Researchers analyzed data from a 1991-1996 survey of approximately 5,000 doctors. Information was gathered from more than 16,000 visits with patients aged 11 to 21. While doctors inquired about cigarette use in approximately 70 percent of these visits, they neglected to counsel the majority of their young patients about the dangerous habit. Indeed, physicians were found to counsel patients about smoking in less than 2 percent of their visits with adolescents. Among patients who were known smokers, doctors discussed tobacco use in only 17 percent of their visits.

“The report … is an important wake-up call to physicians, academic teachers, and researchers,” wrote University of Minnesota Drs.Dorothy K. Hatsukami and Harry A. Lando.

Experts estimate that more than 3,000 American teenagers begin smoking every day. Those who pick up the habit as youngsters are more likely to become lifetime smokers, and as a consequence suffer from smoking-related diseases such as lung cancer and heart disease. Targeting adolescents has been identified as a crucial step in reducing the prevalence of smoking, and doctors can play an important role in these efforts.

“The responsibility of a physician is to prevent disease as much as it is to cure it,” remarked Dr. William G. Cahan, a chest surgeon with Memorial Sloan-Kettering Cancer Center in New York. “Advising adolescents about not smoking is just as important as vaccinating them against polio and other adolescent diseases. There’s no difference.”

The study found that non-white patients were less likely to be questioned about their smoking habits and to receive tobacco counseling than white patients. Doctors were more inclined to discuss tobacco use with older patients, and with those who had asthma, lower respiratory infections or who were pregnant. Researchers also reported that compared to specialists, primary care physicians more often discussed the harms of smoking with their patients.

Guidelines for counseling adolescents and young adults have been provided by the National Cancer Institute and the American Academy of Pediatrics. These guidelines recommend that physicians inquire about the use of tobacco by their young patients, commend non-users and advise patients to quit or abstain from tobacco.

Study authors expressed concern that despite these guidelines and the highly publicized efforts of the public health community to reduce teen smoking, physicians have not assumed their responsibility in discouraging adolescent tobacco use.

“I think a lot of physicians are defeatist about the impact they can have on adolescents,” said Cahan. “Talking to young patients about not smoking can be difficult, but it’s very important,” he added.

Cahan recommended that supplementary materials and a list of referrals be made available to physicians to help them in their efforts to counsel patients about the risks of tobacco use.

“The overwhelming majority of smokers take up smoking as teenagers,” commented Dr. Gilbert Ross, medical director of the American Council on Science and Health. “If we are ever to have an impact on reducing the rate of smoking in this country, we have to educate our young people to its real dangers. Physicians must take a leadership role in this endeavor.”

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Nor was DDT shown to be a human carcinogen, certainly at environmental doses, as stated by A.J. Lehman, M.D., director of pharmacology at the U.S. Food and Drug Administration, in 1965.

Harm to Wildlife — Where?
The propaganda assault on DDT was enormous. Activists alleged that it was harming birds, including declines in bird populations, loss of reproductive capabilities, eggshell thinning, etc. A closer examination of the literature showed different results.

The raptor populations of eagles, hawks and falcons have been the subjects of scorn for decades, prior to the introduction of DDT in the early 1940s. Not only were they viewed as vermin, but because they were at the tops of their food chains, they were also viewed as menaces to other birds — especially game birds. However, as a result of over-hunting and egg-collection, raptor populations were approaching extinction years before the use of DDT.

The ban’s supporters in one case reported DDT in bird tissue taken from stuffed museum birds, which had died before the advent of DDT, a difficult finding to explain. Effects must always follow causes, not before. The analyses were later found to be incorrect, but not before they had been publicized and accepted as fact.

Bird-count data from sources such as the Audubon Society and the Hawk Mountain Sanctuary, showed a steady increase in raptor populations during the years of heavy DDT use. Lawmakers banned the hunting, collection and shooting of raptors, permitting raptor populations to recover. Thus the DDT ban was not responsible for the population increase.

Contrary to the unsupportable musings of Rachel Carson (who triggered the assault on DDT with her book, “Silent Spring”), the robin population increased a stunning 12-fold during the years of heavy DDT use. Even today, alarmists still consider her unscientific words biblical.

Other bird-count data showed that at least 26 varieties of bird populations increased during the years of heavy DDT use (1941 to 1960).

