Physiology

How to lose visceral fat: Best type of exercise to do to reduce the harmful belly fat – Express

Visceral fat increases a persons risk of developing various health conditions, such as hypertension and heart disease. Which exercise is the best at reducing levels of this harmful belly fat?

Researchers from the Duke University Medical Centre have discovered the best type of exercise to cut levels of visceral fat.

Their eight-month study compared how much visceral fat was lost due to aerobic exercise, resistance training or both.

Documenting 196 people, they found aerobic exercise to be the most efficient and effective way to lose the harmful belly fat.

Published in the American Journal of Physiology, lead author physiologist Cris Slentz, Ph.D. said: Our study sought to identify the most effective form of exercise to get rid of that unhealthy fat.

[If] you want to lose belly fat, aerobic exercise is the better choice because it burns more calories."

The study revealed aerobic exercise burned 67 percent more calories than resistance training.

The aerobic group performed an equivalent of 12 miles of jogging per week at 80 percent maximum heart rate.

READ MORE: Vitamin D deficiency symptoms: The sign on your head you need to watch out for

The resistance group, on the other hand, performed three sets of eight, 12 repetitions, three times per week.

What really counts is how much exercise you do, how many miles you walk and how many calories you burn," Slentz said.

If you choose to work at a lower aerobic intensity, it will simply take longer to burn the same amount of unhealthy fat."

Examples of aerobic exercise include anything that gets your heart pumping.

There are free aerobic workout videos to follow on the NHS website, which include dancing.

And aerobic exercises, also known as cardio, include spinning, running, swimming and hiking.

By repeatedly moving large muscles in the arms, legs and hips, breathing will get become rapid.

This maximises the amount of oxygen in your blood, according to the Mayo Clinic.

Additionally, the body will release endorphins natural painkillers which will promote an increased sense of wellbeing.

If youre new to moderate-intensity exercise, its best to start off slowly.

Also, if you have any current health conditions, do discuss your plans to exercise more with your doctor who can advise you further.

The NHS state: Aim to be physically active every day. Any activity is better than none, and more is better still.

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How to lose visceral fat: Best type of exercise to do to reduce the harmful belly fat - Express

Physiology

Stoners Bake Snacks with Scientific Hacks – The LumberJack

Edibles or cannabis-infused foods are a common way to consume marijuana. The process of making edibles, just like baking brownies, is a science. The primary psychoactive compound in marijuana is called cannabinoids. When making edibles, you infuse a fat with cannabinoids to activate the chemical.

Mark Wilson, a Humboldt State University professor with a Ph.D. in microbiology, genetics and toxicology explained that cannabinoids are fat soluble and dont break down in water.

Some substances are water soluble and some substances are fat soluble, Wilson said. THC is primarily composed of carbon-carbon bonds and carbon-hydrogen bonds, so it cant interact well with water, but it can interact well with fats and oils.

This characteristic of THC, tetrahydrocannabinol, limits what can be turned into an edible. THC cant steep in hot water for weed tea. Marijuana would need to be steeped in hot milk instead, where the THC would break down and bond with the milk fats.

Things that dissolve into our fat tend to remain in our system much longer. That is, they slowly diffuse into fat, and slowly diffuse out. The fat acts as a sort of absorption compartment. That makes it detectable in drug tests for weeks.

Many people use butter as the main fatty ingredient in edibles. Dairy-based fats are a good option for infusing cannabinoids, but lactose-free alternatives are also solid options, including coconut and olive oil. Bacon fat can absorb cannabinoid infusions too, if youre looking for a savory option.

Joseph Szewczak, an HSU professor who studies and teaches comparative physiology and physiological ecology explained the physical changes to the body when people eat cannabis-infused fats rather than smoking cannabis plants.

Things that dissolve into our fat tend to remain in our system much longer, Szewcxak said. That is, they slowly diffuse into fat, and slowly diffuse out. The fat acts as a sort of absorption compartment. That makes it detectable in drug tests for weeks.

Whether inhaled or eaten, the THC enters the blood stream and messes with brain-cell functions in a unique way. Since THC is shaped like a chemical in the brain, the brain recognizes the chemical and allows to alter normal brain function. That chemical usually tells brain neurons to rest, but THC forces the brain to keep firing, which leads to deep thoughts, increased creativity and anxiety.

In light of these effects, its important to understand whats going to happen after eating an edible. First, since the body takes some time to digest edibles and since their THC is stored in fat, the high lasts longer. Second, the nature of THC and marijuana may lead to discomfort or anxiety, or may lead to creativity and fun, but thats dependent on many factors.

Co-Director of the Humboldt Institute for Interdisciplinary Marijuana Research Josh Meisel is researching the significance of set and setting, or who youre with and where you are, and how those things impact a high.

Peoples negative experiences may be influenced by edible use, Meisel said. But set and setting may be as influential or more influential than the psychoactive properties of the substance itself.

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Stoners Bake Snacks with Scientific Hacks - The LumberJack

Physiology

An atlas of the protein-coding genes in the human, pig, and mouse brain – Science Magazine

Mapping the mammalian brain

The diverse physiology of the brain is reflected in its complex organization at regional, cellular, and subcellular levels. Sjstedt et al. combined databoth newly acquired and from other large-scale brain mapping projectsfrom transcriptomics, single-cell genomics, in situ hybridization, and antibody-based protein profiling to map the molecular profiles in human, pig, and mouse brain. The analysis is consistent with a conserved basic brain architecture during mammalian evolution, but it does show differences in regional gene expression profiles.

Science, this issue p. eaay5947

The brain is the most complex organ of the mammalian body, boasting a diverse physiology combined with intricate cellular organization. In an effort to expand our basic understanding of the neurobiology of the brain and its diseases, we performed a comprehensive molecular dissection of the main regions of the human, pig, and mouse brain using transcriptomics and antibody-based mapping. With this approach, we have identified regional expression profiles and observed similarities and differences in expression levels between these three mammalian species.

There is a need for a comprehensive overview of genes expressed in the mammalian brain categorized by organ, brain region, and species specificity. To address this need, a brain-centered knowledge resource of RNA and protein expression in the brain of three mammalian species has been created and used for cell topological analysis, systems modeling, and data integration. The regional expression of all protein-coding genes is reported, and this classification is integrated with results from the analysis of tissues and organs of the whole human body. All generated data, including high-resolution images and metadata, have been made publicly available in an open-access Human Protein Atlas (HPA) Brain Atlas.

