2014年4月24日星期四

Semax

Semax is a new heptapeptide nootropic that shares a similar history, potency and chemical make-up with Noopept powder. Semax was developed in 1982 by a research team from the Institute of Molecular Genetics at the Russian Academy of Sciences in Moscow. It was initially pursued as a treatment for stroke victims suffering bran damage but was subsequently determined to promote significant cognitive enhancement in health individuals as well. This nootropic stimulates the Central Nervous System and increases memory, focus, mental and physical performance, and analytical skills. It is regarded as much safer than other stimulants and does not cause negative side effects like Adderall, Ritalin or Ephedrine. How does Semax work and what are some of the benefits of this drug?

Semax Review

Semax is a neuroactive peptide derived from corticotropin with the structure Pro8-Gly9-Pro10 ACTH(4-10). It has been described as 1000 times stronger than Nootropil (Piracetam) which makes it similar in concentration to Noopept, Sunifiram and Unifiram. Since 2011, it has been classified as a Vital and Essential drug in Russia. Clinical uses of Semax are common in Russia and the Ukraine where it is prescribed for its neuroprotective and neurorestorative characteristics. It is particularly beneficial to ischemic stroke victims and individuals who have suffered other forms of head trauma but has also been used in the treatment of cognitive disorders, optic nerve disease and peptic ulcers.
Semax works by modulating receptors in the Limbic Reticular complex and for the neurotransmitters acetylcholine, dopamine, serotonin, adenosine, histamine and others. It also activates NMDA receptors for glutamate in the central and peripheral nervous system and enhances energy metabolism in your neurons. Additionally, Semax increases synthesis of neurotrophins, proteins and biosubstrates to protect and repair neurons while also reducing inflammation. This drug exhibits highly neuroprotective properties and has been recorded to increase mRNA for Nerve Growth Factor by 500% and for Brain Derived Neurotropic Growth Factor by 800%.
The purported benefits of Semax are extensive, promising increased memory, learning, alertness, reasoning, perception, concentration, energy, immune system functioning and even better mood. Many of these benefits are derived from the fact that Semax has a psychostimulant effect, but it lacks the negative side effects that normally go hand-in-hand with CNS stimulants. In some user experiences and reviews of Semax, it is described as lessening the perception of mental strain and allowing you to be more productive. Experience logs often state that this drug makes all of your cognitive tasks seem to flow easier, faster and with less effort.
Other benefits related to learning and memory come from the fact that Semax boosts neuroplasticity and increases Glutamatergic and Cholinergic activity. Semax has been observed to improve the adaptive capacity of the brain to environmental sources of stress and to lessen symptoms of fatigue after long hours of exhaustive mental work. It may be useful as a treatment for depression, anxiety and even sleep disorders by increases Dopamine and Serotonin levels as well. There is also the possibility of using Semax to cure or reduce signs of Alzheimer’s and other degenerative cognitive disorders or memory loss due to aging. With such a wide range of mechanisms of action, Semax should be a fruitful topic of research in the coming years.

Semax Dosage

The effective dosage of Semax is said to be 1000 times smaller than Piracetam by weight. Semax is typically sold in a 0.1% or a 1% nasal spray solution in bottles of 3 ml which contain 60 doses each. Some nootropic users are wary of taking Semax because it is administered as a nasal spray. While this does make it somewhat unique compared to other nootropic powders or pills that are ingested orally or dosed sublingually, you should not avoid Semax solely for this reason. Ultimately this just means that Semax is more effective when absorbed into your system via the nasal mucous membrane as opposed to being passed through your digestive system.
The suggested dose of Semax for cognitive enhancement purposes is two to three drops of 0.1% solution in each nostril taken twice a day. This amounts to 50 mcg of active ingredient per spray which means if you were spraying twice in each nostril you would be getting 200 mcg of Semax per dosing. Users may actually only need one dosage of Semax per day due to the very long half-life of the drug which can range from 12-24 hours. It is recommended that you cycle this drug for 14 days on at a time and then break from using it for 14 days before starting again. The 1% Semax drop solution should be reserved for stroke victims or more serious medical purposes and should not be used for more than 14 days in a row.

Semax Side Effects

semax dropsDespite its extremely high potency, Semax is considered safe with no serious side effects. There are no known interactions with other drugs, signs of addiction or symptoms of withdrawal from this nootropic drug. It has an exceptionally low toxicity profile both in the liver and in the brain. However, it is important to remember that this is still a newer nootropic with less history of use in the world of brain enhancing compounds. As such, there are fewer user reports to go on whendetermining the safety of this drug. This means that there are some inherent risks in taking such a novel substance even if early research indicates it is very safe.


