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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

Fertil Steril. 1999 Mar;71(3):457-61.
Obesity regulates bioavailable testosterone levels in women with or without polycystic ovary syndrome.

Penttila TL, Koskinen P, Penttila TA, Anttila L, Irjala K.

Department of Clinical Chemistry, Turku University Central Hospital, Finland.

OBJECTIVE: To evaluate [1] the effects of levels of sex hormone-binding globulin (SHBG), albumin, and total testosterone on the distribution of testosterone between SHBG-bound and non-SHBG-bound fractions; [2] the independent effects of polycystic ovary syndrome (PCOS) and body mass index on serum levels of total testosterone, non-SHBG-bound testosterone, SHBG, and albumin; and [3] the usefulness of levels of total testosterone and non-SHBG-bound testosterone and of the free androgen index in the diagnosis of PCOS. DESIGN: Retrospective clinical study. SETTING: An academic research environment. PATIENT(S): Forty-three women with oligomenorrhea and PCOS. Twenty-five women with regular menstrual cycles and without hirsutism served as controls. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Levels of non-SHBG-bound testosterone, total testosterone, SHBG, and albumin in serum. RESULT(S): Levels of total testosterone and non-SHBG-bound testosterone, and the free androgen index were higher in patients with PCOS than in healthy controls. PCOS did not have an effect on the levels of SHBG or albumin, or on the percentage of non-SHBG-bound testosterone. Levels of SHBG and albumin were inversely related to body mass index. The percentage and concentration of non-SHBG-bound testosterone and the free androgen index were directly related to body mass index. Hirsutism did not have an effect on any outcome measure. CONCLUSION(S): The distribution of total testosterone into SHBG-bound and non-SHBG-bound fractions is associated with body mass index, not with PCOS. The high levels of non-SHBG-bound testosterone and the high free androgen index in patients with PCOS reflect mainly high levels of total testosterone. Thus, the measurement of levels of non-SHBG-bound testosterone and the calculation of the free androgen index provide no further information in the diagnosis of PCOS beyond that provided by the measurement of levels of total testosterone.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10065782&dopt=Abstract

AJR Am J Roentgenol. 1999 Mar;172(3):759-63.
Sonographic detection of uterine and ovarian abnormalities in female survivors of Wilms' tumor treated with radiotherapy.

Nussbaum Blask AR, Nicholson HS, Markle BM, Wechsler-Jentzch K, O'Donnell R, Byrne J.

Department of Diagnostic Imaging and Radiology, Children's National Medical Center, Washington, DC 20010, USA.

OBJECTIVE: The purpose of this study was to use sonography to evaluate the size of the ovaries and uterus in survivors of Wilms' tumor who underwent radiotherapy. SUBJECTS AND METHODS: Eighteen survivors of Wilms' tumor had their ovaries and uterus measured on sonography. Their ages at diagnosis and treatment ranged from 14 months to 6 years. Four girls were prepubertal (age, 5-9 years), 11 were postpubertal (age, 11-30 years), and three had primary ovarian failure (age, 15-23 years) at the time of imaging. Findings were compared with those of a control group of 25 prepubertal and 25 postpubertal girls and women. Gonadotropin levels were measured. RESULTS: Three patients who underwent whole abdomen radiotherapy had elevated levels of gonadotropin and primary ovarian failure. Neither ovary was seen in two of the three patients and both ovaries were abnormally small (< or = 1 cm3) in the third patient. The uterus was abnormally small (length, < or = 4 cm) in all three of these patients even though two were being treated with hormone replacement therapy. Ten postpubertal patients who underwent hemiabdomen radiotherapy had normal gonadotropin levels and a normal-sized uterus on sonography; the ovary on the side that received radiotherapy was not seen in three of the 10 patients or was abnormally small (< or = 1.4 cm3) in two of the 10 patients compared with all normal ovaries in the postpubertal control group (p < .0001). One postpubertal patient with bilateral renal bed radiotherapy had normal ovaries and a normal-sized uterus. Significantly more patients in the postpubertal and ovarian failure radiotherapy group (5 [36%] of 14 patients) had one or both ovaries not seen than the control group (none [0%] of 25 patients; p = .0014). The uterus was significantly smaller than normal in three (23%) of the 13 patients in the postpubertal hemiabdomen and ovarian failure radiotherapy group versus none of the 25 patients in the postpubertal control group (p = .0339). CONCLUSION: Postpubertal female survivors of Wilm's tumor who underwent radiotherapy as children may have one or two small or absent ovaries and a small uterus that can be detected by sonography. The response of the uterus to hormone replacement therapy can also be assessed on sonography.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10063876&dopt=Abstract

J Hypertens. 2003 Feb;21(2):327-35.
Implication of Ref-1 in the repression of renin gene transcription by intracellular calcium.

Fuchs S, Philippe J, Corvol P, Pinet F.

INSERM U36, College de France, Paris, France and INSERM U508, Pasteur Institut, Lille cedex, France.

