The reproduction of lynxes is highly mysterious. Unlike other wild cats, most lynxes are only receptive for a few days once a year. As scientists from the Leibniz Institute for Zoo and Wildlife Research (Leibniz-IZW) have already shown in the past, this is a consequence of the long life of corpus lutea in the ovaries which prevents further ovulation during the course of the year. The Berlin team has now achieved another breakthrough in solving the puzzle: they were able to isolate several cell types of corpus luteum from domestic cat tissue and characterise their function in detail with the help of cell cultures. The new method can also be applied to endangered felids such as the Iberian lynx and could advance our understanding of the causes and mechanisms of the longevity of corpus lutea in lynxes. The ultimate goal in practical terms is to induce ovulation with the help of corpus luteum hormones. This would enhance the support for the reproduction of the highly endangered Iberian lynx in breeding programmes.

When it comes to reproduction, the felids are usually quite unanimous: most wild cat species go through several sexual cycles per year, so can become pregnant several times a year. However, unlike its relatives, the genus Lynx mainly uses a mono-oestric reproduction strategy. Three of four lynx species can become pregnant for a short time only once per year. This is a burden for endangered species such as the Iberian lynx (Lynx pardinus). If they do not succeed in producing offspring within this time, they have to wait until next year. Artificial insemination also failed, probably because of the lack of knowledge about how to induce ovulation. It is therefore indispensable for the success of the lynx conservation breeding programme to learn more about the mysterious physiology of their reproduction.

In 2014, the reproduction team of the Leibniz-IZW was able to present the first important partial solution of the puzzle. Together with colleagues from several zoological gardens they discovered that the corpus luteum of lynx is continuously active for several years and thus responsible for their unusual reproduction pattern. The corpus luteum is a glandular tissue in the ovaries of mammals that, among other things, produces progesterone - the hormone that supports pregnancy and prevents further ovulation. If the egg is not fertilised, the corpus luteum normally degrades quite quickly and thereby enables a new cycle.

"In lynxes, a mechanism has developed that maintains the corpus luteum for several years. This means that the genus Lynx has the longest known lifespan of functionally active corpora lutea among mammals," says Beate Braun, scientist in the Department of Reproduction Biology at the Leibniz-IZW. "It is astonishing that lynxes are ready for reception in a new season despite the presence of corpus lutea. The activity of the corpus luteum is apparently shut down for a short time, which triggers ovulation. Progesterone production is then resumed and held high beyond pregnancy. In this way, the persistent corpus luteum is likely to prevent further ovulations in the same year."

It is still unclear, how exactly the longevity of the corpus luteum is maintained. However, the scientists from Berlin have now come one step closer to solving the mystery. "We succeeded in isolating and cultivating different cell types from the corpus luteum of domestic cats," explains Michal Hryciuk, PhD student in the Department of Reproduction Biology at the Leibniz-IZW. "The cells originate from tissue taken from domestic cats in animal clinics during castration. Tissues from lynxes or other wild cat species are very rarely available - for example when dead animals are found or animals in zoos are castrated for medical reasons. It was therefore important to us to set up a functioning cultivation system first and then apply it to valuable samples, and that is exactly the system that we have now."

The scientists not only succeeded in cultivating several cell types but also characterised large and small cells of corpus lutea under controlled laboratory conditions. They were able to determine the amount of progesterone and other hormones produced and track the changing activity of genes over time. With the developed cultivation technique, scientific research now has the urgently needed instruments at its disposal to solve the riddle of the long-lived corpus luteum. "Our results will help to identify the hormonal control mechanisms that regulate the growth, maintenance, and degradation of corpus luteum," says Katarina Jewgenow, Head of the Department of Reproduction Biology at the Leibniz-IZW. "This opens up completely new possibilities to enhance the conception of endangered lynxes and other wild cat species in order to support conservation breeding programmes."

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Corpus luteum cells of cats successfully cultivated and comprehensively characterized - Science Codex

Long before Apple watches, grandfather clocks or even sundials, nature provided living things with a way to tell time.

Life evolved on a rotating world that delivered alternating light and darkness on a 24-hour cycle. Over time, cellular chemistry tuned itself to that rhythm. Today, circadian rhythms governed by a master timekeeper in the brain guide sleeping schedules and mealtimes and influence everything from diet to depression to the risk of cancer. While an Apple watch can monitor a few vital functions such as your heart rate, your bodys natural clock controls or affects nearly all of them.

