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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

Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):15154-8. Epub 2002 Oct 24.
Neuroendocrine control of a sexually dimorphic behavior by a few neurons of the pars intercerebralis in Drosophila.

Belgacem YH, Martin JR.

Bases Neurales du Mouvement Chez la Drosophile, Laboratoire de Neurobiologie de l'Apprentissage, de la Memoire et de la Communication, Centre National de la Recherche Scientifique, Unite Mixte de Recherche-8620, Universite Paris-Sud, F-91405 Orsay, France.

In Drosophila, locomotor activity is sexually dimorphic and the brain area controlling this dimorphism has been mapped. The neurons of the pars intercerebralis (PI) have been suggested to participate in such differences between males and females. However, the precise physical nature of the dimorphism, the identity of the PI neurons involved, and the nature of the neuronal signal coding the dimorphism remain unknown. In this study, we used a video-tracking paradigm to characterize further the pattern of locomotor activity in Drosophila. We show that the number of activity/inactivity periods (start/stop bouts) is also sexually dimorphic, and that it can be genetically feminized in males. Moreover, the transplantation of PI neurons from a female, or of feminized PI neurons from a donor male into a receiver wild-type male is sufficient to induce the feminization of locomotor behavior, confirming that this tiny cluster of approximately 10 neurons is directly responsible for the sexual dimorphism in locomotor activity. Finally, feeding males with fluvastatin, a juvenile hormone (JH) inhibitor, also led to start/stop feminization, and this effect is reversible by the simultaneous application of methoprene, a JH analog, suggesting the existence of a neuroendocrine control, by JH, of such behavioral dimorphism.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12399547&dopt=Abstract

Science. 2002 Oct 25;298(5594):843-6.
Reversal of bone loss in mice by nongenotropic signaling of sex steroids.

Kousteni S, Chen JR, Bellido T, Han L, Ali AA, O'Brien CA, Plotkin L, Fu Q, Mancino AT, Wen Y, Vertino AM, Powers CC, Stewart SA, Ebert R, Parfitt AM, Weinstein RS, Jilka RL, Manolagas SC.

Division of Endocrinology and Metabolism, Department of Internal Medicine, and Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

We show that sex steroids protect the adult murine skeleton through a mechanism that is distinct from that used to preserve the mass and function of reproductive organs. The classical genotropic actions of sex steroid receptors are dispensable for their bone protective effects, but essential for their effects on reproductive tissues. A synthetic ligand (4-estren-3alpha,17beta-diol) that reproduces the nongenotropic effects of sex steroids, without affecting classical transcription, increases bone mass and strength in ovariectomized females above the level of the estrogen-replete state and is at least as effective as dihydrotestosterone in orchidectomized males, without affecting reproductive organs. Such ligands merit investigation as potential therapeutic alternatives to hormone replacement for osteoporosis in both women and men [corrected].

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12399595&dopt=Abstract

J Vet Med Sci. 2002 Sep;64(9):773-7.
Steroid hormones do not reactivate Neospora caninum in ovariectomized mice.

Kobayashi A, Katagiri S, Kimura T, Ochiai K, Umemura T.

Laboratory of Comparative Pathology, Department of Veterinary Clinical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapparo, Japan.

The direct effects of three steroid hormones (progesterone, estradiol-17beta and corticosterone) on the growth of Neospora caninum (N. caninum) tachyzoite were examined in Vero cells. Subsequently, ovariectomized BALB/c mice infected with N. caninum were treated with physiological concentrations of the steroid hormones for 1 or 2 weeks. These hormones had no direct effect on the parasite growth in vitro. In the infected mice, there was no significant difference in the parasite distribution and histopathological changes between the hormone-injected and control groups. No mice showed parasitemia at the time of autopsy. These results suggest that physiological levels of steroid hormones (progesterone, estradiol-17beta and corticosterone) do not reactivate N. caninum in mice.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12399600&dopt=Abstract

J Vet Med Sci. 2002 Sep;64(9):835-7.
Parathyroid hormone-related protein (PTHrP) produced by dog lymphoma cells.

