Published17 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, PA MediaSenior doctors in England have ended their pay dispute with the government.Consultants who are members of the British Medical Association (BMA) and the Hospital Consultants and Specialists Association (HCSA) have backed a fresh pay deal.The offer will mean some consultants will receive a pay increase of nearly 20% for the financial year 2023-24.Junior doctors in England remain in dispute with ministers over pay, and have a fresh mandate to strike.Junior doctors and consultants are among several groups of health workers who have been taking industrial action at various points since 2022.New pay offerThe unions said 83% of members voted to back the pay offer, which was made last month.It was the second time a pay offer had been put to members of the BMA. The last one, made in early December, was narrowly voted against.Consultants got a 6% pay rise in April 2023 and were then offered an extra sum worth nearly 5% on average at the end of last year.But the amount extra individual consultants got varied considerably from nothing to an extra 12.8%.The new offer included an extra 2.85% for those between four and seven years into their consultant careers – the group that was getting the smallest rise under the previous offer.This pay rise will be backdated to March 2024, which means some senior doctors will see their pay increase by nearly 20%.On top of this, consultants will be eligible for a separate pay rise for the 2024-25 financial year, which is just starting.NHS consultant strike: How pay compares globallyWhy talk of a UK doctor exodus is prematureDr Vishal Sharma, BMA consultants committee chair, said: “We’ve reached this point not just through our tough negotiations with the Government, but thanks to the resolve of consultants, who took the difficult decision to strike, and did so safely and effectively, on multiple occasions, sending a clear message that they would not back down.”He added: “But the fight is not yet over. This is only the end of the beginning, and we have some way to go before the pay consultants have lost over the last 15 years has been restored.”The Royal College of Nursing has called the amount being handed to consultants as “galling”.Nurses and other health workers ended their strike action last year after receiving a 5% rise and a one-off payment of £1,655.Despite this breakthrough, the government and BMA remain a long way from solving the junior doctors’ pay dispute. Members of the BMA want a 35% pay increase. The BMA has a fresh six-month strike mandate after talks collapsed late last year. However, no new strike dates have been announced yet.Junior doctors in Northern Ireland and Wales remain in dispute with the government over pay and have taken strike action.

Research into the protective effects of two anti-inflammatory molecules, transforming growth factor-beta1 (TGFβ1) and Heligmosomoides polygyrus TGM (HpTGM), following heart attack found that both proteins reduced the inflammatory response within the injured heart and reduced mature scarring. Anti-inflammatory therapy to treat patients following acute myocardial infarction is an exciting prospect that deserves further translational studies, report investigators in The American Journal of Pathology, published by Elsevier.
Patients with acute heart attacks (ST elevation myocardial infarction, or STEMI) are very likely to survive if they undergo timely reopening of the occluded coronary artery (coronary reperfusion) in specialized clinical centers. Despite the given survival rates and major improvements in treatment, progression to heart failure still represents a major clinical problem. The patients’ longer-term outcomes depend on the extent of the damage to their heart tissue.
Lead investigator Helen M. Arthur, PhD, Biosciences Institute, Faculty of Medical Sciences, Newcastle University, explains: “Coronary reperfusion after STEMI is standard therapy to salvage ischemic heart muscle. However, evidence suggests that the subsequent inflammatory response that the body initiates to repair the damaged heart tissue can also cause further loss of viable heart muscle. The more muscle that is lost, the greater the risk of subsequent progression to heart failure. The reason for this study was to investigate the potential protective effects of TGFβ1as a possible intervention to minimize this additional damage to the heart beyond the ischemic damage caused by the heart attack itself.”
The research team found that levels of an important anti-inflammatory protein TGFβ1 in the blood of STEMI patients 24 hours after reperfusion correlated with a reduction in infarct size after three months. To investigate this further they used an established mouse model of a heart attack to test the protective effects of TGFβ1, a protein known to be released in the body in response to tissue injury. They also studied its mimic HpTGM, a protein produced by a parasitic worm to help evade the immune response and thereby enable the worm to live within the tissue lining the gut. Intravascular delivery of either of these naturally occurring anti-inflammatory proteins reduced the injurious inflammatory response within the heart and importantly, the extent of heart injury as evidenced by reduced mature scar size.
The investigators were surprised to find almost identical beneficial effects of TGFβ1 and HpTGM treatment. Although TGFβ1 and HpTGM are evolutionarily unrelated, both these molecules interact with cells in a similar manner by activating the same signalling pathway. The dose of anti-inflammatory therapy was given at the time of reperfusion, which corresponds to a clinically useful time for a therapeutic intervention in humans.
Investigators could attribute the beneficial outcomes to the protective effect of these molecules on endothelial cells — the cells lining the blood vessels that help to regulate the exit of proinflammatory white blood cells from the circulation and enter the injured tissue. TGFβ1 has well-established anti-inflammatory properties, whereas HpTGM is a parasitomimetic with great clinical potential. Recent work in the Maizels laboratory at the University of Glasgow has also shown that delivery of HpTGM has a major anti-inflammatory effect in mouse models of colitis or airway inflammation, taking advantage of the product evolved by a parasite to quell the immune response to its presence.
Dr. Arthur concluded: “The current study shows that exogenous delivery of HpTGM at the time of coronary artery reperfusion dampens the proinflammatory response of coronary endothelial cells and reduces cardiac injury, leading to increased myocardial salvage and reduced scar size with the corollary of improved prospects for long-term cardiac function. The use of HpTGM as an anti-inflammatory therapy in treating heart attack patients is clearly an exciting prospect that requires further translational studies.”