Company Name: PhtdPeptides. Co., Ltd.
Contact: William wang
Email: phtd012@phtdpeptides.com
web:   www.phtdpeptides.com
Skype: william39333
QQ:329284319
Tel : 0086-0371-65741695
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Mobile:0086-13592439230

Heptapeptide Semax

Heptapeptide Semax (MEHFPGP) is the fragment of ACTH(4-10) analogue with prolonged neurotropic activity. The aim of the present work was to study the Semax effects on learning capability and pain sensitivity in white rats following intraperitoneal and intranasal administration in different doses. Semax nootropic effects were studied in the test of acquisition of passive avoidance task. Pain sensitivity was estimated in Randall-Selitto paw-withdrawal test. It was shown that Semax exerts nootropic and analgesic activities following intraperitoneal administration. Analysis of dependence of these effects on dose resulted in different dose-response curves. Following intranasal administration, Semax was more potent in learning improvement compared to intraperitoneal administration. The peptide failed to affect the animal pain sensitivity following intranasal administration as opposed to intraperitoneal administration. The data obtained suggest different mechanisms and brain structures involved in realization of the nootropic and analgesic effects of Semax.

2014年4月23日星期三

Epithalon decelerates aging and suppresses development of breast adenocarcinomas in transgenic her-2/neu mice.

Epithalon decelerates aging and suppresses development of breast adenocarcinomas in transgenic her-2/neu mice.

Abstract

Female transgenic FVB/N mice carrying the breast cancer gene HER-2/neu received epithalon (Ala-Glu-Asp-Gly) in a dose of 1 mg subcutaneously 5 times a week to from the 2nd month of life to death. Epithalon prolonged the average and maximum lifetimes of mice by 13.5 (p<0.05) and 13.9%, respectively. The peptide prolonged the average lifetime of animals without neoplasms (by 34.2%, p<0.05). Epithalon decelerated the development of age-related disturbances in reproductive activity and suppressed the formation of neoplasms. The peptide decreased the incidence of breast adenocarcinomas, lungs metastases (by 1.6 times, p<0.05), and multiple tumors (by 2 times). Epithalon 3.7-fold increased the number of mice without breast tumors (p<0.05), while the number of animals with 6 or more breast tumors decreased by 3 times (p<0.05). Epithalon prolonged the lifetime of mice with breast tumors by 1.4 times (p<0.05). These results indicate that Epithalon possesses geroprotective activity and inhibits breast carcinogenesis in transgenic mice, which is probably related to suppression of HER-2/neu expression.


Company Name: PhtdPeptides. Co., Ltd.
Contact: William wang
Email: phtd012@phtdpeptides.com
web:   www.phtdpeptides.com
Skype: william39333
QQ:329284319
Tel : 0086-0371-65741695
Fax: 0086-0371-66837889
Mobile:0086-13592439230

Effect of Epitalon on biomarkers of aging – PubMed


Effect of Epitalon on biomarkers of aging – PubMed


Here’s some scientific articles about Epitalon effects…

Effect of Epitalon on biomarkers of aging, life span and spontaneous tumor incidence in female Swiss-derived SHR mice.

Abstract

From the age of 3 months until their natural deaths, female outbred Swiss-derived SHR mice were subcutaneously injected on 5 consecutive days every month with 0.1 ml of normal saline (control) or with 1.0 microg/mouse (approximately 30-40 microg/kg) of tetrapeptide Epitalon (Ala-Glu-Asp-Gly) dissolved in 0.1 ml saline. There were 54 mice in each group. The results of this study show that treatment with Epitalon did not influence food consumption, body weight or mean life span of mice. However, it slowed down the age-related switching-off of estrous function and decreased the frequency of chromosome aberrations in bone marrow cells (by 17.1%, P<0.05). It also increased by 13.3% the life span of the last 10% of the survivors (P<0.01) and by 12.3% the maximum life span in comparison with the control group. We also found that treatment with Epitalon did not influence total spontaneous tumor incidence, but inhibited the development of leukemia (6.0-fold), as compared with the control group. The data obtained suggest a geroprotector activity of Epitalon and the safety of its long-term administration in mice.
Source: PubMed

Effect of epitalon and melatonin on life span and spontaneous carcinogenesis in senescence accelerated mice.

