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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







Exp Clin Endocrinol Diabetes. 2002 Oct;110(7):343-7.
Growth hormone secretagogue (GHS) analogue, hexarelin stimulates GH from peripheral lymphocytes.

Poppi L, Dixit VD, Baratta M, Giustina A, Tamanini C, Parvizi N.

Institute of animal science, 31535 Neustadt, Germany.

The role of growth hormone releasing hormone (GHRH) and growth hormone releasing peptide-6 (GHRP-6) analogue hexarelin was investigated in the regulation of GH production from lymphocytes. Porcine and bovine blood mononuclear cells were separated using density gradient centrifugation method by layering the whole blood or buffy coat cells on lymphodex. Cells were incubated for 3 or 5 days with or without phytohemagglutinin (PHA-M), GHRH, GHRP-6 analogue hexarelin, somatostatin or GHRH + hexarelin. Growth hormone was fractionated from supernatants by gel chromatography and further concentrated by lyophilization at - 20 degrees C. A nearly two fold increase in basal secretion of GH (porcine: 3.5 +/- 0.1 ng/ml, bovine: 3.2 +/- 0.2 ng/ml) was achieved by GHRH and hexarelin at concentrations of 0.1, 1.0, 10 and 100 nM in both porcine and bovine cells. Lymphocytic GH release was also stimulated in response to PHA-M (10 micro g/well). Neither a dose dependent nor a synergistic nor an additive effect was apparent on GH secretion from lymphocytes. GHRH stimulated lymphocytic GH secretion, whereas, somatostatin had no effect. This study reports for the first time that hexarelin stimulates the secretion of GH from peripheral lymphocytes.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12397533&dopt=Abstract



Mol Cell Endocrinol. 1999 Jan 25;147(1-2):75-84.
Characterization of membrane estrogen binding proteins from rabbit uterus.

Monje P, Boland R.

Departamento de Biologia, Bioquimica y Farmacia, Universidad Nacional del Sur, Bahia Blanca, Argentina.

Estrogens exert fast non-genomic actions in their target tissues which may involve the participation of receptors located at the cell membrane. Studies were performed to identify and characterize membrane-associated 17beta-estradiol binding proteins in rabbit uterus. Specific and saturable [3H]17beta-estradiol binding sites of high affinity (Kd = 0.36 nM) were detected in uterine microsomes at higher concentration than in cytosol (370 +/- 98 vs. 270 +/- 87 fmol/mg protein, respectively). Various other steroid hormones, the stereoisomer 17alpha-estradiol and the antiestrogen tamoxifen were significantly less effective than 17beta-estradiol to compete with the radioactive ligand for binding to the membranes. The microsome binding sites were trypsin-sensitive and could be extracted to a great extent (80-90%) with 0.4/0.6 M KCl. Assays of the marker enzyme glucose-6-P dehydrogenase excluded membrane contamination with cytosolic soluble components. Immunoblot analysis of particulate and soluble fractions using monoclonal antibodies against the transactivation, heat shock protein recognition, and steroid binding domains of the nuclear estrogen receptor (ER; 67 kDa), revealed lower concentrations of the ER in membranes and the presence of five additional immunoreactive proteins of 57, 50, 32, 28, and 11 kDa which were absent in cytosol. Moreover, the antibody against the steroid binding domain was as effective as an inhibitor for cytosolic and membrane specific radioligand binding. Extraction of microsomes with the nondenaturing detergent CHAPS allowed a 2-fold enrichment of ER-like binding proteins as shown by antibody labeling and [3H]17beta-estradiol binding analysis. The results of this work are consistent with the existence of novel 17beta-estradiol membrane binding proteins structurally related to the intracellular ER. Future studies should investigate whether any of these proteins are involved in the primary events (e.g. receptor function) mediating nongenomic estrogen effects.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10195694&dopt=Abstract



Exp Clin Endocrinol Diabetes. 2002 Oct;110(7):348-54.
Long-term follow-up of thyroid nodule growth.

Quadbeck B, Pruellage J, Roggenbuck U, Hirche H, Janssen OE, Mann K, Hoermann R.

Department of Medicine, University of Essen, Essen, Germany. beate.quadbecni-essen.de

