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Modern cancer therapies have greatly improved survival rates in men of reproductive age and younger; however, surgery, chemotherapy, and irradiation may lead to male infertility. Men with cancer should be counseled about fertility preservation before initiating therapy, when possible. Currently, options for male fertility preservation include cryopreservation of semen or testicular tissue. However, prepubertal boys pose a special problem in this area.

Animal studies have demonstrated the likely role of oxidative tissue damage in the pathophysiology of stone disease; however, the effect of antioxidants on stone formation in the human population is unknown. We evaluated the association between serum antioxidant levels and the self-reported prevalence of kidney stones in a large cross-sectional population in a retrospective cohort study.Serum levels of antioxidants among adult participants in the National Health and Nutrition Examination Survey (NHANES III) 1988-1994 were compared between those with and without a self-reported history of kidney stones, adjusting for covariates of age, sex, body mass index (BMI), race/ethnicity, diabetes, and hypertension.The prevalence of kidney stones was 5.25% (95% confidence interval: 4.60%, 5.90%). The prevalence of kidney stones was higher in males, white/non-Hispanics, diabetics, and those with hypertension. The prevalence of kidney stones increased with BMI. After adjusting for covariates, mean levels of alpha-carotene, beta-carotene, and beta-cryptoxanthin were significantly lower in those with kidney stones (-9.36%, -10.79%, and -8.48%, respectively). When analyzed by quartile, higher serum levels of beta-carotene and beta-cryptoxanthin,, trended toward a decreasing prevalence of stones (P=0.007 and P=0.03, respectively), indicating that the highest levels of these antioxidants may protect against the formation of kidney stones.Lower levels of alpha-carotene, beta-carotene, and beta-cryptoxanthin are associated with a history of kidney stones and may indicate a role for these antioxidants in preventing stone formation.

This study investigated the effect of sildenafil citrate on micro-recanalization and neovascularization, which were previously demonstrated in a rat model using biodegradable grafts (BGs) for vas deferens reconstruction. A total of 24 male rats underwent bilateral vasectomy with removal of a 0.5-cm vasal segment and were randomly assigned to four groups. Groups 1 and 2 underwent immediate vasovasostomy. Groups 3 and 4 underwent interposition of a 0.5-cm BG in the vasal gap. Groups 1 and 3 were given 5 mg kg(-1) day(-1) oral sildenafil. Other groups were given placebo. Rats were housed with females 12 weeks postoperatively. Reconstructed vasal segments were harvested 16 weeks postoperatively and analyzed histologically. Fluid from the distal vasal stump was analyzed for motile sperm. Urine samples obtained 16 weeks postoperatively were analyzed for cGMP levels. cGMP levels in rats treated with sildenafil were significantly higher than in control rats. No pregnancies were sired by grafted groups. In all, 5/6 rats in group 1 and 3/6 rats in group 2 sired litters. No motile sperm were noted in the vasal fluid of the grafted groups. Motile sperm were noted in all rats in group 1 and in 5/6 rats in group 2. In addition, 29 and 4 microcanals were detected in the sildenafil and placebo groups, respectively (P = 0.023). No microcanal exceeded 3 mm in length. An average of 12 and 28 blood vessels per graft were noted in the placebo and sildenafil groups, respectively (P0.0001). In conclusion, sildenafil enhances micro-recanalization and neovascularization in BG used for vas deferens reconstruction, but does not increase the microcanal length after 16 weeks.

Since its discovery in 1995, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a member of the tumor necrosis factor super family, has been under intense focus because of its remarkable ability to induce apoptosis in malignant human cells while leaving normal cells unscathed. Consequently, activation of the apoptotic signaling pathway from the death-inducing TRAIL receptors provides an attractive, biologically-targeted approach to cancer therapy. A great deal of research has focused on deciphering the TRAIL receptor signaling cascade and intracellular regulation of this pathway, as many human tumor cells possess mechanisms of resistance to TRAIL-induced apoptosis. This review focuses on the currently state of knowledge regarding TRAIL signaling and resistance, the preclinical development of therapies targeted at TRAIL receptors and modulators of the pathway, and the results of clinical trials for cancer treatment that have emerged from this base of knowledge. TRAIL-based approaches to cancer therapy vary from systemic administration of recombinant, soluble TRAIL protein with or without the combination of traditional chemotherapy, radiation or novel anticancer agents to agonistic monoclonal antibodies directed against functional TRAIL receptors to TRAIL gene transfer therapy. A better understanding of TRAIL resistance mechanisms may allow for the development of more effective therapies that exploit this cell-mediated pathway to apoptosis.