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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

Biochem Biophys Res Commun. 2002 Apr 26;293(1):622-8.
Leptin mediates a proliferative response in human MCF7 breast cancer cells.

Dieudonne MN, Machinal-Quelin F, Serazin-Leroy V, Leneveu MC, Pecquery R, Giudicelli Y.

Service de Biochimie et Biologie Moleculaire, Faculte de Medecine Paris-Ouest, Centre Hospitalier de Poissy, Universite Descartes Paris V, 78303 Poissy Cedex, France.

Obesity is a risk factor of breast cancers. As leptin, a hormone mainly secreted by white adipocytes, elicits proliferative effects in some cell types, we tested the hypothesis that leptin could influence human breast cancer MCF-7 cell growth. Here we show that MCF-7 cells express leptin receptors and respond to human recombinant leptin by STAT3 and p42/p44 MAPkinase activations and by increased proliferation. These findings suggest that leptin could act in vivo as a paracrine/endocrine growth factor towards mammary epithelial cells thus contributing to explain why obesity is a risk factor of developing breast cancers.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12054648&dopt=Abstract

Biochem Biophys Res Commun. 2002 Apr 26;293(1):629-32.
Polymorphism in exon 4 of the human 3 beta-hydroxysteroid dehydrogenase type I gene (HSD3B1) and blood pressure.

Rosmond R, Chagnon M, Bouchard C, Bjorntorp P.

Department of Clinical Chemistry, Sahlgrenska University Hospital, S-413 45 Goteborg, Sweden. roland.rosmonedic.gu.se

There is growing evidence to the effect that steroid hormones are associated with a complex phenotype of metabolic abnormalities usually referred to as the metabolic syndrome. The 3 beta-hydroxysteroid dehydrogenases/Delta(4,5)-isomerase (3 beta-HSD) is crucial to the biosynthesis of hormonal steroids, including aldosterone, cortisol, and testosterone. The objective of the present study was to examine the potential impact of a T-->C substitution at codon Leu(338) of the type I (HSD3B1) 3 beta-HSD gene on obesity, circulating hormones, and estimates of insulin, glucose, and lipid metabolism as well as blood pressure in 284 unrelated Swedish men born in 1944. The subjects were genotyped by using PCR amplification of exon 4 of the HSD3B1 gene followed by digestion with the restriction enzyme BglII. The frequency of allele T was 0.44 and that of allele C 0.56. Homozygotes for the C allele (n=75) had significantly (P<0.05) higher mean systolic and diastolic blood pressures compared to both heterozygotes (n=143) and homozygotes for the T allele (n=45). In addition, the C allele was significantly (P=0.018) more frequent among subjects with grade 1 hypertension (>140/90 mm Hg) compared to normotensive (<130/85 mm Hg) subjects. These results were all adjusted for the potential confounding effect of body mass index (BMI) and waist-to-hip ratio (WHR). Other measurements such as BMI, WHR, abdominal sagittal diameter, salivary cortisol, total testosterone, serum leptin, fasting insulin and glucose, and serum lipids were not different across the HSD3B1 genotype groups. In conclusion, a T-->C polymorphism at codon Leu(338) of exon 4 of the HSD3B1 gene is associated with elevated systolic and diastolic blood pressures. The pathogenic mechanism underlying this association is, however, uncertain from the present data and further studies are warranted.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12054649&dopt=Abstract

Exp Parasitol. 2002 Feb;100(2):103-11.
Pancreatic hepatocytes in hamsters (Mesocricetus auratus) infected with Trypanosoma cruzi.

dos Santos VM, de Lima MA, Cabrine-Santos M, Marquez Dde S, Reis MG, Pereira Gde A, Lages-Silva E, Ramirez LE.

