Tenofovir Induced Hypokalaemia - A case report

Tenofovir, an important medication for HIV/AIDS, carries the risk of hypokalemia in patients receiving treatment. Factors such as dietary deficits, vomiting, or diarrhea further increase this risk. Tenofovir acts as a mitochondrial toxin by inhibiting the DNA polymerase gamma enzyme, crucial for mitochondrial DNA replication. Consequently, ATP generation is depleted through the aerobic pathway, leading to dysfunction in the proximal tubule. This dysfunction manifests as renal acidosis type 2, which involves reduced bicarbonate excretion by the proximal tubule, resulting in renal bicarbonate wasting and decreased serum bicarbonate levels. Consequently, the lumen of the distal nephron becomes negatively charged, leading to compensatory potassium secretion and ultimately causing severe hypokalemia. Understanding the mechanisms underlying tenofovir-induced hypokalemia is crucial for healthcare providers to monitor and manage electrolyte imbalances in patients undergoing tenofovir treatment

Treatment outcome of tubercular lymphadenopathy cases treated under dots: a five year follow up study

Background: Treatment of tubercular lymphadenopathy consists of at least 6 months of therapy with antitubercular drugs as DOTS in India. Some studies recommend that extension of therapy for some time may lead to lesser recurrence and relapse. This study was planned to assess the outcome of DOTS therapy in lymph node tuberculosis (TB) cases treated under RNTCP and to find out the prevalence of relapse in these patients in southern Rajasthan.Methods: This was a retrospective analysis of 275 cases of lymph node tuberculosis treated with DOTS under RNTCP. An immediate outcome of these cases was recorded and further traceable 81 patients were interviewed for long term outcome.Results: In our study population, treatment completion rate was 93.09%, defaulter rate was 4% and death reported in 3.7% (3/81) cases. We observed relapse rate of 9.1% after treatment completion. A total of 7.04% patients received extended treatment and none of them had relapsed during our follow up.Conclusions: Our study confirms that the efficacy of DOTS treatment is quite good in cases of tubercular lymphadenopathy but still requires review of programmatic strategy. An extension of antitubercular therapy is recommended because patients treated with DOTS had a little higher relapse rate in comparison to whom the treatment extended who had no recurrence and relapse

10,21-Dimethyl-2,7,13,18-tetraphenyl-3,6,14,17-tetraazatricyclo[17.3.1.18,12]tetracosa-1(23),2,6,8(24),9,11,13,17,19,21-decaene-23,24-diol cyclohexane 0.33-solvate

The title compound, C46H40N4O2·0.33C6H12, was obtained unintentionally as a product of an attempted synthesis of a cadmium(II) complex of the [2,6-{PhSe(CH2)2N=CPh}2C6H2(4-Me)(OH)] ligand. The full tetra­imino­diphenol macrocyclic ligand is generated by the application of an inversion centre. The macrocyclic ligand features strong intra­molecular O—H⋯N hydrogen bonds. The dihedral angles formed between the phenyl ring incorporated within the macrocycle and the peripheral phenyl rings are 82.99 (8) and 88.20 (8)°. The cyclo­hexane solvent mol­ecule lies about a site of symmetry. Other solvent within the lattice was disordered and was treated with the SQUEEZE routine [Spek (2009). Acta Cryst. D65, 148–155]

M1 muscarinic receptor is a key target of neuroprotection, neuroregeneration and memory recovery by i-Extract from Withania somnifera

Memory loss is one of the most tragic symptoms of Alzheimer's disease. Our laboratory has recently demonstrated that 'i-Extract' of Ashwagandha (Withania somnifera) restores memory loss in scopolamine (SC)-induced mice. The prime target of i-Extract is obscure. We hypothesize that i-Extract may primarily target muscarinic subtype acetylcholine receptors that regulate memory processes. The present study elucidates key target(s) of i-Extract via cellular, biochemical, and molecular techniques in a relevant amnesia mouse model and primary hippocampal neuronal cultures. Wild type Swiss albino mice were fed i-Extract, and hippocampal cells from naïve mice were treated with i-Extract, followed by muscarinic antagonist (dicyclomine) and agonist (pilocarpine) treatments. We measured dendritic formation and growth by immunocytochemistry, kallikrein 8 (KLK8) mRNA by reverse transcription polymerase chain reaction (RT-PCR), and levels of KLK8 and microtubule-associated protein 2, c isoform (MAP2c) proteins by western blotting. We performed muscarinic receptor radioligand binding. i-Extract stimulated an increase in dendrite growth markers, KLK8 and MAP2. Scopolamine-mediated reduction was significantly reversed by i-Extract in mouse cerebral cortex and hippocampus. Our study identified muscarinic receptor as a key target of i-Extract, providing mechanistic evidence for its clinical application in neurodegenerative cognitive disorders

Impact of Excellence Model Awards on Stock Market Performance -A Study of Selected Indian Companies

Abstract: Busines