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Sci Rep. 2024 Jan 31;14(1):2600. doi: 10.1038/s41598-024-52314-x.

ABSTRACT

Bovine tuberculosis is an infectious disease of global significance that remains endemic in many countries. Mycobacterium bovis infection in cattle is characterized by a cell-mediated immune response (CMI) that precedes humoral responses, however the timing and trajectories of CMI and antibody responses determined by newer generation assays remain undefined. Here we used defined-antigen interferon-gamma release assays (IGRA) and an eleven-antigen multiplex ELISA (Enferplex TB test) alongside traditional tuberculin-based IGRA and IDEXX M. bovis antibody tests to assess immune trajectories following experimental M. bovis infection of cattle. The results show CMI responses developed as early as two-weeks post-infection, with all infected cattle testing positive three weeks post-infection. Interestingly, 6 of 8 infected animals were serologically positive with the Enferplex TB assay as early as 4 weeks post-infection. As expected, application of the tuberculin skin test enhanced subsequent serological reactivity. Infrequent M. bovis faecal shedding was observed but was uncorrelated with observed immune trajectories. Together, the results show that early antibody responses to M. bovis infection are detectable in some individuals and highlight an urgent need to identify biomarkers that better predict infection outcomes, particularly for application in low-and-middle income countries where test-and-slaughter based control methods are largely unfeasible.

PMID:38297023 | PMC:PMC10831113 | DOI:10.1038/s41598-024-52314-x

Bradford Hill Seminar - Social justice and health equity

Register to attend Please note this will be online webinar. Professor Sir Michael Marmot will present online via Teams.

Register on Teams to attend seminar online at https://events.teams.microsoft.com/event/e8489407-d5e4-4d3e-a91e-d95a97ed97e8@49a50445-bdfa-4b79-ade3-547b4f3986e9

Abstract Taking action to reduce health inequalities is a matter of social justice. In developing strategies for tackling health inequalities we need to confront the social gradient in health not just the difference between the worst off and everybody else. There is clear evidence when we look across countries that national policies make a difference and that much can be done in cities, towns and local areas. But policies and interventions must not be confined to the health care system; they need to address the conditions in which people are born, grow, live, work and age. The evidence shows that economic circumstances are important but are not the only drivers of health inequalities. Tackling the health gap will take action, based on sound evidence, across the whole of society.

About Professor Sir Michael Marmot Sir Michael Marmot MBBS , MPH, PhD, FRCP , FFPHM, FMedSci, FBA has been Professor of Epidemiology at University College London since 1985. He is the author of The Health Gap: the challenge of an unequal world (Bloomsbury: 2015), and Status Syndrome: how your place on the social gradient directly affects your health (Bloomsbury: 2004). Professor Marmot is the Advisor to the WHO Director-General, on social determinants of health, in the new WHO Division of Healthier Populations; Distinguished Visiting Professor at Chinese University of Hong Kong (2019-), and co-Director of the of the CUHK Institute of Health Equity. He is the recipient of the WHO Global Hero Award; the Harvard Lown Professorship (2014-2017); the Prince Mahidol Award for Public Health (2015), and 19 honorary doctorates.

Marmot has led research groups on health inequalities for nearly 50 years. He chaired the Commission on Equity and Health Inequalities in the Americas, set up in 2015 by the World Health Organization’s Pan-American Health Organization (PAHO/ WHO ) and chaired the Commission on Social Determinants of Health (CSDH), which was set up by the World Health Organization in 2005, and produced the report entitled: ‘Closing the Gap in a Generation’ in August 2008. At the request of the British Government, he conducted the Strategic Review of Health Inequalities in England post 2010, which published its report ‘Fair Society, Healthy Lives’ in February 2010. This was followed by the European Review of Social Determinants of Health and the Health Divide, for WHO EURO in 2014; Health Equity in England: Marmot Review 10 Years On, in 2020; Build Back Fairer: the COVID -19 Marmot Review in 2021; and the Report of the Commission on Social Determinants of Health in the Eastern Mediterranean Region, for WHO EMRO , also in 2021.

