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Psychoneuroendocrinology. 2002 Aug;27(6):683-91.
Pubertal changes in gonadal hormones do not underlie adolescent dopamine receptor overproduction.

Andersen SL, Thompson AP, Krenzel E, Teicher MH.

Department of Psychiatry, Harvard Medical School, Laboratory of Developmental Psychopharmacology, Mailman Laboratories for Psychiatric Research, McLean Hospital, 115 Mill Street, Belmont, MA 02478, USA. anderseclean.org

Males, but not females, overproduce dopamine receptors in the striatum of rats across the periadolescent period followed by their elimination during young adulthood. In order to investigate the role that gonadal hormones play in this pubertal process, rats were castrated or ovariectomized at postnatal day (P) 28 when estrogen and testosterone levels are beginning to surge. Dopamine D1 and D2 striatal receptor density was then determined with autoradiography at P40 (adolescence) and P80 (young adulthood) to determine if either testosterone stimulates the overproduction of receptors in males or if estrogen inhibits this process in females. Neither castration nor ovariectomy altered dopamine receptor density, although enhanced testosterone levels increased D1 receptor binding 4.2% and 19.5% in males and females, respectively. The results of this study suggest that the endogenous rise in gonadal steroid hormones during puberty is not responsible for the overproduction of receptors in males or the lack of overproduction in females.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12084661&dopt=Abstract

J Biol Chem. 2002 Sep 20;277(38):35422-33. Epub 2002 Jun 25.
Identification of human male germ cell-associated kinase, a kinase transcriptionally activated by androgen in prostate cancer cells.

Xia L, Robinson D, Ma AH, Chen HC, Wu F, Qiu Y, Kung HJ.

Department of Biological Chemistry, School of Medicine, University of California, Davis, California 95616, USA.

Androgen is involved in both normal development and malignant transformation of prostate cells. The signal transduction pathways associated with these processes are not well understood. Using a novel kinase display approach, we have identified a protein kinase, human male germ cell-associated kinase (hMAK), which is transcriptionally induced by the androgenic hormone 5alpha-dihydrotestosterone (DHT). The kinetics of induction is rapid and dose-dependent, and the induction is not blocked by cycloheximide treatment. Real time reverse transcription-PCR studies demonstrated a 9-fold induction of hMAK by 10 nm DHT at 24 h post-stimulation. The expression levels of hMAK in prostate cancer cell lines are in general higher than those of normal prostate epithelial cells. A reverse transcription-PCR product encompassing the entire hMAK open reading frame was isolated. The results from sequencing analysis showed that the hMAK protein is 623 amino acids in length and contains a kinase catalytic domain at its N terminus, followed by a proline/glutamine-rich domain. The catalytic domain of this kinase contains sequence motifs related to both the cyclin-dependent kinase and the mitogen-activated protein kinase families. When expressed in COS1 cells, hMAK is kinase-active as demonstrated by autophosphorylation and phosphorylation of exogenous substrate and is localized in the nucleus. A 3.7-kilobase pair promoter of the hMAK locus was isolated from a human genomic DNA bacterial artificial chromosome clone and was shown to be activated by DHT. This activation can be blocked by an anti-androgen drug bicalutamide (Casodex), implicating the involvement of androgen receptor in this process. Taken together, these data suggest that hMAK is a protein kinase targeted by androgen that may participate in androgen-mediated signaling in prostate cancer cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12084720&dopt=Abstract

J Appl Genet. 2002;43(1):109-14.
Transition C2718T in the AR gene, resulting in generation of a termination codon and truncated form of the androgen receptor, causes complete androgen insensitivity syndrome.

Ignacak M, Niedziela M, Trzeciak WH.

Department of Biochemistry and Molecular Biology, Karol Marcinkowski University of Medical Sciences, Poznan, Poland.

