-3btd0c strong{font-weight:600;}.css-3btd0c em{font-style:italic;}.css-1kpebx{margin:0 auto;font-family:nyt-franklin,helvetica,arial,sans-serif;font-weight:700;font-size:1.125rem;line-height:1.3125rem;color:#121212;}#NYT_BELOW_MAIN_CONTENT_REGION .css-1kpebx{font-family:nyt-cheltenham,georgia,’times new roman’,times,serif;font-weight:700;font-size:1.375rem;line-height:1.625rem;}@media (min-width:740px){#NYT_BELOW_MAIN_CONTENT_REGION .css-1kpebx{font-size:1.6875rem;line-height:1.875rem;}}@media (min-width:740px){.css-1kpebx{font-size:1.25rem;line-height:1.4375rem;}}.css-1gtxqqv{margin-bottom:0;}.css-19zsuqr{display:block;margin-bottom:0.9375rem;}.css-12vbvwq{background-color:white;border:1px solid #e2e2e2;width:calc(100% – 40px);max-width:600px;margin:1.5rem auto 1.9rem;padding:15px;box-sizing:border-box;}@media (min-width:740px){.css-12vbvwq{padding:20px;width:100%;}}.css-12vbvwq:focus{outline:1px solid #e2e2e2;}#NYT_BELOW_MAIN_CONTENT_REGION .css-12vbvwq{border:none;padding:10px 0 0;border-top:2px solid #121212;}.css-12vbvwq[data-truncated] .css-rdoyk0{-webkit-transform:rotate(0deg);-ms-transform:rotate(0deg);transform:rotate(0deg);}.css-12vbvwq[data-truncated] .css-eb027h{max-height:300px;overflow:hidden;-webkit-transition:none;transition:none;}.css-12vbvwq[data-truncated] .css-5gimkt:after{content:’See more’;}.css-12vbvwq[data-truncated] .css-6mllg9{opacity:1;}.css-qjk116{margin:0 auto;overflow:hidden;}.css-qjk116 strong{font-weight:700;}.css-qjk116 em{font-style:italic;}.css-qjk116 a{color:#326891;-webkit-text-decoration:underline;text-decoration:underline;text-underline-offset:1px;-webkit-text-decoration-thickness:1px;text-decoration-thickness:1px;-webkit-text-decoration-color:#326891;text-decoration-color:#326891;}.css-qjk116 a:visited{color:#326891;-webkit-text-decoration-color:#326891;text-decoration-color:#326891;}.css-qjk116 a:hover{-webkit-text-decoration:none;text-decoration:none;}Many pandemic-weary Americans, too, seem unmoved by the administration’s push for boosters. More than 85 percent of the adult population is already eligible, but only about 17 percent has chosen to get them. And those may not be the people most in need of extra protection.As with the initial shots, fully vaccinated white people are more likely to have lined up for a booster shot, compared with other racial and ethnic groups, according to data compiled by the Kaiser Family Foundation.So far, the people who have opted for boosters “tend to be of higher socioeconomic status and more highly educated, and have more access in general to medical care,” said Dr. Celine Gounder, an infectious disease specialist at Bellevue Hospital Center.“That’s not necessarily who’s actually at risk of severe disease, hospitalization or death, and so I think you’re going to have limited public health impact.”

Researchers at The University of Texas at Dallas are investigating the use of whole-cell vaccines to fight urinary tract infection (UTI), part of an effort to tackle the increasingly serious issue of antibiotic-resistant bacteria.
Dr. Nicole De Nisco, assistant professor of biological sciences, and Dr. Jeremiah Gassensmith, associate professor of chemistry and biochemistry, recently demonstrated the use of metal-organic frameworks (MOFs) to encapsulate and inactivate whole bacterial cells to create a “depot” that allows the vaccines to last longer in the body.
The resulting study, published online Sept. 21 in the American Chemical Society’s journal ACS Nano, showed that in mice this method produced substantially enhanced antibody production and significantly higher survival rates compared to standard whole-cell vaccine preparation methods.
“Vaccination as a therapeutic route for recurrent UTIs is being explored because antibiotics aren’t working anymore,” De Nisco said. “Patients are losing their bladders to save their lives because the bacteria cannot be killed by antibiotics or because of an extreme allergy to antibiotics, which is more common in the older population than people may realize.”
The American Urological Association estimates that 150 million UTIs occur yearly worldwide, accounting for $6 billion in medical expenditures. If not successfully treated, a UTI can lead to sepsis, which can be fatal.
Recurrent UTI, De Nisco said, is primarily regarded as a women’s health issue, and although it’s common — especially in postmenopausal women — it’s something many women don’t talk about a lot.

‘Plague sceptics’ are wrong to underestimate the devastating impact that bubonic plague had in the 6th- 8th centuries CE, argues a new study based on ancient texts and recent genetic discoveries.
