About the position

A position as PhD candidate is open at the Cardiac Exercise Research Group, Department of Circulation and Medical Imaging, Faculty of Medicine and Health Sciences, NTNU (Trondheim, Norway). The group is headed by Professor Ulrik Wislff.

The position has fixed-term duration of three years (100%). At CERG we investigate the effects of exercise in chronic diseases, such as heart diseases, diabetes, and Alzheimers disease using a wide range of tools spanning from animal experiments to clinical trials and epidemiological studies. For more information about the Department and the research group, see the following pages:www.ntnu.edu/isbandwww.ntnu.edu/cerg.

This project consists of three complementary studies that aim to (1) explore the effect of increased cardiorespiratory fitness in exercise-trained older adults on their future risk of Alzheimers disease, (2) identify biomarkers in blood that might underlie the expected effect of increased fitness on the risk of Alzheimers disease and that could identify the future Alzheimers disease patients up to 8 years before clinical manifestation of the disease, and (3) detect changes in these biomarkers in early Alzheimers disease patients following treatment with blood plasma from exercise-trained donors. We seek a talented and diligent candidate with a high motivation and commitment to research.

Duties of the position

The successful candidate will be responsible for daily management of the projects, hereunder data collection, analysis and interpretation and communication of results.

Required selection criteria

Medical degree or Master`s degree in Molecular Medicine, Neuroscience, Biology, Biotechnology, Exercise Physiology, or equivalent program:

Preferred selection criteria

Emphasis will also be placed on:

Personal characteristics

NTNU is an equal opportunity employer and welcomes applicants from anywhere in the world. The university is strongly committed to diversity and welcomes applications from members of ethnic minorities. The appointment will be made in accordance with current regulations for employment at universities and university colleges in Norway.

We offer

Salary and conditions

Appointment to a PhD position requires that you are admitted to the PhD programme in within three months of employment, and that you participate in an organized PhD programme during the employment period.

It is a prerequisite you can be present at and accessible to the institution daily.

About the application

Applicants are asked to apply via this page, and to attach all relevant documents, see list below:

Candidates from universities outside Norway are kindly requested to send a Diploma Supplement or a similar document, which describes in detail the study and grade system and the rights for further studies associated with the obtained degree:http://ec.europa.eu/education/tools/diploma-supplement_en.htm

For inquiries regarding the position, please contact:

PhD Atefe R. Tari, Department of Circulation and Medical Imaging, NTNU, email: atefe.r.tari@ntnu.no

Professor Ulrik Wislff, Department of Circulation and Medical Imaging, NTNU, email: ulrik.wisloff@ntnu.no

For inquiries regarding the application procedures, please contact:HR Advisor Julie Hoff, email: julie.hoff@ntnu.no

General information

Working at NTNU

A good work environment is characterized by diversity. We encourage qualified candidates to apply, regardless of their gender, functional capacity or cultural background.

The city of Trondheimis a modern European city with a rich cultural scene. Trondheim is the innovation capital of Norway with a population of 200,000. The Norwegian welfare state, including healthcare, schools, kindergartens and overall equality, is probably the best of its kind in the world. Professional subsidized day-care for children is easily available. Furthermore, Trondheim offers great opportunities for education (including international schools) and possibilities to enjoy nature, culture and family life and has low crime rates and clean air quality.

As an employeeatNTNU, you must at all times adhere to the changes that the development in the subject entails and the organizational changes that are adopted.

In accordance with The Public Information Act (Offentleglova), your name, age, position and municipality may be made public even if you have requested not to have your name entered on the list of applicants.

Please submit your application electronically via jobbnorge.no with your CV, diplomas and certificates. Applications submitted elsewhere will not be considered.

If you are invited for interview you must include certified copies of transcripts and reference letters.

Application deadline: 10.01.2022

NTNU - knowledge for a better world

The Norwegian University of Science and Technology (NTNU) creates knowledge for a better world and solutions that can change everyday life.

The Department of Circulation and Imaging(ISB) has 260 employees, and its research units are at the Cardiothoracic Centre at St. Olavs Hospital, integrated with collaborating clinical divisions. The Department of Circulation and Medical Imaging (ISB) includes anaesthesiology, radiology, radiography, ultrasound, magnetic resonance imaging, exercise physiology, cardiovascular physiology, pulmonary physiology, pulmonary medicine, cardiology, vascular surgery, thoracic surgery and biomedical engineering.