Kubota A, Kano R, Mizuno T, Hisasue M, Moore PF, Watari T, Tsujimoto H, Hasegawa A.

Department of Pathobiology, Nihon University School of Veterinary Medicine, Fujisawa, Kanagawa, Japan.

Parathyroid hormone-related protein (PTHrP) was investigated in a canine lymphoma case with hypercalcemia by means of immunoradiomentric assay (IRMA) and molecular analysis. The plasma calcium level of the patient dog was 13.7 mg/dl. The PTHrP concentration examined by IRMA was 6.1 pmol/L in the plasma sample from the dog, but it was undetectable (< 1.1 pmol/L) in plasma samples from 4 lymphoma cases without hypercalcemia or 5 normal dogs. The PTHrP concentration examined in the culture supernatant of the lymphoma cells from this case was 1.3 pmol/L, whereas those of the lymphoma cells from a lymphoma case without hypercalcemia was undetectable. PTHrP mRNA was clearly detected not only in the lymphoma cells from this dog with hypercalcemia but also in lymphoma cells from 4 lymphoma cases without hypercalcemia and 2 canine lymphoma cell lines.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12399610&dopt=Abstract

Nephron. 2002 Dec;92(4):860-7.
Different effects of castration and estrogen administration on glomerular injury in spontaneously hyperglycemic Otsuka Long-Evans Tokushima Fatty (OLETF) rats.

Tomiyoshi Y, Sakemi T, Aoki S, Miyazono M.

Department of Internal Medicine, Saga Medical School, Nabeshima, Saga, Japan. tomiyoshi-yoshiyukouseikan.saga.saga.jp

AIM: Non-insulin-dependent diabetic mellitus model rats, Otsuka-Long-Evans-Tokushima-Fatty (OLETF), develop diabetic nephropathy presenting with mesangial expansion leading to glomerular sclerosis and thickening of the glomerular basement membrane (GBM), especially in elderly males. The effects of sex hormones and castration on the incidence of diabetes mellitus (DM) have been studied in this strain rat. However, there have been no detailed studies on the effects of castration and sex hormone in the development of diabetic nephropathy. METHODS: In this study we examine the effect of castration or estrogen on the development of glomerular injury in OLETF rats. Thirty male OLETF rats and 10 male long-Evans Tokushima Otsuka (LETO) rats as a normal control were used. OLETF rats were divided into three groups: group 1 received sham-operation, group 2 was castrated at 6 weeks, and group 3 was administered 0.1 mg estrogen subcutaneously once a month from 6 weeks to 58 weeks of age and LETO rats were assigned to group 4. Body weight, urinary protein and fasting blood glucose, serum albumin and other serum constituents were investigated every 12 weeks from 12 weeks to 60 weeks of age. In groups 1-3, glucose tolerance test was performed at 38 weeks. Each group was studied morphologically at the end of the experiment (60 weeks of age). RESULTS: Castration attenuated proteinuria and glomerular sclerosis accompanied by an amelioration of glucose tolerance, a decrease in mesangial expansion and an attenuation of the GBM thickening. In contrast, although estrogen equally ameliorated glucose tolerance and attenuated the mesangial expansion and the GBM thickening, estrogen failed to attenuate proteinuria and glomerulosclerosis. A significant increase in glomerular tuft volume, and serum levels of growth hormone, total cholesterol and triglycerides was observed in the estrogen-treated rats as compared with the castrated rats. CONCLUSION: Besides the mechanisms involved in the development of diabetic nephropathy, other mechanisms may be involved and contribute to the development of glomerulosclerosis in the estrogen-treated rats, leading to a difference in glomerular injury between the castrated and estrogen-treated OLETF rats. 2002 S. Karger AG, Basel

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12399633&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.

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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