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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 Reprod Immunol. 2002 May-Jun;55(1-2):131-9.
Human endometrial receptivity: gene regulation.

Martin J, Dominguez F, Avila S, Castrillo JL, Remohi J, Pellicer A, Simon C.

Instituto Valenciano de Infertilidad (IVI), Valencia University, C/ Guardia Civil 23, 46020 Valencia, Spain.

Endometrial receptivity is a self-limited period in which the endometrial epithelium (EE) acquires a functional and transient ovarian steroid-dependent status that allows blastocyst adhesion. Termed as "the window of implantation", this specific period opens 4-5 days after progesterone production or administration and closes after 9-10 days. Scientific knowledge on the endometrial receptivity process is fundamental for the understanding of human reproduction, but so far none of the proposed biochemical markers for endometrial receptivity has been proven to be clinically useful. In this work, we present strategies of cDNA analysis technologies that aim to clarify the fragmented information in this field. Specifically, the objective is the differential identification, cloning and sequencing of genes linked to endometrial receptivity in humans, combining differential display PCR and cDNA microarray analysis of endometrial epithelial-derived cell lines and endometrial samples obtained in the same patient 2 and 7 days after the luteinizing hormone (LH) surge (day LH+2) and (day LH+7), respectively.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12062828&dopt=Abstract



Mol Cell Endocrinol. 2002 Jun 14;191(2):149-56.
Regulation of the gonadotropin-releasing hormone receptor (GnRHR) by RGS proteins: role of the GnRHR carboxyl-terminus.

Castro-Fernandez C, Conn PM.

Oregon National Primate Research Center and Department of Physiology and Pharmacology, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA.

The cytoplasmic carboxyl-terminus of G-protein coupled receptors (GPCRs), absent in the mammalian gonadotropin-releasing hormone receptor (GnRHR), plays an important role in receptor expression, desensitization, internalization and efficiency of coupling to G proteins. Regulators of G protein signaling (RGS) likewise are involved in regulating GPCR-G protein mediated responses and can regulate transcription of other genes. In this study, we evaluate differential expression, ligand binding and effector coupling of the rat GnRHR (rGnRHR) and a chimera of rGnRHR with the pre-mammalian carboxyl domain (rGnRHR-C-tail). Membrane expression of the chimeric receptor and G(q)alpha and G(s)alpha-mediated signaling was increased 2- and 1.5-fold, respectively by RGS10, while RGS3 did not interfere with rGnRHR and rGnRHR-C-tail cell surface expression in spite of negatively regulating GnRH-stimulated G(q)alpha-mediated signaling by both receptors. The rGnRHR and rGnRHR-C-tail showed similar internalization rates in the presence of either RGS protein, indicating that the modification of rGnRHR expression and regulation in the presence of a carboxyl-terminus by RGS10 was not caused by alteration of the internalization rate. The observations in this study implicate the carboxyl domain of the receptor as a site of interaction for RGS10, but not RGS3. This is the first evidence of an altered cell surface expression and regulation of the GnRHR bearing a carboxyl-terminus by RGS proteins.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12062898&dopt=Abstract



Mol Cell Endocrinol. 2002 Jun 14;191(2):157-66.
Identification and functional characterization of melatonin Mel 1a receptors in pancreatic beta cells: potential role in incretin-mediated cell function by sensitization of cAMP signaling.

Kemp DM, Ubeda M, Habener JF.

Laboratory of Molecular Endocrinology, Massachusetts General Hospital, Howard Hughes Medical Institute, Harvard Medical School, 55 Fruit Street WEL320, Boston, MA 02114, USA.

Melatonin receptors are expressed within the pancreatic islets of Langerhans, and melatonin induces a direct effect on insulin secretion ex-vivo. Here, we report the endogenous expression of the melatonin Mel 1a receptor in the INS-1 pancreatic beta cell line. Pharmacological characterization of the receptor using a CRE-luciferase reporter gene demonstrated its functional activity in INS-1 cells, displaying the characteristic signaling properties of the G(i/o) coupled receptor. Acute melatonin treatment of INS-1 cells in the presence of either forskolin or the incretin hormone glucagon-like peptide 1 (GLP-1) caused an attenuation of the responses in insulin secretion, insulin promoter activity, and CRE mediated gene expression, consistent with its effects in inhibiting cAMP mediated signal transduction. However, prolonged exposure (12 h) of INS-1 cells to melatonin treatment resulted in a sensitization of cAMP mediated responses to forskolin and GLP-1. Insulin secretion, insulin promoter activity and CRE mediated gene expression levels were augmented compared with responses without melatonin pre-treatment in INS-1 cells. In isolated rat islets, insulin secretion was enhanced following melatonin pre-treatment both in the absence and presence of GLP-1 or forskolin. This phenomenon reflects observations reported in other cell types expressing the melatonin Mel 1a receptor, and may represent the first evidence of a specific physiological role for melatonin-induced sensitization.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12062899&dopt=Abstract



Neuropsychopharmacology. 2002 Jul;27(1):12-24.
Ovarian steroid regulation of 5-HT1A receptor binding and G protein activation in female monkeys.

