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Postuar nga darke datė 15 Nëntor 2005 - 23:47:

Re: his brain VS her brain (part 9)

Po citoj ato qė tha NS-6

and thats all of the was a bit long but i think it worth the effort...i have to read it all from the beginning myself becouse when i first read it,it was in italian in the "le scienze" magazine...the results are very interesting and complicate the life of the researchers but at the same time open new ways to understand our body better...

yes it's really interesting. According to this fragment of the article, it could be said that some persons would be more susceptible to suffer squizofrenia just because the form or size of any part of their brain? women are more propense?

Postuar nga NS-6 datė 15 Nëntor 2005 - 23:59:

probably but non absolutely sure... the article says that it may be like this,without leaving the other possibilities...u have to consider even the eziology and the pathogenesis of the disease and a lot of other things to arrive at this conclusion and this is not a simple thing of course...but here the article says that the brain regions concerning that disease are different between men and women...

Postuar nga darke datė 27 Nëntor 2005 - 11:29:

AIDS origin

Cod. A27112005

I received this morning an article in my inbox that surprised me. It's about a theory of the origin of AIDS. It seems that the origin is not in the african monkeys but in some experiments of usa goverment?? I don't know... Just take a look at it. What do you think?

The Gay Experiments That Started AIDS in America


There is no doubt that AIDS erupted in the U.S. shortly after government- sponsored hepatitis B vaccine experiments (1978-1981) using gay men as guinea pigs.

The epidemic was caused by the "introduction" of a new retrovirus (the human immunodeficiency virus, or HIV for short); and the introduction of a new herpes-8 virus, the virus that causes Kaposi’s sarcoma, widely known as the "gay cancer" of AIDS.

The taboo theory that AIDS is a man-made disease is largely based on research showing an intimate connection between government vaccine experiments and the outbreak of "the gay plague."

The widely accepted theory is that HIV/AIDS originated in a monkey or chimpanzee virus that "jumped species" in Africa.

However, it is clear that the first AIDS cases were recorded in gay men in Manhattan in 1979, a few years before the epidemic was first noticed in Africa in 1982.

It is now claimed that the human herpes-8 virus (also called the KS virus), discovered in 1994, also originated when a primate herpes virus jumped species in Africa.

How two African species-jumping viruses ended up exclusively in gay men in Manhattan beginning in the late 1970s has never been satisfactorily explained.

Researchers who claim AIDS is a man-made disease believe it is much more likely that these two primate viruses were introduced and spread during the government’s recruitment of thousands of male homosexuals beginning in 1974.

Large numbers of gay men in Manhattan donated blood for the experimental hepatitis B vaccine trial, which took place at the New York Blood Center in Manhattan in 1978.

Extensive evidence supporting the man-made theory of AIDS is easily found on the Internet by Googling: man-made origin of AIDS; and in my two books, "AIDS and the Doctors of Death" and "Queer Blood: The Secret AIDS Genocide Plot."


Beginning in the mid-1970s, government scientists became interested in the health of gay men, particularly in the realm of sexually- transmitted diseases, and specifically in the sexual transmission of the hepatitis B virus.

The early 1970s was a time when large numbers of gays come out of the closet and identified themselves as homosexuals at government- sponsored health clinics.

Organizations such as the Gay Men’s Health Project were formed at this time. Promiscuous gays were avidly sought as volunteers to test the efficacy of a newly-developed hepatitis B vaccine manufactured by Merck and the National Institutes of Health (NIH).

By 1977 over 13,000 Manhattan gays were screened to secure the final 1083 men who would serve as guinea pigs to test the hepatitis B vaccine.

The vaccine was manufactured from the combined plasma of 30 highly selected gay men who carried the hepatitis B virus in their blood. Developed over a period of 65 weeks during 1977-1978 and tested for six months in chimpanzees (the primate in which HIV is thought to have originated), the first group of gay men were inoculated at the New York Blood Center in November 1978.

That same year a final cohort of 6875 homosexual men at the San Francisco City Clinic was assembled to study hepatitis B virus sexual transmission in that city.

By the end of the decade gays in clinics in Los Angeles, Denver, Chicago, and St. Louis, also came under surveillance by the Centers for Disease Control. An additional 1402 volunteers were finally selected to participate in similar vaccine experiments in those cities beginning in March 1980.

Before 1978 there was no stored blood anywhere in the U.S. that tested positive for HIV or the KS virus. There were no cases of AIDS and no cases of "gay cancer" in young men.

The first cases of AIDS appeared shortly after the experiment began in Manhattan. In June 1981 the epidemic became official and was quickly labeled the "gay–related immune deficiency syndrome," later known as AIDS.

The gay community was the most hated minority in America. After the experiments ended, the gay community was decimated by the "gay plague."

