paris writes in forum and emails

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Author Topic: Hello Again forum (Read 19 times)
PARIS HILTON
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Posts: 10


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Hello Again forum
« on: May 29, 2007, 04:27:32 PM »

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Hello John. and "FORUM" I found some tantalizing interesting information in my collection of notes that maybe of some interest to your forum as it is to me. It is an article from a news paper i don't have the title of it unfortunately, but reading it came from India, no "date" but the month is mentioned, quoting it as follows "Mysore July 24 Hollywood based filmmaker MS. Yin Gazda is in the city and is planning to make a TV serial on the spiritual masters it goes on in saying the filmmaker from California is undergoing ayurvedic treatment" the new paper goes on saying "that the film is and it was about synthesis and the unity of beliefs and faith that are woven around one God and representing the various faces of deity or divine faith or belief according to MS..Gazda the film is about the five major religions are portraying god even thought the in essence they are the same ,they are only different in language and imaginary but the messages are actually identical" the articles go on to say "she asserted that she would contact only those who are witness to God" "she mentions also there are many false guras" also the film will use special effects and big budget.... her other film a T.V Serial which she had produced earlier was called UFO and Cosmic Dimensions a very spiritual film which made one see the unseen dimensions of space time and cosmology that was previewed on Entertainment Tonight" i did see that episode a few years back I brought the topic up also to see if anyone within your forum follows a spiritual path aim looking for lots of information on these topics your Wife would have some Its a lovely website she has thank you; Paris 818XXXXXXXX310XXXXXXXXXXXX

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"all in a day work" MySpace Profile - Paris Hilton, , California, US, The Official Paris Hilton MySpace Page. ... Paris Hilton's Latest Blog Entry [Subscribe to this Blog] ...
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darko
Jr. Member

Posts: 53



Re: Hello Again forum
« Reply #1 on: May 30, 2007, 12:19:38 AM »

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Thanxs Paris This is inportant!!"MS..Gazda the film is about the five major religions are portraying god even thought the in essence they are the same ,they are only different in language and imaginary but the messages are actually INDENTICAL"
Meny thanxs!!

« Last Edit: May 30, 2007, 01:43:01 PM by darko » Report to moderator Logged



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June 03, 2007, 06:12:33 PM

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Hutchison Effect Online 2006
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Life Extension And Related Technologies
106 and telmomerase regulation red peppers apoptosis « previous next »
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Author Topic: 106 and telmomerase regulation red peppers apoptosis (Read 93 times)
john hutchison
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106 and telmomerase regulation red peppers apoptosis
« on: March 16, 2006, 11:01:33 PM »

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ok red peppers it is i looked this up as it rang true ''.. your hHuman endothelial cell life extension by telomerase expression.Human endothelial cell life extension by telomerase expression. ... Apoptosis/drug effects Base Sequence Cell Aging* Cell Cycle Cell Division ...
www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve& db=PubMed&list_uids=10473565&dopt=Abstract - Similar pages
omework 106 what prodct to bye ok is it or what hot peppers as well as vitamin d from my studyies ill email some folks on this thanks

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1o6
Administrator
Hero Member

Posts: 794



Re: 106 and telmomerase regulation red peppers apoptosis
« Reply #1 on: March 16, 2006, 11:38:44 PM »

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Great stuff! I grow my own aeroponic Habs. Tons of Capsaicin!
Great for headaches too. Extact with 100 proof vodka or grain alcohol.
They're excellent raw, if you can stand 'em.
Burning ring of fire. Hehe!

« Last Edit: March 17, 2006, 11:01:18 AM by 106 » Logged

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1o6
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More information on Capsaicin
« Reply #2 on: March 17, 2006, 12:01:10 PM »

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http://sulcus.berkeley.edu/mcb/165_001/papers/manuscripts/_784.html

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Today's anomaly may become tomorrow's technology.


gyftos
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Posts: 25



Re: 106 and telmomerase regulation red peppers apoptosis
« Reply #3 on: July 15, 2006, 10:12:35 PM »

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106 i am super extremely interested in aeroponics could you beam me a link or two thx in advance

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ο βασσιλιασ τον γυφτον


1o6
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Hero Member

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Re: 106 and telmomerase regulation red peppers apoptosis
« Reply #4 on: July 15, 2006, 10:33:29 PM »

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http://www.futuregarden.com/
http://www.jasons-indoor-guide-to-organic-and-hydroponics-gardening.com/
Good for here and beyond!

