Laga HOT PLATE

laga setengah matang merebutkan gorengan mak telur....

perubahan itu tidak dengan ngomong

 

be assured ... she will come

hidup akan terus berjalan , tiada kata kompromi bagi hari kemaren akan terulang kembali...

waktu itu kejam dan sadis...  akan melahab bagi semua orang tanpa kenal status dan kedudukan...

saling pengertian dan memahami adalah kuncinya... 

akrabilah waktu.... maka dia akan mengakrabimu sepanjang waktu..

romantislah dengan waktu.... maka dia akan romantis kepadamu...

24 tahun bukan waktu yang sedikit dalam menikmati waktu...

kuhabiskan dengan senda gurau bersama gerakan jarum jam...

seraya menanti hal yang sesungguhnya diharapkan akan kehadirannya...

karena semua akan indah pada waktunya...

wahai sang Pencipta waktu subuh dan senja.... datangkanlah dia padaku...

berilah ketenanang dimalam ini...

seraya kebahagiaan yang selalu menyertainya...

dan semua akan berjalan sebening embun pagi di waktu sang kokok meyuarakan lagunya...

semoga engakau bisa menjadi inspirasi bagi kehidupan...dan menjadi dunia terindah bagiku..

Toni 10 januari 2012

Cafe Zayzah Malang.

Tugas biomol

Nama : Muhammad Fathoni Hamzah

Nim    : 110690100111016

Paris chinensis dioscin inducer G2/M cel cycle arrest and apoptosis in human gastric cancer SGC-7901 cells

1.      In this paper describes the anti-tumor effect of the Paris chinensis dioscin (PCD) in human gastric cancer and the mechanisms of cell cycle regulation and apoptosis in SGC-7091 cells and signaling pathways involved in apoptosis induction in PCD. But not explain in detail about the effect of PCD on other cells that are also affected from this PCD, that feared any negative effects on other cells if given in a concentration PCD.

2.      Has not specifically set forth PCD influence on cell cycle regulatory mechanisms at the G2-M phase.

Tues gastric treated using PCD with various concentrations of visible fluid in the cell cytoplasm shrinking so that experienced plasmolisis, mediated looks fluffy and when observed under a microscope look blurry. These cells flake off with increasing concentrations of drug (PCD).

PCD administration significantly inhibited cell viability or survival of SGC-7901 cells. It is known that PCD can inhibit cell viability SGC-7901 cells because they contain anti-cancer substances such as saponin steroids polyphylin, dioscin, and balanitin 7 are capable of inhibiting proliferation of tumor cells.

When the active component of the Paris induksikan chinensis in this dioscin will cause the cells lose the ability to defend themselves or experiencing stress, Bcl-2 or Bcl-x will disappear from the mitochondrial membrane and replaced the pro-apoptotis proteins such as Bax, Bak and Bim. When Bcl-2/Bcl-x decreased, an increase in mitochondrial membrane permiabilitas cause the release of several proteins which will activate the caspase cascade. One of these proteins is cytochrome c. In the cytosol cytochrome c binds to Apaf-1 (apoptosis activating factor-1) and activates caspase-9. (Bcl-2 and Bcl-x directly inhibits the activation of Apaf-1 and then disappeared from the cells that cause activation can occur Apaf-1). Other mitochondrial proteins such as apoptosis initiating factor (AIF) into the cytoplasm that would bind to neutralize a wide range of inhibitors of apoptosis. This will activate the caspase cascade.

Release of cytochrome c. Because cytochrome c exit so it will be bound by Apaf-1 (apoptosis activating factor), he will be bound and form a CARD domain and form a apoptoseome. Apoptosome will activate caspase 9 (caspase-activated early cytochrome c release), so it will activate caspase caspase 9 then (3,6,7) to further caspase will activate the other system.

Apoptosis is an intracellular suicide program carried out by activating caspase (a family of cysteine ​​proteases). Two main lines apoptotis are intrinsic and extrinsic pathway. Intrinsic pathway includes the provision of the code that triggers a process-dependent mitochondrial release of cytochrome c and activate caspase-9, and extrinsic pathway involves activation of death receptors (death receptor, DR) such as Fas (tumor necrotic factor receptor 1), DR4 and DR5. Interaction with the appropriate ligand will lead to tranduksi signal coverage beginning with DR molecules associated with death such as Fas-associative domain (FADD) and caspase-8 activates the next. This caspase then catalyzes a series of proteolytic processes that produce biochemical and morphological changes typically associated with the process of apoptosis [15]. Figure 1 shows the process of apoptosis or programmed cell death (PCD), which include signal amplification and involves a wide range of mitochondrial genes such as Bax and Bak.

Figur 1. Mekanisme apoptosis atau programmed cell death (PCD) yang diinduksi oleh sel T sitotoksik melalui sinyal mitokondrial dan melibatkan sejumlah gen.

Inducing genes such as Bax and Fas antigen expression and repression / suppression of genes simultaneously as BCL2 [16]. If severe cell damage, a number of genes for apoptosis controlled by p53 gene also plays a role in regulating the cell cycle. Outcome study showed activation of apoptotic pathways by p53 can be done with transferring malignant type p53 (wild type) recombinants in cancer cells that have no p53 (null) or mutated.