Publisher Health

Education about gene-by-environment interaction (G X E) causes of eating behaviors can have beneficial downstream effects on attitudes toward people with higher weight. A recent study included in the Journal of Nutrition Education and Behavior, published by Elsevier, found that participants who received education about G X E concepts reported higher empathy and held fewer stigmatizing attitudes toward individuals with higher weight. G X E is when two different genotypes respond to variations in the environment in two different ways.
“Discriminatory attitudes against people with higher weight have been observed at comparable rates to racial and gender discrimination and are often more overt because weight stigma is viewed as a more socially acceptable form of negative bias,” says corresponding author Susan Persky, PhD, Social and Behavioral Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD. “However, weight has a sizable genetic component. Our study found that increasing education about the role of genetics in eating behavior may therefore help to alleviate weight stigma by reducing the extent to which individuals are blamed for their weight.”
Participants were recruited via the online platform Prolific and were randomly assigned to watch an educational or a control video. Participants then watched a set of vignette scenarios that depicted what it is like to have a predisposition toward obesogenic eating behaviors from either a first-person or third-person perspective. Participants completed questionnaires measuring G X E knowledge, causal attributions, weight stigma, and empathy post intervention.
Participants who watched the educational video demonstrated greater G X E knowledge, reported higher empathy toward the characters in the vignette scenarios and held fewer stigmatizing attitudes (notably blame) toward individuals with higher weight. Exploratory mediation analyses indicated that the educational video led to these positive downstream effects by increasing the extent to which participants attributed genetic causes to eating behaviors.
Communicating G X E causes of eating behaviors to the public is a useful way to improve attitudes toward people with higher weight. Therefore, the authors envision the potential for similar G X E education to be broadly disseminated as part of public health campaigns. Moreover, a greater understanding of these concepts may help improve patient-provider interactions around healthy eating and weight.
“Focusing on G X E causes of eating may help tackle entrenched weight stigma among the general public and health care providers,” suggests the study’s lead author Alison Jane Martingano, PhD, National Human Genome Research Institute, National Institutes of Health. “This research provides initial evidence that future educational interventions may benefit from focusing on eating behaviors, specifically, when attempting to improve attitudes toward people with higher weight.”
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The risk for poor glycemic control in patients with type 2 diabetes can be predicted with confidence by using machine learning methods, a new study from Finland finds. The most important factors predicting glycemic control include prior glucose levels, duration of type 2 diabetes, and the patient’s existing anti-diabetic medicines.
The researchers examined glycaemic control in patients with type 2 diabetes in North Karelia, Finland, over a period of six years. Patients’ glycemic control was determined on the basis of long-term blood glucose, HbA1c. Three HbA1c trajectories were identified from the data, and based on these, patients were divided into two groups: patients with adequate glycemic control, and patients with inadequate glycemic control. Using machine learning methods, the researchers examined the association of patients’ baseline characteristics, clinical- and treatment-related factors and socio-economic status with glycemic control. The baseline characteristics included more than 200 different variables.
The results showed that by using data on the duration of type 2 diabetes, prior HbA1c levels, fasting blood glucose, existing anti-diabetic medicines and their number, it is possible to reliably identify patients with a persistent risk for hyperglycemia at any point of their disease. In other words, inadequate glycemic control can be predicted from data that is routinely collected as part of diabetes monitoring and management.
The primary objective of treatment in type 2 diabetes is to maintain good glycemic control in order to prevent complications associated with the disease. According to the Finnish Current Care Guidelines for Diabetes, glycemic control should be followed up annually, making it possible to monitor the long-term trajectory of the disease. Early identification of patients with poor glycemic control is of paramount importance in order to target treatment to those in need and to intensify it at the right time. Delayed intensification of treatment increases the risk of complications, which is also reflected in higher costs of care.
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A variety of healthy eating patterns are linked to reduced risk of premature death, according to a new study led by Harvard T.H. Chan School of Public Health researchers. They found that participants who scored high on adherence to at least one of four healthy eating patterns were less likely to die during the study period from any cause and less likely to die from cardiovascular disease, cancer, or respiratory disease, compared with people with lower scores. The findings are consistent with the current Dietary Guidelines for America, which recommend multiple healthy eating patterns.
