Thursday, March 1, 2012

News and Events - 29 Feb 2012




27.02.2012 6:18:12

ADMISSOIN NOTIFICATION 2012 : JAMIA HAMDARD, NEW

Delhi

Online / offline applications (under general categroy and NRI/Sponsored category as per detail given below are invited for admission to the following programmes :

FACULTY OF PHARMACY :
1.

PhD
- Pharmaceutics, Pharmacognosy & Phytochemistry, Pharmaceutical Chemistry, Pharmacology, Pharmaceutical Medicine
2. M Pharm - Pharmacuetical Chemistry, Pharmaceutics, Pharmacognosy & Phytochemistry, Pharmacology, Pharmacy Practice, Quality Assurance, Pharmaceutical

Biotechnology

3. Bachelor of Pharmacy (B.Pharm
4. Diploma of Pharmacy (D.Pharm

FACULTY OF INFORMATION TECHNOLOGY :
1.

M.Tech


Bioinformatics

FACULTY OF SCIENCE :
1.

PhD
-

Biochemistry
,

Biotechnology
,

Botany
, Toxicology
2.

M.Sc
-

Biochemistry
,

Botany
,

Biotechnology
, Toxicology, Bioelectronics & Instrumentation

FACULTY OF ENGINEERING AND INTER-DISCIPLINARY SCIENCES :
1.

PhD
-

Bioinformatics
,

PhD
- Chemoinformatics
2.

M.Tech
- Food Technology



  • Online application form is available on our website :
    www.jamiahamdard.edu w.e.f. 1st february 2012.
  • Offline (Printed application form will be available from 1st march 2012 at Jamia Hamdard counter and form may also be obtained by post from Asst Registrar (Admissions , Jamia Hamdard by sending a draft of Rs 600/- for General Category and Rs 3100/- (for NRI/Sponsored category in favour of Jamia Hamdard payable at New

    Delhi
    by 31.03.12
  • The Entrance Test will be held at Allahabad / Calicut /Lucknow /

    Delhi
    /hyderabad /

    Kolkata
    /Kota / Patna /Pune /Srinagar, Anantnag (J & K

Deadline : 05.04.12

View Original Notification



http://www.biotecnika.org/content/february-2012/admissoin-notification-2012-jamia-hamdard-new-delhi#comments



27.02.2012 8:00:00
Antisense oligonucleotides -- short segments of genetic material designed to target specific areas of a gene or chromosome -- that activated an enzyme to "chew up" toxic RNA could point the way to a treatment for a degenerative muscle disease called myotonic dystrophy, said researchers from Baylor College of Medicine and Isis Pharmaceuticals Inc., in a report in the journal Proceedings of the National Academy of Sciences.



briggsln@ucmail.uc.edu (Lynn Briggs
28.02.2012 3:00:00
Dr. Brian Terpstra and
Dr. Caryl Sortwell have discovered that
allantoin holds great potential as a non-invasive global neuroprotective therapy for Parkinson's disease.



Parkinson's disease (PD is a disorder of the brain that leads to shaking (tremors and difficulty with walking, movement, and coordination. A number of different compounds are being investigated as a treatment, including oral administration of inosine (metabolized to urate , which is currently in Phase II trials (
Safety of Urate Elevation in Parkinson’s Disease, SURE-PD . The goal of the SURE-PD trial is to determine whether oral inosine supplementation can safely elevate plasma urate without leading to hyperuricemia and gout. Urate, or uric acid, is believed to be the neuroprotective agent to slow PD progression. However, the efforts of Drs. Terpstra and Sortwell have shown that neither inosine nor urate is the molecule responsible for neuroprotection in a rodent model of Parkinson's disease. Their research instead shows that when the conversion of urate to allantoin is blocked then the neuroprotection associated with inosine administration is similarly blocked. Further, administration of allantoin alone results in the same level of protection against the motor impairment and nigral dopamine neuron loss (neurons lost by PD normally induced in the rodent PD model. Lastly, in rats with elevated levels of uric acid no neuroprotection was observed. Compared to uric acid, allantoin: 1 has a greater ability to cross the blood brain barrier and access the brain and 2 will not increase the risk of hyperuricemia and gout. Collectively these findings suggest that allantoin administration is potentially better treatment for PD than inosine.



Allantoin is the end product of purine metabolism in most mammals and is also found in botanical extracts of the comfrey plant. It is a normal component of the human diet and can be found in small amounts in eggs, bananas, peas, bread, yams, wax beans and milk, to name just a few. Plasma allantoin levels are significantly elevated during strenuous exercise. The biological activity of allantoin has rarely been scientifically examined and the compound has been widely touted as a biologically inert. It can be found in a number of existing products including toothpaste, mouthwash, shampoos, lipsticks, anti-acne products, and sun care products. However recently there has been more interest in the pharmaceutical use of the compound. For example the FDA has approved it as topical treatment for wound treatment. Additionally in vitro allantoin has been shown to have intrinsic anti-oxidant properties and has been shown to be as potent as ascorbate in quenching hydroxyl radicals. In the studies at UC, allantoin's effect on NADPH oxidase-1 immunoreactivity (NOX-1ir neurons in vivo suggest that allantoin can reduce oxidative stress and be able to modify the underlying disease process of Parkinson's disease.



Allantoin has great potential as a treatment for Parkinson's disease because:
  1. It potentially has a more favorable safety trial and ability to access the brain when compared to oral inosine administration
  2. Our preclinical evidence in a rodent model of PD suggests that allantoin, not inosine or uric acid, is responsible for the neuroprotective effect
  3. Our data in NOX-1ir cells suggested that allantoin will reduce oxidative stress and be able to modify the underlying disease process of Parkinson's disease.
  4. Allantoin is a readily available low cost compound.

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