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Published14 hours agoSharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesPeople on cholesterol-lowering statins can be reassured that it is uncommon for the tablets to cause muscle pain, say the authors of a large study.The pills can protect against heart attacks and strokes, but have had some bad press because of a very rare risk of dangerous muscle inflammation. The British Heart Foundation says patients should not automatically stop their tablets for mild muscle aches. The conclusions are based on data from nearly 155,000 people. They were taking part in a number of statin trials assessing the treatment and possible side effects. Muscle pain or weakness was commonly reported by the participants, regardless of whether or not they were taking a statin tablet. Some of the volunteers received a placebo or dummy tablet instead of the statin, for comparison. About one in four in both groups – statin or placebo – reported some muscle aches.According to the researchers, during the first year of treatment, statin therapy produced a 7% relative increase in muscle pain or weakness compared to placebo, suggesting that only one in 15 of these muscle-related reports by patients given statins were because of the statin. The absolute excess risk of muscle symptoms because of a statin was 11 per 1,000 patients treated during the first year, the researchers calculate.After the first year of treatment, there was no significant difference in reports of muscle pain or weakness between those given statins and those given the placebo. The findings have been published in The Lancet and presented at this year’s European Society of Cardiology Congress in Barcelona. Joint lead author Prof Colin Baigent said: “The idea that statins may cause frequent muscle pain has been a persistent belief among some patients and clinicians. However, our study confirms that the statin is rarely the cause of muscle pain in those taking statins.” He said if a patient on statins does report muscle pain, then it should first be assumed that the symptoms are not because of the statin and are most likely down to other causes. “Statin therapy should continue until other potential causes have been explored.”He said it was still important to be on the lookout for the very rare cases of dangerous muscle damage that can occur as a side effect. “Additionally, in light of our analysis, we believe there is a need to revise the information in the medication label for statins to clarify that most muscle pain experienced during statin therapy is not due to the statins.”Statins are one of the most commonly prescribed drugs in the UK, with millions taking them. Prof Sir Nilesh Samani, from the British Heart Foundation, which funded the work, said the findings “should provide reassurance to the many people taking, or considering taking, these lifesaving drugs that have been proven to protect against heart attacks and strokes”. Cardiovascular disease kills about 160,000 people in the UK each year. More on this storyMost statin problems caused by ‘nocebo effect’15 November 2020Related Internet LinksThe LancetThe BBC is not responsible for the content of external sites.

He helped write the first comprehensive dictionary of American Sign Language and later identified the deaf as a part of society worth examining.Carl Croneberg, a deaf Swedish immigrant who helped write the first comprehensive dictionary of American Sign Language and was the first to outline the idea of Deaf culture as a distinct part of society and one worth studying, died on Aug. 11. He was 92.His death was announced by Gallaudet University in Washington, D.C., the only university for the hearing-impaired in the United States, where he earned a degree and spent his entire career. The university did not specify the cause or say where he died.Mr. Croneberg was a new member of the Gallaudet faculty when, in 1957, the linguist William C. Stokoe Jr., himself recently arrived on campus, recruited him to join his new Linguistics Research Laboratory. Until the late 1950s, many linguists had dismissed sign language as a poor substitute for spoken language, a rigid, imprecise system of gestures that left no room for nuance.Dr. Stokoe, who was hearing, believed otherwise, though he had gone to Gallaudet with no previous training in sign language and no real exposure to a Deaf community — his specialty was Middle English.Yet it didn’t take long for him to confirm his hunch. While undergoing a crash course in American Sign Language, he noticed that the signs he was learning in class were sometimes different from what his students were using among themselves.The difference, he was told, was slang — and in that difference he saw the capacity for A.S.L. to be every bit as capacious as spoken language. Dr. Stokoe committed himself to developing a script, and from that, a dictionary. But to do so he needed colleagues with native-speaker