In the first years of AIDS, the epidemic was largely ignored by the government (see Randy Shilt’s best-seller, "And the Band Played On") and the disease was blamed on gay anal sex, drugs, and promiscuity.

Gays were immediately labeled "high risk."

In my view, what made gay men "high risk" was the fact that they were the exclusive volunteers for government medical experiments that undoubtedly put them at "high risk."

The evidence for this conclusion is outlined in this report. Further evidence can be obtained from abstracts of scientific reports available on the Internet at the PubMed website of the National Library of Medicine.


The experimental hepatitis B vaccine injected into gays was unlike any other vaccine previously made.

As stated, it was developed in chimpanzees and manufactured in a year-long process of sterilization and purification of the pooled blood of 30 gay men who were hepatitis B virus carriers.

The final group of 1083 selected for the first experiment at the Blood Center were inoculated from November 1978 until October 1979. At one point, there was great concern that the vaccine might be contaminated. According to June Goodfield’s "Quest for the Killers," p 86, "This was no theoretical fear, contamination having been suspected in one batch made by the National Institutes of Health, though never in Merck's."

Each gay man was given three inoculations of the vaccine over a period of three months. The vaccine proved successful with 96% of the men developing protective antibodies against the hepatitis B virus.

It has been assumed by some that these men might have been already immunosuppressed due to promiscuity and venereal disease. Although the young men in the study were indeed "promiscuous" (this was a requirement for entrance into the study), they were in excellent health.

Despite many previous sexual partners, these volunteers had never been infected with the hepatitis B virus, which was a requirement for participation in the experiment. Furthermore, the 96% success rate would not have been accomplished if the men were immunosuppressed, because such people often do not respond to the vaccine.

When Robert Gallo's blood test for HIV became available in the mid-1980s, the New York Blood Center's stored gay blood specimens were reexamined.

Most astonishing is the fact that 20% of the gay men who volunteered for the hepatitis B experiment in Manhattan were discovered to be HIV-positive in 1980 (one year before the AIDS epidemic became "official" in 1981).

This signifies that Manhattan gays in 1980 had the highest incidence of HIV anywhere in the world, including Africa, the supposed birthplace of HIV and AIDS.

In addition, we now know that one out of five gay men (20%) tested positive for the new KS herpes-8 virus in 1982 when stored blood samples from an AIDS trial in New York City were re-examined by epidemiologists at the NCI in 1999.

Never mentioned by AIDS historians is the fact that the New York Blood Center established a chimp virus laboratory for viral vaccine research in West Africa in 1974.

One of the purposes of VILAB II, in Robertsfield, Liberia, was to develop the hepatitis B vaccine in chimps. The lab also prides itself by releasing rehabilitated" (but virus-infected) chimps back into the wild, perhaps accounting for some of the ancestors of HIV and the KS virus found in the jungle by some government researchers.


In the decade before AIDS, the Virus Cancer Program (1968-1980), sponsored by the National Institutes of Health, attempted to prove that viruses caused human cancer.

Ultimately the Program was unsuccessful in providing proof, yet it succeeded in building up the field of animal retrovirology, which led to a more complete understanding of how cancer-causing and immunosuppressive viruses in animals might cause disease in humans.

The VCP was also the birthplace of genetic engineering, molecular biology, and the human genome project. As the VCP was winding down in the late 1970s, the gay experiments began in New York City.

The introduction of HIV and the KS herpes virus into gay men during this period (along with some "novel" and now-patented mycoplasmas discovered at the Armed Forces Institute of Pathology) miraculously revived the career of Robert Gallo and made him the most famous virologist in the world.

And, of course, turned the "failure" of the VCP into a triumph by providing proof that these primate-derived viruses could cause disease in humans.


When AIDS began there were scattered reports in the medical journals questioning whether the "gay plague" might have its origin in the hepatitis B experiments.

It was well-known in medical circles that the vaccine was made from the pooled plasma of gay men — and there was fear that the AIDS agent might be in the vaccine. As a result, when the hepatitis B commercial vaccine became available in July 1982, many people refused to be injected with it.

The fear of the vaccine was readily admitted by the CDC. Nevertheless, in detailed reports the CDC concluded that the vaccine was safe. Although it was clear the hepatitis B vaccine eliminated all "known" viruses, this obviously did not apply to "unknown" viruses at the time, such as HIV and the KS virus.

After HIV was discovered in 1984, some of the vaccine was retested and declared free of HIV. Of course, it was impossible to say whether the vaccine contained the KS virus, because this virus was undiscovered until 1994. I am unaware of any subsequent testing of the vaccine for this herpes KS virus.

Possible contamination problems with the hepatitis vaccine was the impetus that led Luc Montagnier to hunt for a virus in the new gay disease in the autumn of 1982. He began testing batches of human plasma for "reverse transcriptase activity", a biochemical sign indicating the possible presence of a retrovirus. (See page 46 of his book "Virus").

