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In December 1981, The Lancet medical journal reported the first Aids-related death in London. The disease claimed thousands of lives throughout the 1980s and 1990s, many of them young, gay men. Although the treatment of HIV has vastly improved, people who lived through the time remember the homophobia and stigma that was attached to the condition. Video by Raphael Sheridan

SharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesThe World Health Organization has said people who are unwell or vulnerable should delay travel if they are not completely vaccinated. In its latest travel advisory, the UN agency includes in that category people over 60, and those with conditions like heart disease, cancer and diabetes.An earlier WHO statement advised against all travel for this group.A corrected version specified that only those more vulnerable and not fully vaccinated should delay travelling.This is in line with the WHO’s previous advice for travel during the pandemic, and comes amid concern about the new Omicron variant.The WHO also restated its position that blanket travel bans do not prevent the spread of the variant.South Africa alerted the world about the variant last week.Many countries then proceeded to impose restrictions on travel from countries in southern Africa. “Blanket travel bans will not prevent the international spread, and they place a heavy burden on lives and livelihoods,” the WHO said in its statement.”In addition, they can adversely impact global health efforts during a pandemic by disincentivising countries to report and share epidemiological and sequencing data.”The WHO advice comes as officials say Omicron was present in the Netherlands earlier than previously thought.How do you detect Omicron?Escaped couple fight Omicron quarantineHow worrying is the new Covid variant?UN Secretary General António Guterres said he was “deeply concerned” about the isolation of southern Africa, adding that “the people of Africa cannot be blamed for the immorally low level of vaccinations available”.Earlier, the head of the WHO, Tedros Adhanom Ghebreyesus, said there were still many questions regarding Omicron, including its transmission, the severity of the disease it might provoke, and the effectiveness of tests and vaccines.In remarks to a closed-door meeting posted on the WHO website, Dr Tedros called on WHO member states to take “rational, proportional” measures.South Africa’s President Cyril Ramaphosa said the wider region had been the victim of unfair discrimination, adding that the bans would not be effective in preventing the spread of the variant.An earlier version of this article stated that the WHO recommended vulnerable people delay all travel, but was updated when the WHO issued a corrected statement to specify delays to travel to areas with community transmission if unwell or not fully vaccinated.This video can not be playedTo play this video you need to enable JavaScript in your browser.

There are few treatment options for children with multiple sclerosis — a condition in which the immune system attacks the protective covering of nerves in the brain and spinal cord — and most therapies for the disease have not been tested in children. An international team of investigators, including researchers at Massachusetts General Hospital (MGH), has conducted a phase 3, randomized, double-blind clinical trial to examine the safety and efficacy of teriflunomide, an oral immunomodulatory drug approved in more than 80 countries for the treatment of adults with relapsing forms of multiple sclerosis. Based on the trial’s results, which appear in Lancet Neurology, teriflunomide was recently approved by the European Commission for children aged 10-17 years with a diagnosis of relapsing remitting multiple sclerosis.
In the trial, called TERIKIDS, 109 children were randomized to receive teriflunomide and 57 were randomized to receive placebo for up to 96 weeks (nearly two years). Early entry in an open-label extension phase (where patients were guaranteed to receive teriflunomide) was possible before the end of the double-blind period for patients who experienced a relapse or demonstrated high disease activity on MRI imaging tests.Importantly, more patients in the placebo group entered the open-label extension phase (because of high MRI activity) than anticipated, with 26% of patients switching from placebo to teriflunomide before 96 weeks.
After 96 weeks, there was no difference in time to first clinical relapse of multiple sclerosis with teriflunomide compared with placebo. Teriflunomide was well tolerated — serious adverse events occurred in 11% of patients in the teriflunomide group and 11% of patients in the placebo group. Nasal inflammation, upper-respiratory-tract infection, hair loss, tingling sensations, abdominal pain, and increased blood creatine phosphokinase (a marker of muscle damage) were more frequent with teriflunomide than with placebo.
“The trial did not meet its primary endpoint — delaying time to the next clinical relapse — possibly because of more frequent switches to the open-label arm due to high MRI activity. However, the study did meet several key secondary endpoints related to teriflunomide’s ability to reduce the number of new or enlarged lesions that are detected through MRI, suggesting that the medication might have beneficial effects in children with relapsing forms of multiple sclerosis,” says lead author Tanuja Chitnis, MD, director of the MGB Pediatric Multiple Sclerosis Center at MGH.
