23 research outputs found

    Synthesis, characterization and photocatalytic dye degradation studies of novel defect pyrochlore, KHf0.5Te1.5O6

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    We report the solid-state synthesis of KHf0.5Te1.5O6 (KHTO), its characterization and employment as photocatalyst for methylene blue and methyl violet degradations in aqueous solution. The material was subjected to X-ray Diffraction (XRD), Field emission-scanning electron microscopy (FE-SEM), Energy dispersive spectroscopy (EDS), Fourier transform infrared spectroscopy (FT-IR), UV-vis diffuse reflectance spectroscopy (UV-vis DRS), N2 adsorption/desorption and XPS measurements. The material was crystallized in a cubic lattice with the   space group. The bandgap energy of the KHTO is 2.60 eV. The photocatalytic methylene blue (MB) and methyl violet (MV) dyes degradation efficiency of KHTO was investigated under the visible light irradiation. The mechanistic dye degradation pathway of MB was studied. The radical quenching experiments reveal that the short-lived species O2●-, OH●, and h+ actively participate in the degradation of MV and MB dyes. An additional terephthalic acid experiment was carried out to establish the participation of OH● radicals in the dye degradation process. The stability and reusability of the KHTO catalyst were also studied

    Synthesis, characterization and photocatalytic dye degradation studies of novel defect pyrochlore, KHf0.5Te1.5O6

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    1092-1099In this study, KHf0.5Te1.5O6 (KHTO) semiconductor has been synthesized by the solid-state method. The synthesized material is characterized using X-ray diffraction, Fourier transform infrared spectroscopy, UV-visible diffuse reflectance spectroscopy, field emission-scanning electron microscopy, energy dispersive spectroscopy, X-ray photoelectron spectroscopy and N2 adsorption/desorption measurements. The material is found to be crystallized in a cubic lattice with the space group Fdm . The bandgap energy of the KHTO is 2.6 eV. The photocatalytic activity of KHTO has been investigated by measuring the degradation of methylene blue (MB) and methyl violet (MV) dyes under the visible light irradiation. The mechanistic dye degradation pathway of MB has been studied. The radical quenching experiments reveal that the short-lived species O2●-, OH●, and h+ actively participate in the degradation of MB and MV dyes. An additional terephthalic acid experiment has been carried out to establish the participation of OH● radicals in the dye degradation. The stability and reusability of the KHTO catalyst are also studied

    Predictors of mortality among hospitalized COVID-19 patients and risk score formulation for prioritizing tertiary care—An experience from South India

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    BACKGROUND: We retrospectively data-mined the case records of Reverse Transcription Polymerase Chain Reaction (RT-PCR) confirmed COVID-19 patients hospitalized to a tertiary care centre to derive mortality predictors and formulate a risk score, for prioritizing admission. METHODS AND FINDINGS: Data on clinical manifestations, comorbidities, vital signs, and basic lab investigations collected as part of routine medical management at admission to a COVID-19 tertiary care centre in Chengalpattu, South India between May and November 2020 were retrospectively analysed to ascertain predictors of mortality in the univariate analysis using their relative difference in distribution among ‘survivors’ and ‘non-survivors’. The regression coefficients of those factors remaining significant in the multivariable logistic regression were utilised for risk score formulation and validated in 1000 bootstrap datasets. Among 746 COVID-19 patients hospitalised [487 “survivors” and 259 “non-survivors” (deaths)], there was a slight male predilection [62.5%, (466/746)], with a higher mortality rate observed among 40–70 years age group [59.1%, (441/746)] and highest among diabetic patients with elevated urea levels [65.4% (68/104)]. The adjusted odds ratios of factors [OR (95% CI)] significant in the multivariable logistic regression were SaO(2)3; 3.01 (1.61–5.83), Age ≥50 years;2.52 (1.45–4.43), Pulse Rate ≥100/min: 2.02 (1.19–3.47) and coexisting Diabetes Mellitus; 1.73 (1.02–2.95) with hypertension and gender not retaining their significance. The individual risk scores for SaO(2)3–11, Age ≥50 years-9, Pulse Rate ≥100/min-7 and coexisting diabetes mellitus-6, acronymed collectively as ‘OUR-ARDs score’ showed that the sum of scores ≥ 25 predicted mortality with a sensitivity-90%, specificity-64% and AUC of 0.85. CONCLUSIONS: The ‘OUR ARDs’ risk score, derived from easily assessable factors predicting mortality, offered a tangible solution for prioritizing admission to COVID-19 tertiary care centre, that enhanced patient care but without unduly straining the health system

    Modeling, Analysis, and Implementation of High Voltage Low Power Flyback Converter Feeding Resistive Loads

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    An Energy-Based Analysis for High Voltage Low Power Flyback Converter Feeding Capacitive Load

