Citation cartels help some mathematicians—and their universities—climb the rankings
Wed 28 Feb 13:00: 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.
Fri 09 Feb 13:00: The Evolving Relative Role of Stratospheric Ozone and Greenhouse Gasses in Modifying the Southern Ocean Carbon Sink from 1950-2100
Southern Ocean winds have strengthened and moved poleward in the latter half of the 20th century, which has been attributed to the depletion of stratospheric ozone and to climate warming from rising greenhouse gas concentrations. Both ozone recovery and changing greenhouse gas concentrations are expected to continue modulating wind structure throughout the 21st century. Here, we quantify the relative roles of ozone and greenhouse gases on Southern Ocean wind structure from 1950-2100 using the UK Earth System Model (UKESM1) model output, with a combination of three scenarios of ozone and two scenarios of greenhouse gas evolution. Both ozone depletion and increases in greenhouse gas concentration act to increase wind speed over the Southern Ocean. The influence of ozone is predominant in summer winds, while the influence of greenhouse gases acts in all seasons. We show that wind speeds return close to their original levels by the end of the 21st century under a low-greenhouse gas scenario with ozone recovery. The influence of ozone on wind speed was dominant in the 1950-2000 time-period, but not in the 21st Century when the influence of greenhouse gases becomes two to three times larger than that of ozone, even in the low emissions scenario. We find significant effects of both ozone scenario and greenhouse gas emissions on physical-oceanographic variables (sea surface temperature, mixed layer depth, and overturning circulation). Finally, we quantify the relative contributions of these physical changes to the evolving carbon sink of the Southern Ocean, and discuss how wind-induced physical changes can alter ecosystem processes and the associated carbon export to the deep ocean.
- Speaker: Tereza Jarníková, University of East Anglia
- Friday 09 February 2024, 13:00-14:00
- Venue: BAS Seminar Room 1; zoom.
- Series: British Antarctic Survey - Polar Oceans seminar series; organiser: Dr Birgit Rogalla.
Thu 01 Feb 16:30: Interested in Nuclear Energy Innovation?
Join us for a panel discussion with nuclear start-ups. Hear about their technologies, mindset and approaches. Take your opportunity to ask questions. Our speakers will be Mark Davies from USNC and Daniel Theobald from Last Energy
- Speaker: Mark Davies from USNC and Daniel Theobald from Last Energy
- Thursday 01 February 2024, 16:30-18:00
- Venue: Cambridge University Engineering Department, Lecture Room 6.
- Series: Engineering Department Nuclear Energy Seminars; organiser: Jo Boyle.
Thu 08 Feb 16:30: The UK Nuclear Road Map
What it means for the next few years and beyond
- Speaker: Tony Roulstone
- Thursday 08 February 2024, 16:30-18:00
- Venue: Cambridge University Engineering Department, Lecture Room 6.
- Series: Engineering Department Nuclear Energy Seminars; organiser: Jo Boyle.
Scientists identify how fasting may protect against inflammation
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.
Scientists identify how fasting may protect against inflammation
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.
Religious people coped better with Covid-19 pandemic, research suggests
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.
Mon 26 Feb 13:00: Data-Driven and Equation-Informed Optimal Control of Lagrangian pairs in turbulent flows
We show how to apply optimal control theory to catch a passive drifting target in a turbulent flow by an autonomous flowing agent with limited maneuverability. For the case of a perfect knowledge of the environment, we show that Optimal Control theory can overcome chaotic dispersion capturing the Lagrangian target in the shortest possible time [1]. We also provide baselines using heuristic policies based on local-only hydrodynamical cues [2]. How to extend this approach to model-free Reinforcement Learning tools is also briefly discussed [3]. Data are open downloadable from TURB Lagr [4], a database of more than 300K three-dimensional trajectories of tracer particles advected by a fully developed homogeneous and isotropic turbulent flow.
