EXPERIMENTAL GESTATIONAL DIABETES DISRUPTS THE FORMATION OF IMMUNE TOLERANCE IN OFFSPRING.

Objective: The aim: To analyze the mRNA gene expression level of Aire, Deaf1, Foxp3, Ctla4, Il10, Nlrp3 and distribution of NLRP3+-cells in mesenteric lymph nodes (MLNs) of the offspring of rats with GD, both untreated and treated with glibenclamide and in conditions of insulin oral tolerance formation.

Patients And Methods: Materials and methods: The study involves 160 male rats, one- or six-month-old. The mRNA genes expression was studied by real time quantitative poly¬merase chain reaction.

[INDICATORS OF GOUT INTERLAYKINS AND THERMOGRAPHY OF JOINTS ON THE BACKGROUND OF ENTEROSORBTION THERAPY].

Gout is a serious medical, social and economic problem of today. The major factor in its pathogenesis is impaired purine metabolism, which leads to an increase in uric acid concentration and the development of monourate-induced inflammation. Disruption of thermoregulation and regional blood flow is an important clinical and pathogenic manifestation of gout, which can be evaluated by the registration of infrared radiation.

The Influence of Metformin to the Transcriptional Activity of the mTOR and FOX3 Genes in Parapancreatic Adipose Tissue of Streptozotocin-Induced Diabetic Rats.

The mammalian target of rapamycin is not only a central regulator of lipid metabolism that controls the processes of adipogenesis and lipolysis but also a regulator of the immunometabolism of immune cells that infiltrate adipose tissue. In turn, the level of progression of diabetes is significantly influenced by the Treg subpopulation, the complexity and heterogeneity of which is confirmed by the detection of numerous tissue-specific Tregs, including the so-called VAT Tregs (visceral adipose tissue CD4+Foxp3+ regulatory T cells). Therefore, the purpose of the study was to determine the mRNA expression levels of mTOR, Foxp3, IL1β, and IL17A genes in rat parapancreatic adipose tissue with experimental streptozotocin-induced diabetes mellitus, with or without metformin administration.

Topical Diagnosis and Determination of the Primary Hyperaldosteronism Variant.

Laboratory diagnosis of primary hyperaldosteronism is based on determining blood levels of aldosterone, renin on request, potassium, and sodium. The results of these studies are significantly influenced by drugs, preparation for the study and blood collection methods, age, gender, and concomitant diseases. The work analyzes the factors influencing the results of the study of aldosterone and identifies the main ways of their exclusion at each stage of the diagnosis.

Laboratory Diagnostics of Primary Hyperaldosteronism and its Peculiarities (Literature Review).

The final stage of the diagnostic of primary hyperaldosteronism is to identify the causes of excessive secretion of aldosterone and determination of its variants. Based on the analysis of literature data, the diagnostic value, sensitivity and specificity of the methods of radiation diagnostics for primary hyperaldosteronism were assessed: ultrasound, computed tomography, magnetic resonance imaging, photon emission tomography, magnetic resonance spectroscopy, scintigraphy with iodine radiopharmaceuticals. The causes of false-positive and false-negative evaluations of changes in adrenal glands in the application of these diagnostics have been analyzed.