First-row transition metal phthalocyanines as catalysts for water electrolysis

Modification of carbon electrodes with first row transition metal phthalocyanines results in the lowering of the potentials needed for water electrolysis in basic media, by 600 to 700 mV when compared to unmodified carbon electrodes. Nickel(II), cobalt(II) and iron(II) phthalocyanines show higher catalytic activity than zinc(II), manganese(II), copper(II) and metal free phthalocyanines

Interactions of cobalt (II) tetrasulfophthalocyanine with nitrite in the presence of nitrate and perchlorate ions

Spectroscopic changes observed on addition of nitrite to solutions of cobalt(II) tetra-sulfophthalocyanine ([Co(II)TSPc]4-) in the presence of N− 3 or ClO− 4 are reported. There is spectroscopic evidence for the oxidation of [Co(II)TSPc]4- to a [Co(III)TSPc]3- species in the presence of nitrite ions. Equilibrium and kinetic studies for the interaction between [Co(II)TSPc]4- and NO− 2 are reported. The rate was found to be first order in both [Co(II)TSPc]4- and NO− 2. The rate constant for the forward reaction, k f=1.6 × 10−4 dm3mol−1s−1 was determined at 20°C for the interaction between nitrite ions and [Co(II)TSPc]4- in the presence of NO3 − or ClO4 − ions

POLYMORPHISMS OF DRUG-METABOLIZING ENZYMES CYP1A2, CYP2D6, GST, NAT2 AND TRANSPORTER MDR1 IN POPULATION OF BELARUS: COMPARISON WITH SELECTED EUROPEAN AND ASIAN POPULATIONS

Drug therapeutic efficiency and development of unfavorable pharmacologic responses as well as the disease predisposition are caused first of all by patient’s genetic features. Genetic variations in genes encoding drug-metabolizing enzymes and transporter proteins are essential to understand the ethnic differences in disease occurrence, development, prognosis, therapeutic response and toxicity of drugs. For that reason, it is necessary to establish the normative frequency distribution of genotypes and alleles of these genes in a particular population. Data on frequency of pharmacogenetic polymorphisms in the of Belarus population are limited. The goal of our investigation was to analyze the frequency distribution of genotypes and alleles of genes encoding drug-metabolizing enzymes (CYP1А2, CYP2D6 – I phase; GSTs, NAT2 – II phase) and transporter protein MDR1 in the population of Belarus and comparisons with other ethnic populations. Our results indicate that clinically important genes are genetically highly variable and differ considerably between populations. Differences in allele frequencies across continents should be considered when designing clinical trials of new drugs continents should be considered when designing clinical trials of new drugs

POLYMORPHISMS OF DRUG-METABOLIZING ENZYMES CYP1A2, CYP2D6, GST, NAT2 AND TRANSPORTER MDR1 IN POPULATION OF BELARUS: COMPARISON WITH SELECTED EUROPEAN AND ASIAN POPULATIONS

Drug therapeutic efficiency and development of unfavorable pharmacologic responses as well as the disease predisposition are caused first of all by patient’s genetic features. Genetic variations in genes encoding drug-metabolizing enzymes and transporter proteins are essential to understand the ethnic differences in disease occurrence, development, prognosis, therapeutic response and toxicity of drugs. For that reason, it is necessary to establish the normative frequency distribution of genotypes and alleles of these genes in a particular population. Data on frequency of pharmacogenetic polymorphisms in the of Belarus population are limited. The goal of our investigation was to analyze the frequency distribution of genotypes and alleles of genes encoding drug-metabolizing enzymes (CYP1А2, CYP2D6 – I phase; GSTs, NAT2 – II phase) and transporter protein MDR1 in the population of Belarus and comparisons with other ethnic populations. Our results indicate that clinically important genes are genetically highly variable and differ considerably between populations. Differences in allele frequencies across continents should be considered when designing clinical trials of new drugs continents should be considered when designing clinical trials of new drugs

Gout: from Hippocrates till the modern time

Gout (podagra) is one of the most ancient articular diseases. Its accurate mechanisms and causes were delineated only during the last century. Major historical investigatory steps are described in relation to causality and pathogenesis of the disease from Hippocrates ages till the modern time. The newest genetic and epidemiologic aspects of the disease are presented in this article

Preliminary study of anti-CD40 and ubiquitin proteasome antibodies in primary podocytopaties

BackgroundMinimal change disease and focal segmental glomerulosclerosis are primary podocytopathies that are clinically presented in adults presenting with severe nephrotic syndrome. The pathogenesis of these diseases is not clear and many questions remain to be answered. A new concept about the role of changes in the antigenic determinant of podocytes and the production of anti-podocyte antibodies that cause podocyte damage is being developed. The aim of the study is to evaluate the levels of anti-CD40 and anti-ubiquitin carboxyl-terminal hydrolase L1 (anti-UCH-L1) antibodies in patients with podocytopathies in comparison with other glomerulopathies.MethodsOne hundred and six patients with glomerulopathy and 11 healthy subjects took part in the study. A histological study revealed primary FSGS in 35 patients (genetic cases of FSGS and secondary FSGS in the absence of NS were excluded), 15 had MCD, 21 - MN, 13 - MPGN, 22 patients - IgA nephropathy. The effect of steroid therapy was evaluated in patients with podocytopathies (FSGS and MCD). The serum levels of anti-UCH-L1 and anti-CD40 antibodies were measured by ELISA before steroid treatment.ResultsThe levels of anti-UCH-L1 antibodies were significantly higher in MCD patients and anti-CD40 antibodies were higher in MCD and FSGS than in the control group and other groups of glomerulopathies. In addition, the level of anti-UCH-L1 antibodies was higher in patients with steroid-sensitive FSGS and MCD, and anti-CD40 antibodies were lower than in patients with steroid-resistant FSGS. An increase in anti-UCH-L1 antibody levels above 6.44 ng/mL may be a prognostic factor of steroid-sensitivity. The ROC curve (AUC = 0.875 [95% CI 0.718–0.999]) for response to therapy showed a sensitivity of 75% and specificity of 87.5%.ConclusionAn increase in the level of anti-UCH-L1 antibodies is specific for steroid-sensitive FSGS and MCD, while an increase in anti-CD40 antibodies – for steroid-resistant FSGS, compared with other glomerulopathies. It suggests that these antibodies could be a potential factor for differential diagnosis and treatment prognosis