Montagnier's research eventually led to the first discovery of the AIDS virus at the Pasteur Institute in Paris.

Although the CDC and the New York Blood Center claimed it was safe, many health professionals refused the hepatitis B vaccine. In 1985, only 23 out of 162 Rhode Island dentists agreed to take the vaccine because of concerns about AIDS.

As late as 1990, 13 out of 14 black nurses at a university hospital refused to take the vaccine for the same reason.


The purpose of the gay experiments was to test a vaccine that could immunize people against hepatitis B virus. Infection with this virus could lead to severe liver disease and sometimes to liver cancer. Ironically, an unprecedented explosion of cancer took place in male homosexuals after the experiment.

Reports of the fate of these men attest to the fact that participating in the government’s experiments was clearly injurious to the health of gay men.

Significantly, there were no reported blood specimens anywhere in the U.S. that were HIV-positive prior to the epidemic in 1979, except in the samples stored at the NYBC.

In a May 12, 1983, letter to the editor of The New England Journal of Medicine, Cladd Stevens (who supervised the NYBC experiment) wrote : "No cases haves occurred in the vaccine recipients from populations at low risk of AIDS, and there is no excess incidence in the high-risk population." But this proved to be incorrect in later reports co-authored by Stevens.

In a 1985 report Cladd Stevens et al. claimed that seven men (out of 1083) were HIV-positive before they received either vaccine or placebo. If true, this indicates that HIV (and possibly the KS virus) was already present in the blood of Manhattan homosexuals and could have contaminated the pooled blood of gays whose plasma was used to make the vaccine in 1977.

As stated previously, a 1986 report in JAMA showed 20% of the men in the experiment were already infected with HIV by the end of 1981; and by 1984, more than 40% of the men were HIV-positive and doomed to death.

Another follow-up study of 8,906 gay men who donated blood for the hepatitis experiments in Manhattan was released in 1992. Statistical analysis of this group showed that mortality rates for men aged 25-44 began to rise in the 1980s, with AIDS the leading cause of death among young men in New York City. Remarkably, "The all-cause mortality in this cohort in 1988 was 24 times higher that the mortality rate in the cohort before the beginning of the AIDS epidemic."


Largely forgotten in AIDS history is the hepatitis B vaccine trial that also took place with 685 gay Dutch volunteers in Amsterdam between November 1980 and December 1981.

Unlike the American vaccine makers, the Dutch researchers heated their experimental hepatitis B vaccine for added safety.

A 1986 report of the trial clearly states the AIDS virus "was not transmitted by the heat inactivated hepatitis B vaccine."

Of the 685 participants, five were already infected with HIV when the trial began. The researchers theorized that HIV entered the Dutch gay population at the end of the 1970s.

Another follow-up Dutch report of this trial in 1993 again suggests the efficacy of heating the vaccine for safety. (The experimental vaccine was not heated in the U.S. until after all the gay experiments were completed.) At the end of 1982, one year after the Dutch experiment had ended, only As stated previously, a 1986 report in JAMA showed 20% of the men in the experiment were already infected with HIV by the end of 1981; and by 1984, more than 40% of the men were HIV-positive and doomed to death.

7.5% of the Amsterdam men were infected. In contrast, 26.8% of the men in the New York experiment were HIV-positive; and a whopping 42.6% of the San Francisco men were HIV-positive.

These statistics showing many men infected in the American trials in 1982 further prove that Cladd Stevens of the NYBC, and the CDC, were incorrect in declaring there was no excess incidence of AIDS in the "high-risk" gay male population.

The fate of all the men who participated in the hepatitis B vaccine trials in six U.S cities has never been revealed. However, it is likely from the statistics presented in JAMA in 1986 that many, if not most, of the men eventually died of AIDS.

The actual number of AIDS deaths has never been revealed, nor have the individual medical records been studied. Attempts to secure this information have been rebuffed by the Blood Center, due to the "confidential" nature of the experiment.


After the introduction of HIV and the KS virus into the U.S. gay male population in the late 1970s, the incidence of KS skyrocketed.

A 1989 report by Biggar found no cases of KS in young men in New York City during the years 1973-1976. But by 1985 the incidence of KS in "never-married men" in Manhattan had increased 1850 times. In San Francisco the rate of KS increased over 2000 times!

KS is now 20,000 times more common in AIDS patients than in the general population. A 1985 autopsy study by Lee Moskowitz of 52 AIDS cases (23 Haitians, 19 gays, 5 intravenous drug abusers, 2 hemophiliacs, and 3 persons at unknown risk) showed that 94% of AIDS patients from the various risk groups had internal KS. The CDC claims KS now occurs in only 15% of gay men (down from 30% at the beginning of the epidemic), but these statistics are not based on current autopsy studies

KS was never a sexually-transmitted disease before the introduction of HIV into gays. For a century after the first reported KS cases were discovered in Vienna in 1872, there was no evidence that KS could be transmitted from person-to-person.