Chitnis notes that an ongoing open-label treatment extension study is continuing to evaluate the long-term effects of teriflunomide in young patients.
Chitnis is also director of the Translational Neuroimmunology Research Center at Brigham and Women’s Hospital and a professor of neurology at Harvard Medical School.
This work was supported by Sanofi.
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A new study led by University of California, Irvine researchers has confirmed a link between altered DNA repair and increased DNA damage associated with spinocerebellar ataxia type 7 (SCA7), a debilitating, sometimes deadly neurodegenerative condition causing movement disorders. Their work also revealed a potential therapeutic target for the currently incurable and difficult to treat condition.
“Our research delves into the mechanistic basis of the cerebellar neuron degeneration and death in SCA7, a specific SCA that causes impaired coordination, like difficulty with walking, talking and eye movement,” said corresponding author Albert La Spada, MD, PhD, Distinguished Professor of pathology, neurology and biological chemistry in the UCI School of Medicine. “Through our efforts, we confirmed the connection between altered DNA repair and DNA damage, and also the importance of the activation of PARP1 enzymes that results.”
Previous research has shown that increased DNA damage can lead to the activation of PARP1 enzymes. These enzymes serve to recruit the DNA repair machinery but can also promote cerebellar neuron dysfunction and death. Fortunately, PARP inhibitors already exist and could prove to be a promising potential new treatment.
“Perhaps more exciting is that the DNA damage and altered DNA repair found in SCA7, is also found in other SCAs. This could mean new therapeutics to treat the devastating effects of many of the forms of spinocerebellar ataxia might be possible,” said LaSpada. “Our next steps will be to test candidate PARP inhibitor drugs in mouse models of SCA7 as well as in neurons derived from pluripotent stem cells generated from human SCA7 human patients.”
SCA7, belongs to a disease category which includes spinobulbar muscular atrophy (SBMA), Huntington disease (HD), dentatorubral-pallidoluysian atrophy (DRPLA), and five other forms of spinocerebellar ataxia (SCA1, 2, 3, 6, and 17).
Each year, 15,000 — 20,000 Americans suffer from spinocerebellar ataxia (SCA), a genetic dominantly inherited neurodegenerative condition, that frequently results in atrophy of the cerebellum and the loss of fine coordination of muscle movements leading to unsteady and clumsy motion, and other symptoms. SCAs can affect anyone of any age. Currently, there are no known effective treatments or cures.
This work was supported by grants from the National Institutes of Health and the Polish Ministry of Science and Higher Education.
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Combining knowledge of chemistry, physics, biology, and engineering, scientists from McGill University develop a biomaterial tough enough to repair the heart, muscles, and vocal cords, representing a major advance in regenerative medicine.
“People recovering from heart damage often face a long and tricky journey. Healing is challenging because of the constant movement tissues must withstand as the heart beats. The same is true for vocal cords. Until now there was no injectable material strong enough for the job,” says Guangyu Bao, a PhD candidate in the Department of Mechanical Engineering at McGill University.
The team, led by Professor Luc Mongeau and Assistant Professor Jianyu Li, developed a new injectable hydrogel for wound repair. The hydrogel is a type of biomaterial that provides room for cells to live and grow. Once injected into the body, the biomaterial forms a stable, porous structure allowing live cells to grow or pass through to repair the injured organs.
“The results are promising, and we hope that one day the new hydrogel will be used as an implant to restore the voice of people with damaged vocal cords, for example laryngeal cancer survivors,” says Guangyu Bao.
Putting it to the test
The scientists tested the durability of their hydrogel in a machine they developed to simulate the extreme biomechanics of human vocal cords. Vibrating at 120 times a second for over 6 million cycles, the new biomaterial remained intact while other standard hydrogels fractured into pieces, unable to deal with the stress of the load.
“We were incredibly excited to see it worked perfectly in our test. Before our work, no injectable hydrogels possessed both high porosity and toughness at the same time. To solve this issue, we introduced a pore-forming polymer to our formula,” says Guangyu Bao.
The innovation also opens new avenues for other applications like drug delivery, tissue engineering, and the creation of model tissues for drug screening, the scientists say. The team is even looking to use the hydrogel technology to create lungs to test COVID-19 drugs.
“Our work highlights the synergy of materials science, mechanical engineering and bioengineering in creating novel biomaterials with unprecedented performance. We are looking forward to translating them into the clinic,” said Professor Jianyu Li, who holds the Canada Research Chair in Biomaterials and Musculoskeletal Health.