ГЕНЕТИЧЕСКИЙ ПОЛИМОРФИЗМ ВНУТРИКЛЕТОЧНЫХ СИГНАЛЬНЫХ ПУТЕЙ У ПАЦИЕНТОВ С НЕМЕЛКОКЛЕТОЧНЫМ РАКОМ ЛЕГКОГО

The key process in the pathogenesis of any malignant neoplasms, including non-small cell lung cancer (NSCLC), is the angiogenesis that is activated by two tyrosine kinase cascades (RAS/RAF/MAPK and PI3K/AKT/mTOR). The main genes controlling these pathways are EGFR, KRAS, PIK3CA and PTEN. The study analyzed the mutations in 18–21 exons of the EGFR gene, 2 exons of the KRAS gene, 9 and 20 exons of the PIK3CA gene and 7 exons of the PTEN gene in patients with NSCLC living in Belarus and their relationship with the clinical and morphological characteristics of the tumor. Our results revealed that mutations in the EGFR gene are significantly frequent more than 5 times in patients with non-small cell lung cancer than those in the control group. Classical mutations in the EGFR gene are found only in patients with lung adenocarcinoma, predominantly in women. Mutations of the KRAS gene are found only in men, and in patients with adenocarcinoma it is 3 times more likely than in patients with squamous cell lung carcinoma. There are no somatic mutations in the PIK3CA and PTEN genes in patients with NSCLC in this study. Ключевым процессом в патогенезе любых злокачественных новообразований, в том числе и немелкоклеточного рака легкого (НМРЛ), является ангиогенез, который активируется двумя тирозинкиназными каскадами (RAS/ RAF/MAPK и PI3K/AKT/mTOR). Основными генами, контролирующими эти пути, являются EGFR, KRAS, PIK3CA и PTEN. В исследовании проанализированы мутации в 18–21 экзонах гена EGFR, 2 экзоне гена KRAS, 9 и 20 экзонах гена PIK3CA и 7 экзоне гена PTEN у пациентов с НМРЛ, проживающих на территории Беларуси, и изучена их связь с клиникоморфологическими характеристиками опухоли. Полученные результаты показали, что мутации в гене EGFR достоверно чаще в 5 раз встречаются у пациентов с НМРЛ, чем в контрольной группе. Классические мутации в гене EGFR обнаружены только у пациентов с аденокарциномой легкого, преимущественно у женщин. Мутации гена KRAS встречаются только у мужчин, причем у пациентов с аденокарциномой в 3 раза чаще, чем у пациентов с плоскоклеточным раком легкого. В данном исследовании не выявлено соматических мутаций в генах PIK3CA и PTEN у пациентов с НМРЛ.

Acute kidney injury and mortality in coronavirus disease 2019: results from a cohort study of 1,280 patients

Background: The development of acute kidney injury (AKI) in patients with coronavirus disease 2019 (COVID-19) is associated with a high risk of death. Published data demonstrate the possibility of severe kidney injury in patients suffering from COVID-19. However, these data are still controversial. Methods: A total of 1,280 patients with a proven diagnosis of COVID-19 were included in our study. COVID-19 was confirmed in all patients using reverse transcriptase polymerase chain reaction test of a nasopharyngeal swab, and based on the typical computed tomography findings. Demographic data, underlying comorbidities, and laboratory blood tests were assessed. We assessed the incidence of AKI and its associated mortality defined by survival status at discharge. Results: Proteinuria was identified with 648 patients (50.6%) with COVID-19. AKI was identified in 371 patients (29.0%). Ten of these patients (2.7%) required dialysis. The risk factors for AKI included age of > 65 years, augmentation of C-reactive protein, ferritin and an increase in values of activated partial thromboplastin time. Overall, 162 of the 1,280 hospitalized patients (12.7%) and 111 of the 371 patients (29.9%) with AKI did not survive. The hazard ratio (HR) for mortality was 3.96 (95% confidence interval, 2.83-5.54) for patients with AKI vs. no AKI. Conclusion: AKI was a relatively common finding among patients with COVID-19. The risk factors for AKI in COVID-19 included old age, the inflammatory response, the severity of lung involvement, and disseminated intravascular coagulation. These same factors, in addition to arterial hypertension, were found to increase the risk of mortality

Acute kidney damage in COVID-19 patients

The presentation of kidney damage in Coronavirus disease 2019 (COVID-19) varies significantly. According to recent studies, the development of acute kidney injury (AKI) in severe cases of COVID-19 infection significantly worsens the prognosis of these patients. The pathological changes in kidneys might be caused directly by the cytopathic effect mediated by local replication of the severe acute respiratory syndrome coronavirus-2 (SARS]CoV-2) or indirectly because of systemic immune response or hypercoagulation, so-called immunothrombosis. Other causes, such as hypovolemia and hypoxia, may also contribute to AKI. Acute kidney disease often develops in elderly patients with underlying comorbidities or in critically ill patients with severe respiratory failure. It is known that AKI is a risk factor for mortality in COVID-19 patients