By 1950, a more aggressive "endemic" form of KS was uncovered in African blacks. Still, there was no evidence the disease was transmissible or contagious. Suddenly with the introduction of HIV into the homosexual community, scientists began to view KS as a contagious "gay cancer" out of Africa.

The new KS virus is closely related to a monkey tumor virus, known as herpes virus saimiri, that was extensively studied by researchers in the VCP in the decade before the epidemic. Initially found only in KS from AIDS patients, the new KS virus has also been found in non-AIDS-related KS tumors and in other forms of cancer, such as lymphoma and multiple myeloma.

HIV is a cancer-causing virus. Infection with HIV (with or without the KS virus) has resulted in a noticeable increase in various forms of cancer.

A 2005 study of over 4000 AIDS patients showed higher rates of melanoma, basal and squamous cell skin carcinomas, anal carcinoma, prostate carcinoma, and Hodgkin disease, when compared with age-adjusted rates for the general United States population.

The KS virus is now in the U.S. blood supply; and blood is not screened routinely for this virus. A 2001 study indicated that 15% of normal Texas blood donors showed evidence of KS virus infection in the blood. A 2002 study of healthy children (ages 4-13) in South Texas showed that 26% had antibodies to the KS virus in their blood.


How did these two viruses of primate origin get into the gay male population to cause AIDS and a contagious form of cancer?

AIDS experts blame monkeys and chimps in the African jungle.

My research indicates it is much more likely these viruses were introduced during government-sponsored hepatitis B experiments using gays as unsuspecting guinea pigs.

Extensive documentation of past "secret medical experiments" by the government can be found on Google.

A recent BBC news report (30 Nov 2004) uncovering unauthorized and dangerous HIV drug experiments on infants and children in New York City orphanages can be found by Googling: BBC + guinea pig kids.

Until proven otherwise, a "new" HIV retrovirus and a "new" KS virus could easily have been developed in a laboratory as part of the Virus Cancer Program.

In the decade before AIDS it was common to transfer and adapt primate retroviruses and herpes viruses into human cells in genetic engineering experiments.

Such viruses were deemed potential "candidate human viruses," as clearly stated in the annual progress reports of the VCP. For further details on the relationship of the VCP to the introduction of HIV, Google: virus cancer program + AIDS.

The connection between the hepatitis experiments and the AIDS epidemic was quickly dismissed by government authorities two decades ago.

However, it is clear from a review of the scientific literature that the "gay plague" began immediately after the government experiments; and the experiments permanently damaged the health of the gay community, and led to continuing spread of HIV into the "general population."

Are we to believe that all this is merely a coincidence — and that AIDS in America resulted simply from two viruses jumping species in the African jungle?

Or is the origin of HIV and AIDS — and the KS virus — related to secret medical research and covert human testing, as suggested here?

* Dr. Alan Cantwell is a retired dermatologist; and the author of five books on the man-made origin of AIDS and the infectious origin of cancer, all published by Aries Rising Press, PO Box 29532, Los Angeles, CA 90029 (


Abstracts of 30 published papers can be found at the PubMed website. Many of his personal writings can be found on by typing in key words "alan cantwell" + articles.

His latest book is Four Women Against Cancer: Bacteria, Cancer and the Origin of Life. His books are available on and through Book Clearing House @ 1-800-431-1579]


Cantwell A. AIDS and the Doctor of Death: An inquiry into the origin of the AIDS epidemic. Aries Rising Press, Los Angeles, 1988.

Cantwell A: Queer Blood: The secret AIDS genocide plot. Aries Rising Press, Los Angeles, 1993.

Miller M.KS enters Y2K still riddled with many questions. J Natl Cancer Inst. 1999 Oct 6;91(19):1612-4.

Szmuness W. Large-scale efficacy trials of hepatitis B vaccines in the USA: baseline data and protocols. J Med Virol. 1979;4(4):327-40.

Szmuness W, Stevens CE, Harley EJ, Zang EA, Oleszko WR, William DC, Sadovsky R, Morrison JM, Kellner. Hepatitis B vaccine: demonstration of efficacy in a controlled clinical trial in a high-risk population in the United States. N Engl J Med. 1980 Oct 9;303(15):833-41.

Szmuness W, Stevens CE, Zang EA, Harley EJ, Kellner A.
A controlled clinical trial of the efficacy of the hepatitis B vaccine (Heptavax B): a final report. Hepatology. 1981 Sep-Oct;1(5):377-85.

Yacovone JA, Weisfeld J. Acceptance of hepatitis B vaccine by Rhode Island dental practitioners. J Am Dent Assoc. 1985 Jul;111(1)5-7.

