DEE FINNEY'S BLOG
STARTED JULY 20. 2011
Tuday's date August 1, 2011 = page 13
NOTE FROM DEE: The issue of age has been debated many times by many people, including myself. Many laws determine what we can do at what age, like going to school, drinking, smoking, age at when adulthood starts, voting, going into othe mmilitary, marriage, driving, the age of reason, and many other thiings.
Some states change those laws as they see fit, like school, marriage, drinking, smoking,,, driving, etc., but the Federal government determines the rest.
Other countries have quite different rules or laws. Some countries allolwo marriage as young as age 8, which to us is ridiculous.
The Bible says that God created Earth in 7 days, but nobody knows how long a day is. Mankind divided it up so that mankind could manage their mundane lives. In the beginning mankind followed the stars, the sun and mon and determined seasons, noted when iti snowed and froze, when it go twarmer, and when they developed farming and didn't have to followo the animals, the learned to plants and grow crops.
As life for mankind became more complicated, they needed to determine days, hours, mnutes, weeks, months, etc. It all makes sense for us.
However, all that is just for Earth. Nowhere else in the Universe, is alll that dividing of time worthwhile. Only here.
As for age, mankiknd has been bamboozled for many years, and even the Bible mentions who bamboozled us. The Bible calls them them Nephilim. Most people recognnize that name.
We also know them by the name of Annuake.
The Annunaki/Nephilm come from a planet that goes around Sirius B. Zechariah Sitchin probably didn't find a piece of clay that spelled that out even though he deciphered a lot of other information about them.
Some people wou8ld rather debate Sitchen's work, rather than accept the facts.
However, its not that simple. Mankiknd was createdin a special frequency that went with Earth and its frequency. When the Anunnaki/Nephilim came here and had sex or impregnated them with test tubes - which is also shown on some of Sitchin's drawings that are copies of drawings on jars they used back then, it messed with the dna of mankind and ever since, mankind has had frequency sickness. Mankind no longer fits with the frequency of Earth.
The Annunaki on the planet going around Sirius B live at least 500 to 600 years, even though they are 9 to 12 feet tall, they look exactly like us and have a working appendix which exudes a fluid that digest raw meat. They don't have to cook anything if they don't want to, but they occasionally do so. They actually cook using crystal slabs that the sun shines through like we would use a magnifying glass. They have two suns, so its very hot there between 80 and 130 all the time. They can grow food all year round if they wish.
They don't eat junk food like we do, and they don't have a company named Monsanto that combines weed killer with their seeds, so when they farm, they go pull their own weeds. Their food is much healthier than ours too.
Our problem now though is our dna, our frequency sickness, and crappy food that is not oright for our bodies. a second problem, because of ET's messing with us over time (there have been many intnefering with us over time - our dna no loonger repllciates properly and over time starts to drop off the good replication and we start to die. Slowly but surely. Actually we start dying the day we are born.
A telomere is a region of repetitive DNA sequences at the end of a chromosome, which protects the end of the chromosome from deterioration or from fusion with neighbouring chromosomes. Its name is derived from the Greek nouns telos (τέλος) "end" and merοs (μέρος, root: μερ-) "part". The telomere regions deter the degradation of genes near the ends of chromosomes by allowing for the shortening of chromosome ends, which necessarily occurs during chromosome replication. Over time, due to each cell division, the telomere ends do become shorter.
During cell division, enzymes that duplicate DNA cannot continue their duplication all the way to the end of chromosomes. If cells divided without telomeres, they would lose the ends of their chromosomes, and the necessary information they contain. The telomeres are disposable buffers blocking the ends of the chromosomes, are consumed during cell division, and are replenished by an enzyme, , telomerase reverse transcriptase.
Telomeres are repetitive DNA sequences located at the termini of linear chromosomes of most eukaryotic organisms. Because most prokaryotes have circular chromosomes, the majority of them do not have telomeres. Telomeres compensate for incomplete semi-conservative DNA replication at chromosomal ends. The protection against homologous recombination (HR) and non-homologous end joining (NHEJ) constitutes the essential “capping” role of telomeres that distinguishes them from DNA double-strand breaks (DSBs).
In most prokaryotes, chromosomes are circular and, thus, do not have ends to suffer premature replication termination. A small fraction of bacterial chromosomes (such as those in Streptomyces and Borrelia) are linear and possess telomeres, which are very different from those of the eukaryotic chromosomes in structure and functions. The known structures of bacterial telomeres take the form of proteins bound to the ends of linear chromosomes, or hairpin loops of single-stranded DNA at the ends of the linear chromosomes.
