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U rubrici zdravlje možete pronaći korisne informacije o procesu tranzicije, hormonima i specifičnostima koje ovaj proces donosi. Da biste pregledali određene delove ove rubrike, molimo vas da napravite korisnički nalog. Ukoliko želite da podelite svoju priču sa čitaocima ovog sajta ili želite da doprinesete prevođenjem, molimo vas da nas kontaktirate na  Ova adresa el. pošte zaštićena je od spam napada, treba omogućiti JavaSkript da biste je videli
 
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FTMIako postoje izvesni zdravstveni rizici u vezi sa hormonskom terapijom, ona ipak može da ima pozitivne i važne efekte na kvalitet života transseksualaca.
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Testosteron (ponekad se naziva „T“) je glavni hormon odgovoran za stvaranje „muških“ fizičkih karakteristika, i obično se koristi za hormonsku „maskulinizaciju“ kod FTM. Testosteron direktno utiče na tkiva u telu (npr. stimuliše rast klitorisa), a takođe indirektno tako što potiskuje produkciju estrogena. Ukoliko menstrualni ciklus ne prestane nakon tri meseca uzimanja testosterona, na svaka tri meseca se mogu uzimati injekcije vrste progestagena (derivata progesterona) dok testosteron ne počne da „radi“.

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hormones1.    Hormoni nisu magične pilule. Nećeš „postati žena“ samo njihovim uzimanjem.
2.    Promene izazvane uzimanjem hormona su prilično suptilne i dešavaju se tokom nekoliko godina.
3.    Ukoliko želiš da te sredina prihvati kao ženu, nemoj se oslanjati samo na hormone.
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Having trouble maintaining an erection from time to time isn't necessarily a cause for concern. What can I do to prevent a heart attack and help my ED? Many of the same steps can be taken to improve both, including: Evidence of an immune-mediated, antitumor effect of PDE5 inhibition is further shown by tetramer analysis on splenocytes obtained from sildenafil-treated, CT26WT tumor- bearing mice, which revealed a higher number of CTLs specific for AH-1 (unpublished data), a CT26 tumor-associated antigen, as compared with their untreated counterparts (19). To confirm immune-mediated antitumor activity in the sildenafil-treated groups, we performed an in vivo cytotoxicity assay. BALB/c mice were injected with PBS (naive), vaccinated with -irradiated CT26WT or C26GM, or challenged with CT26WT or C26GM tumors on day 0. On day 12 (CT26WT) or day 5 (C26GM), all mice received carboxyfluorescein diacetate succinimidyl ester (CFSE)labeled splenocytes pulsed with the MHC class Irestricted AH-1 peptide (CFSEhigh), admixed with CFSE-labeled splenocytes pulsed with the irrelevant hemagglutinin (HA)-peptide (CFSElow). In vivo T cell cytotoxicity was determined 40 h later (Fig. 2). These time points were chosen based on the kinetics of tumor outgrowth observed in Fig. 1 A and Fig. 1 B, respectively, when tumor size significantly differed between untreated and sildenafil-treated mice. As expected, an endogenous AH1-specific immune response was observed in the vaccinated mice as compared with their tumor-bearing counterparts. PDE5 inhibition in the vaccine-primed mice failed to augment antigen-specific CD8 responsiveness compared with no treatment. In contrast, tumor-bearing mice treated with sildenafil early after tumor challenge generated antigen-specific immunity that was significantly greater then that observed in their untreated counterparts and similar, or even superior, to that induced by vaccination. Collectively, this is the first indication that PDE5 inhibitors can modulate antitumor immunity. Because the sildenafil-mediated antitumor immune response does not completely eradicate tumors, tumor escape mechanisms may be associated with their outgrowth. To test this hypothesis, the parental CT26WT cell line, as well as the CT26 tumor removed on day 24 from sildenafil-treated mice (either AH-1 pulsed or unpulsed), and BALB/c splenocytes were incubated with either AH-1 peptide-primed (Fig. S1 C) or tumor-primed (Fig. S1 D) effector T cells. Although effector T cells recognized the parental CT26WT line and released IFN- in the assay, they failed to recognize the sildenafil-derived tumor. Its recognition, however, was restored by loading the sildenafil-derived tumor with the AH-1 peptide. (Fig. S1, C and D). These results suggest that the immune response in sildenafil-treated mice does not result in complete tumor eradication but rather in the selection of antigen-escape variants. Current Article Ratings: In the first study of its kind, New England Research Institutes, Inc. (NERI) in collaboration with the Division of Cardiology, San Francisco General Hospital and the University of California, San Francisco tested whether erectile dysfunction (ED) can be used to reclassify patients according to their future risk of developing cardiovascular disease (CVD) beyond traditional risk factors (such as smoking, high blood pressure, high cholesterol, etc). Results of the 12-year research study are published in the January 26, 2010 issue of the Journal of the American College of Cardiology and show that ED may be a warning sign of a future cardiovascular event like heart attack, stroke, atherosclerosis, coronary artery bypass graft surgery, and congestive heart failure. However, while ED is significantly related to CVD independent of traditional risk factors, it does not improve the prediction of who will and will not develop CVD beyond these risk factors. Have you had any psychological problems such as stress, anxiety and depression? Setting Patients' homes and 19 clinical practice centers in the United States. What you need to know about alprostadil (Caverject, Edex, and Prostin VR) injections and MUSE suppositories. When did you first notice symptoms of ED? Sharlip says he thinks it's dangerous to take your doctor out of the loop by buying Viagra on the Internet, for example. "Internet acquisition of these drugs is the same thing as over-the-counter," he says. "They say there's a physician that's overseeing it, but there's no physician overseeing it very carefully." Reprints: Dr. Setter, Department of Pharmacotherapy, College of Pharmacy, Washington State University/Elder Services, 5125 N. Market St., Spokane, WA 99217-6131, fax 509/458-7459, ssetter@smhca.org undescended testicle buy generic viagra In other words, the complex chemical process behind your erection can be interrupted if the vascular, or blood vessel, system isnt functioning correctly. Atherosclerosis, the build-up of plaque in your blood vessels, can also increase erectile dysfunction risk by reducing blood flow throughout the body. "We think that if men with erectile dysfunction went to see their physicians, it may enable the interaction with the physician to discuss other coronary risk factors," he said. It is been estimated that about 35-75% of men with diabetes will experience at least some degree of erectile dysfunction -- also called impotence -- during their lifetime. Five of seven of the rats that received nanoparticles with nitric oxide and all 11 rats that received nanoparticles with nitric oxide and either silorphin or tadalafil showed significant improvements in erectile function. Sildenafil appeared to control such increases after exercise, reigning in pulmonary blood pressure to markedly lower levels -- higher than at rest, but lower than non-medicated post-exercise readings. And, the non-PAH patients appeared to experience pulmonary blood pressure reductions after taking the drug, both while resting and exercising.

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