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Biological systems can behave as siblings in several ways, including by borrowing something and never giving it back. That appears to be what the human immune system did with a protein that now helps bind and regulate the subunits that make up antibodies, according to a multi-institute research collaboration. They found that, before the immune system evolutionarily co-opted it, the protein originally belonged to gene family responsible for directing cells to move to the right location at the right time to address specific functional needs.
The researchers, including Kazuhiko Kawasaki, associate research professor of anthropology at Penn State, published their findings in the Proceedings of the National Academy of Sciences. According to the team, while this work primarily informs a fundamental understanding of one feature of the immune system and associated genes, it may also help open design pathways future therapeutics, such as personalized immune responses.
“Everything comes from somewhere, and we believe we found the origin of immunoglobin Joining chain (J chain), an important immune molecule,” said corresponding author Martin F. Flajnik, department of microbiology and immunology, University of Maryland, who led the study. Flajnik also earned his undergraduate degree in biology from Penn State in 1978 before completing his graduate degrees at the University of Rochester.
The J chain assembles and stabilizes two types of antibodies, called immunoglobin M (IgM) and immunoglobin A (IgA). It specifically regulates the structures of the IgM and IgA molecules, which have several subunits, and is required for their movement across the mucus-producing tissue lining body structures with external exposure, like the intestine, nasal cavity and lungs. The researchers found that the J chain originated from the CXCL chemokines, a specific family of proteins that regulate the ability of white blood cells to move throughout the body.
“Like immunoglobin itself and human-like adaptive immunity, the J chain emerged in jawed vertebrates, but its origin has remained mysterious since its discovery over 50 years ago,” Flajnik said. “This finding was never anticipated. Chemokine-driven locomotion is a vital function of the immune system, but a totally different function as compared to the J chain!”
Evolutionarily, new genes are often generated from genes that reside physically close together on the chromosome, and those genes typically remain clustered together even as they evolve different yet similar functions, but Kawasaki said location isn’t the only deciding factor to determine origin.
“The evolutionary relationship of genes can usually be detected when two genes retain similar nucleotide sequences or encoded amino acid sequences,” Kawasaki said, referring to the materials comprising an organism’s genetic code. “But previous studies could not detect any genes that show sequence similarities to the J chain gene, probably because the J chain gene sequence was quickly changed at its origin.”
Flajnik said he had a hunch that the J chain was related to a group of secretory calcium-binding phosphoprotein (SCPP) genes due to their similar charges and levels of proline, an amino acid. He knew Kawasaki was an expert on SCPP genes, so he emailed him to assess the idea.

“He told me that, for various good reasons, the SCPPs and J chain were not related,” Flajnik said. “That was sad, as it was my favorite hypothesis.”
However, Kawasaki had noticed that genes on the opposite side of the J chain gene, away from the SCPP genes, did appear to be related to the J chain. Those were the CXCL chemokine genes.
“I immediately checked these CXCL chemokine genes and found that, though these genes do not show sequence similarities to the J chain genes, these genes and the J chain gene resemble each other with other various characteristics,” Kawasaki said.
Those characteristics include the same number of exons, which encode the protein, and phases of introns, which act as interrupters to stop or start splicing of the RNA molecules transcribed from the gene. The second exon encodes the same sequence, which is known as the classical tripeptide Cysteine-X-Cysteine, for both genes. The lengths of three of the exons are also similar.
“No other gene encoding the human secretome, which encompasses all proteins that can be secreted by cells of an organism, shares all three characteristics,” Kawasaki said.
The bonds between the Cysteine molecules encoded by the second exon in each gene are completely different from one another, though, the researchers said.

“This means that a chemokine can change its structure, to a large extent, and take on a new function,” Flajnik said.
Next, the researchers said they plan to investigate if chemokines have taken on other functions, specifically in the immune system. They also want to study if chemokines are pliable in their structure, which could indicate the ability to take on an entirely new secondary structure, adapting in response to different biological needs as required.
“I’ve been around for a long time, for 44 years in science, but this experience was one of the most incredibly satisfying and lucky,” Flajnik said. “I doubt that this similarity would have been uncovered for a long time without the serendipitous interaction between Kazuhiko and me.”
