For many years, the role of testosterone has been perceived to play a role in the development of prostate cancer and certain cardiovascular diseases (Jones et al., 2013); with its general therapeutic roles being much overlooked. Much of this unprecedented assumption was based upon clinical observations showing the benefit of androgen deprivation in prostate cancer patients, and the perceived reports of higher cardiovascular death amongst people abusing steroid therapies (Jones et al., 2013; Basaria et al., 2010). However, there has been compelling evidence that suggests that testosterone administration within physiological ranges does not contribute to prostate cancer or the pathogenesis of cardiovascular disease (Morgentaler et al., 2009; Jones et al., 2013; Traish et al., 2009). Recent evidence actually suggests the protective role of androgens in the management of metabolic conditions, such as: obesity, metabolic syndrome, and type-2 diabetes mellitus, all of which are known to increase the risk of cardiovascular disease (Traish et al., 2009; Morgentaler et al., 2009; Wang et al., 2000). Erectile dysfunction, which is a type of endothelial dysfunction disorder, is defined as the persistent inability to achieve or maintain an erection for satisfactory sexual performance, and it affects an estimated 30 million American men between the ages of 40 to 70 years old, and this prevalence increases with age (Nehra A, 2007; Barkin J, 2011; Guay A, 2007). The male human erection involves a multifactorial interplay between various mechanisms within the body; encompassing psychological, vascular, neural and endocrine factors (Dean et al., 2005; Castela et al, 2011). The human erection involves the increased inflow of blood into the penile arteries, and the subsequent veno-occlusion, all of which occurs at a perfectly orchestrated hormonal environment (Bivalacqua et al, 1998; Castela et al., 2011). Nitric oxide is released from the endothelium, which dilates penile arteries and relaxes the penile smooth muscles, causing the corpora cavernosa of the penis to fill with blood; the ischiocavernosus and bulbospongiosus muscles then compress the veins, which restricts the egress of blood (Bivalacqua et al, 1998; Castela et al., 2011). Nitric oxide increases cGMP, which decreases intracellular calcium uptake, and increases K+ efflux; these all cause a smooth muscle cell relaxation. The decreased venous outflow from the penis helps maintain erection. In addition to nitric oxide, several other mechanisms are involved in the erectile response. The endothelium, which regulates vascular tone and blood flow, is responsible for the cholinergic smooth muscle relaxation observed by the addition of acetylcholine (Furchgott et al., 1983). Chamness et al. (1995) have shown that androgen differentially affects nitric oxide synthase activity in the male reproductive tract endothelium. Thus, the role of androgens, namely testosterone, is of importance in maintaining erectile function. In addition to affecting nitric oxide synthase activity, testosterone is also shown to affect erectile physiology in many more ways, including its role in activating K+ channels to increase the efflux or inhibit calcium channels via hyperpolarization (Yildiz et al., 2009), and even increasing arterial blood flow to the penis (Aversa et al., 2000). Interestingly, testosterone also modulates endothelial function. Endothelial progenitor cells are responsible for the regeneration of the endothelium. The area of study of these progenitor cells is relatively new, thus, it is important to evaluate how they affect endothelial function. Since erectile dysfunction is a form of endothelial dysfunction, it has been found that patients with erectile dysfunction had significantly lower levels of circulating progenitor cells than patients with a normal erectile function (Baumhäkel et al., 2006). Endothelial cells in the penile arteries play a critical role in regulating the physiological function of the erectile response in humans. Modulation of the endothelium in the penis by androgens, thus, is a critical area of research that must be further addressed.

The purpose of this study was to examine the perceived consequences of racism experiences on adult development and overall well-being of highly educated African American males. There were three objectives: to describe African American male responses to experienced racism in four social contexts: on the job, in academia, in the public realm, and statements in the media; to describe African American male social support networks for dealing with racism and to describe their level of satisfaction with those social support network; and to examine the relationship between racism experiences and other variables with two measures of psychological well-being, neuroticism and extraversion. The data used to address the study objectives were derived from a unique sample of responses to questionnaires submitted by 130 African American male college graduates. These men are very extraverted and score within average range on the neuroticism scales. The participants perceived frequent incidences of racism in all four social contexts: on the job, in academic settings, in the public realm, and racist statements in the media. At all developmental levels, the respondents' acknowledged that incidences of racism experiences had occurred in both the "previous year" and "throughout their lifetime. The African American men are acknowledging performing additional tasks during their development that was heretofore never mentioned in developmental theory. The African American male college graduates were very satisfied with the African American supporters European Americans who were a part of their social support network. Results of several regression analyses that entered all independent variables, found that only two variables showed a small but significant negative predictor value for neuroticism. Results of analyses that entered variables for predicting extraversion found that the total number of African American supporters was a small but positive predictor. These graduates provided evidence that they are constantly aware and vigilant about circumstances in American society. They experienced incidences of racism across social contexts and have devised ways to cope, yet they are always looking at themselves through the eyes of others and the negative influences of the ensuing feelings of isolation, hurt and frustration threaten to diminish their sense of well-being.

From the sexual preselection point of view, understanding sex determination/differentiation mechanisms in the bird is critical in both evolutionary and industrial applications. The chicken embryo provides an unique vertebrate model in the field of development biology. Morphological sex development in the chick gonad starts at 6.5 embryonic day (E6.5), however, genetic sex determination and development should occur earlier. In order to comprehend genes and their underlying mechanisms being involved in sex-determination/development during early embryogenesis, we not only made a male-subtract-female and a female-subtract-male cDNA library as early as embryonic day 3 (E3; Hamburger and Hamilton Stage 20), but also examined early transcripts related to male development in chicken embryo and their expression profiles in this study. A total of 89 and 127 candidates of male-development transcripts represented respectively for 83 known and 119 unknown non-redundant sequences, which were characterized in an E3 male- subtract-female complementary DNA library. In this study, thirty-five selected transcripts being validated by quantitative reverse transcription-polymerase chain reaction that the expression levels of 25 transcripts were higher in male E3 whole embryos than in females (P < 0.05). Notably, twelve of these transcripts mapped to the Z chromosome. At 72 weeks of age, twenty transcripts were expressed at higher levels in testes than in ovaries. Meanwhile, four transcripts were expressed at higher levels in brains of male than in brains of female chickens (P < 0.05). By using of methods of whole mount and frozen cross-section in situ hybridization, the expressions of riboflavin kinase (RFK), WD repeat domain 36 (WDR36) and EY505808 transcripts on E7 chicken male gonads were corroborated to be better than female gonads. This result was confirmed by using of western blotting analysis which also showed the expressions were specifically on gonads than other tissues. Treatment with an aromatase inhibitor formestane at E4 depicted the effect of the expression levels at E7 of the coatomer protein complex (subunit beta 1), solute carrier family 35 member F1, LOC427316 and EY505812 transcripts across both sexes (P < 0.05), which was similar to the observed gene expressions for both doublesex and mab-3 related transcription factor 1 gene. Additionally, the interaction effects of sex with formestane treatment were observed in 15 candidate male development transcripts (P < 0.05). This study demonstrated a panel of potentially candidate male development transcripts being identified during early chicken embryogenesis; some might be regulated by sex hormones.

No description available.