Lu NZ, Bethea CL.

Division of Reproductive Sciences, Oregon Regional Primate Research Center, 505 NW 185th Avenue, Beaverton, OR 97006, USA.

Serotonin 5-HT(1A) receptors play an important role in serotonin neurotransmission and mental health. We previously demonstrated that estradiol (E) and progesterone (P) decrease 5-HT(1A) autoreceptor mRNA levels in macaques. In this study, we questioned whether E and P regulate 5-HT(1A) binding and function and G(alpha) subunit protein expression. Quantitative autoradiography for 5-HT(1A) receptors and G proteins using [3H]8-OH-DPAT and [35S]GTP-gamma-S, respectively, was performed on brain sections of rhesus macaques from four treatment groups: ovariectomized controls (OVX), E (28 d), P (28 d), and E (28 d) plus P (the last 14 d) treated. Western blot analysis for G(alpha) subunits was performed on raphe extracts from cynomolgus macaques that were OVX or OVX treated with equine estrogens (EE, 30 months). In the hypothalamus, E or E + P but not P alone decreased postsynaptic 5-HT(1A) binding sites. In the dorsal raphe nucleus (DRN), E, P, and E + P treatments decreased 5-HT(1A) autoreceptor binding. The Kd values for 8-OH-DPAT were the same for each treatment group. Both the basal and the R-(+)-8-OH-DPAT stimulated [35S]GTP-gamma-S binding were decreased during hormone replacement whereas the coupling efficiency between the receptor and G proteins was maintained. Finally, EE treatment reduced the level of G(alphai3), but not G(alphai1), G(alphao), and G(alphaz) in the DRN. In conclusion, these observations suggest that ovarian hormones may increase serotonin neurotransmission, in part, by decreasing 5-HT(1A) autoreceptors, 5-HT(1A) postsynaptic receptors, and the inhibitory G proteins for intracellular signal transduction.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12062903&dopt=Abstract



Thyroid. 2002 Oct;12(10):861-5.
Epidemiology and prevention of thyroid disease in pregnancy.

Lazarus JH.

University of Wales College of Medicine, Cardiff, Wales, United Kingdom. Lazaruf.ac.uk

Pregnancy has variable effects on thyroid hormone concentrations throughout pregnancy as well as being associated with goiter. The latter is largely preventable by ensuring optimal iodine intake of at least 200 microg/d. Immunologic changes in pregnancy include a so-called T(H)2 shift that reverts to T(H)1 status around birth or early in the postpartum period. Hyperthyroidism during gestation, usually caused by Graves' disease, is rare (0.2%) and is best managed medically with propylthiouracil; thyroid-stimulating antibodies should be measured. Prevention of the deleterious effects of Graves' disease includes adequate preconception advice, adequate monitoring during pregnancy, and total avoidance of (131)I therapy during pregnancy. Hypothyroidism during pregnancy has an incidence of 2.5% although there is a 10% incidence of thyroid peroxidase (TPO)-antibody positivity in early gestation. There are convincing epidemiologic data to show that suboptimal thyroid function in pregnancy is associated with impaired neurointellectual development (e.g., 19% with IQ < 85 compared to 5% in one study). Therefore, there is a case for screening for thyroid function in early pregnancy with thyroxine (T(4)) intervention therapy. Maintenance of optimal iodine intake is critical to prevent nonautoimmune gestational maternal hypothyroxinaemia. Postpartum thyroid dysfunction (PPTD) occurs in 5%-9% of women and in up to 50% of TPO-antibody positive women (as ascertained in early pregnancy). Prevention of PPTD at this time could only be achieved by pregestational ablation of the thyroid. Another approach is to at least improve the prediction of postpartum thyroid disease (PPT) because the TPO antibody has a sensitivity of only 50%.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12487768&dopt=Abstract







Natural Herbal Supplement: Hair Million


Hair loss alone does not pose significant health problems. In fact, there are people who opt for baldness as an alternative hair style. However, in general, however, hair loss is not considered desirable.

The most ostensive feature that distinguishes us human from chimps and other primates is the lack of bodily hair. During evolutionary process, we have lost the majority of hair. Hair is no longer a biologically essential part of our body, just like appendix. The hair we still have on our scalp and a few other bodily parts is still regarded as significant for reasons other than biological necessity. Hair loss is naturally accompanied by aging process, although the extent of hair loss and the timing of onset vary widely among individuals. Thus, loss of hair and baldness is considered as a symbol of maturity or old age. Like winkles and other signs of aging, hair loss is not welcome by most people, because we don't welcome aging, and being perceived as an aging person. However, it is alopecia, or premature hair loss that especially concerns certain people.

While the hair loss and resulting baldness in general have not been proven to be related to underlying health problems, there are certain correlations between hair loss and health problems. For instance, premature hair loss could suggest premature aging or nutritional and hormonal imbalance, stressful life, use of drugs that cause hair loss as a side effect, skin disease, or heart disease. The balding appearance could also impart a subdued impression of integrity in bodily health and youthfulness.












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