The global analysis suggests similar regional organization and expression patterns in the three mammalian species, consistent with the view that basic brain architecture is preserved during mammalian evolution. However, there is considerable variability between species for many neurotransmitter receptors, in particular between human and mouse. This calls for caution when using the mouse as a model system for the human brain, for example, in attempts to develop therapeutic strategies. For some of the brain regions, such as the cerebellum and hypothalamus, the human global expression profile is closer to that of the pig than it is to that of the mouse, suggesting that the pig might be considered a preferred animal model to study many brain processes. We show that many signature genes identified previously for specific brain cell types (such as astrocytes, microglia, oligodendrocytes, and neurons) are expressed at even higher levels in peripheral organs. In fact, our results support a view of shared functions between many genes in microglia and immune cells, and a large number of genes previously identified as signature genes for astrocytes are shown to be shared with liver or skeletal muscle. The cerebellum stands out as having a distinct molecular signature with many regionally enriched genes. Several genes suggested to be involved in neuropsychiatric diseases are selectively expressed in the cerebellum.

The integration of data from several sources has allowed us to combine data from transcriptomics, single-cell genomics, in situ hybridization, and antibody-based protein profiling. This integrative approach for mapping the molecular profiles in the human, pig, and mouse brain has generated a detailed multilevel genome-wide view on the protein-coding genes of the mammalian brain, where we compared tissue specificity across the whole body, as classified in the HPA (www.proteinatlas.org). The open-access HPA Brain Atlas resource offers the opportunity to explore individual genes and classes of genes and their expression profiles in the various parts of the mammalian brain.

Multiple regions of the human, pig, and mouse brain were dissected and analyzed. A uniform manifold approximation and projection (UMAP) analysis (middle) shows the global expression patterns of 1710 samples in the human brain, with the cerebellum as the outlier. The HPA Brain Atlas (right) shows the expression of individual genes, for example, synaptosomal-associated protein 25 (SNAP25), in the different brain regions in the three mammalian species.

The brain, with its diverse physiology and intricate cellular organization, is the most complex organ of the mammalian body. To expand our basic understanding of the neurobiology of the brain and its diseases, we performed a comprehensive molecular dissection of 10 major brain regions and multiple subregions using a variety of transcriptomics methods and antibody-based mapping. This analysis was carried out in the human, pig, and mouse brain to allow the identification of regional expression profiles, as well as to study similarities and differences in expression levels between the three species. The resulting data have been made available in an open-access Brain Atlas resource, part of the Human Protein Atlas, to allow exploration and comparison of the expression of individual protein-coding genes in various parts of the mammalian brain.

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An atlas of the protein-coding genes in the human, pig, and mouse brain - Science Magazine

Immunology

How to boost your immune system to avoid colds and coronavirus – The Guardian

Its been a long, wet winter. Everybody has got colds, and now we are braced for a coronavirus epidemic. Boosting our immune system has rarely felt more urgent, but, beyond eating more tangerines and hoping for the best, what else can we do?

Sheena Cruickshank, a professor of immunology at the University of Manchester, has a shocking cold when we speak at a safe distance, over the phone. To know how to take care of your immune system, she says, first you need to understand the weapons in your armoury a cheeringly impressive collection, it turns out.

When you come into contact with a germ youve never met before, she says, youve got various barriers to try to stop it getting into your body. As well as skin, we have mucus snot is a really important barrier and a microbiome, the collective noun for the estimated 100tn microbes that live throughout our bodies, internally and externally. Some of these helpful bugs make antimicrobial chemicals and compete with pathogens for food and space.

Beneath these writhing swamps of mucus and microbes, our bodies are lined with epithelial cells which, says Cruickshank, are really hard to get through. They make antimicrobial products including, most relevant to coronavirus, antiviral compounds that are quite hostile.

If a pathogen breaches these defences, it has to deal with our white blood cells, or immune cells. One type, called macrophages, inhabit all our body tissue and, says Cruickshank, have all these weapons ready to go, but theyre not terribly precise. They report to the cleverer, adaptive white blood cells known as lymphocytes. They are the ones that remember germs, so if you meet that germ again, says Cruickshank, theyll just deal with it probably without you even knowing. Thats when youve got immunity and is the basis of vaccination. Its trying to bypass all the early stuff and create the memory, so you dont have to be sick.

Our immune systems may have blind spots. This might mean that our immune response doesnt recognise certain bugs, she says, or the bugs have sneaky evasion strategies. Personally, my immune system is not necessarily very good at seeing colds. But a healthy lifestyle will ensure your defences are as good as they get.

Seeing as our bodies contain more cells belonging to microbes, such as bacteria and yeasts, than human ones, lets start with the microbiome. We live in a symbiotic relationship with our gut bacteria, says Prof Arne Akbar, the president of the British Society for Immunology and a professor at University College, London. Having the right ones around, that we evolved with, is best for our health. Anything we do that alters that can be detrimental.

Not only do our microbes form protective barriers, they also programme our immune systems. Animals bred with no microbiome have less well developed immune responses. Older people, and those with diseases that are characterised by inflammation, such as allergies, asthma, rheumatoid arthritis and diabetes, tend to have less varied gut microbiomes.

To feed your gut flora, Cruickshank recommends eating a more varied diet with lots of high-fibre foods. Being vegetarian isnt a prerequisite for microbiome health, but the more plant foods you consume, the better. The microbiome really likes fibre, pulses and fermented foods, she adds.

Kefir yoghurt and pickles such as sauerkraut and kimchi are among the fermented delicacies now fashionable thanks to our increasing knowledge of the microbiome. But the evidence for taking probiotic supplements, she says, is mixed. Its not a dead cert that they will survive the journey through your digestive tract, or that they will hang around long enough if they do. Its more effective to change your diet, says Cruickshank.

The skin microbiome is important, too, but we know less about it. High doses of ultraviolet light (usually from the sun) can affect it negatively, weakening any protective functions (as well as triggering immune suppression in the skin itself). Overwashing with strong soaps and using antibacterial products is not friendly to our skin microbiomes. Combinations of perfumes and moisturisers might well also have an effect, says Cruickshank.