Focused laboratory experiments attempted to replicate eggshell thinning in many bird species, and failed to demonstrate eggshell thinning over wide ranges of DDT doses. In a few cases a small increase in eggshell thickness occurred in birds fed high doses of DDT.

The world owes much to the efforts of Africa Fighting Malaria’s Bate and The Malaria Project’s Attaran. Their decision to revisit the use of DDT may prove influential in saving millions of lives. As EPA administrator, Whitman has the opportunity to follow in Bate and Attaran’s footsteps.

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As president-elect Bush selects his cabinet and advisors, his new Administrator of the Environmental Protection Agency, New Jersey Gov. Christie Whitman must become knowledgeable of the dubious, unscientific history of the agency. Historically, the EPA has been very harmful to a lot of people.

The Costs of the Ban
The human and economic costs of the DDT ban have been staggering. The United States should rethink its science and environmental policies and put human health first. It should end its chronic deference to harmful agendas of elitist Greens.

In December 2000, the United Nations Environmental Programme (UNEP) met in Johannesburg, South Africa, to implement a global ban of 12 chemicals the UNEP regarded as harmful. These chemicals, called persistent organic pollutants (POPs) included organo-chlorides such as DDT. UNEP proposed that these chemicals be banned because of their alleged harm. The case for harm hinges upon allegations of persistence, various cancers and reproductive problems. When one examines the specific POP data, cause-and-effect relationships and scientific plausibility, the allegations become very fuzzy.

Thanks to the continuing efforts of a few individuals and organizations, such as Roger Bate, M.D., head of the South African non-government organization Africa Fighting Malaria, and Amir Attaran, M.D., head of the Malaria Project, DDT received a restricted exemption from the UNEP ban.

Johannesburg provided a sobering setting for the UNEP meeting since malaria has increased in South Africa since the 1996 DDT ban. Malaria has returned with a vengeance in South Africa and Mozambique, and in Asian countries. There were 163 malaria deaths in South Africa in 1996 while the total (fatal and non-fatal) cases of malaria there rose to 28,000 in 1999. Globally, the annual malaria death toll is more than 2 million per year, plus hundreds of millions more non-fatal afflictions. Such have been the human costs of the EPA 1972 DDT ban.

The total human costs of the DDT ban have been even higher since foreign companies are reluctant to expand companies into African states, exposing highly trained workforces to these hazardous diseases. This has kept much of the African subcontinent in grinding poverty, while much of the world increases in productivity and prosperity. Further, chemical substitutes for DDT such as Larvex-100 have been invariably more costly and less effective.

DDT remains the premier insecticide effective against the anopheles mosquito, which is the known carrier of the organism that causes malaria.

DDT is also effective against several potentially fatal insect-borne diseases such as typhus, plague, yellow fever and sleeping sickness. These are carried by a variety of flies, aphids, lice, and mosquitoes, among others.

The controversy surrounding the DDT ban featured so called “junk science” in many areas. The controversy, the flood of bad science, the subsequent DDT ban and the deaths of hundreds of millions that followed should serve as a warning to all policy makers, especially those in the new administration. The ban demonstrates the harm of poorly reasoned health and science policies. Junk science will never protect the environment or people.

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Exercise, in fact, is the closest thing to an anti-aging potion. A Tufts University study, for instance, found women who did strength exercises twice a week for one year had bodies that were 15 to 20 years more youthful than when they began. Furthermore, exercise has been shown to prevent falls, promote independence and reduce sick time and the need for nursing home care. Exercise also has been proven to stimulate the brain to release hormones that alleviate pain and produce a sense of well-being, which reduces fatigue and relieves depression.

Many older adults not only know the value of exercise, they have fully embraced it, committing themselves to the rigors and rewards of a fitness program. Leo Weil of Sun City Palm Desert bicycled 600 miles in 11 days at the age of 66. Sam Gadless of Florida finished the 1998 New York Marathon at the age of 91. Seventy-three-year-old John House of Sun City Grand near Phoenix bicycles 40 miles every day.

Residents of Del Webb Corporation’s Sun City adult communities have developed “10 Far-Out Fitness Fundamentals” to help seniors across the country get off their rockers and have some fun:

Play the “skin game” with your partner to look for melanoma or abrasions. And remember to wear your sunscreen.

Work on those abdominal muscles and rediscover your belly button! Try chair aerobics.

