30 research outputs found

    Proanthocyanidin to prevent formation of the reexpansion pulmonary edema

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    <p>Abstract</p> <p>Background</p> <p>We aimed to investigate the preventive effect of Proanthocyanidine (PC) in the prevention of RPE formation.</p> <p>Methods</p> <p>Subjects were divided into four groups each containing 10 rats. In the Control Group (CG): RPE wasn't performed. Then subjects were followed up for three days and they were sacrificed after the follow up period. Samplings were made from tissues for measurement of biochemical and histopathologic parameters. In the Second Group (PCG): The same protocol as CG was applied, except the administration of PC to the subjects. In the third RPE Group (RPEG): Again the same protocol as CG was applied, but as a difference, RPE was performed. In the Treatment Group (TG): The same protocol as RPEG was applied except the administration of PC to the subjects.</p> <p>Results</p> <p>In RPEG group, the most important histopathological finding was severe pulmonary edema with alveolar damage and acute inflammatory cells. These findings were less in the TG group. RPE caused increased MDA levels, and decreased GPx, SOD and CAT activity significantly in lung tissue.</p> <p>Conclusion</p> <p>PC decreased MDA levels. Oxidative stress plays an important role in pathophysiology of RPE and PC treatment was shown to be useful to prevent formation of RPE.</p

    Protective efficiacy of taurine against pulmonary edema progression: experimental study

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    Re-expansion pulmonary edema (RPE) is an acute, rare and potentially lethal complication [1,2]. Its beginning is sudden and dramatic. The mechanism is not yet fully understood [1]. Some authors suggest that it may occur after rapid re-inflation of a collapsed lung [1]. It was reported by other authors that it may relate to surfactant depletion or may result from hypoxic capillary damage, leading to increased capillary permeability [1,3]. In RPE, unilateral lung injury is initiated by cytotoxic oxygen metabolites and temporally associated with an influx of polymorphonuclear neutrophils [1]. These toxic oxygen products are the results of re-oxygenation of a collapsed lung. Treatment of re-expansion pulmonary edema is basically preventive [4]

    Protective efficiacy of taurine against pulmonary edema progression: experimental study

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    Re-expansion pulmonary edema (RPE) is an acute, rare and potentially lethal complication [1,2]. Its beginning is sudden and dramatic. The mechanism is not yet fully understood [1]. Some authors suggest that it may occur after rapid re-inflation of a collapsed lung [1]. It was reported by other authors that it may relate to surfactant depletion or may result from hypoxic capillary damage, leading to increased capillary permeability [1,3]. In RPE, unilateral lung injury is initiated by cytotoxic oxygen metabolites and temporally associated with an influx of polymorphonuclear neutrophils [1]. These toxic oxygen products are the results of re-oxygenation of a collapsed lung. Treatment of re-expansion pulmonary edema is basically preventive [4]

    Epigenetic perturbations in the pathogenesis of mustard toxicity; hypothesis and preliminary results

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    Among the most readily available chemical warfare agents, sulfur mustard (SM), also known as mustard gas, has been the most widely used chemical weapon. SM causes debilitating effects that can leave an exposed individual incapacitated for days to months; therefore delayed SM toxicity is of much greater importance than its ability to cause lethality. Although not fully understood, acute toxicity of SM is related to reactive oxygen and nitrogen species, oxidative stress, DNA damage, poly(ADP-ribose) polymerase (PARP) activation and energy depletion within the affected cell. Therefore several antioxidants and PARP inhibitors show beneficial effects against acute SM toxicity. The delayed toxicity of SM however, currently has no clear mechanistic explanation. One third of the 100,000 Iranian casualties are still suffering from the detrimental effects of SM in spite of the extensive treatment. We, therefore, made an attempt whether epigenetic aberrations may contribute to pathogenesis of mustard poisoning. Preliminary evidence reveals that mechlorethamine (a nitrogen mustard derivative) exposure may not only cause oxidative stress, DNA damage, but epigenetic perturbations as well. Epigenetic refers to the study of changes that influence the phenotype without causing alteration of the genotype. It involves changes in the properties of a cell that are inherited but do not involve a change in DNA sequence. It is now known that in addition to mutations, epimutations contribute to a variety of human diseases. Under light of preliminary results, the current hypothesis will focus on epigenetic regulations to clarify mustard toxicity and the use of drugs to correct possible epigenetic defects