experience.Mr. Croneberg, left, with his mentor William C. Stokoe. Their work together led to a dictionary of American sigh language.Gallaudet ArchivesHe chose Mr. Croneberg and a second colleague, Dorothy Casterline, both young instructors at Gallaudet, not only because of their intelligence, but also because, in a way, they were outsiders, too: Mr. Croneberg grew up in Sweden, Ms. Casterline in Hawaii.That made it possible for them to both analyze the language in a way that Dr. Stokoe could not access, yet also examine its use with a certain amount of detachment.Mr. Croneberg’s charge was to assess how Deaf people deploy sign language in everyday life and around the country. He traveled throughout New England and the South, interviewing Deaf residents and conducting ethnographic investigations, paying attention to how the language informed their lives.What he found may not have surprised his research subjects, but it astounded other linguists. He identified significant regional variations; the sign for cheese, for example, was different in Washington, D.C., and Virginia. Catholics and Protestants had different words for the same religious objects. And he found different dialects among old and young, and between Black and white people.“The community of Deaf people who use sign language and who have more or less frequent social contact with each other extends all over North America,” he wrote. “But the whole divides into local and regional groups which can be mapped geographically.”Mr. Croneberg published his results as two appendices to “A Dictionary of American Sign Language on Linguistic Principles” (1965), which he wrote with Dr. Stokoe and Ms. Casterline, and which became a seminal text among Deaf scholars.“Stokoe would not have been able to do the work without his colleagues, Carl and Dorothy,” Pamela Wright, who teaches linguistics at Gallaudet, said in an email. “It was a perfect mix of skills that pulled together to study A.S.L. as an authentic language. Stokoe didn’t know signs, he was still learning, and Carl and Dorothy were his connection to the community.”Ever the linguist, Mr. Croneberg saw American Sign Language as the core of what he coined “Deaf culture,” a term that later generations of researchers built into an entire field of study. And he was among the first to outline Black American Sign Language as a distinct dialect.In recognition of their contributions, Gallaudet presented Mr. Croneberg and Ms. Casterline with honorary degrees in May 2022.“Deaf scholars like the ones who stand before us today are enjoying opportunities for a better life thanks to the painstaking research conducted in the 1950s and early 1960s by Mr. Croneberg and his colleagues,” the university said in announcing the awards.Carl Gustav Arvid Olof Croneberg was born on April 26, 1930, in Norrbacka, a small town about 30 miles northeast of Stockholm. Deaf from birth, he was sent by his parents to a specialized school, where, in addition to learning Swedish sign language in class, he taught himself written English and German through a correspondence school.A chance encounter with Leonard M. Elstad, the president of Gallaudet, who was traveling in Europe, persuaded Mr. Croneberg to come to America to study at the university, according to research by Carey Ballard, a doctoral student in linguistics at Boston University. Mr. Croneberg arrived in 1951 and graduated with a degree in English four years later.He was immediately hired as a junior faculty member while he took graduate studies at the nearby Catholic University of America. He received a master’s degree in English there in 1959, but despite high grades and Dr. Stokoe’s strong recommendation, he was not admitted to the university’s doctoral program in anthropology because its director thought it would be too difficult for a deaf person.He continued to teach English at Gallaudet, and over time became an inspiration for a new generation of linguists and scholars of Deaf studies, who created programs and departments at Boston University; California State University, Northridge; and other institutions.Mr. Croneberg retired in 1986. Survivors include his wife, Eleanor (Wetzel) Croneberg, and his daughter, Lisa Croneberg.

An estimated five to ten percent of blindness worldwide is caused by the rare inflammatory eye disease uveitis. Posterior uveitis in particular is often associated with severe disease progression and the need for immunosuppressive therapy. In posterior uveitis, inflammation occurs in the retina and in the underlying choroid that supplies it with nutrients. Researchers at the Ophthalmology Department at the University of Bonn have tested color-coded fundus autofluorescence as a supportive novel diagnostic method. Fluorescence of the retina can be used to infer the uveitis subtype. This is an essential prerequisite for accurate diagnosis and treatment of the disease. The results have now been published in Scientific Reports.