« Last Edit: July 15, 2006, 10:40:01 PM by 1o6 » Logged

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Today's anomaly may become tomorrow's technology.


gyftos
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Posts: 25



Re: 106 and telmomerase regulation red peppers apoptosis
« Reply #5 on: July 15, 2006, 10:37:45 PM »

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thanks again 106

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ο βασσιλιασ τον γυφτον


1o6
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Re: 106 and telmomerase regulation red peppers apoptosis
« Reply #6 on: July 15, 2006, 10:40:41 PM »

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June 03, 2007, 06:14:31 PM

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ACTIVATION OF TELOMERASE IN NORMAL HUMAN CELLS EXTENDS THEIR LIFE-SPAN IMPORTANT « previous next »
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Author Topic: ACTIVATION OF TELOMERASE IN NORMAL HUMAN CELLS EXTENDS THEIR LIFE-SPAN IMPORTANT (Read 63 times)
ICY
Jr. Member

Posts: 96



ACTIVATION OF TELOMERASE IN NORMAL HUMAN CELLS EXTENDS THEIR LIFE-SPAN IMPORTANT
« on: August 01, 2006, 11:54:52 PM »

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ACTIVATION OF TELOMERASE IN NORMAL HUMAN CELLS EXTENDS THEIR LIFE-SPAN IMPORTANT IMPLICATIONS FOR MEDICINE

Extension of the life-span of normal human cells is a critical milestone on Geron's path to discovering treatments for age-related disorders that strike at a fundamental mechanism of aging: cell senescence. This achievement, which was accomplished by introducing the enzyme telomerase into normal mortal cells, provides definitive evidence that the triggering mechanism for aging, or senescence, in human cells is telomere shortening. The demonstration that telomerase activity can extend cell life-span identifies a central mechanism and a point for intervention in age-related diseases at the cellular level.

Telomerase, Telomeres, and the Extension of Cell Life-Span

Most normal human cells can divide only a finite number of times. Cells from various tissues in the body, such as osteoblasts in the bone, endothelial cells in the blood vessels, retinal pigment epithelial cells in the eye, fibroblasts in the skin, and lymphocytes in the blood are mortal, that is to say, they divide 20-100 times (depending on the tissue and age of the donor) and then cease dividing in a process called cell senescence. This phenomenon of cell aging was first described by Leonard Hayflick in 1961, and therefore the limit of cell proliferation is often called the "Hayflick Limit". Since, it is widely believed that we age in large part because our cells age, the National Institute on Aging has sponsored a significant amount of research into the biological mechanisms of cell aging.

In the decades that followed Hayflick's discovery that human cells are mortal and age in the laboratory dish, a theory for the mechanism of a cellular clock that counts how many times a cell has divided has emerged, called the telomere hypothesis.

According to this theory, the clock of cellular aging resides at the linear ends of the DNA molecule, a region called the telomere (tea'-low-meer). The linear end of each DNA strand ends with a sequence of DNA (TTAGGG) that repeats hundreds of times, effectively "capping" the ends of chromosomes in a manner similar to the way the plastic on the ends of shoelaces "caps" and protects the shoelaces from unraveling.

The telomere hypothesis proposes that as mortal cells divide, terminal DNA or telomeres are progressively lost with each cell division, shortening like a burning fuse. When a critical amount of telomere shortening has occurred, the genetic program of cell senescence, or cell aging, is triggered.

Among normal cells, only the reproductive cells do not senesce; the telomere clock does not "tick", telomeres do not shorten, and the cells can apparently divide indefinitely, a characteristic referred to as immortality. Cellular immortality does not mean that the cells cannot die; like all cells, they must be carefully nourished to remain viable. Instead, immortality refers to the fact that these cells are not limited to a finite number of doublings. Immortal cells, provided they are properly fed and maintained, can divide indefinitely.

