The role of long non-coding RNAs in the development of adipose cells.

In recent times, the rising prevalence of obesity and its associated comorbidities have had a severe impact on human health and social progress. Therefore, scientists are delving deeper into the pathogenesis of obesity, exploring the role of non-coding RNAs. Long non-coding RNAs (lncRNAs), once regarded as mere "noise" during genome transcription, have now been confirmed through numerous studies to regulate gene expression and contribute to the occurrence and progression of several human diseases. LncRNAs can interact with protein, DNA, and RNA, respectively, and participate in regulating gene expression by modulating the levels of visible modification, transcription, post-transcription, and biological environment. Increasingly, researchers have established the involvement of lncRNAs in regulating adipogenesis, development, and energy metabolism of adipose tissue (white and brown fat). In this article, we present a literature review of the role of lncRNAs in the development of adipose cells.

Studies on the role of non-coding RNAs in controlling the activity of T cells in asthma.

Bronchial asthma, commonly known as asthma, is a chronic inflammatory disease characterized by airway inflammation, increased responsiveness and changes in airway structure. T cells, particularly T helper cells, play a crucial role in the disease. Non-coding RNAs, which are RNAs that do not code for proteins, mainly include microRNAs, long non-coding RNAs, and circular RNAs, play a role in regulating various biological processes. Studies have shown that non-coding RNAs have an important role in the activation and transformation of T cells and other biological processes in asthma. The specific mechanisms and clinical applications are worth further examination. This article reviews the recent research on the role of microRNAs, long non-coding RNAs and circular RNAs in T cells in asthma.

Clinical manifestations and risk factors of coronary artery disease in patients with diabetes mellitus in western Siberia.

OBJECTIVE: To compare the prevalence of cardiovascular risk factors and clinical manifestations of coronary artery disease (CAD) between patients with type 2 diabetes mellitus (DM) and CAD who lived at northern latitudes vs. those who resided at southern latitudes in the Tyumen region, western Siberia. STUDY DESIGN: This retrospective study involved 382 patients with type 2 DM selected from 8,573 patients with angiographic CAD (>50% stenosis). Out of the total, 243 patients were permanent residents at the high latitudes of the Tyumen region ("northern patients"), and 139 patients were permanent residents in areas south of the Tyumen region ("southern patients"). RESULTS: On average, northern patients were younger than southern patients (53 vs. 57 years, respectively). The odds ratio (OR) for living in the north was 2.1 (95% CI 0.99-4.53) for obesity (BMI>or=30 kg/m2), 1.87 (95% CI 1.05-3.31) for smoking, 0.93 (95% CI 0.89-0.96) per 1 year increase in age, 0.84 (95% CI 0.76-0.94) per 1 mmol/L increase of fasting plasma glucose, and 1.15 (95% CI 1.04-1.28) per 1 mm increase of right ventricular end-diastolic diameter. The proportion of patients with 3 or more CAD risk factors was higher in the north. Most patients in both groups had a history of myocardial infarction, severe angina in class III/IV as defined by the Canadian Cardiovascular System (CCS), heart failure in class II/IV as defined by the New York Heart Association (NYHA) and hypertension. CONCLUSIONS: A north-south gradient was observed in cardiovascular risk factors among patients with DM and CAD in the Tyumen region. The clinical manifestations of CAD in DM patients at high latitudes were comparable with those of patients who reside south of the Tyumen region of western Siberia, despite the younger age of northern patients.

Asymmetric septal hypertrophy in patients with coronary artery disease.

AIMS: To assess the relationship between asymmetric septal hypertrophy (ASH) and manifestations of coronary artery disease (CAD). METHODS AND RESULTS: A total of 5128 consecutive patients with proven diagnosis of CAD were examined. There were 2469 patients with left ventricular (LV) hypertrophy (LVH) (48.2%), among whom 297 (5.8%) had ASH (echocardiographic ventricular septum thickness to LV posterior wall thickness ratio > or =1.3). There were more male patients with ASH than patients with symmetric LVH (SLVH). ASH patients were significantly older and more obese, more of them were in NYHA class III/IV compared with SLVH patients. The prevalence of prior myocardial infarction (MI), systemic hypertension, heart rhythm disorders were higher in patients with ASH compared with SLVH patients. The groups differed significantly in echocardiographic parameters: LV and right ventricular (RV) end-diastolic dimensions, LV ejection fraction, left atrial dimension, extent of LV wall motion abnormalities, wall motion score index, LV mass/body surface area, signs of prior MI, and frequency of moderate mitral regurgitation. The frequency of stenosis and more severe (>90% stenosis) lesion of right coronary artery (RCA) and left circumflex artery (LCA) were higher in patients with ASH. Multivariate analysis identified that heart rhythm disorder, LV and RV end-diastolic dimensions, aortic root diameter, impaired LV ejection fraction, echocardiographic signs of previous MI, LV mass, and severe lesions of RCA were independently associated with ASH. CONCLUSION: In patients with CAD, ASH is associated with significant atherosclerosis of RCA and LCA, and more severe clinical manifestations of CAD and impaired LV function.

Characterization of the mouse myeloid-associated differentiation marker (MYADM) gene: promoter analysis and protein localization.

Hematopoietic differentiation is a complex process involving many genes inducing functional changes and characteristics of different cell lineages. To understand this process, it is important to identify genes involved in lineage commitment and maturation of hematopoietic progenitor cells. Recently we isolated the novel gene MYADM which is strongly up-regulated as multipotent progenitor cells differentiate towards myeloid cells. Because it is not expressed in lymphocytes, understanding the transcriptional control of MYADM could further explain differences in gene expression between myeloid and lymphoid cells. To identify regulatory elements controlling its restricted expression, we have analyzed the 5'-flanking region of the MYADM gene. The proximal promoter was found to lack both TATA and CCAAT boxes, but contained several potential binding sites for both ubiquitous and myeloid-specific transcription factors. Maximal promoter activity was contained within 800 bp from the tentative transcription initiation site, which was reduced as portions of the 5'-end were deleted, and completely abolished when the transcription initiation site was deleted. This promoter sequence had higher activity in myeloid cells compared to B cells, and activity was enhanced during myeloid differentiation, suggesting that we have identified the MYADM core promoter. Computer predictions had suggested MYADM to encode a protein with multiple transmembrane domains. By immunofluorescence and confocal microscopy we demonstrate that the protein is localized to the nuclear envelope and to intracytoplasmic membranes, indicating that MYADM constitutes an integral membrane protein.