Spence MR, Dash GP. Hepatitis B: perceptions, knowledge and vaccine acceptance among registered nurses in high-risk occupations in a university hospital. Infect Control Hosp Epidemiol. 1990 Mar;11(3):129-33.

O'Brien TR, Kedes D, Ganem D, Macrae DR, Rosenberg PS, Molden J, Goedert JJ. Evidence for concurrent epidemics of human herpesvirus 8 and human immunodeficiency virus type 1 in US homosexual men: rates, risk factors, and relationship to Kaposi's sarcoma. J Infect Dis. 1999 Oct;180(4):1010-7.

Dollard SC, Nelson KE, Ness PM, Stambolis V, Kuehnert MJ, Pellett PE, Cannon MJ. Possible transmission of human herpesvirus-8 by blood transfusion in a historical United States cohort. Transfusion. 2005 Apr;45(4):463-5.

Sacks HS, Rose DN, Chalmers TC. Should the risk of acquired immunodeficiency syndrome deter hepatitis B vaccination? A decision analysis. JAMA. 1984 Dec 28;252(24):3375-7.

Stevens CE, Taylor PE, Zang EA, Morrison JM, Harley EJ, Rodriguez de Cordoba S, Bacino C, Ting RC, Bodner AJ, Sarngadharan MG, et al. Human T-cell lymphotropic virus type III infection in a cohort of homosexual men in New York City. JAMA. 1986 Apr 25;255(16):2167-72.

Stevens CE, Taylor PE, Rubinstein P, Ting RC, Bodner AJ, Sarngadharan MG, Gallo RC. Safety of the hepatitis B vaccine. N Engl J Med. 1985 Feb 7;312(6):375-6.

van Griensven GJ, Hessol NA, Koblin BA, Byers RH, O'Malley PM, Albercht-van Lent N, Buchbinder SP, Taylor PE, Stevens CE, Coutinho RA. Epidemiology of human immunodeficiency virus type 1 infection amonghomosexual men participating in hepatitis B vaccine trials in Amsterdam, New York City, and San Francisco, 1978-1990. Am J Epidemiol. 1993 Apr 15;137(8):909-15.

Biggar RJ, Burnett W, Mikl J, Nasca P. Cancer among New York men at risk of acquired immunodeficiency syndrome. Int J Cancer. 1989 Jun 15;43(6):979-85.

Moskowitz LB, Hensley GT, Gould EW, Weiss SD. Frequency and anatomic distribution of lymphadenopathic Kaposi's sarcoma in the acquired immunodeficiency syndrome: an autopsy series. Hum Pathol. 1985 May;16(5):447-56.

Barahona H, Melendez LV, Hunt RD, Daniel MD. The owl monkey (Aotus trivirgatus) as an animal model for viral diseases and oncologic studies. Lab Anim Sci. 1976 Dec;26(6 Pt 2):1104-12.

Koblin BA, Hessol NA, Zauber AG, Taylor PE, Buchbinder SP, Katz MH, Stevens CE. Increased incidence of cancer among homosexual men, New York City and San Francisco, 1978-1990. Am J Epidemiol. 1996 Nov 15;144(10):916-23.

Burgi A, Brodine S, Wegner S, Milazzo M, Wallace MR, Spooner K, Blazes DL, Agan BK, Armstrong A, Fraser S, Crum NF. Incidence and risk factors for the occurrence of non-AIDS-defining cancers among human immunodeficiency virus-infected individuals. Cancer. 2005 Oct 1;104(7):1505-11.

Baillargeon J, Deng JH, Hettler E, Harrison C, Grady JJ, Korte LG, Alexander J, Montalvo E, Jenson HB, Gao SJ. Seroprevalence of Kaposi's sarcoma-associated herpesvirus infection among blood donors from Texas. Ann Epidemiol. 2001 Oct;11(7):512-8.

Baillargeon J, Leach CT, Deng JH, Gao SJ, Jenson HB. High prevalence of human herpesvirus 8 (HHV-8) infection in south Texas children. J Med Virol. 2002 Aug;67(4):542-8.

The Virus Cancer Program: Birthplace of AIDS by ALAN CANTWELL MD
Vaccines: Cure or Another Cause of Disease? by DR. ALAN CANTWELL, MD
Govt Conspiracy, Political Paranoia' & Bill Frist by ALAN CANTWELL, MD
HIV-AIDS: Why Gays Will Not Consider It Man-Made by ALAN CANTWELL MD
Breast Cancer Microbe Research May Yield Cure by ALAN R. CANTWELL, M.D.
Prostate Cancer: Why No Bacteria/Microbe Research? by ALAN CANTWELL, M.D.