Professor Marmot also chaired the Expert Panel for the WCRF /AICR 2007 Second Expert Report on Food, Nutrition, Physical Activity and the Prevention of Cancer: a Global Perspective; the Breast Screening Review for the NHS National Cancer Action Team, and was a member of The Lancet-University of Oslo Commission on Global Governance for Health. Early in his career, he set up and led a number of longitudinal cohort studies on the social gradient in health in the UCL Department of Epidemiology & Public Health (where he was head of department for 25 years): the Whitehall II Studies of British Civil Servants, investigating explanations for the striking inverse social gradient in morbidity and mortality; the English Longitudinal Study of Ageing (ELSA), and several international research efforts on the social determinants of health. He served as President of the British Medical Association (BMA) in 2010-2011, and as President of the World Medical Association in 2015. He is President of the British Lung Foundation. He is an Honorary Fellow of the American College of Epidemiology; a Fellow of the Academy of Medical Sciences; an Honorary Fellow of the British Academy, and an Honorary Fellow of the Faculty of Public Health of the Royal College of Physicians. He was a member of the Royal Commission on Environmental Pollution for six years and in 2000 he was knighted by Her Majesty The Queen, for services to epidemiology and the understanding of health inequalities. Professor Marmot is a Member of the National Academy of Medicine.

• Speaker: Professor Sir Michael Marmot, Institute of Health Equity and UCL Department of Epidemiology & Public Health
• Wednesday 28 February 2024, 13:00-14:00
• Venue: Webinar (via Teams).
• Series: Bradford Hill Seminars; organiser: Paul Browne.

Add to your calendar or Include in your list

Bradford Hill Seminar - Social justice and health equity

Register to attend Please note this will be online webinar. Professor Sir Michael Marmot will present online via Teams.

Register on Teams to attend seminar online at https://events.teams.microsoft.com/event/e8489407-d5e4-4d3e-a91e-d95a97ed97e8@49a50445-bdfa-4b79-ade3-547b4f3986e9

Abstract Taking action to reduce health inequalities is a matter of social justice. In developing strategies for tackling health inequalities we need to confront the social gradient in health not just the difference between the worst off and everybody else. There is clear evidence when we look across countries that national policies make a difference and that much can be done in cities, towns and local areas. But policies and interventions must not be confined to the health care system; they need to address the conditions in which people are born, grow, live, work and age. The evidence shows that economic circumstances are important but are not the only drivers of health inequalities. Tackling the health gap will take action, based on sound evidence, across the whole of society.

About Professor Sir Michael Marmot Sir Michael Marmot MBBS , MPH, PhD, FRCP , FFPHM, FMedSci, FBA has been Professor of Epidemiology at University College London since 1985. He is the author of The Health Gap: the challenge of an unequal world (Bloomsbury: 2015), and Status Syndrome: how your place on the social gradient directly affects your health (Bloomsbury: 2004). Professor Marmot is the Advisor to the WHO Director-General, on social determinants of health, in the new WHO Division of Healthier Populations; Distinguished Visiting Professor at Chinese University of Hong Kong (2019-), and co-Director of the of the CUHK Institute of Health Equity. He is the recipient of the WHO Global Hero Award; the Harvard Lown Professorship (2014-2017); the Prince Mahidol Award for Public Health (2015), and 19 honorary doctorates.

Marmot has led research groups on health inequalities for nearly 50 years. He chaired the Commission on Equity and Health Inequalities in the Americas, set up in 2015 by the World Health Organization’s Pan-American Health Organization (PAHO/ WHO ) and chaired the Commission on Social Determinants of Health (CSDH), which was set up by the World Health Organization in 2005, and produced the report entitled: ‘Closing the Gap in a Generation’ in August 2008. At the request of the British Government, he conducted the Strategic Review of Health Inequalities in England post 2010, which published its report ‘Fair Society, Healthy Lives’ in February 2010. This was followed by the European Review of Social Determinants of Health and the Health Divide, for WHO EURO in 2014; Health Equity in England: Marmot Review 10 Years On, in 2020; Build Back Fairer: the COVID -19 Marmot Review in 2021; and the Report of the Commission on Social Determinants of Health in the Eastern Mediterranean Region, for WHO EMRO , also in 2021.