Blurred vision, floaters and unusual light perception — those affected by the rare disease posterior uveitis feel no pain. “But the consequences can be severe: About five to ten percent of blindness worldwide is caused by uveitis. Uveitis is a rare disease, but posterior uveitis in particular potentially has a poor prognosis and often requires immunosuppressive therapy,” explains Dr. Maximilian Wintergerst of the Ophthalmology Department at the University of Bonn. There are different forms of the disease. In posterior uveitis, the retina or choroid in the eye becomes inflamed. While the retina converts the incident light into nerve impulses, the choroid supplies the outer layers of the retina with nutrients.
Different therapeutic management
“It’s not easy to distinguish between the numerous subtypes of uveitis,” says Wintergerst. However, since the different subtypes often require a different therapeutic approach, a reliable diagnosis is all the more important. This is why researchers from the Ophthalmology Department at the University of Bonn, together with colleagues from the Medical Biometry and Rheumatology Departments at the University Hospital Bonn and the University Hospital of Ophthalmology in Bern (Switzerland), investigated a new imaging technique that can assist in the diagnosis of posterior uveitis.
The team evaluated color-coded fundus autofluorescence (Spectrally Resolved Autofluorescence Imaging). The CenterVue (iCare) company from Padua (Italy) provided the newly developed device to the researchers for the examinations. This process involves illuminating the retina with bluish light. The retina absorbs the light and emits it again at a different wavelength. The device measures this fluorescence and splits the signals into a green and a red component.
“The green-to-red ratio of the light emitted from each inflammatory focus depends, among other factors, on the exact posterior uveitis subtype involved,” Wintergerst explains. The researchers examined the eyes of 45 study participants. In all of them, the exact subtype of uveitis was diagnosed beforehand. This included ophthalmologic examination findings, laboratory investigations, serologic and radiologic findings, and in some cases genetic and interdisciplinary clinical examinations.
More reliable diagnoses with color-coded fundus autofluorescence
The researchers evaluated the green-red ratio in the fluorescence of the fundus of the eye for about 800 inflammatory foci in the eyes of the patients. “Our results indicate, that this ratio can be very characteristic and helpful as a marker for differentiating the various posterior uveitis subtypes,” states Prof. Dr. Dr. Robert Finger, co-author of the study and head of the uveitis clinic at the Ophthalmology Department at the University Hospital Bonn. “It could allow us to make more confident diagnoses in the future.” This is a big step for the Ophthalmology Department at the University of Bonn, especially since Finger coordinates the Germany-wide uveitis registry “TOFU” (Treatment exit options for non-infectious uveitis) together with colleagues from Münster. The aim is to document disease progression on a long-term basis and to develop recommendations for treatment guidelines.
“In the current study, we present the precise technical background of color-coded fundus autofluorescence in ophthalmology in collaboration with our international partners,” says head of department Prof. Dr. Frank Holz. “This technology may also allow better monitoring of posterior uveitis in the future, in addition to more reliable diagnoses.”
The study was funded by the BONFOR-GEROK program of the Faculty of Medicine of the University of Bonn.
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In Gram-negative bacteria, which include some of the most devastating human pathogens, just two mechanisms for the export of polysaccharides have been identified so far. Now a Max Planck research team led by Lotte Søgaard-Andersen has identified an entirely novel third mechanism for how polysaccharides are exported. These findings pave the way toward a complete understanding of the mechanisms that mediate the protection, motility and interaction of many bacterial pathogens.
Bacteria not only thrive on sugar as a carbon and energy source — they also produce and secrete a wide variety of so-called polysaccharides. Polysaccharides are strings of sugars and are the most abundant biopolymers on earth. The long sugar chains play vital roles in free-living, commensal, and pathogenic bacteria. They are also crucial for bacterial protection, sheathing the cells against environmental stresses such as desiccation, immune effectors, and predators. In addition, their adhesive and structural functions contribute to surface colonization and biofilm formation. They are also important for the successful application of anti-bacterial vaccines. Thus, they hold the keys to understanding and controlling both beneficial and pathogenic human, animal- and plant-microbe interactions. And last but not least, polysaccharides are used in the food, pharmaceutical and medical industries.