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Biomedical engineers at Duke University have engineered a holographic system capable of imaging and analyzing tens of thousands of cells per minute to both discover and recognize signs of disease.
In the proof-of-concept demonstration, the technique distinguished between healthy samples and either cancerous or carcinogen-exposed, pre-cancerous cells with nearly 100% accuracy, using just four basic cellular physical parameters out of a holographic panel of 25. The results point toward a promising screening or diagnostic technology that is simpler and cheaper to use than current standard practices, making it a potential target for use in remote, low-resource settings.
The research appears online on November 30 in the journal Frontiers in Physics.
“The cells are flying through the scanner so fast that if the computer didn’t slow them down on the screen, you wouldn’t even be able to see them,” said Adam Wax, professor of biomedical engineering at Duke. “We were very excited to be able to image this many cells at once because it points toward this technology’s potential for point-of-care diagnostics.”
In a traditional cellular diagnostic process, cells obtained from tissue scraping or fine needle biopsies are put on a slide and stained for a trained physician to carefully magnify and inspect. But in some cases, the staining process can damage the cells, and getting the slides to the eyes of trained experts can take days if not weeks.
In the new holographic imaging approach, sample cells could be rinsed off of the collection instrument into a biocompatible solution and inserted into a microfluidic chip. The small device diverts the sample into a series of parallel channels that pass beneath a line camera, kind of like a conveyor belt passing newly manufactured items beneath an autonomous scanner for inspection. When slowed down, the march of cell images is reminiscent of green characters cascading down a computer screen in The Matrix.

To an immunologist, autoimmune diseases like Type 1 diabetes are the polar opposite of cancer. In the former, the immune system goes into overdrive and attacks the body’s own organs in a relentless manner, eventually causing disease; with cancer, the immune system shuts down and fails to mount an aggressive attack to stop cancer from forming.
Why does the immune system behave so differently in the two cases? No one knows.
“This is a real mystery in the field,” says Andrea Schietinger, a tumor immunologist in the Sloan Kettering Institute (SKI) at Memorial Sloan Kettering Cancer Center who studies the phenomenon of immune cell dysfunction in cancer.
“We thought if we could figure out how autoimmune T cells are programmed, then we could take that information and apply it to tumor-specific T cells to make them more effective cancer killers.”
It was a bit of a long shot. To pursue this ambitious research project, Dr. Schietinger was awarded a National Institutes of Health (NIH) Director’s New Innovator Award in 2017, a funding opportunity that specifically supports high-risk, high-reward science. The project became a collaborative effort between Dr. Schietinger’s research team, particularly Sofia Vaccarino Gearty, an MD/PhD student in the lab, and scientists Doron Betel, Friederike Dündar, and Paul Zumbo from Weill Cornell Medicine.
Now, four years later, the results are in. Researchers reported in the journal Nature, on November 30, 2021, that the ability of autoimmune T cells to continue fighting is dependent upon a population of stem-like T cells that perpetually resupply the stock of self-reactive T cells. This type of stem-like T cell has never been seen before in autoimmune diseases, and the researchers think it could hold important lessons for improving the treatment of both autoimmune diseases and cancer.

Ever since the first barcode appeared on a pack of chewing gum in 1974, the now-ubiquitous system has enabled manufacturers, retailers and consumers to quickly and effectively identify, characterize, locate and track products and materials. In a paper first posted online Nov. 26, 2021, in the journal Cell, researchers at Johns Hopkins Medicine and The Johns Hopkins University demonstrate how they can do the same thing at the molecular level, studying the ways cancer cells “talk” with one another using a different kind of barcode system — one made up of combinations of patterns and colors, with each set tied to a specific biochemical activity in the communication network.
“When cancer cells communicate, numerous proteins constantly change how they interact with one another,” says senior study author Chuan-Hsiang (Bear) Huang, M.D., Ph.D., assistant professor of pathology at the Johns Hopkins University School of Medicine. “Studying this signaling in depth and in real time has traditionally been difficult, so we needed a method that could simultaneously image, track and analyze everything happening in the network, and therefore, reveal the true relationships among these activities.”
Genetically encoded fluorescent biosensors were previously used to study cellular protein functions, including signaling activities in cancer cells, says Huang. The biosensors are protein fragments tagged with fluorophores — fluorescent molecules that glow by absorbing light energy of a specific wavelength and then emitting light at a longer wavelength — and each color is linked to a specific activity in the cell. Using a fluorescent microscope to image the type, location and intensity of the colors exhibited by these sensors, researchers can accurately and precisely document proteins in action in different cell regions.