    Elective cancer surgery in COVID-19-free surgical pathways during the SARS-CoV-2 pandemic: An international, multicenter, comparative cohort study

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    PURPOSE As cancer surgery restarts after the first COVID-19 wave, health care providers urgently require data to determine where elective surgery is best performed. This study aimed to determine whether COVID-19–free surgical pathways were associated with lower postoperative pulmonary complication rates compared with hospitals with no defined pathway. PATIENTS AND METHODS This international, multicenter cohort study included patients who underwent elective surgery for 10 solid cancer types without preoperative suspicion of SARS-CoV-2. Participating hospitals included patients from local emergence of SARS-CoV-2 until April 19, 2020. At the time of surgery, hospitals were defined as having a COVID-19–free surgical pathway (complete segregation of the operating theater, critical care, and inpatient ward areas) or no defined pathway (incomplete or no segregation, areas shared with patients with COVID-19). The primary outcome was 30-day postoperative pulmonary complications (pneumonia, acute respiratory distress syndrome, unexpected ventilation). RESULTS Of 9,171 patients from 447 hospitals in 55 countries, 2,481 were operated on in COVID-19–free surgical pathways. Patients who underwent surgery within COVID-19–free surgical pathways were younger with fewer comorbidities than those in hospitals with no defined pathway but with similar proportions of major surgery. After adjustment, pulmonary complication rates were lower with COVID-19–free surgical pathways (2.2% v 4.9%; adjusted odds ratio [aOR], 0.62; 95% CI, 0.44 to 0.86). This was consistent in sensitivity analyses for low-risk patients (American Society of Anesthesiologists grade 1/2), propensity score–matched models, and patients with negative SARS-CoV-2 preoperative tests. The postoperative SARS-CoV-2 infection rate was also lower in COVID-19–free surgical pathways (2.1% v 3.6%; aOR, 0.53; 95% CI, 0.36 to 0.76). CONCLUSION Within available resources, dedicated COVID-19–free surgical pathways should be established to provide safe elective cancer surgery during current and before future SARS-CoV-2 outbreaks

    Elective Cancer Surgery in COVID-19-Free Surgical Pathways During the SARS-CoV-2 Pandemic: An International, Multicenter, Comparative Cohort Study.

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    PURPOSE: As cancer surgery restarts after the first COVID-19 wave, health care providers urgently require data to determine where elective surgery is best performed. This study aimed to determine whether COVID-19-free surgical pathways were associated with lower postoperative pulmonary complication rates compared with hospitals with no defined pathway. PATIENTS AND METHODS: This international, multicenter cohort study included patients who underwent elective surgery for 10 solid cancer types without preoperative suspicion of SARS-CoV-2. Participating hospitals included patients from local emergence of SARS-CoV-2 until April 19, 2020. At the time of surgery, hospitals were defined as having a COVID-19-free surgical pathway (complete segregation of the operating theater, critical care, and inpatient ward areas) or no defined pathway (incomplete or no segregation, areas shared with patients with COVID-19). The primary outcome was 30-day postoperative pulmonary complications (pneumonia, acute respiratory distress syndrome, unexpected ventilation). RESULTS: Of 9,171 patients from 447 hospitals in 55 countries, 2,481 were operated on in COVID-19-free surgical pathways. Patients who underwent surgery within COVID-19-free surgical pathways were younger with fewer comorbidities than those in hospitals with no defined pathway but with similar proportions of major surgery. After adjustment, pulmonary complication rates were lower with COVID-19-free surgical pathways (2.2% v 4.9%; adjusted odds ratio [aOR], 0.62; 95% CI, 0.44 to 0.86). This was consistent in sensitivity analyses for low-risk patients (American Society of Anesthesiologists grade 1/2), propensity score-matched models, and patients with negative SARS-CoV-2 preoperative tests. The postoperative SARS-CoV-2 infection rate was also lower in COVID-19-free surgical pathways (2.1% v 3.6%; aOR, 0.53; 95% CI, 0.36 to 0.76). CONCLUSION: Within available resources, dedicated COVID-19-free surgical pathways should be established to provide safe elective cancer surgery during current and before future SARS-CoV-2 outbreaks

