64 research outputs found

    Six Sigma in Human Resource Management of Selected Organisation in Bangalore

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    The aim of the study is to examine the six sigma practices and its impact on strategic decision. Six sigma as a business process is now allowing organizations to improve their bottom line by designing and monitoring business activities in a way that minimizes wastes and resources without, however, compromising with customer satisfaction. Most of the companies attempted to implement this methodology and got backward from attempt in middle of the process or beginning due to the challenges in implementing Six Sigma in HRM. Measurability of a process depends on the perception of an individual HR person. HR is that it is not considered as a major line function in many organizations. This is mainly due to the non-measurable nature of HR processes, Most of the organizations not considered Human resources as human capital. HR must ensure that there’s good return on investment in human capital’. This paper made an attempt to frame a Five C’s concept for easy and better implementing of Six Sigma in HRM by putting the outcome of discussion with five black belt experts, who worked on six sigma projects as the tools to successful implementation of six sigma methodologies in HR functions. Research on significance of Six Sigma and implementing of Six Sigma in HR functions abounds in the literature. The paper shall review the opportunity and challenges in implementing Six Sigma in HRM

    Relation of COVID-19 with acute ischemic bowel disease: A retrospective observational study

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    Introduction: COVID-19 is a serious respiratory disease caused by SARS-CoV-2, aside from the respiratory system, the gastrointestinal system is the most common site of SARS-COV-2 infection. The study aimed to assess relation between COVID and ischemic bowel disease by analysing length of hospital stay and mortality rates between COVID and non-COVID groups. Methods: The study was conducted from June 2020 to November 2021 in the surgical wards of Seth GS Medical College and KEM Hospital, Mumbai. Included patients presented to emergency room with acute abdomen which diagnosed as acute ischemic bowel disease during the period of study and then compared the outcomes between COVID and non-COVID groups. Results: Out of 40 patients, 16 had no history of COVID and remaining 24 had either previous history of COVID or diagnosed presently with COVID. In both COVID and non-COVID population, distribution of comorbidities were almost equal exception being stroke, where both the cases had previous history of COVID, diabetes was the most common comorbidity in both the groups followed by hypertension. Patients with active COVID infection had higher mortality of 75% (3 out of 4) followed by patients with past history of infection with mortality rate of 65% (13 out of 20) whereas the mortality rate in non-COVID patients were 37.5% (6 out of 16). Conclusion: Ischemic bowel disease among COVID-19 patients is rare, but its association with high mortality rates and prolonged length of stay necessitates clinical suspicion and prompt intervention

    Macrophages Facilitate Resistance to Anti-VEGF Therapy by Altered VEGFR Expression

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    Abstract Purpose: VEGF-targeted therapies have modest efficacy in cancerpatients, butacquiredresistance iscommon. Themechanisms underlying such resistance are poorly understood. Experimental Design: To evaluate the potential role of immune cells in the development of resistance to VEGF blockade, we first established a preclinical model of adaptive resistance to anti-VEGF therapy. Additional in vitro and in vivo studies were carried out to characterize the role of macrophages in such resistance. Results: Using murine cancer models of adaptive resistance to anti-VEGF antibody (AVA), we found a previously unrecognized roleofmacrophagesinsuchresistance.Macrophageswereactively recruited to the tumor microenvironment and were responsible for the emergence of AVA resistance. Depletion of macrophages following emergence of resistance halted tumor growth and prolonged survival of tumor-bearing mice. In a macrophagedeficient mouse model, resistance to AVA failed to develop, but could be induced by injection of macrophages. Downregulation of macrophage VEGFR-1 and VEGFR-3 expression accompanied upregulation of alternative angiogenic pathways, facilitating escape from anti-VEGF therapy. Conclusions: These findings provide a new understanding of the mechanisms underlying the modest efficacy of current antiangiogenesis therapies and identify new opportunities for combinationapproachesforovarianandothercancers. ClinCancerRes; 23(22); 7034–46. �2017 AACR

    Hematogenous Metastasis of Ovarian Cancer: Rethinking Mode of Spread

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    SummaryOvarian cancer has a clear predilection for metastasis to the omentum, but the underlying mechanisms involved in ovarian cancer spread are not well understood. Here, we used a parabiosis model that demonstrates preferential hematogenous metastasis of ovarian cancer to the omentum. Our studies revealed that the ErbB3-neuregulin 1 (NRG1) axis is a dominant pathway responsible for hematogenous omental metastasis. Elevated levels of ErbB3 in ovarian cancer cells and NRG1 in the omentum allowed for tumor cell localization and growth in the omentum. Depletion of ErbB3 in ovarian cancer impaired omental metastasis. Our results highlight hematogenous metastasis as an important mode of ovarian cancer metastasis. These findings have implications for designing alternative strategies aimed at preventing and treating ovarian cancer metastasis

    2′-OMe-phosphorodithioate-modified siRNAs show increased loading into the RISC complex and enhanced anti-tumour activity

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    Improving small interfering RNA (siRNA) efficacy in target cell populations remains a challenge to its clinical implementation. Here, we report a chemical modification, consisting of phosphorodithioate (PS2) and 2′-O-Methyl (2′-OMe) MePS2 on one nucleotide that significantly enhances potency and resistance to degradation for various siRNAs. We find enhanced potency stems from an unforeseen increase in siRNA loading to the RNA-induced silencing complex, likely due to the unique interaction mediated by 2′-OMe and PS2. We demonstrate the therapeutic utility of MePS2 siRNAs in chemoresistant ovarian cancer mouse models via targeting GRAM domain containing 1B (GRAMD1B), a protein involved in chemoresistance. GRAMD1B silencing is achieved in tumours following MePS2-modified siRNA treatment, leading to a synergistic anti-tumour effect in combination with paclitaxel. Given the previously limited success in enhancing siRNA potency with chemically modified siRNAs, our findings represent an important advance in siRNA design with the potential for application in numerous cancer types