Department of Internal Medicine, Faculdade de Medicina do Triangulo Mineiro, Uberaba, MG, Brazil

Hepatocytic metaplasia may be induced in hamsters by carcinogens, and associated with aging, diabetes or chronic pancreatitis. By means of histopathologic and immunohistochemic studies, we observed pancreatic hepatocytes in hamsters infected and reinfected with Trypanosoma cruzi. The change was seen in 18 (19%) out of 94 infected animals, and was not found among 53 controls, Normal islet cells were immunoreactive for neuron-specific enolase and not reactive for NCL-HAS. Metaplastic cells were immunoreactive for NCL-HAS and not reactive for islet hormones and enolase. No relationship was observed between number of inoculations and metaplasia; however, the intensity of the inflammatory process and sequels seems to favor the development of metaplastic cells. Hamsters infected with T. cruzi may be useful to study hepatocytic metaplasia, and contribute to clarify aspects of Chagas' disease and pancreatic changes. Our data indicate that aging, in addition to inflammation and atrophy, plays a role in this change. (c) 2002 Elsevier Science (USA).

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12054700&dopt=Abstract

J Exp Zool. 2002 Oct 1;293(5):525-31.
Induction of parturition in snow skinks: can low temperatures inhibit the actions of AVT?

Girling JE, Jones SM, Swain R.

Centre for Women's Health Research, Monash University, Department of Obstetrics and Gynaecology, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria, Australia 3168. jane.girlined.monash.edu.au

The influence of environmental factors on the timing of parturition has not been investigated in viviparous squamates. We investigated the interaction between temperature and parturition in two viviparous skink species, the southern snow skink (Niveoscincus microlepidotus) and the metallic skink (N. metallicus). In these species, the timing of parturition is separated from the completion of embryonic development; the delay is attributed to their cool and variable habitats. We examined whether the neurohypophyseal hormone arginine vasotocin (AVT) stimulated parturition in southern snow skinks with late stage embryos in autumn (approximately 6-7 months prior to parturition) and in metallic skinks with late stage embryos in summer (approximately 2-3 weeks prior to parturition). The experiments were conducted at a range of environmentally relevant temperatures (6 degrees C, 15 degrees C, 22 degrees C, and 28 degrees C). AVT induced parturition in both species at all temperatures; time until birth, however, occurred more quickly at warmer temperatures (22 degrees and 28 degrees C), whereas cooler temperatures delayed parturition. We hypothesize that if cool temperatures are preventing parturition, then temperature must act at some level within the brain to prevent or slow the secretion of AVT. Future experiments will need to determine how temperature influences AVT production. Further research is also required to determine how the timing of parturition is influenced by interactions between temperature, photoperiod, and seasonal hormone patterns.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12486812&dopt=Abstract

Biochem Biophys Res Commun. 2002 May 31;294(1):11-5.
Luteinizing hormone-releasing hormone induces JunD-DNA binding and extends cell cycle in human ovarian cancer cells.

Gunthert AR, Grundker C, Hollmann K, Emons G.

Department of Gynecology and Obstetrics, Georg-August-University, Robert-Koch-Street 40, D-37075 Gottingen, Germany.

Expression of luteinizing hormone-releasing hormone (LHRH) and its receptor as part of an autocrine regulatory system of cell proliferation has been demonstrated in a number of human malignant tumors, including cancers of the ovary. This study was conducted to investigate whether LHRH induces activation of JunD and affects cell cycle regulation and DNA synthesis. Treatment of primary human ovarian cancer cells and human ovarian cancer cell lines EFO-21 and EFO-27 with LHRH agonist triptorelin (100 nM) resulted in an increase in G(0/1) phase and a decrease in G(2/S) phase of cell cycle. Treatment of quiescent EFO-21 or EFO-27 cells with triptorelin (100 nM) resulted in a 46.7 or 44.2-fold increase of AP-1 activation, respectively (p<0.001). Maximal binding of JunD on DNA consensus sequence was found after 4 h of treatment of quiescent EFO-21 or EFO-27 cells with triptorelin (100 nM). DNA synthesis was significantly decreased to 45.5+/-11.4% (day 0=control=100%; p<0.001) after 3 days of triptorelin (1 nM) treatment. These results suggest that LHRH agonist triptorelin induces JunD-DNA binding, resulting in reduced proliferation as indicated by increased G(0/1) phase of cell cycle and decreased DNA synthesis. Since LHRH activates nucleus factor kappa B (NF kappa B) and protects ovarian cancer cells from doxorubicin-induced apoptosis and JunD is shown to decrease cell cycle and cell proliferation, we propose that JunD activated by LHRH acts as a modulator of cell proliferation and cooperates with the anti-apoptotic and anti-mitogenic functions of LHRH.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12054733&dopt=Abstract

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