Circadian rhythms impact almost every aspect of biology, says neuroscientist Joseph Takahashi of the University of Texas Southwestern Medical Center.

Lately, research by Takahashi and others has suggested strategies for manipulating the bodys clock to correct circadian-controlled chemistry when it goes awry. Such circadian interventions could lead to relief for shift workers, antidotes for jet lag, and novel treatments for mood disorders and obesity, not to mention the prospect of counteracting aging.

Prime weapons for the assault on clock-related maladies, Takahashi believes, can be recruited from an arsenal of small molecules, including some existing medical drugs.

Researchers are increasingly interested in developing small molecules to target the circadian system directly for therapeutic gains, Takahashi and coauthors Zheng Chen and Seung-Hee Yoo wrote in the 2018 Annual Review of Pharmacology and Toxicology.

In sophisticated life-forms (such as mammals), central control of the bodys clock resides in a small cluster of nerve cells within the brains hypothalamus. That cluster, called the suprachiasmatic nucleus SCN for short is tuned to the day-night signal by light transmitted via the eyes and the optic nerve.

But the SCN does not do the job alone. Its the master clock, for sure, but satellite timekeepers operate in all kinds of cells and body tissues.

There isnt just an SCN clock in the brain, Takahashi said at a recent meeting of the Society for Neuroscience. There are clocks throughout the entire body. Every major organ system has its own intrinsic clock.

The proliferation of clocks throughout the body makes circadian chemistry relevant to various behaviors and physiological processes, such as metabolism and blood flow. Maintaining healthy physiology requires all the bodys various clocks to be synchronized by signals (in the form of hormones and nerve impulses) from the SCN. SCN signals govern the timing of genetic activity responsible for the production of numerous clock-related proteins. Studies mainly in mice have shown how those proteins participate in complex chemical feedback loops, perpetuating rhythmic genetic activity in which proteins are first produced and then degraded to drive circadian cycles. Similar chemistry operates in humans.

Key molecular players in keeping the bodys clocks ticking are the proteins known as CLOCK and BMAL1. Studies of liver cells in mice show that CLOCK partners with BMAL1 to regulate gene activity, driving all the important circadian chemical reactions. Generally in many cells you see a similar kind of picture, in the brain or other tissues, Takahashi said.

The CLOCK-BMAL1 tandem activates genes that produce several forms of the circadian proteins period and cryptochrome. In mice, that process starts work in daytime, leading to a substantial buildup of period (PER) and cryptochrome (CRY) by evening. At night, PER and CRY migrate into the cells nucleus and block the action of CLOCK-BMAL1, thereby halting production of PER and CRY themselves. PER and CRY amounts then diminish as other molecules degrade them. By morning, PER and CRY levels drop so low that CLOCK and BMAL1 are no longer disabled and can begin producing PER and CRY anew.

Many other molecules participate in circadian chemistry; the exact molecular participants differ from tissue type to tissue type. In the (mouse) liver alone, the activity of thousands of genes fluctuates on a circadian schedule.

An hourglass uses the flow of sand to mark time. The body uses the build-up and flow of proteins to keep its rhythms. Although there are numerous different players in the bodys many clocks, the workings of the circadian proteins period (PER) and cryptochrome (CRY) (and their counterparts CLOCK and BMAL1) exemplify the kind of feedback loop that keeps the body in sync with the day-night cycle.

While signals from the SCN set the daily schedule for circadian chemistry, various small molecules, such as many medicinal drugs, can disrupt cellular timing. (Thats one reason certain drugs such as blood thinners and chemotherapy treatments are more or less effective depending on the time of day that they are administered.) Researchers have identified dozens of small molecules that can influence circadian processes.

Some such molecules change the length of the circadian period. Some alter the precise timing of specific processes during the cycle. Others help maintain robust signals for synchronizing the bodys clocks. Circadian signaling weakens with age, possibly contributing to many age-related disorders such as impaired metabolism or sleep problems.

Among the common drugs that exert effects on the circadian system are opsinamides, sulfur-containing compounds that suppress the amount of light input into the SCN. Nobiletin, found in the peels of citrus fruits, manipulates circadian rhythms to improve metabolism in obese mice. (Nobiletin also counters tumors and inflammation.) Resveratrol is a well-known compound that alters the activity of certain clock genes, with some possible human health benefits.

Scientists have discovered a long list of existing medicines and small molecules now under investigation that act on or influence the bodys circadian system.