The department is also responsible for the Centre for Innovative Ultrasound Solutions (CIUS), the Medical Simulation Centre and the MR Centre. More information about the department is available at http://www.ntnu.edu/isb

Deadline10th January 2022EmployerNTNU - Norwegian University of Science and TechnologyMunicipalityTrondheimScopeFulltimeDurationTemporaryPlace of serviceya cmapus

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PhD Position in the Project, Molecular Secrets of Fitness to Prevent Diagnose and Treat Alzheimer's job with NORWEGIAN UNIVERSITY OF SCIENCE &...

DUBLIN--(BUSINESS WIRE)--The "Global Regenerative Medicine Market Size, Share & Trends Analysis Report by Product (Cell-based Immunotherapies, Gene Therapies), by Therapeutic Category (Cardiovascular, Oncology), and Segment Forecasts, 2021-2027" report has been added to ResearchAndMarkets.com's offering.

The global regenerative medicine market size is expected to reach USD 57.08 billion by 2027, growing at a CAGR of 11.27% over the forecast period.

Recent advancements in biological therapies have resulted in a gradual shift in preference toward personalized medicinal strategies over the conventional treatment approach. This has resulted in rising R&D activities in the regenerative medicine arena for the development of novel regenerative therapies.

Furthermore, advancements in cell biology, genomics research, and gene-editing technology are anticipated to fuel the growth of the industry. Stem cell-based regenerative therapies are in clinical trials, which may help restore damaged specialized cells in many serious and fatal diseases, such as cancer, Alzheimer's, neurodegenerative diseases, and spinal cord injuries.

For instance, various research institutes have adopted Human Embryonic Stem Cells (hESCs) to develop a treatment for Age-related Macular Degeneration (AMD).

Constant advancements in molecular medicines have led to the development of gene-based therapy, which utilizes targeted delivery of DNA as a medicine to fight against various disorders.

Gene therapy developments are high in oncology due to the rising prevalence and genetically driven pathophysiology of cancer. The steady commercial success of gene therapies is expected to accelerate the growth of the global market over the forecast period.

Regenerative Medicine Market Report Highlights

Key Topics Covered:

Market Variables, Trends, & Scope

Competitive Analysis

Covid-19 Impact Analysis

Regenerative Medicine Market: Product Business Analysis

Regenerative Medicine Market: Therapeutic Category Business Analysis

Regenerative Medicine Market: Regional Business Analysis

Companies Mentioned

For more information about this report visit https://www.researchandmarkets.com/r/kovhgl

Link:
Global Regenerative Medicine Market is Expected to Reach USD 57.08 Billion by 2027, Growing at a CAGR of 11.27% Over the Forecast Period. -...

STOCKHOLM, Dec. 23, 2021 /PRNewswire/ -- Betagenon AB a Sweden-based company focused on development of AMPK activator compounds, today announced the publication by co-founder Helena Edlund of a new study demonstrating the prevention and reversal of gene expression and epigenetic changes to beta cells in diet-induced obese mice. Treatment with O304 prevented genome-wide gene expression changes associated with high fat diet and remodelled active and repressive chromatin markers in beta cells, the cells responsible for producing the body's insulin. Glucose control was restored in the animals and markers of stress were reduced and markers of function increased in the beta cells.

The data are published in Scientific Reports, a member of the Nature family of journals.

"Obesity and associated insulin resistance stresses our beta-cells. If this persists long enough it will lead to beta-cell failure and the body will not be able to produce and secrete insulin, resulting in the development of diabetes. Our work identifies changes at the genetic level as the beta cells become stressed and show that these changes can be prevented by treatment with O304" said Prof. Helena Edlund of the Ume Centre for Molecular Medicine, and one of the senior authors of the study.

"A narrow window exists after diabetes onset when stressed beta cells can be rescued and their function normalized. These important results give us insight into the genetic changes involved in this process and are a key part in understanding the treatment potential of O304 in helping diabetic patients to remission" said Dr. James Hall, Betagenon CEO.

O304 is a first in class non-allosteric pan-AMPK activator. O304 sodium salt is in clinical development to treat Heart Failure, Renal Disease and Insulin Resistance.