To be immunologically fit, you need to be physically fit. White blood cells can be quite sedentary, says Akbar. Exercise mobilises them by increasing your blood flow, so they can do their surveillance jobs and seek and destroy in other parts of the body. The NHS says adults should be physically active in some way every day, and do at least 150 minutes a week of moderate aerobic activity (hiking, gardening, cycling) or 75 minutes of vigorous activity (running, swimming fast, an aerobics class).

The advice for older people, who are more vulnerable to infection, is to do whatever exercise is possible. Anythings better than nothing, says Akbar. But a lifetimes exercise could significantly slow your immune system declining with age. In 2018, a study by University of Birmingham and Kings College London found that 125 non-smoking amateur cyclists aged 55 to 79 still had the immune systems of young people.

The other side of the coin, says Akbar, is elite athletes who become very susceptible to infections because you can exercise to a point where it has a negative impact on your immune system. This problem is unlikely to affect most of us unless, says Cruickshank, youre a couch potato and suddenly try and run a marathon, this could introduce stress hormones and be quite bad for your immune system.

One of the many happy side-effects of exercise is that it reduces stress, which is next on our list of immune-boosting priorities. Stress hormones such as cortisol can compromise immune function, a common example of which, says Akbar, is when chickenpox strikes twice. If you have had it, the virus never completely goes away. During periods of stress, he says, it can reactivate again and we get shingles.

Forget boozing through the coronavirus crisis, because heavy drinking also depletes our immune cells. Some studies have suggested that the first-line-of-defence macrophages are not as effective in people who have had a lot of alcohol, says Cruickshank. And theres been suggestions that high alcohol consumption can lead to a reduction of the lymphocytes as well. So if the bug gets into you, youre not going to be as good at containing and fighting it off.

Cruickshank says that vitamin D has become a hot topic in immunology. It is used by our macrophages, and is something that people in Britain can get quite low on in the winter. Necking extra vitamin C, however, is probably a waste of time for well-fed westerners. Its not that vitamin C isnt crucial to immune function (and other things, such as bone structure). All the vitamins are important, says Cruickshank, but vitamin C is water soluble, its not one that your body stores. Eating your five a day of fruits and vegetables is the best way to maintain necessary levels.

Exercising and eating well will have the likely knock-on effect of helping you sleep better, which is a bonus because a tired body is more susceptible to bugs. One study last year found that lack of sleep impaired the disease-fighting ability of a type of lymphocyte called T cells, and research is demonstrating the importance of our natural biorhythms overall.

Janet Lord, a professor at the University of Birmingham, recently showed that vaccinating people in the morning is more effective than doing so in the afternoon. Your natural biorhythms are, to some extent, dictated by sleep, says Akbar. If youve got a regular sleep pattern, you have natural body rhythms and everythings fine. If they go out of kilter, then youve got problems.

The seriousness of an infection largely depends on the dose you are hit with, which could in turn depend on how contagious the carrier is when they cough near you. Were constantly exposed to germs, and we only get sick from a handful of those, says Cruickshank.

If youre reasonably young and healthy, says Akbar, the mild benefits you may achieve from being extra good probably wont fend off a severe dose of coronavirus or flu. The likely scenario if you catch the infection is, he says, youll be sick for a while and you will recover.

From a public-health perspective, when nasty viruses such as coronavirus are doing the rounds, Akbars priority is not boosting already healthy peoples immune systems, but protecting the vulnerable people. Older people dont respond that well to the flu jab, though its better for them to have it than not. Its a general problem of immune decline with ageing.

When we get older, he says, the barrier function in the gut doesnt work that well, so you have something called leaky gut syndrome, where bugs creep into our bodies causing mild infections. This causes inflammation around the body, as does the natural accumulation of old zombie cells, called senescent cells, and inflammation compromises the immune response.

Akbar is working on developing drug treatments to reduce inflammation in older people but they are a way off yet. Age 65 is when, medically, one is considered older, but thats arbitrary, says Akbar. Some old people might get problems much earlier. And there are older people who are totally healthy.

In terms of coronavirus, says Cruickshank, its mostly spread by droplet transmission, as far as we can tell, so the biggest thing is hygiene. So wash your hands, and sneeze and cough into tissues, she suggests, between sniffles. No one can completely avoid getting sick, not even top immunologists.

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How to boost your immune system to avoid colds and coronavirus - The Guardian

Immunology

Coronavirus Market Correction: Where to Invest $1,000 Right Now – Motley Fool

What should I do?

That's the question that's on the mind of many investors right now. Fears about the global coronavirus outbreak have caused a market correction. A natural instinct is to flee -- run as fast as you can away from the stock market. But I suspect most investors know that this natural instinct isn't the best choice. The smarter approach is to take advantage of the buying opportunity that the market correction presents.

And that leads to another question: What stocks should I buy? There are actually plenty of good answers to that question because there are plenty of great stocks.

My view is that there are three kinds of stocks that you should consider buying during the market downturn. First, look at stocks that have held up well despite the overall market downturn -- the exceptions to the rule. Second, check out stocks that are dirt cheap because of the correction. And third, invest in stocks that are simply great businesses to own no matter what happens with the overall market.

If you have some available cash, I think that investing $1,000 in each of the following three stocks that represent each of those categories is a great place to start.

Image source: Getty Images.

Few stocks have been able to defy the gravity of the overall stock market decline in recent days. But Gilead Sciences (NASDAQ:GILD) is one of them. It helped a lot that a World Health Organization (WHO) official stated recently that Gilead's experimental drug remdesivir appears to have the most potential in being effective at treating COVID-19, the disease caused by the novel coronavirus.

While Gilead's promising antiviral drug remdesivir is the reason why the stock has risen by a double-digit percentage this year, it's not the main reason I like the biotech stock. There are actually four other things that I like even more about Gilead than its coronavirus program. The first three relate to the company's current drugs and pipeline candidates.

