Publications by authors named "D K Sinha"

Background:  Acute kidney injury (AKI) and sepsis are well-recognized complications of steroid-responsive nephrotic syndrome. Systemic inflammatory response syndrome (SIRS) initiates inflammation and oxidative stress, which eventually results in septic acute kidney injury (SAKI). A few papers are available in the literature regarding the clinical profile of AKI in nephrotic syndrome; however, there are hardly any data on SAKI in steroid-responsive nephrotic syndrome.

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NEDD4-2 (human NEDD4L), a ubiquitin ligase, plays an essential role in regulating a number of membrane proteins, including ion channels and transporters. In the kidney, NEDD4-2 deletion results in a progressive loss of tubular cells and salt-sensitive chronic kidney disease. While deregulation of sodium homeostasis due to increased levels and function of the epithelial sodium channel (ENaC) and sodium chloride transporter (NCC), both NEDD4-2 substrates, plays a critical role in kidney damage in this model, other ubiquitination targets may also be important.

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Context: The increasing prevalence of antibiotic resistance and concerns regarding adverse drug reactions have prompted interest in natural alternatives for antimicrobial treatments, particularly in endodontics.

Aims: This study aimed to evaluate the antimicrobial effectiveness of mangosteen, chitosan, and their combination as intracanal medicaments against .

Settings And Design: A double-blind, randomized clinical trial was conducted involving 40 patients with single-rooted nonvital teeth ( = 10 per group).

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A dental implant is a surgical fixture that is placed into the jawbone and allowed to fuse with the bone over the span of a few months. It acts as an alternative for a lacking teeth.The implant surgical guide comprises a teeth formed contour which stimulates natural teeth and prosthesis.

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Premature termination codons (PTCs) are associated with rare genetic disorders. Inducing targeted read-through of these 'nonsense mutations' presents a potential therapeutic strategy for modifying disease outcomes. We previously reported that one such PTC, W53X, in the gene causes blindness and Leber congenital amaurosis type-16 (LCA-16) due to loss of function of the inwardly rectifying potassium channel 7.

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