    Erythropoietin Stimulates Tumor Growth via EphB4

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    While recombinant human erythropoietin (rhEpo) has been widely used to treat anemia in cancer patients, concerns about its adverse effects on patient survival have emerged. A lack of correlation between expression of the canonical EpoR and rhEpo’s effects on cancer cells prompted us to consider the existence of an alternative Epo receptor. Here, we identified EphB4 as an Epo receptor that triggers downstream signaling via STAT3 and promotes rhEpo induced tumor growth and progression. In human ovarian and breast cancer samples, expression of EphB4 rather than the canonical EpoR correlated with decreased disease-specific survival in rhEpo-treated patients. These results identify EphB4 as a critical mediator of erythropoietin-induced tumor progression and further provide clinically significant dimension to the biology of erythropoietin

    Investigation of in vitro and in vivo antioxidant potential of secoisolariciresinol diglucoside

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    The present study was designed to evaluate the in vitro and in vivo ameliorative antioxidant potential of secoisolariciresinol diglucoside (SDG). In vitro antioxidant activity of synthetic SDG was carried out using DPPH, reducing power potency, and DNA protection assays. Wistar albino rats weighing 180-220 g were used for in vivo studies and liver damage was induced in the experimental animals by a single intraperitoneal (I.P.) injection of CCl 4 (2 g/kg b.w.). Intoxicated animals were treated orally with synthetic SDG at (12.5 and 25 mg/kg b.w.) and Silymarin (25 mg/kg) for 14 consecutive days. The levels of catalase (CAT), superoxide dismutase (SOD), peroxidase (POX), and lipid peroxidase (LPO) were measured in liver and kidney homogenates. The synthetic SDG exerts high in vitro antioxidant potency as it could scavenge DPPH at a IC50 value of 78.9 μg/ml and has dose-dependent reducing power potency and protected DNA at 0.5 mg/ml concentration. Oral administration of synthetic SDG at 12.5 and 25 mg/kg b.w. showed significant protection compared to Silymarin (25 mg/kg) and the activities of CAT, SOD, and POX were markedly increased (P < 0.05), whereas LPO significantly decreased (P < 0.001) in a dose-dependent manner in liver and kidney in both pre- and post-treatment groups when compared to toxin-treated group. The results of in vitro and in vivo investigations revealed that synthetic SDG at 25 mg/kg b.w. is associated with beneficial changes in hepatic enzyme activities and thereby plays a key role in the prevention of oxidative damage in immunologic system

    Antidiabetic effect of secoisolariciresinol diglucoside in streptozotocin-induced diabetic rats

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    Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycaemia. Its complications such as neuropathy, cardiopathy, nephropathy, and micro and macro vascular diseases are believed to be due to the increase in oxidative stress and decrease in the level of antioxidants. The aim of this study was to determine the antihyperglycemic activity of synthetic Secoisolariciresinol diglucoside (SDG) in streptozotocin (STZ)-induced diabetic rats. The synthetic SDG in a single-dose (20 mg/kg b.w.) two-day study showed dose-dependent reduction in glucose levels with maximum effect of 64.62% at 48 h post drug treatment (p \textless 0.05), which is comparable to that of the standard drug tolbutamide (20 mg/kg b.w.). In a multi-dose fourteen-day study, lower doses of SDG (5 and 10 mg/kg b.w.) exhibited moderate reduction in glucose levels, lipid profile, restoration of antioxidant enzymes and improvement of the insulin and c-peptide levels which shows the regeneration of β-cell which secretes insulin. Altered levels of lipids and enzymatic antioxidants were also restored by the SDG to the considerable levels in diabetic rats. Results of the present investigation suggest that diabetes is associated with an increase in oxidative stress as shown by increase in serum malondialdehyde (MDA), decreased levels of catalase (CAT), superoxide dismutase (SOD), and glutathione (GSH). Also, diabetes is associated with an increase in serum total cholesterol as well as triglycerides levels and decrease in insulin and c-peptide levels. SDG is effective in retarding the development of diabetic complications. We propose that synthetic SDG exerts anti hyperglycemic effect by preventing the liver from peroxidation damage through inhibition of ROS level mediated increased level of enzymatic and non-enzymatic antioxidants. And, also maintaining tissue function which results in improving the sensitivity and response of target cells in STZ-induced diabetic rats to insulin

    Evidence for presence of Zn<SUP>+2</SUP>-binding site in acetylcholinesterase

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    The purified electric eel acetylcholinesterase (AChE) was able to bind to the Zn<SUP>+2</SUP>-chelate-Sepharose affinity column only on treatment with EDTA. However goat brain and cobra venom AChE were binding to the column even without EDTA treatment. But all these enzymes were eluted from Zn<SUP>+2</SUP>-chelate-Sepharose affinity column by EDTA. Modification of histidine residues of AChEs by diethylpyrocarbonate resulted in abolition of its binding to Zn<SUP>+2</SUP>-chelate-Sepharose affinity column. Further the thermal stability of such EDTA-treated enzymes was decreased at 37 &#176;C. Dot-blot studies involving <SUP>65</SUP>Zn<SUP>+2</SUP> further demonstrated the zinc binding property of AChE proteins. These results confirm the presence of Zn<SUP>+2</SUP>-binding site on AChE and further removal of metal from binding site with chelators resulted in loss of its catalytic function. Presence of metal-binding sequences HXXE...H in AChE, similar to many other metal containing enzymes supports our findings
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