Published in the journal Cortex, the study is the first to investigate, and first to identify, the association between body image and the brain’s processing of internal signals that occur unconsciously.

Carried out by a team of psychologists and neuroscientists at Anglia Ruskin University (ARU), the study found that adults whose brains are less efficient at detecting these internal messages are more likely to experience body shame and weight preoccupation.

This research could have therapeutic implications for people suffering with conditions in which body image plays a significant role. For example, the unconscious signals could be made conscious. Further research could even be applied to the clinic as it may be the case that brain responses to gut signals could indicate a predisposition to eating disorders.

The study participants — a group of healthy UK adults — first took part in four body image assessments to measure their feelings of body appreciation, body functionality appreciation, body shame, and weight preoccupation.

The researchers then carried out measurements of the participants’ internal signals. Some of the messages from the heart and gut are processed at an unconscious level and the nervous system interprets these signals to provide the brain with continuously updated information about the body’s internal state.

The strength of the connection between the gut and the brain was measured by recording the electrical activity of both regions at the same time. The researchers also measured brain responses to heartbeats.

They found that weaker brain responses to the gut and heart were both significantly associated with greater levels of body shame and weight preoccupation amongst the participants.

Senior author Dr Jane Aspell, Associate Professor of Cognitive Neuroscience at Anglia Ruskin University (ARU), said: “We experience our body both from the inside and out: we can be aware of how our skin and limbs look, but also of how hungry we feel or how strongly our heart is beating during exercise. The brain also continuously processes internal signals that we are not conscious of.

“We found that when the brain is less responsive to these implicit signals from inside the body, individuals are more likely to hold negative views about their external bodily appearance. It may be that when the brain has a weaker connection to the internal body, the brain puts more emphasis on the external body and so appearance becomes much more important for self-evaluation.”

Lead author Dr Jennifer Todd, a Postdoctoral Research Fellow at Anglia Ruskin University (ARU), said: “Our research could have implications for those experiencing negative body image, which can have a serious impact on people’s lives.

“The gut and heart signal measurements used in our study could potentially act as a biomarker to help identify, or even predict, negative body image and associated conditions, such as eating disorders. Additionally, by training people to become more aware of internal sensations, it might be possible to amplify these unconscious signals.

“We need to understand why some brains are better at detecting these internal signals than others. We expect it is partly due to differences in neuro-anatomical connections between the brain and internal organs, and this will be the subject of future research.”

Meanwhile, Dr Jane Aspell will be speaking about her research on the body and sense of self in a talk at the British Science Festival 2021, 7-11 September hosted by the British Science Association at Anglia Ruskin University. The talk will explore research on out of body experiences (OBEs), and she will share case studies from neurological patients.

Dr Aspell’s work investigates what happens in the brain during an OBE and she will present evidence that these are caused by abnormal functioning in parts of the brain that process and combine signals from our bodies. This research on neurological patients sheds light on how the healthy brain generates the experience of one’s self, and what happens when that construction temporarily goes ‘wrong’.

The tool, developed through analysis of CT scans from nearly 900 COVID-19 patients diagnosed in 2020, was able to predict ventilator need with 84% accuracy.

“That could be important for physicians as they plan how to care for a patient — and, of course, for the patient and their family to know,” said Anant Madabhushi, the Donnell Institute Professor of Biomedical Engineering at Case Western Reserve and head of the Center for Computational Imaging and Personalized Diagnostics (CCIPD). “It could also be important for hospitals as they determine how many ventilators they’ll need.”

Next, Madabhushi said he hopes to use those results to try out the computational tool in real time at University Hospitals and Louis Stokes Cleveland VA Medical Center with COVID-19 patients.

If successful, he said medical staff at the two hospitals could upload a digitized image of the chest scan to a cloud-based application, where the AI at Case Western Reserve would analyze it and predict whether that patient would likely need a ventilator.

Dire need for ventilators

Among the more common symptoms of severe COVID-19 cases is the need for patients to be placed on ventilators to ensure they will be able to continue to take in enough oxygen as they breathe.

Yet, almost from the start of the pandemic, the number of ventilators needed to support such patients far outpaced available supplies — to the point that hospitals began “splitting” ventilators — a practice in which a ventilator assists more than one patient.

While 2021’s climbing vaccination rates dramatically reduced COVID-19 hospitalization rates — and, in turn, the need for ventilators — the recent emergence of the Delta variant has again led to shortages in some areas of the United States and in other countries.

“These can be gut-wrenching decisions for hospitals — deciding who is going to get the most help against an aggressive disease,” Madabhushi said.