Gilead continues to be a juggernaut in HIV. Biktarvy appears destined to become the most successful HIV drug in history. Thanks to the company's 2017 acquisition of Kite Pharma, Gilead is a leader in cancer cell therapy -- an area that I think will gain momentum in the future. The biotech is also poised to enter the immunology market if filgotinib wins FDA approval later this year in treating rheumatoid arthritis. Some analysts project that filgotinib could generate peak annual sales of close to $6 billion if approved for multiple indications.

That leaves the fourth reason I like Gilead: Its dividend. Most biotechs don't pay dividends, but Gilead is yet again an exception to the rule. Its dividend yield currently stands at close to 3.6%. Gilead has increased its dividend payout by 58% since initiating its dividend program in 2015. With more dividend increases probably on the way and growth drivers in HIV, oncology, and immunology (plus potentially with its coronavirus drug), Gilead should provide market-beating returns over the long run.

TD Ameritrade Holding (NASDAQ:AMTD) has fallen hard during the market downturn. Shares of the online brokerage are down nearly 30%, a significantly worse performance than its peers. TD Ameritrade stock now trades at less than 14 times expected earnings.

Granted, it's not just worries about the coronavirus outbreak that have caused TD Ameritrade's stock to drop. The antitrust division of the Department of Justice is investigating the pending acquisition of TD Ameritrade by Charles Schwab (NYSE:SCHW). There's a possibility that the deal could be blocked.

But those fears could be overblown. Schwab and TD Ameritrade say they're cooperating fully with the DOJ and expect the transaction to close in the second half of this year.

What if the DOJ prevents the acquisition? I still think the future for TD Ameritrade looks bright. Investors continue to flock to online brokerages. The greatest generational transfer of wealth is on the way. Research firm Cerulli Associates estimates that over the next 25 years $68 trillion will shift from older parents to their children. A lot of that money will be invested in stocks, creating a major opportunity for TD Ameritrade whether it remains an independent entity or not.

Last -- and certainly not least -- Brookfield Infrastructure Partners (NYSE:BIP) is just a great business to own. I'd make that claim even if the stock hasn't performed pretty well this year (which it has).

If you can think of a type of infrastructure asset, Brookfield Infrastructure probably owns it. Cell towers, data centers, electricity transmission systems, natural gas pipelines, ports, railroads, toll roads, and more are all in the company's portfolio.

I personally bought shares of Brookfield Infrastructure earlier this year, mainly because I think the company's business model is rock-solid. Brookfield doesn't have to worry about a viral epidemic impacting its financial strength. Close to 95% of its adjusted EBITDA comes from regulated or contracted revenue that won't change with twists and turns in the overall economy.

Brookfield Infrastructure also pays a dividend that yields more than 4%. The company has boosted its dividend payout by 52% over the last five years. With Brookfield's strategy of selling lower-performing assets to reinvest in more promising assets, I look for solid earnings growth plus more dividend increases in the future.

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Coronavirus Market Correction: Where to Invest $1,000 Right Now - Motley Fool

Immunology

Hinojosa: Working Together to Beat Cancer – Rio Grande Guardian

Cancer is the second most common cause of death in Texas adults, and the same is true inthe Rio Grande Valley.

According to the Texas Cancer Registry Annual Report 2019, anestimated 124,383 new cases of cancer will be diagnosed in Texas and an estimated45,524 Texans will die from cancer.

In 2017, Hidalgo County had2,411 cancer cases of which 814 resulted in death.

Last year, Dr. John Krouse, dean of the University of Texas Rio Grande Valley School ofMedicine, stated that cervical cancer in women occurs more frequently in the Valley andwhen it occurs the mortality rate is much higher in the Valley. That is just unacceptable.That is something we need to address, and we need to fix.I completely agreeand we have been taking the necessary steps to tackle these challenges.

The first step in this process was passing a bill in 2013 that created the University of TexasRio Grande Valley (UTRGV) and the accompanying School of Medicine (SOM).Thistransformational institution has brought millions of dollars in state and federalfunding to our region, increased our health care infrastructure and personnel, and hasallowed us to begin addressing many of our health care needs.

It has also opened the doors to public-private partnerships that benefit us all, such as theopening of the UTRGV Biomedical Research Building. This opening was made possible due to thecollaboration between the SOM, the City of McAllen, and DHR Health (DHR). This building,located in McAllen, is home to the South Texas Center of Excellence in CancerResearch and a new cancer immunology team that will focus on womens cancerstarting with cervical cancer and transitioning to breast cancer. I appreciate the City ofMcAllens financial contribution and commitment to fund this research program.Thiscooperative effort will lead to new treatment opportunities for patients with cancer.

To continue making progress to address the challenge with Breast and Cervical Cancer, I secured $2.7 million in State funds to support the Cervical Dysplasia and Cancer Immunology Center.We have been working to transfer the Center from the University of Texas Medical Branch to UTRGV School of Medicine. This will improve cooperation and coordination of diagnoses, treatment and research to fight Breast and Cervical Cancer.

Another program that could help improve cancer diagnosis and prognosis for those in theValley is a biorepository for cancer research. DHR is currently working to obtain a Cancer Prevention and Research Institute of Texas (CPRIT) grant that will allow them to expand the current BorderBioRepository at DHR to establish a cancer biorepository.

These efforts will be of great benefit to the women in the Valley and South Texas, but there is still more to bedone. Cancer has no boundaries and can impact anyone regardless of age, gender, or race.For this reason, we are working with community leaders in both the public and privatesector on establishing a world-class cancer treatment clinic that will provide care toValley patients here at home. We are pursuing partnerships with the best entities in thefield, to make this vision a reality.

In the past six months, we have met with CPRIT leadership to advocate not only for additional funding to help prevent cancer, but also for financial support to recruit oncologists and expand our cancer treatment infrastructure in South Texas. CPRIT is a key funding source for cancer research and treatment provided to our universities, medical schools, and other entities committed to fighting cancer. For this reason, I advocated for and supported the appointment of Dr. Ambrosio Hernandez to the CPRIT Board. He is a physician with extensive experience in public health, is a dedicated public servant, and understands the needs of our communities.

We have also pushed for additional partnerships with the best entities in the field, such as M.D. Anderson. UTRGV is currently in the process of developing an oncology program that will assist in actively recruiting clinical oncologists to increase our clinical workforce in this field and provide guidance and expertise in developing best practices and treatments for patient care.