Researchers at the University of Helsinki and HUS Helsinki University Hospital have succeeded in correcting a gene defect that causes a hereditary liver disease and its adverse effects on cells.
Argininosuccinate lyase deficiency (ASLD), also known as argininosuccinic aciduria, is a disease that has been enriched in the Finnish genetic heritage. In this severe metabolic disease, the body does not process proteins normally, instead resulting in a very dangerous accumulation of argininosuccinic acid and ammonia. Excess ammonia causes disturbances of consciousness, coma and even death.
In Finland, infants are screened for ASLD to determine the disease risk before symptoms develop. The treatment is an extremely strict lifelong diet and, in severe cases, a liver transplant.
Researchers from the University of Helsinki and HUS Helsinki University Hospital have succeeded in correcting the gene defect associated with argininosuccinic aciduria and demonstrated that the harmful metabolism caused by the disease can be cured.
In their recently completed study, they initially modified the skin cells of patients with ASLD into stem cells. Subsequently, the researchers reprogrammed the disease-causing gene defects in the stem cells using the CRISPR-Cas9 technique, known as gene scissors. Finally, the researchers guided the corrected stem cells to differentiate into liver cells to see whether the disease that impairs hepatic function was actually cured and that the fixed cells no longer produced the harmful argininosuccinic acid.
“In our study, we demonstrated for the first time that the gene defect causing ASLD can be corrected with gene scissors without any adverse effects visible in the cells. The gene-corrected cells were also metabolically improved,” says Docent of Stem Cell Biology Kirmo Wartiovaara, specialist in medical genetics, from the University of Helsinki and HUS.
The study was published in the American Journal of Human Genetics.

Researchers discover a suitable “gene mixture” in a drug already in use
In the study, the researchers used mRNA encapsulated inside lipid nanoparticles to get the gene scissors inside the cultured cells.
“This ‘gene mixture’ we produced is based on the formula of a pharmaceutical product already in use, which may facilitate its clinical use in the future. Our next goal is to cure ASLD in mice,” says Doctoral Researcher Timo Keskinen from the University of Helsinki.
“The same gene editing technique works on living animals and humans, but we don’t yet know how safe it is. This is why the matter has to be investigated first in laboratory animals,” Keskinen adds.
Therapeutic potential at last for hereditary diseases
There are already more than 7,000 hereditary diseases in the world. Finns, as well as other populations originating in small groups of people, have their own genetic disease variants that are more common in the population than elsewhere in the world. Many of these gene variants of our distant ancestors are such that if a child inherits the same variant from both parents, they may develop a severe disease.
Treatments are available for only a handful of hereditary diseases, and curative therapies are even more rare.
“However, a cure could be possible if the gene defect causing the disease is eliminated entirely. Thanks to basic research carried out with the help of gene scissors and other precise gene-editing techniques, permanent fixes are gradually starting to emerge,” Wartiovaara says.
The study is part of the doctoral theses of Sami Jalil and Timo Keskinen, supervised at the Biomedicum Stem Cell Center of the Biomedicum Helsinki research institute by Docent Kirmo Wartiovaara and Mervi Hyvönen, DMedSc.

