DetIk MAsa

Wednesday, November 9, 2011

Immortal?????????

Is Human can achieve Immortality?

Assalamualaikum w.b.t…

If you're alive in 20 years, you may be able to live forever.

By Gary Vey ©2011 Viewzone


Pada tahun 1786, jangka hayat purata hanya 24 tahun. Seratus tahun kemudian (1886), jangka hayat purata ini meningkat dua kali ganda kepada 48. Pada masa ini, bayi yang baru lahir boleh mengharapkan untuk hidup purata 76 selama tahun. Dengan penemuan terkini dalam biologi, banyak saintis meramalkan bahawa jangka hayat akan terus selama tiga-digit. Malah jika mereka adalah betul,manusia tidak sepatutnya mati pada semua pada masa akan datang.

"Lebih separuh bayi boomers di sini di Amerika akan melihat hari jadi seratus dan seterusnya mereka dalam kesihatan yang cemerlang. Kami melihat tempoh hayat untuk boomers bayi dan generasi selepas boomers bayi berusia 120 hingga 150 tahun." – Dr Ronald Klatz Akademi Anti-Penuaan Amerika.

Di Amerika,mereka berusaha hari ini bagi menggalakkan belia mengambil alih ahli-ahli sains di dalam struktur genetik sel-sel dan memberi perhatian yang kurang kepada peranan tekanan dan diet jangka hayat.Adakah manusia akan abadi??? dan manusia akan berduyun-duyun pergi ke klinik anti-penuaan dan sanggup keluar duit sebanyak $ 20,000 dolar setahun untuk rawatan yang merangkumi terapi hormon, analisis DNA,malah anti-penuaan pembedahan kosmetik. Terapi eksperimen menawarkan tiada jaminan keabadian - hanya janji untuk memanjangkan hayat.

"Anti-aging medicine is not about stretching out the last years of life. It's about stretching out the middle years of life... and actually compressing those last years few years of life so that diseases of aging happen very, very late in the life cycle, just before death, or don't happen at all." -- Dr. Klatz.

Mengapa kita tua dan mati?

Sebab apa yang kita panggil "penuaan" kini sedang difahami. Ini pemahaman baru tidak lama lagi boleh bergerak mencipta produk anti-penuaan dan pembedahan kepada penggunaan minyak ular dan yogurt Siberia sebagai lanjutan untuk panjangan aliran hayat.Terdapat beberapa halangan yang perlu ditangani.

Hanya apabila ada yg berfikir fikir bahawa TV hologram dan pelancongan angkasa lepas di ufuk masa depan merupakan teknologi moden, keabadian juga menjadi 1 kemodenan & menarik minat ahli-ahli sains seperti Doktor John Langmore dari Universiti Jabatan Michigan Biologi.

Dr Langmore dan kumpulannya melihat dalam sel-sel manusia, pada dasarnya kehidupan manusia melalui molekul DNA. Khususnya, Dr. Langmore melihat tips molekul DNA – yg menfokuskan molekul double-helix - yang mengandungi sejenis rantai mengulangi sepasang enzyme.

Dipanggil telomeres, rantaian molekul ini sering dibandingkan dengan ruang-ruang kosong terdapat pada filem dan pita rakaman. Sesungguhnya, telomeres seolah-olah untuk melaksanakan fungsi yang serupa. Semasa proses replikasi molekul lingkaran DNA mesti berpecah pada separuh dan pasang semula salinan itu sendiri.Melindungi molekul DNA yang penting daripada disalin keluar daripada synch, telomeres menyediakan zon penampan di mana salah penjajaran (yang tidak dapat dielakkan) tidak akan menyebabkan mana-mana kod DNA penting yang hilang.

Perhaps the best analogy I have heard is to compare the telomeres to the white margin surrounding an important type written document. In this analogy, the printed text is the vital DNA code while the white space is the "blank" telomeres. Imagine that this paper is repeatedly slapped on a copy machine, a copy is made, and then that copy is used to make another copy. Each time the paper is subject to errors of alignment and these errors accumulate. After enough copying, it is probable that the white space will diminish and some of the actual text will not be copied. That's what happens inside our cells and it is the reason we get old and die.

As any cell gets older, it is under attack by oxides and free-radicals in the body and environment. We survive as living beings because our cells have the ability to duplicate and replace themselves before being killed by these natural causes. Each time our cells divide, the DNA molecule makes a new copy of itself.



[DNA is a complex molecule that resembles a spiral ladder. When it divides, it splits along the "rungs" then each half of this "ladder" rebuilds the missing half --voila! -- two DNA molecules. Now the cell can divide. The old cell dies and the new cell continues on.]

But the procedure is very complex and not perfect. Usually a small portion of the DNA molecule is lost, misaligned and not copied. Since errors are more frequent on the ends of the DNA molecule, this area, the telomere, does not contain any important DNA information and the effect is insignificant.

Telomeres -- programmed to die!


Scientists observe that the length of telomere chains becomes shorter as we grow older. Eventually the telomeres become so short that cell replication produces lethal errors or missing pieces in the DNA sequence, ending the cell's ability to replace itself. This point, when the cell has lost vital DNA code and cannot reproduce, is called the Hayflick limit. It's the measure of how many times a cell can copy itself before it dies.

Some cells in our body have a very high hayflick limit. Cells that line the inside of your mouth and intestines, for example, are constantly being worn away and replaced. Indeed these cells appear to have the ability to regrow telomeres even in aged bodies. Scientists were curious why some cells shut down telomere growth with age, and some do not.

Dr. Langmore used physical, biochemical, and genetic techniques to study the structure and function of telomeres. His group developed a cell-free system to reconstitute functional model telomeres using synthetic DNA, and studied the mechanism by which telomeres normally stabilize chromosomes and how shortening of the telomeres could cause instability.

The protein factors responsible for stabilizing the ends of chromosomes are being identified, cloned, and studied. Electron microscopy is used to directly visualize the structure of the model telomeres. Dr. Langmore's group used new enzymatic assays to determine the structure of telomere DNA in normal and abnormal cells grown in vivo and in vitro, in order to address specific hypotheses about the role of telomeres in aging and cancer. It's exciting research, for sure, and there have been some promising discoveries.
Scientists have discovered an important enzyme that can turn the telomere production on the DNA molecule "on" and "off." It's called telomerase. Not surprisingly, it seems that as we get older, the amount of telomerase in our cells decreases.

Progeren?



Scientists now believe that the protein calledprogerin, causing rapid aging symptons in progeria victims, is the same protein that causes our own more standard aging.
Progerin stems from a gene mutation that shows up in abundance in the disease but in more manageable quantities in all of us. It causes extreme premature aging.

"When the telomeres become too short and frayed, this triggers the production of progerin, signaling to the body that the cell is at the end of its useful life." -- Dr. Francis Collins, director of the National Institutes of Health

Studies are underway to block the excess production of the protein in children with progeria, which may in turn lead to slowing our own aging and preventing age-related diseases such as cancer, heart disease, and Alzheimer's.[10].

Sekian dulu.. Akan ada sambungan… Wassalam

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