Effect of Corticotropin-Releasing Hormone Antagonist on Oestrogen-Dependent Glucoprivic Suppression of Luteinizing Hormone Secretion in Female Rats

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75477/1/j.1365-2826.1999.00312.x.pd

Peripheral or Central Administration of Motilin Suppresses LH Release in Female Rats: A Novel Role for Motilin

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72420/1/j.1365-2826.2000.00467.x.pd

Central Mechanism Controlling Pubertal Onset in Mammals: A Triggering Role of Kisspeptin

Pubertal onset is thought to be timed by an increase in pulsatile gonadotropin-releasing hormone (GnRH)/gonadotropin secretion in mammals. The underlying mechanism of pubertal onset in mammals is still an open question. Evidence accumulated in the last 15 years suggests that kisspeptin/neurokinin B/dynorphin A (KNDy) neurons in the hypothalamic arcuate nucleus play a key role in pubertal onset by triggering pulsatile GnRH/gonadotropin secretin in mammals. Specifically, KNDy neurons are now considered a part of GnRH pulse generator, in which neurokinin B facilitates and dynorphin A inhibits, the synchronized discharge of KNDy neurons in autocrine and/or paracrine manners. Kisspeptin serves as a potent secretagogue of GnRH secretion and thus its release is fundamental to pubertal increase in GnRH/gonadotropin secretion in mammals. Proposed mechanisms inhibiting Kiss1 (kisspeptin gene) expression during childhood to juvenile varies from species to species: we envisage that negative feedback action of estrogen plays a key role in the inhibition of Kiss1 expression in KNDy neurons in rodents and sheep, whereas estrogen-independent inhibition of kisspeptin secretion by γ-amino butyric acid or neuropeptide Y are suggested to be responsible for the pre-pubertal suppression of GnRH/gonadotropin secretion in primates. Taken together, the timing of pubertal onset is postulated to be controlled by upstream regulators for kisspeptin biosynthesis and secretion in mammals

Design and synthesis of fluorescent probes for GPR54.

Kisspeptins are neuropeptides that induce the secretion of gonadotropin-releasing hormone via the activation of the cognate receptor, G-protein coupled receptor 54 (GPR54). The kisspeptin-GPR54 axis is associated with the onset of puberty and the maintenance of the reproductive system. In this study, several fluorescent probes have been designed and synthesized for rat GPR54 through the modification of the N-terminus of rat kisspeptins to allow for the visualization of the expression and localization of kisspeptin receptor(s) in living cells and native tissues. The tetramethylrhodamine (TMR) and rhodamine green (RG)-labeled kisspeptins exhibited good binding and agonistic activities towards GPR54, and the results of the application studies demonstrated that these fluorescent probes could be used effectively for the detection of GPR54 receptors in flow cytometry and confocal microscopy experiments

Profiling Mycobacterium ulcerans with hsp65

Univ Fed Sao Paulo, Escola Paulista Med, Dept Microbiol, BR-04023062 Sao Paulo, BrazilInst Trop Med, B-2000 Antwerp, BelgiumUniv Fed Sao Paulo, Escola Paulista Med, Dept Microbiol, BR-04023062 Sao Paulo, BrazilWeb of Scienc

Aerobic biotransformation of alkyl branched aromatic alkanoic naphthenic acids via two different pathways by a new isolate of Mycobacterium

Naphthenic acids (NAs) are complex mixtures of carboxylic acids found in weathered crude oils and oil sands, and are toxic, corrosive and persistent. However, little is known about the microorganisms and mechanisms involved in NA degradation. We isolated a sediment bacterium (designated strain IS2.3), with 100% 16S rRNA gene sequence identity to Mycobacterium aurum, which degraded synthetic NAs (4′-n-butylphenyl)-4-butanoic acid (n-BPBA) and (4′-t-butylphenyl)-4-butanoic acid (t-BPBA). n-BPBA was readily oxidized with almost complete degradation (96.8%±0.3) compared with t-BPBA (77.8%±3.7 degraded) by day 49. Cell counts increased fourfold by day 14 but decreased after day 14 for both n- and t-BPBA. At day 14, (4′-butylphenyl)ethanoic acid (BPEA) metabolites were detected. Additional metabolites produced during t-BPBA degradation were identified by mass spectrometry of derivatives as (4′-carboxy-t-butylphenyl)-4-butanoic acid and (4′-carboxy-t-butylphenyl)ethanoic acid; suggesting that strain IS2.3 used omega oxidation of t-BPEA to oxidize the tert-butyl side-chain to produce (4′-carboxy-t-butylphenyl)ethanoic acid, as the primary route for biodegradation. However, strain IS2.3 also produced this metabolite through initial omega oxidation of the tert-butyl side-chain of t-BPBA, followed by beta-oxidation of the alkanoic acid side-chain. In conclusion, an isolate belonging to the genus Mycobacterium degraded highly branched aromatic NAs via two different pathways. © 2011 Society for Applied Microbiology and Blackwell Publishing Ltd

Mycobacterium ulcerans Disease (Buruli Ulcer) in Rural Hospital, Southern Benin, 1997–2001

Hospital data show that Buruli ulcer is highly endemic in southern Benin