Professor Marmot also chaired the Expert Panel for the WCRF /AICR 2007 Second Expert Report on Food, Nutrition, Physical Activity and the Prevention of Cancer: a Global Perspective; the Breast Screening Review for the NHS National Cancer Action Team, and was a member of The Lancet-University of Oslo Commission on Global Governance for Health. Early in his career, he set up and led a number of longitudinal cohort studies on the social gradient in health in the UCL Department of Epidemiology & Public Health (where he was head of department for 25 years): the Whitehall II Studies of British Civil Servants, investigating explanations for the striking inverse social gradient in morbidity and mortality; the English Longitudinal Study of Ageing (ELSA), and several international research efforts on the social determinants of health. He served as President of the British Medical Association (BMA) in 2010-2011, and as President of the World Medical Association in 2015. He is President of the British Lung Foundation. He is an Honorary Fellow of the American College of Epidemiology; a Fellow of the Academy of Medical Sciences; an Honorary Fellow of the British Academy, and an Honorary Fellow of the Faculty of Public Health of the Royal College of Physicians. He was a member of the Royal Commission on Environmental Pollution for six years and in 2000 he was knighted by Her Majesty The Queen, for services to epidemiology and the understanding of health inequalities. Professor Marmot is a Member of the National Academy of Medicine.

• Speaker: Professor Sir Michael Marmot, Institute of Health Equity and UCL Department of Epidemiology & Public Health
• Wednesday 28 February 2024, 13:00-14:00
• Venue: Webinar (via Teams).
• Series: Bradford Hill Seminars; organiser: Paul Browne.

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The visit took place at Cambridge Innovation Capital and was hosted by Innovate Cambridge – an initiative which is bringing together partners across the city region to deliver an inclusive future for Cambridge and its science and technology cluster. The Shadow Minister met with experts on AI from the University and from industry, discussing both the challenges it presents, as well as the enormous potential for AI to serve science, people, and society.

At the opening roundtable, academics including Professor Dame Diane Coyle (Director of the Bennett Institute of Public Policy), Professor Neil Lawrence (DeepMind Professor of Machine Learning), and Professor John Aston (Professor of Statistics in Public Life), provided expert analysis on AI policy challenges as well as the role AI can play in public service reform. The group discussed how governance systems need to evolve for the AI era, and how an increasingly complex information infrastructure can be managed. In addition, they considered the opportunity that AI presents for improving public services and breaking down siloed decision-making within government.

Mr Kyle took part in a series of ‘flash talks’, focused on areas where research in AI is delivering benefits to society. These included work by Dr Ronita Bardhan, from the University’s Department of Architecture, on a new deep-learning model which makes it far easier and cheaper to identify ‘hard-to-decarbonise’ houses and develop strategies to improve their green credentials. Dr Anna Moore presented her work in the Department of Psychiatry, using AI systems to speed up the diagnosis of mental health conditions in children.

In the afternoon, Mr Kyle met with leaders representing civic institutions, academia and business organisations from across the city, including Councillor Mike Davey, Leader of Cambridge City Council, and Andrew Williamson, Managing Partner at Cambridge Innovation Capital. They spoke about their shared vision and strategy for the region to ensure Cambridge remains a globally leading innovation centre, and a collective desire to deliver benefits both locally and across the UK.

The day concluded with a spin-out and business roundtable at which participants discussed the need for government and the private sector to be active in ensuring AI benefits all parts of the UK, and people are re-skilled as jobs change. Mr Kyle was also interested to explore how the UK can become a more attractive place to scale companies. Key considerations included the need to improve access to talent, capital and infrastructure, as well tackling the regulatory barriers which can make the UK less competitive.

Peter Kyle MP, the Shadow Secretary of State for Science, Innovation and Technology, met academics from the University of Cambridge and leaders from the Cambridge community for a day focused on AI policy and innovation.

The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Yes

Nat Commun. 2024 Jan 30;15(1):888. doi: 10.1038/s41467-024-44701-9.

ABSTRACT

To date only a fraction of the genetic footprint of thyroid function has been clarified. We report a genome-wide association study meta-analysis of thyroid function in up to 271,040 individuals of European ancestry, including reference range thyrotropin (TSH), free thyroxine (FT4), free and total triiodothyronine (T3), proxies for metabolism (T3/FT4 ratio) as well as dichotomized high and low TSH levels. We revealed 259 independent significant associations for TSH (61% novel), 85 for FT4 (67% novel), and 62 novel signals for the T3 related traits. The loci explained 14.1%, 6.0%, 9.5% and 1.1% of the total variation in TSH, FT4, total T3 and free T3 concentrations, respectively. Genetic correlations indicate that TSH associated loci reflect the thyroid function determined by free T3, whereas the FT4 associations represent the thyroid hormone metabolism. Polygenic risk score and Mendelian randomization analyses showed the effects of genetically determined variation in thyroid function on various clinical outcomes, including cardiovascular risk factors and diseases, autoimmune diseases, and cancer. In conclusion, our results improve the understanding of thyroid hormone physiology and highlight the pleiotropic effects of thyroid function on various diseases.

