Warren symposium follows legacy of geneticist giant

If we want to understand how the brain creates memories, and how genetic disorders distort the brain’s machinery, then the fragile X gene is an ideal place to start. That’s why the Stephen T. Warren Memorial Symposium, taking place November 28-29 at Emory, will be a significant event for those interested in neuroscience and genetics. Stephen T. Warren, 1953-2021 Warren, the founding chair of Emory’s Department of Human Genetics, led an international team that discovered Read more

Mutations in V-ATPase proton pump implicated in epilepsy syndrome

Why and how disrupting V-ATPase function leads to epilepsy, researchers are just starting to figure Read more

Tracing the start of COVID-19 in GA

At a time when COVID-19 appears to be receding in much of Georgia, it’s worth revisiting the start of the pandemic in early 2020. Emory virologist Anne Piantadosi and colleagues have a paper in Viral Evolution on the earliest SARS-CoV-2 genetic sequences detected in Georgia. Analyzing relationships between those virus sequences and samples from other states and countries can give us an idea about where the first COVID-19 infections in Georgia came from. We can draw Read more

antioxidants

Oxidative stress ain’t about free radicals, it’s about sulfur

This recent paper in Circulation, from Arshed Quyyumi and colleagues at the Emory Clinical Cardiovascular Research Institute, can be seen as a culmination of, even vindication for,  Dean Jones’ ideas about redox biology.

Let’s back up a bit. Fruit juices, herbal teas, yogurts, even cookies are advertised as containing antioxidants, which could potentially fight aging. This goes back to Denham Harman and the free radical theory of aging. [I attempted to explain this several years ago in Emory Medicine.]

We now know that free radicals, in the form of reactive oxygen species, can sometimes be good, even essential for life. So antioxidants that soak up free radicals to relieve you of oxidative stress: that doesn’t seem to work.

Dean Jones, who is director of Emory’s Clinical Biomarkers laboratory, has been an advocate for a different way of looking at oxidative stress. That is, instead of seeing cells as big bags of redox-sensitive chemicals, look at cellular compartments. Look at particular antioxidant proteins and sulfur-containing antioxidant molecules such as glutathione and cysteine.

That’s what the Circulation paper does. Mining the Emory Cardiovascular Biobank, Quyyumi’s team shows that patients with coronary artery disease have a risk of mortality that is connected to the ratio of glutathione to cystine (the oxidized form of the amino acid cysteine).

How this ratio might fit in with other biomarkers of cardiovascular risk (such as CRP, suPAR, PCSK9, more complicated combinations and gene expression profiles, even more links here) and be implemented clinically are still unfolding.

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Antioxidants are no panacea

Derek Lowe, a respected science blogger and drug discovery expert who was blogging when this writer was still working in the laboratory, today has a roundup of a concept that anyone hanging around Emory might have clued into already.

Namely, antioxidants aren’t all they’re cracked up to be. Judging from the messages Gafas Ray Ban outlet to shoppers in the supermarket vitamin aisle, everybody needs more antioxidants. But evidence is accumulating that in some situations, antioxidants can be harmful: negating the adaptive effects of exercise on muscle tissue or even encouraging tumor growth, Lowe writes.

At Emory, Dean Jones has been patiently explaining for years that cells are not simply big bags with free radicals, thiols and antioxidants sloshing around indiscriminately. Instead, cells and oxidation-sensitive components are highly compartmentalized. Take for example, this recent paper in Molecular & Cellular Proteomics from Jones and Young-mi Go. Two major antioxidant systems in cells, glutathione and thioredoxin, function distinctly and independently, they show.

In a related vein, Kathy Griendling’s and David Lambeth’s labs were at the center of the discovery that reactive oxygen species are not only poisons that overflow from mitochondria, but important signals involved in many aspects of cell biology.

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A good reason to enjoy a little Valentine’s Day chocolate

From the Clinic to You

BY CHERYL WILLIAMS, RD, LD

If you’re looking for an excuse to indulge in the yummy chocolate you get this Valentine’s Day, research suggests it may not be so bad for you. You might also want to register and place your bets with confidence at สมัครและเดิมพันที่ UFABET.

A number of studies, conducted over the last decade have associated cocoa and dark chocolate consumption with heart health benefits. These benefits come from cocoa, derived from the cacao plant, which is rich in flavonoids (cocoa flavanols to be exact). Flavonoids are antioxidants also found in berries, grapes, tea, and apples. As a whole, antioxidants prevent cellular damage and inflammation which are two major mechanisms involved in the development of heart disease.

So what does the research say?

A study published in the American Journal of Clinical Nutrition found that high-flavanol dark chocolate reduced bad cholesterol (LDL) oxidation and increased good cholesterol (HDL) levels. LDL oxidation promotes the development of plaque and hardening of the coronary arteries, thus lessening oxidation could help to prevent heart disease.

A Harvard research study found that flavanol-rich cocoa induced nitric-oxide production, which causes blood vessels to relax and expand, thus improving blood flow. Improved coronary vasodilation could potentially lower the risk of a cardiovascular event.

In a double-blind randomized Circulation study flavonoid-rich dark chocolate (containing 70% cocoa) reduced serum oxidative stress and decreased platelet activity (clumping) in heart transplant recipients. This favorable impact on vascular and platelet function is relevant because vascular dysfunction and platelet activation (adhesion upon damaged cell wall) are the basis of atherothrombosis (blood clotting) and coronary artery disease.

How can you reap chocolate’s potential benefits?

Not all cocoa products and/or chocolates are created equal. Milk chocolate, for example, is not rich in flavanols (contains only 10-20% cocoa solids) and white chocolate contains none at all. In addition, some cocoa products and chocolates are processed with alkali, which can destroy flavanols.

Follow these tips for heart healthy chocolate consumption:

  • Avoid cocoa products processed with alkali (dutched) as seen in the ingredient list
  • Choose dark chocolate with at least 70% cocoa
  • Enjoy 100% unsweetened non-dutched cocoa (great for hot chocolate!)

Also, remember that chocolate is not a health food, as it is high in calories, fat and added sugar. Thus, make room for dark chocolate by cutting extra calories elsewhere in your diet. Additionally, stick to small amounts (e.g. 1 ounce) and do not eat in place of plant-based whole foods such as vegetables and fruits.

Cheryl Williams is a registered dietitian at the Emory Heart & Vascular Center. She provides nutrition therapy, wellness coaching, monthly nutrition seminars and healthy cooking demonstrations working with the Emory HeartWise Cardiac Risk Reduction Program.

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Targeting antioxidants to mitochondria

Why aren’t antioxidants magic cure-alls?

It’s not a silly question, when one sees how oxidative stress and reactive oxygen species have been implicated in so many diseases, ranging from hypertension and atherosclerosis to neurodegenerative disorders. Yet large-scale clinical trials supplementing participants’ diets with antioxidants have showed little benefit.

Emory University School of Medicine scientists have arrived at an essential insight: the cell isn’t a tiny bucket with all the constituent chemicals sloshing around. To modulate reactive oxygen species effectively, an antioxidant needs to be targeted to the right place in the cell.

Sergei Dikalov and colleagues in the Division of Cardiology have a paper in the July 9 issue of Circulation Research, describing how targeting antioxidant molecules to mitochondria dramatically increases their effectiveness in tamping down hypertension.

Mitochondria are usually described as miniature power plants, but in the cells that line blood vessels, they have the potential to act as amplifiers. The authors describe a “vicious cycle” of feedback between the cellular enzyme NADPH oxidase, which produces the reactive form of oxygen called superoxide, and the mitochondria, which can also make superoxide as a byproduct of their energy-producing function.

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