To date, physicians have lacked a consistent and reliable way to identify which newly admitted COVID-19 patients are likely to need ventilators — information that could prove invaluable to hospitals managing limited supplies.

Researchers in Madabhushi’s lab began their efforts to provide such a tool by evaluating the initial scans taken in 2020 from nearly 900 patients from the U.S. and from Wuhan, China — among the first known cases of the disease caused by the novel coronavirus.

Madabhushi said those CT scans revealed — with the help of deep-learning computers, or Artificial Intelligence (AI) — distinctive features for patients who later ended up in the intensive care unit (ICU) and needed help breathing.

The research behind the tool appeared this month in the IEEE Journal of Biomedical and Health Informatics.

Amogh Hiremath, a graduate student in Madabhushi’s lab and lead author on the paper, said patterns on the CT scans couldn’t be seen by the naked eye, but were revealed only by the computers.

“This tool would allow for medical workers to administer medications or supportive interventions sooner to slow down disease progression,” Hiremath said. “And it would allow for early identification of those at increased risk of developing severe acute respiratory distress syndrome — or death. These are the patients who are ideal ventilator candidates.”

Further research into ‘immune architecture’

Madabhushi’s lab also recently published research comparing autopsy tissues scans taken from patients who died from the H1N1 virus (Swine Flu) and from COVID-19. While the results are preliminary, they do appear to reveal information about what Madabhushi called the “immune architecture” of the human body in response to the viruses.

“This is important because the computer has given us information that enriches our understanding of the mechanisms in the body against viruses,” he said. “That can play a role in how we develop vaccines, for example.”

Germán Corredor Prada, a research associate in Madabhushi’s lab who was the primary author on the paper, said computer vision and AI techniques allowed the scientists to study how certain immune cells organize in the lung tissue of some patients.

“This allowed us to find information that may not be obvious by simple visual inspection of the samples,” Corredor said. “These COVID-19-related patterns seem to be different from those of other diseases such as H1N1, a comparable viral disease.”

Eventually, when combined with other clinical work and further tests in larger sets of patients, this discovery could serve to improve the world’s understanding of these diseases and maybe others, he said.

Madabhushi established the CCIPD at Case Western Reserve in 2012. The lab now includes more than 60 researchers. Some were involved in this most recent COVID-19 work, including graduate students Hiremath, Pranjal Vaidya; research associates Corredor and Paula Toro; and research faculty Cheng Lu and Mehdi Alilou.

The intestinal epithelium, a single layer of cells, plays a critical role in human health by providing a barrier while also allowing nutrient and water absorption. Intestinal epithelial cells are needed for regulating immune function, communicating with the intestinal microbiota, and protecting the gut from pathogen infection — all of which critically depend on an intact epithelial barrier.

Affecting roughly 3 million Americans, IBD is a set of chronic intestinal diseases in which the lining of the gut becomes inflamed and leaky. Increased gut leakiness has recently been confirmed to increase the risk of developing IBD.

“This new publication is a culmination of a body of work from my lab identifying how loss-of-function mutations in PTPN2 can increase gut permeability or leakiness,” said Declan F. McCole, a professor of biomedical sciences in the UCR School of Medicine, who led the study published in the Journal of Clinical Investigation. The journal has selected the research paper as an “Editor’s highlight.”

In the study, which was conducted in mice, human cells, and tissue from IBD patients, McCole and his colleagues showed that in IBD patients carrying a loss-of-function PTPN2 mutation, the expression of claudin-2, a protein that causes loss of water and sodium into the gut and promotes diarrhea, is increased. Using mouse models, the McCole lab identified a dual mechanism that explains how claudin-2 expression increases and contributes to fluid loss.

PTPN2 typically acts as a brake on the expression of claudin-2, McCole explained. The loss-of-function mutation in PTPN2 that occurs in IBD removes this brake and allows increased fluid loss.

“In addition, PTPN2 also promotes an endogenous factor, called matriptase, that removes claudin-2 from the area of the cell membrane where it mediates its effects in allowing fluid loss to occur,” McCole said.

The cumulative effect of reduced PTPN2 activity on both mechanisms was elevated fluid loss. The researchers proved this defect could be reversed by treating cells lacking PTPN2 with recombinant — or synthetic — matriptase.

“Our work improves understanding of how the genetics of IBD can contribute to the altered physiology in patients that drives their symptoms,” McCole said. “It also supports our related work identifying how the class of drugs, called JAK inhibitors, may be used to rescue ‘leaky gut,’ particularly in patients with loss-of-function mutations in the PTPN2 gene.