Abstract

Female senescence accelerated mice SAMP-1. (prone) and SAMR-1 (resistant) were exposed 5 times a week monthly to melatonin (with drinking water 20mg/ml during the night hours) or to s.c. injections of epitalon (Ala-Glu-Asp-Gly) at a single dose 1mkg/mouse. Control mice were intact or exposed to injection of 0.1 ml normal saline. The body weight and temperature, food consumption, estrous function were monitored regularly. The life span and tumor incidence were evaluated as well. As age advanced, the weight increased whereas food consumption and body temperature did not change. There was no significant substrain difference in these parameters. Exposure to melatonin or epitalon also failed to influence those indices. As age advanced, the incidence of irregular estrous cycles increased both in SAMP-1 and SAMR-1, whereas the treatment with both melatonin andepitalon prevented such disturbances. SAMP-1 revealed some features of accelerated aging as compared to SAMR-1. The mean life span of the 10% of the last survivors among treated SAMP-1 was shorter than that of SAMR-1, aging rate increased and mortality doubling time decreased. There was a direct correlation between body mass of the two substrains at the age of 3 and 12 months matched by body mass increase and longer life span. Melatonin or epitalon treatment was followed by longer mean and maximum survival in the 10% of the last survivors among SAMP-1. Melatonin involved decreased aging rate and increased mortality doubling time. Malignant lymphomas predominated in SAM without any significant difference in frequency between the substrains. While melatonin failed to influence tumor incidence or term of detection in SAMP-1, neither didepitalon affect frequency. However, it was followed by longer survival in tumor-free animals. No link between melatonin or epitalon treatment, on the one hand, and carcinogenesis, on the other, was reported in SAMR-1.
Source: PubMed

Epitalon telomerase activator

Epitalon telomerase activator

Pure Epitalon compound is a telomerase activator, a very small peptide of four amino acids. There are numerous scientific studies that show teleomeres do lengthen with Epitalon peptide. In fact, the whole cell’s biological clock is reset and cells start to multiply to repair immune system. That way the body can function properly and can maintain organs optimaly, the body itself can continue growing and repairing.
Telomeretelomere is a region of repetitive nucleotide sequences at each end of a chromatid, which protects the end of the chromosome from deterioration or from fusion with neighboring chromosomes. Its name is derived from the Greek nouns telos (τέλος) ‘end’ and merοs (μέρος, root: μερ-) ‘part.’ Telomere regions deter the degradation of genes near the ends of chromosomes by allowing chromosome ends to shorten, which necessarily occurs duringchromosome replication.[1] Without telomeres, the genomes would progressively lose information and be truncated after cell division because the synthesis of Okazaki strands requires RNA primers attaching ahead on the lagging strand. Over time, due to each cell division, the telomere ends become shorter.[2] During cell divisionenzymes 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.
Source: Wikipedia
Here’s a video for you to watch. A Nobel laureate Carol Greider, Ph.D., presents the seventh annual Jeffrey M. Trent Lectureship in Cancer Research. Learn about the groundbreaking research that won her the 2009 Nobel Prize in Physiology or Medicine:
Some interesting comments from the video:
Q: Can the telomerase activator drugs act as anti-ageing drugs? Seems that not much research has been done into them but also that the shortening telomeres are a reasonable factor in ageing.
A: Researchers are actively studying telomeres impact on cell aging (and thus aging of the organism), but they need to be careful to not convert cells into cancers by altering the enzymes regulating telomere length. Cancer cells are immortal because their telomeres do not shorten during cell reproduction. Not sure we want to live forever as a giant tumor.
Here’s another interesting video titled “Extension of Life-Span by Introduction of Telomerase into Normal Human Cells”:
What is life extension exactly?
Here’s an excerpt from Wikipedia:
Life extension science, also known as anti-aging medicine, indefinite life extension, experimental gerontology, and biomedical gerontology, is the study of slowing down or reversing the processes of aging to extend both the maximum and average lifespan. Some researchers in this area, and “life extensionists” or “longevists” (those who wish to achieve longer lives themselves), believe that future breakthroughs in tissue rejuvenation with stem cells, molecular repair, and organ replacement (such as with artificial organs or xenotransplantations) will eventually enable humans to have indefinite lifespans (agerasia[1]) through complete rejuvenation to a healthy youthful condition.
The sale of putative anti-aging products such as nutrition, physical fitness, skin care, hormone replacements, vitamins, supplements and herbs is a lucrative global industry, with the US market generating about $50 billion of revenue each year.[2] Some medical experts state that the use of such products has not been proven to affect the aging process, and many claims of anti-aging medicine advocates have been roundly criticized by medical experts, including the American Medical Association.[2][3][4][5][6]
However, it has not been shown that the goal of indefinite human lifespans itself is necessarily unfeasible; some animals such as lobsters and certain jellyfish do not die of old age, and an award was offered to anyone who could prove life extensionist Aubrey de Grey’s hopes were ‘unworthy of learned debate’; nobody won the prize.[7] The ethical ramifications of life extension are debated by bioethicists.
To learn more about telomerase activators, read the homepage article too.
If you’re wondering where to buy Epitalon, here is your chance.

