StemCell Therapy

New research by Dorothy P. Schafer, PhD, at the University of Massachusetts Medical School, reveals the molecular process in which synaptic connections in the brain are damaged in multiple sclerosis and how this contributes to neurodegenerative symptoms. The paper, published in Immunity, also shows how gene therapy may be used to preserve neural circuits and protect against vision loss in the disease.

These findings suggest a path for developing therapies that may protect synapses from the damaging effects of MS and could be broadly applicable to other neurodegenerative disorders, according to Dr. Schafer, assistant professor of neurobiology, and Sebastian Werneburg, PhD, a postdoctoral fellow in the Schafer lab.

"Most MS research and FDA-approved treatments focus on demyelination and axon death," said Schafer. "Far less is known about what happens to the synaptic connections between neurons, which has proven to be a key aspect of neurodegeneration likely leading to cognitive decline in other diseases such as Alzheimer's disease."

Multiple sclerosis is a neurological disease of the central nervous system affecting more than 2 million people worldwide. The disease involves an abnormal response of the body's peripheral immune system against the brain, spinal cord and optic nerves, which damages the fatty substance surrounding nerve fibers called myelin. Recurrent episodes of inflammation result in demyelination. As the myelin is stripped away, the nerve fibers are exposed to inflammatory attacks from the immune system and the transmission of nerve signals within the central nervous system are altered or stopped completely. A small subset of MS patients experience chronic progressive neurodegenerative symptoms accompanied by significant synaptic loss and central nervous system atrophy. This version of the disease is called progressive MS.

FDA-approved medications for treating MS have been developed to limit and reduce the number of relapses, which delay progression of the disease and minimize demyelination, but there is no cure for the disease and patients are still left with disability. Current therapies work to inhibit peripheral immune attack of the central nervous system and inflammatory demyelination, but the neurodegenerative aspects of the disease have proven harder to decelerate, particularly for patients with progressive MS.

Vison loss is one of the most common symptoms of MS and is often one of the first that patients notice. Problems with vision result from damage to the optic nerve that connects the eye to the brain or from lack of coordination in the eye muscle.

"The retinogeniculate system, which comprises neurons that extend their axons via the optic nerve to the thalamus in the brain, is an ideal model for investigating MS because it's easy to access for therapeutic intervention, subtle changes can be readily detected and the visional pathway is affected in almost half of all patients with the disease," said Dr. Werneburg.

Profound synaptic loss was observed in animal models as microglia engulfed and eliminated presynaptic connections. Microglia are the immune cells of the central nervous system and are emerging as key players in regulating neural circuit structure in health and disease. One of the vast number of functions microglia perform in the brain is similar to the role macrophages perform in the immune system: clearing cellular decay and dead neurons from tissue.

"We found the protein C3 in abundance at synapses," said Werneburg.

C3 is not normally found in adult brain tissue. C3 protein usually only shows up in neural tissue during the developmental stages of the brain when synapses are being pruned. Synaptic pruning eliminates weak or unused synapsis as the brain matures to help efficiency and conserve energy.

In the case of demyelinating disease, it is not known why C3 is being produced and activated. This complement protein binds to synapses, sending the signal to microglia that the otherwise healthy-seeming synapse should be eliminated. This leads microglia to attack synapses.

Schafer, in collaboration with Guangping Gao, PhD, the Penelope Booth Rockwell Professor in Biomedical Research, professor of microbiology & physiological systems, director of the UMMS Horae Gene Therapy Center and Viral Vector Core, and co-director of the Li Weibo Institute of Rare Disease, used a gene therapy approach and adeno-associated virus to deliver Crry, an inhibitor of C3, specifically to synapses in the visual system while leaving the rest of the brain untouched, to see if synapses could be spared and vision preserved. Crry is a natural inhibitor of complement proteins such as C3. These regulators help protect cells or tissue from unwanted attack by the immune system.

After injection of the AAV into the circuit, Crry localized to synapses and successfully preserved them by binding to C3 so microglia couldn't damage them.

"As a result of this inhibition, we saw improved visional function in mice," said Werneburg.

Schafer said the protective effects of the AAV-delivered inhibitor were specific to the visual circuit. "It's possible that therapies targeting different circuits of the brain can be used to protect against synaptic damage in other neurodegenerative diseases such as Alzheimer's."

The next step for Schafer and colleagues will be to determine how the C3 protein is being activated and produced during MS and other neurodegenerative diseases.

Reference: Werneburg, S., Jung, J., Kunjamma, R. B., Ha, S.-K., Luciano, N. J., Willis, C. M., Gao, G., Biscola, N. P., Havton, L. A., Crocker, S. J., Popko, B., Reich, D. S., & Schafer, D. P. (2020). Targeted Complement Inhibition at Synapses Prevents Microglial Synaptic Engulfment and Synapse Loss in Demyelinating Disease. Immunity, 52(1), 167-182.e7. https://doi.org/10.1016/j.immuni.2019.12.004

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

Link:
Gene Therapy Protects Eyesight in Models of Multiple Sclerosis - Technology Networks

Early research in animal models and human samples reveals how loss of communication between nerve cells contributes to the symptoms of multiple sclerosis (MS), and shows how gene therapy could be used to preserve such connections and protect againstvision loss.

Researchers say their work identifies a new approach for developing MS therapies that target nerve cell communication, rather than myelin loss, and could be applicable to other neurodegenerative disorders.

The study, Targeted Complement Inhibition at Synapses Prevents Microglial Synaptic Engulfment and Synapse Loss in Demyelinating Disease, was published in the journal Immunity.

MS is a neurological disease marked by inflammation and a self-attack of the immune system against a persons brain, spinal cord, and optic nerves.

This attack damages the protective fatty substance covering nerve fibers (axons), which are necessary for proper transmission of nerve signals called myelin. As the myelin sheath is lost (demyelination), the communication between nerve cells is damaged or even interrupted, and nerve cell death occurs, leading to a range of disease symptoms.

Some MS patients experience a version of the disease called progressive MS, in which symptoms continuously worsen over time while their central nervous system (brain and spinal cord) shrinks (atrophies), and the junctions at which nerve cell terminals meet to communicate with each other, called synapses, are lost.

The majority of MS medications work to inhibit the self-attacking immune responses and inflammatory demyelination, but the neurodegenerative aspects of the disease have been more difficult to stop, particularly for patients with progressive MS.

Most MS research and FDA-approved treatments focus on demyelination and axon death, Dorothy P. Schafer, PhD, professor at the University of Massachusetts Medical School, said in a press release.

Far less is known about what happens to the synaptic connections between neurons, which has proven to be a key aspect of neurodegeneration likely leading to cognitive decline in other diseases such as Alzheimers disease, Schafer said.

Using tissue samples from deceased MS patients, a primate model of MS, and mice models of demyelinating disease, Schafer and colleagues investigated how synapses change during MS.They specifically looked at synapses involved in transmitting visual information from the eye to the brain via the optic nerve.

According to the studys first author, Sebastian Werneburg, PhD, a postdoctoral researcher at Schafers lab, the visual system is an ideal model for investigating MS because its easy to access for therapeutic intervention, subtle changes can be readily detected, and the visional pathway is affected in almost half of all patients with the disease.

Most MS patients experience vision problems at some point, which result from damage to the optic nerve or from lack of coordination in the eye muscle. These problems can be the first indication of the disease.

Similar to other neurodegenerative diseases, researchers found a profound synaptic loss in patient samples as a consequence of immune cells called microgliaeating nerve cell connections.