Most human nerve cells last a lifetime without renewal. A trait echoed within the cells’ components, some enduring as long as the organism itself. New research by Martin Hetzer, molecular biologist and president of the Institute of Science and Technology Austria (ISTA), and colleagues discovered RNA, a typical transient molecule, in the nerve cells of mice that remain stable for their entire lives. Published in Science, these findings contribute to unraveling the complexities of brain aging and associated diseases.
After two decades in the United States, Martin Hetzer returned home to Austria in 2023 to become the 2nd President of the Institute of Science and Technology Austria (ISTA). A year into his new role, the molecular biologist remains engaged in the realm of aging research.
Hetzer is fascinated by the biological puzzles surrounding the aging processes in organs like the brain, heart, and pancreas. Most cells comprising these organs are not renewed throughout a human’s entire life span. Nerve cells (neurons) in the human brain, for instance, can be as old as the organism, even up to more than a century, and must function for a lifetime. This remarkable age of neurons might be a major risk factor for neurodegenerative disorders such as Alzheimer’s disease. Crucial to comprehending these kinds of ailments is a deeper understanding of how nerve cells function over time and maintain control. This potentially opens doors to therapeutically counteract the aging processes of these specific cells.
The latest collaborative publication by Hetzer, Tomohisa Toda from the Friedrich-Alexander University Erlangen-Nürnberg (FAU), who is also associated with the Max Planck Center for Physics and Medicine, Erlangen, and colleagues, gives new insights into this underexplored field of intricate mechanisms. For the first time in mammals, the study shows that RNA — an essential group of molecules important for various biological processes inside the cell — can persist throughout life. The scientists identified specific RNAs with genome-protecting functions in the nuclei of nerve cells of mice that remain stable for two years, covering their entire lives. The findings, published in the journal Science, underpin the importance of long-lived key molecules for maintaining a cell’s function.
Longevity of key molecules
The inside of cells is a very dynamic place. Some components are constantly renewed and updated; others stay the same their whole lives. It is like a city in which the old buildings blend in with the new ones. DNA found in the nucleus — the city’s heart — for instance, is as old as the organism. “DNA in our nerve cells is identical to DNA within the developing nerve cells in our mother’s womb,” explains Hetzer.
Unlike stable DNA, which is constantly being repaired, RNA, especially messenger RNA (mRNA), which forms proteins upon DNA’s information, is characterized by its transient nature. The cellular scope, however, extends beyond mRNA to a group of so-called non-coding RNAs. They do not turn into proteins; instead, they have specific duties to contribute to the overall organization and function of the cell. Intriguingly, their lifespan remained a mystery. Until now.

RNAs that last the whole life
Hetzer and Co. set out to decipher that secret. Therefore, RNAs were labeled, i.e. “marked,” in the brains of newborn mice. “For this labeling, we used RNA analogs — structurally similar molecules — with little chemical hooks that click fluorescent molecules on the actual RNAs,” explains Hetzer. This assured efficient tracking of the molecules and powerful microscopic snapshots at any given time point in the mice’s lives.
“Surprisingly, our initial images revealed the presence of long-lived RNAs, in various cell types within the brain. We had to further dissect the data to identify the ones in the nerve cells,” Hetzer explains. “Fruitful collaboration with Toda’s lab enabled us to make sense of that chaos during brain mapping.” Collaboratively, the researchers were able to focus solely on long-lived RNAs in neurons. They quantified the molecules’ concentration throughout a mouse’s life, examined their composition and analyzed their positions.
While humans have an average life expectancy of around 70 years, the typical lifespan of a mouse is 2.5 years. After one year, the concentration of long-lived RNAs was slightly reduced compared to newborns. However, even after two years, they remained detectable indicating a lifelong persistence of these molecules.
RNAs help protect the genome
Additionally, the scientists proved long-lived RNAs’ prominent role in cellular longevity. They found out that long-lived RNAs in neurons consist of mRNAs and non-coding RNAs and accumulate near the heterochromatin — the densely packed region of the genome, typically homing inactive genes. Next they further investigated the function of these long-lived RNAs.
In molecular biology, the most effective approach to achieve this is by reducing the molecule of interest and observing its subsequent effects. “As their name and our previous experiments suggest, these long-lived RNAs are extremely stable,” says Hetzer. The scientists, therefore, employed an in vitro (outside a living organism) approach, using neuronal progenitor cells — stem cells with the capacity to give rise to neural cells, including neurons. The model system allowed them to effectively intervene with these long-lived RNAs. A lower amount of long-lived RNAs caused problems in the heterochromatin architecture and stability of genetic material, eventually affecting the cells’ viability. Thus, the important role of long-lived RNAs’ in cellular longevity was clarified.
The study highlights that long-lived RNAs may function in the lasting regulation of genome stability. “Lifelong cellular maintenance during aging involves an extended life span of key molecules like the long-lived RNAs, we just identified,” Hetzer adds. The precise mechanism, however, remains unclear. “Together with unidentified proteins, long-lived RNAs likely form a stable structure that somehow interacts with the heterochromatin.” Upcoming research projects in Hetzer’s lab are set on finding these missing links and understanding the biological characteristics of these long-lived RNAs.