“The Dietary Guidelines for Americans are intended to provide science-based dietary advice that promotes good health and reduces major chronic diseases. Thus, it is critical to examine the associations between DGAs-recommended dietary patterns and long-term health outcomes, especially mortality,” said corresponding author Frank Hu, Fredrick J. Stare Professor of Nutrition and Epidemiology and chair of the Department of Nutrition.
The study will be published online January 9, 2023, in JAMA Internal Medicine.
Few studies have evaluated whether greater adherence to the DGAs-recommended dietary patterns is associated with long-term risk of total and cause-specific mortality. The researchers used health data collected over 36 years from 75,230 women participating in the Nurses’ Health Study and 44,085 men in the Health Professionals Follow-up Study. All participants were free of cardiovascular disease or cancer at the beginning of the study and completed dietary questionnaires every four years. Their information was scored based on each of the four dietary pattern indexes (Healthy Eating Index 2015, Alternate Mediterranean Diet, Healthful Plant-based Diet Index, and Alternate Healthy Eating Index). All share key components including whole grains, fruits, vegetables, nuts, and legumes, although other components differ across different eating patterns.
A higher score on at least one of the indexes was associated with lower risk of premature death from all causes, and from cardiovascular disease, cancer, and respiratory disease. Higher scores on the AMED and the AHEI were associated with lower risk of death from neurogenerative disease. The results were consistent for non-Hispanic white, non-Hispanic Black, and Hispanic people.
The current DGAs (2015-2020) recommend multiple healthy eating patterns that can be adapted toindividual food traditions and preferences. An updated version of the Guidelines is released every five years by the U.S. Departments of Health and Human Services (HHS) and Agriculture (USDA).
“It is important to evaluate adherence to DGAs-recommended eating patterns and health outcomes, including mortality, so that timely updates can be made,” said Hu. “Our findings will be valuable for the 2025-2030 Dietary Guidelines Advisory Committee, which is being formed to evaluate current evidence surrounding different eating patterns and health outcomes.”
Other Harvard Chan School co-authors of the study included Zhilei Shan, Fenglei Wang, Yanping Li, Megu Baden, Shilpa Bhupathiraju, Dong Wang, Qi Sun, Eric Rimm, Lu Qi, Fred Tabung, Edward Giovannucci, Walter Willett, JoAnn Manson, and Qibin Qi.
Funding for the study came from grant R01HL060712 from the NHLBI. The Nurses’ Health Studies and Health Professional Follow-up Studies are supported by the grants UM1 CA186107, P01 CA87969, R01 CA49449, R01 HL034594, R01 HL088521, U01 CA176726, R01 CA67262, U01 CA167552, R01 HL35464, and U01 H145386 from the NIH. Q. Qi is supported by grants K01HL129892 and R01 HL140976 from the NHLBI and grant R01 DK119268 and R01 DK120870 from the National Institute of Diabetes and Digestive and Kidney Diseases. F. Wang is supported by postdoctoral fellowship grant 897161 from the American Heart Association.

Research led by Queen Mary University of London, King’s College London and the Francis Crick Institute has identified a protein that makes melanoma, the most serious type of skin cancer, more aggressive by giving cancer cells the ability to change the shape of their nucleus — a characteristic which allows the cells to migrate and spread around the body.
The study, published today in Nature Cell Biology, modelled the behaviour of aggressive melanoma cells that are able to change the shape of their nucleus to overcome the physical constraints that cancer cells encounter when they migrate through tissues. The study found that these aggressive melanoma cells harboured high levels of a protein called LAP1 and that increased levels of this protein were linked to poor prognosis in melanoma patients.
Melanoma is a type of skin cancer that can spread to other organs in the body. Cancer spread or ‘metastasis’ is the leading cause of cancer-related deaths. While metastasis has been extensively studied, the mechanisms by which it occurs are poorly understood. The findings from the study shed new light on a mechanism of melanoma progression and could pave the way for the development of new ways to target melanoma spread.
The study
The study was co-led by Professor Victoria Sanz-Moreno from Queen Mary’s Barts Cancer Institute and Dr Jeremy Carlton from King’s College London and The Francis Crick Institute, and primarily funded by Cancer Research UK, the Wellcome Trust and Barts Charity.
