The present study embodies a detailed investigation of the binding modes of a potential anticancer and neuroprotective fluorescent drug, 2-(5-selenocyanato-pentyl)-6-chloro benzo[de]isoquinoline-1,3-dione (NPOS) with calf thymus DNA (ctDNA). Experimental results based on spectroscopy, isothermal calorimetry, electrochemistry aided with DNA-melting, and circular dichroism studies unambiguously established the formation of a groove binding network between the NPOS and ctDNA. Molecular docking analysis ascertained a hydrogen bonding mediated 'A-T rich region of B-DNA' as the preferential docking site for NPOS. The cellular uptake and binding of NPOS with DNA from "Ehrlich Ascites Carcinoma" cells confirmed its biocompatibility within tumor cells. Experimental and ex vivo cell imaging studies vividly signify the importance of NPOS as a potential prerequisite for its use in therapeutic purposes.

The intracellular parasite Cryptosporidium is responsible for severe diarrhea in immunocompromised persons in developing countries. Few studies on the characterization of the parasite in India are available. In this study, molecular characterization of the parasite from diarrheic children was carried out by PCR-restriction fragment length polymorphism analysis. At least three genotypes were identified. Out of 40 positive samples, 35 were positive for C. hominis, 4 were positive for C. parvum, and 1 was positive for C. felis. This study clearly suggests that cryptosporidiosis in this region is caused largely by anthroponotic transmission.

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The clinical use of multiple classes of cancer chemotherapeutics is limited by irreversible, dose-dependent, and sometimes life-threatening cardiotoxicity. Though distinct in their mechanisms of action, doxorubicin, paclitaxel, and 5-FU all induce rapid and robust upregulation of atypical G protein Gβ in the myocardium correlating with oxidative stress, myocyte apoptosis, and the accumulation of proinflammatory and profibrotic cytokines. In ventricular cardiac myocytes (VCM), Gβ deficiency provided substantial protection against the cytotoxic actions of chemotherapeutics, including reductions in oxidative stress and simultaneous attenuation of ROS-dependent activation of the ATM and CaMKII proapoptotic signaling cascades. In addition, Gβ loss allowed for maintenance of Δψ, basal mitochondrial calcium uniporter expression, and mitochondrial Ca levels, effects likely to preserve functional myocyte excitation-contraction coupling. The deleterious effects of Gβ are not restricted to VCM, however, as Gβ knockdown also reduces chemotherapy-induced release of proinflammatory cytokines (e.g., TNFα), hypertrophic factors (e.g., ANP), and profibrotic factors (e.g., TGFβ1) from both VCM and ventricular cardiac fibroblasts, with the most dramatic reduction occurring in cocultured cells. Our experiments suggest that Gβ facilitates the myofibroblast transition, the persistence of which contributes to pathologic remodeling and heart failure. The convergence of Gβ-mediated, ROS-dependent signaling pathways in both cell types represents a critical etiological factor in the pathogenesis of chemotherapy-induced cardiotoxicity. Indeed, intracardiac injection of Gβ-targeted shRNA allowed for heart-specific protection against the damaging impact of chronic chemotherapy. Together, our results suggest that inhibition of Gβ might represent a novel means to circumvent cardiotoxicity in cancer patients whose treatment regimens include anthracyclines, taxanes, or fluoropyrimidines. These findings suggest that inhibiting an atypical G-protein might provide a strategy to limit the cardiotoxicity in cancer patients treated with anthracyclines, taxanes, or fluoropyrimidines. .