Hypokalemic paralysis is an important and reversible cause of acute flaccid paralysis. The treating physician faces unique diagnostic and therapeutic challenges. We did a prospective study and included all patients with acute flaccid weakness and documented serum potassium of <3.5 mEq/L during the period between January 2009 and August 2015. We studied the incidence, etiology, clinical profile, and acid–base disturbances in patients presenting with hypokalemic paralysis and analyzed the significance of periodic and non-periodic forms of hypokalemic paralysis on patient's outcome. Two hundred and six patients were studied with a mean follow-up of 3.6 ± 1.2 years. Mean age was 37.61 ± 2.2 years (range 18–50 years). Males were predominant (M:F ratio 2.1:1). The nonperiodic form of hypokalemic paralysis was the most common (61%). Eighty-one (39%) patients had metabolic acidosis, 78 (38%) had normal acid–base status, and 47 (23%) patients had metabolic alkalosis. The most common secondary cause was distal renal tubular acidosis (RTA) (n = 75, 36%), followed by Gitelman syndrome (n = 39, 18%), thyrotoxic paralysis (n = 8, 4%), hyperaldosteronism (n = 7, 3%), and proximal RTA (n = 6, 4%). Patients with non-periodic paralysis had more urinary loss (40.1 vs. 12.2 mmol, P = 0.04), more requirement of potassium replacement (120 vs. 48 mmol, P = 0.05), and longer recovery time of weakness (48.1 vs. 16.5 h, P = 0.05) than patients with periodic paralysis. Non-periodic form of hypokalemic paralysis was the most common variant in our study. Patients with periodic paralysis had significant incidence of rebound hyperkalemia.

Leelamine (LEE) has recently attracted significant attention for its growth inhibitory effects against melanoma, breast cancer, and prostate cancer cells; however, its impact on hematological malignancies remains unclear. Here, we first investigate the cytotoxic effects of LEE on several human chronic myeloid leukemia (CML) cells. We noted that LEE stimulated both apoptosis and autophagy in CML cells. In addition, the constitutive activation of signal transducer and activator of transcription 5 (STAT5) was suppressed substantially upon LEE treatment. Moreover, STAT5 knockdown with small interfering RNA (siRNA) increased LEE-induced apoptosis as well as autophagy and affected the levels of various oncogenic proteins. Thus, the targeted mitigation of STAT5 activation by LEE can contribute to its diverse anticancer effects by enhancing two distinct cell death pathways.

Objectives: The current research explores the anticancer effects of pH sensitive CVC-ZnO QDs (Carvacrol-loaded Zinc Oxide Quantum Dots) on DMBA induced mammary carcinoma in rats. Methods: Female SD rats were used, and mammary cancer was induced by chemical carcinogen via subcutaneous injection near the mammary gland. Different concentrations of CVC-ZnO QDs were orally supplemented to evaluate the optimum dose. We assessed the growth rate, body weight changes, tumor volume, tumor incidence and tumor burden in both the inducer and treatment groups. We also evaluated the biochemical parameters (antioxidant status, lipid peroxidation, detoxification enzymes, and lipid profile) and histopathological changes in the kidney and mammary tissues. Results: Our findings indicate that CVC-ZnO QDs treated rats significantly decreased the tumor weight, incidence, burden, lipid peroxidation levels, phase I detoxification enzyme activities and increased the body weight, phase II detoxification enzyme activities, and antioxidant status compared to the DMBA alone treated rats. CVC-ZnO QDs treatment also altered the lipid profile of plasma and mammary tissue. Furthermore, histopathological results confirmed that the CVC-ZnO QDs protect against DMBA-mediated damage to the mammary and kidney. Conclusion: The findings indicate that the CVC-ZnO QDs administered at 4 mg/kg b.w exhibited a significant anticancer effect against DMBA-induced mammary cancer.

Background and Objectives: Hereditary hearing loss is the most common genetic disorder in children. Nearly 120 genes associated with auditory impairment have been identified. Although the disease is clinically and genetically complex, the chances of identifying deafness-causing loci increase when studying consanguineous families.Materials and Methods: Whole-exome sequencing was performed to identify genetic variants underlying sensorineural hearing loss in affected individuals from a family with third-degree consanguineous practices.Results: A homozygous deletion of 250.285 kb was identified in the 16p12.2 region encompassing three genes, METTL9, IGSF6, and OTOA, and a partial deletion of the NPIPB4 gene co-segregated within the family.Conclusions: This study highlighted the genetic heterogeneity of hearing loss in consanguineous families. Future research should focus on the OTOA mutational spectrum in South Indian populations with hearing loss.