We must give our South Texas patients all the help they can get from modern medicine in the fight against cancer here at home. We will keep working to secure the partnerships and investments necessary so that in the future our patients in South Texas will have access to top notch facilities and world-class doctors. By working together, we can ensure that Valley residents have all of these resourcesavailable to them during their battle. Working together, we can beat cancer.

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Immunology

New ‘Immuno-Engineering to Improve Immunotherapy’ Center formed to advance cancer therapy – The Medical News

Harvard University's Wyss Institute of Biologically Inspired Engineering and its collaborating institutions, the Harvard John A. Paulson School of Engineering and Applied Sciences (SEAS), Dana-Farber Cancer Institute (Dana-Farber), and Harvard's Department of Stem Cell and Regenerative Biology, announce the formation of a new NIH-funded Immuno-Engineering to Improve Immunotherapy (i3) Center. The cross-institutional and cross-disciplinary i3 Center includes world-leading researchers in the cancer immunology and bioengineering fields and will create biomaterials-based approaches to enable anti-cancer immuno-therapy in settings where it currently is limited, such as in myeloid malignancies and solid tumors.

The Harvard i3 Center is part of NIH's Cancer MoonshotSM initiative that was formed to accelerate cancer research to make more therapies available to more patients, while also improving the ability to prevent cancer and detect it at an early stage.

We aim to develop new technologies that induce robust anti-cancer T cell immunity, and we also hope that the i3 Center's highly cross-disciplinary and cross-fertilizing mechanisms will provide a center of gravity for many future efforts in the immuno-therapy space across and beyond our collaborating institutions."

David Mooney, Ph.D., Wyss Institute Founding Core Faculty member, one of the two principal investigators (PIs) of the i3 Center

Mooney also is the Robert P. Pinkas Family Professor of Bioengineering at SEAS and leads the Wyss Institute's broader Immuno-Materials Initiative. His team has developed a number of strategies that use immune-modulating biomaterials to trigger and enhance T cell-mediated immune responses against tumors. Most notably, together with clinical collaborators, they succeeded in creating the first implantable vaccine ever to eliminate melanoma tumors in mice, which the Wyss Institute and Dana-Farber are investigating in an ongoing Phase I clinical trial at the Dana-Farber.

F. Steven Hodi, Jr., M.D., Director of Melanoma Center and The Center for Immuno-Oncology at Dana-Farber, and Professor of Medicine at Harvard Medical School (HMS), is leading the clinical cancer vaccine trial, and is the i3 Center's other PI. Hodi has been at the forefront of developing cancer immunotherapies using "immune checkpoint inhibitors," a class of drugs able to re-activate tumor-destroying T cells that are muted in the tumor microenvironment. "The funding for this center provides a unique opportunity to unite key investigators for translating fundamental advancements in immunology and biomedical engineering into highly synergistic approaches to improve the treatments for cancer patients," said Hodi.

Using both in vivo and ex vivo biomaterials-based approaches, the i3 Center aims to boost tumor-specific activities of cytotoxic T cells, by boosting different stages of the normal process by which T cells develop, and acquire anti-cancer activity. T cells' normal development starts in the bone marrow where hematopoietic stem cells generate T cell progenitor cells. These migrate to the thymus to differentiate into nave T cells, which then travel further to lymph nodes. There, they encounter cancer-derived antigens presented to them by specialized antigen-presenting cells (APCs) that can activate T cells to recognize and eliminate cancer cells.

In relation to "adoptive T cell" therapies in which T cells are given to patients to fight their cancers, one team at the i3 Center will be led by Dana-Farber researchers Catherine J. Wu, M.D., and Jerome Ritz, M.D., who along with Mooney, will develop and test biomaterials that can better mimic normal APCs in activating and directing the function of patient-derived T cells outside the human body, prior to their transplantation. Wu is Chief of the Division of Stem Cell Transplantation and Cellular Therapies, and Ritz is Executive Director of the Connell and O'Reilly Families Cell Manipulation Core Facility at Dana-Farber.

"We need to make efforts to enhance the ability of the immune system to recognize tumor cells. One direction my laboratory is taking makes use of innovative biomaterials to help us to efficiently expand polyclonal tumor-specific functionally-effective T cells ex vivo in a way that can be readily translated to the clinical setting. In our studies, we are currently focusing on melanoma and acute myeloid leukemia," said Wu, whose research interests include understanding the basis of effective human anti-tumor responses, including the identification and targeting of the tumor-specific antigens.

A second project explores the use of DNA origami, biocompatible nanostructures composed of DNA, to create cancer vaccines. DNA origami could provide significant advantages in presenting tumor-specific antigens and immune-enhancing adjuvants to APCs because the concentrations, ratios, and geometries of all components can be modulated with nano-scale precision to determine configurations that are more effective than other vaccination strategies. The project will be run by Wyss Institute Core Faculty member William Shih, Ph.D., Derin Keskin, Ph.D., lead immunologist at Dana-Farber's Translational Immunogenomics Lab, and Mooney.

In a third project, David Scadden, M.D., the Gerald and Darlene Jordan Professor of Medicine at Harvard University, and Professor at Harvard's Department of Stem Cell and Regenerative Biology, and Mooney, based on their previous work, will engineer biomaterials that recreate key features of the normal hematopoietic stem cell niche in the bone marrow. Such implantable biomaterials could help rapidly amplify T cell progenitor cells, and enhance T cell-mediated anti-cancer immunity.

The i3 Center's investigators anticipate that it will stimulate additional cross-disciplinary concepts and research, due to the culture of continuous interactions, sharing of findings, data and samples between all investigators, as well strong biostatistical expertise provided by Donna Neuberg, Sc.D., a senior biostatistician broadly involved with exploring immune-modulating cancer interventions at the Dana-Farber.

"This new i3 Center for cancer immunotherapy innovation really embodies how the Wyss Institute with its unparalleled capabilities in bioengineering and serving as a site for multidisciplinary collaboration, and can liaise with clinicians and researchers at our collaborating institutions to confront major medical problems and bring about transformative change," said Wyss Founding Director Donald Ingber, M.D., Ph.D. He is also the Judah Folkman Professor of Vascular Biology at HMS and the Vascular Biology Program at Boston Children's Hospital, and Professor of Bioengineering at SEAS.