In the study, the team challenged aggressive and less-aggressive melanoma cells in laboratory experiments to migrate through pores in an artificial membrane that were smaller than the size of their nucleus. The aggressive cells were from a site of metastasis in a patient with melanoma, and the less-aggressive cells were from the original or ‘primary’ melanoma tumour of the same patient.

To metastasise, cancer cells need to break away from the primary tumour, travel to another part of the body and start growing there. However, the dense surroundings of a tumour make this physically difficult for cancer cells.
Cells contain a large, stiff structure called the nucleus that stores the cell’s genetic information, but which also restricts the ability of a cell to move through the tight gaps in the tumour’s environment. For cancer cells to squeeze through these gaps, they need to make their nucleus more malleable.
Imaging conducted after the migration experiments showed that the aggressive cells were able to move through the pores more effectively than the less-aggressive ones by forming bulges at the edge of their nucleus called ‘blebs’. Genetic analyses of the melanoma cells revealed that the aggressive cells that formed the blebs contained higher levels of the LAP1 protein, which sits within the membrane that surrounds the nucleus (called the nuclear envelope).
Dr Jeremy Carlton, whose laboratory is interested in understanding the dynamics of membrane-bound structures within cells, said:
“The nuclear envelope is tethered to the underlying nucleus, and our investigations show that the LAP1 protein loosens this tethering, allowing the nuclear envelope to bulge away and form blebs that make the nucleus more fluid. As a result, the cancer cells could squeeze through gaps that would normally stop them.”
When the team blocked the production of the LAP1 protein in aggressive cells and re-challenged them to migrate through pores in laboratory experiments, they found that the cells were less able to form nuclear envelope blebs and less able to squeeze through these gaps.

The team also observed the same pattern of LAP1 expression in melanoma samples from patients. LAP1 levels were higher in tissue samples taken from sites of metastasis in melanoma patients compared to the levels found in primary tumours. The patients that had high levels of LAP1 in the cells around the edge of the primary tumour had more aggressive cancer and poorer outcomes, suggesting that the protein could be used to identify subpopulations of melanoma patients that may be at higher risk of aggressive disease.
Professor Sanz-Moreno, whose research group is interested in understanding how cancer cells communicate with their environment to promote their growth and spread, said:
“Melanoma is the most aggressive and deadly type of skin cancer. By combining the expertise of my laboratory with that of Dr Carlton’s, we have gained new mechanistic understanding of how LAP1 contributes to melanoma progression, and have shown that LAP1 is a key regulator of melanoma aggressiveness in laboratory and patient models.”
“Because LAP1 is expressed in such high levels in metastatic cells, interfering with this molecular machinery could have a big impact on cancer spread. There are currently no drugs that target LAP1 directly, so looking to the future we would like to investigate ways to target LAP1 and nuclear envelope blebbing to see if it is possible to block this mechanism of melanoma progression.”
The team would like to investigate whether nuclear envelope blebbing driven by LAP1 occurs in other cells that make up and move through a tumour’s environment, such as immune cells, to determine if this process in other cells helps or hinders the progression of cancer.
Dr Iain Foulkes, Executive Director of Research and Innovation at Cancer Research UK, which partly funded the study, said:
“Studies like this one are a perfect example of why Cancer Research UK is passionate about funding research that furthers our knowledge of what cancer does to the biology of our bodies, in addition to research that focuses on what’s happening in the clinic.
This new understanding of how the nucleus of a melanoma cell can become more fluid to move around the body is useful for building our knowledge of how cancer works and opens up a new avenue of investigation into ways to make it harder for cancer to spread.”
The first author of the study, Dr Yaiza Jung, conducted the work as part of her PhD funded by The Francis Crick Institute and King’s College London.

Investigators at Cedars-Sinai have created a unique and detailed molecular profile of endometriosis to help improve therapeutic options for the millions of women suffering from the disease.
The study is published today in the journal Nature Genetics.
“Endometriosis has been an understudied disease in part because of limited cellular data that has hindered the development of effective treatments. In this study we applied a new technology called single-cell genomics,which allowed us to profile the many different cell types contributing to the disease,” said Kate Lawrenson, PhD, an associate professor in the Department of Obstetrics and Gynecology at Cedars-Sinai, and co-senior and corresponding author of the study.