Other co-authors include Yuko Ohta, assistant professor of microbiology and immunology at the University of Maryland, and Caitlin D. Castro, a research fellow in the Department of Biochemistry and Molecular Biology at the University of Chicago.
The National Institutes of Health supported this research.

Researchers at the National Institutes of Health observed rapid and distinct immune system changes in a small study of people who switched to a vegan or a ketogenic (also called keto) diet. Scientists closely monitored various biological responses of people sequentially eating vegan and keto diets for two weeks, in random order. They found that the vegan diet prompted responses linked to innate immunity — the body’s non-specific first line of defense against pathogens — while the keto diet prompted responses associated with adaptive immunity — pathogen-specific immunity built through exposures in daily life and vaccination. Metabolic changes and shifts in the participants’ microbiomes — communities of bacteria living in the gut — were also observed. More research is needed to determine if these changes are beneficial or detrimental and what effect they could have on nutritional interventions for diseases such as cancer or inflammatory conditions.
Scientific understanding of how different diets impact the human immune system and microbiome is limited. Therapeutic nutritional interventions — which involve changing the diet to improve health — are not well understood, and few studies have directly compared the effects of more than one diet. The keto diet is a low-carbohydrate diet that is generally high in fat. The vegan diet eliminates animal products and tends to be high in fiber and low in fat.
The study was conducted by researchers from the NIH’s National Institute of Allergy and Infectious Diseases (NIAID) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) at the Metabolic Clinical Research Unit in the NIH Clinical Center. The 20 participants were diverse with respect to ethnicity, race, gender, body mass index (BMI), and age. Each person ate as much as desired of one diet (vegan or keto) for two weeks, followed by as much as desired of the other diet for two weeks. People on the vegan diet, which contained about 10% fat and 75% carbohydrates, chose to consume fewer calories than those on the keto diet, which contained about 76% fat and 10% carbohydrates. Throughout the study period, blood, urine, and stool were collected for analysis. The effects of the diets were examined using a “multi-omics” approach that analyzed multiple data sets to assess the body’s biochemical, cellular, metabolic, and immune responses, as well as changes to the microbiome. Participants remained on site for the entire month-long study, allowing for careful control of the dietary interventions.
Switching exclusively to the study diets caused notable changes in all participants. The vegan diet significantly impacted pathways linked to the innate immune system, including antiviral responses. On the other hand, the keto diet led to significant increases in biochemical and cellular processes linked to adaptive immunity, such as pathways associated with T and B cells. The keto diet affected levels of more proteins in the blood plasma than the vegan diet, as well as proteins from a wider range of tissues, such as the blood, brain and bone marrow. The vegan diet promoted more red blood cell-linked pathways, including those involved in heme metabolism, which could be due to the higher iron content of this diet. Additionally, both diets produced changes in the microbiomes of the participants, causing shifts in the abundance of gut bacterial species that previously had been linked to the diets. The keto diet was associated with changes in amino acid metabolism — an increase in human metabolic pathways for the production and degradation of amino acids and a reduction in microbial pathways for these processes — which might reflect the higher amounts of protein consumed by people on this diet.
The distinct metabolic and immune system changes caused by the two diets were observed despite the diversity of the participants, which shows that dietary changes consistently affect widespread and interconnected pathways in the body. More study is needed to examine how these nutritional interventions affect specific components of the immune system. According to the authors, the results of this study demonstrate that the immune system responds surprisingly rapidly to nutritional interventions. The authors suggest that it may be possible to tailor diets to prevent disease or complement disease treatments, such as by slowing processes associated with cancer or neurodegenerative disorders.

The composition of microbiota found in the gut influences how susceptible mice are to respiratory virus infections and the severity of these infections, according to researchers from the Center for Translational Antiviral Research in the Institute for Biomedical Sciences at Georgia State University.
The findings, published in the journal Cell Host & Microbe, report that segmented filamentous bacteria, a bacterial species found in the intestines, protected mice against influenza virus infection when these bacteria were either naturally acquired or administered.
This protection against infection also applied to respiratory syncytial virus (RSV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes COVID-19. To maintain this protection, the study noted that segmented filamentous bacteria required immune cells in the lungs called basally resident alveolar macrophages.
