Hypertrichosis is defined as excessive hair growth anywhere on the body in either males or females. It is important to distinguish hypertrichosis from hirsutism, which is a term reserved for females who grow an excessive amount of terminal hairs in androgen-dependent sites.[1][2][3] There are several ways of classifying hypertrichosis. These are based on distribution (generalized vs. localized), the age of onset (congenital versus acquired), and the type of hair (vellus versus terminal). Forms of generalized hypertrichosis include, but are not limited to, congenital generalized hypertrichosis (which is further divided into congenital hypertrichosis lanuginosa, universal hypertrichosis, and hypertrichosis universalis congenita), prepubertal hypertrichosis, acquired generalized hypertrichosis, and acquired hypertrichosis lanuginosa. They each differ in their etiology and clinical findings.[4][5][6][7][8] Forms of localized hypertrichosis include, but are not limited to, congenital localized hypertrichosis (congenital nevi, plexiform neurofibromas, Becker melanosis/nevus, nevoid hypertrichosis, spinal dysraphism, and the hair collar sign), localized hypertrichosis in hereditary and acquired systemic disease, and acquired localized hypertrichosis.[9][10][11][12][13] An understanding of lanugo, vellus, and terminal hair is integral in evaluating a patient with presumed hypertrichosis. Lanugo hair is fine, non-pigmented hair that covers the normal fetus. It is often several centimeters long. By the first few weeks of life, lanugo hair should be replaced by vellus hair on the body and terminal hair on the scalp.  Vellus hair is lightly pigmented, fine, short hair, often referred to as “peach fuzz” that is found on the face, arms, stomach, and legs. Terminal hair is coarse, thick hair that is found on the scalp, underarms, and pubic area. In men, terminal hair is also found on the face. During puberty, vellus hair is replaced with terminal hair in androgen-dependent sites under the influence of testosterone.[1]

Hypogonadism is seen in 19% of men in their 60s, 28% of men in their 70s, and 49% of men in their 80s.[1] Testosterone is FDA-approved as replacement therapy in men who have low testosterone levels and those with symptoms of hypogonadism. It is important to distinguish between primary (testicular) and secondary (pituitary-hypothalamic) hypogonadism. Symptoms highly suggestive of hypogonadism include decreased spontaneous erections, decreased nocturnal penile tumescence, decreased libido, decreased beard growth, and shrinking testicles. The normal range for early morning testosterone in a male is between 300 ng/dL to 1000 ng/dL.[2]

Low circulating testosterone is associated with an increased risk of developing type 2 diabetes (T2DM) in overweight men with impaired glucose tolerance (IGT).

Polycystic ovary syndrome (PCOS), known as a common endocrine disorder among females, plagues many PCOS patients. The current study aimed to explore the correlations of sex hormone-binding globulin (SHBG) polymorphisms with the outcome of in vitro fertilization-embryo transfer (IVF-ET) in PCOS patients. PCOS patients who underwent IVF-ET and patients with non-PCOS-related infertility were selected in the study. Correlations of SHBG rs6259 and rs727428 with the risk factors in PCOS were analyzed, followed by the evaluation of the effect of SHBG polymorphisms on the outcome of IVF-ET in PCOS patients. At last, unconditional logistic regression analysis was performed to study the risk factors for IVF-ET treatment outcome. Compared with SHBG rs6259 GG carriers, the incidence of PCOS was found to be elevated in SHBG rs6259 GA+AA carriers which indicated that the A allele was a risk factor for PCOS. Compared with SHBG rs6259 TT carriers, the number of retrieved oocytes and embryo as well as the fertility rate in SHBG rs6259 GA+AA carriers was found to be decreased, while the abortion rate, incidence of ovarian hyperstimulation syndrome, transplant rejection rate, estradiol, and testosterone in serum, as well as testosterone in follicular fluid were elevated. The luteal hormone, serum testosterone, and progesterone and GA+AA genotype of rs6259 were the risk factors for IVF-ET treatment outcome. Taken together, the study showed that SHBG rs6259 polymorphisms might be correlated with the risk of PCOS and the outcome of IVF-ET treatment.

