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Genetic Basis For Some Birth Defects Uncovered

ScienceDaily (Nov. 12, 2008) — A multidisciplinary research team at Case 
Western Reserve University led by Gary Landreth, Ph.D., a professor in the 
School of Medicine's Department of Neurosciences, has uncovered a common 
genetic pathway for a number of birth defects that affect the development of 
the heart and head.

Abnormal development of the jaw, palate, brain and heart are relatively common 
congenital defects and frequently arise due to genetic errors that affect a key 
developmental pathway.

Landreth, also the senior author of the study, developed a mouse model of these 
disorders by removing a gene central to this developmental pathway, called 
ERK2. He, together with Dr. William Snider at the University of North Carolina, 
discovered that the mice missing the gene for ERK2 in neural crest cells had 
developmental defects resembling those of human patients with a deletion that 
includes this gene. The patients have features that are similar to DiGeorge 
syndrome, which is associated with cardiac and palate defects. Interestingly, 
the ERK2 gene is central to a well-known pathway already associated with a 
different distinct group of cardiac and craniofacial syndromes that include 
Noonan, Costello, Cardiofaciocutaneous syndrome, and LEOPARD syndrome.

Landreth enlisted the help of Michiko Watanabe, Ph.D., professor of Pediatrics 
at Case Western Reserve University School of Medicine to look at the mouse 
hearts. She and her team found that they had characteristic heart defects 
resembling those seen in the patients with ERK2 deletions.

"Given Dr. Watanabe's findings, we determined that we had in fact developed 
animal models that mimicked the human deletion syndrome," said Landreth. "This 
work sheds light on how these developmental errors occur."

Remarkably, Dr. Sulagna Saitta, a human geneticist at Children's Hospital of 
Philadelphia had identified children who had comparable heart defects as well 
as subtle facial differences. These children were all missing a very small 
region of chromosome 22 that contained the ERK2 gene.

Saitta agreed that the similarity in the anatomic structures affected in the 
mice and those in the patients who have lost one copy of this gene suggest that 
ERK2 and its pathway members are essential for normal development and might 
lead to these birth defects. These findings link together several distinct 
syndromes that are each characterized by cardiac and craniofacial abnormalities 
and show that they can result from perturbations of the ERK cascade.

Landreth and his team will take these findings back to the lab and find out 
exactly why cells need ERK2 during embryogenesis.

Funding was provided by the National Institutes of Health, the National Science 
Foundation, the National Heart Lung Blood Institue and a National Research 
Service Award.

Journal reference:

   1. Jason Newbern et al. Mouse and human phenotypes indicate a critical 
conserved role for ERK2 signaling in neural crest development. PNAS, 
105:17115-17120; published ahead of print October 24, 2008 DOI: 

Adapted from materials provided by Case Western Reserve University, via 
EurekAlert!, a service of AAAS.
Need to cite this story in your essay, paper, or report? Use one of the 
following formats:

Case Western Reserve University (2008, November 12). Genetic Basis For Some 
Birth Defects Uncovered. ScienceDaily. Retrieved November 12, 2008, from 
http://www.sciencedaily.com­ /releases/2008/11/081110190653.htm

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