PMID:38291025 | PMC:PMC10828500 | DOI:10.1038/s41467-024-44701-9

J Virol. 2024 Jan 30:e0177723. doi: 10.1128/jvi.01777-23. Online ahead of print.

ABSTRACT

Rubella virus encodes a nonstructural polyprotein with RNA polymerase, methyltransferase, and papain-like cysteine protease activities, along with a putative macrodomain of unknown function. Macrodomains bind ADP-ribose adducts, a post-translational modification that plays a key role in host-virus conflicts. Some macrodomains can also remove the mono-ADP-ribose adduct or degrade poly-ADP-ribose chains. Here, we report high-resolution crystal structures of the macrodomain from rubella virus nonstructural protein p150, with and without ADP-ribose binding. The overall fold is most similar to macroD-type macrodomains from various nonviral species. The specific composition and structure of the residues that coordinate ADP-ribose in the rubella virus macrodomain are most similar to those of macrodomains from alphaviruses. Isothermal calorimetry shows that the rubella virus macrodomain binds ADP-ribose in solution. Enzyme assays show that the rubella virus macrodomain can hydrolyze both mono- and poly-ADP-ribose adducts. Site-directed mutagenesis identifies Asn39 and Cys49 required for mono-ADP-ribosylhydrolase (de-MARylation) activity.IMPORTANCERubella virus remains a global health threat. Rubella infections during pregnancy can cause serious congenital pathology, for which no antiviral treatments are available. Our work demonstrates that, like alpha- and coronaviruses, rubiviruses encode a mono-ADP-ribosylhydrolase with a structurally conserved macrodomain fold to counteract MARylation by poly (ADP-ribose) polymerases (PARPs) in the host innate immune response. Our structural data will guide future efforts to develop novel antiviral therapeutics against rubella or infections with related viruses.

PMID:38289106 | DOI:10.1128/jvi.01777-23

Title - TBC

This Cambridge Immunology and Medicine Seminar will take place on Friday 22 March 2024, starting at 1:00 pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC):

Speaker: Dr Sara Ghorashian, Honorary Senior Clinical Lecturer, University College London and Consultant Paediatric Haematologist, Great Ormond Street Hospital

Host: Professor Rahul Roychoudhuri, Professor of Cancer Immunology, University of Cambridge.

For anyone who can’t attend in person, please join the Cambridge Immunology and Medicine Seminar on Zoom Refreshments will be available following the Seminar.

This talk is part of the Immunology and Medicine Seminars series.

If you have a question about this talk, please contact Ruth Paton

• Speaker: Sara Ghorashian, Honorary Associate Professor, University College London
• Friday 22 March 2024, 13:00-14:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Immunology and Medicine Seminars; organiser: Ruth Paton.

Add to your calendar or Include in your list

Title - TBC

This Cambridge Immunology and Medicine Seminar will take place on Friday 22 March 2024, starting at 1:00 pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC):

Speaker: Dr Sara Ghorashian, Honorary Senior Clinical Lecturer, University College London and Consultant Paediatric Haematologist, Great Ormond Street Hospital

Host: Professor Rahul Roychoudhuri, Professor of Cancer Immunology, University of Cambridge.

For anyone who can’t attend in person, please join the Cambridge Immunology and Medicine Seminar on Zoom Refreshments will be available following the Seminar.

This talk is part of the Immunology and Medicine Seminars series.

If you have a question about this talk, please contact Ruth Paton

• Speaker: Sara Ghorashian, Honorary Associate Professor, University College London
• Friday 22 March 2024, 13:00-14:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Immunology and Medicine Seminars; organiser: Ruth Paton.

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In research published in Cell Reports, the team describes how fasting raises levels of a chemical in the blood known as arachidonic acid, which inhibits inflammation. The researchers say it may also help explain some of the beneficial effects of drugs such as aspirin.

Scientists have known for some time that our diet – particular a high calorie Western diet – can increase our risk of diseases including obesity, type 2 diabetes and heart disease, which are linked to chronic inflammation in the body.

Inflammation is our body’s natural response to injury or infection, but this process can be triggered by other mechanisms, including by the so-called ‘inflammasome’, which acts like an alarm within our body’s cells, triggering inflammation to help protect our body when it senses damage. But the inflammasome can trigger inflammation in unintentional ways – one of its functions is to destroy unwanted cells, which can result in the release of the cell’s contents into the body, where they trigger inflammation.