Polysaccharide export is a major challenge because the molecules are chemically diverse and very large. In Gram-negative bacteria, which include some of the most devastating human pathogens, just two known mechanisms for export of polysaccharides have been known so far: an outer membrane OPX protein (in the so-called Wzx/Wzy- and ABC transporter-dependent pathways), and an outer membrane β-barrel protein (in the so-called synthase-dependent pathways). Yet there are examples of pathways that do not seem to follow these simple schemes: In particular, in some Wzx/Wzy-pathways, outer membrane β-barrel proteins were known to be important for polysaccharide export, for instance in Vibrio cholerae and Myxococcus xanthus, but the exact mechanism was unclear. In addition, other studies describe short OPX proteins that lack the part that integrates into the outer membrane. Here, it is unclear how these proteins could support polysaccharide export.
A research team at the Max-Planck-Institute for Terrestrial Microbiology led by Lotte Søgaard-Andersen was able to shed new light on these questions. Using experiments and computational structural biology, the scientists provide evidence for an entirely novel mechanism for how bacteria can export polysaccharides across the outer membrane. Johannes Schwabe, a graduate student and lead author of the study, and Dr. María Pérez-Burgos say: “We started by taking a close look at the Wzx/Wzy-dependent pathway for the synthesis of a secreted polysaccharide called EPS in M. xanthus.” According to current knowledge, EPS would be secreted across the outer membrane by an OPX protein that is integrated into the membrane. However, the group found that an outer membrane β-barrel protein named EpsX is also important for EPS export. “Then, surprisingly, we discovered a corresponding periplasmic short OPX protein EpsY that completely lacks the part to span the outer membrane. Together with Dr. Timo Glatter, we also found that EpsX and EpsY directly interact.”
Based on their observations and computational structural biology, the scientists propose that EpsX and EpsY represent a novel type of translocon for polysaccharide export across the outer membrane, where a β-barrel protein functions explicitly as the outer membrane-spanning part in a bipartite complex with an entirely periplasmic OPX protein.
According to Lotte Søgaard-Andersen, this detailed knowledge might open up new ways of controlling pathogenic bacteria. She explains: “Marco Herfurth, a graduate student in my research group, found using computational genomics that similar composite systems are widespread in Gram-negative bacteria. For instance, this new system explains how V. cholerae secretes its VPS polysaccharide, which is important for biofilm formation and virulence. Thus, our findings not only have significant implications for our understanding of polysaccharide export in M. xanthus but also profound implications for our understanding of polysaccharide export in general in Gram-negative bacteria.”
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Heart attacks are one of the leading causes of death worldwide, and women who suffer a heart attack have a higher mortality rate than men. This has been a matter of concern to cardiologists for decades and has led to controversy in the medical field about the causes and effects of possible gaps in treatment. The problem starts with the symptoms: unlike men, who usually experience chest pain with radiation to the left arm, a heart attack in women often manifests as abdominal pain radiating to the back or as nausea and vomiting. These symptoms are unfortunately often misinterpreted by the patients and healthcare personnel — with disastrous consequences.
Risk profile and clinical picture is different in women
An international research team led by Thomas F. Lüscher, professor at the Center for Molecular Cardiology at the University of Zurich (UZH), has now investigated the role of biological sex in heart attacks in more detail. “Indeed, there are notable differences in the disease phenotype observed in females and males. Our study shows that women and men differ significantly in their risk factor profile at hospital admission,” says Lüscher. When age differences at admission and existing risk factors such as hypertension and diabetes are disregarded, female heart-attack patients have higher mortality than male patients. “However, when these differences are taken into account statistically, women and men have similar mortality,” the cardiologist adds.
Current risk models favor under-treatment of female patients
In their study, published in the journal The Lancet, researchers from Switzerland and the United Kingdom analyzed data from 420,781 patients across Europe who had suffered the most common type of heart attack. “The study shows that established risk models which guide current patient management are less accurate in females and favor the undertreatment of female patients,” says first author Florian A. Wenzl of the Center for Molecular Medicine at UZH. “Using a machine learning algorithm and the largest datasets in Europe we were able to develop a novel artificial- intelligence-based risk score which accounts for sex-related differences in the baseline risk profile and improves the prediction of mortality in both sexes,” Wenzl says.