The study also showed that a recently identified and rare novel mutation in PTPN2, which causes gut epithelial damage in children, also increases gut epithelial leakiness — but without causing epithelial cell death.

“This suggests that patients who develop this condition may exhibit ‘leaky gut’ before full-blown disease occurs,” McCole said.

McCole was supported in the study by co-first authors Moorthy Krishnan and Marianne R. Spalinger of UCR, and Ronald Marchelletta of UC San Diego. Other co-authors are Anica Sayoc-Becerra, Vinicius Canale, Rocio Alvarez, and Ali Shawki of UCR; as well as colleagues at UC San Diego, Cedars-Sinai Medical Center Los Angeles, the University of Chicago, the National Institutes of Health, University Hospital Zurich in Switzerland, and McGill University in Montreal.

The study was supported by the National Institutes of Health, the Crohn’s and Colitis Foundation, the Swiss National Science Foundation, and Pfizer Inc.

Last year, researchers from Charité and the MPIMG made a surprising discovery. They were the first to report that individuals with no prior exposure to SARS-CoV-2 nonetheless had immunological memory cells capable of recognizing this novel virus. The researchers concluded that these ‘T helper cells’ must have been generated to deal with mostly harmless common cold coronaviruses and that, thanks to the structural similarities between coronaviruses (in particular the characteristic spike protein found on their outer surface), these T helper cells will also attack the novel coronavirus. This ‘cross reactivity’ hypothesis has since been confirmed by a range of studies.

Still unclear, however — and the object of intense debate — is the question of whether these immune cells affect the course of subsequent SARS-CoV-2 infections. “Our assumption at the time was that cross-reactive T helper cells have a protective effect, and that prior exposure to endemic (i.e. long-established and widely circulating) coronaviruses therefore reduces the severity of COVID-19 symptoms,” says the study’s (and the previous study’s) first author, Dr. Lucie Loyal, a researcher based at both the Si-M (‘Der Simulierte Mensch — literally ‘The Simulated Human’, a joint research space of Charité and Technische Universität Berlin) and the BIH Center for Regenerative Therapies (BCRT). She adds: “However, the opposite could have been true. With some viruses, a second infection involving a similar strain can lead to a misdirected immune response and a negative impact on clinical course.” In the current study, the Berlin-based research team presents evidence to support their previous assumptions regarding the existence of a protective effect. According to their data, cross-reactive immunity could be one of several reasons for the variability in disease severity seen with COVID-19 but might also explain differences in vaccine efficacy seen in different age groups.

For the current study, the researchers recruited individuals with no prior exposure to SARS-CoV-2, testing them at regular intervals to establish whether they had contracted the infection. Out of a total of nearly 800 participants who were recruited from mid-2020 onwards, 17 persons tested positive. The researchers studied the affected individuals’ immune systems in detail. Their analyses showed that the immune response against SARS-CoV-2 also included the mobilization of T helper cells which had been generated in response to endemic common cold viruses. The researchers also showed that the quality of the immune response against SARS-CoV-2 was linked to the quantity of cross-reactive cells which had been present in the body prior to infection. These cells were particularly effective at recognizing a certain area of the spike protein. In both the endemic viruses and the new coronavirus, this site was characterized by sequence similarities which were particularly well ‘preserved’. “During infections with the more harmless coronaviruses, the immune system builds up a kind of protective ‘universal coronavirus’ memory,” explains the study’s corresponding author, Dr. Claudia Giesecke-Thiel, Head of the Flow Cytometry Service Group at the MPIMG. “Once exposed to SARS-CoV-2, these memory cells are reactivated and kick-start the response against the new pathogen. This could help accelerate the initial immune response to SARS-CoV-2 and limit viral propagation during the early stages of the infection and is therefore likely to have a positive effect on the course of the disease.” Taking a more cautionary tone, the researcher adds: “This does not mean that prior exposure to common cold viruses will definitely protect an individual against SARS-CoV-2, nor does it change the course of the pandemic as of now because these underlying mechanisms have been operating all along. It in no way diminishes the importance of getting vaccinated. Our study provides one of several explanations for an observation made since the beginning of the pandemic, namely that the symptoms of SARS-CoV-2 infection can vary greatly between individuals.”