    Panniculitis in juvenile dermatomyositis: Report of a case and review of the published work

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    We report a 15-year-old girl who presented with indurated, subcutaneous nodules in addition to classical findings of juvenile dermatomyositis. Histopathological examination confirmed the diagnosis of panniculitis associated with juvenile dermatomyositis. Considering that panniculitis is a rare cutaneous manifestation of juvenile dermatomyositis, we present a patient with a brief review of the published work to highlight the importance of keeping juvenile dermatomyositis in mind among the etiologies of pediatric panniculitis

    The diagnostic efficiency of whole-body bedside ultrasonography protocol for syncope patients in the emergency department

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    © 2023 Elsevier Inc.Background: The emergency physician should diagnose and treat the critical illnesses that cause syncope/presyncope in patients presenting to the emergency department (ED). Whole-body ultrasonography can detect the critical etiology of syncope with high diagnostic sensitivity. We aimed to reveal whether whole-body ultrasonography for syncope (WHOBUS-Syncope) protocol recognizes high-risk syncope patients and the effect of WHOBUS-Syncope protocol on the management of patients. Method: This is a prospective, cross-sectional study. Patients over the age of 18 years who presented to the ED with syncope or near syncope were included consecutively. Carotid, lung, cardiac, collapsibility of inferior vena cava, abdominal and compression ultrasonography of the lower extremity veins was performed among the WHOBUS-Syncope protocol. Frequency of abnormal sonographic findings associated with syncope/presyncope and requirement of critical intervention for abnormal sonographic findings were assessed. Results: 152 patients were included in the study. The median age of the patients was 61.5 years (IQR: 41–71.8) and 52.6% were female. The most common (64.3%) abnormal sonographic finding was >50% collapse of vena cava inferior during inspiration. In addition, abnormal sonographic findings thought to cause syncope/presyncope were detected in 35.5% of the patients. Bolus fluid resuscitation were given in in 62 patients (40.8%) with increased inferior vena cava collapse. Critical interventions other than fluid resuscitation were performed for abnormal sonographic findings in 35 (23%) of the patients. Advanced age, increased heart rate and the presence of high-risk criteria in the ‘European Society of Cardiology Guidelines for Syncope’ were independent risk factors for detection of abnormal ultrasonographic findings related to syncope/presyncope. Conclusion: WHOBUS-Syncope protocol can be included in emergency practice as part of the standard evaluation in patients with syncope or presyncope presenting to the ED

    Pulmonary hypertension in sickle-cell disease: Comorbidities and echocardiographic findings

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    Background: Our aim is to determine comorbidities associated with pulmonary hypertension (PHT) in clinically stable sickle-cell disease (SCD) patients and to evaluate left ventricular (LV) and right ventricular (RV) function in those patients. Methods: Echocardiography was performed in 87 SCD patients that were divided into group I (without PHT) and group II (with PHT). Both groups were compared with healthy controls. Results: A history of retinopathy and leg ulcer was more frequent in group II than group I (p < 0.01). Haemoglobin levels were lower (p < 0.05), whereas blood urea nitrogen, lactate dehydrogenase and total bilirubin levels were higher in group II (p < 0.01). Although group II patients had larger LV end-diastolic, LV end-systolic and RV diastolic diameters compared with group I patients and controls (p < 0.05), LV ejection fraction was similar in the three groups. The mitral peak early diastolic inflow velocity to peak late diastolic inflow velocity (E/A) ratio was similar in group I, group II and the control group. The tricuspid E/A ratio was lower in group II than group I and controls (p < 0.05). Conclusion: End organ damage occurs more often and haemolysis is severer in SCD patients with PHT than SCD patients without PHT. Although LV systolic and diastolic function is well preserved, RV diastolic function is disturbed in those patients with PHT. Copyright (c) 2007 S. Karger AG, Basel

    Can cathepsin-D a new inflammation biomarker in detection of lysosomal storage diseases?

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    FEBS EMBO 2014 Conference -- AUG 30-SEP 04, 2014 -- Paris, FRANCEWOS: 000359666801105FEBS, EMB
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