While replicating of DNA, the eukaryotic DNA replication enzymes (the DNA polymerase protein complex) cannot replicate the sequences present at the ends of the chromosomes (or more precisely the chromatid fibres). Hence these sequences and the information they carry may get lost. This is the reason why telomeres are so important in context of successful cell division, because they "cap" the end-sequences and themselves get lost in the process of DNA replication. But the cell has an enzyme called telomerase which carries out the task of adding repetitive nucleotide sequences to the ends of the DNA. Telomerase thus "replenishes" the telomere "cap" of the DNA. In most multicellular eukaryotic organisms, telomerase is active only in germ cells, stem cells and certain white blood cells. There are theories that claim that the steady shortening of telomeres with each replication in somatic (body) cells may have a role in senescence and in the prevention of cancer. This is because the telomeres act as a sort of time-delay "fuse", eventually running out after a certain number of cell divisions and resulting in the eventual loss of vital genetic information from the cell's chromosome with future divisions.
Telomere length varies greatly between species, from approximately 300 base pairs in yeast to many kilobases in humans, and usually is composed of arrays of guanine-rich, six- to eight-base-pair-long repeats. Eukaryotic telomeres normally terminate with 3′ single-stranded-DNA overhang, which is essential for telomere maintenance and capping. Multiple proteins binding single- and double-stranded telomere DNA have been identified. These function in both telomere maintenance and capping. Telomeres form large loop structures called telomere loops, or T-loops. Here, the single-stranded DNA curls around in a long circle stabilized by telomere-binding proteins. At the very end of the T-loop, the single-stranded telomere DNA is held onto a region of double-stranded DNA by the telomere strand disrupting the double-helical DNA and base pairing to one of the two strands. This triple-stranded structure is called a displacement loop or D-loop.
Telomere shortening in humans can induce replicative senescence, which blocks cell division. This mechanism appears to prevent genomic instability and development of cancer in human aged cells by limiting the number of cell divisions. However, shortened telomeres impair immune function which might also increase cancer susceptibility. Malignant cells that bypass this arrest become immortalized by telomere extension due mostly to the activation of telomerase, the reverse transcriptase enzyme responsible for synthesis of telomeres. However, 5–10% of human cancers activate the Alternative Lengthening of Telomeres (ALT) pathway, which relies on recombination-mediated elongation.
Since shorter telomeres are thought to be a cause of poorer health and aging, this raises the question of why longer telomeres are not selected for to ameliorate these effects. A prominent explanation suggests that inheriting longer telomeres would cause increased cancer rates (e.g. Weinstein and Ciszek, 2002). However, a recent literature review and analysis  suggests this is unlikely, because shorter telomeres and telomerase inactivation is more often associated with increased cancer rates, and the mortality from cancer occurs late in life when the force of natural selection is very low. An alternative explanation to the hypothesis that long telomeres are selected against due to their cancer promoting effects is the "thrifty telomere" hypothesis which suggests that the cellular proliferation effects of longer telomeres causes increased energy expenditures. In environments of energetic limitation, shorter telomeres might be an energy sparing mechanism.
Human somatic cells without telomerase gradually lose telomeric sequences as a result of incomplete replication (Counter et al., 1992). As human telomeres grow shorter, eventually cells reach the limit of their replicative capacity and progress into senescence or old age. Senescence involves p53 and pRb pathways and leads to the halting of cell proliferation (Campisi, 2005). Senescence may play an important role in suppression of cancer emergence, although inheriting shorter telomeres probably does not protect against cancer. With critically shortened telomeres, further cell proliferation can be achieved by inactivation of p53 and pRb pathways. Cells entering proliferation after inactivation of p53 and pRb pathways undergo crisis. Crisis is characterized by gross chromosomal rearrangements and genome instability, and almost all cells die. Rare cells emerge from crisis immortalized through telomere lengthening by either activated telomerase or ALT (Colgina and Reddel, 1999; Reddel and Bryan, 2003). The first description of an ALT cell line demonstrated that their telomeres are highly heterogeneous in length and predicted a mechanism involving recombination (Murnane et al., 1994). Subsequent studies have confirmed a role for recombination in telomere maintenance by ALT (Dunham et al., 2000), however the exact mechanism of this pathway is yet to be determined. ALT cells produce abundant t-circles, possible products of intratelomeric recombination and t-loop resolution (Tomaska et al., 2000; 2009; Cesare and Griffith, 2004; Wang et al., 2004).