The same study suggests that bubonic plague may have reached England before its first recorded case in the Mediterranean via a currently unknown route, possibly involving the Baltic and Scandinavia.
The Justinianic Plague is the first known outbreak of bubonic plague in west Eurasian history and struck the Mediterranean world at a pivotal moment in its historical development, when the Emperor Justinian was trying to restore Roman imperial power.
For decades, historians have argued about the lethality of the disease; its social and economic impact; and the routes by which it spread. In 2019-20, several studies, widely publicised in the media, argued that historians had massively exaggerated the impact of the Justinianic Plague and described it as an ‘inconsequential pandemic’. In a subsequent piece of journalism, written just before COVID-19 took hold in the West, two researchers suggested that the Justinianic Plague was ‘not unlike our flu outbreaks’.
In a new study, published in Past & Present, Cambridge historian Professor Peter Sarris argues that these studies ignored or downplayed new genetic findings, offered misleading statistical analysis and misrepresented the evidence provided by ancient texts.
Sarris says: “Some historians remain deeply hostile to regarding external factors such as disease as having a major impact on the development of human society, and ‘plague scepticism’ has had a lot of attention in recent years.”
Sarris, a Fellow of Trinity College, is critical of the way that some studies have used search engines to calculate that only a small percentage of ancient literature discusses the plague and then crudely argue that this proves the disease was considered insignificant at the time.

New research shows how genetic variations linked to severe cases of COVID-19 affect our immune cells.
The study, led by scientists at La Jolla Institute for Immunology (LJI), is one of the first in-depth look at the connections between COVID-19 severity and gene expression in many types of immune cells. This work could guide the development of new COVID-19 therapies to boost immune cell function.
Among their findings, the researchers report that a gene in a cell type called non-classical monocytes, which are part of the body’s “first responder” team of innate immune cells, could be a potential target for COVID-19 therapies.
“This study highlights the power of human genetics to uncover novel pathways linked to disease,” says LJI Professor Pandurangan Vijayanand, M.D., Ph.D., senior author of the Nature Communications study.
The science community has identified many genetic differences, called polymorphisms, they call “severe COVID-19-risk variants.” These genetic variants are associated with gene expression and appear to influence case severity. Yet scientists didn’t know which immune cells are most affected by these risk variants.
For the new study, Vijayanand and his colleagues combined patient genetic data from the COVID-19 Host Genetic Initiative and LJI’s open-access Database of Immune Cell Epigenomes (DICE) to define the genes and susceptible cell types affected by these risk variants. The team looked at 13 subtypes of the body’s key protective and virus-fighting cells: T cells, B cells, NK cells and monocytes.

A study led by researchers at Children’s Hospital of Philadelphia (CHOP) has implicated several genes involved in a variety of bodily functions associated with the hypothalamus, a notoriously difficult-to-study region of the brain. The findings could help clinicians identify potential causes of dysfunction for many important traits regulated by the hypothalamus, such as sleep, stress, and reproduction.
The findings were published today in the journal Nature Communications.
The hypothalamus helps maintain health and stable metabolism by influencing a variety of vital functions, including appetite and thirst, puberty and reproductive timing, sleep cycles, and body temperature. However, the hypothalamus is located in the center of the brain, making it extremely difficult to study the gene regulation associated with these traits.
To overcome that hurdle, the researchers used an embryonic stem cell (ESC) model to study gene expression during development of the hypothalamus. This model allowed them to study the genetic architecture first in hypothalamic progenitor cells — cells prior to their full development into a hypothalamus — and then in arcuate nucleus-like hypothalamic neurons. The hypothalamus contains several different subtypes of neurons, and the researchers integrated results from various genome-wide association studies (GWAS) to implicate genes driving particular traits regulated by the hypothalamus.
“By studying the three-dimensional genomic architecture of these cell models, we can see the dynamic process of how the hypothalamus is formed over different stages of development,” said senior study author Struan F.A. Grant, PhD, Director of the Center for Spatial and Functional Genomics and the Daniel B. Burke Endowed Chair for Diabetes Research at CHOP. “The information we yielded in this study provides us with more concrete information about diseases that are relevant to hypothalamic function.”
Grant and his collaborators assessed variants associated with puberty, body mass index, height, bipolar disorder, sleep, and major depressive disorder, among others. They identified both known and novel genes associated with these traits. For example, their data confirmed the role of the BDNF of gene in influencing body mass index and obesity risk. Another gene of interest identified in the study was PER2, which was implicated in sleep regulation.
All the data ascertained from this study will be made publicly available. Many of the disorders studied can be caused by other factors, so the findings will help researchers distinguish which genes play a more central role in this tissue and in turn inform clinical practice. For example, body mass index can be affected by variants in genes conferring their effects in hypothalamus or fat tissue cells, so being able to distinguish the context in which genes and subsequent tissues or hormones operate can lead to more personalized treatment options.