Epitalon Research Article – Part 1

Epitalon Research Article – Part 1

Today we are presenting to you Part 1 Epitalon research article.
Title: Effect of Epitalon on biomarkers of aging, life span and spontaneous tumor incidence in female Swiss-derived SHR mice
Part 1 - Introduction
The search for new effective and safe means to prevent premature aging is one of the priorities in gerontology (Anisimov 2001; Butler et al. 2002; De Grey et al. 2002). During the last decade a number of reports have appeared on the role of the pineal gland in aging (Armstrong and Redman 1991; Reiter 1995; Reppert and Weaver 1995; Pierpaoli 1998; Reiter et al. 2002).
Pineal Gland
Pineal Gland
A modulating effect of the pineal gland on theneuroendocrine and the immune system was shown to change during aging (Arendt 1995). Pinealectomized rats showed a reduced life span (Malm et al. 1956; Reiter et al. 1999), whereas the administration of the pineal hormonemelatonin to rodents or syngeneic transplantation of pineal glands from young donors into the thymus orin situof old mice prolonged the life span of the recipients (Pierpaoli and Regelson 1994; Lesnikov and Pierpaoli 1994; Anisimov et al. 2001b; Oxenkrug et al. 2001).
Most investigators invoked melatonin as a primary mediator of the endocrine capabilities of the pineal gland. However, some of the effects of the pineal gland might have obviously resulted from pineal peptide secretion (Benson 1977; Bartsch et al. 1992; Yuwiler and Brammer 1993; Arendt 1995). Some crude peptide extracts or purified peptides isolated from pineal glands were
shown to have antigonadotropic, metabolic and anti-194 tumor activity (Anisimov et al. 1994; Bartsch et al. 1992; Lapin and Ebels 1979).
One of the complex peptide bioregulators isolated from the pineal gland, Epithalamin , was shown to slow down aging rate, prolong life span in fruit flies, mice and rats, and inhibit spontaneous and induced carcinogenesis in rodents (Anisimov et al. 1994; Khavinson et al. 2001c; Khavinson 2002). Tetrapeptide Epitalon (Ala-Glu-Asp-Gly, molecular weight 390.35 dalton) was designed on the basis of Epithalamin amino acid analysis and synthesized (Khavinson et al. 2000).
The geroprotective activity of Epitalon was studied in three strains of Drosophila melanogaster(Khavinson et al. 2000; Mylnikov and Lyubimova 2000). Epitalon increased the life span of imagoes significantly by 11–16% when applied at unprecedentedly low concentrations – from 0.001×10 −6 to 5 ×10 −6 wt% of the culture medium. A recent study by us demonstrated a geroprotective effect of long-term Epitalon administration in female inbred CBA mice (Anisimov et al. 2001a).
The bioregulator slowed down aging of the reproductive function, inhibited free radical processes, and decreased total spontaneous tumor incidence in female CBA mice (Anisimov et al. 2001a). Epitalon inhibited mammary carcinogenesis and metastasis in transgenic HER-2/neumice (Anisimov et al. 2002b) and colon and small intestine carcinogenesis induced by 1,2-dimethylhydrazine in rats (Anisimov et al. 2002a).
Administration of Epitalon to young (6–8 years old) and senescent (20–26 years old) female monkeysMacaca mulattarestored the evening level of melatonin and the circadian rhythm of cortisol in the blood serum of senescent monkeys (Khavinson et al. 2001a).
This paper presents data on the effect of Epitalon on life span, estrous function, incidence of chromosome aberration in the bone marrow cells and spontaneous tumorigenesis in outbred Swiss-derived SHR mice.