In this study, the researchers investigated how differences in specific microbial species can impact outcomes of respiratory virus infections and how they might do so, which hasn’t been well defined previously. They studied mice with discrete microbiome differences and mice differing in only the presence or absence of segmented filamentous bacteria. Viral titers in the lung were measured several days after infection and varied significantly depending on the nature of the microbiome of the different animal groups.
“These findings uncover complex interactions that mechanistically link the intestinal microbiota with the functionality of basally resident alveolar macrophages and severity of respiratory virus infection,” said Dr. Andrew Gewirtz, co-senior author of the study and Regents’ Professor in the Institute for Biomedical Sciences at Georgia State.
The study found that in segmented filamentous bacteria-negative mice, basally resident alveolar macrophages were quickly depleted as respiratory virus infection progressed. However, in segmented filamentous bacteria-colonized mice, basally resident alveolar macrophages were altered to resist influenza virus infection depletion and inflammatory signaling.
The basally resident alveolar macrophages disabled influenza virus, in large part by activating a component of the immune system referred to as the complement system.

“We find it remarkable that the presence of a single common commensal bacterial species, amidst the thousands of different microbial species that inhabit the mouse gut, had such strong impacts in respiratory virus infection models and that such impacts were largely attributable to reprogramming of basally resident alveolar macrophages,” said Dr. Richard Plemper, co-senior author of the study, Regents’ Professor and director of the Center for Translational Antiviral Research at Georgia State. “If applicable to human infections, these findings will have major implications for the future risk assessment of a patient to advance to severe disease.”
“We find it highly unlikely that segmented filamentous bacteria is the only gut microbe capable of impacting the phenotype of alveolar macrophages, and consequently, proneness to respiratory virus infection,” Gewirtz said. “Rather, we hypothesize that gut microbiota composition broadly influences proneness to respiratory virus infection. Microbiota mediated programming of basally resident alveolar macrophages may not only influence the severity of acute respiratory virus infection, but may also be a long-term post-respiratory virus infection health determinant.”
The study’s primary authors were virologist Carolin M. Lieber from the Center for Translational Antiviral Research and immunologist Vu L. Ngo from the Institute for Biomedical Sciences at Georgia State. Other contributing authors were Hae-ji Kang and Michal Kuczma of the Institute for Biomedical Sciences at Georgia State and Kaori Sakamoto of the University of Georgia.
The study is funded by the National Institutes of Health’s National Institute of Allergy and Infectious Diseases.

The human genome, an intricate tapestry of genetic information for life, has proven to be a treasure trove of strange features. Among them are segments of DNA that can “jump around” and move within the genome, known as “transposable elements” (TEs).
As they change their position within the genome, TEs can potentially cause mutations and alter the cell’s genetic profile, but also are master orchestrators of our genome’s organization and expression. For example, TEs contribute to regulatory elements, transcription factor binding sites, and the creation of chimeric transcripts — genetic sequences created when segments from two different genes or parts of the genome join together to form a new, hybrid RNA molecule.
Matching their functional importance, TEs have been recognized to account for half of the human DNA. However, as they move and age, TEs pick up changes that mask their original form. Over time, TEs “degenerate” and become less recognizable, making it difficult for scientists to identify and track them in our genetic blueprint.
In a new study, researchers in the group of Didier Trono at EPFL have found a way to improve the detection of TEs in the human genome by using reconstructed ancestral genomes from various species, which allowed them to identify previously undetectable degenerate TEs in the human genome. The study is published in Cell Genomics.
The scientists used a database of reconstructed ancestral genomes from different kinds of species, like a genomic “time machine.” By comparing the human genome with the reconstructed ancestral genomes, they could identify TEs in the latter that, over millions of years, have become degenerate (worn out) in humans.
This comparison allowed them to detect (“annotate”) TEs that might have been missed in previous studies that used data only from the human genome.
Using this approach, the scientists uncovered a larger number of TEs than previously known, adding significantly to the share of our DNA that is contributed by TEs. Furthermore, they could demonstrate that these newly unearthed TE sequences played all the same regulatory roles as their more recent, already identified relatives.
The potential applications are vast: “Better understanding TEs and their regulators could lead to insights into human diseases, many of which are believed to be influenced by genetic factors,” says Didier Trono. “First and foremost, cancer, but also auto-immune and metabolic disorders, and more generally our body’s response to environmental stresses and aging.”