Betagenon isa clinical stage company that develops its proprietary AMPK activators as therapies for diseases and conditions associated with the global epidemic in metabolic disorders and an aging population.

For more information, contact:

James Hall, CEO Betagenon AB

james.hall@betagenon.com+46 70 5775300

Helena Edlund received funding from Vetenskapsrdet, Familjen Erling-Perssons stiftelse, and

Knut och Alice Wallenbergs Stiftelse for the study.

This information was brought to you by Cision http://news.cision.com

https://news.cision.com/betagenon-ab/r/betagenon-co-founder-publishes-that-ampk-activator-o304-prevents-gene-expression-changes-and-remobil,c3478094

The following files are available for download:

View original content:https://www.prnewswire.com/news-releases/betagenon-co-founder-publishes-that-ampk-activator-o304-prevents-gene-expression-changes-and-remobilisation-of-histone-marks-in-islets-of-diet-induced-obese-mice-301450397.html

SOURCE Betagenon AB

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Betagenon co-founder publishes that AMPK activator O304 prevents gene expression changes and remobilisation of histone marks in islets of diet-induced...

CDC's "Nowcast" estimates that omicron likely became the dominant variant in the United States late last week. But experts say that America's understanding of the variant's spread is limited and comes with considerable uncertainty, underscoring the shortcomings of the United States' Covid-19 surveillance.

The policies Biden and states could use to control the omicron variant

Data from the World Health Organization's (WHO) newest weeklyepidemiological report showed the United States had the highest number of new cases in the world last weekat 725,750, between Dec. 13 and Dec. 19CNN reports. On a global level, WHO estimated there were 4.1 million new Covid-19 cases over that same time frame.

According to CNN, the delta variant remains the dominant coronavirus strain globally. However, WHO's weekly report showed that the omicron variant, which has been confirmed in 106 countries, is surging and poses a significant risk.

"Recent evidence indicates that [the] omicron variant has a growth advantage over the delta variant and is spreading rapidly, even in countries with documented community transmission and high levels of population immunity," WHO said.

This data appeared to align with new CDC data released Monday via the agency's "Nowcast" variant surveillance data, STAT News reports. According to "Nowcast," the omicron variant likely became the most common variant in the United States at the end of last week.

That said, some experts caution that CDC's numbers from the last two weeks have been estimated using models that likely contain sizable margins for error. Nonetheless, the estimates seem comparable to the limited real-world data from countries where omicron was detected early on, STAT News reports.

Notably, STAT News said CDC estimates indicated that hospitalizations are increasing at a more modest rate than the increase in overall casesalthough this could change going forward, as hospitalizations tend to lag behind case reports.

For its part, WHO said of the recent global surge in cases, "Given rapidly increasing case numbers, it is possible that health care systems may become overwhelmed. Preliminary data suggest that there is a reduction in neutralization of omicron in those who have received a primary vaccination series or in those who have had prior SARS-CoV-2 infection, which may suggest a level of humoral immune evasion."

As a result, WHO said that "the overall risk related to the new variant of concern omicron remains very high."

Amid surging omicron cases, health officials and scientists in the United States still struggle to gather reliable data almost two years into the pandemic, Politico reports.

Part of the issue is that even though most Covid-19 tests can detect the coronavirus, they can't identify each individual variant. That's because the tests detect parts of the virus that don't typically change. To determine which variant is present, a sample needs to be sent out to a lab to be genetically sequenced. According to experts, this has created a weakness in the United States' surveillance of coronavirus variants, leaving the country to rely mostly on data from other countries.

According to Politico, this continued dependence on international dataeven now, nearly two years into the pandemichighlights the degree to which U.S. public health data has failed to produce accurate, timely data on both the spread of the virus and the degree to which it evades the vaccine.

"I think we've done a horrible job from day one in data tracking for the pandemic," said Eric Topol, a professor of molecular medicine at Scripps Research and former advisory board member of theCovid Tracking Project. "We're not tracking all the things that we need to get a handle on what's going on. It is embarrassing."

Separately, National Institute of Allergy and Infectious DiseasesDirector Anthony Fauci said there's data "coming in from the U.K., from Israel, [and] from South Africa, which is ahead of the rest of the world in the experience they're having with omicron." But while that's enabled the United States to get the "virus either in the live virus form or in the pseudo virus form, we don't have enough of this in the United States to be able to bank on our own clinical experience which is in contrast to the South Africans who are in real time experiencing the clinical impact of omicron."