OBJECTIVE The production of renin, which catalyzes the rate-limiting step of the renin-angiotensin system, is tightly regulated by intracellular second messengers. Among them, an increase of intracellular calcium represses renin gene expression. This inhibition of gene expression by intracellular calcium is exceptional, and the molecular mechanism supporting this phenomenon has not yet been identified. As the renin gene is negatively regulated by calcium in the same way as the parathormone (PTH) gene, we hypothesized that a similar molecular transcriptional mechanism could be involved.RESULTS Analysis of the human renin proximal promoter led to the identification of a negative calcium response element (nCaRE), which is identical to the region of the PTH promoter and is involved in its repression by calcium. Transfection experiments in renin-expressing chorio-decidual cells demonstrated the transcriptional functionality of the human renin promoter nCaRE. In addition, mutation of nCaRE suppressed the sensitivity of the renin promoter to the increase in intracellular calcium. Gel shift assays demonstrated that Redox factor 1, a multifunctional protein involved in the repair of damaged DNA and the redox activation of AP-1 transcriptional factors, binds specifically to nCaRE. Immunostaining showed that this factor is translocated from the cytoplasm to the nucleus in response to an increase in the intracellular calcium concentration.CONCLUSION Thus, the repression of renin expression by intracellular calcium may be mediated by the calcium-induced translocation of Ref-1 to the nucleus, where it binds to the renin promoter nCaRE, to repress the transcription of the renin gene.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12569263&dopt=Abstract [PubMed - in process]

Nephrol Dial Transplant. 1999 Feb;14(2):400-5.
Leptin in CAPD patients: serum concentrations and peritoneal loss.

Kagan A, Haran N, Leschinsky L, Shuali N, Rapoport J.

Department of Nephrology and Hypertension, Kaplan Medical Center, Rehovot, Israel.

BACKGROUND: To determine whether serum leptin concentrations in patients undergoing continuous ambulatory peritoneal dialysis (CAPD) are influenced by peritoneal loss of leptin and to compare serum leptin levels of normal subjects with those of patients receiving renal replacement therapy such as haemodialysis (HD), CAPD, or kidney transplantation. SUBJECTS AND METHODS: Eighty-four individuals were investigated: six females and 14 males on standard CAPD; 13 females and 13 males on chronic HD; 10 female and eight male kidney transplant recipients, and 10 female and 10 male subjects as controls. Morning serum, 8-h and 24-h samples of peritoneal fluid concentrated to 6-20-fold by Centricon 3 (cutoff 3000 daltons), and 24-h urinary concentrations of leptin were measured with commercial RIA (Linco Research, Inc., USA). Venous blood and peritoneal fluid samples of albumin, beta2-microglobulin, glucose, urea, and creatinine were determined by standard laboratory techniques. Serum insulin levels were measured by radioimmunoassay. RESULTS: Patients (men and women) on CAPD and after kidney transplantation exhibited significantly higher serum concentrations of leptin and leptin/BMI ratios than control subjects. These increased values did not reach statistical significance in HD patients. Serum leptin concentrations were correlated very significantly with BMI in all cases (r=0.380, P<0.001). Moreover, in CAPD patients (r=0.630, P<0.007) and in HD patients (r=0.668, P<0.005), but not in kidney transplant recipients or control subjects, significant correlations were observed between serum leptin and insulin concentrations. Residual renal function (RRF) in the range 0-12.8 ml/min and serum beta2-microglobulin levels in the range 7.9-47.1 mg/l did not influence serum leptin levels in CAPD and HD patients. As expected, leptin was detected in the peritoneal fluid of CAPD patients. Twenty-four-hour peritoneal loss (30.95+/-21.05 ng/min) and 24-h peritoneal clearance (0.01+/-0.01 ml/kg/min) of leptin account for only 3.9% of estimated whole-body leptin production rate and 0.7% of leptin clearance from plasma respectively. Twenty-four-hour urinary losses of leptin in CAPD patients were negligible, accounting for 5.6+/-1.8% (range 0.3-15.2%) of total (peritoneal and urinary) loss of this hormone. CONCLUSIONS: These findings suggest that serum leptin levels are not affected by continuous peritoneal loss of leptin during CAPD and that insulin resistance and hyperinsulinaemia contribute to elevated serum leptin concentrations in CAPD and HD patients. The aetiology of increased serum leptin levels in kidney transplant recipients is probably different from that in dialysis patients.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10069196&dopt=Abstract

Biochim Biophys Acta. 1999 Feb 25;1437(2):257-64.
Short-time effects of neuroactive steroids on rat cortical Ca2+-ATPase activity.

Zylinska L, Gromadzinska E, Lachowicz L.

Neurochemical Laboratory, Department of Biochemistry, Medical University of Lodz, 6 Lindley Street, 90-131, Lodz, Poland.

Recent experimental evidence indicates that some steroid hormones, apart from their well-documented genomic actions, could produce non-genomic rapid effects, and are potent modulators of the plasma membrane proteins, including voltage- and ligand-operated ion channels or G protein-coupled receptors. Neuroactive steroids, 17beta-estradiol, testosterone, pregnenolone sulfate and dehydroepiandrosterone sulfate, after a short-time incubation directly modulated the activity of plasma membrane Ca2+-ATPase purified from synaptosomal membranes of rat cortex. The sulfate derivatives of dehydroepiandrosterone and pregnenolone applied at concentrations of 10-11-10-6 M, showed an inverted U-shape potency in the regulation of Ca2+-ATPase activity. At physiologically relevant concentrations (10-8-10-9 M) a maximal enhancement of the basal activity reached 200%. Testosterone (10-11-10-6 M) and 17beta-estradiol (10-12-10-9 M) caused a dose-dependent increase in the hydrolytic ability of Ca2+-ATPase, and the activity with the highest concentration of steroids reached 470% and 200%, respectively. All examined steroids decreased the stimulatory effect of a naturally existing activator of the calcium pump, calmodulin. The present study strongly suggests that the plasma membrane calcium pump could be one of the possible membrane targets for a non-genomic neuroactive steroid action.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10064908&dopt=Abstract

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