Lose the remote control. Get up, get out, get involved.

Accumulate your frequent miles on a treadmill, stationary bicycle, cross-trainer or stair climber, or just jog in place.

Forget fast food; it is fried fat. Try stir-fried, steamed or raw vegetables. And remember, all calories count, even if they are off your spouse’s plate. (Snacks, too.)

Take a nap. Restorative naps improve alertness, sharpen your memory skills and generally reduce symptoms of fatigue.

Understand your hereditary risk for osteoporosis. Exercise your bones, increase your calcium intake, avoid alcohol and make your skeleton a nonsmoking section.

Where there is smoke, there is ? emphysema, lung cancer, heart disease, halitosis, gum disease and burned holes in the couch.

Mark Twain said it best: “Wrinkles should merely indicate where smiles have been.” Take time to reminisce. Encourage intergenerational events. Continue to seek stimulation and thought-provoking activities to nurture your spiritual self.

Danny McCoy, a fitness expert employed at Sun City, Georgetown, Texas, pointed to another fitting Mark Twain quote: “I may wear out, but I’ll be darned if I’m going to rust out!”

Take this advice to heart — and keep it going the whole year long!

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1. Local Factors: Although each injurious agent could disturb the ecosystem of the liver by a different route, there are, however, common sets of responses that lead to excess deposition of extracellular matrix components. As illustrated in Figure 1, there are two key players in the fibrogenic process. These are: a) the stellate cells (HSC) that are activated to produce cytokines, growth factors and extracellular matrix components, including type I collagen and b) activated Kupffer cells (KC) (and other inflammatory cells) which secrete reactive oxygen intermediates and produce several cytokines and growth factors. Of all the cytokines and growth factors produced, transforming growth factor _ (TGF-_) and interleukin-6 are the two main fibrogenic cytokines. TGF-_ is produced by KC and HSC, it up-regulates the transcription of the _1(I) and _2(I) collagen genes and induces the expression of TIMP-1, a tissue inhibitor of metalloproteinases involved in collagen degradation. Moreover, TGF-_ induces its own mRNA and establishes key autocrine and paracrine loops to sustain high levels of this cytokine in local sites of liver injury and/or inflammation. IL-6 which is produced by HSC and KC, also induces the transcriptional activation of the type I collagen genes. However, while IL-6 is unable to induce its own mRNA in HSC from normal or cirrhotic livers, it up-regulates the expression of TGF-_ in HSC from cirrhotic livers. Accordingly, it enhances the fibrogenic actions of TGF-_. The molecular mechanisms by which TGF-_ up-regulates the expression of the type I collagen genes have not been completely defined. However, recent work from our laboratory indicates that reactive oxygen intermediates in general, and H2O2 in particular, are important mediators of TGF-_ actions in HSC.

2. Systemic Factors: It has been recently established that cytokines released during an acute phase response episode, mainly IL-6 and tumor necrosis factor-___TNF-___play a key role in liver regeneration and in fibrogenesis. In this regard, we have shown that a single acute phase episode suffices to increase the expression of _1(I) procollagen mRNA in rat liver, and that IL-6 is the cytokine responsible for this up-regulation. Moreover, repeated acute phase episodes in rats receiving CCl4 to produce cirrhosis, enhance the expression of _1(I) procollagen and TIMP 1 mRNAs and increase further the deposition of liver collagen (see Figure 2). In this regard, it is noteworthy to mention that many non-specific inflammatory stimuli are capable of inducing acute phase response episodes. Accordingly, they could play an important role in fibrogenesis by enhancing the production of liver collagen.

In spite of the complexity of the fibrogenic process, several investigators have dissected individual paths leading to activation of KC and HSC and to excess collagen deposition. Thus, the concept of antifibrogenic therapy that was introduced by our group in the early 1970’s could now become a reality in the 1990’s. A better knowledge of the fibrogenic routes could help in designing drugs that will specifically block single fibrogenic pathways. Thus, the development of combined therapies to block two or more fibrogenic routes, may prove to be more efficient and less toxic.

Figure 2

C = Control liver T = Liver from rats with weekly (x3) acute phase response episodes CCl4 = Liver from rats receiving weekly (3x) injections of CCl4 to produce fibrosis CCl4 + T= Liver from rats receiving the combined treatment (acute phase response and CCl4) for 3 weeks.