A new study led by researchers at UCLA may change the way clinicians and scientists understand, diagnose and treat placenta accreta spectrum disorder, a serious condition in which the placenta fails to separate from the uterus at birth, jeopardizing the life and health of both mother and baby.
Researchers previously believed that certain overly invasive placental cells, called trophoblasts, were responsible for keeping the connection intact. But this new research, which identifies genetic and cellular changes within single cells where the placenta and uterus join, shifts the focus to how the structural support of tissues, and the blood vessels of the uterus, can cause a “loss of normal boundary limits” between the placenta and the uterus.
“We utilized two new techniques in single-cell analysis to create an atlas of cells involved in placenta accreta to better understand this increasingly prevalent disorder that can have devastating implications for maternal and neonatal health,” said Dr. Yalda Afshar, a maternal-fetal medicine specialist and researcher at the David Geffen School of Medicine at UCLA, and the first and corresponding author of an article describing the findings in the American Journal of Obstetrics & Gynecology.
“This work revealed a subset of genes differentially expressed in placenta accreta spectrum disorder, which provides the basis for the ‘permissive environment’ for the placenta to attach to the uterine lining,” said Dr. Deborah Krakow, a maternal-fetal medicine specialist and researcher, chair of the Department of Obstetrics and Gynecology at the David Geffen School of Medicine at UCLA, and the paper’s senior author.
The research showed that the decidua, the layer of the uterine lining that forms during pregnancy, and blood vessels, are sending different signals to the placenta when a pregnant person has placenta accreta. Normally, the placenta — the temporary organ that provides support for a fetus — is shed after birth. In placenta accreta, it is stuck on too tight, which becomes the reason for many of the maternal complications of placenta accreta.
“Our goal was to characterize the intimate relationship between the maternal and fetal tissue at the site of accreta or malfunction,” Afshar said. “The genes and signaling pathways we identified go beyond providing a better understanding of the mechanism of the disease; they may be used as targets to help us refine diagnostic tests, track disease progression over time, and discover new, more effective therapies.”
The incidence of placenta accreta spectrum (PAS) disorders has increased dramatically in recent decades, the cause of which is not certain, though cesarean deliveries, is one of several risk factors. Today, incidence is estimated at 1 in 272 births in the U.S., up from 1 in about 30,000 pregnancies in the 1960s, researchers say.
For this study, the research team performed multiple placental biopsies on 12 placentas — six with PAS disorder and six controls — conducting single-cell RNA analysis on 31,406 individual cells. The researchers also applied spatial transcriptomics to 36 regions of interest — 12 in PAS-adherent, 12 in PAS-nonadherent, and 12 in controls. Spatial transcriptomics allow researchers to precisely measure and map the gene activity within a single tissue sample.
“At the end of the day, understanding the biology of pregnancy and pregnancy-related diseases, like accreta, is inspired by only one thing — finding ways to improve the care we can provide to pregnant people and their families,” said Afshar, a physician-scientist who manages the care of many patients with placenta accreta spectrum disorders at UCLA Health.

Image source, GettyEleanor LawsonBBC News, West MidlandsPublished21 minutes agoThree quarters of measles cases reported in England since October have been in the West Midlands, new data shows.Figures released by the UK Health Security Agency (UKHSA) reveal the region had 260 out of 347 cases across the country, between 1 October and 23 January.Meanwhile, 13% of cases have been in London and 7% in Yorkshire and the Humber.A consultant epidemiologist at the UKHSA said the outbreak in the region “remains a concern”.Of the 347 cases in England, 127 of these were confirmed in January.The majority of these cases (67%) were in children under the age of 10 (67%).’Vaccination best protection’Dr Vanessa Saliba, UKHSA consultant epidemiologist, said: “MMR vaccine coverage has been falling for the last decade with one out of 10 children starting school in England not protected and so there is a real risk that this outbreak could spread to other towns and cities.“Measles is a nasty illness for most children and for some can be serious, but it is completely preventable.””Vaccination is the best way to protect yourself and your children.”Symptoms of measles,

Cases have risen by 80 percent since 2018, the C.D.C. reported. But chlamydia remains by far the most common sexually transmitted infection.Syphilis, once nearly eliminated in the United States, continues to resurge, reaching the highest rate of new infections recorded since 1950, the Centers for Disease Control and Prevention said on Tuesday.More than 207,000 cases were diagnosed in 2022, the last year for which data are available. That represents an 80 percent increase since 2018, and 17 percent over the previous year’s tally, according to a new C.D.C. report.The rates soared in every age group, including newborns. In November, the C.D.C. said more than 3,700 cases of congenital syphilis were reported in 2022, roughly 11 times the number recorded a decade ago. The disease caused 231 stillbirths and 51 infant deaths in 2022.Experts pointed to a slew of reasons for the continued increases in syphilis and other S.T.I.s.Substance use, which is tied to risky sexual behavior, has risen. With better prevention and treatment for H.I.V., condom use has fallen out of vogue — decreasing by about 8 percentage points between 2011 and 2021 among high school students, for example.And, crucially, there are far fewer sexual health clinics, along with the disease-intervention specialists and nurses who staffed them.Syphilis has been increasing even in countries with national health care, because “sexual health services remain inadequate relative to the need pretty much everywhere,” said Dr. Jay Varma, chief medical officer at Siga Technologies and a former deputy commissioner of health for New York City.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? 