Endometriosis is a condition in which cells of the uterine lining, or ones similar to endometrial tissue, are found growing in the wrong places, most commonly on the ovaries, fallopian tubes and in the abdominal cavity. The disease impacts about 10% of women, usually during their reproductive years. Patients with the disorder can experience chronic pain, infertility, headaches, fatigue, and bowel and bladder dysfunction.
Currently, there are few good treatment options for women diagnosed with endometriosis. Lawrenson and her co-investigators were able to profile endometriosis using state-of-the-art methods permitting them to gather an immense amount of data from the cells of just 21 patients, some of whom had the gynecological disorder and others who were disease-free.
“We generated a cellular atlas of endometriosis after analyzing nearly 400,000 individual cells from these patients. We were able to identify the molecular differences between the major subtypes of endometriosis, including peritoneal disease and ovarian endometrioma,” said Lawrenson, who is also an associate professor in the Department of Biomedical Sciences.

Investigators expect this critical new database will lead to improved care.
“Identifying these cellular differences at such a detailed level should allow us to better understand the origins, natural progression, and potential therapeutic targets for treatment. We are currently limited to hormonal therapy and surgical excision, with variable success and frequent recurrence of disease,” said Matthew Siedhoff, MD, MSCR, vice chair of Gynecology at Cedars-Sinai and a co-author of the study.
Endometriosis has been associated with a slightly elevated risk for developing certain cancers. Medical scientists have often observed similarities in the way the disorders operate.
“The disease can travel throughout the body, so in many ways it behaves like cancer. But why does endometriosis behave like cancer while rarely becoming cancer? Large-scale next generation sequencing projects have been incredibly helpful in understanding how cancer works and in designing targeted therapeutics. We expect it can do the same for endometriosis,” said Lawrenson, co-director of the Women’s Cancer Research Program at Cedars-Sinai Cancer.
Investigators at Cedars-Sinai have already begun using the new cellular atlas of endometriosis to test therapeutic targets in a mouse model of the disease.
“This resource can now be used by researchers all throughout the world to study specific cell types that they specialize in, which will hopefully lead to more efficient and effective diagnosis and treatment for endometriosis patients. It really is a game changer,” said Lawrenson.
Funding was provided by the Leon Fine Translational Science Award from Cedars-Sinai. Additional support came from the National Institutes of Health, the American Cancer Society, the Canadian Cancer Society Research Institute, the Canadian Institutes of Health Research, and the Michael Smith Foundation for Health Research.

Afamitresgene autoleucel (afami-cel; formerly ADP-A2M4), an adoptive T cell receptor (TCR) therapy targeting the MAGE-A4 cancer antigen, achieved clinically significant results for patients with multiple solid tumor types in a Phase I clinical trial led by researchers at The University of Texas MD Anderson Cancer Center.
The outcomes, published today in Nature Medicine, were especially noteworthy in the subgroup of patients with synovial sarcoma, where afami-cel achieved an objective response rate of 44% compared to the overall response rate of 24% across all cancer types. Initial data from this trial were presented at the 2020 American Society of Clinical Oncology (ASCO) Annual Meeting.
According to principal investigator David S. Hong, M.D., professor of Investigational Cancer Therapeutics, these early results demonstrate a proof-of-concept for this novel cell therapy approach in solid tumors.
“These high response rates are significant because patients with synovial sarcoma really have very few options after high-dose chemotherapy with ifosfamide,” Hong said. “The overall toxicity from afami-cel was manageable, and we saw evidence of early activity in other cancer types. These results suggest this is an approach with the potential to work in solid tumors where there are currently no approved cellular therapies.”
The goal of TCR therapies is to more accurately target solid tumor cells without the toxicities to normal cells often associated with chimeric antigen receptor (CAR)-based cell therapies. Unlike CAR-based cell therapies, which recognize designated surface proteins, TCR therapies like afami-cel can target proteins normally found inside the cell. Using the T cell’s native receptor, TCR therapies can recognize protein fragments — in this case from MAGE-A4 — bound to immune-related proteins on the cell surface.
A total of 38 patients were treated with afami-cel on the study, with an average of three prior lines of therapy. Participants were 58% male; 92% of participants were white and the rest were Asian. The study included 16 patients with synovial sarcoma, nine with ovarian cancer, three with head and neck cancer, two each with esophageal cancer, non-small cell lung cancer, urothelial cancer and myxoid/round cell liposarcoma, and one each with gastric cancer and melanoma.