Professor Clare Bryant from the Department of Medicine at the University of Cambridge said: “We’re very interested in trying to understand the causes of chronic inflammation in the context of many human diseases, and in particular the role of the inflammasome.

“What's become apparent over recent years is that one inflammasome in particular – the NLRP3 inflammasome – is very important in a number of major diseases such as obesity and atherosclerosis, but also in diseases like Alzheimer's and Parkinson's disease, many of the diseases of older age people, particularly in the Western world.”

Fasting can help reduce inflammation, but the reason why has not been clear. To help answer this question, a team led by Professor Bryant and colleagues at the University of Cambridge and National Institute for Health in the USA studied blood samples from a group of 21 volunteers, who ate a 500kcal meal then fasted for 24 hours before consuming a second 500kcal meal. 

The team found that restricting calorie intake increased levels of a lipid known as arachidonic acid. Lipids are molecules that play important roles in our bodies, such as storing energy and transmitting information between cells. As soon as individuals ate a meal again, levels of arachidonic acid dropped.

When the researchers studied arachidonic acid’s effect in immune cells cultured in the lab, they found that it turns down the activity of the NLRP3 inflammasome. This surprised the team as arachidonic acid was previously thought to be linked with increased levels of inflammation, not decreased.

Professor Bryant, a Fellow of Queens’ College, Cambridge, added: “This provides a potential explanation for how changing our diet – in particular by fasting – protects us from inflammation, especially the damaging form that underpins many diseases related to a Western high calorie diet.

“It’s too early to say whether fasting protects against diseases like Alzheimer's and Parkinson's disease as the effects of arachidonic acid are only short-lived, but our work adds to a growing amount of scientific literature that points to the health benefits of calorie restriction. It suggests that regular fasting over a long period could help reduce the chronic inflammation we associate with these conditions. It's certainly an attractive idea.”

The findings also hint at one mechanism whereby a high calorie diet might increase the risk of these diseases. Studies have shown that some patients that have a high fat diet have increased levels of inflammasome activity.

“There could be a yin and yang effect going on here, whereby too much of the wrong thing is increasing your inflammasome activity and too little is decreasing it,” said Professor Bryant. “Arachidonic acid could be one way in which this is happening.”

The researchers say the discovery may also offer clues to an unexpected way in which so-called non-steroidal anti-inflammatory drugs such as aspirin work. Normally, arachidonic acid is rapidly broken down in the body, but aspirin stops this process, which can lead to an increase in levels of arachidonic acid, which in turn reduce inflammasome activity and hence inflammation.

Professor Bryant said: “It’s important to stress that aspirin should not be taken to reduce risk of long terms diseases without medical guidance as it can have side-effects such as stomach bleeds if taken over a long period.”

The research was funded by Wellcome, the Medical Research Council and the US National Heart, Lung, and Blood Institute Division of Intramural Research.

Reference
Pereira, M & Liang, J et al. Arachidonic acid inhibition of the NLRP3 inflammasome is a mechanism to explain the anti-inflammatory effects of fasting. Cell Reports; 23 Jan 2024; DOI: 10.1016/j.celrep.2024.113700

Cambridge scientists may have discovered a new way in which fasting helps reduce inflammation – a potentially damaging side-effect of the body’s immune system that underlies a number of chronic diseases.

Our work adds to a growing amount of scientific literature that points to the health benefits of calorie restrictionClare BryantCarol Yepes (Getty Images)Intermittent fasting conceptual image

The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Yes

Title - TBC

The next Cambridge Immunology and Medicine Seminar will take place on Friday 8th March 2024, starting at 1:00 pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC)

Speaker: Professor Luca Gattinoni, Division of Functional Immune Cell Modulation, Leibniz Institute for Immunotherapy

Host: Professor Rahul Roychoudhuri, Professor of Cancer Immunology (Department of Pathology) and Director (non-clinical) of the CRUK Cambridge Centre Training Programme, at the University of Cambridge.

For anyone who can’t attend in person, please join the Cambridge Immunology and Medicine Seminar on Zoom:

Join Zoom Meeting: https://cam-ac-uk.zoom.us/j/89741634903?pwd=dzcxbU45NjAwQXo1dmlNMjR3V0lUUT09

Meeting ID: 897 4163 4903 Passcode: 539740

Refreshments will be available following the Seminar.

