Orang Yahudi yang pada hal lagi dikepung orang Arab !yang memang rata-rta dungu 
kayak anjing itu) masih ada waktu dan kecerdasan untuk  melakukan, penelitian 
yang begini pelik...

Jelas agama Islam yagn dianut kebanyakan orang Arab itu adalah salah satu sebab 
utama kenap aorang Arab itu nggk sanggup make otak lagi......

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    Web address:
     http://www.sciencedaily.com/releases/2008/12/
     081221220328.htm     
Mechanism That Triggers Differentiation Of Embryo Cells Discovered

Prof. Yehudit Bergman. Professors Yehudit Bergman and Howard Cedar of the 
Hebrew University-Hadassah Medical School have deciphered the mechanism whereby 
embryonic cells stop being flexible and turn into more mature cells that can 
differentiate into specific tissues. (Credit: Image courtesy of Hebrew 
University of Jerusalem)

ScienceDaily (Dec. 22, 2008) — The mechanism whereby embryonic cells stop being 
flexible and turn into more mature cells that can develop into specific tissues 
has been discovered by scientists at the Hebrew University of Jerusalem. The 
discovery has significant consequences towards furthering research that will 
eventually make possible medical cell replacement therapy based on the use of 
embryonic cells.

At a very early stage of human development, all cells of the embryo are 
identical, but unlike adult cells are very flexible and carry within them the 
potential to become any tissue type, whether it be muscle, skin, liver or brain.

This cell differentiation process begins at about the time that the embryo 
settles into the uterus. In terms of the inner workings of the cell, this 
involves two main control mechanisms. On the one hand, the genes that keep the 
embryo in their fully potent state are turned off, and at the same time, 
tissue-specific genes are turned on. By activating a certain set of genes, the 
embryo can make muscle cells. By turning on a different set, these same 
immature cells can become liver. Other gene sets are responsible for additional 
tissues.

In a recent paper, published in the journal, Nature Structural and Molecular 
Biology, Professors Yehudit Bergman and Howard Cedar of the Hebrew 
University-Hadassah Medical School have deciphered the mechanism whereby 
embryonic cells stop being flexible and turn into more mature cells that can 
differentiate into specific tissues. Bergman is the Morley Goldblatt Professor 
of Cancer Research and Experimental Medicine and Cedar is the Harry and Helen 
L. Brenner Professor of Molecular Biology at the Medical School.

They found in their experiments, using embryos from laboratory mice and cells 
that grow in culture, that this entire process is actually controlled by a 
single gene, called G9a, which itself is capable of directing a whole program 
of changes that involves turning off a large set of genes so that they remain 
locked for the entire lifetime of the organism, thereby unable to activate any 
further cell flexibility.

Their studies shed light not only on this central process, but also can have 
consequences for medical treatment. One of the biggest challenges today is to 
generate new tissues for replacing damaged cells in a variety of different 
diseases, such as Parkinson’s disease or diabetes. Many efforts have been aimed 
at “reprogramming” readily-available adult cells, but scientists have 
discovered that it is almost impossible to do this, mainly because normal 
tissues are locked in their fixed program and have lost their ability to 
convert back to fully potent, flexible, embryonic cells.

Now, with the new information discovered by Bergman and Cedar, the molecular 
program that is responsible for turning off cell flexibility has been 
identified, and this may clear the way towards developing new approaches to 
program cells in a controlled and specific manner.
Adapted from materials provided by Hebrew University of Jerusalem, via 
AlphaGalileo.
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Hebrew University of Jerusalem (2008, December 22). Mechanism That Triggers 
Differentiation Of Embryo Cells Discovered. ScienceDaily. Retrieved December 
23, 2008, from http://www.sciencedaily.com­ /releases/2008/12/081221220328.htm


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