Genomics and proteomics can complement each other in clinical app

Genomics and proteomics can complement each other in clinical applications by balancing the strengths and weaknesses of each individual technology. Several proteomics approaches have been exploited to shed more light on the molecular pathophysiology of several hereditary tubular disorders, such as Fanconi

and Gitelman syndromes, and have provided important insights into the defective molecular mechanisms underlying these tubulopathies. Here we summarize several of the most important discoveries arising from molecular genetic and proteomic studies on hereditary tubular dysfunctions and show how these results can complement each other to increase our comprehension of these disorders at the molecular level.”
“Opioids are widely used for their analgesic properties for the AZD9291 mw management of acute and chronic pain related to a variety of illnesses. Opioid usage is associated with adverse effects on respiration which are often attributed

to depression of the central nervous system. Recent data indicate that opioid use has increased over the last two decades. There is also increasing evidence that opioids have a variety of effects on the lungs besides suppression of respiration. Opioids can affect immune cells function, increase histamine release GNS-1480 causing bronchospasm, vaso-constriction and hypersensitivity reactions. Together, these actions have a variety of effects on lung function. Here, we provide a comprehensive review of the effects of opioids on the lungs including the respiratory centre, immune function, airways and pulmonary vasculature.”
“The formation of various types of kidney stones is strongly influenced by urinary pH. An alkaline pH favors the crystallization of calcium- and phosphate-containing stones, whereas and acidic urine pH promotes uric acid or cystine stones. The activity of many transport processes involved in calcium, citrate and phosphate

handling are sensitive to changes in systemic or local pH as shown for several phosphate transporters, the citrate transporter NaDC1 and the TRPV5 calcium channel. Defects in urinary acidification NVP-BSK805 (excretion of inappropriately alkaline or acidic urines, respectively) contribute to kidney stone disease. The low excretion of ammonium in patients with metabolic syndrome has been linked to more acidic urine and a higher incidence of uric acid stones. In this state, insulin resistance may reduce ammonium excretion by the proximal tubule. On the other hand, defensive mechanisms may protect from kidney stone formation in conditions such as hypercalciuria where high luminal calcium concentrations stimulate urinary acidification and reduce urinary concentration via a calcium-sensing receptor, resulting in the excretion of acidic and diluted urine.

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