Epitalon Research Article – Part 2

Epitalon Research Article – Part 2

This is the Epitalon Research Aticle – Part 2
Part 2 - Materials and methods
Animals
Swiss-derived SHR miceFemale outbred Swiss-derived SHR 2-month-old mice (108 specimens) were purchased from the Rappolovo Animal Farm of the Russian Academy of Medical Sciences (St. Petersburg). The mice were kept in polypropylene cages (30×21×9 cm), 5 mice to a cage, at a temperature of 22±2◦ C. A regimen was followed of 12 hours of light and 12 hours of dark.
The animals received sterilized standard laboratory  feed (Anisimov et al. 2003) and tap water ad libitum. Mice were checked daily by animal care personnel and weekly by a veterinarian. The study was conducted in accordance with the regulations for ensuring the humane treatment of animals under the approval of the Committee on Animal Research of the N.N. Petrov Research Institute of Oncology.
Experiment
At the age of 3 months the mice were randomly divided into two groups, 54 animals in each, and they were individually marked. Mice of the control group were subcutaneously injected with 0.1 ml of 0.9% normal saline for 5 consecutive days every month, whereas the mice of the second group received subcutaneously 1.0 µg of Epitalon dissolved in 0.1 ml of saline. This treatment dosage and regimen were effective for the inhibition of spontaneous tumorigenesis in female CBA mice (Anisimov et al. 2001a).
Epitalon was synthesised in St. Petersburg, Institute of Bioregulation and Gerontology, by E.I. Grigoriev and was 99.8% pure. Four intact female SHR mice were euthanized at the age of three months to evaluate the initial level of chromosome aberrations. Additionally four mice from each group were euthanized at the age of 12 months for a cytogenetic study of chromosome aberrations in bone marrow cells (see below).
Once every 3 months, simultaneously with weighing, the amount of food consumed was measured. Thirty grams of food were given in each cage after cleaning and twenty-four hours thereafter the food that had not been consumed was collected from each cage and weighed. The mean amount of food (grams) consumed per mouse during this day was calculated for each group.
Once every three months, vaginal smears taken daily for two weeks from the animals were examined cytologically to estimate the phases of their estrous functions. In the same period, the rectal body temperatures of the mice were measured with an electronic thermometer, TPEM (KMIZ, Russia). Animals were observed until their natural death. The date of each death was recorded, and the mean life span, the age by which 90% of the animals died, and the maximum life span were estimated.
Cytogenetic study
Chromosomal aberrations in bone marrow cells were studied by a modified Ford’s method, described by Rosenfeld et al. (2001). Mice were sacrificed by etheranaesthesia. Both femurs of each mouse were dissected and bone marrow cells were flushed gently with 0.56% KCl solution into a centrifuge tube. Cells were treated for 20 min with hypotonic solution and fixed with an ethanol : acetic acid mixture (3:1). Slides were stained with 4% acetoorseine: 20–30 well spread anaphases were analyzedfor each animal and cells with chromosome breaks,acentric fragments, and other aberrations were evaluated at 1000×magnification under a light microscope (Leitz, Germany).
Pathomorphological examination
All animals that died, or were sacrificed when moribund, were autopsied and their skin and internal organs were examined. Neoplasias were classified according to the recommendations of the International Agency of Research on Cancer (IARC) as ‘fatal’ (i.e., those that directly caused the death of the animal) or ‘incidental’ (in cases where the animal died of a different cause) (Gart et al. 1986). All tumors, as well as tissues and organs with suspected tumors, were excised and fixed in 10% neutral formalin.
After routine histological processing, tissues were embedded in paraffin. Thin, 5–7 µm histological sections were stained with hematoxylin-eosine and examined microscopically. The experimental group to which the mouse belonged was blinded. Tumors were classified according to IARC recommendations (Turusov and Mohr 1994).
Statistics
Experimental results were statistically processed by the methods of variation statistics (Goubler 1978). The significance of discrepancies was defined according to Student’s t-criterion, Fischer’s exact method,χ2-analysis, and the non-parametric criterion of Wilcoxon–Mann–Whitney (Goubler 1978). To estimate discrepancies in neoplasm incidence, an IARC method of combined contingency tables calculated individually for the fatal and incidental tumors (Gart et al. 1986). For survival analysis, Cox’s method (Cox and Oakes 1996) was used. All reported test values for survival analyses are two-sided.
Survival models and estimations
The mathematical model used to describe survival is the Gompertz model with the survival function:
Survival models and estimations
where parametersαandβare associated with demographic aging and initial mortality rate, respectively.
Parameters for the model were estimated from data using the maximum likelihood method implemented in the GAUSS statistical system (Gauss System 1994). Confidence intervals for the aging rate parameter estimates were calculated using log-likelihood functions (Cox and Oakes 1994).

How to Reverse Aging?

