Incidental Diagnosis of Williams Syndrome in an Adult With Recurrent Hypercalcemia.

Williams syndrome (WS) is a rare genetic disorder with multisystem involvement associated with hypercalcemia. The cause of this hypercalcemia is poorly understood and while primarily associated with WS children, it is also observed in adults. A 51-year-old woman with intellectual disability, renal insufficiency, recurrent pancreatitis, and intermittent hypercalcemia despite partial parathyroidectomy presented with hypercalcemia to 14 mg/dL (3.

Role of free nitrogen and oxygen radicals in the pathogenesis of lipopolysaccharide-induced endotoxemia.

We studied molecular mechanisms of changes in oxidative metabolism under conditions of experimental lipopolysaccharide-induced endotoxemia. Generation of reactive nitrogen and oxygen species in mice increased 18 h after treatment with lipopolysaccharide. These changes contributed to inactivation of enzymes and enzyme complexes (ribonucleotide reductase, NADH-ubiquinone oxidoreductase, and cytochrome c oxidase), dysfunction of the mitochondrial electron transport chain, and development of oxidative stress.

[Comparative study of the influence of renal endogenic factors on the proliferation activity of epithelial cells].

The proliferation activity of monolayer culture of Madin Darby Canine Kidney (MDSK) cells is suppressed by a thermostable protein factor of renal tissue of white rats and of humans. Under the influence of renal factors (RF), a decrease in cell number, and suppression of DNA synthesis and mitotic activity in MDCK cells occur. The inhibition of proliferative activity of cultured cells under the influence of RF was substantiated also by MTT assay.

[Effectiveness of plaferon LB in gamma-radiotherapy].

Free radical oxidation plays important role in the radiation-induced cell and tissue damage. Numerous studies evidence a decrease in body antioxidant system activity and changes in nitric oxide levels during irradiation. It has been demonstrated that in the process of radiation damage NO may play either radioprotective or radiotoxic role depending on body redox status.

[Role of NO and several mechanisms of plaferon lb action in the regulation of arterial blood pressure during hemorrhagic shock].

The present study aimed to establish the role of NO and mechanisms of plaferon LB (PLB) (USA patent N WO 02/12444 A2) effectiveness in the regulation of arterial blood pressure (ABP) during hemorrhagic shock (HS). As it follows from the results of our study and literary data analysis, stress-hormone mediated receptor-induced accumulation of Ca2+ ions in vascular cells occurs during experimental HS. At that, rapid release of large amount of NO due to Ca-dependent eNOS activation in endothelium results in the prevalence of NO-dependent relaxation mechanisms over Ca2+-dependent constriction in smooth muscle cells with subsequent abrupt decrease in ABP.