Geron Scientific Discoveries

Geron and collaborators have discovered that the capacity of reproductive cells to divide in an immortal fashion is due to the presence of a protein, telomerase (tel-om'-er-ase). This enzyme is actually a complex of at least two distinct molecules, one made of RNA and another made of protein. The RNA component is designated hTR (human Telomerase RNA), and the protein component is designated hTRT (for human Telomerase Reverse Transcriptase). Telomerase uses the RNA component to direct the synthesis of the repeated sequence (TTAGGG), and the fusion of the building blocks of DNA is accomplished by the catalytic compound hTRT. The combination of hTR and hTRT makes active telomerase that can lengthen telomeres, "rewind the clock" of cell aging, and extend the replicative life-span of cells.

Geron, in collaboration with Cold Spring Harbor Laboratory, reported the isolation of the RNA component of telomerase in 1995 (Science September 1, 1995) and has received a U.S. patent on the molecule on December 10, 1996. Geron and the University of Colorado at Boulder were the first to report the isolation of the protein component hTRT (Science August 15, 1997). Geron has filed for patents to protect this discovery. While the RNA component is present in both mortal and immortal cells, the catalytic protein component is observed to be expressed only in immortal cells, leading to the logical question - what would happen if the telomerase hTRT gene were introduced into mortal cells in an active form? In the December 1, 1997 issue of Nature Genetics, Geron, in collaboration with the University of Texas Southwestern Medical Center at Dallas, demonstrated that the expression of hTRT in normal human cells is sufficient to produce active telomerase. The final questions were - would it extend telomeres and would that reverse the aging of human cells?

In a breakthrough accomplishment, Geron and its collaborators have now reported in Science (January 16, 1998) that the introduction of hTRT into mortal cells leads to the extension of telomeres and also the extension of cell life-span. As of the writing of the paper, three different types of cells were observed to substantially pass their normal limits of replicative life-span. These cells are continuing to grow and may be immortal.

Implications of Cell Life-Span Extension for Age-Related Disorders

Senescent cells are not only incapable of dividing, they also exhibit an altered pattern of gene expression, leading to a number of changes in their structure and function. The effects of senescence on cell function can damage the surrounding tissues, contributing to age-related pathologies. For example, senescent skin fibroblasts produce lesser amounts of important skin matrix elements such as collagen and elastin and elevated levels of enzymes such as collagenase that break down the skin matrix. These changes contribute to atrophy of the skin and, ultimately, age-related skin disorders. Similarly, metabolic changes in senescent retinal pigmented epithelium cells, and the loss of proliferative capacity and overexpression of hypertensive and thrombotic factors in endothelial cells are considered contributors to the pathologies of age-related macular degeneration (AMD) and atherosclerosis, respectively.

Skin disorders, AMD, and atherosclerosis are major diseases in the aging population. Skin atrophy, for example, affects virtually all aging individuals, with 40 percent of the population over 75 years of age seeking treatment for at least one skin disorder. These disorders range from photoaging and wrinkling to increased wounding and, ultimately, skin ulceration. The latter disease can be life-threatening. The major class of drugs for treating age-related skin disorders, the retinoids, produces mainly palliative or "cosmeceutical" effects. In the case of AMD, one third of the population at age 70 is affected and, in most patients, the disease is currently untreatable.

The delay or prevention of cell senescence through the extension of cell life-span is expected to have important beneficial effects in diseases to which cell senescence contributes. In addition to skin disorders, AMD and atherosclerosis, this group is thought to include osteoporosis, immune dysfunction, arthritis, and neurodegenerative disorders. The improvement in the health of the elderly through the more effective treatment of age-related diseases is expected to increase the length of healthy life. There is no evidence that this will translate into an extension of the maximum human life-span, which is now believed to be about 120 years.

Implications of Life-Span Extension in Other Health-Related Areas

In addition to the application of cell life-span extension to the development of therapeutics for age-related disorders, there are other health-related uses of this technology which could be pursued in a much shorter time frame. These uses relate to extension of the life-span of cells grown outside of the body. Cell senescence was, in fact, first described by Hayflick in human cells grown in the laboratory.