AI-based risk profiling improves individualized care
Many researchers and biotech companies agree that artificial intelligence and Big Data analytics are the next step on the road to personalized patient care. “Our study heralds the era of artificial intelligence in the treatment of heart attacks,” says Wenzl. Modern computer algorithms can learn from large data sets to make accurate predictions about the prognosis of individual patients — the key to individualized treatments.
Thomas F. Lüscher and his team see huge potential in the application of artificial intelligence for the management of heart disease both in male and female patients. “I hope the implementation of this novel score in treatment algorithms will refine current treatment strategies, reduce sex inequalities, and eventually improve the survival of patients with heart attacks — both male and female,” says Lüscher.
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The earlier individuals develop Type 2 diabetes or hypertension in life, the earlier they are likely to develop primary open-angle glaucoma (POAG), the leading cause of irreversible blindness worldwide, researchers from UT Southwestern reported in a recent study. The findings, published in Clinical Ophthalmology, could lead to better screening protocols for POAG, which accounts for up to 90% of all cases of glaucoma.
“Currently, we lack the tools to cure glaucoma, but with enough advanced notice, we can preserve patients’ vision. Early detection of glaucoma is the key to better control of intraocular pressure and preventing blindness,” said study leader Karanjit Kooner, M.D., Ph.D., M.B.A., Associate Professor of Ophthalmology at UTSW.
Tens of millions of people have POAG around the globe. Because this disease has few symptoms in its earliest stages, Dr. Kooner explained, patients are frequently diagnosed in its later stages when vision has already been permanently damaged. Although researchers have identified several risk factors for POAG — including Type 2 diabetes, hypertension, migraines, and obstructive sleep apnea — how they might influence the onset of POAG is not well understood.
To answer this question, Dr. Kooner and his colleagues collected data from the medical records of 389 POAG patients, all seen by Dr. Kooner between June 2019 and December 2019 at the UTSW Eye Clinic. Using statistical modeling, the researchers found no connection between migraines and/or obstructive sleep apnea and the age of POAG onset. However, the researchers found that the age of Type 2 diabetes and/or hypertension diagnosis was significantly linked with the onset of POAG — the earlier patients presented with either or both of these conditions, the earlier they tended to develop POAG.
Dr. Kooner noted that both Type 2 diabetes and hypertension are diseases that affect blood vessels of both the optic nerve and retina, thus potentially causing changes that predispose patients to POAG, another condition with a vascular root. If these connections hold up in future research, he said, Type 2 diabetes and hypertension could be added to the list of factors that can trigger POAG screening — including a family history of POAG, elevated intraocular pressure, and Black race — and lead to earlier diagnosis of POAG, preserving patients’ vision and quality of life.
Other UTSW researchers who contributed to this study include Jeffrey Wooliscroft, Rubeel Akram, Hafsa Zuberi, Betty Tong, Jane Gu, and Aaron Hurd.
This research was funded by grants from Research to Prevent Blindness, the National Institutes of Health (P30 EY030413, UL1TR001105), and the UT Southwestern Medical Student Research Program.
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Inactivation of a particular protein complex that plays a key role in keeping genes switched off leads to nerve cells not producing enough essential neurotransmitters. This could be part of the explanation for diseases such as Parkinson’s and anxiety disorders. This is the result of a discovery by researchers at Umeå University, Lund University and Karolinska Institutet, Sweden.
“We have seen that if this protein complex is inactivated, the ability to keep genes that control other functions switched off is impaired. This, in turn, shuts down genes needed to maintain the function of nerve cells. In animal studies, we can see a change in the animals’ behaviour that is similar to those that occur in Parkinson’s disease,’ says Johan Holmberg,” professor at the Department of Molecular Biology, Umeå University and one of the study’s lead authors.