Microglia are cells that serve as one of the first and main forms of immune defense in the central nervous system, acting to clear cellular debris and dead neurons via phagocytosis a process by which some cells engulf other cells or particles.

In mice, synapse loss occurred independently of local demyelination and neuronal degeneration, but coincided with a rise in a specific immune factor called C3. C3 is part of the complement system, and is normally not present in the brains of adults. It is produced and activated during demyelinating diseases, but it is not clear why.

As C3 was seen to bind to synapses in models of MS, researchers reasoned this complement protein might be involved with the ongoing destruction of synapses in mice with MS-like disease.

To test this hypothesis, they specifically neutralized C3 at synapses of the visual pathway using gene therapy in mice. The strategy basically worked by delivering genetic material to synapses that provided instructions for the production of a C3 inhibitor.

After injection of the therapy, the inhibitor successfully blocked C3, reduced microglia engulfment, and preserved nerve cell connections, which improved eyesight in mice.

As a result of this inhibition, we saw improved visional function in mice, Werneburg said.

Overall, based on the results, the team believes that C3 probably is sending a signal to microglia telling them to eliminate synapses.

The next step will be to determine how C3 turns active during MS and other neurodegenerative diseases.

Its possible that therapies targeting different circuits of the brain can be used to protect against synaptic damage in other neurodegenerative diseases such as Alzheimers, Schafer said.

Ana is a molecular biologist with a passion for discovery and communication. As a science writer she looks for connecting the public, in particular patient and healthcare communities, with clear and quality information about the latest medical advances. Ana holds a PhD in Biomedical Sciences from the University of Lisbon, Portugal, where she specialized in genetics, molecular biology, and infectious diseases

Total Posts: 1,053

Patrcia holds her PhD in Medical Microbiology and Infectious Diseases from the Leiden University Medical Center in Leiden, The Netherlands. She has studied Applied Biology at Universidade do Minho and was a postdoctoral research fellow at Instituto de Medicina Molecular in Lisbon, Portugal. Her work has been focused on molecular genetic traits of infectious agents such as viruses and parasites.

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Gene Therapy Recovers Vision in Mice Models of MS, Uncovers How... - Multiple Sclerosis News Today

Glaucoma is a serious and lifetime eye disease that can cause permanent vision loss if not controlled before time. The Australian researchers have studied 107 genes that are involved in increasing the risk of eye disease glaucoma and identified a genetic test for those who are at the risk of getting blind.

The researchers are in search of many other genes that cause eye disease. The research conducted by the QIMR Berghofer Medical Research Institute and FlinUniversity finds that glaucoma-related blindness happens due to optic nerve degeneration and it is the most important cause of blindness in the whole world and researchers predicts that 76 million people will be affected by it in 2020. Possible cure for glaucoma is not found yet and fifty percent of people dont know that they are living with glaucoma.

This research was published in the journal Nature Genetics.

Stuart MacGregor, an associate professor of QIMR Berghofers Statistical Genetics Group explains that with the help of newly identified genes the people with eye disease can be identified with the help of a glaucoma polygenic risk score (PRS).

MacGregor finds that the only way to stop the loss of eyesight from genetic disease glaucoma is the discovery and the treatment of disease before time.

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It can be determined which person has eye disease or who will have in the future and need early treatment by analyzing the DNA taken from blood or saliva. If the people came to know before the time that in the future they will get glaucoma, they can take basic precautions that can prevent them from getting glaucoma.

Professor Jamie Craig, a clinical lead researcher and Academic Head of Ophthalmology at Flinders University, hopes that mass screening will be accessible for glaucoma in the next years.

Professor Craig finds that if the people are given a proper treatment earlier can be prevented from blindness. Many people come to know about glaucoma when visits the optometrist for a normal eye check-up or the loss of vision is felt by them. The early detection of glaucoma is necessary because the lost vision cant be restored even if the treatments are provided. The late detection is the main reason for blindness.

Most of the people are affected with glaucoma in older age but it can occur at any time of age. The researchers want to suggest blood tests to the older people that will help in the detection of glaucoma and will protect them from blindness.

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To identify the more genes the researchers want to sign up twenty thousand people with the record of disease in family or person to connect them with the Genetics of Glaucoma Study

This will benefit the researchers to approach all those people who are at high risk of disease or to those who are at lower risk and can be protected from getting blind by providing them the existing treatments. This study provides new insights for people with weak eyesight who are near to fifty to pay more attention to regularly visit the optometrist. It would protect their eyes and reduce the risk of permanent blindness in later years.

Link:
Early Detection And Prevention Of Blindness Associated With Glaucoma - TheHealthMania

A Mayo woman is raising funds for her niece who is losing her sight from three different eye conditions.

Magdalena Krawiec, originally from Poland, wants to help her goddaughter Zuzia Krawiec to get the best care possible.

Zuzia, four, was born with an eye disease called congenital nystagmus, which can be caused with the eye itself or by a problem with the visual pathway from the eye to the brain.

Around four months after she was born, Zuzia was then diagnosed with hyperopia astigmatism.

The condition affects Zuzias sight so that objects close to her are out of focus.

This along with her mcular hypoplasia, which she was only diagnosed with recently, make it impossible for her to see anything in detail.

Her aunt told Extra.ie: The macular hypoplasia is the worst because theres not much we can do about it.

It affects the vision clarity and because of it she will never be able to see clearly. She can only see as far as one metre and its basically shadows and lights

Were working on her sight so that she will eventually be able to see 10 or 15 metres in front of her but thats going to be over many years.

Zuzia has to take medication and do exercises to help her eyes improve but shes also had to have surgeries.

Shes had one of ten surgeries so far and the family are looking into stem cell treatment, which more people are interested in in recent years.

The family hope to schedule her second operation soon as the masses are really loose behind her eye and they need to tighten those muslces.

This operation will held Zuzias eyeball become more steady and so help her look straight because right now theyre all over the place.

Theyre kind of shaky, Magdalena continued. Thats the problem.

Zuzia is currently in play school but once a week she goes to a special school where she does two hours of different exercises for children with disabilities.

One hour she learns how to use her hands to recognise objects and another hour Zuzia uses an optical enlarger, something her family hopes to buy her so she can see things better.

It will be able to help her see better as it makes pictures at least 50 times larger, Magdalena said.

Zuzia needs constant care, her aunt tells Extra.ie, so that she doesnt hurt herself as she walks around.

Magdalena said: She needs help going to the toilet or going outside, anything where there may be obstacles in her way.

She cant see so she could walk into a wall or something, she could hurt herself.

Zuzia will never have the same sight the average person has, but with the operations she may gain better sight.

Magdalena revealed that she and her family dont know the root of the problem and hope genetic tests will help them get an idea of what is going on.

The genetic tests have to be done through the national health service and can take two to three years, but another huge hit is the cost of the tests.

Its around 2,500, Magdalena said. Its ridiculous because shes young, we need to do it as quick as possible.

The brain is getting used to the eyes not working, so the quicker we get it fixed the better. We want her to actually see something.

Despite her eyesight, Zuzia is a happy child and a big sister to her baby brother.

However, Zuzia has started asking about her brothers sight, wondering: How come he can see and I cant?

Its heartbreaking, Magdalena admitted. Its hard to explain to her that her eyes are sick.

To help her family, Magdalena set up a GoFundMe page to raise money for Zuzias operation and her care, which you can donate to here.

Magdalena has also has a collection point in The Breadski Brothers store in Westport to help raise funds.

She really needs specialised care, especially during these early years in her development, to improve her chances of avoiding total blindness and giving her the childhood she deserves.