Todays challenge, Takahashi and coauthors say, is to identify the precise targets where small molecules exert their influence. Knowing the targets should help researchers find ways to repair defects in the circadian system or alleviate temporary inconveniences such as jet lag.

Jet lag occurs when sudden changes in time zone generate a mismatch between the body clocks expectations and the actual day-night cycle (not to mention timing of meals and social activities). While it is usually just an annoyance for travelers, shift workers face long-term consequences for working when the body clock advises sleep. Shift workers, Chen, Yoo and Takahashi point out, are at risk for sleep problems, gastrointestinal disorders, obesity, cardiovascular disease, cancer and mood disorders. Molecules tested in mice have shown promise for reconciling expectations with reality, getting the clock back in phase with the bodys environment.

Clock malfunction also affects the bodys disease-fighting immune system, and certain clock components have been identified as potential targets for alleviating autoimmune disease and excessive inflammation. Other recent studies have shown that molecular intervention with clock components can aid proper functioning of mitochondria, the cellular structures responsible for energy production.

While most of the details about circadian chemistry come from studies in mice, studies of human sleep disorders indicate that the basic circadian story is similar in people. A mutation in the human gene responsible for making one of the period proteins has been linked, for example, to familial advanced sleep phase disorder. (In people with that mutation, the normal sleep-wake cycles shift by several hours.) Other research has shown that a variant version of the human gene for cryptochrome protein increases the risk of diabetes.

An especially intriguing possibility is that body clock management could provide strategies for slowing down aging.

Many studies have shown that aging in some animal can be slowed by restricting food intake. Fewer calories can lead to longer lives. But work by Takahashi and others has found that (in mice, at least) timing of ingesting the calories can be almost as important as the quantity.

Mice allowed to eat a normal amount of calories, but only within restricted hours, have lived about 15 percent longer than usual, Takahashi reported at the neuroscience meeting. In humans, that would correspond to a life span increase from 80 years to 92.

Were super excited about these results, because these are the first experiments to show that you can extend life span by restriction of time of nutrient intake only without a reduction of calories, Takahashi said.

For us its much easier to restrict the time that we eat than the amount that we eat. Now if you can do both, thats even better. I think that this, I hope, could have benefit for human health and longevity in the future.

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Winding the body's clock - Knowable Magazine

Application closing date:13/01/2020Faculty / School or Service:Faculty of Health and Life SciencesSalary:51,044.00 - 63,684.00 per annumPackage:As one of Coventry's biggest employers, we offer some pretty impressive benefits including an excellent pension scheme and generous holiday allowances.Job category/type:Academic

Job description

Research within the Centre for Sport, Exercise and Life Sciences (CSELS), at Coventry University, reflects a broad range of sport, exercise and biological sciences to understand life from the molecular level through to the whole body. The Centre has considerable expertise, ranging from microbiology, cell biology, genomic and molecular biology, biochemistry,nutritionand food science, safety pharmacology, physiology, physical activity and sport performance.

As part of Coventry Universitys Research Strategy 2021 it is increasing its investment in quality research excellence with impact. As a result the Centre is looking to appoint a range of senior academic staff to provide strategic leadership in the management of our research. The fields of research expertise include; Therapeutics and Disease Prevention, Clinical and Molecular Exercise Physiology and Physical Activity, Exercise and Sport.

The following vacancies are currently available:

The successful candidates will have a PhD in a relevant subject, along with a track record of securing significant external funding and a substantial record of research and publications or other forms of dissemination (such as policy advice) in a relevant field, commensurate with a 3* REF rating. The post holders would be expected to have an international reputation with the ability to attract world-class academics to collaborate within their field of Research.

In addition you will be expected to seek and obtain funding to support the development of further research activities, conduct and publish original research and supervise research students working in this field. Developing the academic and commercial potential within the Centre to ensure this continues to reflect the leadership of Interdisciplinary Research whilst delivering excellence with impact in line with our Corporate Strategy.

These role provides a unique opportunity to join one of the UKs most forward thinking and successful modern Universities at a time of rapid expansion in our research capacity. The positions will be based in our new purpose-built research laboratories on the Coventry city campus.

If would like to find out more about this exciting opportunity please contact, Executive Director of the Centre, Professor Helen Maddockhelen.maddock@coventry.ac.ukTo find out more about our work and to tell us more about how you can contribute, visit ourwebsite

Click here for Job Description and Person Specification

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Associate Professor in Psychology of Physical Activity and Health job with COVENTRY UNIVERSITY | 190233 - Times Higher Education (THE)

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Newswise SILVER SPRING, Md.--A new analysis suggests that the increasing average body size of people on Earth, in addition to the growing world population may further challenge attempts to reduce man-made carbon dioxide emissions, according to a paper published online inObesity, the flagship journal of The Obesity Society.