After neurons are formed during fetal development, they often retain their identity and function for the rest of life. In addition to the need for gene programmes necessary to form and maintain the nerve cell to be active, genes controlling other properties are also required to be permanently “silenced.” The current study shows that this silencing of irrelevant genes depends on a specific protein complex, PRC2.
Without a functioning PRC2 complex, mature neurons that produce the important neurotransmitters dopamine and serotonin gradually lose their identity and function. In Parkinson’s disease, the cells that produce dopamine die, while a lack of serotonin is associated with mental health problems. When tested on mice the researchers observed a progressive change in the behaviour of the mice, such as motor symptoms typical of Parkinson’s disease.
“If we can see that mechanisms controlling the regulation of genes are part of the reason why diseases that damage the nervous system occur, this could open up interesting new possibilities for diagnosis and treatment, but there is still a long way to go,” says Johan Holmberg.
The study was done by knocking out a vital component of the PRC2 protein complex in the nerve cell types of interest in mice. The effects were then investigated using microscopy, behavioural studies, electrophysiology and a combined analysis of gene expression and modifications of histones, the proteins around which the long DNA coils of chromosomes are wound.
The researchers now plan to go further and investigate whether the mechanisms studied in mouse models are indeed involved in neurodegenerative or mental disorders. In addition, the researchers want to find out what exactly controls the downregulation of genes when the PRC2 complex is inactivated. An interesting observation made in the study is that the very subtype of dopamine-producing neurons that die in Parkinson’s disease exhibit a particular sensitivity to loss of PRC2 activity, and they exhibited significantly greater changes in gene expression than other neurons. The mechanisms behind this selective sensitivity are one of the things they want to explain.
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A study led by LSU Health New Orleans cancer researchers describes a novel therapeutic strategy to overcome tumor-induced immunosuppression. For the first time, the research team identified a critical immunosuppressive pathway and a promising approach to intervene, protecting the ability of T-cells to attack cancer cells. Results are published in Frontiers in Immunology.
“Immunotherapy is one of the most promising areas in oncology,” notes senior author Lucio Miele, MD, PhD, Assistant Dean for Translational Research at LSU Health New Orleans School of Medicine, who is also a cancer researcher. “Our immune systems are capable of destroying cancer cells, and several approved and experimental drugs stimulate cancer immunity. But cancers fight back, producing substances that weaken immune cells.”
The immune system cells that kill cancer cells are called CD8 T-cells. To be effective, CD8 T-cells need a protein made by the NOTCH1 gene.
“We had already described how adenosine, an immune-suppressive substance released by tumor cells, causes the breakdown of NOTCH1, weakening T-cells,” says Dr. Miele.
Using a proteomics strategy, the LSU Health New Orleans research team led by postdoctoral researcher Giulia Monticone, PhD, determined what causes the breakdown of NOTCH1 in T-cells. It is an enzyme called CBL-B. Collaborating with a Massachusetts biotech firm that is developing CBL-B inhibitors, the scientists were able to show that their experimental inhibitors do protect NOTCH1 from breaking down in CD8 T-cells and make them far more effective in killing breast and colorectal cancer cells.
“When added to existing immunotherapeutics, these CBL-B inhibitors greatly increased their potency,” Dr. Miele adds. “This new strategy could expand the efficacy of cancer immunotherapy by making patients’ T-cells able to evade the immune-suppressive defenses of tumors.”
Co-authors also included Drs. Deniz Ucar, Fokhrul Hossain, Salome Ibba, Hamid Boulares, Zhi Huang, and Samarpan Majumder at LSU Health New Orleans; Drs. Fred Csibi, David Ciccone, Silvana Leit, and Christine Loh from Nimbus Therapeutics; Dr. Ameya Champhekar from the University of California; Jermaine Austin from the University of Virginia; Dr. Nick Carpino from Stony Brook University; Dr. Keli Xu from the University of Mississippi Medical Center; and Dr. Barbara Osborne from the University of Massachusetts Amherst.
The research was supported by a grant from the National Cancer Institute.