Benign thyroid nodules are common in iodine deficient countries. Although many recent studies have addressed the molecular basis and short-term outcome of treatment in nodular thyroid disease, data on the long-term follow-up of thyroid nodule growth are widely lacking. The aim of the present study was to evaluate the long-term behaviour of benign thyroid nodules growth. We followed 109 consecutive patients seen at yearly intervals in our Outpatient Clinic for at least 3 years (range 3-12 years, mean 4.9 +/- 2.6 years) presenting with 139 benign nodules in uni- or multinodular goiters. The size of the nodules and thyroid glands was analysed retrospectively. The study included a spectrum of benign thyroid nodules, 86 functioning and 53 non-functioning. 27 patients were treated with levothyroxine, 8 with iodide and 16 with a combination of both. 58 patients were not treated mainly because of thyroid functional autonomy. Patients with overt hyperthyroidism or suspected malignancy by fine-needle aspiration were excluded from the study. The nodules and glands were assessed by ultrasonography at yearly intervals and documented by photoprints. Relevant growth was defined as an increase in nodule volume of at least 30%. For statistical analyses, Cox Proportional Hazard Model and life-table analyses according to Kaplan-Meier were performed. Most thyroid nodules grew slowly but continuously during follow-up. After about 3 years, half of the nodules had increased their volume by at least 30%. Growth of the nodules was significantly faster than of the corresponding thyroid glands (p < 0.0001). Age and sex of the patients and size or function of the nodules at initial presentation were not significantly related to their growth. Suppression of TSH did not affect growth of the nodules irrespective of the source of thyroid hormones, endogenous or by administration of levothyroxine. In conclusion, benign thyroid nodules have a slow intrinsic growth potential, which is apparently higher than that of the non-nodular tissue. In this study, not only nodular but even non-nodular goiter growth continues in the majority of patients. Exogeneous factors, including therapy with levothyroxine and/or iodide, appear to have little effect on the growth behaviour.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12397534&dopt=Abstract



Exp Clin Endocrinol Diabetes. 2002 Oct;110(7):361-3.
Effect of growth hormone on high plasma levels of glucagon-like peptide-1 (GLP-1) in hypophysectomized rats.

Tateishi K, Kitayama N, Ishikawa H, Mitsudome A, Hirose S.

Department of Biochemistry, Fukuoka University School of Medicine, Fukuoka, Japan. tateishukuoa-u.ac.jp

Fasting plasma GLP-1 levels were significantly higher in hypophysectomized (hypox) rats (n = 6) than in intact (normal) rats (n = 7) (54.3 +/- 5.2 vs. 33.3 +/- 2.4 pmol/L, p < 0.001). To examine the influence of pituitary hormones on plasma GLP-1 levels, concentrations of plasma glucose, insulin and GLP-1 after an oral glucose load to hypox rats that were given either rat growth hormone (rGH) (n = 7), cortisol and thyroxine (n = 7) or no substitution (n = 6) were compared with those of normal rats (n = 7). Plasma glucose levels in the fasting state and after the glucose ingestion were significantly lower in hypox rats, but the hormonal replacements to hypox rats increased their total glucose levels to those of normal rats, although the increasing patterns were different from those in normal rats. Insulin levels both in the fasting state and after the glucose ingestion were significantly decreased in hypox rats and the fasting and total GLP-1 levels were significantly increased in those rats. rGH substitution significantly increased the total insulin levels in hypox rats and decreased the fasting and total GLP-1 levels closely to levels in normal rats, while substitution with cortisol and thyroxine failed to introduce such a significant effect. These results suggested that secretion of GLP-1 might be influenced by the function of GH.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12397536&dopt=Abstract



Hepatogastroenterology. 2002 Nov-Dec;49(48):1597-601.
Liver metastases from breast cancer. Results of surgical resection.

Carlini M, Lonardo MT, Carboni F, Petric M, Vitucci C, Santoro R, Lepiane P, Ettorre GM, Santoro E.

Department of Surgery, Division of Digestive Surgery and Liver Transplant, Regina Elena Institute for Cancer Research, Rome, Italy. maxcarliniscali.it

BACKGROUND/AIMS: Purpose of this study is to define the effectiveness of surgical resection of liver metastases from operated breast cancer. METHODOLOGY: Nineteen patients underwent surgical exploration to resect liver metastases from previously operated breast carcinoma. Seventeen patients were resected: 15 patients had unique metastases and were submitted to a wedge liver resection while 2 had multiple lesions; in these cases a V-VI segmentectomy and a right hepatectomy was required. After liver resection 11 patients received chemotherapy, 2 chemotherapy plus hormone therapy, 2 hormone therapy alone and in the remaining 2 no adjuvant treatment was done. RESULTS: Postoperative mortality was nil and morbidity consisted of 1 subphrenic abscess and 1 pleural effusion. Actuarial 5-year survival rate was 46%. Eight patients are still alive, 7 of whom are disease-free. Nine patients died for neoplastic progression. CONCLUSIONS: Surgical resection of liver metastases from breast cancer seems to be able to improve long-term survival in selected patients with unique and isolated lesions especially in association to systemic chemotherapy and hormone therapy.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12397744&dopt=Abstract








Like developmental biology of any part of our body, hair growth is a complicated process. Hence the homework for modern science to yet unravel the process and mechanism to a completion. There exist a number of traditional and alternative therapeutic methods that include drugs, surgery, suppelements, and even snake oils that have been developed and used for those who lose hair. No understanding, and there is no solution. Of course, none of these approaches are perfect for all hair loss problems, especially due to the heterogeneity of the causes underlying hair losses. Most of chemical drugs and hair transplantation surgeries are accompanied by undesirable side effects.
















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