All oxygen-dependent organisms on the planet produce carbon dioxide as a result of metabolic processes necessary to sustain life. Total carbon dioxide production from any species is linked to the average metabolic rate, the average body size and the total number of individuals of the species.

People with obesity have greater carbon dioxide production from oxidative metabolism than individuals with normal weight. Also, maintenance of greater body weights requires more food and drinks to be produced and transported to the consumers. Similarly, transportation of heavier people is associated with increased consumption of fossil fuels. This results in additional carbon dioxide emissions related to food production and transportation processes. Globally, obesity was estimated to contribute to an extra 700 megatons of carbon dioxide emissions per year or about 1.6 percent of all man-made emissions.

The authors emphasize that it is critically important that this new information does not lead to more weight stigmatization. People with obesity already suffer from negative attitudes and discrimination, and numerous studies have documented several prevalent stereotypes.

"This study makes it clear that we pay a steep price for making it difficult to access care for obesity. Not only does obesity affect the health of the individuals who have it, untreated obesity might also contribute to environmental issues," said Ted Kyle, RPh, MBA, founder of ConscienHealth, who was not involved in the research.

Physical activity is also associated with much more carbon dioxide being produced compared with rest, but no one will ever think of stigmatizing people who exercise for having a negative effect on the environment, according to Boyd Swinburn, MB ChB, FRACP, MD, FNZCPHM, in the School of Population Health at the University of Auckland in New Zealand. Swinburn wrote a commentary on the paper.

"Our analysis suggests that, in addition to beneficial effects on morbidity, mortality, and healthcare costs, managing obesity can favorably affect the environment as well," said Faidon Magkos, of the Department of Nutrition, Exercise and Sports at the University of Copenhagen in Denmark. "This has important implications for all those involved in the management of obesity." Magkos is the corresponding author of the paper.

To assess the impact of obesity on the environment, researchers used the standard definitions of obesity (body mass index of greater than or equal to 30 kg/m2) and normal weight (body mass index of less than 25). Calculations were made of the extra emission of greenhouse gases (carbon dioxide, methane, and nitrous oxide) from the increased oxidative metabolism, the increased food production and consumption and the increased fuel used to transport the greater body weight of people with obesity.

Compared with an individual with normal weight, researchers found an individual with obesity produces an extra 81 kg/y of carbon dioxide emissions from higher metabolism, an extra 593 kg/y of carbon dioxide emissions from greater food and drink consumption and an extra 476 kg/y of carbon dioxide emissions from car and air transportation. Overall, obesity is associated with approximately 20 percent greater greenhouse gas emissions when compared to people with normal weight.

"Harmonizing data from epidemiology (prevalence rates of obesity), physiology (total energy intake and expenditure) and environmental science (carbon dioxide emissions from different sources) is not a straightforward task, and we emphasize that our estimates are not intended to be precise, but rather be reasonable enough," said Magkos.

In the commentary accompanying the paper, Swinburn said the estimates add valuable information to the growing literature examining the nexus between obesity and climate change. He added, "while the contribution of obesity to greenhouse gas emissions is small, acting on the underlying drivers of them both is of paramount importance."

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Other authors of the study include Inge Tetens, Simon Ronnow Schacht, Susanne Gjedsted Bgel and Arne Astrup of the Department of Nutrition, Exercise and Sports at the University of Copenhagen in Denmark. Claus Felby of the Department of Geosciences and Natural Resource Management at the University of Copenhagen also co-authored the paper. Other authors include James Hill of the University of Alabama at Birmingham and Eric Ravussin of Louisiana State University's Pennington Biomedical Research Center in Baton Rouge, La.

The study, titled "The Environmental Foodprint of Obesity" will be published in the January 2020 print issue.

The Obesity Society (TOS) is the leading organization of scientists and health professionals devoted to understanding and reversing the epidemic of obesity and its adverse health, economic and societal effects. Combining the perspective of researchers, clinicians, policymakers and patients, TOS promotes innovative research, education, and evidence-based clinical care to improve the health and well-being of all people with obesity. For more information, visithttp://www.obesity.organd connect with us onFacebook,TwitterandLinkedIn.

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Study suggests obesity associated with greater greenhouse gas emissions - Newswise