All patients experienced treatment-related adverse events, with low blood cell counts (lymphopenia, leukopenia, neutropenia, anemia and thrombocytopenia) the most common. Prolonged cytopenia persisting at four weeks after afami-cel treatment occurred in 17 patients (45%). Two patients had trial-related deaths, which resulted in the lowering of the maximum age at screening and discontinued use of the high-dose cyclophosphamide lymphodepletion regimen.
The median duration of response was 26 weeks across all patients and 28 weeks in the synovial sarcoma subgroup. These results in synovial sarcoma led to an ongoing Phase II trial of afami-cel for patients with advanced synovial sarcoma or myxoid/round cell liposarcoma that also is being led by MD Anderson.
Early results of afami-cel led to another Phase I trial, also led by Hong, evaluating the next generation of afami-cel, known as ADP-A2M4CD8. This new TCR therapy expresses a CD8 co-receptor with the goal of broadening the immune response in solid tumors. Hong shared encouraging early data from that trial at the European Society for Medical Oncology (ESMO) Congress 2022.
These trials are part of an ongoing strategic alliance between MD Anderson and Adaptimmune, which aims to expedite the development of novel T cell therapies in multiple cancer types.
This study was supported by Adaptimmune.

Fewer cases of melanoma were observed among regular users of vitamin D supplements than among non-users, a new study finds. People taking vitamin D supplements regularly also had a considerably lower risk of skin cancer, according to estimates by experienced dermatologists. The study, conducted in collaboration between the University of Eastern Finland and Kuopio University Hospital and published in Melanoma Research, included nearly 500 people with an increased risk of skin cancer.
Vitamin D plays a key role in the normal function of the human body, and it may also play a role in many diseases. The link between vitamin D and skin cancers has been studied abundantly in the past, but these studies have mainly focused on serum levels of calcidiol, which is a metabolite of vitamin D, and its association with skin cancers. Findings from these studies have been inconclusive and even contradictory at times, as serum calcidiol levels have been associated with both a slightly higher and with a slightly lower risk of different skin cancers. This may, in part, be explained by the fact that serum calcidiol analyses do not provide information on the metabolism of vitamin D in the human skin, which can express enzymes that generate biologically active vitamin D metabolites or inactivate them.
The new study, conducted under the North Savo Skin Cancer Programme, took a different approach: 498 adult patients estimated to have an increased risk of a skin cancer, such as basal cell carcinoma, squamous cell carcinoma or melanoma, were recruited at the dermatological outpatient clinic of Kuopio University Hospital. Experienced dermatologists at the University of Eastern Finland carefully analysed the patients’ background information and medical history and examined their skin. The dermatologists also classified the patients into different skin cancer risk classes, namely low risk, moderate risk and high risk. Based on their use of oral vitamin D supplements, the patients were divided into three groups: non-users, occasional users and regular users. Serum calcidiol levels were analysed in half of the patients and found to correspond to their self-reported use of vitamin D.
A key finding of the study is that there were considerably fewer cases of melanoma among regular users of vitamin D than among non-users, and that the skin cancer risk classification of regular users was considerably better than non-users’. Logistic regression analysis showed that the risk for melanoma among regular users was considerably reduced, more than halved, compared to non-users.
The findings suggest that even occasional users of vitamin D may have a lower risk for melanoma than non-users. However, there was no statistically significant association between the use of vitamin D and the severity of photoaging, facial photoaging, actinic keratoses, nevus count, basal cell carcinoma and squamous cell carcinoma. Serum calcidiol levels were not significantly associated with these skin changes, either. Since the research design was cross-sectional, the researchers were unable to demonstrate a causal relationship.
Other relatively recent studies, too, have provided evidence of the benefits of vitamin D in melanoma, such as of the association of vitamin D with a less aggressive melanoma.
“These earlier studies back our new findings from the North Savo region here in Finland. However, the question about the optimal dose of oral vitamin D in order to for it to have beneficial effects remains to be answered. Until we know more, national intake recommendations should be followed,” Professor of Dermatology and Allergology Ilkka Harvima of the University of Eastern Finland notes.
Researchers at the University of Eastern Finland and Kuopio University Hospital have previously reported (BMC Cancer 2021) that the melanoma mortality rate in North Savo is relatively high in relation to its incidence.
