The presence of quinolinic acid in the structures of the rat brain]

The brain tissue extracts from chronically alcoholized (15% ethanol intake for more than 18 months) rats were studied by mass spectrometry. The mass spectra for the striatum of control and alcohol-consuming rats were identical, while those for the hippocampus showed a significant difference: a great increase in the intensity of peaks typical of mass spectra for quinolinic acid.     

The importance of virus drug-resistance in the treatment of influenza with rimantadine

Rimantadine is the first specific antiviral agent widely used in the Soviet Union for the treatment and prophylaxis of influenza A in adults. Development of resistance of influenza A virus to rimantadine has been observed. Concern has been expressed about the development of resistance during treatment of large populations with the antiviral. The efficacy of rimantadine in the treatment of various outbreaks caused by different serotypes of influenza virus has been followed over a period of 20 years in 142,227 patients with influenza. No diminution in efficacy that could be contributed to the development of drug-resistant virus strains was observed.     

Transport of urea and amino acids through the isolated human placenta

By means of a method of two-way perfusion of the isolated human placenta the transport of urea from the fetal to the maternal placental circulation and the transport of amino acids in the opposite direction were studied. Experiments showed that the method provides for sufficiently complete perfusion of the intervillous space and creates suitable conditions for the study of placental transport. If the amino nitrogen concentrations in the two circulatory systems are equal, its concentration in the fetal circulation rises in the course of the experiment. On the addition of an amino acid to the maternal circulation, this increase develops to a greater degree. The results of these experiments confirm the view that amino acids are secreted by trophoblast cells into the fetal circulation.Laboratory of Biochemistry, Institute of Obstetrics and Gynecology, Academy of Medical Sciences of the USSR, Leningrad. (Presented by Academician of the Academy of Medical Sciences of the USSR M. A. Petrov-Maslakov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 81, No. 4, pp. 394–397, April, 1976     

Temporal profile of potassium channel dysfunction in cerebrovascular smooth muscle after experimental subarachnoid haemorrhage

The pathogenesis of cerebral vasospasm after subarachnoid haemorrhage (SAH) involves sustained contraction of arterial smooth muscle cells that is maximal 6–8 days after SAH. We reported that function of voltage-gated K⁺ (K_V) channels was significantly decreased during vasospasm 7 days after SAH in dogs. Since arterial constriction is regulated by membrane potential that in turn is determined predominately by K⁺ conductance, the compromised K⁺ channel dysfunction may cause vasospasm. Additional support for this hypothesis would be demonstration that K⁺ channel dysfunction is temporally coincident with vasospasm. To test this hypothesis, SAH was created using the double haemorrhage model in dogs and smooth muscle cells from the basilar artery, which develops vasospasm, were isolated 4 days (early vasospasm), 7 days (during vasospasm) and 21 days (after vasospasm) after SAH and studied using patch-clamp electrophysiology. We investigated the two main K⁺ channels (K_V and large-conductance voltage/Ca²⁺-activated (K_Ca) channels). Electrophysiologic function of K_Ca channels was preserved at all times after SAH. In contrast, function of K_V channels was significantly decreased at all times after SAH. The decrease in cell size and degree of K_V channel dysfunction was maximal 7 days after SAH. The results suggest that K_V channel dysfunction either only partially contributes to vasospasm after SAH or that compensatory mechanisms develop that lead to resolution of vasospasm before K_V channels recover their function.     

Dendritic polyglycerol nanoparticles show charge dependent bio-distribution in early human placental explants and reduce hCG secretion

A thorough understanding of nanoparticle bio-distribution at the feto-maternal interface will be a prerequisite for their diagnostic or therapeutic application in women of childbearing age and for teratologic risk assessment. Therefore, the tissue interaction of biocompatible dendritic polyglycerol nanoparticles (dPG-NPs) with first- trimester human placental explants were analyzed and compared to less sophisticated trophoblast-cell based models. First-trimester human placental explants, BeWo cells and primary trophoblast cells from human term placenta were exposed to fluorescence labeled, ～5?nm dPG-NPs, with differently charged surfaces, at concentrations of 1 µM and 10?nM, for 6 and 24?h. Accumulation of dPGs was visualized by fluorescence microscopy. To assess the impact of dPG-NP on trophoblast integrity and endocrine function, LDH, and hCG releases were measured. A dose- and charge-dependent accumulation of dPG-NPs was observed at the early placental barrier and in cell lines, with positive dPG-NP-surface causing deposits even in the mesenchymal core of the placental villi. No signs of plasma membrane damage could be detected. After 24?h we observed a significant reduction of hCG secretion in placental explants, without significant changes in trophoblast apoptosis, at low concentrations of charged dPG-NPs. In conclusion, dPG-NP’s surface charge substantially influences their bio-distribution at the feto-maternal interface, with positive charge facilitating trans-trophoblast passage, and in contrast to more artificial models, the first-trimester placental explant culture model reveals potentially hazardous influences of charged dPG-NPs on early placental physiology.