How To Reverse Aging
Michio Kaku – How To Reverse Aging
Here’s a very interesting video you really need to see. It is about aging, or how to reverse aging. I am sure you are already familiar with Mr. Michio Kaku. If not, you should definitely watch this video now because there’s lots in common with what this website is all about, anti aging and life extension with the help of Pure Epitalon.
I am sure you will love it as much as I did. Enjoy!
And here’s the transcription of the “how to reverse aging” video if you prefer reading it:
Enzymes like Telomerase and Resveratrol, though not the Fountain of Youth unto themselves, offer tantalizing clues to how we might someday soon unravel the aging process.
Question: Do you think the enzyme Telomerase could be used to reverse the aging process in our lifetime? (Submitted by Paul Cellura)
Michio Kaku: Paul, Telomerase hit the headlines; however, I think we have to put it into perspective. It is not the fountain of youth; however, it is a significant breakthrough. We have to put it into a much larger perspective.
First of all, we know that DNA is sort of like a shoelace. It has plastic tips at the end.Every time a cell reproduces, the tips get shorter and shorter and shorter until finally they fray. And you know that your shoelace, without the plastic tips will simply fall apart. That’s what happens inside a cell. A cell, for example, your skin cell, will divide about 60 times, that’s called a Hayflick Limit. Then the cell goes into senescence and eventually dies.
Hayflick Limit
Hayflick Limit
So in some sense, every cell has a biological clock. It is doomed to die after about 60 reproductions. However, Telomerase can eliminate some of the contraction of thechromosomes and the chromosomes can maintain their length. So at first you may say, “ah-ha! We can now defeat the biological clock.”
But not so fast, first of all, cancer cells also use Telomerase. Cancer cells are immortal. Cancer cells are immortal and that’s precisely why they kill you. Why are cancer cells so dangerous? Because they are immortal. They grow and they grow and they grow until they take over huge chunks of your body, meaning that your bodily functions cannot be performed and you die. So we have to make sure that when you hit ordinary cells with Telomerase that you don’t also trigger cancer in the process.
Now, also you have to realize that genes are also very essential for the aging process. It turns out that we know what aging is. Aging is the buildup of error. That’s all aging is. The build up of genetic and cellular error. And cells begin to age; they begin to get sluggish because genetic mistakes start to build up. Now cells; however, have a repair mechanism. They can repair damage to their cells; otherwise we would all basically rot very soon after birth.
However, even the repair mechanisms eventually get gummed up and then the cell really starts to get old as a consequence. So then the question is, can you accelerate cell repair? That is another branch of gerontology which is being looked at using genes and using chemicals to accelerate the repair mechanisms.
For example, if I take any organism on the planet Earth from yeast cells to spiders, insects, rabbits, dogs, and even monkeys now. And I reduce their caloric intake by 30%, they live 30% longer. In fact the only organism which has not yet been deliberately tested by scientists are homo sapiens. All the other species obey this basic rule. You starve them to death, they live longer. This is independent of Telomerase. This is a function of the wear and tear that we have on the cells. And this is the only known way of actually deliberately extending the lifespan of any organisms almost at will.
Now, what we want is a genetic way of mimicking this mechanism without having to starve yourself because how many people do you know would be willing to starve themselves in order to live 30% longer? Not too many. So then the question is, are there genes that control this process. And the answer is apparently, yes.
There’s something called the Sirtuin genes, Sir2 being the most prominent of them. They in turn stimulate certain enzymes, among them Resveratrol, which is found in red wine, for example. So this does not mean that drinking red wine or taking Telomerase is the fountain of youth. I don’t think that anyone has the fountain of youth yet.

Abstract

Sirtuin genes function as anti-aging genes in yeast, Caenorhabditis elegans, and Drosophila. The NAD requirement for sirtuin function indicates a link between aging and metabolism, and a boost in sirtuin activity may in part explain how calorie restriction extends life span. In mammals, one of the substrates of the SIR2 ortholog, SIRT1, is a regulator of mitochondrial biogenesis, PGC-1alpha. Indeed, the putative SIRT1 activator resveratrol has been shown to stimulate mitochondrial biogenesis and deliver health benefits in treated mice. I explore here how mitochondrial biogenesis may have beneficial effects on aging and, perhaps, diseases of aging. In particular, I speculate that SIRT1-mediated mitochondrial biogenesis may reduce the production of reactive oxygen species, a possible cause of aging, and offer two possible mechanisms for this effect. An understanding of how calorie restriction works may lead to novel drugs to combat diseases of aging. Source: http://www.ncbi.nlm.nih.gov/pubmed/18419308
What I am saying is, we are now finding pieces of the fountain of youth, tantalizing clues that mean that perhaps in the coming decades, we might be able to actually unravel the aging process. We don’t have it yet. Don’t go out to the drug store and stock up on these kinds of chemicals and enzymes thinking you’re going to live forever. However it is conceivable that in the coming decades we’ll come very close to finding it.
So, how to reverse aging naturally?
Pure Epitalon is very close to reversing aging, to the fountain of youth and now you too have a chance to try it and experience its numerous benefits.