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Mayo woman raising funds for niece, 4, who is losing her sight from three different eye conditions - Extra.ie

Dr Ezekiel Tallam with patients who have undergone surgery to treat trachoma, on January 14. [Mercy Kahenda, Standard]For a 70-year-old with impaired vision and no one to help him back up when he stumbles, life can be a punishment. Asman Chepochepunjo has been living alone inChemsarel village in Tiaty, Baringo County, after he was abandoned by his family when he became blind.He resorted to traditional herbs, but the condition worsened, making it hard for him to look after his livestock in the rocky locality.On the verge of becoming blind, Mr Chepochepunjo learnt he was suffering from trachoma, a neglected tropical disease in Baringo County.

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Hope in sight for locals as cases of punishing eye disease reduce - Standard Digital

A new study suggests its time you stopped worrying about cutting carbs or limiting the amount of fat in your diet. To live longer, its more important to focus on the quality of the foods than the quantity of carbs or fats they contain, according to a study from the JAMA Internal Medicine journal.

This means limiting processed carbohydrates, sugar, red meat and processed meats, and emphasizing whole grains, nuts, fruits and vegetables.

In the study, researchers asked more than 37,000 adults in the United States what they ate in the course of a 24-hour period in 1999 then followed them for 15 years.

At the end of the study the average age of the participants was 50 years old, and 4,866 of them had died around 13 percent of the group. Justless than half of those who died succumbed to heart disease (849 people) or cancer (1,068 people), certain types of which have been linked to diet.

Researchers found no difference in the risk of death between people on low-fat versus low-carb diets. Instead, the sources of those carbs or fats was what either risked or helped prevent an early death.

Low-fat diets full of unhealthy foods such as white bread, processed meats and sugary soda were associated with a 12 percent elevated risk of death, while similarly unhealthy low-carb diets made people 16 percent more likely to die.

People eating low-fat and low-carb diets composed of healthy foods including vegetables, fruits, legumes and whole grains lived longer, enjoying a 27 percent decreased risk of death.

Low-carb or low-fat diets can be good or bad depending on the foods that go into them, researcher Andrew Mente, who wasnt involved in the study, told Reuters.

Its more about selecting whole natural or minimally-processed foods, regardless of the amount of carbs or fat, Mente told Reuters. This would translate into a diet that may include a variety of whole foods in various combinations including fruit, vegetables, legumes, nuts and fish as well as whole fat dairy and unprocessed red meat and poultry.

Originally posted here:
New study says low-carb and low-fat diets don't boost longevity. Here's what does. - The Hill

(Editors note: This article is part of an editorial partnership between Next Avenue and The American Federation for Aging Research (AFAR), a national nonprofit whose mission is to support and advance healthy aging through biomedical research.)

Are you as old as you feel, as old as you look or as old as your birth certificate says? The best answer may be none of the above.

Actually, you may be as biologically old as your blood says you are.

For many years, aging researchers have sought markers of biological age, or biomarkers simple signals that reveal the expected length of your future health. The expected length of future health, after all, is the key biological difference between younger and older people.

Some people have called such markers biological clocks. I dont know about you, but I dont typically calculate my age by thinking of clocks. I think of calendars. So, I prefer to call these hypothetical signals biological calendars.

Plasma proteins may turn out to be just the type of biological calendar we are seeking.

The importance of these calendars is that they potentially allow researchers to quickly see whether a new drug, diet or other treatment that purports to slow, or even possibly reverse, aging is actually doing so.

Biological calendars of aging can also provide rapid feedback on how a lifestyle change, such as in diet or exercise habits, is affecting your biological age. This insight can motivate people to stick with that change.

Now, as a biological calendar, blood is a devilishly complex stew. Like a stew, it is liquid with lumps in it. We call the liquid plasma; the lumps, cells. Physicians for the past century have been using chemical analysis of plasma and counts of the various blood cell types to diagnose diseases. But we are now entering a brave new world of blood analysis.

Plasma contains not just the dozen or two chemicals that standard laboratory tests measure; it contains a constantly changing mixture of vitamins, nutrients, waste products, hormones and thousands of different proteins.

A hint that plasma might hold secrets about aging has come from research in which the plasma from young mice (or humans!) was found to rejuvenate the function of muscles, brain, heart and other organs of old mice. Dracula, it turns out, may have been onto something.

Recent advances in chemical analysis allow us to measure thousands of plasma chemicals at once, and advances in machine learning are helping make sense of that torrent of information. Plasma proteins may turn out to be just the type of biological calendar we are seeking.

I say this because a recent study of about 3,000 plasma proteins found that a specific combination of 373 of these proteins could accurately tell the age of the person from whom it was drawn. The study was conducted by AFAR Scientific Director Dr. Nir Barzilai with AFAR grantees David Gate of Stanford University and Dr. Sofiya Milman and Dr. Joe Verghese, both from the Albert Einstein College of Medicine in New York.

On top of that, people who were judged by their proteins to be younger than their real age scored better on a panel of physical and mental tests. We dont know yet how well these proteins might predict future health or life, but those studies will soon follow.

Blood cells, in addition to plasma, might have an even more promising aging tale to tell.

Your white blood cells (but not your red cells) contain your DNA, which provides the instruction manual for pretty much everything that goes on in your body. A few years ago, it was hoped that telomeres those protective DNA caps at the ends of your chromosomes from white blood cells might be a useful biological calendar. But telomeres as predictors of future health have not held up to scientific scrutiny.

However, we may have just been looking at the wrong part of our DNA.

Although we tend to think of DNA as little more than a long-coded sequence of DNA letters, there is a bit more to it. In particular, there are a number of small chemical tags that attach to DNA at specific sites to help turn off, or turn on, genes.

In recent years, combinations of particular tags called DNA methylation have, like plasma proteins, been shown to be good predictors of age and health in people and animals. These tags have even been shown to predict time to death and the development of later life diseases in people.

Perhaps even more exciting, a small, very preliminary study of 10 middle-aged men taking a hormone cocktail designed to stimulate the immune system showed a one-and-a-half-year regression in their DNA methylation calendar.

Lets not get too excited about this result yet. It is easy to overinterpret such very preliminary results, as some of the media have done. We have no idea at present what a small backward trend in DNA methylation age means, and this study has more than a few limitations. But it is without doubt provocative.

Stay tuned. Analysis of blood cells and blood plasma may hold secrets of aging that we are just beginning to discover.

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Does Our Blood Hold the Secrets of Our Longevity? - Next Avenue

SOPHIA Natural Health Center in Brookfield will be holding anupcoming FREE lecture, "The 6 Dynamics of Health and Longevity". This lecture willbe held exclusively at the Danbury Library.

Register online at the Danbury Library: https://bit.ly/30LIZyJ

Or RSVP at 203-797-4505

What is your health plan? Are you confused about all the different health information out there? Would you like to take charge of your health? This presentation will share the ancient secrets that you can apply TODAY that will help you take action. You will learn tools to start resolving your health issues naturally, regain energy, lose weight, balance hormones, restore health and regain vitality.

When: Thursday, February 13, 2020 - 5:30 PM 6:30 PM

Where: Danbury Library: 170 Main Street, Danbury, CT in the Farioly Program Room Cost: FREE

Visit our website: https://bit.ly/2vhaQLs

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Feb 13 | The 6 Dynamics of Health and Longevity Lecture | Brookfield - Patch.com

While we know that its important to watch exactly what were putting in our bodies, this study proves that when implemented correctly and nutritiously, a low-carb diet can boost longevity.