Published15 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Angus CochraneBBC Scotland NewsScotland’s former deputy first minister has told the UK Covid inquiry that he manually deleted messages sent to Nicola Sturgeon during the pandemic.John Swinney said the texts with the ex-first minister were “not available”.The SNP MSP said they had been removed in line with his understanding of Scottish government records policy. Mr Swinney also denied a suggestion that Scottish cabinet meetings were “driven” by Ms Sturgeon’s “strong mindedness”.It came after ex-finance secretary Kate Forbes said she was surprised no minutes were kept from top-level meetings during the Covid crisis.Mr Swinney served as deputy first minister and education secretary until May 2021. Following a reshuffle, he left the latter role to become Covid recovery secretary. He stepped down from government in March 2023.Swinney tells Covid inquiry he deleted messages to SturgeonGove denies government played politics in pandemicSturgeon called Johnson a ‘clown’, inquiry hearsThe inquiry had already heard that none of his WhatsApps or “similar messages” had been retained. A document supplied to the inquiry stated the texts had been either deleted manually or by using an auto-delete function.The former deputy first minister told the inquiry he rarely spoke to Ms Sturgeon via text messages or other informal means. He said texts were generally only used to set up a phone call.Mr Swinney told the inquiry that since entering government in 2007 he had “deleted material after I have made sure any relevant information was placed on the official record of the government, and that was the approach I was advised to take”.He said this approach was never “questioned” in previous years in government and was “consistent” with the ministerial code. Image source, PA MediaThe former deputy first minister conceded that it “might well be the case” that all the information needed by the inquiry might not be retained. He said he would apologise “unreservedly” if he had “misunderstood” the government’s records management policy.”My intention was never to do anything other than ensure the official record was furnished with all of the information that it needed to have,” Mr Swinney said. The inquiry was sent 18 pages of WhatsApp messages between Mr Swinney and current First Minister Humza Yousaf from during the pandemic. They were recovered from an old handset of Mr Yousaf’s after Mr Swinney erased his messages, the inquiry heard. “They would be deleted by periodic deletion once I was satisfied I had told my private office any info that was relevant so that I was not facing a large number of messages that I would potentially have to delete on one occasion,” Mr Swinney added.Freeman will regret Covid care home deaths ‘for rest of my life’Derogatory texts between Yousaf and Leitch releasedThe inquiry was also shown messages from 14 December 2021, following cabinet talks, between then health secretary Mr Yousaf and national clinical director Jason Leitch.At the meeting, Mr Yousaf had suggested unexpectedly that he may be able to make £100m from the health budget available for business support as the government considered another lockdown. In the messages, Mr Yousaf told Mr Leitch that Ms Sturgeon had been “ranting” at him and he had taken “one hell of a bullet”. Mr Leitch said Ms Sturgeon was being “ridiculous, absolutely ridiculous” and that he “almost intervened”.Image source, UK Covid Inquiry Lead counsel to the inquiry, Jamie Dawson KC, put it to Mr Swinney that the culture of the Scottish cabinet was driven by Ms Sturgeon’s “strong mindedness when challenging her was seen as taking a bullet”. Mr Swinney said: “No, because I think that particular morning, the first minister was a little bit surprised that the health portfolio had been able to find £100m to transfer to business support.”In all my 10 years of handling the public finances of Scotland, the health secretary never offered me £100m in exchange for anything.”He insisted the cabinet had “open and full discussions”. Ms Forbes, in messages about the same cabinet meeting, said she had “never seen the FM this angry in all my cabinets for good reason”.She told the inquiry that while “surprises” were not typically welcome at cabinet, Mr Yousaf had tried to be “helpful” and had not tried to “undermine the process”. Earlier, the inquiry heard that the Scottish government’s equivalent of Cobra meetings – the Scottish Government Resilience Room (SGoRR) – had not been minuted.Image source, PA MediaNeither were records kept for so-called “gold command” meetings – attended by Ms Sturgeon, a small group of advisers