“The data set we derived from this study allows other researchers to determine which diseases or conditions are relevant when doing a genetic workup of the patient,” Grant said. “As more information about the hypothalamus is known, that information can be queried against this data set and potentially identify therapeutic targets for multiple disorders.”
This research was supported by the National Center for Research Resources (UL1RR024134) and the National Center for Advancing Translational Sciences (UL1TR000003). This research was also supported in part by the Institute for Translational Medicine and Therapeutics (ITMAT) Transdisciplinary Program in Translational Medicine and Therapeutics, the Eunice Kennedy Shriver National Institute of Child Health (NIH1K99HD099330-01), and National Institutes of Health grants DK52431-23, P30DK026687-41, R01 HD056465, R01 HG010067, R01 HL143790, and the Daniel B. Burke Endowed Chair for Diabetes Research.
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Identifying specific facial features that can be used to distinguish a child’s face from an adult’s may offer a useful tool for determining whether children are depicted in indecent images of children, according to research led by the University of Birmingham.
The shape of our nose and eyebrows contains critical information used to identify adult faces, while the eye and jawline are used to identify a child’s face, according to the study, published in Frontiers in Psychology. Understanding these visual cues could lead to improvements in the automation techniques and training developed to identify and classify indecent images of children.
Researchers in the University of Birmingham’s School of Psychology and the Department of Psychology at the University of Montreal designed an experiment to determine how people make judgements about whether the person depicted was a child or adult from specific facial features. Their aim was to find out whether focusing on these features could enable more accurate distinction between child and adult faces.
Current processes to identify indecent images of children require digital forensics analysts in police forces to review images and make a decision. This is a time-consuming and emotionally challenging task and work is already well underway to design computer algorithms to automate part of the process. It is anticipated that the findings from this new study will inform and contribute to that development.
In this study, the researchers worked with 16 volunteers, including digital forensic analysts from West Midlands Police. Each volunteer was shown a series of images depicting faces of either children or adults, each revealed through a filter that excluded non-facial cues such as ears, hair and neck. They were asked to identify the faces as belonging to either children or adults.
The researchers used image processing techniques to analyse which facial attributes of both children and adults the volunteers used to make their identifications. They found that information around the nasal bone and eyebrows were most commonly used to classify adult faces, while the eyes, nose and jawline were more likely to be used to classify a child’s face.
Dr Juliane Kloess, at the University of Birmingham, explained: “The number of indecent images of children in circulation has dramatically increased over the past 25 years. We hope that our findings may assist with the way computer algorithms prioritise images for human attention, which will help to partially automate the process of identifying and classifying this material. This would alleviate the pressures on existing resources within policing, and reduce the exposure of analysts to this type of material.”
Professor Jessica Woodhams, also at the University of Birmingham, added: “There are many physical changes which happen as faces mature. While it can be difficult even for experts to distinguish between faces of similar-aged children, by using the specific facial features we identified, the task of discriminating between child and adult faces may become easier.”
The researchers suggest their findings could be used to develop artificial intelligence algorithms to make the job of identifying children in indecent images of children easier. They may also be used to inform the current national grading training course, with a view to teaching digital forensics analysts that certain facial features are more indicative of children’s faces than adult’s faces.
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SharecloseShare pageCopy linkAbout sharingImage source, ReutersDays after Austria imposed a lockdown on the unvaccinated, it has announced a full national Covid-19 lockdown starting on Monday.Chancellor Alexander Schallenberg said it would last a maximum of 20 days and there would be a legal requirement to get vaccinated from 1 February 2022.He was responding to record cases numbers and one of the lowest vaccination levels in Western Europe.Many other European countries are imposing restrictions as cases rise.”We don’t want a fifth wave,” said Mr Schallenberg after meeting the governors of Austria’s nine provinces at a resort in western Austria. Latest figures show an incidence rate of 990.7 cases per 100,000 people in the past week, and Health Minister Wolfgang Mückstein said imposing a lockdown was a “last resort”. Under the measures, Austrians will be told to work from home, non-essential shops will close, and schools will remain open for children who require face-to-face learning. They will continue until 12 December, but will be reassessed after 10 days.Slovak Prime Minister Eduard Heger announced that what he called a lockdown for the unvaccinated would start on Monday, and the Czech government is also limiting access to a variety of services. The Netherlands introduced a partial lockdown last weekend.German leaders have agreed to introduce restrictions for unvaccinated people in areas with high Covid hospital admissions that would affect 12 of Germany’s 16 states. Austria’s is the first full lockdown imposed by an EU country this winter. The Europe regional director of the World Health Organization, Hans Kluge, has warned of a hard winter ahead. He blamed insufficient vaccination coverage along with “the easing of preventive measures and the spread of the more transmissible Delta variant”.