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A new study conducted by the National Institutes of Health (NIH) RECOVER Pediatric Electronic Health Records (EHR) Cohort and authored by Suchitra Rao, MD, infectious disease specialist at Children’s Hospital Colorado, found that the risk of post-acute sequelae of SARS-CoV-2 infection (PASC), or long COVID, in children appears to be lower than what has been reported in adults. However, more children have long COVID than those kids who are hospitalized with acute COVID-19. The study is featured in JAMA Pediatrics.
“We concluded that many of the symptoms children experience post-COVID-19 are similar to what is seen in adults, but there are some features more unique to children, such as myocarditis, abnormal liver enzymes, hair loss, skin rashes and diarrhea,” said Rao. “There has been a critical need to understand the impact of COVID-19 in children both in the short as well as long-term. This is one of biggest studies we know of to explore what the post-acute sequelae look like in kids. Studies using electronic health record data are a great way to explore research questions that require further confirmation in longer term prospective studies.”
While the presentation has some overlap compared with adults, distinct features exist in children. The risk for PASC appears to be higher in children younger than five years of age, those with medical complexity and those admitted to the intensive care unit with their initial COVID-19 infection.
The exploratory study, “Syndromic, Systemic and Medication Features of Post-acute Sequelae of SARS-CoV-2 Infection in Children and Adolescents: EHR-based Cohort Study from the RECOVER Program,” used electronic health record data from PEDSnet member institutions of 659,286 children tested for SARS-CoV-2 and compared 59,893 children who tested positive with those who tested negative.
The NIH RECOVER Pediatric EHR Cohort investigators conducted a multistate analysis using EHR data of children and people younger than 21 years of age who underwent testing for SARS-CoV-2 at one of eight pediatric health systems in the country between March 1, 2020, and Oct. 31, 2021. Clinicians identified conditions, symptoms and medications associated with PASC in the one to six months following testing. Out of 660,000 children who underwent testing, 9% were positive and most were tested as outpatients.
Symptoms most strongly associated with infection included changes in loss of smell and taste, hair loss, chest pain, abnormal liver enzymes, skin rashes, fever and chills, fatigue and malaise. Conditions most strongly associated with infection included myocarditis, acute respiratory distress and myositis. There was also a higher association with mental health treatment among children who tested positive for PASC compared with those who tested negative.
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An international consortium of researchers has identified genetic variants in 10 genes that elevate a person’s susceptibility to Crohn’s disease, a form of inflammatory bowel disease.
Led by researchers from the Wellcome Sanger Institute and the Broad Institute of MIT and Harvard, the study is the largest to date to focus on rare variants associated with Crohn’s disease and is published today (29 August) in Nature Genetics. These discoveries highlight the causal role of mesenchymal cells in intestinal inflammation, helping to zero in on the genetic roots of inflammatory bowel disease and providing better data with which to develop the next generation of treatments.
Crohn’s disease (CD) is a debilitating condition characterised by chronic inflammation of the gastrointestinal tract. The causes of the disease are poorly understood, but it is believed to be triggered by a hyperactive immune response against gut bacteria in genetically susceptible individuals. Though drugs are available that improve symptoms for many patients, there is no cure and relapsing bouts of severe illness are common.
With a few rare exceptions, there is no single genetic cause of CD. Environment, diet and genetic variation collectively shape an individual’s risk of disease. Previous genome-wide association studies (GWAS) have identified around 250 regions of the genome that influence an individual’s susceptibility to CD. Unfortunately, GWAS studies are somewhat restricted to testing sites in the human genome that frequently vary between individuals.
In this study, researchers at the Wellcome Sanger Institute and the Broad Institute set out to identify rare genetic variants within protein-coding genes that are associated with Crohn’s disease susceptibility. They performed exome sequencing1 on around 30,000 patients with Crohn’s and compared these to exome sequences from around 80,000 individuals without the condition.
This identified genetic variation within six genes in regions of the genome that had not been previously connected to Crohn’s disease. Several of these genes are known to play important roles in a type of stem cell in the gut called mesenchymal cells2, suggesting that disruption of these cells contributes to the initiation and maintenance of intestinal inflammation.