The action of testosterone and 5 alpha-dihydrotestosterone are essential to the development of the male phenotype. Patients with karyotype 46,XY, resistant to these hormones, exhibit a wide spectrum of phenotypes: from phenotypic female, through a range of incomplete masculinization, to under-virilized, infertile man. These disturbances are caused by mutations in the androgen receptor gene (AR). We studied a 46,XY fenotypic female with typical symptoms of Complete Androgen Insensitivity Syndrome (CAIS). Multiple temperature single-stranded conformation polymorphism (MSSCP) and sequence analysis of exon 6 of the AR gene in a patient revealed a C2718T transition causing R786X mutation in the loop between helices VII and VIII of the LBD of the androgen receptor. The R786X mutation has been described in a patient with CAIS only once and no such mutations have been described in Eastern Europe.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12084976&dopt=Abstract

Asian J Androl. 2002 Jun;4(2):117-21.
Bone mineral density in hypogonadal men remains low after long-term testosterone replacement.

Ishizaka K, Suzuki M, Kageyama Y, Kihara K, Yoshida K.

Department of Urology, Kanto Central Hospital, Tokyo 158-8531, Japan. E-mail: kazziarkcity.ne.jp

AIM: In 11 congenital hypogonadal men, the bone mineral density (BMD) values were determined to assess the effect of long-term androgen replacement therapy (ART) on skeletal integrity. METHODS: Eleven congenital hypogonadal men, including 8 isolated gonadotropin deficiency patients, 2 Kallmann's syndrome and 1 vanishing testes syndrome were recruited and treated with 250 mg of testosterone enanthate intramuscularly every 4 weeks for 7-43 years (mean+/-SD: 21.5 +/-13 years). In these patients and a group of 10 healthy young men (controls), the whole and trabecular BMDs were examined at the distal end of radius by means of a peripheral quantitative computerized tomography device. RESULTS: The whole radial BMD in hypogonadal men was significantly less in the patients than in the healthy men (498+/-115 and 725+/-134 mg/cm(3), respectively; P<0.01); the trabecular BMD was also lower in the hypogonadal men (199+/-80 and 375+/-89 mg/cm(3); P< 0.01). The whole radial BMD values in 10 of 11 hypogonadal men were at least 1 SD below the mean value for healthy young men; 2 hypogonadal men had BMD values more than 2.5 SD lower than the healthy mean. Additionally, the whole radial BMD showed a significant negative correlation with the patient's age at the initiation of ART (r = 0.748, P<0.01). The serum level of bone-specific alkaline phosphatase and the urinary level of deoxypyridinoline were not significantly different between the two groups. CONCLUSION: Osteopenia persists in the hypogonadal men after long-term ART, suggesting that such patients have a persistent defect in bone development not alleviated by androgen replacement.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12085102&dopt=Abstract

The average human scalp is covered by approximatey 100,000 hair follicles. Each hair undergoes hair cycle and normally 50-100 hairs randomly fall out a day, which is unnoticeable because lost hair is replaced by as many new hairs springing up daily. Hair loss results from the fall out of hair from the hair follicle. Alopecia or excessive, premature hair loss is the condition caused by many factors. Loss of hair itself does not pose critical health problems because biological role of human hair is relatively marginal. Hair on our scalp protects the head from mechanical shock, heat loss, and exposure to UV-light. The eyelashes and eyebrowes protect the eyes, and hair in the ear canal or the nasal passages help filter out particles and pathogens, thus protecting our internal organs. However, hair does play important social role: it is one of the major determinants of our appearance and identity in daily life. Fullness of hair also implicates or manifests physical integrity and youthfulness of the person. Losing hair could have more than just emotional impacts on individuals. The hair is a unique organ that goes through a characteristic cycle consisting of an immature phase, a growing phase called anagen, a transitional phase between the growing phase and the resting phase called catagen, and finally a resting phase called telogen in which the hair stops growing, waiting to fall out. 85-90% of hairs on our body are in anagen phase or growing phase, which lasts anywhere from two to five years. This phase is followed by a short regression phase, or catagen, which lasts 2-3 weeks. Approximately 1% of hair follicles are in catagen. Approximately 10-15% of hair follicles are in the resting phase, the telogen, which lasts about 3-5 months. Hair follicles typically goes through 10-20 asynchronous cycles during the lifetime. Persistent loss of more than 150 hairs would consist a state of hair loss, or alopecia, albeit it could be temporary.

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