• Speaker: Luca Gattinoni, Division of Functional Immune Cell Modulation, Leibniz Institute for Immunotherapy (LIT), Regensburg, Germany
• Friday 08 March 2024, 13:00-14:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Immunology and Medicine Seminars; organiser: Ruth Paton.

Add to your calendar or Include in your list

Title - TBC

The next Cambridge Immunology and Medicine Seminar will take place on Friday 8th March 2024, starting at 1:00 pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC)

Speaker: Professor Luca Gattinoni, Division of Functional Immune Cell Modulation, Leibniz Institute for Immunotherapy

Host: Professor Rahul Roychoudhuri, Professor of Cancer Immunology (Department of Pathology) and Director (non-clinical) of the CRUK Cambridge Centre Training Programme, at the University of Cambridge.

For anyone who can’t attend in person, please join the Cambridge Immunology and Medicine Seminar on Zoom:

Join Zoom Meeting: https://cam-ac-uk.zoom.us/j/89741634903?pwd=dzcxbU45NjAwQXo1dmlNMjR3V0lUUT09

Meeting ID: 897 4163 4903 Passcode: 539740

Refreshments will be available following the Seminar.

• Speaker: Luca Gattinoni, Division of Functional Immune Cell Modulation, Leibniz Institute for Immunotherapy (LIT), Regensburg, Germany
• Friday 08 March 2024, 13:00-14:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Immunology and Medicine Seminars; organiser: Ruth Paton.

Add to your calendar or Include in your list

People of religious faith may have experienced lower levels of unhappiness and stress than secular people during the UK’s Covid-19 lockdowns in 2020 and 2021, according to a new University of Cambridge study released as a working paper.

The findings follow recently published Cambridge-led research suggesting that worsening mental health after experiencing Covid infection – either personally or in those close to you – was also somewhat ameliorated by religious belief. This study looked at the US population during early 2021.

University of Cambridge economists argue that – taken together – these studies show that religion may act as a bulwark against increased distress and reduced wellbeing during times of crisis, such as a global public health emergency.

“Selection biases make the wellbeing effects of religion difficult to study,” said Prof Shaun Larcom from Cambridge’s Department of Land Economy, and co-author of the latest study. “People may become religious due to family backgrounds, innate traits, or to cope with new or existing struggles.”

“However, the Covid-19 pandemic was an extraordinary event affecting everyone at around the same time, so we could gauge the impact of a negative shock to wellbeing right across society. This provided a unique opportunity to measure whether religion was important for how some people deal with a crisis.”

Larcom and his Cambridge colleagues Prof Sriya Iyer and Dr Po-Wen She analysed survey data collected from 3,884 people in the UK during the first two national lockdowns, and compared it to three waves of data prior to the pandemic.

They found that while lockdowns were associated with a universal uptick in unhappiness, the average increase in feeling miserable was 29% lower for people who described themselves as belonging to a religion.*

The researchers also analysed the data by “religiosity”: the extent of an individual’s commitment to religious beliefs, and how central it is to their life. Those for whom religion makes “some or a great difference” in their lives experienced around half the increase in unhappiness seen in those for whom religion makes little or no difference.**

“The study suggests that it is not just being religious, but the intensity of religiosity that is important when coping with a crisis,” said Larcom.

Those self-identifying as religious in the UK are more likely to have certain characteristics, such as being older and female. The research team “controlled” for these statistically to try and isolate the effects caused by faith alone, and still found that the probability of religious people having an increase in depression was around 20% lower than non-religious people.

There was little overall difference between Christians, Muslims and Hindus – followers of the three biggest religions in the UK. However, the team did find that wellbeing among some religious groups appeared to suffer more than others when places of worship were closed during the first lockdown.

“The denial of weekly communal attendance appears to have been particularly affecting for Catholics and Muslims,” said Larcom.

For the earlier study, authored by Prof Sriya Iyer, along with colleagues Kishen Shastry, Girish Bahal and Anand Shrivastava from Australia and India, researchers used online surveys to investigate Covid-19 infections among respondents or their immediate family and friends, as well as religious beliefs, and mental health. 

The study was conducted during February and March 2021, and involved 5,178 people right across the United States, with findings published in the journal European Economic Review in November 2023.

Researchers found that almost half those who reported a Covid-19 infection either in themselves or their immediate social network experienced an associated reduction in wellbeing.

Where mental health declined, it was around 60% worse on average for the non-religious compared to people of faith with typical levels of “religiosity”.***

Interestingly, the positive effects of religion were not found in areas with strictest lockdowns, suggesting access to places of worship might be even more important in a US context. The study also found significant uptake of online religious services, and a 40% lower association between Covid-19 and mental health for those who used them****.