“For this reason, too, it is worth paying attention to sufficient intake of vitamin D in the population in this region,” Harvima concludes.
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Inspired by digital art generators like DALL-E, biologists are building artificial intelligences that can fight cancer, flu and Covid.An example of an animated diffusion model of A.I.-generated proteins. Video by Ian C. Haydon/University of Washington Institute for Protein DesignLast spring, an artificial intelligence lab called OpenAI unveiled technology that lets you create digital images simply by describing what you want to see. Called DALL-E, it sparked a wave of similar tools with names like Midjourney and Stable Diffusion. Promising to speed the work of digital artists, this new breed of artificial intelligence captured the imagination of both the public and the pundits — and threated to generate new levels of online disinformation.Social media is now teeming with the surprisingly conceptual, in whichshockingly detailed, often photorealistic images generated by DALL-E and other tools. “Photo of a teddy bear riding a skateboard in Times Square.” “Cute corgi in a house made out of sushi.” “Jeflon Zuckergates.”But when some scientists consider this technology, they see more than just a way of creating fake photos. They see a path to a new cancer treatment or a new flu vaccine or a new pill that helps you digest gluten.Using many of the same techniques that underpin DALL-E and other art generators, these scientists are generating blueprints for new proteins — tiny biological mechanisms that can change the way of our bodies behave.Our bodies naturally produce about 20,000 proteins, which handle everything from digesting food to moving oxygen through the bloodstream. Now, researchers are working to create proteins that are not found in nature, hoping to improve our ability to fight disease and do things that our bodies cannot on their own.David Baker, the director of the Institute for Protein Design at the University of Washington, has been working to build artisanal proteins for more than 30 years. By 2017, he and his team had shown this was possible. But they did not anticipate how the rise of new A.I. technologies would suddenly accelerate this work, shrinking the time needed to generate new blueprints from years down to weeks.“What we need are new proteins that can solve modern-day problems, like cancer and viral pandemics,” Dr. Baker said. “We can’t wait for evolution.” He added, “Now, we can design these proteins much faster, and with much higher success rates, and create much more sophisticated molecules that can help solve these problems.”David Baker of the University of Washington.Evan McGlinn for The New York TimesLast year, Dr. Baker and his fellow researchers published a pair of papers in the journal Science describing how various A.I. techniques could accelerate protein design. But these papers have already been eclipsed by a newer one that draws on the techniques that drive tools like DALL-E, showing how new proteins can be generated from scratch much like digital photos.“One of the most powerful things about this technology is that, like DALL-E, it does what you tell it to do,” said Nate Bennett, one of the researchers working in the University of Washington lab. “From a single prompt, it can generate an endless number of designs.”The Rise of OpenAIThe San Francisco company is one of the world’s most ambitious artificial intelligence labs. Here’s a look at some recent developments.ChatGPT: The new cutting-edge chatbot is inspiring awe, fear, stunts and attempts to circumvent its guardrails, our technology columnist writes.DALL-E 2: The system lets you create digital images simply by describing what you want to see. But for some, image generators are worrisome.GPT-3: With mind-boggling fluency, the natural-language system can write, argue and code. The implications for the future could be profound.To generate images, DALL-E relies on what artificial intelligence researchers call a neural network, a mathematical system loosely modeled on the network of neurons in the brain. This is the same technology that recognizes the commands you bark into your smartphone, enables self-driving cars to identify (and avoid) pedestrians and translates languages on services like Skype.A neural network learns skills by analyzing vast amounts of digital data. By pinpointing patterns in thousands of corgi photos, for instance, it can learn to recognize a corgi. With DALL-E, researchers built a neural network that looked for patterns as it analyzed millions of digital images and the text captions that described what each of these images depicted. In this way, it learned to recognize the links between the images and the words.When you describe an image for DALL-E, a neural network generates a set of key features that this image may include. One feature might be the curve of a teddy bear’s ear. Another might be the line at the edge of a skateboard. Then, a second neural network — called a diffusion model — generates the pixels needed to realize these features.The diffusion model is trained on a series of images in which noise — imperfection — is gradually added to a photograph until it becomes a sea of random pixels. As it analyzes these images, the model learns to run this process in reverse. When you feed it random pixels, it removes the noise, transforming these pixels into a