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New 'Immuno-Engineering to Improve Immunotherapy' Center formed to advance cancer therapy - The Medical News

Genetics

$100 Genome Sequencing Will Yield a Treasure Trove of Genetic Data – Singularity Hub

What would the implications be if decoding your genes cost less than a pair of designer jeans? We might soon find out after a Chinese company claimed it can sequence the human genome for $100.

The speed at which the price of genetic sequencing has fallen has been astonishing, from $50,000 a decade ago to roughly $600 today. For a long time, the industry saw the $1,000 genome as the inflection point at which we would enter the genomic agewhere getting a read out of your DNA would be within reach for huge swathes of the population.

That milestone has come and gone, but progress hasnt stopped. And now Chinese firm BGI says it has created a system that can sequence a full genome for just $100. If the claims hold up, thats a roughly six times improvement over state-of-the-art technology.

The key to the breakthrough is a significant increase in the size of the chip that is used to analyze genetic data, so twice as many genomes can be processed at once. Their machine also uses a robotic arm to dunk the chip into baths of the chemicals used to carry out the sequencing process, which allows them to be reused multiple times.

The company says the system, which will be made available to customers late this year, is aimed at large-scale genomics projects and could make it possible to decode the DNA of 100,000 people a year.

The breakthrough could spur further price falls as well by breaking the stranglehold that industry leader Illumina has had on the market. Dennis Grishin, co-founder of startup Nebula Genomics, told MIT Tech Review that he believed the reason the price of genetic sequencing had remained stuck around $1,000 in recent years was due to Illuminas near monopoly.

A $100 genome could significantly broaden the scope of what we can do with genetic data. The growing field of population genetics promises to uncover the genetic quirks that set different groups of people apart, which can prove vital for developing new medicines and understanding the susceptibility of different groups to certain conditions.

While some ambitious projects, such as the UK Biobank project aimed at collating genetic data on 500,000 people, are already underway, the cost of sequencing has so far limited the scope of these projects. A dramatically cheaper system could see these kinds of initiatives become far more commonplace, greatly expanding our understanding of genetic diversity among humans.

By bringing the cost of full genome sequencing within reach of everyday people, the approach could also dramatically expand the scope of personalized medicine. While services like 23andMe have seen a huge expansion in consumer genetic testing, these services only decode a small fraction of the genome that isnt particularly useful for medical purposes.

DNA sequencing is already used to tailor cancer treatment by determining how peoples genetics are likely to influence their response to certain treatments, but it is still far from standard practice. At $100 the practice could become far more common and also be expanded to predict responses to a host of other treatments, ushering in a new era of personalized medicine.

Theres also hope that it would enable new tests that could provide early warning of susceptibility to a host of genetic diseases, or even sequence the DNA of patients microbiomes to detect imbalances in their gut flora that might be responsible for certain conditions or impact their responses to certain treatments.

Rade Drmanac, chief scientific officer of Complete Genomics, a division of BGI, told MIT Tech Review that at $100 it could soon be common to sequence the DNA of every child at birth. This could provide unprecedented early-warning for a host of diseases, but would also open up a Pandoras box of ethical concerns.

The movie Gattaca already explored the potential for discrimination when genetic testing becomes trivially easy, particularly when paired with increasingly powerful genetic engineering that is bringing the potential for designer babies ever closer.

Perhaps more importantly though, our understanding of how our genetics impact our lives is still very hazy. While we have identified some genes that strongly influence propensity for certain diseases, most human characteristics are governed by complex interactions between multiple genes whose activity can vary throughout our lives in response to environmental pressures.

Our ability to read our DNA is far ahead of our ability to understand it, which could lead to all sorts of problemsfrom creating a new class of worried well flagged as at risk of certain conditions that never come to be, to unnecessarily medicalizing or stigmatizing patients in ways that alter the trajectories of their lives.

With a $100 genome now within reach, we will have to tackle these issues with urgency to make sure the genomic age is one to look forward to rather than one to fear.

Image Credit: Pete Linforth from Pixabay

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Genetics

Coronaviruss Genetics Hint at its Cryptic Spread in Communities – The Scientist

When Emma Hodcroft read that, seemingly out of nowhere, a rash of cases of the novel coronavirus had popped up in Britain in late January, she started collecting media reports on them, searching the articles for clues as to how it had moved to the island nation. Early reports suggested that a lone traveler from Singapore, who was unaware he was infected with virus, had visited a French chalet for a few days and had spread the virus to others at the ski resort. This intrigued Hodcroft, who is half British and a postdoctoral researcher in evolutionary biologist Richard Nehers lab at the University of Basel in Switzerland, where she uses genetics to study and track diseases. She took notes on the cases that were associated with the infected traveler. At first, there wasnt that much information and the story was simple, she tells The Scientist. But more and more cases kept appearing, and she found it hard to keep track of who had traveled to which country and when they were diagnosed.

Hodcroft decided to generate an infographic showing the connections between the traveler from Singapore and the other coronavirus cases emerging in Europe. I thought, Ill make an image and see if anyone else finds this useful, she says. She posted the image on Twitter, and somewhat unexpectedly, it got a lot of attention, she says. People were definitely really, really interested in this. So I kept that image updated over the next week or so. As she updated it, the graphic showed that at least 21 people were exposed to the virus at the ski resort the traveler from Singapore visited; 13 of those people ended up developing COVID-19, the disease caused by the virus. After shed finished the preliminary work, a colleague of Hodcroft saw it and suggested she write it up for publication. She posted the paper on February 26; the next day it appeared in Swiss Medical Weekly.

Hodcroft talked with The Scientist about the work, how its conclusions have been supported by genetic testing of viral strains from patients, and what it tells us about the spread of the virus, SARS-CoV-2, in other countries.

Emma Hodcroft: Firstly, that it seems like so many people [at least 13] could be infected by a single person. It seems like they were infected by the man who traveled from Singapore. So thats quite a lot of forward transmission on his part in a fairly short time period; he was only in France for about four days. Of course, this could be some unusual event that doesnt normally happen, but it lets us put an outer bound on what is possible even if it is not common.