“Religious beliefs may be used by some as psychological resources that can shore up self-esteem and add coping skills, combined with practices that provide social support,” said Prof Iyer, from Cambridge’s Faculty of Economics.

“The pandemic presented an opportunity to glean further evidence of this in both the United Kingdom and the United States, two nations characterised by enormous religious diversity.” 

Added Larcom: “These studies show a relationship between religion and lower levels of distress during a global crisis. It may be that religious faith builds resilience, and helps people cope with adversity by providing hope, consolation and meaning in tumultuous times.”  

Two Cambridge-led studies suggest that the psychological distress caused by lockdowns (UK) and experience of infection (US) was reduced among those of faith compared to non-religious people.  

Getty/Luis AlvarezPeople in church praying with covid-19 restrictions Notes

* The increase in the mean measure for unhappiness was 6.1 percent for people who do not identify with a religion during the lockdown, compared to an increase of 4.3 percent for those who do belong to a religion – a difference of 29%.

**For those that religion makes little or no difference, the increase was 6.3 percent.  For those for whom religion makes some or a great difference, the increase was around half that, at 3 percent and 3.5 percent respectively.

*** This was after controlling for various demographic and environmental traits, including age, race, income, and average mental health rates prior to the pandemic.

**** The interpretation is from Column 1 of Table 5: Determinants of mental health, online access to religion. Where the coefficients of Covid {Not accessed online service} is 2.265 and Covid {Accessed online service} is 1.344. Hence the difference is 2.265-1.344 = 0.921 which is 40% of 2.265.

The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Yes

Mechanisms controlling gene expression in hypoxia and inflammation

Professor Sonia Rocha, Executive Dean of the Institute of Systems Molecular and Integrative Biology, University of Liverpool.

The next Cambridge Immunology and Medicine Seminar will take place on Friday 16th February 2024, starting at 1:00 pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC)

Host: Professor James Nathan, Wellcome Senior Clinical Fellow, Professor of Respiratory Medicine, University of Cambridge.

For anyone who can’t attend in person, please join the Cambridge Immunology and Medicine Seminar on Zoom:

Join Zoom Meeting: https://cam-ac-uk.zoom.us/j/89741634903?pwd=dzcxbU45NjAwQXo1dmlNMjR3V0lUUT09

Meeting ID: 897 4163 4903 Passcode: 539740

Refreshments will be available following the Seminar.

If you have a question about this talk, please contact Ruth Paton.

• Speaker: Professor Sonia Rocha, Executive Dean of the Institute of Systems Molecular and Integrative Biology, University of Liverpool
• Friday 16 February 2024, 13:00-14:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Immunology and Medicine Seminars; organiser: Ruth Paton.

Add to your calendar or Include in your list

Mechanisms controlling gene expression in hypoxia and inflammation

Professor Sonia Rocha, Executive Dean of the Institute of Systems Molecular and Integrative Biology, University of Liverpool.

The next Cambridge Immunology and Medicine Seminar will take place on Friday 16th February 2024, starting at 1:00 pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC)

Host: Professor James Nathan, Wellcome Senior Clinical Fellow, Professor of Respiratory Medicine, University of Cambridge.

For anyone who can’t attend in person, please join the Cambridge Immunology and Medicine Seminar on Zoom:

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• Speaker: Professor Sonia Rocha, Executive Dean of the Institute of Systems Molecular and Integrative Biology, University of Liverpool
• Friday 16 February 2024, 13:00-14:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Immunology and Medicine Seminars; organiser: Ruth Paton.

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EMBO Rep. 2024 Jan 29. doi: 10.1038/s44319-024-00063-3. Online ahead of print.

ABSTRACT

The exquisite specificity of antibodies can be harnessed to effect targeted degradation of membrane proteins. Here, we demonstrate targeted protein removal utilising a protein degradation domain derived from the endogenous human protein Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9). Recombinant antibodies genetically fused to this domain drive the degradation of membrane proteins that undergo constitutive internalisation and recycling, including the transferrin receptor and the human cytomegalovirus latency-associated protein US28. We term this approach PACTAC (PCSK9-Antibody Clearance-Targeting Chimeras).

PMID:38287192 | DOI:10.1038/s44319-024-00063-3

The research team, from the University of Cambridge, used machine learning algorithms to teach a robotic sensor to quickly slide over lines of braille text. The robot was able to read the braille at 315 words per minute at close to 90% accuracy.