Telomerase is a "ribonucleoprotein complex" composed of a protein component and an RNA primer sequence that acts to protect the terminal ends of chromosomes. The actions of telomerase are necessary because, during replication, DNA polymerase can synthesize DNA in only a 5' to 3' direction and can do so only by adding polynucleotides to an RNA primer that has already been placed at various points along the length of the DNA. These RNA strands must later be replaced with DNA. This replacement of the RNA primers is not a problem at origins of replication within the chromosome because DNA polymerase can use a previous stretch of DNA 5' to the RNA template as a template to backfill the sequence where the RNA primer was; at the terminal end of the chromosome, however, DNA polymerase cannot replace the RNA primer because there is no position 5' of the RNA primer where another primer can be placed, nor is there DNA upstream that can be used as a primer so that DNA polymerase can replace the RNA primer. Without telomeres at the end of DNA, this genetic sequence at the end of the chromosome would be deleted. The chromosome would grow shorter and shorter in subsequent replications and genetic information would be lost. The telomere prevents this problem by employing a different mechanism to synthesize DNA at this point, thereby preserving the sequence at the terminal of the chromosome. This prevents chromosomal fraying and prevents the ends of the chromosome from being processed as a double-strand DNA break, which could lead to chromosome-to-chromosome telomere fusions. Telomeres are extended by telomerases, part of a protein subgroup of specialized reverse transcriptase enzymes known as TERT (TElomerase Reverse Transcriptases) that are involved in synthesis of telomeres in humans and many other, but not all, organisms. However, because of DNA replication mechanisms, oxidative stress, and, because TERT expression is very low in many types of human cells, the telomeres of these cells shrink a little bit every time a cell divides, although, in other cellular compartments that require extensive cell division, such as stem cells and certain white blood cells, TERT is expressed at higher levels and telomere shortening is partially or fully prevented.
In addition to its TERT protein component, telomerase also contains a piece of template RNA known as the TERC (TElomerase RNA Component) or TR (Telomerase RNA). In humans, this TERC telomere sequence is a repeating string of TTAGGG, between 3 and 20 kilobases in length. There are an additional 100-300 kilobases of telomere-associated repeats between the telomere and the rest of the chromosome. Telomere sequences vary from species to species, but, in general, one strand is rich in G with fewer Cs. These G-rich sequences can form four-stranded structures (G-quadruplexes), with sets of four bases held in plane and then stacked on top of each other with either a sodium or a potassium ion between the planar quadruplexes.
If telomeres become too short, they have the potential to unfold from their presumed closed structure. The cell may detect this uncapping as DNA damage and then either stop growing, enter cellular old age (senescence), or begin programmed cell self-destruction (apoptosis) depending on the cell's genetic background (p53 status). Uncapped telomeres also result in chromosomal fusions. Since this damage cannot be repaired in normal somatic cells, the cell may even go into apoptosis. Many aging-related diseases are linked to shortened telomeres. Organs deteriorate as more and more of their cells die off or enter cellular senescence.
At the very distal end of the telomere is a 300 bp single-stranded portion, which forms the T-Loop. This loop is analogous to a knot, which stabilizes the telomere, preventing the telomere ends from being recognized as break points by the DNA repair machinery. Should non-homologous end joining occur at the telomeric ends, chromosomal fusion will result. The T-loop is held together by seven known proteins, the most notable ones being TRF1, TRF2, POT1, TIN1, and TIN2, collectively referred to as the shelterin complex.
The phenomenon of limited cellular division was first observed by Leonard Hayflick, and is now referred to as the Hayflick Limit. Significant discoveries were made by the team led by Professor Elizabeth Blackburn at the University of California, San Francisco (UCSF).
Advocates of human life extension promote the idea of lengthening the telomeres in certain cells through temporary activation of telomerase (by drugs), or possibly permanently by gene therapy. They reason that this would extend human life because it would extend the Hayflick Limit. So far these ideas have not been proven in humans, but it has been demonstrated that telomere extension has successfully reversed some signs of aging in laboratory mice  and the nematode worm species Caenorhabditis elegans. However, it has been hypothesized that longer telomeres and especially telomerase activation might cause increased cancer (e.g. Weinstein and Ciszek, 2002). Paradoxically, longer telomeres might also protect against cancer, because short telomeres are associated with cancer. It has also been suggested that longer telomeres might cause increased energy consumption.
Techniques to extend telomeres could be useful for tissue engineering, because they might permit healthy, noncancerous mammalian cells to be cultured in amounts large enough to be engineering materials for biomedical repairs.
However, there are several issues that still need to be cleared up. First, it is not even certain whether the relationship between telomeres and aging is causal. Changing telomere lengths are usually associated with changing speed of senescence. This telomere shortening, however, might be a consequence of, and not a reason for, aging.
