Really? I had a heart attack?

Discrepancy between patients' recollection and medical records touches on an issue of concern for clinical cardiology research

Test of megadose vitamin D in intubated critical care patients

Jenny Han presenting her vitamin D research this week at American Thoracic Society meeting. Hat tip to Greg Martin for picture!

A few links for BEINGS2015

Three links relevant to #BEINGS2015

Really? I had a heart attack?

A recent Harvard study, published in Circulation, found a surprising level of inconsistency between what medical records say about whether people had a heart attack and what they report themselves in surveys.

About a quarter of Medicare patients who said in a survey that they previously had a heart attack have no record of having any heart-related hospital admission. Conversely, about one-third of patients who, according to Medicare, experienced a heart attack said they hadn’t.

This finding is consistent with an Emory study from cardiologists Neal Dickert and Habib Samady, in which participants in a clinical trial were interviewed just a couple days after the initial procedure. The trial was testing a “post-conditioning” modification of angioplasty+stenting performed during treatment for a heart attack. Just over half (55 percent) of the participants initially remembered being asked to participate when asked. Read more

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Test of megadose vitamin D in intubated critical care patients

Whether dietary supplementation with vitamin D is beneficial, in terms of preventing disease, has been controversial. However, vitamin D has been reported to increase immune cells’ production of microbe-fighting proteins. That’s why Emory doctors have been testing whether high doses of vitamin D could be helpful for critical care patients, who need to ward off infections.

The results of a small-scale clinical trial, presented in Denver this week at the American Thoracic Society meeting, suggest that high doses of vitamin D could decrease the length of hospital stays in critically ill patients with respiratory failure. Read more

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A few links for BEINGS2015

Several well-known authors, scientists and bioethicists are in downtown Atlanta’s Tabernacle for the #BEINGS2015 conference. Paul Wolpe and the Center for Ethics have been central to organizing the event, and several Emory biomedical and genetics researchers will be involved in shaping the consensus documents that will emerge.

I won’t attempt to summarize the ongoing discussion at this point; with biotechnology, it is difficult to draw a circle around certain topics and say “we’re going to focus on this, but not this” and today was a good example. The border between existing agricultural biotechnology and new organisms seems hard to define.

Three interesting relevant links:

The National Academy of Sciences is launching an effort to guide decision making on human gene editing technologies such as Cas9/CRISPR

Collection of scientists’ comments on human gene editing and Cas9/CRISPR in Nature Biotechnology

Nature Chem Bio paper on engineered yeast that “paves way for home brew heroin”. Interesting role of FBI in overseeing this emerging area, and note that full production of opiates in yeast may look close, but is still not yet possible.

 

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Spotlight on liver fibrosis

For a May explainer, we’d like to spotlight liver fibrosis. Two recent papers from Emory research teams in the journal Hepatology focus on this process.

Liver fibrosis is an accumulation of scar tissue and proteins outside cells that occurs as a result of chronic damage to the liver. It involves inflammation and immune cells, as well as activation of a type of cell in the liver (hepatic stellate cells), which usually stores fat and vitamin A. Fibrosis and cirrhosis are not the same. Think of it this way: cirrhosis is the late stage of the disease, but fibrosis is how someone can get there.

The liver has a remarkable, even mythical, ability to regenerate, but there is a long list of ways that someone can injure this most vital organ. Quickly – take too much acetaminophen (the most common cause of acute liver failure in the United States). More slowly – develop a hepatitis C infection. Drink large quantities of alcohol. Or something with more subtle effects: consume a diet high in sugar, which can lead to fatty liver. The relationship between fatty liver and more serious liver disease is currently under investigation.

One of the Hepatology papers comes at liver fibrosis from a malaria angle. Patrice Mimche, Tracey Lamb and colleagues show the involvement of EphB2 tyrosine kinase, a signaling molecule not previously known to be involved in liver fibrosis.

Malaria parasites have a complex life cycle, growing in the liver and then in the blood. Lamb says an important part of her paper was the finding that in mouse malaria infection, EphB2 is activated during the blood stage on immune cells infiltrating into the liver. EphB2 (an active drug discovery target) may be acting as a tissue-specific adhesion molecule, she says.

Read more

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Education is a life preserver, after heart attack

For the last decade, cardiology researchers have been collecting detailed information on the patients who come through Emory’s catheterization labs. The density of data (close to 7000 people) can make it possible to achieve some insights about mortality in American society.

Cardiology research fellow Salim Hayek, MD, presented some provocative findings yesterday in a poster competition at the American College of Physicians meeting in Boston. He has been working with Arshed Quyyumi, MD and colleagues at Emory’s Clinical Cardiovascular Research Institute.

Their analysis shows “college education as a discrete indicator of socioeconomic status was an independent predictor of survival.”