In conversations with Politico, several public health experts said the federal government needs to invest more in the nation's surveillance systems so they can better handle another surge in Covid-19 surge or a new pandemic.

CDC has made recent financial investments to improve genomic sequencing and data systems. However, the agencyas well as various state and local public health departmentsrely on outdated data systems that are often dependent on manual data input, subject to slow lab turnaround times, and suffering from a shortage of public health workers. And Politico reports that, according to state officials, CDC's recent financial investments on this front will likely take "several years to implement" as well as sufficient federal funding.

"It will be very important that we identify ways to have sustainable support for these non-categorical activities like data modernization," said Dan Jernigan, the deputy director of the CDC's Public Health Science and Surveillance office. He added, "That's something that we look to our partners in Congress to identify how best to support the ongoing need for maintaining a good data infrastructure."

And until the United States has a sufficient data-tracking system for this type of surveillance, experts told Politico the country will still depend on other nations' data.

"We're relying on everyone else's data. We should be providing data to the world and we are not," said Zeke Emanuel, a bioethicist and former member of President Joe Biden's transition Covid-19 advisory board. "We started [the pandemic] with a serious problem of not enough data and bad data infrastructure. We have not made the structural investments we need. The ideal is that we have real time data. And we don't have that. We're not even close to that." (Langmaid, CNN, 12/21 [1]; Parker, STAT News, 12/21; Langmaid, CNN, 12/21 [2]; Banco, Politico, 12/21)

The rest is here:
Why some experts say Covid-19 surveillance in the US 'is embarrassing' - The Daily Briefing

Inflammatory lesion in the spinal cord of a mouse model of multiple sclerosis demonstrating the presence of ILC3 (green) or T cells (red). Credit: Image courtesy of Dr. Christopher N. Parkhurst

A group of immune cells that normally protect against inflammation in the gastrointestinal tract may have the opposite effect in multiple sclerosis (MS) and other brain inflammation-related conditions, according to a new study by Weill Cornell Medicine and NewYork-Presbyterian researchers. The results suggest that countering the activity of these cells could be a new therapeutic approach for such conditions.

The researchers, who reported their findings on December 1, 2021, in the journal Nature, were studying a set of immune cells called group 3 innate lymphoid cells (ILC3s), which help the immune system tolerate beneficial microbes and suppress inflammation in the intestines and other organs throughout the body. They discovered a unique subset of these ILC3s that circulate in the bloodstream and can infiltrate the brainand, to their surprise, do not quench inflammation but instead ignite it.

The scientists called this subset inflammatory ILC3s, and found them in the central nervous system of mice with a condition modeling MS. Instead of constraining the immune response, this subset of ILC3s spurred another group of immune cells called T cells to attack myelinated nerve fibers, leading to MS-like disease symptoms. The researchers detected similar inflammatory ILC3s in the peripheral blood and cerebrospinal fluid of MS patients.

This work has the potential to inform our understanding of, and potential treatments for, a broad variety of conditions involving T-cell infiltration of the brain, said senior author Dr. Gregory Sonnenberg, associate professor of microbiology and immunology in medicine in the Division of Gastroenterology and Hepatology and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine.

MS affects more than two million people worldwide. Other conditions that feature chronic brain inflammation afflict tens of millions more and include Alzheimers and Parkinsons diseases. There is also evidence that neuroinflammation develops naturally with aging and is a major factor in age-related cognitive decline, and more recently inflammatory T-cell responses in the brain have been linked to neurological symptoms associated with SARS-CoV-2 infection.

The researchers have shown in recent work that ILC3s residing in the gut act as sentinels and immune regulators, suppressing inflammationincluding inflammatory T-cell activityand warding off cancer. In the new study, they examined the roles of ILC3s in the brain, and found, contrary to their expectation, that ILC3s are not normally present in the brain under healthy conditions but can infiltrate the brain from the bloodstream during inflammation. When they do infiltrate the central nervous system, they have pro-inflammatory rather than anti-inflammatory effects.