Epitalon Research Article – Part 3

Epitalon Research Article – Part 3

This is the Epitalon Research Aticle – Part 3
Part 3 – The results
Results
Age-related body weight dynamics
Mean values of body weight for mice at different ages in the control and treated withEpithalon groups are displayed in Table 1.
Table 1
The body weight of the mice in both groups increased with age, exceeding by 13 months the body weight of 3-month-old animals by 44.5% in the control group (P<0.001), and by 48.5% in the group given Epitalon (P<0.01). There were no differences in the body weight between groups at any period of observation.
Age-related dynamics of food consumption
Measurements showed that the amount of food consumed by the mice in the control (saline) group was practically stable from the age of 5 months to the age of 16 months, increasing slightly at the age of 18 months. Mice treated with Epitalon consumed more food from the 5th to the 16th months of their life than the control group (Table 2).
Age-related dynamics of estrous function in mice
The estrous function in the animals of both age groups was examined every three months, starting when the mice were three months old. The following parameters of estrous function were estimated: the length of the estrus, the relative rate of estrous cycle phases (in percent); and the relative number of short (5 days) estrous cycles. The relative number of animals with regular cycles and irregular cycles (persistent estrus and anestrus) were also calculated. Judging by the data presented in Table 3, the length of estrous cycle in the control female SHR mice increased with advancing age (P<0.05; Student’sttest).
Thus, no essential age-related alterations in the rate of estrous cycle phases were observed. However, the relative number of short estrous cycles decreased significantly with age (37.1% at the age of 3 months, 9.4% at the age of 12 months (P<0.05; Fischer’s exact test) and zero at the age of 15 months, whereas the number of long cycles rose (5.1% at the age of 6 months and 36% at the age of 15 months,P<0.05; Fischer’s exact test).
In the group of mice exposed to Epitalon the length of estrous cycles did not change with the age of the animals and decreased in comparison with the agematched controls at the age of 15 months (P<0.05). There was no significant age-related decrease in the number of short cycles, or an increase in the number of long cycles. The number of mice with regular cycles did not change significantly with age in both groups (Table 3).
Table 3
Age-related dynamics of body temperature in mice
Data on body temperature alterations in the mice exposed to saline or Epitalon are presented in Table 4. The control mice and mice treated with Epitalon revealed a significant decrease in body temperature with age, both on the whole (irrespective of the estrous cycle phases) and in any of the phases. No cyclic alterations in rectal body temperature during the estrus cycle were observed in mice of the control group, but the temperature at diestrus was significantly higher than that in estrus in mice treated with Epitalon at the age of 15 months (P<0.05). It should be noted that the average body temperature in the mice treated with Epitalon was not significantly different from the control mice during the entire period of observation (Table 4).
Table 4
Chromosome aberrations in mouse bone marrow cells
The incidence of chromosome aberrations in bone marrow cells of 3-month-old female SHR was 2.1 ±0.29%. At the age of 12 months this parameter increased to 8.2 ±0.41% (P<0.001; Wilcoxon–Mann–Whitney test) in the group injected with saline. In mice treated from the age of 3 months with Epitalon the incidence of chromosome aberrations at the age of 12 months was 6.8±0.21(-17.1%;P<0.05).
Survival and longevity of female SHR mice
Survival dynamics in the mice treated with either saline or DSIP are demonstrated in Table 5 and Figure 1.
Figure 1
The survival dynamics were in general similar in all groups up to the age of 22 months. However, thereafter, the number of survivors was much higher in Epitalon-treated groups. The last mouse in the control group died at the age of 739 days (24.3 months), whereas in the groups treated with Epitalon 12% of mice survived to this age, and the maximum life span was 830 days (27.3 months, + 12.3%). The mean life span of mice treated with Epitalon did not change as compared with controls. However, the life span in the last 10% of the mice increased for the duration of Epitalon treatment by 3.1 months (+ 13.3%,P<0.01; Student’st-test) (Table 6).
Table 5
Table 6
Spontaneous tumor development in female SHR mice
The total tumor incidence in the control female mice was 36%. Mammary carcinomas and leukemias developed most frequently, corresponding to the oncological characteristics of female SHR mice (Anisimov et al. 1989). The treatment with Epitalon failed to influence the total or malignant tumor incidence in comparison with that of the control group.
However, the incidence of leukemias during the treatment with Epitalon decreased 6-fold (P<0.01; Fischer’s exact test). There was no significant difference in the incidence of any other tumors between the group of mice
treated with the peptide and saline (Table 7). The treatment with Epitalon significantly shifted to right the total tumor yield curve as compared with the control group (Figure 2).
Table 7
Figure 2
Mathematical model and estimations of survival of tumor-free and tumor-bearing mice
A mathematical analysis of the survival data of the mice from the control and melatonin-treated groups has been done separately for three different contexts:
for all animals in each group (total cases); (2) for fatal tumor-bearing mice, and (3) for fatal tumor-free mice. We composed the groups of animals without consideration of possible effects caused by dependence between these groups.
The Gompertz model shows a slowdown (by 29.0.4%) of the population aging rate (calculated as αin the Gompertz equation) and a corresponding increase in MRTD under the influence of Epitalon. The mortality rate in the group of fatal tumor-free mice treated with Epithalon was decreased by 32.5% as compared with the controls (P<0.05, Table 8).
Table 8