Although the robot braille reader was not developed as an assistive technology, the researchers say the high sensitivity required to read braille makes it an ideal test in the development of robot hands or prosthetics with comparable sensitivity to human fingertips. The results are reported in the journal IEEE Robotics and Automation Letters.

Human fingertips are remarkably sensitive and help us gather information about the world around us. Our fingertips can detect tiny changes in the texture of a material or help us know how much force to use when grasping an object: for example, picking up an egg without breaking it or a bowling ball without dropping it.

Reproducing that level of sensitivity in a robotic hand, in an energy-efficient way, is a big engineering challenge. In Professor Fumiya Iida’s lab in Cambridge’s Department of Engineering, researchers are developing solutions to this and other skills that humans find easy, but robots find difficult.

“The softness of human fingertips is one of the reasons we’re able to grip things with the right amount of pressure,” said Parth Potdar from Cambridge’s Department of Engineering and an undergraduate at Pembroke College, the paper’s first author. “For robotics, softness is a useful characteristic, but you also need lots of sensor information, and it’s tricky to have both at once, especially when dealing with flexible or deformable surfaces.”

Braille is an ideal test for a robot ‘fingertip’ as reading it requires high sensitivity, since the dots in each representative letter pattern are so close together. The researchers used an off-the-shelf sensor to develop a robotic braille reader that more accurately replicates human reading behaviour.

“There are existing robotic braille readers, but they only read one letter at a time, which is not how humans read,” said co-author David Hardman, also from the Department of Engineering. “Existing robotic braille readers work in a static way: they touch one letter pattern, read it, pull up from the surface, move over, lower onto the next letter pattern, and so on. We want something that’s more realistic and far more efficient.”

The robotic sensor the researchers used has a camera in its ‘fingertip’, and reads by using a combination of the information from the camera and the sensors. “This is a hard problem for roboticists as there’s a lot of image processing that needs to be done to remove motion blur, which is time and energy-consuming,” said Potdar.

The team developed machine learning algorithms so the robotic reader would be able to ‘deblur’ the images before the sensor attempted to recognise the letters. They trained the algorithm on a set of sharp images of braille with fake blur applied. After the algorithm had learned to deblur the letters, they used a computer vision model to detect and classify each character.

Once the algorithms were incorporated, the researchers tested their reader by sliding it quickly along rows of braille characters. The robotic braille reader could read at 315 words per minute at 87% accuracy, which is twice as fast and about as accurate as a human Braille reader.

“Considering that we used fake blur the train the algorithm, it was surprising how accurate it was at reading braille,” said Hardman. “We found a nice trade-off between speed and accuracy, which is also the case with human readers.”

“Braille reading speed is a great way to measure the dynamic performance of tactile sensing systems, so our findings could be applicable beyond braille, for applications like detecting surface textures or slippage in robotic manipulation,” said Potdar.

In future, the researchers are hoping to scale the technology to the size of a humanoid hand or skin. The research was supported in part by the Samsung Global Research Outreach Program.

 

Reference:
Parth Potdar et al. ‘High-Speed Tactile Braille Reading via Biomimetic Sliding Interactions.’ IEEE Robotics and Automation Letters (2024). DOI: 10.1109/LRA.2024.3356978

Researchers have developed a robotic sensor that incorporates artificial intelligence techniques to read braille at speeds roughly double that of most human readers.

Parth PotdarRobot braille reader

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• Speaker: Ross Waller
• Friday 08 March 2024, 15:00-16:00
• Venue: Jean Thomas Lecture theatre, Sanger Building, Tennis Court Road.
• Series: Biochemistry Friday Seminars; organiser: reception.

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• Speaker: Ross Waller
• Friday 08 March 2024, 15:00-16:00
• Venue: Jean Thomas Lecture theatre, Sanger Building, Tennis Court Road.
• Series: Biochemistry Friday Seminars; organiser: reception.

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• Speaker: Chris Smith
• Friday 01 March 2024, 15:00-16:00
• Venue: Jean Thomas Lecture theatre, Sanger Building, Tennis Court Road.
• Series: Biochemistry Friday Seminars; organiser: Becky Bowers.

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• Speaker: Chris Smith
• Friday 01 March 2024, 15:00-16:00
• Venue: Jean Thomas Lecture theatre, Sanger Building, Tennis Court Road.
• Series: Biochemistry Friday Seminars; organiser: Becky Bowers.

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