Postuar nga NS-6 datė 28 Nëntor 2005 - 23:17:


this is the fifth version i hear about the origin of AIDS and all of them seem havin good bases on what they tell...this version is quite interesting but in order to accept this version we have to search whether there is any other article that speaks whether there have been any case, or at least suspect, of AIDS in the african population during the time of this experiment becouse i have read somewhere that there might have been cases concerning this disease before the time of the experiment...i'll try a search any other article that speaks about the origins of AIDS...there was one,last year on the scientific american magazine (but in italian ) talkin about the AIDS distribution and its probable causes...i hope i find the english version...

p.s:darke just smth : try to split the article when it is too long...sometimes it helps havin more clear the ideas

Postuar nga ~Enigme~ datė 04 Dhjetor 2005 - 19:29:

Research Shows Laser Surgery Effective for Liver Cancer

Cod. A04122005

(The New York Times News Service):November 29, 2005

Long-term research has found that laser surgery using magnetic resonance guidance is effective in treating cancerous liver tumors in some patients, German researchers report.

In this 12-year study, 839 patients at the University of Frankfurt received magnetic resonance-guided, laser-induced thermotherapy for the treatment of liver tumors resulting from colorectal cancer. Under the procedure, laser light is used to destroy tumor tissue.

In the trial, lead researcher Dr. Martin Mack, an associate professor in the university's department of diagnostic and interventional radiology, and his colleagues treated 2,506 liver tumors and tracked patient survival to evaluate the long-term results of the procedure.

Using the laser technology, the average survival rate from the date of diagnosis was 3.8 years, which compared well with survival rates after traditional surgery, which are usually 1.5 to 5.0 years, the researchers reported.

According to Mack, laser ablation has many advantages over other treatments. In addition, laser surgery can be used to treat tumors in both halves of the liver -- often during the same procedure. This is practically impossible in a traditional surgery where only the left or right lobe is surgically excised, the researchers note. Moreover, if new tumors are found during follow-up exams, it is easier to do another laser treatment than to subject the patient to another invasive surgery.

"Many surgeons are already performing local ablation instead of resection, because they have already recognized the positive effect of local ablation," Mack says. "I believe that minimally invasive tumor ablation together with chemotherapy will play the most important role in the treatment of tumors in the years to come."

One expert, however, doesn't think this method is as good as standard surgery for the treatment of liver cancer.

"I would be wary of making too much out of this new technology," says Dr. Charles Cha, an assistant professor of gastrointestinal surgery and surgical oncology at Yale University School of Medicine. "The long-term survival presented by Mack's group is impressive and does demonstrate some promise for this new and experimental technology."

But, Cha notes, "the five-year survival after resection for metastatic colon cancer is around 40 percent, much higher than the 24 percent reported. In addition, there was no surgical arm to compare to, and the conclusion that this technology is better than resection is a bit of a stretch."

The results with either cold (cryotherapy) or heat (radiofrequency ablation) for the treatment of metastatic colorectal cancer have not yet matched the results of surgery, which remains the gold standard, Cha adds. "Until more definitive evidence is available, patients should not consider this technology as a replacement for standard surgical therapy, but rather as an alternative if surgery is not possible."

Another expert agrees.

"This is the only group that has really done this procedure," says Dr. Ronald W. Busuttil, chief of the division of liver and pancreas transplant at the University of California, Los Angeles School of Medicine. "It has not been duplicated." Busuttil says he thought that there are a lot of other methods that can be used to treat liver tumors caused by colorectal cancer that do not include surgery.

"For this technique to really come to the fore, it needs to be compared against surgery and radiofrequency ablation," he says. "It's interesting," Busuttil says, "but I don't know if it's ready for prime time."

Postuar nga ~Enigme~ datė 09 Dhjetor 2005 - 13:49:

Post The Dog Shares Most Genes with Humans

Cod. A09122005

(The New York Times News Service) --
Scientists are publishing Thursday the complete DNA sequence that makes a dog a dog, and it turns out to be uncannily close to what makes a person a person.

Genome sequencers at Harvard University, MIT and their affiliated Whitehead Institute for Biomedical Research in Cambridge, Mass., led an international team of scientists through a unique landscape of doggie DNA.

About 2.4 billion chemical units of DNA define a species uniquely shaped by people ever since dogs left the wolf pack and joined our human ancestors at least 15,000 years ago. Accurately mapping the dog genome took about two years and $30 million. Canis familiaris is the latest species to have its genetic code mapped, following that of the rat, mouse, fruit fly and, most famously, the human.

A report on the work appears today in Nature, the British science journal.

Simultaneously, Cold Spring Harbor Laboratory on Long Island devoted the December issue of its journal "Genome Research," exclusively to canine studies, and produced a book, "The Dog and Its Genome," co-edited by the Whitehead Institute's Kerstin Lindblad-Toh, lead author of the genome study.