coherent image.At the University of Washington, other academic labs and new start-ups, researchers are using similar techniques in their effort to create new proteins.Proteins begin as strings of chemical compounds, which then twist and fold into three-dimensional shapes that define how they behave. In recent years, artificial intelligence labs like DeepMind, owned by Alphabet, the same parent company as Google, have shown that neural networks can accurately guess the three-dimensional shape of any protein in the body based just on the smaller compounds it contains — an enormous scientific advance.Now, researchers like Dr. Baker are taking another step, using these systems to generate blueprints for entirely new proteins that do not exist in nature. The goal is to create proteins that take on very specific shapes; a particular shape can serve a particular task, such as fighting the virus that causes Covid.Much as DALL-E leverages the relationship between captions and photographs, similar systems can leverage the relationship between a description of what the protein can do and the shape it adopts. Researchers can provide a rough outline for the protein they want, then a diffusion model can generate its three-dimensional shape.A protein diffusion model doing unconditional generation, converting noise into plausible structures. Video by Namrata AnandNamrata Anand, a former Stanford University researcher. She is now building a company in generative A.I. protein design.Herve Philippe/TerrificShot Photography“With DALL-E, you can ask for an image of a panda eating a shoot of bamboo,” said Namrata Anand, a former Stanford University researcher who is also an entrepreneur, building a company in this area of research. “Equivalently, protein engineers can ask for a protein that binds to another in a particular way — or some other design constraint — and the generative model can build it.”The difference is that the human eye can instantly judge the fidelity of a DALL-E image. It cannot do the same with a protein structure. After artificial intelligence technologies produce these protein blueprints, scientists must still take them into a wet lab — where experiments can be done with real chemical compounds — and make sure they do what they are supposed to do.For this reason, some experts say that the latest artificial intelligence technologies should be taken with a grain of salt. “Making a new structure is just a game,” said Frances Arnold, a Nobel Laureate who is a professor specializing in protein engineering at the California Institute of Technology. “What really matters is: What can that structure actually do?”But for many researchers, these new techniques are not just accelerating the creation of new protein candidates for the wet lab. They provide a way of exploring new innovations that researchers could not previously explore on their own.“What’s exciting isn’t just that they are creative and explore unexpected possibilities, but that they are creative while satisfying certain design objectives or constraints,” said Jue Wang, a researcher at the University of Washington. “This saves you from needing to check every possible protein in the universe.”Often, artificially intelligent machines are developed to perform skills that come naturally to humans, like piecing together images, writing text or playing board games. Protein-designing bots pose a more profound question, Dr. Wang said: “What can machines do that humans can’t do at all?”

Published5 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Nicholas YongBBC NewsNearly 90% of people in Henan, China’s third most populous province, have now been infected with Covid, local health officials say.Provincial official Kan Quancheng revealed the figure – amounting to about 88.5 million people – at a press conference.China is battling an unprecedented surge in cases after abandoning zero-Covid policies in December.The move followed rare protests against lockdowns, quarantines and mass tests.Mr Kan did not specify a timeline for when all the infections happened – but as China’s previous zero-Covid policy kept cases to a minimum, it’s likely the vast majority of Henan’s infections occurred in the past few weeks.He said visits to fever clinics in Henan province peaked on 19 December “after which it showed a continuous downward trend”.The Henan provincial figures are in stark contrast to Covid figures from the central governmentAccording to official data, just 120,000 people in the country of 1.4 billion have been infected and 30 died since the shift in Covid policy. Meanwhile on Sunday, authorities reported three Covid deaths in mainland China, one more than the day before.However, with the definition of Covid deaths narrowed and mass testing no longer compulsory, government data is no longer reflective of the true scale of the outbreak.Other local and provincial officials have also been providing very different data to that from the central government. On Christmas Eve, a senior health official in the port city of Qingdao reported that half a million people were being infected each day. Those case figures were swiftly removed from news reports. Young Chinese self-infect amid Covid fears for elderlyCelebrity deaths spark fears over China Covid tollMeanwhile Chinese health officials said they would not include Pfizer’s antiviral Covid medicine Paxlovid in its basic medical insurance schemes as a result of the high price quoted by