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Sudden cardiac arrests are more likely to happen on any day at any time : Study

Raghu Kshitiz



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A new study has showed that sudden cardiac arrests are more likely to happen on any day at any time, challenging previous claims that weekday mornings — especially Mondays — were the danger zones.

Previously heart experts have long believed that weekday mornings were the danger zones for unexpected deaths from sudden cardiac arrests.

“While there are likely several reasons to explain why more cardiac arrests happen outside of previously identified peak times, stress is likely a major factor,” said Sumeet Chugh, a Professor of medicine from the Smidt Heart Institute in the US.

“We now live in a fast-paced, ‘always on’ era that causes increased psycho-social stress and possibly an increase in the likelihood of sudden cardiac arrest,” Chugh added.

Almost 17 million cardiac deaths occur annually worldwide while the survival rate from sudden cardiac arrest is less than one per cent.

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For the study, published in the journal Heart Rhythm, Chugh’s team analysed data on 1,535 from the community-based Oregon Sudden Unexpected Death Study between 2004 to 2014, among which only 13.9 per cent died in the early morning hours, the findings revealed.

All reported cases were based on emergency medical service reports containing detailed information regarding the cause of the cardiac arrest.

“Because sudden cardiac arrest is usually fatal, we have to prevent it before it strikes,” Chugh said. “Our next steps are to conclusively determine the underlying reasons behind this shift, then identify public health implications as a result,” he added.

Apart from stress, other contributing factors may be a shift in how high-risk patients are being treated, as well as inadequacies in how past studies have measured time of death caused by sudden cardiac arrest.

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Scientists find genetic risk factor for erectile dysfunction

Raghu Kshitiz



WASHINGTON — For the first time, scientists have found a specific place in the human genome that raises a man’s risk of erectile dysfunction.

The researchers, in the study published on Monday in the journal Proceedings of the National Academy of Sciences, analyzed data from hundreds of thousands of men.

They found that gene variations in a specific spot in the human genome near the SIM1 gene that are significantly associated with an increased risk of impotence.

The finding is a significant progress in the understanding of the genetics underlying erectile dysfunction (ED), the inability to obtain and maintain an erection sufficient for sexual activity, which is a common condition of men of primarily in middle and older ages.

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“Identifying this SIM1 locus as a risk factor for erectile dysfunction is a big deal because it provides the long sought-after proof that there is a genetic component to the disease,” said study author Eric Jorgenson, a research scientist at Kaiser Permanente Northern California’s division of research.

The disease is linked to many causes, such as neurological, hormonal and vascular factors. Many men don’t respond to therapies based on these factors however.

Genetics has been suspected to be a factor in about one-third of ED cases, but researchers have failed to make any link with any specific genomic locations until now.

The new study found that variations in a genetic locus near the SIM1 gene are significantly associated with an increased risk of erectile dysfunction.

The researchers ruled out that the risk was due to other known risk factors for erectile dysfunction, such as body mass index.

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The study also demonstrated a biological role for the genetic location in regulating sexual function, strongly suggesting that these variations can cause erectile dysfunction.

The study found that variations in the SIM1 locus were associated with a 26-percent increased risk of erectile dysfunction. This risk was independent of known erectile dysfunction risk factors.

The SIM1 gene is known to be part of a signaling pathway that plays a central role in body weight regulation and sexual function.


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