A key thing to remember when looking at this data is that most of the people in the cath lab at a given moment are not actually having a heart attack — just 13 percent are. (Abstract/poster available upon request). However, there’s enough suspicion or history of heart disease for doctors to take a look inside; most of them have hypertension and coronary artery disease, and many have had a heart attack in the past. The group is mostly men, average age 63. Read more

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Six beautiful images — choose your favorites

WoodruffMatthew1

Matthew Woodruff — Bali Pulendran lab

ImageJ=1.48g unit=micron

Kenneth Myers — James Zheng lab

Joshua_Strauss_OPE_Image

Joshua Strauss — Elizabeth Wright lab

AndersonJoAnna

JoAnna Anderson — Francisco Alvarez lab

AlexTamas

Alexey Tamas — Charles Searles lab

Emory’s Office of Postdoctoral Education is holding a Best Image contest. The deadline to vote is this Thursday, April 30. You can look at these beautiful images (and guess exactly what they are, based on what lab they come from), but to VOTE, you need to go to the OPE site.

This is part of the run up to their Postdoctoral Research Symposium at the end of May.

(Hat tip to Ashley Freeman in Dept of Medicine!)

Read more

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Congratulations to AAAS Mass Media fellows

Two Emory graduate students, Anzar Abbas and Katie Strong, will be spending the summer testing their communication skills as part of the AAAS Mass Media fellowship program. The program is supposed to promote science communication by giving young scientists a taste of what life is like at media organizations around the country. Both of Emory’s fellows have already gained some experience in this realm.

Abbas, a Neuroscience student who recently joined brain imaging number cruncher Shella Keilholz‘s lab, will be at Howard Hughes Medical Institute. He is part of the group that recently revived the Science Writers at Emory publication In Scripto.

Strong, a Chemistry student working with Dennis Liotta on selective NMDA receptor drugs, will be at the Sacramento Bee. She has been quite prolific at the American Journal of Bioethics Neuroscience and its Neuroethics Blog.

(Thanks to Ian Campbell, a previous AAAS Mass Media fellow from Emory who worked at the Oregonian, for notifying me on this!)

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Risk triangle: immune gene, insecticide, Parkinson’s

Genetic variation and exposure to pesticides both appear to affect risk for Parkinson’s disease. A new study has found a connection between these two risk factors, in a way that highlights a role for immune responses in progression of the disease.

The results are published in the inaugural issue of NPJ Parkinson’s Disease.

The findings implicate a type of pesticide called pyrethroids, which are found in the majority of commercial household insecticides, and are being used more in agriculture as other insecticides are being phased out. Although pyrethroids are neurotoxic for insects, exposure to them is generally considered safe for humans by federal authorities.

The study is the first making the connection between pyrethroid exposure and genetic risk for Parkinson’s, and thus needs follow-up investigation, says co-senior author Malu Tansey, PhD, associate professor of physiology at Emory University School of Medicine.

The genetic variation the team probed, which has been previously tied to Parkinson’s in larger genome-wide association studies, was in a non-coding region of a MHC II (major histocompatibility complex class II) gene, part of a group of genes that regulate the immune system.

“We did not expect to find a specific association with pyrethroids,” Tansey says. “It was known that acute exposure to pyrethroids could lead to immune dysfunction, and that the molecules they act on can be found in immune cells; now we need to know more about how longer-term exposure affects the immune system in a way that increases risk for Parkinson’s.”

“There is already ample evidence that brain inflammation or an overactive immune system can drive the progression of Parkinson’s. What we think may be happening here is that environmental exposures may be altering some people’s immune responses, in a way that promotes chronic inflammation in the brain.”

For this study, Emory investigators led by Tansey and Jeremy Boss, PhD, chair of microbiology and immunology, teamed up with Stewart Factor, DO, head of Emory’s Comprehensive Parkinson’s Disease Center, and public health researchers from UCLA led by Beate Ritz, MD, PhD. The first author of the paper is MD/PhD student George T. Kannarkat.

The UCLA researchers used a California state geographical database covering 30 years of pesticide use in agriculture. They defined exposure based on proximity (someone’s work and home addresses), but did not measure levels of pesticides in the body. Pyrethroids are thought to decay relatively quickly, especially in sunlight, with half-lives in soil of days to weeks. Read more

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Fragile X syndrome: building a case for a treatment strategy

New research in mice strengthens a potential strategy for treating fragile X syndrome, the most common inherited form of intellectual disability and a major single-gene cause of autism spectrum disorder.

The results, published April 23 in Cell Reports, suggest that a drug strategy targeting a form of the enzyme PI3 (phosphoinositide-3) kinase could improve learning and behavioral flexibility in people with fragile X syndrome. The PI3 kinase strategy represents an alternative to one based on drugs targeting mGluR5 glutamate receptors, which have had difficulty showing benefits in clinical trials.

Research led by Emory scientists Gary Bassell, PhD and Christina Gross, PhD had previously found that the p110β form of PI3 kinase is overactivated in the brain in a mouse fragile X model, and in blood cells from human patients with fragile X syndrome.

Now they have shown that dialing back PI3 kinase overactivation by using genetic tools can alleviate some of the cognitive deficits and behavioral alterations observed in the mouse model. Drugs that target the p110β form of PI3 kinase are already in clinical trials for cancer.

“Further progress in this direction could lead to a clinical trial in fragile X,” says Bassell, who is chair of Cell Biology at Emory University School of Medicine. “The next step is to test whether this type of drug can be effective in the mouse model and in human patient cells.” Read more

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