Publications by authors named "Raja S Mahidhara"

Background: Esophageal stent placement for acute esophageal perforation has become part of the treatment algorithm for many thoracic surgery programs. Despite high success rates, there are patients for which stent placement is not successful. This investigation summarizes the outcomes of a relatively large group of such patients.

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Objectives: Palliative care is a medical specialty focused on improving the quality of life of patients and their families with life threatening illness by preventing or relieving suffering. An assessment of a thoracic surgery service was performed to identify the scope and frequency of care that was considered palliative and any implications the findings might have on the current thoracic surgery residency curriculum.

Methods: A retrospective review of a prospectively collected database of general thoracic surgery procedures performed over a 5-year period at a single institution was performed.

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Background: A prospective, multidisciplinary care conference (MDC) has been shown to result in measurable benefits for patients with non-small cell lung cancer (NSCLC). However whether a MDC also results in a difference in resource utilization and cost as well as whether these benefits persist across a multiinstitutional system has not been reported. This investigation compared propensity-matched patients with NSCLC whose care was coordinated through a MDC to patients without access to an MDC across a geographically diverse system of hospitals.

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Background: Esophageal stent for the treatment of a perforation or anastomotic leak has been shown to be effective and safe. However, the optimal timing for stent removal is in question. This purpose of this investigation was to identify a time for stent removal in patients treated for an acute perforation or anastomotic leak that resulted in sealing of the leak while minimizing the incidence of stent-related complications.

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Objectives: Esophageal stent placement has been shown to be a safe and effective treatment for acute esophageal perforation in selected patients. However, a comparison between surgical repair and stent placement has not been reported. This investigation compares the outcomes and costs of the 2 treatment modalities.

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Background: Patients with severe heart failure often have recurrent pleural effusions that produce dyspnea and shortness of breath. It is unclear whether chemical pleurodesis or the placement of a tunneled pleural catheter that can be used for intermittent pleural drainage produces superior palliation, a shorter hospital stay, and less morbidity. This investigation compares these two treatments.

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Background: Surgical repair of esophageal perforation has been the mainstay of therapy for patients without associated esophageal malignancy or diffuse mediastinal necrosis. However, the leak rate after primary surgical repair is reported to range between 15% and 20% and increases to 45% and 70% in patients whose repair is delayed beyond 24 hours. This analysis reviews patients who experienced a leak after the operative repair of an esophageal perforation treated with esophageal stent placement.

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Background: Readmission to the hospital has become a focus for payers with the threat of nonpayment for preventable readmissions and a global penalty for excessive readmissions rates. This study compares readmission rates with lengths of stay (LOS) for patients undergoing lobectomy of the lung and the potential impact on reimbursement.

Methods: The Premier database for a single health system's hospitals was used to identify patients undergoing lobectomy for non-small cell lung cancer by cardiothoracic surgeons over a 5-year period.

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Background: Patients with a suspected malignant pleural effusion occasionally require thoracoscopy to achieve a diagnosis. It is unclear whether chemical pleurodesis or the placement of a tunneled pleural catheter (TPC) that can be used for intermittent pleural drainage produces superior palliation, a shorter hospital stay, and less morbidity. This investigation compares these 2 treatment groups.

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We have shown that the ectopic expression of Interferon Regulatory Factor 1 (IRF-1) results in human cancer cell death accompanied by the down-regulation of the Inhibitor of Apoptosis Protein (IAP) survivin and the induction of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1). In this report, we investigated the direct role of p21 in the suppression of survivin. We show that IRF-1 down-regulates cyclin B1, cdc-2, cyclin E, E2F1, Cdk2, Cdk4, and results in p21-mediated G1 cell cycle arrest.

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Background: Decreased cell-surface expression of Fas (CD95) results in resistance to Fas-mediated apoptosis in esophageal adenocarcinoma (EA). Because p53 is known to increase transcription of Fas and also may induce trafficking of the protein to the plasma membrane, we investigated whether the loss of wild-type (wt)-p53 function accounts for our previous findings.

Materials And Methods: Surgical specimens of Barrett's Esophagus containing areas of dysplasia were immunostained for p53 and Fas protein expression.

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T lymphocyte activation and proliferation is involved in many pathological processes. We have recently shown that carbon monoxide (CO), an enzymatic product of heme oxygenase-1 (HO-1), confers potent antiproliferative effects in airway and vascular smooth muscle cells. The purpose of this study was to determine whether CO can inhibit T lymphocyte proliferation and then to determine the mechanism by which CO can modulate T lymphocyte proliferation.

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Purpose: Vascular injury and inflammation are associated with elaboration of a number of cytokines that signal through multiple pathways to act as smooth muscle cell (SMC) mitogens. Activation of the nuclear factor-kappa B (NF-kappaB) transcription factor is essential for SMC proliferation in vitro and is activated by vascular injury in vivo. Activation of NF-kappaB is controlled by several upstream regulators, including the inhibitors of kappa B (IkappaB).

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Nitric oxide (NO), a pleiotropic signaling molecule produced at sites of inflammation, is a powerful inhibitor of lymphocyte proliferation. Caspases, central effector proteases in apoptosis, have recently been implicated as critical mediators of T cell activation. We and others have shown that NO can inhibit caspases by S-nitrosylation, which is reversible by the reducing agent dithiothreitol (DTT).

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The gaseous molecule carbon monoxide (CO) is elevated in the breath of individuals with asthma. The physiologic function of CO in asthma is poorly understood. Here we demonstrate that CO (250 ppm) markedly inhibits human airway smooth muscle cell (HASMC) proliferation, arresting cells at the G0/G1 phase.

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Background: On antigenic stimulation, CD4 T cells generally proliferate more readily than CD8 T cells. The purpose of the present experiments was to determine whether nitric oxide (NO) might differentially modulate CD4 vs. CD8 T-cell proliferation.

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