Just because someone is on a low-carb diet, however, does not mean that they are necessarily being healthy. According to the study, These findings suggest that the associations of low-carbohydrate and low-fat diets with mortality may depend on the quality and food sources of macronutrients.

The study brings into conversation the important aspect of certain diets like these: the sources of carbs and fats arent well-enough defined to thrive off of only counting carbs or calories. Head researcher Zhilei Shan, Ph.D. says, The debate on the health consequences of low-fat or low-carbohydrate diets is largely moot unless the food sources of fats or carbohydrates are clearly defined.

This research may be especially relevant to those just starting on the keto dietwhile limiting your daily carb intake may keep you in ketosis, its also essential to make sure youre utilizing those few carbs to get nutrientsthings like fruits, veggies, nuts, and grains.

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Low Carb Diets Can Boost Longevity, But Only If You Do This - mindbodygreen.com

Cara Santana opened up about how she made her romance with ex-fianc Jesse Metcalfework just a few hours before they split.

The Santa Clarita Diet alum, 35, told Us Weekly exclusively on January 4 that maintaining balance in her relationship with Metcalfe, 41, has allowed them to be successful after 13 years together. Its the thing that really, like, probably has given us such longevity in our relationship, she told Us at the Art of Elysiums 13th annual celebration, where she and Metcalfe made their last appearance as a couple.

We both have such fulfilling professional lives and were both so ambitious and Im really focused, she continued. So, I think thats something that we really respect in one another and that creates balance, because youre separate and then you really value the time that you have together. I think its all part and parcel of, like, what makes us work.

Us broke the newson Wednesday, January 22,that Metcalfe and Santana split on January 4andare not together. A source added,They are not even living together. He did not cheat on her.

On Wednesday, the Daily Mail posted photos of the Desperate Housewives alum cozying up with two different women weeks after Santanas comments to Us. He was photographed holding hands with model Livia Pillmann while dining at Gracias Madre in West Hollywood. Hours later, he was spotted getting close to another woman while visiting Attic bar in Sherman Oaks, California.

In August 2016, Us exclusively reported Metcalfe and Santana were engaged after dating for a decade. The John Tucker Must Die actor asked for his former longtime loves hand in marriage with a 5.5-carat diamond sparkler while aboard a sailboat on the Hudson River in New York. Metcalfe told Us at the time that their engagement was a long time coming and that they couldnt be happier.

More than two years into their engagement, Santana confirmed to Us exclusively in March 2019 that the exes were nowhere in their wedding planning process.

At this months Art of Elysium event, Santana talked about how she and Metcalfe have done their relationship on their own terms over the years. In a modern couple, its nice to be able to be like, Hes 41, Im 34 and were taking our time, the fashion blogger. And its just easy.

Santana added that it would be hard to imagine their lives without children in the picture. But she had no desire to start a family at the time.

Thats like the worst sound bite ever, but I have to have two amazing dogs. Were fostering a medically fragile French Bulldog right now and so those three dogs feel like my children, she continued. Jesse, hes like a grown man child. So, you know, theres that too.

With reporting by Carly Sloane

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Cara Santana Opened Up About the Longevity in Jesse Metcalfe Relationship Just Hours Before Split - Us Weekly

Its good to always be thinking however new research shows you may want to give your brain a break sometimes.

Healthy cognition is made possible by two opposing functions: neural excitation and neural inhibition. The former makes nerves more active while the latter achieves just the opposite.

Up until very recently the effects of this counter-balance were relatively unknown but a preliminary new report published in the journal Naturemotions an intriguing correlation.

The physiological activities that regulate metabolism also play a huge role in exciting our nervous system. According to the new paper prolonged hyper-activity bears the potential to shorten our lifespan.

This hypothesis began with an examination of brain tissue extracted from deceased humans. Subjects that evidenced increased neural activity died younger than those who did not. Because the disparity was upwards of ten years, the researchers set out to identify a primary effect.

From the report: Here we show that extended longevity in humans is associated with a distinct transcriptome signature in the cerebral cortex that is characterized by downregulation of genes related to neural excitation and synaptic function. Furthermore, longevity is dynamically regulated by the excitatory-inhibitory balance of neural circuits.

Depending on the objectivesome species are more conducive to human translation than others. Since the researchers wanted to examine the impact neural hyperactivity has on lifespan, worm models served the criteria well, given they do not live very long.

Following several follow-up trails, the Harvard researchers were confident about excitation being a crucial correlate of longevity.

As the worms aged their brain activity naturally increased, as is the case with humans. When administered a drug that inhibited neural activity the worms lived longer than the control group. When the researchers administered a drug that stimulated neural activity the inverse was demonstrated.

This meant excitation produced a profound effect on lifespan all on its own. To locate the specific protein that was at play, the researchers swapped the worms for mice models; animals frequently employed in the service of degenerative disease research. Mice and humans share many genetic similarities. Ninety-seven percent of our working DNA is identical to be more precise.

The deceased mice analyzed showcased a neurological journey parallel to the dead worm models. Moreover, after examining the genetic material of the living rodents with a complex computer algorithm an influencing CEO protein was successfully isolated.

The expression of a protein previously linked to the progression of dementia called REST, directly surged or diminished neural activity in the mouse models.

The transcription factor REST is upregulated in humans with extended longevity and represses excitation-related genes. Notably, REST-deficient mice exhibit increased cortical activity and neuronal excitability during aging, the report continued. These findings reveal a conserved mechanism of ageing that is mediated by neural circuit activity and regulated by REST.

Though pioneering, the data is leagues away from human application. The increased and decreased REST expression was engineered for the purpose of research but there are lifestyle changes you can make to pump the brakes on neural excitation. For more on these methods please refer to an article published by Ladders on the proven benefits of interception.

When we over-expressed or turned up, this protein in the worm, the worm now, interestingly, reduced the amount of nervous system excitation and lived longer. When we did the opposite, when we turned it down, we actually got more excitation and the worm lived a shorter lifespan, the studys co-author Dr. Bruce Yankner, a professor of genetics and neurology at Harvard Medical School explained toTime Magazine.

In the same press release the professor expressed interest in furnishing the ways in which a persons thoughts, personality and behavior affect their overall health and longevity.

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Harvard scientists find people with more brain activity have shorter lives - Ladders

KEY POINTS

The human race has always been on the lookout for better ways to improve health and longevity. While it is an undeniable fact that no one is going to live forever, there is always that desire to add just a little bit more years to their lives.

In fact, many people want to enjoy their retirement and watch their grandchildren grow without having to worry about acquiring serious health ailments or diseases. The good news is that this is possible with the help of carefully chosen foods and diet.

A new study has shown that particular food groups could help you live longer. Two of these food groups even came as a surprise to researchers. food groups for increase of life expectancy Photo: ExplorerBob - Pixabay

A New Study

Fresh evidence has been offered by a recent study conducted by US researchers. Involving over 37,200 adults, the new study provides strong evidence that both low-fat and low-carb diets aid in improving longevity. Their findings may put to rest the never-ending low-fat versus low-carb diet when it comes to eating healthy.

According to the new study, diets that contain lots of processed meats and refined carbs may shorten your lifespan. At the same time, researchers say that whole grains, healthy fats, vegetables, and nuts are among the best foods to consume to enjoy a longer and healthier life.

Evidence from the study strengthens the findings of earlier studies proving that diets rich in both healthy carbs and healthy fats could help you live life past 100.The study also took note of the fact that mortality may strongly depend on the quality, as well as food sources, of macronutrients. Life longevity with these types of foods is hugely determined on whether they are loaded with low-quality carbs and processed fats. Many are aware these low-quality carbs and processed fats are bad for the health. These include red meat, white bread, and sugar.

