Pseudohipoaldosteronismo tipo 1 secundario a reflujo vesicoureteral: una urgencia endocrinológica / Pseudohypoaldosteronism type 1 secondary to vesicoureteral reflux: An endocrinologic emergency

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Alcalosis metabólica con hiponatremia, hipopotasemia e hipocloremia como forma de presentación de fibrosis quística en un adulto / Metabolic alkalosis with hyponatremia, hypokalemia and hypochloremia as the initial presentation of cystic fibrosis in an adult patient

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Activation of farnesoid X receptor induces RECK expression in mouse liver.

Farnesoid X receptor (FXR) belongs to the ligand-activated nuclear receptor superfamily, and functions as a transcription factor regulating the transcription of numerous genes involved in bile acid homeostasis, lipoprotein and glucose metabolism. In the present study, we identified RECK, a membrane-anchored inhibitor of matrix metalloproteinases, as a novel target gene of FXR in mouse liver. We found that FXR agonist substantially augmented hepatic RECK mRNA and protein expression in vivo and in vitro. FXR regulated the transcription of RECK through directly binding to FXR response element located within intron 1 of the mouse RECK gene. Moreover, FXR agonist reversed the down-regulation of RECK in the livers from mice fed a methionine and choline deficient diet. In summary, our data suggest that RECK is a novel transcriptional target of FXR in mouse liver, and provide clues to better understanding the function of FXR in liver.

Burkholderia pseudomallei in unchlorinated domestic bore water, Tropical Northern Australia.

To determine whether unchlorinated bore water in northern Australia contained Burkholderia pseudomallei organisms, we sampled 55 bores; 18 (33%) were culture positive. Multilocus sequence typing identified 15 sequence types. The B. pseudomallei sequence type from 1 water sample matched a clinical isolate from a resident with melioidosis on the same property.

Mitochondrial dysfunction in rat with nonalcoholic fatty liver Involvement of complex I, reactive oxygen species and cardiolipin.

Mitochondrial dysfunction and oxidative stress play a central role in the pathophysiology of nonalcoholic fatty liver disease (NAFLD). This study aimed to elucidate the mechanism(s) responsible for mitochondrial dysfunction in nonalcoholic fatty liver. Fatty liver was induced in rats with a choline-deficient (CD) diet for 30 days. We examined the effect of CD diet on various parameters related to mitochondrial function such as complex I activity, oxygen consumption, reactive oxygen species (ROS) generation and cardiolipin content and oxidation. The activity of complex I was reduced by 35% in mitochondria isolated from CD livers compared with the controls. These changes in complex I activity were associated with parallel changes in state 3 respiration. Hydrogen peroxide (H(2)O(2)) generation was significantly increased in mitochondria isolated from CD livers. The mitochondrial content of cardiolipin, a phospholipid required for optimal activity of complex I, decreased by 38% as function of CD diet, while there was a significantly increase in the level of peroxidized cardiolipin. The lower complex I activity in mitochondria from CD livers could be completely restored to the level of control livers by exogenously added cardiolipin. This effect of cardiolipin could not be replaced by other phospholipids nor by peroxidized cardiolipin. It is concluded that CD diet causes mitochondrial complex I dysfunction which can be attributed to ROS-induced cardiolipin oxidation. These findings provide new insights into the alterations underlying mitochondrial dysfunction in NAFLD.

2,3-butanedione monoxime (BDM), a potent inhibitor of actin-myosin interaction, induces ion and fluid transport in MDCK monolayers.

Membrane-cytoskeleton interactions have been shown to be crucial to modulate polarity, cell shape and the paracellular pathway in epithelial MDCK cell monolayers. In particular, actin organization and myosin-dependent contractility play an important role in the regulation of these functions. Participation of myosin in vectorial transport, expressed as formation of domes, was investigated in confluent monolayers of high transepithelial electrical resistance (TER) plated on non-permeable supports. Cells exposed to 2,3-butanedione monoxime, a selective inhibitor of myosin ATPase, showed a remarkable increase in the number of domes. Replacement of extracellular Na+ and Cl- and inhibition of Na+-K+-ATPase blocked the induction of domes. The monoxime also caused a reduction of the TER leading to an increase in the paracellular flux of small molecular weight dextran. However, immunofluorescence microscopy of drug-treated cells showed that the localization and staining pattern of tight junction proteins ZO-1, occludin, and claudin 1, or the actin-myosin ring at the zonula adherens, were not modified. Treatment with the drug produced striking re-arrangements of actin filaments at the microvilli and at the basal level of the cells. Our data show that disruption of actin-myosin interaction at several cellular sites contributed importantly to the increased transport activity and the formation of the domes. These results point to the relevant role or actin-myosin dynamics and actin organization in the regulation of ion and water channel activity in these cells.