The endogenous opioid system has received attention and extensive research for its effects on reward, pleasure, and pain. However, relative to other neurochemicals, such as oxytocin, vasopressin and dopamine, the function of opioids in regulating human attachment, sociosexuality, and other aspects of human sociality has not received much consideration. For example, nonapeptides (oxytocin and vasopressin) have been extensively studied in animals and humans for their possible roles in mother-offspring attachment, romantic attachment, fatherhood, and social cognition. Likewise, others have proposed models wherein oxytocin and vasopressin are moderators of the relationship between steroid hormones and human social behaviors. Recently, opioids have generated renewed interest in relation to social pain, and importantly, the brain opioid hypothesis of social attachment (BOTSA), which suggests that endogenous opioids are a key implementer in primate and human bonding, has received some support. Here we focus on romantic bonds by proposing that endogenous opioids are an important mechanism mediating reproductive trade-offs through their inhibitory effects on testosterone production.

Background: Docetaxel (DOC), or Taxotere, is an anthracycline antibiotic used to treat multiple types of cancer. It is a first-line chemotherapy treatment for patients with metastasized, hormone-resistant prostate cancer (PCa) or for patients with high-risk, localized PCa that could benefit from early chemotherapy treatment. Previously, we showed that stearidonic acid (SDA), an omega-3 fatty acid, enhances the cytotoxicity of doxorubicin (DOX) in human PCa cells. This observation suggests that PCa therapies using SDA and chemotherapeutic drugs in combination offer attractive possibilities for developing treatments that ameliorate toxic side effects of some commonly used chemotherapy drugs. Objectives: We used androgen-resistant PC3 and DU 145 cells derived from human prostate cancer to quantify the effects of combined SDA and DOC on proliferation/viability and on the production of pro-apoptotic caspases 9 and 3. We also compared the effects of SDA with those of BAY, a pharmacological inhibitor of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-ĸB), in androgen-sensitive LNCaP cells. Finally, we qualitatively and quantitatively assessed the drug combination on androgen receptor (AR) and peroxisome proliferator-activated receptor gamma (PPARγ) expression in LNCaP and PC3 cells, respectively. Methods: The half maximal inhibitory concentration (IC50) and combination indices of SDA and DOC in PC3 and DU 145 cells were determined using the MTT cell viability assay. To quantify the effects of SDA and BAY on NF-ĸB activity, we used luciferase reporter assays in LNCaP cells that were stably transduced with lentiviral vectors carrying NF-ĸB response element sequence upstream of the luciferase gene sequence. AR and PPARγ expression were assessed by western blotting and immunocytochemistry. We considered caspase 9 and 3 cleavage to be apoptosis markers and determined the drug combination effect on the extent of that cleavage by western blot analysis. Results: The cytotoxic effects of DOC were synergistically enhanced by SDA when the two were added to DU145 and PC3 cell cultures. Combination index (CI) analyses based on the Chou-Talalay method and mass action law showed synergistic interaction with CI <1. SDA suppressed TNFα-induced NF-κB activity similarly to BAY. The SDA/DOC combination down regulated testosterone (T)-induced AR and troglitazone-induced PPARγ protein expression when compared to using the drugs singly. Similarly, the SDA/DOC combination induced caspase 9 and 3 production and cleavage suggesting apoptosis induction. Like our DOX studies, this work provides proof-of-concept for using SDA and DOC in combination to reduce the dose, and therefore the toxicity, of DOC and possibly increasing the survival benefit in DOC clinical translation studies.

Qianlie Tongqiao Capsule (QTC) is clinically confirmed to be efficacious and safe in treating lower urinary tract syndromes and bladder dysfunction that are induced by benign prostatic hyperplasia (BPH). However, the functional mechanisms of QTC remain unclear. We aim to investigate the effects of QTC on both bladder weight and several growth factors in the bladder tissue of rats with testosterone-induced BPH. BPH in the rats was established through bilateral orchiectomy and subcutaneous administration of testosterone propionate (5 mg/kg) dissolved in corn oil. At the end of the study, all bladder tissues were collected and weighed, and a histological examination was conducted using H&E staining. Immunohistochemistry and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) were applied to detect the expression of nerve growth factor (NGF), basic fibroblast growth factor (bFGF), and transformation growth factor-β1 (TGF-β1) in the bladder tissue. The expression of Bcl-2 and Bax in the bladder tissue was tested by Western Blot and qRT-PCR. We found that QTC, especially when administered in high-dosages, had a significant inhibitory effect on bladder weight gain and overexpression of NGF, bFGF, and TGF-β1 in rats with BPH. In addition, QTC downregulated and upregulated protein and mRNA expression of Bcl-2 and Bax in the bladder after prostatic obstruction, respectively. Furthermore, QTC balanced the Bcl-2/Bax ratio. Overall, these results reveal possible functional mechanisms of QTC in treating BPH-caused bladder dysfunction, and further studies are needed.