Friday, 10 June 2011

News letter

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Cabinet gives nod for lowering of age for pension under Old Age Scheme

Lowering the age limit from 65 years to 60 years under Indira Gandhi National Old Age Pension Scheme and increase in rate of pension to persons of 80 years and above
The Cabinet today approved lowering the age limit for the Indira Gandhi National Old Age Pension Scheme (IGNOAPS) from 65 years to 60 years and increasing the rate of pension from  Rs. 200 to Rs. 500 to persons of 80 years and above. The revised norms would be applicable with effect from 1st April, 2011.
It is estimated that lowering of the age limit would benefit about an additional 72.32 lakh persons in the age group of 60-64 years and living below the poverty line. It is estimated that 26.49 lakh persons above the age of 80 years and living below the poverty line, would become eligible to receive enhanced central assistance @ Rs. 500 per month. At present 169 lakh persons above the age of 65 years and living below poverty line are receiving central assistance under IGNOAPS.
The additional funds required will be Rs. 1,736 crore for providing old age pension @ Rs. 200 per month per beneficiary in the age group of 60-64 years and Rs. 953 crore for providing enhanced pension @ Rs. 500 per month per beneficiary of age 80 years and above. Thus the total additional requirement will be Rs. 2,770 crore including 3% administrative expenses.
As a result of change in the eligibility criteria for receiving old age pension, eligibility criteria for widowpension under IGNWPS and disability pension under IGNDPS will get revised from 40-64 years to 40-59 years and from 18-64 years to 18-59 years respectively.


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Scientists developing treatments for the devastating brain disorder
Creutzfeldt- Jakob Disease (CJD) have unexpectedly blocked the onset of
Alzheimer's disease, the most common cause of dementia.

Researchers said they were "thrilled" at the unexpected discovery that two
antibodies – extensively studied in relation to CJD – may also have an
affect on Alzheimer's disease. Almost 500,000 people a year in the
UK and 20
million worldwide suffer from Alzheimer's.

The finding, published in Nature Communications, represents a "significant
step forward in the battle to develop drugs to treat Alzheimer's disease,"
they say. The lead came from an American study by researchers at
in 2009, which showed prion proteins causing CJD also play a role
in Alzheimer's disease.

The finding triggered a race by scientists to discover whether antibodies
being developed as a treatment for CJD might also work against Alzheimer's.
Now a study on mice at the Medical Research Council Prion Unit at
London has indicated the antibodies block the damaging effects of a
toxic substance called "amyloid beta", a protein which accumulates and
becomes attached to the nerve cells in the brain.

Over time, through its interaction with prion proteins, amyloid stops the
nerve cells from communicating, causing memory loss, the distinctive symptom
of Alzheimer's.

Professor John Collinge, the director of the MRC Prion Unit at
London who led the study published in Nature Communications, said:
"There is an urgent need for new drugs which will help to preserve brain
function and prevent memory loss, the symptom which most characterises the
devastating impact of Alzheimer's. We're thrilled that this discovery shows
in mice that these two antibodies which we are developing to treat CJD may
also have a role in treating more common forms of dementia like Alzheimer's

"If these antibody drugs prove to be safe in use to treat CJD we will
consider whether studies in Alzheimer's disease should be carried out."

Professor Dominic Walsh, a co-author of the study from
University College
Dublin, said: "A unique aspect of this study is that we used amyloid beta
extracted from human brain, the same material we believe is causing memory
loss in patients with this devastating disease and we identified two
antibodies that could block this effect.

"The use of these specific antibodies is particularly exciting since they
have already undergone extensive pre-clinical testing for use in treating
CJD. Thus a lot of basic work has already been done and could fast-track
these antibodies for use in humans. The next step is further validation in
other disease models of Alzheimer's and then safety trials in humans."

The two antibodies, ICSM 18 and 35, target the prion protein that is
implicated as a cause of CJD. Clinical trials of drugs based on the
antibodies are due to begin in humans next year as a treatment for CJD. If
they are successful, the trials could be repeated for patients with
Alzheimer's disease.

One in 14 adults over aged 65 and one in six over aged 80 has dementia,
which in most cases is Alzheimer's disease. The incidence is growing as the
population ages.

Er.S C Maheshwari
Former DEN C.Rly.
Secretary (Railway)
Bharat Pensioners Samaj (Member SCOVA)
Genl. Secy. RREWA
490A/16 Gurudwara Road;Civil Lines .Gurgaon-122001
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