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    Reprocessing of Contaminated MGIT 960 Cultures to Improve Availability of Valid Results for Mycobacteria

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    Optimal recovery of mycobacteria from the contaminated liquid culture is a challenge. While alternative methods have been suggested to reduce the rate of contamination in the BACTEC MGIT 960 system, reprocessing the contaminated liquid culture improves recovery of Mycobacterium tuberculosis. Among 793 MGIT cultures raised from as many sputum specimens after primary decontamination by the standard NaLC-NaOH method, valid results were available for 687 (86.6%) as 106 (13.4%) were contaminated. Reprocessing and reculturing of the contaminated cultures increased valid results to 739 (93.2%) and reduced the contamination rate to 6.8%. Both values were statistically significant. Recovery of the Mycobacterium tuberculosis complex increased from 45.6% to 48.4%. Valid negative results were available for an additional 3.4%. The method may be adopted to reduce the rate of contamination and to improve the valid culture results for mycobacteria

    Role of Microtubules in Osteogenic Differentiation of Mesenchymal Stem Cells on 3D Nanofibrous Scaffolds

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    Human bone marrow mesenchymal stem cells (MSCs) cultured on three-dimensional (3D) nanofibrous scaffolds are known to undergo osteogenic differentiation even in the absence of soluble osteoinductive factors. Although this process of differentiation has been attributed to the shape that cells assume on the fibrous scaffolds, it is unclear how constriction of cell shape would contribute to the differentiation phenotype. Here, we quantitatively compared cell and nuclear morphologies of cells cultured on 3D poly­(ε-caprolactone) (PCL) nanofibers (NF) and two-dimensional (2D) flat films using confocal fluorescence microscopy. We discovered that while cells on the 2D films exhibited cellular and nuclear morphologies similar to those cultured on tissue culture polystyrene, cells cultured on the 3D NF showed distinct cell and nuclear morphologies, with lower areas and perimeters, but higher aspect ratios. We next tested the effect of treatment of cells with actin-depolymerizing cytochalasin D and microtubule-depolymerizing nocodazole on these morphologies. In both 2D and 3D scaffolds, actin depolymerization brought about gross changes in cell and nuclear morphologies. Remarkably, microtubule depolymerization resulted in a phenotype similar to actin depolymerization in cells cultured on 3D NF alone, indicating a significant role for the microtubule cytoskeleton in the maintenance of cell shape and structure in 3D. The morphological changes of the nucleus that were apparent upon cytoskeletal perturbation were reflected in the organization of heterochromatin in the nucleus, with MSCs on 3D alone exhibiting a differentiation phenotype. Finally, we tested the effect of cytoskeletal depolymerization on mineralization of cells. Again, we observed higher mineralization in cells cultured on 3D NF, which was lost in cells treated with either cytochalasin D or nocodazole. Taken together, our results suggest that both the actin and microtubule cytoskeletons contribute significantly toward maintenance of cell and nuclear shape in cells cultured on 3D scaffolds, and consequently to their osteogenic differentiation

    Inflammation-induced PELP1 expression promotes tumorigenesis by activating GM-CSF paracrine secretion in the tumor microenvironment

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    The inflammatory tumor microenvironment has been implicated as a major player fueling tumor progression and an enabling characteristic of cancer, proline, glutamic acid, and leucine-rich protein 1 (PELP1) is a novel nuclear receptor coregulator that signals across diverse signaling networks, and its expression is altered in several cancers. However, investigations to find the role of PELP1 in inflammation-driven oncogenesis are limited. Molecular studies here, utilizing macrophage cell lines and animal models upon stimulation with lipopolysaccharide (LPS) or necrotic cells, showed that PELP1 is an inflammation-inducible gene. Studies on the PELP1 promoter and its mutant identified potential binding of c-Rel, an NF-κB transcription factor subunit, to PELP1 promoter upon LPS stimulation in macrophages. Recruitment of c-Rel onto the PELP1 promoter was validated by chromatin immunoprecipitation, further confirming LPS mediated PELP1 expression through c-Rel–specific transcriptional regulation. Macrophages that overexpress PELP1 induces granulocyte–macrophage colony-stimulating factor secretion, which mediates cancer progression in a paracrine manner. Results from preclinical studies with normal–inflammatory–tumor progression models demonstrated a progressive increase in the PELP1 expression, supporting this link between inflammation and cancer. In addition, animal studies demonstrated the connection of PELP1 in inflammation-directed cancer progression. Taken together, our findings provide the first report on c-Rel–specific transcriptional regulation of PELP1 in inflammation and possible granulocyte–macrophage colony-stimulating factor–mediated transformation potential of activated macrophages on epithelial cells in the inflammatory tumor microenvironment, reiterating the link between PELP1 and inflammation-induced oncogenesis. Understanding the regulatory mechanisms of PELP1 may help in designing better therapeutics to cure various inflammation-associated malignancies
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