Zhilei Shan, the author of the study and a Harvard University research scientist, said that it does not matter whether people opt for low-fat or low-carb diets. What matters most is the quality of the macronutrients they receive.

Another food expert, Dane Buettner, agreed and also said that every longevity diet in the world has four pillars, namely, greens, beans, whole grains, and nuts. Buettner has examined the diets of people living in the Blue Zones all over the world, which saw people living over 100 with regularity.

Foods to Be Consumed

The studys findings solidified past researches and studies pointing to plant-based diets. This diet contains lots of nutritious phytochemicals, vitamins, fiber, and minerals. In short, consume only foods that come straight from the earth and not out of some machine sitting in a factory.

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Improve Your Life Expectancy By Including These 2 Surprising Food Groups - International Business Times

Later this evening, the latest inductees to the Baseball of the Fame will be announced, with one or perhaps two voted in by the BBWAA. The only question with Derek Jeter is whether hell be a second unanimous inductee, and Larry Walker likely to end up right on the knifes edge in his last year of eligibility (my gut is hell fall short despite sitting at over 83% of the 211 known ballots at the time this was published).

Its particularly interesting that these two could make up the 2020 class. At a high level, they had a very similar level of on-field value, with Walker actually edging out Jeter by bWAR 72.7 to 72.4 (Jeter has a more significant edge in fWAR, 73 to 68.7). They even rate similarly by Jay Jaffes JAWS system, with Walker coming in at 58.7 to Jeters 57.4. Of course, off-field factors all the dominant reason to explain the discrepancy in support: Jeter being a career Yankees (Re2pect and all that jazz); Walkers numbers discounted for a significant amount of his career coming in Coors.

In a broader sense however, the way that similar level of on-field production was achieved couldnt have been more different. Jeter played a 20 year career, in which he came to the plate 700 or more times in 10 of them and at least 600 in 17 of them. His 12,602 plate appearances rank 10th all-time as a result of that combination of durability and longevity.

To some extent then Jeter was a compiler: he amassed big counting totals not because of an elite level of productivity, but by being on the field. Its not an entirely fair label since he was objectively very good in terms of productivity, but it shows up in his lack of black ink looking at his player page. Twice he led the league (and in fact MLB) in hits, another time in runs (which isnt even totally a reflection of him), and then the other five are for PA. Never did he lead the league in a rate statistic.

By contrast, Walker was not blessed with such durability, routinely missing time with injuries. While his 17 seasons is not that far behind Jeter, only once did he come to the plate more than 601 times. Thus he only came to the plate 8,030 times, ranking 277th all-time. Thats still a pretty prolific total, speaking to how good he was and hence the quotation marks, but its a low total by Hall of Fame standards. For players active after World War II, theres only 11 inductees with less than 8,000 PA, and most of those involve contextual factors (military service, catchers, colour barrier).

But when he was on the field, he was really good. Even adjusting for Coors Field, he was roughly 40% more productive than the average player per PA (including defensive value). I dont think theres a term for the opposite of a compiler, but Im inclined towards the metaphor of a shooting star: a dazzling bright light arcing across the sky, but that doesnt last long.

Should one prefer a Walker to a Jeter or vice versa? Fundamentally, this is a normative question about what the Hall of Fame should be; everyones mileage will vary especially when it comes to the margin. Descriptively however, its clear that compilers prevail. With Harold Baines inducted last year, Rusty Staub is the only non-active/non-ballot player with at least 10,800 PA not in the Hall of Fame (other than Rafael Palmeiro for PED reasons).

To some extent this is logical theres a very high minimum baseline required to just be able to accrue 10,000 plate appearances. By contrast, absent a contextual factor like those described above, a player under 9,000 career PA making the Hall of Fame is very much an exception regardless of how high the level of productivity (Bobby Grich, Dick Allen, Reggie Smith, etc).

The epitome of this dynamic is actually playing out with two players on the ballot for the third time. Omar Vizquel played 24 big league seasons thanks to his defensive wizardry, his 12,013 PA slotting in 21st all-time. As a result, despite being almost 250 runs below average as a hitter, he ended up just shy of the mythical 3,000 hits (2,877) that represents automatic enshrinement which is supporters point to.

Lets be clear, he had a wonderful career, and hes easily in the top 5% of baseball players historically. This isnt to run him down. But with 45 WAR, hes well shy of Cooperstown standard. Equally, it is almost certain he will one day be inducted. Hes currently sitting at just about 50% support, which actually tends to be increase when non-public votes are tallied. He might not build to the 75% needed, but hell build from this point and only one player ever to get 50% on a writers ballot hasnt been subsequently inducted.

On the flip side is Andruw Jones, who played 17 seasons with just 8,663 PA, but nonetheless put up around 65 WAR (63 bWAR, 67 fWAR). Thats already on the short end by Hall of Fame standards, but its compounded by six of those were partial seasons mostly at the end of his career as a complementary player. Almost all of his value came from his 1997-2007 peak. Not only was he at least Vizquels defensive equal in centre, but he was an impact middle of the order hitter.

Yet even with some big gains this year, hes only at about 25% support (and probably closer to 20% in the end). Its not impossible, but its hard to see him gaining enough support to make it in. Perhaps in the end the productive part of his career was just too short longevity certainly counts. But it speaks volumes I think that if you add the two careers together, you get 41 seasons of which Vizquel contributes 60%. But if you make a list of the top 10 single seasons, perhaps two of them belong to Vizquel (1999 for sure)?

When it comes to balancing peak and longevity, Im definitely in the camp of the former. Give me Jones over Vizquel. Give me Grich over Luis Aparicio. Give me Johan Santana over Jack Morris (or better yet, Dave Steib over Morris). We havent even got to pitchers.

While historically a lot of this was based on achieving counting milestones that required longevity, more recently I think part of the problem is the prevalence of WAR. Dont get me wrong, its a very useful construct. But its an artificial one all the components are measured relative to average, and then at the end theres a translation to make zero replacement level, roughly the level where talent is readily available.

This is very useful most analysis, but it doesnt really apply at the Hall of Fame level though. Routinely, players who were solid everyday regulars (or better) dont get any support or are even left off the ballot. That is to say, for purposes of the Hall of Fame, average is replacement level. And maybe even well higher than that (Rafael Furcal and Eric Chavez were both almost 40 WAR and 10+ WAA, and have a combined one vote on a ballot that isnt crazy crowded).

So in my view, a much better standard for the Hall of Fame is Wins Above Average (WAA). By this measure, Jones (36 WAA) far outclasses Vizquel (5 WAA). Walkers 48 WAA is far ahead of Jeters 31. Using WAA sharpens the contrast longevity and star level productivity.

To finish up and perhaps further elicudate the contrast, I made two starting lineups. The first is compilers who are in the Hall of Fame (not all dont belong objectively, theyre just on the compiling end of the spectrum). The second is shooting stars who have been passed over for Cooperstown.

Overall, shorter career players actually end up a slightly higher WAR total even in a much smaller amount of playing time. Even if all the missing playing time had to be backfilled with ordinary players rather than all-time greats, I think they come out ahead.

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The Baseball Hall of Fame, and longevity versus peak - Bluebird Banter

Turns out you can start fighting the biological agents of aging with your morning cup of coffee. According to new research published in the journal ofOxidative Medicine and Cellular Longevity,the simple decision to opt for skim or 1% milk as opposed to whole milk can add years to your life.

