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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5





J Neurosci. 2003 Jun 1;23(11):4785-90.
The glucocorticoid receptor as a potential target to reduce cocaine abuse.

Deroche-Gamonet V, Sillaber I, Aouizerate B, Izawa R, Jaber M, Ghozland S, Kellendonk C, Le Moal M, Spanagel R, Schutz G, Tronche F, Piazza PV.

Institut National de la Sante et de la Recherche Medicale, Unite 588, Bordeaux 33077, France.

Several findings suggest that glucocorticoid hormones are involved in determining the propensity of an individual to develop cocaine abuse. These hormones activate two related transcription factors, the glucocorticoid receptor (GR) and the mineralocorticoid receptor. In this study, we show that the selective inactivation of the GR gene in the brains of mice profoundly flattened the dose-response function for cocaine intravenous self-administration and suppressed sensitization, two experimental procedures considered relevant models of addiction. Furthermore, administration of a GR antagonist dose-dependently reduced the motivation to self-administer cocaine. Importantly, the absence of GR did not modify the basal behavioral and molecular effects of cocaine but selectively modified the excessive response to the drug spontaneously present in certain vulnerable individuals or induced by repeated drug exposure in others. In conclusion, we provide the first genetic evidence that the GR gene can modulate cocaine abuse. This suggests that targeting GR function in the brain could provide new therapeutic strategies to treat cocaine addiction for which there is no available treatment.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12805318&dopt=Abstract



Obes Res. 2003 Jun;11(6):689-94.
Sex hormones and sexual function in obese men losing weight.

Kaukua J, Pekkarinen T, Sane T, Mustajoki P.

Department of Internal Medicine, Helsinki University Central Hospital, Peijas Hospital, Vantaa, Finland and. Department of Endocrinology, Helsinki University Central Hospital, Helsinki, Finland.

OBJECTIVE: To study the impact of a weight-loss program on sex hormones and sexual function among 38 middle-aged obese men (BMI >/=35 kg/m(2)). RESEARCH METHODS AND PROCEDURES: A randomized controlled clinical trial was conducted. The treatment group (n = 19) participated in a 4-month weight-loss program including 10 weeks on a very-low-energy diet (VLED) and 17 behavior modification visits. There was no intervention in the control group (n = 19). Both groups were followed for 8 months, i.e., 22 weeks after the active weight loss in the treatment group. The outcome measures (weight, sex hormones, sexual function, leptin, and metabolic variables) were obtained at baseline and at three time-points during follow-up. RESULTS: The mean weight loss in the treatment group was 21 kg at the end of the 10-week VLED. At the end of follow-up, the maintained weight loss was 17 kg of baseline weight. The control group was weight stable throughout the study. In the treatment group, increases in sex hormone-binding globulin, testosterone, and high-density lipoprotein-cholesterol, as well as decreases in insulin and leptin, were maintained until the end of follow-up, although with VLED, the level of several hormones and metabolic variables improved transiently during the rapid weight loss. There were no significant changes in the questionnaire scores on sexual function in either group. DISCUSSION: We conclude that obese men lose weight and increase their serum testosterone level on a weight-loss program with VLED and behavior modification. However, they do not change their sexual function scores.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12805389&dopt=Abstract [PubMed - in process]



Obes Res. 2003 Jun;11(6):776-82.
High serum leptin is associated with attenuated coronary vasoreactivity.

Sundell J, Huupponen R, Raitakari OT, Nuutila P, Knuuti J.

Turku PET Centre and Departments of. Medicine, Clinical Pharmacology, and. Clinical Physiology, Turku University, Turku, Finland.

OBJECTIVE: Hyperleptinemia, a hallmark of obesity, appears to be a risk factor for coronary artery disease. However, although leptin is a vasoactive hormone, no studies addressing leptin's effect on coronary perfusion have been performed. We examined the association between circulating leptin concentration and coronary vasoreactivity in young obese and nonobese males. RESEARCH METHODS AND PROCEDURES: Myocardial blood flow was quantitated in 10 obese men (age 31 +/- 7 years, BMI 34 +/- 2 kg/m(2)) and 10 healthy matched nonobese men (age 33 +/- 8 years, BMI 24 +/- 2 kg/m(2)) using positron emission tomography and O-15-water. The measurements were performed basally and during adenosine infusion (140 micro g/kg per minute). RESULTS: Serum leptin was significantly higher in obese than nonobese subjects (10.3 +/- 5.6 vs. 4.3 +/- 2.5 ng/mL, p < 0.01). Basal myocardial blood flow was not significantly different between obese and nonobese subjects. Adenosine-stimulated flow was blunted in obese (3.2 +/- 0.6 mL/g per minute) when compared with nonobese subjects (4.0 +/- 1.1 mL/g per minute, p < 0.05). Serum leptin concentration was inversely associated with adenosine-stimulated flow in study subjects (r = -0.50, p < 0.05). This association was no longer observed after adjustment for obesity and/or hyperinsulinemia. DISCUSSION: Hyperleptinemia and reduced coronary vasoreactivity occur concomitantly in young obese but otherwise healthy men. Moreover, the adenosine-stimulated myocardial flow is inversely related to prevailing concentration of serum leptin. Although this relationship appears to be explained by obesity and/or hyperinsulinemia, leptin might have a role in regulation of myocardial blood supply.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12805399&dopt=Abstract [PubMed - in process]



Mol Endocrinol. 2003 Sep;17(9):1777-91. Epub 2003 Jun 12.
Thyrotropin-releasing hormone receptor processing: role of ubiquitination and proteasomal degradation.