the US firm.The drug, temporarily covered by China’s broad healthcare insurance scheme until 31 March, has seen a sharp increase in demand since China’s Covid cases surged last month.Pfizer would continue to collaborate with the Chinese government and all relevant stakeholders to “secure and adequate supply” of the medicine in China, the company said in a statement.On Sunday, Beijing also lifted mandatory quarantine for all international arrivals and opened its border with Hong Kong.In the first wave of pre-holiday travel, official data showed that 34.7 million people travelled domestically on Saturday. This represented an increase of more than a third compared to last year, according to state media.Infections are expected to soar as the country celebrates Lunar New Year later this month, with millions expected to travel from big cities to visit older relatives in the countryside.Overall, more than two billion individual journeys are expected to take place, officials have said.Listen to more on what we know about China’s Covid numbers: More or Less- Behind the Stats – Can China’s data on Covid deaths be trusted- on BBC SoundsMore on this storyCelebrity deaths spark fears over China Covid toll4 days agoYoung Chinese self-infect amid Covid fears for elderly3 days ago

Published17 hours agoShareclose panelShare pageCopy linkAbout sharingThis video can not be playedTo play this video you need to enable JavaScript in your browser.By Antoinette Radford & Martin YipBBC News London & Hong KongChina has reopened its borders to international visitors for the first time since it imposed travel restrictions in March 2020.Incoming travellers will no longer need to quarantine – marking a significant change in the country’s Covid policy as it battles a surge in cases.They will still require proof of a negative PCR test taken within 48 hours of travelling.The move has been welcomed by many eager to reunite with family.In Hong Kong, 400,000 people are expected to travel into mainland China in the coming weeks with long queues for flights into cities including Beijing and Xiamen.On Sunday, double-decker coaches packed with travellers arrived at the Hong Kong-Zhuhai-Macau Bridge to catch buses to the Guangdong province – among them were college students returning home.One man told the BBC he hadn’t seen his extended family in three years and could not hold back his excitement, having just bought a ticket back to the mainland.A woman told news agency Reuters she had not seen her parents in years – despite one of them suffering from colon cancer – and said she was “so, so happy”.Image source, JEROME FAVRE/EPA-EFE/REX/ShutterstockThe country’s reopening comes at the start of “Chunyun”, the first period of Lunar New Year travel. Before the pandemic, it was the largest annual worldwide migration of people returning home to spend time with family. Two billion trips are expected to be made this Lunar New Year, double the number that travelled last year. Li Hua, who travelled from the UK to China – where her family lives – for the festival said it had been “too long” since she had returned, “I’m so happy to be back, and breathe Chinese air. So happy, so happy”.Mark Clayton returned home to Zhuhai, in Guandong, with his wife and baby after visiting Hong Kong. He told the BBC his trip home had been “nearly as smooth as it used to be pre-Covid”. “We didn’t even show them the PCR, we simply scanned a code and put in a very quick customs declaration… And then straight through,” he said. Young people in China self-infect as fears for elderly growChina under-representing Covid deaths, WHO warnsHow many Covid cases are there in China?But there is concern from some that opening the borders will result in more transmission of Covid-19. Some local bus drivers told the BBC they are worried they might get the virus from incoming travellers, and want their companies to provide them with more protection.Over the past three years, China had one of the world’s strictest Covid health policies that saw numerous lockdowns, frequent testing requirements and had a significant impact on the nation’s economy.The government recently walked back that policy after mass protests across the country, triggered by a fire in a high-rise block in the Xinjiang region that killed 10 people. Many Chinese believed the long-running Covid restrictions contributed to the deaths, but authorities denied this.Since China abandoned the key elements of its Covid zero policy there have been reports of hospitals and crematoriums being overwhelmed, but the country has stopped publishing its case numbers and reported only two deaths on Saturday.On the same day, the Chinese government banned over 1,000 social media accounts critical of its handling of the virus. The anticipated surge in cases and travel out of China has prompted many countries – including the UK – to impose requirements for a negative COVID-19 test on people arriving from China, drawing the ire of the Chinese government.Listen to more on what we know about China’s Covid numbers: More or Less- Behind the Stats – Can China’s data on covid deaths be trusted- on BBC SoundsMore on this storyUS demands Covid tests for visitors from China29 December 2022Celebrity deaths spark fears over China Covid toll3 days agoHow many Covid cases are there in China?29 December 2022China under-representing Covid deaths, WHO warns4 days agoHong Kong to lift Covid ban on hamster imports3 days ago