The new pioneering study conducted at Brigham Young University effectively knee-caps recent reports challenging dairys contribution to optimal health.

The authors write in the reports abstract:Investigations evaluating the effect of adult milk consumption on health and disease have produced inconsistent findings. Some studies indicate that the consumption of cows milk promotes health, while others show that it increases risk of disease and mortality. Numerous investigations highlight the mixed results. Overall, the findings highlight an association of increased biological aging in U.S. adults who consumed high-fat milk. The results support the latest Dietary Guidelines for Americans (20152020), which recommend consumption of low-fat milk, but not high-fat milk, as part of a healthy diet.

A lengthy analysis of the beverage habits of 5,834 Americans not only motioned low-fat milks impact on longevity, but it also uncovered a slew of other benefits.

Nearly 50% of the entire study pool drank some form of milk every single day and a quarter consumed dairy on a weekly basis. Of these, a little more than 30% drank whole milk, exactly 30% drank 2%, 17% drank skim, 13% preferred non-dairy alternatives like soy or almond and a modest 10% regularly drank 1% milk.

Participants who routinely drank either skim or 1% milk aged around four and half years slower than their 2% milk-loving counterparts.

The low-fat milk drinkers even demonstrated slower genetic aging markers than the individuals that privileged nondairy milk. Of course, this adverse correlation was the most pronounced among habitual whole milk drinkers.

You might recall Ladders recent mediation on the physiological hallmarks of aging. It was an in-depth look at the function of telomerestheends of chromosomes that gradually shrink as a result of repeat cell replication. In other words, the older we get, the shorter they get.

This process was thought to be an unalterable one butin the last few decades,experts have motioned several different ways we can protect these chrome-caps and fend off aging.

The researchers behind this new report, for instance, concluded that every 1% increase in milk fat imbibed was associated with a 69 base pair telomere length-decrease. This is the equivalent offour and a half years of increased aging.

Participants who drank whole milk considerably more often than they drank skim or 1% milk expressed a 145 base pair telomere length decrease. Even with these insightful citations in the chamber, the studys lead author, professor Larry A. Tucker,has no doubt that the scholarly wrangle surrounding the health merits of long-time dairy consumption will survive. And rightly so. On the key question, theres still a fair share of unknown left to discover.

Milk is probably the most controversial food in our country, Tucker said in a press release . If someone asked me to put together a presentation on the value of drinking milk, I could put together a one-hour presentation that would knock your socks off. Youd think, Whoa, everybody should be drinking more milk. If someone said do the opposite, I could also do that. At the very least, the findings of this study are definitely worth pondering. Maybe theres something here that requires a little more attention.

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Drinking this every day can reverse the effects of aging - Ladders

Modern diet science is much more charitable towards carbs than fads of old. New data assures us thatcarbohydrates areessential to a balanced dieteven when weight loss is an immediate objective.

But a new study published by Harvard researchers in the JAMA Internal Medicine Journal found that not all carbs are equal.

The study, which featured more than 35,000 Ameican adults aged 20 and older, found that the quality of a food group impacted longevity significantly more than the presence of a food group in a given regimen. Despite past studies, a low-fat diet isnt indicative of an effect, sustainable diet.

In this study, overall low-carbohydrate-diet and low-fat-diet scores were not associated with total mortality, researchers said. Unhealthy low-carbohydrate-diet and low-fat-diet scores were associated with higher total mortality, whereas healthy low-carbohydrate-diet and low-fat-diet scores were associated with lower total mortality.

These findings suggest that the associations of low-carbohydrate and low-fat diets with mortality may depend on the quality and food sources of macronutrients.

Since the weight loss market is such a lucrative industry and the medias obsession with diets, it has been argued by some that the market makes a point to blur the line between personal objectives and dietary guidelines. If someone needs to lose weight for health reasons or even for cosmetic purposes, there are healthyand expedient ways to do so.

While carbohydrates give us energy, if the energy isnt used after consumption then theyre stored in our muscles and liver for later. Eventually, if unused, the carbohydrates will turn into fat. Low-carb diets, if adhered to correctly, promote weight loss by limiting the number of carbs we need to use before they become stored as fat. This method works for about six months but fails to be a sustainable system in the long term.

Relying on meats for energy at the expense of carbs is linked toa higher risk for cancer and early death.Restricting carbohydrates is the quickest way to drop weight as long as you apply this restriction to a considered timeline.The Dietary Guidelines for Americas recommend that carbohydrates make up between 45% to 65% of your daily calories. Thats about225 grams for women and to 325 grams for men.

Unlike previous studies, the researchers not only took the number of carbs into account but also the source of carbs consumed. This prerequisite provided an important insight into the role balance plays into longevity and dietary guidelines. When accounting for the total number of person-years (297,768), 4,866 total deaths occurred. Researchers said low-carbohydrate-diet and low-fat-diet scores were not associated with total mortality, but a healthy low-carbohydrate diet and a healthy low-fat diet were associated with lower total mortality.

Our findings show clearly that the quality rather than the quantity of macronutrients in our diet has an important impact on our health, said Zhilei Shan, a postdoctoral researcher at Harvards Department of Nutrition, in a press release. The debate on the health consequences of low-fat or low-carbohydrate diets is largely moot unless the food sources of fats or carbohydrates are clearly defined.

The recommended carb intake can be obtained in three different ways: sugars, starches, and fibers. Each has its own set of health benefits. In addition, fruits, vegetables, milk, grains, seeds, and nuts are a good varied placed as well. When it comes to addressing mortality statistics, there are confounding factors to consider. Carbs, for instance, primarily provide our bodies with energy. If fibers are consumed in your daily carb intake, you lower your risk for cardiovascular disease and type-2 diabetes.

One recent study found that people who ate at least five fruits a day lived roughly three-years longer than those who didnt. Earlier this week, a new report about habitually consuming skim milk reversed the aging process by an average of four-and-a-half-years.

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This Harvard study might put the end to the carbohydrates war - Ladders

Image Credit: SeventyFour/Shutterstock.com

Tribology refers to the science of how surfaces in natural and artificial systems interact in relative motion. The principles of lubrication, friction, and wear are key to the discipline. As it is a highly interdisciplinary field, scientists from different areas of the scientific community are often drawn together to help solve problems in tribology.

To advance knowledge of tribology and to make innovations in this area, collaborative efforts from experts in biomedical science, chemistry, chemical engineering, computer science, mechanics, engineering, manufacturing, mathematics, physics, and more are needed.

While the science of tribology influences numerous industries, the automotive and medical sectors are those that particularly rely on its knowledge and innovations to improve its products and raise its level of quality.

Problems presented by the automotive industry are mostly fueled by the growing demand to produce components that have lifetime guarantees. The products need to be created with higher levels of quality, as consumers require parts with longevity, not only in terms of how long it will last without breaking but also in terms of how the components function over their lifetime.

The demands of the medical industry are similar. There is a growing demand for medical prosthetics, for example, that are easy to install and last a lifetime. Both industries are facing challenges in tribology; they need to develop components with surfaces that do not cause wear as they interact with each other over extended periods. Components also need to be developed in a way that prevents a change in how they behave as they continue to be in constant contact with their surroundings, offering the ability to do the same job repeatedly and to the same level of quality.

The solution relies heavily on understanding how two surfaces interact with each other. Recent advances in tribology have seen the increase in the development of surface texture of coatings to offer friction-free use.

The monitoring of these coatings is essential to understanding how effective they are, and how this may influence the longevity of a component. The task of monitoring can be difficult, but recently, sensors have been employed to conduct this task efficiently and accurately.