Cook LB, Zhu CC, Hinkle PM.

Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York 14642, USA.

These studies were designed to characterize ubiquitination of the G protein-coupled TRH receptor (TRHR). TRHRs and ubiquitin coprecipitated with antibodies to either receptor or ubiquitin in Chinese hamster ovary or pituitary GHFT cells. Inhibition of the proteasome with MG-132 resulted in an accumulation of total TRHRs and the appearance of a small amount of cytosolic receptor. MG-132 caused an increase in newly synthesized receptors, detected by microscopy using a TRHR coupled to Timer, a DsRed that undergoes a spontaneous time-dependent color change. Misfolded TRHRs were particularly heavily ubiquitinated. These results show that the proteasome participates in TRHR quality control early after receptor synthesis. Under normal circumstances, most ubiquitinated TRHRs were absorbed to wheat germ agglutinin, indicating that they had undergone complex glycosylation in the Golgi apparatus. When cells were treated with tunicamycin to block glycosylation, a ladder of ubiquitinated species was detectable. Cell surface receptors, which were labeled selectively with either radioligand or antibody, showed no detectable ubiquitin modification. To determine if ubiqutination plays a role in TRH-induced receptor endocytosis, the receptor was expressed in Ts20 cells, which have a temperature-sensitive ubiquitin pathway. TRH induced a significant calcium response and rapid and extensive receptor internalization at both the permissive and nonpermissive temperatures, indicating that ligand-dependent ubiquitination of the receptor, or any other protein, is not necessary for TRHR signaling or internalization. These results show that ubiquitin modification targets misfolded receptors for degradation and suggest a possible role for ubiquitination in receptor trafficking.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12805411&dopt=Abstract [PubMed - in process]



Mol Endocrinol. 2003 Sep;17(9):1751-66. Epub 2003 Jun 12.
Thyroid hormone activates fibroblast growth factor receptor-1 in bone.

Stevens DA, Harvey CB, Scott AJ, O'Shea PJ, Barnard JC, Williams AJ, Brady G, Samarut J, Chassande O, Williams GR.

Molecular Endocrinology Group, Medical Research Council Clinical Sciences Centre, Clinical Research Building, 5th Floor, Hammersmith Hospital, Du Cane Road, London W12 0NN, United Kingdom.

Thyroid hormone (T3) and the T3 receptor (TR) alpha gene are essential for bone development whereas adult hyperthyroidism increases the risk of osteoporotic fracture. We isolated fibroblast growth factor receptor-1 (FGFR1) as a T3-target gene in osteoblasts by subtraction hybridization. FGFR1 mRNA was induced 2- to 3-fold in osteoblasts treated with T3 for 6-48 h, and FGFR1 protein was stimulated 2- to 4-fold. Induction of FGFR1 was independent of mRNA half-life and abolished by actinomycin D and cycloheximide, indicating the involvement of an intermediary protein. Fibroblast growth factor 2 (FGF2) stimulated MAPK in osteoblasts, and pretreatment with T3 for 6 h induced a more rapid response to FGF that was increased in magnitude by 2- to 3-fold. Similarly, T3 enhanced FGF2-activated autophosphorylation of FGFR1, but did not modify FGF2-induced phosphorylation of the docking protein FRS2. These effects were abolished by the FGFR-selective inhibitors PD166866 and PD161570. In situ hybridization analyses of TRalpha-knockout mice, which have impaired ossification and skeletal mineralization, revealed reduced FGFR1 mRNA expression in osteoblasts and osteocytes, whereas T3 failed to stimulate FGFR1 mRNA or enhance FGF2-activated MAPK signaling in TRalpha-null osteoblasts. These findings implicate FGFR1 signaling in T3-dependent bone development and the pathogenesis of skeletal disorders resulting from thyroid disease.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12805413&dopt=Abstract [PubMed - in process]







Concerned about losing hair? Hair loss and baldness is indeed a visible problem, and could be more than just the matter of change in appearance.
Saw palmetto berry is a widely known herbal supplement for hair loss problems. However, there are a number of great anecdotal herbs that people used for thousands of years stop hair loss and start hair growth. Numerous anecdotal cases have demonstrated that this herbal formula based on Chinese herbs actually improves the age-related hair thinning and hair loss for a significant fraction of people who take it diligently. It is unknown how Hair Million herbs actually stop hair loss, and promote hair growth, No scientific research or placebo controlled clinical trials have been conducted. Nonetheless, a number of people agree that it works.












DHEA is a natural hormone, and it is produced in our body by the adrenal glands. DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells. Our bodies produce decreasing amount of DHEA as we get older. various health benefits: To deter aging, improve sexual function/erectile dysfunction, treat cognitive decline, enhance athletic performance, facilitate weight loss, improve strength, prevent osteoporosis, enhance immunomodulation for rheumatic conditions, and treat depression.





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