SARS-CoV-2 genomics: An Indian perspective on sequencing viral variants.

Since its emergence as a pneumonia-like outbreak in the Chinese city of Wuhan in late 2019, the novel coronavirus disease COVID-19 has spread widely to become a global pandemic. The first case of COVID-19 in India was reported on 30 January 2020 and since then it has affected more than ten million people and resulted in around 150,000 deaths in the country. Over time, the viral genome has accumulated mutations as it passes through its human hosts, a common evolutionary mechanism found in all microorganisms. This has implications for disease surveillance and management, vaccines and therapeutics, and the emergence of reinfections. Sequencing the viral genome can help monitor these changes and provides an extraordinary opportunity to understand the genetic epidemiology and evolution of the virus as well as tracking its spread in a population. Here we review the past year in the context of the phylogenetic analysis of variants isolated over the course of the pandemic in India and highlight the importance of continued sequencing-based surveillance in the country.

CoCl2 simulated hypoxia induce cell proliferation and alter the expression pattern of hypoxia associated genes involved in angiogenesis and apoptosis.

BACKGROUND/AIMS: Hypoxia microenvironment plays a crucial role during tumor progression and it tends to exhibit poor prognosis and make resistant to various conventional therapies. HIF-1α acts as an important transcriptional regulator directly or indirectly associated with genes involved in cell proliferation, angiogenesis, apoptosis and energy metabolism during tumor progression in hypoxic microenvironment. This study was aimed to investigate the expression pattern of the hypoxia associated genes and their association during breast cancer progression under hypoxic microenvironment in breast cancer cells. METHODS: Cell proliferation in MCF-7 and MDA-MB-231 cell lines treated with different concentration of CoCl2 was analyzed by MTT assay. Flow cytometry was performed to check cell cycle distribution, whereas cell morphology was examined by phase contrast microscopy in both the cells during hypoxia induction. Expression of hypoxia associated genes HIF-1α, VEGF, p53 and BAX were determined by semiquantitative RT-PCR and real-time PCR. Western blotting was performed to detect the expression at protein level. RESULTS: Our study revealed that cell proliferation in CoCl2 treated breast cancer cells were concentration dependent and varies with different cell types, further increase in CoCl2 concentration leads to apoptotic cell death. Further, accumulation of p53 protein in response to hypoxia as compare to normoxia showed that induction of p53 in breast cancer cells is HIF-1α dependent. HIF-1α dependent BAX expression during hypoxia revealed that after certain extent of hypoxia induction, over expression of BAX conquers the effect of anti-apoptotic proteins and ultimately leads to apoptosis in breast cancer cells. CONCLUSION: In conclusion our results clearly indicate that CoCl2 simulated hypoxia induce the accumulation of HIF-1α protein and alter the expression of hypoxia associated genes involved in angiogenesis and apoptosis.

CoCl2 simulated hypoxia induce cell proliferation and alter the expression pattern of hypoxia associated genes involved in angiogenesis and apoptosis

BACKGROUND/AIMS: Hypoxia microenvironment plays a crucial role during tumor progression and it tends to exhibit poor prognosis and make resistant to various conventional therapies. HIF-1α acts as an important transcriptional regulator directly or indirectly associated with genes involved in cell proliferation, angiogenesis, apoptosis and energy metabolism during tumor progression in hypoxic microenvironment. This study was aimed to investigate the expression pattern of the hypoxia associated genes and their association during breast cancer progression under hypoxic microenvironment in breast cancer cells. METHODS: Cell proliferation in MCF-7 and MDA-MB-231 cell lines treated with different concentration of CoCl2 was analyzed by MTT assay. Flow cytometry was performed to check cell cycle distribution, whereas cell morphology was examined by phase contrast microscopy in both the cells during hypoxia induction. Expression of hypoxia associated genes HIF-1α, VEGF, p53 and BAX were determined by semiquantitative RT-PCR and real-time PCR. Western blotting was performed to detect the expression at protein level. RESULTS: Our study revealed that cell proliferation in CoCl2 treated breast cancer cells were concentration dependent and varies with different cell types, further increase in CoCl2 concentration leads to apoptotic cell death. Further, accumulation of p53 protein in response to hypoxia as compare to normoxia showed that induction of p53 in breast cancer cells is HIF-1α dependent. HIF-1α dependent BAX expression during hypoxia revealed that after certain extent of hypoxia induction, over expression of BAX conquers the effect of anti-apoptotic proteins and ultimately leads to apoptosis in breast cancer cells. CONCLUSION: In conclusion our results clearly indicate that CoCl2 simulated hypoxia induce the accumulation of HIF-1α protein and alter the expression of hypoxia associated genes involved in angiogenesis and apoptosis.

Cardioprotective effect of Bombax ceiba flowers against acute adriamycin-induced myocardial infarction in rats

The present study was designed to evaluate the cardioprotective potential of aqueous flower extract of Bombax ceiba L., Malvaceae (BC), on the basis of biochemical and histopathological parameters in Adriamycin (Adr) induced myocardial infarction in rats and to compare with vitamin E, a known cardioprotective antioxidant. Male Wister rats were used as in vivo model for the study. BC was administered orally to Wister rats at different doses (150 mg/kg, 300 mg/kg and 450 mg/kg, b.w.) for six days/week for four weeks. Thereafter, all the groups except saline were administered Adr (20 mg/kg, i.p.). There was a significant decrease in myocardial superoxide dismutase, catalase and reduced glutathione in animals treated with Adr. Concurrently marked increase in extent of lipid peroxidation was reported. Co-treatment of BC/vitamin E and Adr resulted in an increase in the cardiac antioxidant enzymes and reduction in lipid peroxidation as compared to Adr-treated animals. Adr showed significant decrease (p<0.001) in the level of cardiac marker enzymes [Lactate dehydrogenase (LDH) and Serum glutamic oxaloacetic transaminase (SGOT)] in heart homogenate with corresponding increase in their level in serum. In BC/vitamin E treated groups significant increase (p<0.001) of LDH in heart homogenate and decrease of SGOT and LDH in serum were observed. Microscopic studies in Adr-treated animals revealed mitochondrial swelling, leukocyte infiltration, lipid inclusions and myofibrillar loss whereas the pre-treatment with BC/vitamin E led to a lesser degree of Adr-induced histological alterations. These findings suggest that aqueous flower extract of BC has protective effect against Adr-induced cardiotoxicity and may have potential as a cardioprotective agent.