Scientists at King’s College London have discovered a new cause for asthma that sparks hope for treatment that could prevent the life-threatening disease.
Most current asthma treatments stem from the idea that it is an inflammatory disease. Yet, the life-threatening feature of asthma is the attack or the constriction of airways, making breathing difficult. The new study, published today in Science, shows for the first time that many features of an asthma attack — inflammation, mucus secretion, and damage to the airway barrier that prevents infections — result from this mechanical constriction in a mouse model.
The findings suggest that blocking a process that normally causes epithelial cell death could prevent the damage, inflammation, and mucus that result from an asthma attack.
Professor Jody Rosenblatt from King’s College London said: “Our discovery is the culmination of more than ten years work. As cell biologists who watch processes, we could see that the physical constriction of an asthma attack causes widespread destruction of the airway barrier. Without this barrier, asthma sufferers are far more likely to get long-term inflammation, wound healing, and infections that cause more attacks. By understanding this fundamental mechanism, we are now in a better position to prevent all these events.”
In the UK, 5.4 million people have asthma and can suffer from symptoms such as wheezing, coughing, feeling breathlessness and a tight chest. Triggers such as pollen or dust can make asthma symptoms worse and can lead to a life-threatening asthma attack.
Despite the disease commonality, the causes of asthma are still not understood. Current medications treat the consequences of an asthma attack by opening the airways, calming inflammation, and breaking up the sticky mucus which clogs the airway, which help control asthma, but do not prevent it.
The answer to stopping asthma symptoms may lie in cell extrusion, a process the researchers discovered that drives most epithelial cell death. Scientists used mouse lung models and human airway tissue to discover that when the airways contract, known as bronchoconstriction, the epithelial cells that line the airway get squeezed out to later die.

Because bronchoconstriction causes so many cell extrusions, it damages the airway barrier which causes inflammation and excess mucus.
In previous studies, the scientists found that the chemical compound gadolinium can block extrusion. In this study, they found it could work in mice to prevent the excess extrusion that causes damage and inflammation after an asthma attack. The authors note that gadolinium has not been tested in humans and has not been deemed to be safe or efficacious.
Professor Rosenblatt said: “This constriction and destruction of the airways causes the post-attack inflammation and excess mucus secretion that makes it difficult for people with asthma to breathe.
“Current therapies do not prevent this destruction — an inhaler such as Albuterol opens the airways, which is critical to breathing but, dishearteningly, we found it does not prevent the damage and the symptoms that follow an attack. Fortunately, we found that we can use an inexpensive compound, gadolinium which is frequently used for MRI imaging, to stop the airway damage in mice models as well as the ensuing inflammation and mucus secretion. Preventing this damage could then prevent the build-up of musculature that cause future attacks.”
Professor Chris Brightling from the University of Leicester and one of the co-authors of the study said: “In the last decade there has been tremendous progress in therapies for asthma particularly directed towards airway inflammation. However, there remains ongoing symptoms and attacks in many people with asthma. This study identifies a new process known as epithelial extrusion whereby damage to the lining of the airway occurs as a consequence of mechanical constriction and can drive many of the key features of asthma. Better understanding of this process is likely to lead to new therapies for asthma.”
Dr Samantha Walker, Director of Research and Innovation at Asthma + Lung UK, said: “Only two per cent of public health funding is allocated to developing new treatments for the 12 million people living with lung conditions in the UK so new research that can help in the treatment or prevention of asthma is good news.