That the role of telomeres is far from being understood is demonstrated by two recent studies on long-lived seabirds. In 2003, scientists observed that the telomeres of Leach's Storm-petrel (Oceanodroma leucorhoa) seem to lengthen with chronological age, the first observed instance of such behaviour of telomeres. In 2006, Juola et al. reported that in another unrelated, long-lived seabird species, the Great Frigatebird (Fregata minor), telomere length did decrease until at least c.40 years of age (i.e. probably over the entire lifespan), but the speed of decrease slowed down massively with increasing ages, and that rates of telomere length decrease varied strongly between individual birds. They concluded that in this species (and probably in frigatebirds and their relatives in general), telomere length could not be used to determine a bird's age sufficiently well. Thus, it seems that there is much more variation in the behavior of telomere length than initially believed.
The telomere length varies in cloned animals. Sometimes the clones end up with shorter telomeres since the DNA has already divided countless times. Occasionally, the telomeres in a clone's DNA are longer because they get "reprogrammed
As a cell begins to become cancerous, it divides more often and its telomeres become very short. If its telomeres get too short, the cell may die. It can escape this fate by up-regulating an enzyme called telomerase, which can prevent telomeres from getting shorter and even elongate them.
Studies have found shortened telomeres in many cancers, including pancreatic, bone, prostate, bladder, lung, kidney, and head and neck. In addition, people with many types of cancer have been found to possess shorter leukocyte telomeres than healthy controls.
Cancer cells require a mechanism to maintain their telomeric DNA in order to continue dividing indefinitely (immortalization). A mechanism for telomere elongation or maintenance is one of the key steps in cellular immortalization and can be used as a diagnostic marker in the clinic. Telomerase, the enzyme complex responsible for elongating telomeres, is activated in approximately 90% of tumors. However, a sizeable fraction of cancerous cells employ alternative lengthening of telomeres (ALT), a non-conservative telomere lengthening pathway involving the transfer of telomere tandem repeats between sister-chromatids.
Telomerase is the natural enzyme that promotes telomere repair. It is active in stem cells, germ cells, hair follicles, and 90 percent of cancer cells, but its expression is low or absent in somatic cells. Telomerase functions by adding bases to the ends of the telomeres. Cells with sufficient telomerase activity are considered immortal in the sense that they can divide past the Hayflick limit without entering senescence or apoptosis. For this reason, telomerase is viewed as a potential target for anti-cancer drugs.
Studies using knockout mice have demonstrated that the role of telomeres in cancer can both be limiting to tumor growth, as well as promote tumorigenesis, depending on the cell type and genomic contex
CHARTS AND MORE DETAILS ARE AVAILANLE HERE http://en.wikipedia.org/wiki/Telomere
THE BEST HEALTH INFORMATION
Unfortunately, the best health infmation is not found in your doctors office if you choose to go to an M.D. They don't get any training in good nutrition. All they do is folloow FDA rules and give you all the pills you are willing to take because your don't know any better, and because you like sugar and fat so much, the most you will do is drink DIET soda full of chemicals and take drugs tat reduces yyour cholesterol levels when your doctor tells you that you don't fit into the FDA guidelines which change rather frequently.
Did you know that if you don't have enough cholesterol in your body, your brain stops functioning? Lots of foods we are given now do that - including ASPERTAME and other chimicallhy changed sugars and fats.
We need to learn to eat well so our AGE doesn't showo in the mirror. Actually, if you don't look i the mirror and you don't have a lot of aches and pains, you can't tell how old you are.
It's only when we don't feel well that we start to feel old.
Most of that is our own fault.
We can fix that if we really try and get the right advice.
We can live a lot longer if we eat right.
The best food to eat is RAW FOOD, as long as its not grown by MONSANTO.
Second choice is vegetarian - which has cooked vegetables in it.
Third choice is t oeat a lot of vegetables andfruits, with a small amount of chicken and fish.
let me say here SOY IS NOT GOOD FOR YOU EITHER. Many people are allergic to it, and much o fit is grown in unhealthy ways - especially the MONSANTO brands.
I can't stress that enough.
The best food you can eat is what you grow yourself, and I realize how hard that is to do because I've tried it myself. Not every state has good growing seasons, good soil, or good climate. So the next best thing is to buy food that is organically grown even if its shipped in.
I realize too that organic food is more expensive, but do you want to live longer or die younger?
we won't even get into drinkikng alcohol, takikng illegal drugs, or smmoking cigarettes here.
As far as I'm concerned HEMP and marijuana are okay to use, especially if you have pain or nausea from other problems.
let me give you some links that mmight help you live lnger.
RAW FOOD DIET
WEIGHT LOSS DIET
DOCTOR LEONARD HOROWITZ
THIS BLOG CONTINUES ON PAGE`` 14