Deletion of altered transcriptomic and metabolomic profiles of Dahl salt-sensitive rats.

The inwardly rectifying K channel K5.1 () is essential in renal salt handling and blood pressure control. However, the underlying mechanisms are not fully understood.

Effects of zinc in podocytes and cortical collecting duct in vitro and Dahl salt-sensitive rats in vivo.

Zinc is one of the essential divalent cations in the human body and a fundamental microelement involved in the regulation of many cellular and subcellular functions. Experimental studies reported that zinc deficiency is associated with renal damage and could increase blood pressure. It was proposed that zinc dietary supplementation plays a renoprotective role.

Small airways response to bronchodilators as the marker of the uncontrolled asthma in children.

Objective: Aim: To develop the criteria of small airways response to bronchodilators (by spirometry indices maximal expiratory flow (MEF50 and MEF25) as the markers of uncontrolled asthma course.

Patients And Methods: Materials and Methods: The study involved 92 participants (64 boys and 28 girls) aged 6 to 17 years (60 were less than 12 years old) with diagnosed asthma. Asthma control was assessed with the use of Asthma Control Test and Asthma Control Questionnaire.

The presence of xanthine dehydrogenase is crucial for the maturation of the rat kidneys.

The development of the kidney involves essential cellular processes, such as cell proliferation and differentiation, which are led by interactions between multiple signaling pathways. Xanthine dehydrogenase (XDH) catalyzes the reaction producing uric acid in the purine catabolism, which plays a multifaceted role in cellular metabolism. Our previous study revealed that the genetic ablation of the Xdh gene in rats leads to smaller kidneys, kidney damage, decline of renal functions, and failure to thrive.

Metabolic Communication by SGLT2 Inhibition.

Background: SGLT2 (sodium-glucose cotransporter 2) inhibitors (SGLT2i) can protect the kidneys and heart, but the underlying mechanism remains poorly understood.

Methods: To gain insights on primary effects of SGLT2i that are not confounded by pathophysiologic processes or are secondary to improvement by SGLT2i, we performed an in-depth proteomics, phosphoproteomics, and metabolomics analysis by integrating signatures from multiple metabolic organs and body fluids after 1 week of SGLT2i treatment of nondiabetic as well as diabetic mice with early and uncomplicated hyperglycemia.

Results: Kidneys of nondiabetic mice reacted most strongly to SGLT2i in terms of proteomic reconfiguration, including evidence for less early proximal tubule glucotoxicity and a broad downregulation of the apical uptake transport machinery (including sodium, glucose, urate, purine bases, and amino acids), supported by mouse and human SGLT2 interactome studies.