and a revolving group of ministers.Ms Forbes confirmed to the inquiry she not attend any of the “gold command” discussions in 2020.Asked by inquiry chair Lady Hallett why she was not invited despite her seniority, Ms Forbes said she was “not even sure” they existed at the time. Ms Forbes added: “I would have expected to be invited to any meeting where there were significant financial implications.” ‘Difficult to understand’She said she understood “frustration” at the lack of minutes from SGoRR and gold command meetings.Mr Dawson suggested the lack of minutes made it “difficult” to understand decision making processes during the pandemic.”I understand that,” Ms Forbes replied, adding: “I think every meeting of that nature in Scottish government should be minuted. I’m surprised to hear that they weren’t.”The former minister, who left government in March 2023, said it was her “expectation” that minutes were recorded in the same way that cabinet was. Ms Sturgeon is due to give evidence to the inquiry, which is holding special evidence sessions in Edinburgh this month, on Wednesday.Scottish Secretary Alister Jack is expected to appear in front of the inquiry on Thursday. More on this storyCovid inquiry: Five things we learned last weekPublished1 day agoCovid inquiry: Five things we learned this weekPublished20 JanuaryCovid inquiry turns spotlight on Scottish decisionsPublished16 January

Published1 hour agoShareclose panelShare pageCopy linkAbout sharingBy Beth RoseBBC Access AllMollie Pearce might have fallen at the final hurdle of The Traitors and lost the £95k prize, but the model and healthcare assistant finds some comfort in what she achieved in opening up on her “double whammy” of disability – limb difference and living with a stoma. “I call my stoma Sid,” Mollie makes clear on the BBC’s Access All podcast. “I’m very proud of Sid. He’s helped me in a lot of ways.”Sid the stoma came into Mollie’s life just a few years ago when she was 18 (she turned 22 on Sunday, 48 hours after the epic TV final).Mollie had been diagnosed with ulcerative colitis aged 11. The autoimmune condition causes inflammation in the large intestine triggering ulcers and debilitating pain. It came to dominate her teenage years stopping certain basic activities and the number of school days missed.”When I was suffering with ulcerative colitis I couldn’t be away from a toilet,” she says.Aged 18 she underwent “massive” surgery to have her colon removed and her small intestine diverted out of an opening in her abdomen known as a stoma. “That colons in the bin,” she says theatrically. “Now, my small intestine sticks outside of my stomach and I have a stoma bag over the top, which collects my waste. “I would never have been able to do the missions in the middle of a field or the middle of a loch. So actually having a stoma bag is the best thing I’ve ever done.”Listen to the Access All podcast with Molly Pearce from The Traitors, and spot the moment when the tables turn and Michael starts to interview Access All’s blind presenter , Emma Tracey, about her experiences…It was something the Bristolian opened up about in the penultimate episode of this year’s series when the final five were enjoying a celebratory dinner. “I really struggled to get my head around the fact that I was going to have a stoma,” she told her fellow finalists. “I wasn’t prepared for it. Eighteen-years-old, you kind of want to be out enjoying yourself with your friends, not having this life changing surgery.” She says it felt right to open up at that point in the game.”We’d got to the final and we were just celebrating. It just made me realise how far I’d come from that girl who was so unwell and couldn’t leave the house.”An energetic island hopping trip around Greece two summers ago with her boyfriend, had given Mollie the confidence to take up the offer of appearing on The Traitors and take on the physical challenges including swimming and climbing, while wearing a stoma bag. “I loved the physical missions,” she says. “They were such a good break from all the mind games and it was a really good bonding experience. Sid’s given me the kind of option to do these things.”In terms of the practicalities, Mollie says she didn’t need any extra support throughout the series, and she got into a good routine. She changed her bag every three to four days and emptied it whenever she visited the loo. Having ulcerative colitis was something going on inside her body whereas she has a much more visible impairment too.She says living with an invisible illness has been much harder to explain to people than her limb difference on her right hand. Without the visual evidence she