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To provide an overview of current concepts of liver fibrosis, with special emphasis on the role of hepatic stellate cells (Ito cells, fat-storing cells or lipocytes) on collagen deposition
To review basic molecular mechanisms whereby the genes encoding the type I collagen chains are up regulated
To describe the contribution of non-specific, systemic events on liver fibrosis
To briefly indicate possible targets for anti-fibrogenic therapy.

Abstract:

The liver behaves as an ecological system in which all its elements contribute to the function of the organ. Injurious agents capable of inducing alterations in any of its cell populations, and/or in its extracellular matrix components will trigger an immediate response in an attempt to establish homeostasis. Irrespectively of the mechanisms induced, two main types of response are observed: there is either regeneration with complete restoration of liver architecture and function, or there is sustained scarring of the tissue that will result in fibrosis and organ failure. Many factors, including the genetic make-up of the individual, the nature of the injurious agent and the intensity and duration of the stimulus, will determine whether regeneration or scarring occurs. It is generally accepted that a single, strong injury capable of inducing a significant reduction in functional mass (>50%), will result in regeneration. However, if the injury is repetitive, of small intensity, and it is not accompanied by a significant loses of functional mass, scarring of the liver will be the predominant form of response. The molecular mechanisms involved in each type of response are currently unknown, but are under investigation in many laboratories around the world. Fibrosis that accompanies liver cirrhosis is characterized by excess deposition of most components of the extracellular matrix. However, type I collagen is the predominant type found in all terminal cirrhotic livers. Therefore, in this presentation, we shall analyze important mechanisms involved in excess collagen deposition in the liver, with special emphasis on type I. Collagen deposition is a complex process that depends on the amount of collagen produced and that, which is degraded by specific interstitial collagenases (metalloproteinases or MMPs). Accordingly, excess collagen deposition will result from an imbalance between its synthesis and its degradation.

Although local mechanisms triggered within the liver play a key role in liver fibrogenesis, nonetheless, systemic factors could influence the outcome of the disease. Figure 1 depicts some of the steps involved in upregulation of the type I collagen genes that could result in excess deposition of collagen. Although the figure was designed to explain how alcohol induces excess collagen deposition, with some minor modifications, it could be adapted for many liver injurious agents including virus, endotoxin and metals. The figure illustrates that both local and systemic factors contribute to excess collagen deposition in the liver. While the local events depend mostly on the nature of the injurious agent and on the cell type that is its primary target, systemic effects depend primarily on the intensity of the stimulus.

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Your activity level and metabolism play a role in determining caloric needs during pregnancy. An active, normal weight woman who burns calories quickly may need to increase her intake by 800 calories a day. A sedentary, overweight woman may need only 300 additional calories for optimal weight gain during pregnancy.

Your pre-pregnancy weight also affects caloric needs during pregnancy. Overweight, underweight and normal weight women have different caloric needs. This will affect the amount of weight you should gain while pregnant. Women who start out their pregnancy underweight may need to eat a little more than women who start out overweight.

Your health-care provider will inform you of the weight gain that is appropriate for you. He or she will assess the progress of your weight gain during prenatal visits. If there is a problem, such as too great a weight gain or too little, your physician or midwife will let you know. Do not restrict your caloric intake during pregnancy unless recommended by a health-care provider.

Some calories are nutrient-rich; others are empty. Taking in additional calories with sweets and chips will not do you or your baby any good. Increase your caloric intake to meet the needs of your developing baby by increasing the low-fat portions of your meals such as fish, lean meats and vegetables, while consuming healthy snacks in-between meals such as fruit or raw vegetables. Dips for carrots and celery sticks can be made low-fat and healthy by substituting yogurt for sour cream in the recipe.

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Estimates by the U.S. FDA as to the percentage of patients using NSAIDs for arthritis who experience adverse GI reactions, which include, ulceration, bleeding and perforation, ranges from one to two percent, after three months of NSAID use, to two to five percent after one year of NSAID use.

While these percentages appear relatively low, GI reactions cause significant co-morbid medical problems in those experiencing these problems. Reluctance to continue NSAID use by these patients often results in an exacerbation of the inflammatory symptoms of arthritis. To allow for continuation of NSAID use by these patients, those experiencing significant GI side effects are often also maintained on additional drugs including, antacids, H2 blockers or muscosa protecting agents such as misoprostol, a synthetic prostaglandin.

