4 research outputs found

    Role of prophylactic midurethral sling in preventing post-operative stress urinary incontinence following repair of anterior vaginal wall prolapse

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    Objective: This study was conducted to find whether, among women without preoperative stress incontinence who underwent surgery for repair of anterior vaginal wall prolapse, the placement of a prophylactic midurethral mesh along with the prolapse correction surgery helped to reduce the incidence of post-operative stress urinary incontinence (POSUI). Materials & Methods: 145 women with anterior vaginal compartment prolapse were randomly assigned to receive either suitable corrective surgery for prolapse or corrective surgery along with concurrent placement of a prophylactic midurethral sling by a transobturator Prolene tape. The primary endpoint was urinary incontinence at three months and twelve months post surgery. Secondary outcomes included expected and unexpected adverse events. Results: At three months follow up the symptoms of urinary incontinence and/or positive cough test did not differ significantly between the two groups. But at twelve months, both the symptoms of urinary incontinence (9.59% versus 23.61%, p = 0.025, 95% CI = -25.93% to -2.11%, CMLE OR =0.346) and positive cough test (8.22% versus 25%, p = 0.007, 95% CI = -28.60% to -4.96%, CMLE OR = 0.271) were significantly lower in the study group compared to the control group. Expected and unexpected adverse events during operation and through the first year after surgery were comparable in both groups Conclusion: Placement of a midurethral sling by a Prolene mesh at the time of prolapse repair surgery significantly reduces the incidence of POSUI in women who were continent preoperatively. For this, the transobturator tape method is safe and effective with a low rate of complications

    An inventory model to study the effect of the probabilistic rate of carbon emission on the profit earned by a supplier

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    Sensitivity analysis of parameters is usually more important than the optimal solution when it comes to linear programming. Nevertheless, in the analysis of traditional sensitivities for a coefficient, a range of changes is found to maintain the optimal solution. These changes can be functional constraints in the coefficients, such as good values or technical coefficients, of the objective function. When real-world problems are highly inaccurate due to limited data and limited information, the method of grey systems is used to perform the needed optimisation. Several algorithms for solving grey linear programming have been developed to entertain involved inaccuracies in the model parameters; these methods are complex and require much computational time. In this paper, the sensitivity of a series of grey linear programming problems is analysed by using the definitions and operators of grey numbers. Also, uncertainties in parameters are preserved in the solutions obtained from the sensitivity analysis. To evaluate the efficiency and importance of the developed method, an applied numerical example is solved

    N-acetyl cysteine enhances imatinib-induced apoptosis of Bcr-Abl+ cells by endothelial nitric oxide synthase-mediated production of nitric oxide

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    Introduction Imatinib, a small-molecule inhibitor of the Bcr-Abl kinase, is a successful drug for treating chronic myeloid leukemia (CML). Bcr-Abl kinase stimulates the production of H2O2, which in turn activates Abl kinase. We therefore evaluated whether N-acetyl cysteine (NAC), a ROS scavenger improves imatinib efficacy. Materials and methods Effects of imatinib and NAC either alone or in combination were assessed on Bcr-Abl? cells to measure apoptosis. Role of nitric oxide (NO) in NAC-induced enhanced cytotoxicity was assessed using pharmacological inhibitors and siRNAs of nitric oxide synthase isoforms. We report that imatinib-induced apoptosis of imatinib-resistant and imatinib-sensitive Bcr-Abl? CML cell lines and primary cells from CML patients significantly enhanced by co-treatment with NAC compared to imatinib treatment alone. In contrast, another ROS scavenger glutathione reversed imatinib-mediated killing. NAC-mediated enhanced killing correlated with cleavage of caspases, PARP and up-regulation and down regulation of pro- and anti-apoptotic family of proteins, respectively. Co-treatment with NAC leads to enhanced production of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS). Involvement of eNOS dependent NO in NACmediated enhancement of imatinib-induced cell death was confirmed by nitric oxide synthase (NOS) specific pharmacological inhibitors and siRNAs. Indeed, NO donor sodium nitroprusside (SNP) also enhanced imatinib-mediated apoptosis of Bcr-Abl? cells. Conclusion NAC enhances imatinib-induced apoptosis of Bcr-Abl? cells by endothelial nitric oxide synthasemediated production of nitric oxide
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