Stuffs of science fiction and Bollywood movies are rapidly coming to pass.  Photochemical tissue bonding, or laser-assisted nanosuturing is a novel technique that allows the surgeon to close the epidermal defect with laser following the application of a light-sensitive dye to the wound edges eliminating the need for epidermal suture placement.

As this article extols it as a new cutting-edge technology that may rewrite the surgical books in terms of standard surgical closure procedures. After the clinical trials the results are described thus:

Results showed that a vast majority of the patients preferred the laser-assisted approach. In all cases, the tensile strength was comparable if not better than the traditional closure technique, and the scar appearance of the laser-treated side in many of the patients was near imperceptible.

Though in a few cases, the scar was not clinically and aesthetically attractive, Dr. Tsao says, the laser-treated side was always the better appearing side. There were no complications, infections or dehiscence associated with either the traditional or the laser-assisted treated wound edges.

Patients were evaluated at two weeks, three months and at six months. Study endpoints included efficacy of wound closure, vascularity, pigmentation, elevation, atrophy and scar appearance. The surgical sites were evaluated by two blinded physicians and patients were also asked to make an evaluation based on the same attributes.

You can read the complete article here at Modern Medicine.

dermatology, no scars

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Mayo”s long-standing practice had been for doctors to give patients detailed oral explanations of the risks, benefits and alternatives to a procedure and to get verbal consent and document it in patients” charts, spokesman Brian Anderson said. Patients weren”t asked to sign specific consent forms, he said. “We”ve always had an informed consent process,” Anderson said. “That is certainly critical, ethically paramount.”

Similarly one of my former institution required a hand written consent of few lines basically stating that the patient was aware of the possible complications including death (which is true though rare) and consented for the procedure. I would be surprised if the patients who indeed developed complications did feel informed later in retrospect. The sad thing is; there is no escape from law- the form is the only thing that matters 6 months hence. Image courtesy: Fannie-Annie

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Must have been a pleasant surprise for the commuters and what a great excuse for being late to office!!

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I am already using an ebook reader – my bebook a variant of Hanlin v3 which is marketed by Mybebook.com from Netherlands. I have been using it for the last 3 months and  it has been great. I need not carry a handful of books each time I travel and  what is even better; I carry this around with me and can read while waiting- in  clinics, on road basically whenever i wish. It supports most ebook formats from pdf, mobi, lit, epub, doc, html, txt, prc, fb2, jpg files besides playing mp3. I have a preference for reading in lit or rtf formats with a tiny clock running at the top of the page.

I have downloaded a great number of books for free from Project Gutenberg with no DRMs  and few new ones from mobipocket directly onto ereader using USB.And one thing is for sure- reading on eink or viziplex (as both the BeBook and Kindle use) is waaaay easier on the eyes rather than reading on the computer or cellphone reader and you do need a nightlamp/ light for reading in bed at night.

The great features of Kindle 2.0 is wireless connectivity with basic browsing and storage of library on their network. They have also removed SD card storage present in the first Kindle and is present in the Bebook. A lot of features of Kindle is available only in the US and for me that is a minus. The downside is that the complex pdf files do not display so well and that is true for mybebook as well.

If you love reading and do not yet have a ereader I would suggest you get one as early as possible and enjoy the pleasure of reading!

Ebook reader, eink

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As advances in genetics are made the influence of genes on individual’s health is all the more apparent. It is quite well known that people of South Asian origin are inordinately susceptible to heart diseases besides diabetes and associated metabolic syndromes.

Today’s Genetics Nature carries a paper delineating the high incidence of genetic mutation among Indians which is associated with Cardiomyopathy and heart failure.Heart failure is a leading cause of mortality in South Asians. However, its genetic etiology remains largely unknown¹. Cardiomyopathies due to sarcomeric mutations are a major monogenic cause for heart failure (MIM600958). Here, we describe a deletion of 25 bp in the gene encoding cardiac myosin binding protein C (MYBPC3) that is associated with heritable cardiomyopathies and an increased risk of heart failure in Indian populations (initial study OR = 5.3 (95% CI = 2.3–13), P = 2 10^-6; replication study OR = 8.59 (3.19–25.05), P = 3 10^-8; combined OR = 6.99 (3.68–13.57), P = 4 ^-11) and that disrupts cardiomyocyte structure in vitro. Its prevalence was found to be high (4%) in populations of Indian subcontinental ancestry. The finding of a common risk factor implicated in South Asian subjects with cardiomyopathy will help in identifying and counseling individuals predisposed to cardiac diseases in this region.

This article was further reported in Medical News Today

The Worst Luck In The World? The Heart Disease Mutation Carried By 60 Million

Heart disease is the number one killer in the world and India carries more than its share of this burden. Moreover, the problem is set to rise: it is predicted that by 2010 India’s population will suffer approximately 60% of the world’s heart disease. Today, an international team of 25 scientists from four countries provides a clue to why this is so: 1% of the world’s population carries a mutation almost guaranteed to lead to heart problems and most of these come from the Indian subcontinent, where the mutation reaches a frequency of 4%.

Considering that the mutation is so dangerous; how come it is so common? Well-

The combination of such a large risk with such a high frequency is, fortunately, unique. “How can such a harmful mutation be so common?” asks Chris Tyler-Smith from The Wellcome Trust Sanger Institute, Hinxton, UK. “We might expect such a deleterious change to have ‘died out’.

“We think that the mutation arose around 30,000 years ago in India, and has been able to spread because its effects usually develop only after people have had their children. A case of chance genetic drift: simply terribly bad luck for the carriers.”

The original advanced online paper is here( in pdf)

Image: topher76

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