The researchers’ findings furthermore confirmed that the immunity-enhancing effects of cross-reactive T cells also occur following vaccination with the BioNTech COVID-19 vaccine. Just like natural infection, the vaccine prompts the body to produce the SARS-CoV-2 spike protein (including the well-preserved section of it) and present it to the immune system. An analysis of the immune responses of 31 healthy individuals before and after vaccination revealed that, while the activation of normal T helper cells took place gradually over the course of two weeks, the activation of cross-reactive T helper cells was extremely rapid, taking place within one week of vaccination. Naturally, this also had a positive effect on the generation of antibodies. Even after the first dose of the vaccine, the body was able to produce antibodies against the preserved section of the spike protein at a rate normally only seen after booster vaccinations. “Even following vaccination, the body is able to utilize at least some of its immunological memory — provided it has had previous exposure to endemic coronaviruses,” says co-corresponding author Prof. Dr. Andreas Thiel, a Charité researcher based at both the Si-M and the BCRT. He adds: “This might explain the surprisingly rapid and extremely strong protective effect we see after the initial dose of the COVID-19 vaccine, at least in younger individuals.”

In a second part of the study, the researchers analyzed T helper cells in approximately 570 healthy individuals. They were able to show that cross-reactive immunity declines in older adults. In fact, both the number of cross-reactive T cells and the strength of their binding interactions was shown to be lower in older participants than in younger participants. According to the authors, this decline in cross-reactive immunity is caused by normal, age-related changes. “Infection with an endemic coronavirus represents a benefit in younger people, helping them fight off SARS-CoV-2 or develop immunity following vaccination. Sadly, this benefit is less pronounced in older adults,” says Prof. Thiel. He adds: “It is likely that a third (or booster) dose would be able to compensate for this weaker immune response, ensuring that members of this high-risk group have adequate immunity.”

Common cold coronaviruses

The four endemic coronaviruses which have been circulating in humans for some time are generally referred to as human endemic coronaviruses (HCoV). The four viruses, all of which usually cause symptoms of the common cold, are known as HCoV-OC43, HCoV-229E, HCoV-HKU1, and HCoV-NL63. Estimates suggest they are responsible for up to 30 percent of all seasonal colds.

T helper cells

T helper cells are responsible for regulating and coordinating the body’s immune response. Once a pathogen invades the body, cells known as macrophages and dendritic cells engulf the pathogen, break it up and present fragments of it (‘antigens’) on their cell surface. T helper cells scour these fragments. If the T helper cell carries a receptor which recognizes these activating fragments, the T helper cell is activated. Activated T helper cells then prompt other immune cells to mount a direct response against the pathogen and produce precisely fitting antibodies. Most immune responses will also generate memory T cells, which can persist in the body for many years and are responsible for the body’s ability to mount a faster and more effective immune response upon re-exposure to the same pathogen. One characteristic feature of T helper cells is that their activation is not dependent on pathogens which are a perfect match. Rather, they can be activated by pathogens with ‘sufficient similarity’.

On this study

This research is based on the ‘Charité Corona Cross’ study, which was launched in 2020, and is being led by Charité and conducted in cooperation with Technische Universität Berlin and the MPIMG. Funded by the Federal Ministry of Health (BMG), the ‘Charité Corona Cross’ study investigates the impact of cross-reactive T helper cells on the course of COVID-19. Elements of this research formed part of a collaborative project known as ‘COVIM — Determining and using immunity to SARS-CoV-2’. The aim of the COVIM consortium is to study who has protective immunity to SARS-CoV-2, how this is achieved and how long it lasts. A further aim is to study how to transfer the protective immunity of a few individuals to a large number of people without such immunity. The project is being coordinated by Charité and University Hospital Cologne. COVIM is one of 13 large collaborative research projects conducted under the auspices of the NUM academic research network. Initiated and coordinated by Charité, the NUM is funded by the Federal Ministry of Education and Research (BMBF). The NUM brings together the combined strength of Germany’s 36 university hospitals.

Researchers at King’s College London analysed data from participants logging their symptoms, tests and vaccines on the UK ZOE COVID Symptom Study app between 8th December 2020 and 4 July 2021, including 1,240,009 (first dose) and 971,504 (second dose) vaccinated UK adults. The research team assessed a range of factors, including age, frailty and areas of deprivation and compared that with post-vaccination infection.

The study, published today in The Lancet Infectious Diseases, found that in the unlikely event of catching COVID-19 after being double vaccinated, the risk of Long COVID was reduced by almost half. There were also fewer hospitalisations (73% less likely) and lower burden of acute symptoms (31% less likely) among those fully vaccinated. The nature of the most common symptoms were similar to unvaccinated adults — e.g. anosmia,(loss of smell) cough, fever, headaches, and fatigue. All these symptoms were milder and less frequently reported by people who were vaccinated, and they were half as likely to get multiple symptoms in the first week of illness. Sneezing was the only symptom which was more commonly reported in vaccinated people with COVID-19.