The past decade or so has seen the advent of the use of sensors to help solve tribology problems. The coatings that are being tested for use in numerous applications have benefited from the addition of embedded sensor layers within the coating.

These sensor layers have been designed to produce distinctive luminescence spectra in response to laser illumination, which makes it possible to measure the wearing of the coating by measuring changes in the amount of light transmitted back. This offers information on the changing thickness of the coating.

Coatings are designed to ideally last a lifetime, protecting the component from wear and extending the longevity of the product. Using embedded sensors to measure wear methodologically allows scientists to make accurate calculations about how coatings will influence the products that they are intended for. It also helps scientists to innovate new and better coatings by allowing them to see how different coating compositions function. It also enables them to make these innovations faster because they have a direct and accurate way of measuring the coatings effectiveness.

Tribology will likely be positively impacted by the use of sensors to help develop more effective coatings. This may lead to the development of more superior products in the automotive and medical industry, as well as others. Sensors will likely play a role in the continuing improvement of quality and longevity of a wide range of components and products.

https://www.sciencedirect.com/science/article/abs/pii/S0167892208700300

https://www.sciencedirect.com/science/article/abs/pii/S0043164808000471#!

Disclaimer: The views expressed here are those of the author expressed in their private capacity and do not necessarily represent the views of AZoM.com Limited T/A AZoNetwork the owner and operator of this website. This disclaimer forms part of the Terms and conditions of use of this website.

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Solving Problems in Tribology with Sensors - AZoSensors

David Hogness

courtesy stanford medicine

David Hogness, a biochemist, geneticist, and developmental biologist at Stanford University, died at his home on December 24. He was 94 years old.

Hogness is well known for a series of experiments during the 1970s and 1980s that were instrumental in launching both molecular genetics and genomics, according to a university statement.

His lab brought molecular biology to Drosophila, discovered the first core promotor element in eukaryotes, cloned the Hox genes, studied the basis of steroid hormone signaling, the list goes on and on. He was a giant, says biologist Mark Peifer of the University of North Carolina in a tweet.

Hogness was born in Oakland, California, on November 17, 1925, and grew up in Chicago. In 1949, he received his bachelors degree in chemistry from Caltech, where he also earned his PhD in biology and chemistry in 1952.

While a faculty member at Washington University in St. Louis, Hogness studied bacteriophage lambda and created the first physical maps of genes along DNA, according to the statement. He joined Stanfords newly formed biochemistry department in 1959, and during a sabbatical in 1968, shifted his focus to Drosophila.

In a 1972 grant proposal, Hogness described the concept of chromosomal walkingnow known as positional cloninga technological breakthrough that many consider to be the founding of genomics, according to Stanfords statement.Hognesss 1975 paper published in PNAS detailed colony hybridization, a novel method of isolating cloned DNA. Three years later, Hogness discovered the Goldberg-Hogness box, now called the TATA box, a non-coding promoter sequence where transcription is initiated in archaea and eukaryotes (prokaryotes have a homolog called the Pribnow box). Another landmark study published in the early 1980s demonstrated the ability to clone the gene underlying any genetic trait, and simultaneously proved there were genes specifically devoted to regulating normal development, says Richard Lifton, the president of Rockefeller University and a former student of Hogness, in the press release. Its one of the great papers in the history of biology.

Daves genius was to realize that the recombinant DNA technologies newly developed at Stanford, which allowed researchers to isolate and replicate to very high copy numbers distinct segments of DNA, could be used to map the locations of the DNA segments to specific bands on the polytene chromosomes, developmental biologist Philip Beachy says in the statement.

Hognesss awards include the March of Dimes Prize in Developmental Biology in 1997, the Lifetime Achievement Award of the Society for Developmental Biology in 2002, the Thomas Hunt Morgan Medal in 2003, and the Warren Alpert Foundation Prize in 2013.

Hogness is survived by his sons.

Amy Schleunes is an intern atThe Scientist. Email her ataschleunes@the-scientist.com.

Read more:
David Hogness, Revolutionary of 20th Century Genetics, Dies - The Scientist

Over the years, the Simons Foundation Autism Research Initiative (SFARI) has made contributions to selected Gordon Research Conferences (GRCs) with the aim of helping to defray the travel and/or conference costs for graduate students, postdoctoral fellows, trainees and other scientists attending these conferences.

As part of SFARIs efforts to encourage diversity and inclusion at scientific meetings and in autism research, SFARI will now require that GRCs organizers allocate all SFARI-donated funds to support attendance specifically of early career (pre-tenure) women, early career trainees from historically underrepresented groups, and scientists from the following ethnic and racial groups: Hispanic or Latino, American Indian or Alaska Native, Black or African American, Native Hawaiian or Other Pacific Islander.

We hope that, by lowering barriers to conferences attendance, SFARI support will promote opportunities for scientific growth and collaborations that can help build a more inclusive research community and advance the field, says SFARI director Louis Reichardt.

SFARI supports GRCs that are focused on topics of relevance to the study of autism spectrum disorder. These may include but are not limited to genetics, molecular mechanisms, brain circuits, systems and behavior, as well as novel technological advances in neuroscience. GRCs may be organized and/or attended by SFARI Investigators and provide unique opportunities to network with leaders in autism research and learn more about the latest findings in the field.

Eligible researchers who are planning to attend SFARI-supported GRCs this year are encouraged to contact the conference chairs to inquire about funding availability.

In 2020, GRCs for which SFARI funds may be available include:

Thalamic circuits for perception, cognition and actionVentura, California, United StatesFebruary 1621, 2020

Functions of the basal ganglia from thought to actionVentura, California, United StatesMarch 813, 2020

Systems neuroscience and genetic approaches to study sleep regulation and functionLucca (Barga), ItalyMarch 813, 2020

Novel technologies to advance discovery of disease mechanisms and therapeutics for fragile X and autismLucca (Barga), ItalyMay 31June 5, 2020

Context-specific synaptic functionLucca (Barga), ItalyJune 2126, 2020

Emerging technologies to study nervous system development, function and neurological diseaseHong Kong, ChinaJuly 510, 2020

Circuits and specializations for behavioral interactions in acoustic communicationNewry, Maine, United StatesJuly 1924, 2020

Linking brain circuits to behavior: Novel methods and biological insights derived from optogenetic approachesNewry, Maine, United StatesJuly 1924, 2020

Neural circuits, dynamics and computations of cognition and behaviorNewry, Maine, United StatesJuly 2631, 2020

Building the nervous system: Insights from development, evolution and diseaseNewport, Rhode Island, United StatesAugust 914, 2020

Molecular and network complexity in the epileptic brainCastelldefels, SpainAugust 1621, 2020

See the article here:
SFARI funds to support diversity at Gordon Research Conferences - SFARI News

Each week, The Dailys Science & Tech section produces a roundup of the most exciting and influential research happening on campus or otherwise related to Stanford. Heres our digest for the week of Jan. 12 Jan. 18.

The Human Screenome Project collects 30 million data points

The Human Screenome Project, a multidimensional map of peoples digital lives, collects data and records which websites users browse online, a Jan. 15 commentary article in Nature reports.

Previous screen studies have relied on people self-reporting their screen time, which can lead to inaccuracies. Although studies have been using software to log total screen time and time between mobile applications, there is no method used to monitor digital interactions of how people use mobile applications.

The Stanford Screenomics Lab currently has 600 participants in the study and over 30 million data points.

No matter what you study, whether its politics, addiction, health, relationships or climate action, if you really want to understand peoples beliefs and behaviors, you really need to look at their screenome, because so much of our lives is now filtered through our digital devices, pediatrics and medicine professor Thomas Robinson told Stanford News.

