Intestinal Coccidiosis in a Patient with Alpha-chain Disease

During an ultrastructural study of small-intestinal mucosa from a patient suffering from alpha-chain disease organisms were identified within the epithelial cytoplasm which showed the fine structural features of the coccidian group. Though coccidiosis is well recognized as causing a diarrhoeal and often lethal illness in animals it has been neglected as a cause of disease in man. Thus this finding may be significant and warrants further investigation into its possible role in the pathogenesis of alpha-chain disease.     

Effects of 1-ethynylpyrene and related inhibitors of P450 isozymes upon benzo[a]pyrene metabolism by liver microsomes

The effects of three aryl acetylenes, 1-ethynylpyrene (EP), 2-ethynylnaphthalene (EN) and 3-ethynylperylene (EPE), upon the metabolism of benzo[a]pyrene (BaP) by microsomes isolated from rat liver were investigated. These aryl acetylenes all inhibited the total metabolism of BaP. Formation of BaP 7,8-dihydrodiol and BaP tetrol products by microsomal preparations from rats that had been pretreated with 3-methylcholanthrene (3MC) were preferentially inhibited. The effects of EP upon the metabolism of BaP 7,8-dihydrodiol by microsomes from rat liver were also studied. This aryl acetylene strongly inhibited the formation of BaP tetrols from BaP 7,8-dihydrodiol by liver microsomes both from untreated rats and from rats pretreated with 3MC, but enhanced the conversion of the BaP dihydrodiol into other metabolites.     

Tissue glycogen concentrations in hypophysectomized pig fetuses following infusion with cortisol

The role of cortisol as a factor controlling the deposition of glycogen in the pig fetus was examined by infusing either a low dose (1 mg/day) or a high dose (3 mg/day) of cortisol into chronically-catheterized hypophysectomized fetal pigs for five days beginning on day 100-104 of gestation. After infusion, liver glycogen was significantly higher (P less than 0.05) and lung glycogen significantly lower (P less than 0.05) than in uninfused hypophysectomized litter mates although concentrations were significantly different from intact litter mates (P less than 0.05). Although skeletal and cardiac muscle content increased after infusion this difference was not significant. Changes in tissue glycogen content were similar for both the low and high rates of infusion. These observations indicate that exogenous cortisol alone is able to stimulate liver glycogen deposition and reverse the effect of hypophysectomy. Although other factors may be necessary for maximal response this suggests that cortisol is an important stimulant for liver glycogen deposition in the fetal pig. The effect of cortisol on muscle glycogen was equivocal suggesting that other hormones may play a more important role in this tissue.     

The first record of the shore fly Paracoenia fumosalis (Diptera, Ephydridae) in the Palaearctic region

Paracoenia fumosalis Cresson previously known only from the USA and Canada is recorded in the Palaearctic Region for the first time. The adults were collected near a thermal hydrosulfuric spring in the Geiser Valley in Kamchatka. A key to species of the genus Paracoenia occurring in Russia is given.     

Cyclo(His-Pro) up-regulates heme oxygenase 1 via activation of Nrf2-ARE signalling

Paraquat (1,1'-dimethyl-4,4'-bipyridinium), a widely used non-selective herbicide, is a redox cycling agent with adverse effects on dopamine systems. Epidemiological data have shown that exposure to paraquat is one of the several risk factors for Parkinson's disease. We have already shown that cyclo(His-Pro), an endogenous cyclic dipeptide produced by the cleavage of the thyrotropin releasing hormone, has a cytoprotective effect through a mechanism involving Nrf2 activation that decreases production of reactive oxygen species and increases glutathione synthesis. Using primary neuronal cultures and PC12 cells as targets of paraquat neurotoxicity, we addressed whether and how cyclo(His-Pro) causes cellular protective response against paraquat-mediated cell death. We found that cyclo(His-Pro) attenuated reactive oxygen species production, and prevented glutathione depletion by up-regulating Nrf2 gene expression, triggering its nuclear accumulation and activating the expression of heme oxygenase1. These protective effects were abolished by RNA interference-mediated Nrf2 knock down whereas were unaffected by RNA interference-mediated Keap1 knock down. Inhibition of heme oxygenase activity decreased cyclo(His-Pro)-induced neuroprotection. These results suggest that cyclo(His-Pro), acting as a selective activator of the brain modulable Nrf2 pathway, may be a promising candidate as neuroprotective agent that act through induction of phase II genes.