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Remember that fees for the first color figure will be waived when both the first and last authors are members in good standing in the Society for the Study of Reproduction at the time of initial submission of a manuscript! At least one must be a Regular member; the other may be a Trainee member. Contact the SSR Business office at http://www.ssr.org if you have any questions.
Toll-Like Receptor 4 in Rat Prostate: Modulation by Testosterone and Acute Bacterial Infection in Epithelial and Stromal Cells
Amado Alfredo Quintar, Felix Daniel Roth, Ana Lucía De Paul, Agustin Aoki, and Cristina Alicia Maldonado. Biol Reprod 2006; 75:664–672. Published online ahead of print 26 July 2006; DOI 10.1095/biolreprod.106.053967
The prostate tolls for infection
The prostate gland is the most inflammation prone organ in the male reproductive tract. Prostatitis is a common clinical condition in men and chronic prostatic inflammation may lead to prostate cancer. The first line of defense against microbial infection is the rapidly responsive and evolutionarily conserved system of innate immunity. Host defense proteins acting in the male reproductive tract are receiving considerable attention, due to their role in protecting against sexually transmitted diseases and possible function in cellular recognition during fertilization (for review, see Hall et al., 2002, J Androl 23:585). Now, in a paper on p. 664, Quintar and colleagues show that Toll-like receptor 4 (TLR4), an important mediator of the innate immune response, is present in the rat prostate. They used an experimental model for bacterial prostatitis to show increase in TLR4 expression and polarization of localization to the apical cytoplasm of epithelial cells, as expected for a mediator of host defense. But, TLR4 is also regulated by androgen: castrated rats exhibited increased levels of TLR4. These interesting results suggest a role for prostatic TLR4 in defense against microbial infection and also that testosterone has suppressive effects on the immune response.
Barusiban, an Effective Long-term Treatment of Oxytocin-induced Preterm Labor in Nonhuman Primates
Torsten M Reinheimer, Gary J. Chellman, John C. Resendez, Julie K. Meyer, and Walter H. Bee. Biol Reprod 2006; 75:809–814. Published online ahead of print 16 August 2006; DOI 10.1095/biolreprod.106.053637
Preventing early labor
Preterm labor is considered a leading cause of premature delivery, which results in increased morbidity and mortality of neonates, and is the outcome of up to 5 to 12 percent of pregnancies in developed countries, including the U.S., and up to 25 percent of pregnancies in developing countries. Preterm labor is associated with release of endogenous oxytocin from the posterior pituitary and pregnant uterus acting via oxytocin receptors expressed by the myometrium. In a paper on p. 809, Reinheimer et al. report that an oxytocin receptor antagonist, barusiban, effectively suppresses oxytocin-induced, preterm-like myometrial contractions and early delivery of babies to cynomologus monkeys. These results suggest that barusiban may be an effective treatment for preventing preterm labor and associated morbidity and mortality of newborn humans. In addition, barusiban may prove to be an effective oxytocin receptor antagonist for experimentation to understand the role of oxytocin in a variety of reproductive paradigms, including the pulsatile release of prostaglandins required for luteolysis and other physiological events.
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