“This research using an experimental mouse model shows that constricting the airways leads to damage to the lung lining and inflammation, like that seen in asthma. It is this constriction and resulting damage that makes it difficult for people with asthma to breathe.
“Current medications for asthma work by treating the inflammation, but this isn’t effective for everyone. Treatments aim to prevent future asthma attacks and improve asthma control by taking inhalers every day, but we know that ~31 per cent of people with asthma don’t have treatment options that work for them, putting them at risk of potentially life-threatening asthma attacks.
“This discovery opens important new doors to explore possible new treatment options desperately needed for people with asthma rather than focusing solely on inflammation.”
The discovery of the mechanics behind cell extrusion could underlie other inflammatory diseases that also feature constriction such as cramping of the gut and inflammatory bowel disease.
The paper is in collaboration with the University of Leicester and funded by Wellcome, Howard Hughes Medical Institute and the American Asthma Foundation.

Psychology researchers at The University of Texas at El Paso are making progress towards understanding the biological underpinnings of depression, a leading cause of disability that affects approximately 280 million people around the world.
In a study published this April in the Journal of Affective Disorders, UTEP psychologist Sergio Iñiguez, Ph.D., and his co-authors make the case that prairie voles, small rodents that are found throughout the central United States and Canada, can be effectively used as animal models to further the study of clinical depression.
“The findings of this investigation are important because we show, for the first time, that prairie voles display some of the core symptoms of depression after chronic stress exposure — just like humans,” Iñiguez said. “This is exciting because we can now use this animal model to potentially uncover the biological factors that underlie illnesses like depression and anxiety.”
The UTEP study focuses on the impact of “bullying” on voles’ behavioral patterns. Researchers observed what happened when individual male voles were bullied by more aggressive males over the course of ten days, inducing what Iñiguez refers to as “social defeat stress.”
Iñiguez explained that that the voles who were bullied exhibited changes in body weight, performed worse on spatial memory tests and were less sociable with other voles compared to those who were not bullied. Where voles generally show a preference for sugar water, the bullied voles showed no preference when given a choice between regular water and sugar water, a pattern known as anhedonia, or loss of pleasure in regular activities, Iñiguez said.
Iñiguez and his fellow researchers concluded that “social defeat” activated the voles’ stress response and became a risk factor for symptoms that mirrored those of depression in humans.
Iñiguez, a professor in the Department of Psychology at UTEP who studies behavioral neuroscience, said that while depression has certain defining characteristics — such as sadness, lack of pleasure in normal activities, and disruption in sleep and eating patterns — researchers don’t yet have a full picture of what causes it.

“We have some information about the many factors that contribute to depression, but the ethical implications of doing neurobiological research in humans make it difficult to pinpoint the biology behind this debilitating condition,” Iñiguez said.
Rats and mice are often used in psychology studies, but prairie voles share several unique characteristics with humans that make them better candidates for research, such as having monogamous relationships, raising vole pups in pairs, and even taking on parental roles for orphaned pups.
Psychology doctoral student Minerva Rodriguez is the lead author of the study.
“These unique and specialanimals have opened doors to understanding aspects of depression we simply could not with mice and rats,” Rodriguez said. “Their distinct social behaviors provide fresh research avenues, demonstrating the prairie vole’s immense value as a model for delving into the neurobiology of social stress-induced depression.”
Future studies will examine how the voles rebound from depression-like experiences and how they respond to antidepressant medications like Prozac or ketamine.
The project is funded by a grant from the National Institutes of Health.

