The World Health Organisation (WHO) has removed India from the list of countries with active endemic wild poliovirus transmission.

In written reply to a question in the Rajya Sabha, Minister of State for Health and Family Welfare Abu Hasem Khan Choudhury said Polio free is certified for WHO regions by the Regional Certification Commission and not for individual country.

The South-East Asia Regional Commission for Polio Eradication (SEA-RCCPE) has examined the data of 31 states/Union Territories of India and has accepted the report of the Indian National Certification Committee for Polio Eradication and has concluded that the wild polio virus is not circulating in these states.

Each region can consider certification only when all countries in the area demonstrate the absence of wild poliovirus transmission for at least three consecutive years in the presence of certification standard surveillance.

In addition, all facilities holding wild poliovirus infectious and potentially infectious materials must have implemented bio-containment measures for laboratory containment of wild poliovirus.

A task force for laboratory containment of wild polioviruses has been constituted. The first phase of laboratory containment started by surveying laboratory to identify laboratory with wild poliovirus, infectious materials or potential wild poliovirus infectious materials and encourage them for destruction of all unneeded materials.

All States/UTs have been communicated about the successful interruption of wild poliovirus transmission in India and the possible certification in 2014 and requested for political and administrative support required for completion of laboratory containment activities in their respective States.

Support of WHOs National Polio Surveillance Project (NPSP) is also being obtained to survey all laboratories in their database and provide information of the Laboratories to the Task Force.

An inventory of laboratories/Institutes of Department of Bio Technology (DBT) / Department of Science and Technology (DST), Council of Scientific and Industrial Research (CSIR) and Indian Institutes of Technology (IITS)/ National Institute of Information Technology (NIITs), databases of bio-medical laboratories in Department of Health Research (DHR), bio-tech laboratories in Biotechnology Industry Research Assistance Council (BIRAC) database has been prepared for information on storage of potentially infectious material.

Adding the carotenoids lutein and zeaxanthin, the omega-3 fatty acids DHA and EPA, or both to a formulation of antioxidant vitamins and minerals that has shown effectiveness in reducing risk of progression to advanced age-related macular degeneration (AMD) did not further help reduce the risk, a new study has found.

Age-related macular degeneration is the leading cause of blindness in the developed world, according to background information in the article.

Without more effective ways of slowing progression, the number of persons with advanced AMD is expected to double over the next 20 years, resulting in increasing socioeconomic burden, the researchers wrote.

"Oral supplementation with the Age-Related Eye Disease Study (AREDS) formulation (antioxidant vitamins C, E, and beta carotene and zinc) has been shown to reduce the risk of progression to advanced AMD. Observational data suggest that increased dietary intake of lutein and zeaxanthin, omega-3 long-chain polyunsaturated fatty acids (docosahexaenoic acid [DHA] and eicosapentaenoic acid [EPA]), or both might further reduce this risk," they said.

Emily Y. Chew, M.D., of the National Eye Institute, National Institutes of Health, Bethesda, Md., and colleagues with the Age-Related Eye Disease Study 2 (AREDS2) Research Group examined whether adding lutein + zeaxanthin, DHA + EPA, or both to the AREDS formulation might further reduce the risk of progression to advanced AMD.

A secondary goal was to evaluate the effect of eliminating beta carotene, lowering zinc doses, or both in the AREDS formulation. AREDS2, a multicenter, randomized phase 3 study was conducted in 2006-2012, enrolling 4,203 participants 50 to 85 years of age at risk for progression to advanced AMD with bilateral large drusen (tiny yellow or white deposits in the retina of the eye or on the optic nerve head) or large drusen in 1 eye and advanced AMD in the fellow eye.

Participants were randomized to receive lutein (10 mg) and zeaxanthin (2 mg), DHA (350 mg) + EPA (650 mg), lutein + zeaxanthin and DHA + EPA, or placebo. All participants were also asked to take the original AREDS formulation or accept a secondary randomization to 4 variations of the AREDS formulation, including elimination of beta carotene, lowering of zinc dose, or both.

A total of 1,608 participants had experienced at least 1 advanced AMD event by the end of the study (1,940 events in 6,891 study eyes). The researchers found that the probabilities of progression to advanced AMD by 5 years were 31 percent for placebo, 29 percent for lutein + zeaxanthin, 31 percent for DHA + EPA, and 30 percent for lutein + zeaxanthin and DHA + EPA. In the primary analyses, comparisons with placebo demonstrated no statistically significant reductions in progression to advanced AMD.

"There was no apparent effect of beta carotene elimination or lower-dose zinc on progression to advanced AMD. More lung cancers were noted in the beta carotene vs. no beta carotene group (23 [2 percent] vs. 11 [0.9 percent]), mostly in former smokers," the authors wrote.

None of the nutrients affected development of moderate or worse vision loss.

The researchers added, "these null results may be attributable to the true lack of efficacy. Other factors to consider include inadequate dose, inadequate duration of treatment, or both."

"Based on apparent risks of beta carotene and possible benefits that are only evident within exploratory subgroup analyses, lutein + zeaxanthin requires further investigation for potential inclusion in the AREDS supplements."