Laboratory culturing of human cells is the basis of several important current, and anticipated, therapies. One example is reconstitution of the blood and immune system following high-dose chemotherapy for cancer. In this approach, cells removed from the patient before the therapy or obtained from a donor are increased in number (expanded) by culturing in the laboratory, and reimplanted into the patient after the chemotherapy. Following reimplantation, the cells undergo further divisions to replace the blood and immune cells destroyed by the chemotherapy. Other cell therapy, as well as gene therapy approaches, also require cell expansion both in culture and after reintroduction in order to be effective.

Because of the large number of cell divisions required by cell and gene therapy approaches, cell senescence is a significant limiting factor in their success. For example, in reconstitution of the blood and immune system after chemotherapy, the cells exhaust the equivalent of an estimated 40 years of their life-span. This restricts the use of this approach in older patients, reduces the number of courses of therapy which can be given, and may produce problems in blood and immune functions for recipients later in life. The ability to extend the life-span of normal human cells in culture, preventing the loss of replicative capacity that now accompanies cell and gene therapy approaches, should dramatically increase their utility and probability of success.

Senescence in normal human cells also has a significant impact on the production of human biological material for medical use. Many human biological products are made in "transformed" cell lines derived from cancer or virally infected cells because they do not senesce. Whenever normal human cells are used, cultures must be replaced every time senescence occurs. These methods for production of biological materials introduce the risk of contamination of viral products or other pathogens, result in high production costs, and may affect the quality of the material produced, particularly when transformed cells are used. Normal human cell strains with an extended life-span can replace the cells currently used to produce biological materials, resulting in safer, economical, and more efficacious therapeutics.

Telomerase, Telomeres, and Cancer

Activation of telomerase does not transform normal cells into cancer cells. As described in the January 16, 1998 Science paper, cells maintain normal growth characteristics following the activation of telomerase. In fact, there are certain types of cells in the body, such as the reproductive cells, in which telomerase is normally activated. Conversely, lack of telomerase activity does not prevent cells from becoming transformed into cancer cells, as has been demonstrated in "knockout" mice. Telomerase activation, if done in a transient fashion, would simply allow normal cells to undergo more divisions, under normal growth conditions, before they become senescent. Inhibition of telomerase activity in cancer cells, on the other hand, causes them to stop growing and die once their telomeres become so short that their chromosomes are unstable.

Geron Corporation January 13, 1998

The Company desires to take advantage of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995. Specifically, the Company wishes to alert readers the matters discussed in this white paper may constitute certain forward-looking statements that are dependent on certain risks and uncertainties. Actual results may differ materially from the results anticipated in these forward-looking statements. Additional information on potential factors that could affect the Company's results are included in the Company's Quarterly Report on Form 10-Q for the quarter ended September 30, 1997.

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John Hutchinson
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Re: ACTIVATION OF TELOMERASE IN NORMAL HUMAN CELLS EXTENDS THEIR LIFE-SPAN IMPORTANT
« Reply #1 on: August 02, 2006, 05:11:11 AM »

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please thanks geron talks lot and mega c but telomerase was modified and is in the dark areas thank you so take vitamin c at 10 gramsa a day also a high orac factor product thank you for posting this

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ICY
Jr. Member

Posts: 96



Re: ACTIVATION OF TELOMERASE IN NORMAL HUMAN CELLS EXTENDS THEIR LIFE-SPAN IMPORTANT
« Reply #2 on: August 02, 2006, 01:50:41 PM »

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Your are welcome.

I wonder how far along Geron is with their research by now?

Here's some orac info:
http://www.applepolyphenols.com/news/prnewswire_mar302005.htm

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John Hutchison
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Re: ACTIVATION OF TELOMERASE IN NORMAL HUMAN CELLS EXTENDS THEIR LIFE-SPAN IMPORTANT
« Reply #3 on: August 05, 2006, 11:18:55 PM »

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they got it but dont want to talk yet

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