It is possible to leave most of the lymph nodes in the armpit, even if one or two of them have metastases larger than two millimetres? This is shown in a trial enrolling women from five countries, led by researchers at Karolinska Institutet and published in the New England Journal of Medicine. The results open up for gentler surgery for patients with breast cancer.
Breast cancer can spread to the lymph nodes in the armpit. However, tumours found only in the breast and armpit lymph nodes are considered a localized disease, with the goal of curing the patient.
A challenging question for breast cancer surgeons revolves around what should be done when patients have metastases in the armpit, first detected during examination of tissue removed during surgery. Performing a so-called axillary dissection (removing many lymph nodes in the armpit) increases the risk of arm lymphedema. This occurs when lymph fluid cannot flow as freely as before, resulting in swelling in the arm and potentially causing pain and restriction of mobility.
“We want to perform less extensive procedures to spare patients from troublesome side effects. But we need to know that it’s safe,” says Jana de Boniface, breast cancer surgeon at Capio S:t Görans’s Hospital and researcher at the Department of Molecular Medicine and Surgery at Karolinska Institutet.
When it is known before the breast cancer surgery that there are metastases in the armpit, different treatment paths are chosen. Those patients are not included in this trial. However, when no lymphatic spread is suspected, the surgeon usually removes the so-called sentinel lymph nodes (the node or nodes first reached by lymph fluid from the breast). If these contain single tumour cells or metastases that are a maximum of two millimetres in size, the rest of the lymph nodes in the armpit are left intact. Previous trials have shown that this is safe for the patient.
Now, a large trial led from Karolinska Institutet has clarified the situation even for larger metastases. It includes nearly 2,800 patients from five different countries. All had metastases larger than two millimetres, so-called macrometastases, in one or two sentinel lymph nodes.
After sentinel node surgery, the patients were randomly assigned to undergo a completion axillary dissection (previously standard practice for all) or to leave the rest of the armpit undisturbed. Nearly all patients received some postoperative treatment with chemotherapy and/or anti-hormonal therapy, plus radiation therapy according to guidelines in each respective country. More than one-third of patients who underwent axillary dissection were found to have additional metastases than the maximum two in the sentinel lymph nodes. This must be assumed to be the same for those who kept the remaining lymph nodes. Still, recurrences were equally common in both groups, indicating that postoperative treatment seems sufficient to eliminate remaining tumour cells.
At the same time, a previous publication from the trial showed that 13 per cent of those who underwent axillary dissection reported serious or very serious problems with their arm function, compared to 4 per cent among those who only had the sentinel lymph nodes removed.
“Our assessment is that it is safe for patients to forgo axillary dissection if there are a maximum of two macrometastases in the sentinel lymph nodes. In these cases, axillary dissection is replaced with radiation therapy to the armpit, which results in less arm-related complications. This has now been implemented in clinical practice in Sweden,” says Jana de Boniface.
The trial is called SENOMAC and is funded by grants from the Swedish Research Council, the Swedish Cancer Society, the Nordic Cancer Union, and the Swedish Breast Cancer Association.

Published1 hour agoShareclose panelShare pageCopy linkAbout sharingImage source, Science Photo LibraryBy Michelle RobertsDigital health editorUK scientists say they have found a new cause behind much of the damage asthma causes. Cells lining the airways are squeezed to destruction during an attack, their research shows.And drugs to prevent this, rather than manage its aftermath, might break the cycle of harm, the Kings College London researchers told the Science journal. The airways of people with asthma are sensitive to triggers such as pollen, pets and exercise.They become inflamed or swollen, causing symptoms including coughing, wheezing and breathlessness. Existing drugs or inhalers can reduce this inflammation and help keep the airways open. But repeated attacks can cause permanent scarring and narrowing of the airways. Mum makes plea to parents after son’s asthma death’For asthma to take her life was unbelievable’During an attack, the smooth muscle surrounding the airways starts to squeeze and tighten, known as bronchoconstriction. The Kings College London team studied this process in detail, using mice and human lung-tissue samples. Lead researcher Prof Jody Rosenblatt said bronchoconstriction damaged the airway lining, resulting in long-term inflammation, wound healing, and infections that cause more attacks. Until now, this lining damage had been overlooked, she told BBC News.”This epithelial lining is the body’s first line of defence against things like infections and yet it is getting damaged during asthma attacks,” Prof Rosenblatt said.”There’s this constant wounding going on – it’s a vicious cycle.”If we can block the damage, we are hoping that might stop attacks from happening at all.” ‘Desperately needed’One possible preventive treatment the researchers are exploring is a compound called gadolinium, which appears to help – at least in mice. But much more work is needed to see if it might be safe and effective enough to try in people – and that will take years. Asthma and Lung UK research and innovation director Dr Samantha Walker said: “This discovery opens important new doors to explore possible new treatment options desperately needed for people with asthma.”The charity says it’s essential that people with asthma continue to use their prescribed medications correctly – many should be able to get on with their lives without symptoms getting in the way, and for those who are still having symptoms it is important that they talk to their healthcare professional. “We know that there are many people for whom existing asthma treatments don’t work as well, so it’s vital we continue to fund research to find new treatments that better tackle the causes of asthma.”In the UK, more than five million people have asthma, about one in every 12 adults and one in every 11 children.Most people with asthma have two inhalers:a preventer to use regularly, to reduce inflammation and prevent symptomsa reliever, to quickly open the airwaysThose having an attack should not delay seeking help and call 999 if:their reliever is not helpingthe attack lasts four hoursthey are worried at any timeMore on this storyBoy’s asthma death prompts records sharing reviewPublished26 March’Asthma can kill if you don’t look after yourself’Published2 May 2023Related Internet LinksScience journalManaging asthma attacks – Asthma and Lung UKThe BBC is not responsible for the content of external sites.