“For example, changes in the intensity of specific colors, their locations within cells and the ratio of one color to another shed light on the activity levels of the proteins being studied and how they interact with one another in real time,” says Huang.
However, Huang says the usefulness of fluorescent biosensors was limited when researchers needed to track a complex system like a cancer cell communications network. This, he explains, was because different biosensors often had very similar colors and could not be distinguished from one another when imaged together.
“In the past, if you wanted to look at dozens of biosensors that tracked the activities of different proteins in a signaling network, each biosensor had to be imaged in separate experiments that lasted hours,” says study lead author Jr-Ming Yang, Ph.D., a research associate at the Johns Hopkins University School of Medicine. “Moreover, to understand the communication network’s properties, those experiments had to be repeated. Besides the time investment, separate imaging runs increased the likelihood of variations popping up, making it difficult to ascertain that the changes in activity were from real effects.”
Huang and his colleagues overcame these problems by combining fluorescent proteins of different colors and localization patterns to create “biosensor barcodes,” tools that can concurrently identify and track a larger number of biosensors for various proteins, including those driving cancer formation.

New clinical research indicates that a widely used food additive, carboxymethylcellulose, alters the intestinal environment of healthy persons, perturbing levels of beneficial bacteria and nutrients. These findings, published in Gastroenterology, demonstrate the need for further study of the long-term impacts of this food additive on health.
The research was led by a collaborative team of scientists from Georgia State University’s Institute for Biomedical Sciences, INSERM (France) and the University of Pennsylvania. Key contributions also came from researchers at Penn State University and Max Planck Institute (Germany).
Carboxymethylcellulose (CMC) is a synthetic member of a widely used class of food additives, termed emulsifiers, which are added to many processed foods to enhance texture and promote shelf life. CMC has not been extensively tested in humans but has been increasingly used in processed foods since the 1960s. It had long been assumed that CMC was safe to ingest because it is eliminated in the feces without being absorbed. However, increasing appreciation of the health benefits provided by bacteria that normally live in the colon, and thus would interact with non-absorbed additives, has led scientists to challenge this assumption. Experiments in mice found that CMC, and some other emulsifiers, altered gut bacteria resulting in more severe disease in a range of chronic inflammatory conditions, including colitis, metabolic syndrome and colon cancer. However, the extent to which such results are applicable to humans had not been previously investigated.
The team performed a randomized controlled-feeding study in healthy volunteers. Participants, housed at the study site, consumed an additive-free diet or an identical diet supplemented with carboxymethylcellulose (CMC). Because the diseases CMC promotes in mice take years to arise in humans, the researchers focused here on intestinal bacteria and metabolites. They found that CMC consumption changed the make-up of bacteria populating the colon, reducing select species. Furthermore, fecal samples from CMC-treated participants displayed a stark depletion of beneficial metabolites that are thought to normally maintain a healthy colon.
Lastly, the researchers performed colonoscopies on subjects at the beginning and end of the study and noticed that a subset of subjects consuming CMC displayed gut bacteria encroaching into the mucus, which has previously been observed to be a feature of inflammatory bowel diseases and type 2 diabetes. Thus, while CMC consumption did not result in any disease per se in this two week study, collectively the results support the conclusions of animal studies that long-term consumption of this additive might promote chronic inflammatory diseases. Therefore, further studies of this additive are warranted.
“It certainly disproves the ‘it just passes through’ argument used to justify the lack of clinical study on additives,” said Georgia State University’s Dr. Andrew Gewirtz, one of the paper’s senior authors. Beyond supporting the need for further study of carboxymethylcellulose, the study “provides a general blueprint to carefully test individual food additives in humans in a well-controlled manner,” said co-senior author Dr. James Lewis, of the University of Pennsylvania, where the subjects were enrolled.
Lead author Dr. Benoit Chassaing, research director at INSERM, University of Paris, France, noted that such studies need to be large enough to account for a high degree of subject heterogeneity. “Indeed, our results suggest that responses to CMC and likely other food additives are highly personalized and we are now designing approaches to predict which individuals might be sensitive to specific additives,” Chassaing said.
This study was funded by the National Institutes of Health, the European Research Council, the Max Planck Society, the INSERM and the Kenneth Rainin Foundation.
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