The other thing thats surprising is that, according to the patient statement that he released, the focal patient never had any symptoms. In his own words, he never felt sick. So he did all of this transmission without ever having any indication that he was unwell or that he should be taking any precautions to modify his behavior. It tells us that some infections might be from people who never even know that theyre sick.

Text continues below infographic

Contact tracing showing the spread of SARS-CoV-2 in a particular cluster of patients in Europe.

EH: As far as we can tell, no one from this cluster had severe symptoms. It seems like some people did have some symptoms, but they were never serious. And thats also interesting because it shows that if we didn't know about this outbreak, its pretty likely that these people would have kind of written this off as a bad cold or the flu. None of them would have ended up going to hospital or significantly changing their behavior. And again, this indicates that it might be quite hard, and it is becoming quite hard, to contain this virus because some people don't feel very unwell, such that they would change their behavior or go for testing.

EH: In the US, from the information available, it still doesnt seem like the US has really ramped up testing. We dont know the number of tests that have been performed because its come down off of the CDC website, which is a little concerning. But at least the last reports that were given to us show the US was really lagging behind most countries in the number of tests that it had done.

A few days ago, the research group called the Seattle Flu Study, which is designed to take community samples from random people who have any kind of cough, runny nose, or cold-like symptoms and look for the fluthey pivoted and started testing some of the samples for coronavirus. They found a case in the Seattle area and sequenced the viral genome of the infected person [posted on NextStrain] and showed it links very closely with another case in the Seattle area thats from mid-January. And so this strongly suggests (though we dont yet know for certain) that there has been ongoing undetected transmission in Seattle since mid-January and wasnt picked up because we werent looking for it. This has become clearer in the last few days, as more cases and even deaths have been reported in Washington State. That tells us the virus hasnt just appeared in the last few days in the area.

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The viral genome of the first case in Washington (USA/WA1/2020) is identical to Fujian/8/2020. The genome of the virus from a second case in Washington (USA/WA2/2020) is identical to the first Washington case, except it has three additional mutations. This suggests WA1 was a traveler from China bringing the virus to Snohomish County, Washington in mid-January, where the virus circulated undetected for about five weeks, a timespan that explains why WA2 is so similar genetically, with a few mutations. The graphic shows the connection to the other cases with viral sequences now available.

EH: This virus causes respiratory illness, which can make you feel unwell for a few days and then you get better or it can progress. If the illness progresses it can cause lung damage that makes the person more susceptible to other illnesses, such as bacterial infection. This can be treated too and for many people that treatment turns the course of the infection, but some dont and the effort can essentially delay their death. So the infection may have occurred weeks [before a person dies]. This is not something intrinsic to this virus, however. With respiratory illness, its usually something that takes a substantial amount of infection and lung damage before you succumb to it.

EH: Sequencing can tell us a lot about what is happening with the virus right now. The Washington samples are a perfect example. . . . Without having these genomes, we never would have seen this signal of ongoing transmission, which we saw just before the case explosion in Washington. And on the flip side we can tell when cases are coming in from other countries. We have another genome from Washington State thats grouping with genomes that we know have a travel history to Italyso it seems like this could be a case where [an infected person] came back from Italy.

When you have a very small number of cases of a disease, you can do this just through epidemiological contact tracing: you can go to everyone and ask questions and find out the connections between the cases. As the case numbers scale up, this becomes very hard to do. With genetic sequencing, we can do this without having to go and try and figure out where everyone was at the time of infection. Weve had an influx of sequences from Brazil, Switzerland, Mexico, Scotland, Germany. These have clustered with sequences from Italy and have a travel history from Italy and so from that we can show that Italy really is now exporting cases around the world to multiple countries.

EH:Theres been a lot of modeling, not only with genetics but epidemiologically in the last few weeks, and we had pretty strong indications that circulation was wider than publicly thought. At the time, we did try to some extent to get this message out to government health agencies and the public in general. I do think that in the future, incorporating a little bit more of that scientific expertise perhaps into the public dialogue and government decision-making could make a big difference. The earlier that you can act in an epidemic, you have more effect you can have, because one person goes on to infect a few more people who go on to infect a few more people. Its much harder once that has gone up to 10 [infected] people, than if you can stop with person one.

One thing I would note is that studies have shown that limiting transportation really doesnt make much of an impact for outbreaks. Quarantining particular cities, if they seem to be epicenters, can work as a preventive measure, but as the epidemic scales up, you move past being able to contain it in this sense, [and] what you end up doing is just disrupting supply routes, interrupting business, making all of these things much harder.

Editors note: This interview has been edited for brevity.

Ashley Yeager is an associate editor atThe Scientist. Email her at ayeager@the-scientist.com. Follow her on Twitter @AshleyJYeager.

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Genetics

Genetic testing is helping prevent cancer and changing treatment plans – PhillyVoice.com

It is a truth universally acknowledged that cancer prevention and early cancer detection saves lives.

As scientists and physicians at the major cancer centers work together to unravel the link betweengenetic alterations and cancer risk, genetic testing is rapidly becoming an impactful tool for matching patients to individualized cancer screening programs.

Often called the Angelina Jolie effect based on the actor'slaudable effort to enhance understanding of increased cancer risk for patients with alterations in the BRCA1 or BRCA2 genes the general public has become appropriately more aware of the importance that genetics can play in cancer risk.

Put most simply, genetic testing utilizes DNA usually obtained from small amounts of saliva or blood to identify a genetic mutation, or change, in your DNA that may increase your risk of developing certain cancers. This is determined by sequencing the DNA, which reads the specific DNA code for a subset of genes known to be important for affecting cancer development.

Individuals with a strong family history of cancer or those of a certain ancestry, such as Ashkenazi Jewish ancestry, might be more likely to carry these genetic mutations, but lack of a family cancer history does not mean that someone wont be a carrier. In many cases, genetic risk of cancer arises spontaneously through DNA errors that occur in developing embryos. In other words, genetic risk can result from a spot of ill-timed bad luck, on or before your journey began at the single cell stage.

Being aware that you have a genetic mutation that might increase your risk of developing cancer can help you and your doctor work together and create a personalized plan to help increase your chance of prevention or early detection.