However, people living in most deprived areas were at greater risk of infection after a single vaccination. While age on its own was not a risk factor, individuals who had health conditions that limited their independence — such as frailty — were up to two times more likely to contract COVID-19 infection after vaccination, and of getting sick.

The findings demonstrate the need to target at-risk groups. Frail adults have already been shown to be disproportionately affected by COVID-19. The research team suggests strategies such as a timely booster programme, targeted infection control measures and more research into the immune response to vaccination in this group could help address the issue.

Lead researcher Dr Claire Steves from King’s College London said: “In terms of the burden of Long COVID, it’s good news that our research has found that having a double vaccination significantly reduces the risk of both catching the virus and if you do, developing long standing symptoms. However, among our frail, older adults and those living in deprived areas the risk is still significant and they should be urgently prioritised for second and booster vaccinations.”

Professor Tim Spector from King’s College London and Lead investigator of ZOE COVID Study comments: “Vaccinations are massively reducing the chances of people getting Long COVID in two ways. Firstly, by reducing the risk of any symptoms by 8 to 10 fold and then by halving the chances of any infection turning into Long COVID, if it does happen. Whatever the duration of symptoms we are seeing that infections after two vaccinations are also much milder, so vaccines are really changing the disease and for the better. We are encouraging people to get their 2nd jab as soon as they can.”

Health and Social Care Secretary, Sajid Javid said: “COVID-19 vaccines have saved more than 105,000 lives and prevented over 24 million infections in England alone. This research is encouraging, suggesting vaccines are not only preventing deaths but could also help prevent some of the longer lasting symptoms.

“We have invested £50 million in research to better understand the lasting effects of COVID and over 80 long COVID assessment services have opened across England as part of a £100 million expansion of care for those suffering the effects.

“It is clear vaccines are building a wall of defence against the virus and are the best way to protect people from serious illness. I encourage everyone who is eligible to come forward for both their jabs as quickly as possible.”

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Materials provided by King’s College London. Note: Content may be edited for style and length.

Without improving its management, the right whale populations will decline and potentially become extinct in the coming decades, according to a Cornell- and University of South Carolina-led report in the journal Oceanography.

“Most of the warming in the Gulf of Maine is not coming from the atmosphere or ocean surface, as one may think,” said senior author Charles Greene, professor emeritus in the Department of Earth and Atmospheric Sciences at Cornell. “It is coming from invading slope water many hundreds of feet below the ocean surface, forcing the right whales to abandon their traditional habitat.”

Since 2010, the calving rate has declined and the right whale population has dropped by an estimated 26%, according to the paper. At the beginning of the decade, the North Atlantic right whale population had numbered over 500. Now, the North Atlantic Right Whale Consortium estimates the population at just 356 whales.

The species is considered critically endangered by the International Union for Conservation of Nature Red List of Threatened Species.

The warm slope water entering the Gulf of Maine at depth derives its heat from the Gulf Stream. As the tail end of the Atlantic Meridional Overturning Circulation, the Gulf Stream has changed its trajectory dramatically during the past ten years.

“Due to a warming climate, the Atlantic Meridional Overturning Circulation is slowing down, causing the Gulf Stream to move North, injecting warmer and saltier slope water into the Gulf of Maine,” Greene said.

The warming Gulf of Maine has reduced the abundance of copepods, the tiny crustaceans that serve as the right whales’ favorite snack. This has reduced right whale calving rates and forced the whales to abandon their mid-summer feeding grounds in the Gulf of Maine. Instead, the whales have headed north to the cooler waters of the Gulf of St. Lawrence.

Since 2015, scientists have witnessed an increased number of right whales feeding in the Gulf of St. Lawrence, where there were no protections in place to prevent ship strikes and fishing gear entanglement. This has led to an Unusual Mortality Event declared by NOAA in 2017, when 17 right whale deaths were confirmed, mostly in the Gulf of St. Lawrence. Ten right whales were found dead in 2019, while for 2020 and 2021, four deaths have occurred thus far.

“Right whales continue to die each year,” said lead author Erin Meyer-Gutbrod, assistant professor at the University of South Carolina. “Protective policies must be strengthened immediately before this species declines past the point of no-return.”

Ocean scientists are hoping for new policies on rope-free fishing gear, vessel speed limit enforcement and money for monitoring and ecosystem forecasting.

Funding for this research was provided by the Lenfest Ocean Program.

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Materials provided by Cornell University. Original written by Blaine Friedlander. Note: Content may be edited for style and length.