Researchers note that dogs share many of the same gene-related health conditions as humans, including cancer and obesity. They have about 19,300 genes, scientists estimate, all but a handful close copies of human genes. Although humans have half a billion more DNA units, or "base pairs," that's mostly because humans are thought to have more silent stretches of so-called junk DNA.

Dogs attract keen research interest in part because of their astounding variety of sizes, physical forms, coat colors and, of course, behavioral traits. If some of these variations can be traced to genes, results may shed light on more subtle variability in other species, including humans.

The task is made more manageable because the same breeding programs that generated the 350 or so modern dog breeds also left precise records of lineages going back many generations. These are tied in some cases to detailed medical records and observations by trainers and owners -- a treasure trove in the era of comparative genomics.

After hundreds of years of selective inbreeding, many of the most prized purebreds have a high risk of genetic maladies.

Discovery of a narcolepsy gene in Dobermans, for instance, helped scientists understand what caused the human form of the sleep disorder.

"The dog is a good model for human disease," Lindblad-Toh said. "They are highly intelligent, social animals, and we interact with them in the same environment."

In veterinary medicine, one of the big tricks now will be to see what disease susceptibilities might be linked genetically to traits that help define a breed.

"There are genes that make a Dalmatian look like a Dalmatian, and that could be very similar to genes that make a disease," said Erika Werne, director of canine research and education at the American Kennel Club Canine Health Foundation in Raleigh, N.C. "If we can see what sort of susceptibility an individual (dog) has, then we may be able to tailor therapies to that individual animal."

The full dog genome sequence was based on DNA samples taken from a female boxer named Tasha, chosen for technical reasons as the best reference breed for widespread use. Ten other breeds were then surveyed for gene variants important as mapping tools, including the dog's great ancestor, the gray wolf, and coyote cousin.

Having all these data in hand may help other researchers sniff out such mysteries as why some dogs, even after extensive training, fail to make the grade as reliable companions for blind and disabled people.

One other canine mystery came nearer to being solved today in a study, also appearing in Nature, on the astounding cornering capacity of greyhounds.

Two researchers in the United Kingdom, James Usherwood and Alan Wilson, used high-speed video to analyze the speed and footfall timings of 40 greyhounds tearing around a track after a mechanical hare. Results showed the dogs derive their power from their hips and back muscles while weight support on banked turns shifts to the forelimbs.

A human track star has to slow down on a sharply banked turn to compensate for rising forces of centripetal acceleration.

Greyhounds can attack a bend full-speed, tilting into a turn like a cyclist, because "the muscles that provide the power are mechanically divorced from the structures that support weight," the scientists found.

"When you watch them run, you're in awe," commented Helen Hamilton, a Fremont veterinarian and longtime greyhound fancier, who likened the dogs to "Ferrari engines on four legs."

Genetically hardwired to run pell-mell, the dogs seem to get despondent if forced to slow down. Still, the speedy gene set comes at the price of shattered bones and torn tendons, Hamilton said, injuries whose incidence jumps dramatically in an environment full of two-legged track hounds laying wagers.

Postuar nga NS-6 datė 15 Dhjetor 2005 - 23:18:

How does someone get two different-colored eyes

Cod. A16122005

How does someone get two different-colored eyes?
question by Jessica,
Mead, Wash.

Susan J. Gross, co-director of the Division of Reproductive Genetics at the Montefiore Medical Center and an associate professor at Albert Einstein College of Medicine, provides this explanation.

Eye color is a manifestation of the pigment that is present in the iris. Brown eyes are rich in melanin deposits, and blue eyes indicate a lack of melanin. The melanocytes of the iris rest in a richly innervated psuedosyncytium, which is necessary to maintain eye color. Two genes control eye color: EYCL3, found on chromosome 15, which codes for brown/blue eye color (BEY), and EYCL1, found on chromosome 19, which codes for green/blue eye color (GEY). Although previously believed to be inherited in simple Mendelian fashion, eye color has proved to be a polygenic trait. Precisely how these genes interact to provide the full constellation of colors, such as hazel and gray, is as yet unknown. Furthermore, other genes may determine the pattern and placement of pigment in the iris, thereby accounting for solid brown as opposed to rays of color.

Heterochromia iridium (two different-colored eyes within a single individual) and heterochromia iridis (a variety of color within a single iris) are relatively rare in humans and result from increased or decreased pigmentation of the iris. Most cases are isolated and sporadic, conceivably resulting from an alteration in the expression of the above-mentioned genes (and those we have yet to find) within the cells of the entire iris or even a particular section. Other potential causes include trauma around the time of birth or later in life, congenital pigmented nevi or even medications such as those used in the treatment of glaucoma. There are a few well-known syndromes of which heterochromia iridis is a striking feature. Waardenburg syndrome type 1, an autosomal dominant disorder caused by mutations in the PAX3 gene, is characterized by pigmentary disturbances of the iris, hair and skin, as well as congenital sensorineural hearing loss. But two different eye colors tends to be an isolated finding, which adds to the seemingly endless and fascinating variation in humans' physical characteristics.