Many of the things we once did face-to-face are now reflected and recorded on our screens, whether it is banking or deciding what to eat or making friends or playing games or dating or exercising or discussing politics, and so on. Robinson added.

Four aging metabolic pathways identified in humans

To better understand the biological mechanisms behind aging, a Jan. 13 Nature Medicine study defined four ageotypes that indicate how an individuals molecular makeup changes as one ages.

Our study captures a much more comprehensive view of how we age by studying a broad range of molecules and taking multiple samples across years from each participant, genetics professor and chair Michael Snyder told Stanford Medicine News. Were able to see clear patterns of how individuals experience aging on a molecular level, and theres quite a bit of difference.

The researchers used 43 men and women between 34 and 68 years old to identify four ageotypes in which aging biomarkers are commonly observed in metabolic, immune, hepatic and nephrotic pathways. For example, people who are metabolic agers may be at a higher risk for developing diabetes or have elevated blood sugar levels as they become older.

The ageotype is more than a label; it can help individuals zero in on health-risk factors and find the areas in which theyre most likely to encounter problems down the line, Snyder told Stanford Medicine News. Most importantly, our study shows that its possible to change the way you age for the better. Were starting to understand how that happens with behavior, but well need more participants and more measurements over time to fully flesh it out.

Analyzing DNA in soil samples to track animals

Analyzing DNA left behind by animals in soil samples may be more effective in tracking animals than the traditional camera traps currently used, a study published on Jan. 14 in Proceedings of the Royal Society B found.

Led by environmental biology professor Elizabeth Hadly, the team is studying how to better monitor biodiversity, which is crucial to conservation efforts. The researchers studied environmental DNA (eDNA) found in soil samples derived from animal hair, feces, skin and saliva.

The findings suggest that studying eDNA provides certain advantages over the traditional camera traps, hidden recording devices used to track animal activity. eDNA can detect genetic traces of animals that were too small for the camera trap to visually capture an image. Additionally, eDNA is useful in distinguishing similar-looking species compared to using cameras.

Its overall accuracy, combined with decreasing costs of genetic sequencing and new portable sequencers, makes eDNA a likely candidate to become the standard for biodiversity surveys in the next decade, Kevin Leempoel, a postdoctoral research fellow in biology, told Stanford News.

Contact Derek Chen at derekc8 at stanford.edu.

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Research Roundup: Human Screenome Project, four pathways in aging and a new DNA-based method to track animals - The Stanford Daily

FRANTZ PNC Bank

AARON NIVERT Howard Gardner AARON NIVERT Howard Gardner AARON NIVERT Howard Gardner

Allied Services Integrated Health System

The health system recently welcomed four new board members.

The health system welcomed two new members to its board of directors. Christina Mueller and Jill Murray, Ph.D., will serve on the Allied Services Foundation board of directors.

Mueller, a native of Clarks Summit, earned her undergraduate degree from St. Marys College in Notre Dame, Indiana. The early years of her career were spent in Chicago, where she earned her Master of Business of Administration at Loyola University. While studying at Loyola, Mueller began her career with McDonalds. After graduating, she returned to Northeast Pennsylvania, where she trained and became a McDonalds operator. Today, she assists her family in operating 16 local McDonalds stores. Mueller is actively involved in supporting the work of the Ronald McDonald House of Scranton and in supporting local schools through the McTeacher nights at local McDonalds restaurants.

Murray is incoming president of Lackawanna College. Before accepting this position, Murray served as executive vice president and chief innovation officer for Lackawanna College. Murray earned her Ph.D. in human development from Marywood University and has held teaching positions at Walden University, Kaplan University, Marywood University and the University of Phoenix. She is currently on the board of Maternal and Family Health Services and received the 2018 Non-Profit Board Member of the Year award from the Wilkes-Barre Chamber of Commerce.

The health system welcomed two new members to its board of directors. Jay Brislin, MSPT, and Dr. Sandra Krokos-Kislan will serve on the hospital board of directors responsible for oversight of Allied Services Scranton Rehab Hospital and Heinz Rehab Hospital.

Brislin, vice president of Quantum Rehab, a division of Pride Mobility Products, brings an unrivaled depth of knowledge of complex rehab needs to his role on the rehabilitation hospital boards. Brislin began with Quantum Rehab in 2000 as a rehab specialist, quickly becoming a leader and educator in the arena of complex rehab needs. Brislin was part of the team instrumental in launching some of Quantum Rehabs most innovative products. Today, he oversees a clinically based team dedicated to the most innovative products and inspiring client outcomes. As an industry leader, Brislin is a RESNA member, Friend of NRRTS and NCART participant.

Krokos-Kislan, of Hazleton, is a graduate of Coughlin High School. She received her Bachelor of Science from Wilkes College before earning her Doctor of Optometry degree from the Pennsylvania College of Optometry. Sandra and her husband, Dr. Thomas Kislan, own and manage Stroudsburg Eye Specialists and Hazleton Eye Specialists. Kroskos-Kislan is a member of the board of directors of Burnley Employment and Rehab Services, a division of Allied Services providing employment services for individuals with disabilities in the Poconos.

American Society of Public

Administration

David Allen Hines was recently reelected to the board of directors for the Keystone State (Pennsylvania state) chapter. Hines holds a Master of Public Administration degree from Marywood University in Scranton, and for many years was the deputy director for budget administration for the government of the District of Columbia in Washington, D.C. After returning to the area, for the past several years he has been director of operations for the city of Pittston. A 40-year resident of Kingston, Hines also serves on the national budget and financial policy committee for the Government Finance Officers Association and the board of directors for the Greater Pittston Historical Society.

Healthy Steps Podiatry Center

Dr. Diane Stchur Bray has recently opened the center on Chocolate Avenue in Hershey. Bray, a graduate of Hanover Area High School, received her Bachelor of Science degree in biology and molecular genetics from Kings College, and her doctorate in podiatric medicine from Temple University.

After doing a three-year intensive surgical residency at Our Lady of Lourdes Hospital in Binghamton, New York, Bray then joined a group practice where she provided podiatric care and served as a wound care specialist for the patients of upstate New York for 16 years.

Howard Gardner Multiple

Intelligence

Charter School

The school welcomed four new trustees to its board. New trustees are Laurie Cadden, owner, Laurie Cadden LLC; Sam Ceccacci, former executive director, Scranton-Lackawanna Human Development Agency; Susan Hennemuth, development director, Childrens Service Center; and Aaron Nivert, executive vice president, Nivert Metal Supply.

PNC Bank

The bank recently announced that Judith Frantz, branch manager, has been promoted to vice president.

Frantz is a graduate of Misericordia University with a bachelors degree in business administration. She is also a graduate of Wilkes University, where she went to earn her MBA. She resides in Luzerne.

Carly Caroselli has joined PNC Wealth Management as a vice president and investment adviser.

Caroselli is a graduate of Drexel University with a Bachelor of Science degree in behavioral health. She resides in Scranton.

University

of Scranton

The university has named Julie Schumacher Cohen assistant vice president for community engagement and government affairs. In this position, she will report to the vice president for enrollment management and external affairs and will also work closely with the provost and senior vice president for academic affairs.

In her new role, Schumacher Cohen will work to deepen the universitys community engagement efforts and government affairs activities and strengthen the mission of the university as an anchor institution in our city and region.

Since 2010, she has served as the universitys director of community and government relations.

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Link:
People on the Move - News - Wilkes-Barre Citizens Voice