(1) Calascibetta et al., Commun. Phys. 6, 256 (2023). (2) Monthiller et al., Phys. Rev. Lett. 129, 064502 (2022). (3) Calascibetta et al., Eur. Phys. J. E 46, 9 (2023). (4) smart-turb.roma2.infn.it
- Speaker: Chiara Calascibetta
- Monday 26 February 2024, 13:00-14:00
- Venue: MR5, CMS.
- Series: Geophysical and Environmental Processes; organiser: Prof. John R. Taylor.
In a big bet on science, the U.S. just created 10 new ‘innovation engines’
Mon 12 Feb 13:00: The Influence of Lateral Spreading upon Solitary Wave Formation by Internal Tides
Abstract not available
- Speaker: Bruce Sutherland, University of Alberta
- Monday 12 February 2024, 13:00-14:00
- Venue: MR5, CMS.
- Series: Geophysical and Environmental Processes; organiser: Prof. John R. Taylor.
Mon 04 Mar 13:00: TBA
Abstract not available
- Speaker: Molly Menzel, NASA GIS
- Monday 04 March 2024, 13:00-14:00
- Venue: MR5, CMS.
- Series: Geophysical and Environmental Processes; organiser: Prof. John R. Taylor.
Mon 26 Feb 13:00: TBA
Abstract not available
- Speaker: Chiara Calascibetta
- Monday 26 February 2024, 13:00-14:00
- Venue: MR5, CMS.
- Series: Geophysical and Environmental Processes; organiser: Prof. John R. Taylor.
Mon 19 Feb 13:00: TBA
Abstract not available
- Speaker: Luke Kearney, University of Oxford
- Monday 19 February 2024, 13:00-14:00
- Venue: MR5, CMS.
- Series: Geophysical and Environmental Processes; organiser: Prof. John R. Taylor.
Mon 05 Feb 13:00: TBA
Abstract not available
- Speaker: Costanza Rodda, Imperial College
- Monday 05 February 2024, 13:00-14:00
- Venue: MR5, CMS.
- Series: Geophysical and Environmental Processes; organiser: Prof. John R. Taylor.
Mon 12 Feb 13:00: TBA
Abstract not available
- Speaker: Bruce Sutherland, University of Alberta
- Monday 12 February 2024, 13:00-14:00
- Venue: MR5, CMS.
- Series: Geophysical and Environmental Processes; organiser: Prof. John R. Taylor.
Thu 01 Feb 11:30: Transport and Settling of Buoyant Microplastics in Turbidity Currents
Although tens of millions of tons of plastic waste are released into the ocean each year, less than 300 kilotons remain on or near the ocean surface. This is particularly puzzling because more than half of plastics that are produced are buoyant in sea water. One mechanism that can result in buoyant plastic settling is the process of biofouling in which microbes and other organic material can accumulate on the plastics rendering them more dense. Less studied is the accumulation of inorganic material on the plastics. For example, clay has recently been shown to attach to plastics, particularly in the presence of surfactants. Here we report on laboratory experiments showing that plastic particles which are less dense than fresh water can settle due to the accumulation of glass spheres (“sand”) on their surface. This process is shown to occur dynamically as sand and plastic particles mix turbulently during the impulsive release of a turbidity current, which can carry some of the plastic particles to depth along with the settling sand. [This work reports on experiments performed by Woods Hole Oceanographic Institute (WHOI) Geophysical Fluid Dynamics (GFD) Fellow Quentin Kriaa during the WHOI GFD Summer Program 2023, co-supervised by Claudia Cenedese and Jim McElwaine.]
- Speaker: Professor Bruce Sutherland, Uni of Alberta
- Thursday 01 February 2024, 11:30-12:30
- Venue: Open Plan Area, Institute for Energy and Environmental Flows, Madingley Rise CB3 0EZ.
- Series: Institute for Energy and Environmental Flows (IEEF); organiser: Catherine Pearson.
Mon 29 Jan 13:00: Negative effective viscosity in strongly stratified turbulence
Abstract not available
- Speaker: Qi Zhou, University of Calgary
- Monday 29 January 2024, 13:00-14:00
- Venue: MR5, CMS.
- Series: Geophysical and Environmental Processes; organiser: Prof. John R. Taylor.