If COX-2 inhibitors were developed, in part, to reduce potential GI side effects inherent with the use of conventional NSAIDs, has the clinical data compiled thus far indicated that adverse GI events have been suppressed or eliminated by COX-2 inhibitors? First, patients who have a risk factor for GI side effects concomitant with conventional chronic NSAID use cannot always be predicted ahead of time. In order to avoid potential complications, these patients are generally candidates for acetaminophen therapy. In fact, acetaminophen is prescribed to almost one-half of patients with rheumatoid arthritis, in addition to other anti-rheumatic medications. Patients with osteoarthritis also frequently use acetaminophen or salsalates. Thus, many physicians use acetaminophen to avoid GI complications knowing full well that the inflammatory components of arthritis will be generally unaffected by the use of acetaminophen alone.

Celecoxib (Celebrex) or refecoxib (Vioxx) are members of the COX-2 inhibitor class. The medical management strategy employed suggests that COX-2 inhibitors be considered when patients do not respond to conventional NSAIDs for treatment of rheumatoid arthritis or osteoarthritis, or when adverse GI outcomes occur early from conventional NSAID therapy. Of interest in this regard, the use of low-dose aspirin in combination with conventional NSAIDs such as ibuprofen or diclofenac did not appear to significantly increase the risk for GI toxicity. However, according to Dr. Fred Silverstein and colleagues, publishing in The Journal of the American Medical Association (September 13, 2000), results from the CLASS (Celecoxib Long-term Arthritis Safety Study), clinical trials showed that celecoxib at dosages even greater than those normally employed clinically for the therapy of arthritis was associated with a low rate of GI complications (i.e., ulcers) when compared to conventional NSAID at standard dosages. The reduction in upper GI toxicity was greatest in patients who were not also using aspirin. These results of this study support the view that COX-2 inhibition, which suppresses the inflammation of arthritis, also results in fewer and less severe GI reactions when compared to COX-1 inhibitors. These results have important ramifications in consideration of long-term arthritis therapy with COX-2 inhibitors. The results of follow-up clinical trials will likely influence how COX-2 inhibitors are employed for aggressively treating inflammation during the very early stages of active arthritis.

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NSAIDs inhibit the activity of the enzyme cyclooxygenase found in many tissues. Cyclooxygenase converts arachidonic acid to molecules called prostaglandins. Prostaglandin production is critical for the normal function of the GI mucosa. Thus, NSAID inhibition of GI cyclooxygenase is correlated with the demonstrable adverse GI side effects when NSAIDs are employed as the primary medical therapy of arthritis.

The recent discovery of a second form of cyclooxygenase produced only at sites of inflammation led to the development of a class of cyclooxygenase inhibitors that would control the activities of inflammatory cells, and in theory, reduce the severity of concomitant GI reactions associated with conventional NSAID use. Thus, the cyclooxygenase produced constitutively (i.e., COX-1) would be spared by these new NSAIDs, whereas the cyclooxygenase type produced by human rheumatoid arthritis synovium or inflamed synovium of osteoarthritic joints (i.e., COX-2) would be inhibited. Since COX-2 biosynthesis is also stimulated by pro-inflammatory cytokines, which up-regulate the synthesis of extracellular matrix metalloproteinases, enzymes responsible for the destruction of cartilage and bone in arthritis, it followed that COX-2 inhibitors would be critical in the medical therapy of arthritis. Other strategies for suppressing cytokine activity, which contributes to arthritis symptoms, have been previously addressed.

The relative strength of NSAID inhibition of COX-1 and COX-2 have been extensively studied in order to establish effective dose and duration of use in clinical practice. In general, according to Drs. Paulus and Bulpitt, writing in the “Primer on the Rheumatic Diseases,” Edition 11, published by The Arthritis Foundation, the conventional NSAIDs, aspirin, indomethacin, tolmetin, naproxen, piroxicam and ibuprofen inhibit COX-1 at much lower concentrations than concentrations required to inhibit COX-2. By contrast, diclofenac and non-acetylated salicylate inhibit COX-1 and COX-2 approximately equally, whereas etodolac inhibits COX-2 at somewhat lower concentrations than concentrations required to inhibit COX-1.

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