Lobose amoebae are abundant free‐living protists and important pathogenic agents, yet their evolutionary history and position in the universal tree of life are poorly known. Molecular data for lobose amoebae are limited to a few species, and all phylogenetic studies published so far lacked representatives of many of their taxonomic groups. Here we analyse actin and small‐subunit ribosomal RNA (SSU rRNA) gene sequences of a broad taxon sampling of naked, lobose amoebae. Our results support the existence of a monophyletic Amoebozoa clade, which comprises all lobose amoebae examined so far, as well as the amitochondriate pelobionts and entamoebids, and the slime molds. Both actin and SSU rRNA phylogenies distinguish two well‐defined clades of amoebae, the “Gymnamoebia sensu stricto” and the Archamoebae (pelobionts+entamoebids), and one weakly supported and ill‐resolved group comprising some naked, lobose amoebae and the Mycetozoa.
In recent years, the definitions and classifications of congenital tubulo-interstitial kidney diseases have been significantly revised. This is primarily due to the achievements in the molecular biology and genetics, which made it possible to significantly clarify the role of a number of genes encoding certain proteins that are closely involved in kidney functions. In 2015, KDIGO proposed to unify the terminology, diagnostic criteria and approaches to monitoring conditions associated with mutations of the MUC1, UMOD, HNF1B and REN genes, which led to the development of ideas about the new nosology - autosomal dominant tubulointerstitial kidney disease (ADTKD). A brief description of the basic information about the ADTKD compiled the content of this message.
Arterial hypertension is the important reason of the morbidity and mortality of the patients with chronic kidney disease. The aim of this study was to estimate the feature of the arterial hypertension, vasomotor form endothelial dysfunction and level of VCAM1 at patients with chronic kidney disease at groups with achievement and not achievement target arterial pressure. At the moment of the survey the target arterial pressure was achieved at 70 (1 group) and not achieved at 31 patients (2 group). During investigation it was applied the complex of biochemical, immune-enzyme and instrumental methods. The vasomotor form of endothelial dysfunction was detected at all of patients. The improvement of endothelium-dependent vasodilatation was defined at patients with achieved target arterial pressure. The VCAM1 concentration was elevated only at the patients 2 group. This group was differ from the 1 group with more high arterial pressure, left ventricular hypertrophy, atrium enlargement, complex intima-media enlargement, decrease glomerular filtration rate. It was made the conclusion that achievement target arterial pressure facilitate the correction of vasomotor form of endothelial dysfunction.
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