The researchers showed with a mouse model of MS that these inflammatory ILC3s in the brain function as antigen-presenting cells: They display bits of myelin protein, the main ingredient in the insulating layer around nerve fibers, to T cellsprompting them to attack myelin, causing the nerve damage that gives rise to disease signs. They found the inflammatory ILC3s in close association with T cells in regions of active inflammation and nerve damage in the mouse brains.

The infiltration of these inflammatory ILC3s to the brains and spinal cords of mice coincides with the onset and peak of disease, said first author John Benji Grigg, a Weill Cornell Graduate School of Medical Sciences doctoral candidate in the Sonnenberg laboratory. Further, our experimental data in mice demonstrate these immune cells play a key role in driving the pathogenesis of neuro-inflammation.

The researchers discovered that they could prevent MS-like disease in the animals by removing from the ILC3s a key molecule called MHCII, which normally is used in the antigen-presenting processthe removal essentially blocks the cells ability to activate myelin-attacking T cells.

Despite our very best disease-modifying therapies for MS, patients continue to progress, and since disease onset is early in life, they face the prospect of permanent physical and cognitive disability, said co-author Dr. Tim Vartanian, professor of neuroscience in the Feil Family Brain and Mind Institute at Weill Cornell Medicine, chief of the division of multiple sclerosis and neuro-immunology and a professor of neurology in the Department of Neurology at Weill Cornell Medicine and NewYork-Presbyterian/Weill Cornell Medical Center. Identification of inflammatory ILC3s with antigen presentation capabilities in the central nervous system of people with MS offers a new strategic target to prevent nervous system injury.

Finally, the researchers discovered that ILC3s that reside in other tissues in the body can be programmed, in effect, to counter the activity of brain-infiltrating T cells, preventing the MS-like condition disease in mice.

This work was completed in close collaboration with Dr. Ari Waisman, director of the Institute for Molecular Medicine at the University Medical Center of Johannes Gutenberg University Mainz, where the researchers built on prior research demonstrating that there are gut-resident ILC3s that display antigens to T cells in a slightly different way to promote T-cell inactivity, or tolerance. The researchers demonstrated that by experimentally exposing these tolerance-inducing intestinal ILC3s to myelin, they could block neuroinflammatory T-cell activity and the development of MS-like disease in the mice.

The work therefore points to the possibility that MS and potentially many other inflammatory conditions could someday be treated either by directly inhibiting the activity of inflammatory ILC3s that infiltrate the brain, or by targeting self-antigens to the intestinal ILC3s that promote tolerance in other tissues, Dr. Sonnenberg said.

Reference: Antigen-presenting innate lymphoid cells orchestrate neuroinflammation by John B. Grigg, Arthi Shanmugavadivu, Tommy Regen, Christopher N. Parkhurst, Anees Ahmed, Ann M. Joseph, Michael Mazzucco, Konrad Gronke, Andreas Diefenbach, Gerard Eberl, Timothy Vartanian, Ari Waisman and Gregory F. Sonnenberg, 1 December 2021, Nature.DOI: 10.1038/s41586-021-04136-4

The Sonnenberg Laboratory is supported by the National Institutes of Health (R01AI143842, R01AI123368, R01AI145989, R01AI162936, R21CA249284 and U01AI095608), the NIAID Mucosal Immunology Studies Team (MIST), the Crohns and Colitis Foundation, the Searle Scholars Program, the American Asthma Foundation Scholar Award, Pilot Project Funding from the Center for Advanced Digestive Care (CADC), an Investigators in the Pathogenesis of Infectious Disease Award from the Burroughs Wellcome Fund, a Wade F.B. Thompson/Cancer Research Institute (CRI) CLIP Investigator grant, the Meyer Cancer Center Collaborative Research Initiative, the Dalton Family Foundation, Linda and Glenn Greenberg, and the Roberts Institute for Research in IBD. Gregory F. Sonnenberg is a CRI Lloyd J. Old STAR. John Benji Grigg is supported by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health under Award Number F31AI138389-01A1. Support for human sample acquisition through the JRI IBD Live Cell Bank is provided by the JRI, Jill Roberts Center for IBD, Cure for IBD, the Rosanne H. Silbermann Foundation and Weill Cornell Medicine Division of Pediatric Gastroenterology and Nutrition.

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Enigmatic Immune Cells May Ignite Inflammation in Multiple Sclerosis and Other Brain Disorders - SciTechDaily