The study has been published online by JAMA to coincide with its presentation at the Association for Research in Vision and Ophthalmology annual meeting.

In a landmark surgery in the UAE, a hospital carried out a kidney transfer and transplant from a deceased donor from Saudi Arabia to a 23-year-old woman patient from Abu Dhabi.

The surgery was done at the Sheikh Khalifa Medical City (SKMC), owned and operated by the Abu Dhabi Health Services Company (SEHA).

The health of the patient, Latifa Sai`ed, who had suffered kidney problems for 16 years, is said to be improving daily. The organ is functioning normally and she is no longer on dialysis.

Ali Abdulkareem al-Obaidli, chief clinical officer at SEHA, spoke about the patient recipient.

Latifa Sai`ed, born and raised in the UAE, suffered from a rare syndrome that resulted in kidney failure at the age of seven. She was on dialysis for 16 years ever since and endured multiple problems common to long-term dialysis patients, such as blood clots, inflammation and painful procedures such as cathertization.

Word was received that a young man died in a traffic accident in Saudi Arabia, and his family decided to donate his organs to help save the lives of those needing organ transplants.

Tests showed that Latifa was a near perfect match for the kidney and arrangements were made to rush it from Saudi Arabia to the UAE by a jet.

Al Qubaisi praised the medical team, and thanked the family of the donor for their generous and selfless act of kindness.

Sheikh Khalifa Medical City has conducted 75 kidney transplants, all from living related donors in the past. Among them were seven children, the youngest being four years old, while the oldest person was 64 years old. However, this was the first transplant from a deceased donor.

Babies whose growth is at either extreme in the womb, either very small or very large, are at greater risk of developing autism, a new study has revealed.

It is the first time that a clear link has been made between babies who grow to above average size at birth and risk of Autism Spectrum Disorder and follows from a study of more than 40,000 child health records in Sweden.

The research, led by The University of Manchester, also confirmed earlier research which reported that premature and poorly grown, low weight babies appear more susceptible to the condition.

Autism affects how individuals interact with the world and with other people and there is no known cure. Researchers believe it has origins in both genetic and environmental causes.

Professor Kathryn Abel, from the University`s Centre for Women`s Mental Health and Institute of Brain, Behaviour and Mental Health, who led the research said: "The processes that leads to ASD probably begin during fetal life; signs of the disorder can occur as early as three years of age. Fetal growth is influenced by genetic and non-genetic factors. A detailed understanding of how fetal growth is controlled and the ways in which it is associated with ASD are therefore important if we are to advance the search for cures.

Researchers looked at data from the Stockholm Youth Cohort in Sweden, where early ultrasound dating provides detailed weights of the baby`s progression in pregnancy. Infants and children then also take part in structured clinical assessments of their social, motor, language and cognitive abilities.

The cohort contained records of 589,114 children aged 0-17 in Sweden between 2001 and 2007. Certain child data was removed, including children too young to have a diagnosis for ASD, adopted children and non Swedish or Stockholm County residents, children not born in Sweden and twins.

From the remaining available data, researchers found 4,283 young people with autism and 36,588 who did not have the condition and who acted as the control.

The study found that bigger babies who were born weighing over 4.5kg (or 9lb 14) showed a higher incidence of autism, as did smaller infants who were born weighing less than 2.5kg (5.5lb).

A baby who had poor fetal growth would therefore have a 63 percent greater risk of developing autism compared to normally grown babies. A baby who was large at birth would have a 60 percent greater risk. This effect was independent of whether or not the baby was born pre or post term.

Professor Abel added: "We think that this increase in risk associated with extreme abnormal growth of the fetus shows that something is going wrong during development, possibly with the function of the placenta.

"Anything which encourages abnormalities of development and growth is likely to also affect development of the baby`s brain. Risk appeared particularly high in those babies where they were growing poorly and continued in utero until after 40 weeks. This may be because these infants were exposed the longest to unhealthy conditions within the mother`s womb," she stated.
The research was published in The American Journal of Psychiatry this month.

Brigham Young University chemistry professor Emily Bates has identified mutations in a gene that makes people more susceptible to migraine headaches.

The study is the first demonstration of a genetic cause for the common migraine and is an important step in the search for a cure.

"I had migraines really frequently and severely. I would lose my vision, vomit uncontrollably - it would wipe out an entire day," Bates said.

She decided then as a high school student that she was going to work on migraines, that she was going to figure them out and help find a cure.

After earning a Ph.D. in genetics from Harvard, Bates did post-doctoral research with a team of geneticists led by Louis Ptacek at University of California San Francisco`s medical school.

This gene hunting party worked with two families that appeared to have a dominantly inherited form of the affliction.

The researchers zeroed in on genetic mutations these families had in common - mutations that affect production of a protein known as casein kinase delta.

To test whether this was a cause or a coincidence, Bates designed an experiment to determine whether the same genetic trait led to migraine symptoms in mice.

"All sensations become amplified with migraines, including touch, heat, sound and light," Bates, who continued work on the project when she took a position at BYU in 2009, said.

The researchers observed this heightened sensitivity in the migraine mice in very subtle ways - from the warmth of a tiny light and the pressure of a single hair-like filament.

The findings are set to be published in Science Translational Medicine.