A study found that when farsighted workers in Bangladesh were given free reading glasses, they earned 33 percent more than those who had not.If you’re 50 or older and reading this article, chances are you are wearing a pair of inexpensive reading glasses to correct your presbyopia, or farsightedness, the age-related decline in vision that makes it progressively more difficult to see fine print and tiny objects.Eventually, everyone gets the condition.But for nearly a billion people in the developing world, reading glasses are a luxury that many cannot afford. According to the World Health Organization, the lack of access to corrective eyewear inhibits learning among young students, increases the likelihood of traffic accidents and forces millions of middle-age factory workers and farmers to leave the work force too early.Uncorrected presbyopia, not surprisingly, makes it harder for breadwinners to support their families. That’s the conclusion of a new study which found that garment workers, artisans and tailors in Bangladesh who were provided with free reading glasses experienced a 33 percent increase in income compared to those who were not given glasses.The study, published on Wednesday in the journal PLOS One, included more than 800 adults in rural Bangladesh, many of whom work in jobs that require intense attention to detail. Half of the participants — a mix of tea pickers, weavers and seamstresses between 35 and 65 — were randomly chosen to receive a free pair of reading glasses. The others were not given glasses.Researchers followed up eight months later and found that the group with glasses had experienced a significant bump in income, receiving an average monthly income of $47.10, compared to $35.30 for the participants who did not have glasses.The study subjects were evenly divided between male and female, and slightly more than a third were literate.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

A register-based study from Finland identified three distinct BMI trajectory groups among patients with newly diagnosed type 2 diabetes. In a four-year follow-up, most patients followed a stable trajectory without much weight change. Only 10% of patients lost weight, whereas 3% gained weight. Mean BMI exceeded the threshold of obesity in all groups at baseline. Weight loss is a central treatment goal in type 2 diabetes, but the study shows that few patients succeed in it.
The study was carried out by researchers at the University of Eastern Finland, and the results were published in Clinical Epidemiology.
Patients belonging to each trajectory group were followed up for another eight years for diabetes complications. During the follow-up, 13% of all patients developed microvascular complications, 21% developed macrovascular complications and 20% of patients deceased. The risk of microvascular complications was 2.9 times higher and the risk of macrovascular complications 2.5 times higher among patients with an increasing BMI compared to those with a stable BMI. Micro- and macrovascular complications of diabetes can include, for example, retinopathy, nephropathy and neuropathy, as well as cardiovascular diseases.
“These results underscore the significance of continuous BMI monitoring and weight management in patients with type 2 diabetes. Tailored treatments and support with lifestyle changes are crucial for efficiently preventing weight gain and reducing the risk of diabetes complications,” says Doctoral Researcher Zhiting Wang of the University of Eastern Finland.
The study was carried out in North Karelia, Finland, using electronic health records from both primary and specialised health care. The study included a total of 889 adults with newly diagnosed type 2 diabetes in 2011 or 2012. The participants were grouped based on individual BMI trajectories from the diagnosis until 2014. Risks for microvascular complications, macrovascular complications, any diabetes complications and all-cause mortality from 2015 to 2022 across BMI trajectory groups were estimated.