For a man carrying specific alterations in the BRCA2 gene, there may be concern for increased risk of prostate or pancreatic cancer development. The team approach is then taken. After meeting with a genetic counselor, a personalized plan for that patient may entail earlier or more frequent prostate cancer screening, and support for helping the patient change behaviors that may further enhance pancreatic cancer risk, like smoking.

At the Sidney Kimmel Cancer Center at Jefferson, the Mens Genetic Risk centralizes these plans, and coordinates with the patients care team to tailor the individual health plan. Further discussions are also had with regard to cascade testing, or testing family members who may also be at risk. As such, genetic testing can impact not just the patient themselves, but family members as well.

Genetic testing might be recommended to someone if they have a strong family history of cancer, which may include several first-degree relatives parents, siblings and children with cancer; many relatives with the same type of cancer; relatives who were diagnosed at a younger-than-normal age; or a relative diagnosed with a rare cancer, such as a male with breast cancer.

Someone who has already been diagnosed with cancer may benefit from genetic testing as well, especially if they were diagnosed at a young age or have a family history of cancer. Cancers with a known hereditary component include breast, ovarian, uterine, prostate, colorectal, melanoma, pancreatic and stomach cancers.

Having a family history of cancer is not limited to a having a family history of thesamecancer. For example, and related to our case above, a man whose mother or sister had breast cancer might be at risk himself for prostate cancer.

It is also important to note that the presence of a gene mutation is also relevant when treating existing cancer. Certain genetic mutations are also associated with a greater risk of having an aggressive cancer and resistance to certain therapies, which can help your doctor manage specific tumor types.

Your results may help your doctor decide on the best treatment regimen, because researchers have found that some treatments are more effective in people with certain gene mutations. In fact, the FDA has recently approved cancer therapies that are only for patients whose tumors have specific gene alterations and it is expected that many more such targeted therapies will be approved and ready for use in treating cancer.

So what if you have been tested and you do not have an identified genetic risk? It is important to note that not having a family history of cancer or genetic risk of cancer does not guarantee that you will never develop cancer. With regard to family history, the National Cancer Institute notes that only 5-10% of cancers are due to inherited gene mutations.

Additionally, having a family history of cancer does not mean that you are certain to be diagnosed with cancer one day yourself. Genetic testing can help inform you of your genetic risk for certain diseases, but it does not inform you of your overall risk. Other factors that contribute to an increased risk for cancer include environmental factors and lifestyle choices, many of which are modifiable.

If you are considering genetic testing or have questions about whether you or your family should undergo testing, talk to your doctor or other health care providers. Talking to a health professional or genetic counselor can help you decide whether you would benefit from testing. They will collect your family and personal health history, explain what kind of information the test can provide you, and help you decide whether the test is right for you.

After undergoing genetic testing, it is important that you talk to your health care provider about what the results mean for you, whether positive or negative. The results can be confusing, and they can help you interpret your results, allay any fears, discuss potential implications for your family, and help you make an informed decision about how to proceed based on the results. Discussion with a specialist is important for future care decisions.

If appropriate, your doctor may discuss cancer risk-reduction strategies with you, like preventive surgery, medications that help reduce risk or lifestyle changes. They also may recommend alternative screening options to help detect the cancer early, such as beginning mammograms before age 40 or having a colonoscopy at 45 rather than 50.

In addition to the clinical genetic testing, a growing number of companies are making tests available to consumers that can provide insight into ones ancestry, as well as certain health information. There are a few things to keep in mind regarding these direct-to-consumer tests if you decide to go ahead with one.

Ancestry DNA tests are typically not clinical grade, meaning that the information is not of the established quality required to change someones health plan. Even if a cancer gene is suspected on these tests, confirmation would be required using a clinical-grade test that has been deemed valid and reliable for detecting cancer gene alterations.

In addition, many at-home tests are very small in scale, and leave out testing of many genes known to be influential in determining cancer risk. For example, an at-home test might screen for mutations in the BRCA1 and BRCA1 genes, but not for the genes associated with Lynch syndrome, an inherited disorder that increases the risk of several cancer types, including colorectal cancer.

There is a growing concern that negative results from an at-home test can provide consumers with a false sense of security. These tests should not be used as a substitute for the genetic counseling and testing you would receive from your health care provider, who will usually re-order a clinical test to confirm the results, and help you understand the results of the test.

Despite the importance of understanding personal genetic risk of cancer, there are justifiable concerns about privacy. This is an important concept for every person to consider. The Health Insurance Portability and Accountability Act protects your genetic data if you were tested through your health care provider. However, there are fewer protections with the direct-to-consumer DNA testing companies, so be sure to understand the companys privacy policy when signing up for services. Some companies may share your results with third parties, such as medical or pharmaceutical researchers.

A common concern for people considering genetic testing is discrimination based on their genetics. The Genetic Information Nondiscrimination Act is a federal law that protects individuals from genetic discrimination. GINA prohibits health insurers from discrimination based on the genetic information of enrollees, meaning they may not use genetic information to make decisions regarding eligibility, coverage, underwriting or premium-setting. However, GINA does not cover disability, life and long-term care insurance.

GINA also prevents employers who have at least 15 employees from using genetic information in employment decisions such as hiring, firing, promotions, pay and job assignments. Additionally, some states have enacted laws that offer additional protections against genetic discrimination. For more information on GINA and genetic discrimination, click here

In sum, cancer genetics is a rapidly evolving field, and the era is upon us wherein individual wellness plans will be as guided by genetic information as they are by vital signs. It was not long ago when the only genetic testing option was examining the BRCA1 and BRCA2 genes for inherited mutations associated with breast and ovarian cancers.

Fast-forwarding to 2020, we not only understand more about BRCA mutations, but we have discovered that there are many hundreds of other genes related to cancer development and progression. If you had BRCA testing many years ago or were told previously that you were ineligible for genetic testing, talk to your doctor.

As we learn more about genetic mutations and we continue to expand the recommendations for testing to include more people, your doctor might recommend that you undergo genetic testing now or consider additional genetic testing. Understanding your genetic code just might be a life saver!

Karen E. Knudsen, Ph.D., enterprise director at the Sidney Kimmel Cancer Center Jefferson Health, oversees cancer care and cancer research at all SKCC sites in the Greater Philadelphia region. She writes occasionally on topics related to cancer.

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