Epitalon Research Article – Part 4


Epitalon Research Article – Part 4


This is the Epitalon Research Article – Part 4
Part 4 – Discussion
The results of our study show that the long-term administration of Epitalon slows down demographic aging rate, increases survival and maximum life span and decreases the development of spontaneous leukemias in female SHR mice.
Treatment with Epitalon increased the food consumption in comparison to the controls between the 5th and 16th months of their life, but the body weight was similar in both the control and Epitalon treated group.
Epithalon
Epithalon
Administration of Epitalon to female CBA mice failed to influence the body weight, and increased food consumption at the age of 12 months (Anisimov et al. 2001a). No significant differences in the age-related dynamics of body temperature between both groups were observed in SHR mice. In CBA mice a slight decrease in the body temperature under the influence of Epitalon has been observed (Anisimov et al. 2001a).
Thus, it could be suggested that increased food consumption induced by Epitalon was not followed by an increase in the basal metabolic rate, because both the body weight and the body temperature were not different from the controls.
The administration of Epitalon was followed by a slowing down of the age-related disturbances in estrous function in female SHR mice. These observations are in agreement with data obtained with Epitalon in other strains of mice – CBA and FVB/N (Anisimov et al. 2001a, 2002b).
MelatoninIt is worth nothing that long-term administration of melatoninor pineal peptide preparation Epithalamin was also followed by a slowdown of age-related switching-off of reproductive function in SHR, C3H/Sn and CBA mice and rats (Anisimov et al. 1989, 1998, 2001a, b; Meredith et al. 2000).
The aging process predisposes cells to accumulate mutations, some of which are necessary for initiation of tumor growth in target tissues (Vijg 2000; Bodyak et al. 2002). The incidence of chromosome aberrations increases with age in different strains of mice (Crowley and Curtis 1963; Sato et al. 1995).
Previously we found age-related increases in chromosome aberrations in bone marrow cells and in primary spermatocytes in male SHR mice (Rosenfeld et al. 2001). In this study we observed a significant increase in the frequency of chromosome aberrations in the bone marrow cells in 12-month-old female SHR mice compared to 3-month-old specimens.
Long-term treatment with Epitalon significantly decreased the age-associated increase in chromosome aberrations in female SHR mice. It was shown earlier that Epitalon also inhibited the incidence of chromosome aberration in one-year-old senescence-accelerated mice (Rosenfeld et al. 2002).
The long-term administration of Epitalon failed to influence total spontaneous tumor incidence in female SHR mice, but it significantly inhibited the development of leukemias (P<0.001) (Table 7).
Table 7
Treatment with Epitalon inhibited the growth of transplanted sarcoma M-1 (Khavinson et al. 2001b), decreased spontaneous tumor incidence in female CBA mice (mainly lung adenomas) (Anisimov et al. 2001a) and inHER-2/neutransgenic mice (Anisimov et al. 2002b). It also inhibited colon carcinogenesis induced by 1,2-dimethylhydtrazine in rats (Anisimov et al. 2002a).
It possible to suggest that the capacity of Epitalon to prevent the development of spontaneous leukemias in female SHR mice can be related to its antioxidative activity.
It has been shown that Epitalon inhibits free radical processes inD. melanogasterand CBA mice (Anisimov et al. 2001a; Khavinson and Mylnikov 2000).
Our observation of the positive effect of Epitalon on the life span of SHR mice is in agreement with observations of similar activities of Epithalamin in SHR and C3H/Sn mice and rats (Anisimov et al. 1989, 1994) and of Epitalon in female CBA mice (Anisimov et al. 2001a). The effective concentration of Epitalon was 1000–5000 times less than that of Epithalamin.
Aging
In experiments with two strains of D. melanogaster, Epithalon treatment was followed by an increase in their mean life span (Khavinson and Mylnikov 2000). It is noteworthy that effective concentrations of the tetrapeptide were 1000 times less than of Epithalamin and 16,000–80 ×106 times less than that of melatonin (Khavinson and Mylnikov 2000).
Epithalon increased catalase activity and decreased the level of conjugated hydroperoxides in fruit flies (Mylnikov and Lyubimova 2000). The results of this investigation agree with data obtained in previous observations on the safety of long-term administration of peptide preparations isolated from the pineal gland on their geroprotective and anti-tumour effects (Anisimov et al. 1994; Khavinson et al. 2001c; Khavinson 2002).
Thus, the results obtained confirm a geroprotective potential of the peptide preparation Epithalon (AlaGlu-Asp-Gly). In the heart of CBA mice, the expression of 15,247 transcripts from the cDNA library was studied by the microarray technique (Anisimov S et al. 2002).
The analysis of the results of hybridizing the cDNA clone containing microarrays with the heart samples of the control and Epitalon-exposed mice revealed intensified expression of 194 clones and reduced expression of 48 clones. The analysis identified the multiple genes involved in cell division (14 genes), cell signaling/communication (14), cell structure/motility (6), cell/organism defense (13), gene/protein expression (17), metabolism (11), and genes encoded by mitochondrial DNA (5). These subgroups may include gene products that can explain some of the physiological effects described above, and form a molecular basis for the geroprotective effects of these peptides.
Acknowledgements
This study was supported by grants 99-04-48023 and 02-04-07573 from the Russian Foundation for Basic Research. The authors are very grateful to James W. Vaupel for the opportunityto use the facilities of the Max Planck Institute for Demographic Researchto complete this paper, and to I. I. Mikhailova and O.V. Novikova for their excellent technical assistance.
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