has found people often think “you look so healthy but, really you are suffering so much.”As well as working as a hospital healthcare assistant in Bristol, it was Mollie’s limb difference which landed her a glamorous side hustle – what she describes as “disability modelling”. “I saw a model in Primark who had one arm and I’d never seen a disability model before,” she says.”The way that model made me feel in that moment…I was like ‘that is how I want to be for other people’.”Molly was initially signed as a model with limb difference, but now she is very comfortable showing off Sid too. “It’s a double whammy,” she jokes. “Who doesn’t want someone with one hand and a stoma bag?”She says the reaction from her sto-mates, people who also have stomas, to her being on the show and modelling has been “amazing”. “It can be a bit of a taboo and I think it’s super important that we do advocate for it, especially when it comes to younger people.” Molly says it was a “strange” time between finishing filming The Traitors and it coming out on TV – a gap of several months.”You have this crazy experience and this massive adventure and then that’s it. I was back working as a healthcare assistant at the hospital and you obviously can’t talk to anyone about it.”At that point she was still coming to terms with the treachery Harry Clarke had served her, and which the nation had yet to see.Harry – one of the original three traitors – and, faithful, Mollie were the last players standing, after both voted to eliminate faithful Jaz Singh.In the final moments of the series, Mollie had started to write Harry’s name down for banishment, before changing her mind and voting for Jaz, leaving just her and Harry standing.Her decision meant Harry won all £95,150 of the prize money – as if any traitors remain at the end of the game they take all the gold for themselves.”Me and Harry are fine,” she insists for the umpteenth time since leaving the castle. “As a group we were super close. We were together every day, all day. You do build real bonds and also you don’t have communication with your family and friends, they are your support system.”It’s hard finding out your friend’s been lying to you, but I stuck with my heart and I am not going to hate myself for that.”More on this storyThe Traitors final: I trusted the wrong personPublished2 days ago

Vertex Pharmaceuticals said its medicine could address moderate to severe acute pain, and might be able to avoid the risk of addiction.Vertex Pharmaceuticals of Boston announced Tuesday that it had developed an experimental drug that relieves moderate to severe pain, blocking pain signals before they can get to the brain. It works only on peripheral nerves — those outside the brain and the spinal cord — making it unlike opioids. Vertex says its new drug is expected to avoid opioids’ potential to lead to addiction.The company reported that it had completed two randomized studies, the first in 1,118 people who had abdominoplasties and the other in 1,073 people who had bunion surgery. The two procedures are commonly used in studies of people with acute pain, the temporary kind that is brought on by something like a surgical procedure and is likely to ease with time.In its clinical trials, Vertex measured the drug’s effect with a standard pain scale in which patients rated pain severity from 1 to 10, with 10 the most severe. Those taking its drug had a statistically and clinically meaningful reduction in pain, it reports. A third study looked at safety and tolerability of the drug in people experiencing pain from a variety of conditions.Buoyed by the results, which are yet to be published or presented at a meeting, Vertex plans to apply to the Food and Drug Administration by midyear for approval to market the drug, a pill that, for now, is called VX-548.“This has the potential to be a blockbuster,” said Dr. Stephen Waxman, a professor of neurology, neuroscience and pharmacology at Yale. Dr. Waxman was not associated with the study but was paid a speaking honorarium by the company. He predicted that the Vertex drug would be only the first foray into this new area.“I like to think it’s the beginning of nonaddictive medicines for pain,” he said.For now, most people needing relief from moderate to severe pain have two options: drugs like ibuprofen and COX-2 inhibitors, or opioids. The drugs like ibuprofen are not very effective, and the opioids, as is well known, can be addictive because of the way they work. There is no way to separate the effects of opioids — pain relief — from the side effects: changes in thinking, cognition, energy and emotions.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?