Answer posted on November 03, 2001

Postuar nga ~Enigme~ datė 16 Dhjetor 2005 - 01:25:

Post Flu Vaccine Prototype Tests Look Promising

Cod. B16122005

News brought to you by: New York Times on The Web
December 15, 2005

Scientists said Thursday that preliminary tests on a prototype of a pandemic flu vaccine based on the deadly H5N1 strain of bird flu have shown promise. Scientists at Sanofi-Pasteur, the French pharmaceutical company developing the vaccine, said adding another ingredient to the flu shot seemed to boost the potency of lower doses. That would mean that supplies of the key element of the vaccine -- known as the antigen -- could be stretched further, allowing more people to obtain the shots in an emergency.

Since 2003, the deadly bird flu strain has killed at least 69 people in Asia -- most of them farm workers who came into close contact with infected birds.
One of the major challenges in producing a vaccine suitable for a global flu pandemic has been the short supply of antigen. Flu vaccine factories have the capacity to cater to the demands of regular flu seasons, when only a small proportion of the population gets shots. However, many more vaccines would be needed if there were a pandemic.

One solution would be to build more factories or increase the production capacity of existing ones, but that takes time. Another, quicker option is to develop technology that allows the manufacturers to use less antigen per dose of vaccine. Both options are being pursued in preparation for a possible flu pandemic, which experts agree is only a matter of time.

Seasonal flu vaccines, which combine the three most dominant strains, use about 15 micrograms of antigen per strain contained in the shot. Researchers found that the H5N1 bird flu strain -- the one scientists believe is most likely to spawn a potential pandemic -- is so alien to the human body it takes two injections of vaccine using 90 micrograms of antigen apiece to get an adequate response from the human immune system.

In the latest study, an ingredient called alum was added to the vaccine in an attempt to reduce the amount of antigen needed in the shot. Scientists tested the new vaccine on 300 people and found they could get a decent immune response from two injections using only 30 micrograms of antigen each. Provoking an immune system response is not proof the vaccine will protect against infection, but it is the first step. The other major problem -- the need for two shots spread over weeks -- also needs to be addressed.

In addition, it's impossible to perfect a pandemic flu vaccine before the pandemic starts because the vaccine must exactly match the strain, which is unknown until it arrives. However, much of the scientific groundwork, such as perfecting the dose and the amount of antigen needed, can be done using another flu strain.

Postuar nga NS-6 datė 19 Janar 2006 - 22:53:

How Does Sodium Contribute to High Blood Pressure?

Cod. A19012006

In a complex way, increased salt intake causes more fluid to be contained in the blood vessels. This increased volume of blood requires the heart to work harder to pump blood to all the tissues in the body. Increasing the bloods volume within the enclosure of the circulatory system is one way that salt increases blood pressure. Another way salt may help elevate blood pressure is through the action of the arterioles. Arterioles are blood vessels that dilate and constrict to regulate blood pressure and blood flow. By contracting under the influence of sodium, arterioles effectively increase the resistance to blood movement and lessen the volume of blood that is returned to the heart. This action also increases blood pressure. Other mechanisms linking sodium with hypertension are less well understood. The extent to which each person responds to high intake of salt is probably genetically determined. Some people are more susceptible to the effects of sodium than others, and sodium sensitivity appears to increase with age.

Postuar nga NS-6 datė 26 Janar 2006 - 11:18:

why CO is toxic for the human being?

Cod. A26012006

To explain this aspect, we need to explain how the body uses oxygen from the air. Oxygen is transported around the body via the red blood cells. Specifically, oxygen binds to a substance within the red blood cells called haemoglobin, which is also responsible for their red colour.
Haemoglobin takes up oxygen as blood passes through the lungs, and at the same time carbon dioxide, produced by the body's metabolism, is released from the blood into the exhaled breath. The combination of oxygen with haemoglobin is called oxyhaemoglobin and this 'oxygenated' blood is carried away from the lungs through the bloodstream to all the tissues of the body.

Carbon monoxide can also bind to haemoglobin but does so about 240 times more tightly than oxygen, forming a compound called carboxyhaemoglobin. This means that if both carbon monoxide and oxygen are inhaled, carbon monoxide will preferentially bind to haemoglobin. This reduces the amount of haemoglobin available to bind to oxygen, so the body and tissues become starved of oxygen.

Carboxyhaemoglobin also has direct effects on the blood vessels of the body - causing them to become 'leaky'. This is seen especially in the brain, causing the brain to swell, leading to unconsciousness and neurological damage.

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