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Träfflista för sökning "WFRF:(Bhiladvala Pallonji) "

Search: WFRF:(Bhiladvala Pallonji)

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1.
  • Belfrage, Hans, et al. (author)
  • Combined activation of murine lymphocytes with staphylococcal enterotoxin and interleukin-2 results in additive cytotoxic activity
  • 1994
  • In: Cancer Immunology and Immunotherapy. - 1432-0851. ; 38:4, s. 71-265
  • Journal article (peer-reviewed)abstract
    • This report demonstrates that in vitro activation of murine spleen cells with interleukin-2 (IL-2) or the bacterial superantigen staphylococcal enterotoxin A (SEA) results in different patterns of activation and function of cytotoxic cells. Lymphokine-activated killer activity and antibody-dependent cellular cytotoxicity (ADCC) are mainly mediated by IL-2 activated natural killer (NK) cells. SEA is the most powerful T cell mitogen known so far and retargets cytotoxic T lymphocytes (CTL) to tumors expressing major histocompatibility complex (MHC) class II in staphylococcal-enterotoxin-dependent cellular cytotoxicity (SDCC). Culture of mouse spleen cells with SEA led to expansion and activation of T cells, which demonstrated strong SDCC activity and some NK-like cytotoxicity after 5 days in culture. Cell sorting revealed that both CD8+ and CD4+ T cells mediated SDCC but the former were more effective. Phenotypic analysis showed that SEA preferentially stimulated and expanded T cells expressing T cell receptor V beta 11, in particular CD8+ T cells. Combined activation with SEA and IL-2 resulted in simultaneous induction of T and NK cell cytotoxicity. Moreover, IL-2 had additive effects on SEA-induced SDCC. Combined treatment with SEA and IL-2 might therefore be an approach to induce maximal cytotoxicity against tumors and to recruit both T and NK cells in tumor therapy.
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2.
  • Belfrage, Hans, et al. (author)
  • Functionally involved cell surface antigens on murine lymphokine activated killer cells
  • 1987
  • In: Immunology Letters. ; 14:4, s. 8-293
  • Journal article (peer-reviewed)abstract
    • To investigate the possible involvement of some cell surface structures on lymphoid cells in the functional activity of lymphokine activated killer (LAK) cells, a number of monoclonal antibodies (Mab) against such structures was studied for their ability to inhibit LAK activity in a standard cytotoxicity assay against the natural killer-insensitive target cell EL-4. Almost complete inhibition of LAK activity resulted from incubation with antibodies to the LFA-1 antigen, while blocking of the Lyt 2 antigen reduced cytotoxic activity about 50%. Mab to T-200 gave a weak and inconsistent inhibitory activity, while antibodies to Thy 1, L3T4, IL-2 receptor and MHC class I antigens were without effect. Mab to LFA-1 and Lyt 2 inhibited LAK activity towards EL-4, YAC-1 and differentiated F-9 teratocarcinoma cells, but did not affect LAK-mediated killing of undifferentiated F-9 cells. Experiments with separate preincubation of effector and target cells revealed that both LFA-1 and Lyt 2 inhibited LAK activity at the effector cell level only.
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3.
  • Bhiladvala, Pallonji, et al. (author)
  • Early identification of acute myocardial infarction by activated protein C-protein C inhibitor complex.
  • 2006
  • In: Thrombosis Research. - : Elsevier BV. - 1879-2472 .- 0049-3848. ; 118:Aug 10, s. 213-219
  • Journal article (peer-reviewed)abstract
    • Introduction: Increased coagulation activity due to coronary thrombosis in a ruptured plaque should result in activation of the protein C anticoagulant system with formation of complexes between activated protein C (APC) and,the protein C inhibitor (PCI), which reflects coagulation activity. We hypothesized that elevated APC-PCI concentration might allow earlier detection of ongoing myocardial infarction than traditional biochemical markers. We have evaluated a newly devised immunofluorimetric assay for measuring plasma concentration of APC-PCI complexes among patients with suspected acute coronary syndrome. Materials and methods: Blood samples were taken from 340 patients (median 71 years, range 31-97) with suspected acute coronary syndrome at first presentation in the emergency department. Electrocardiogram was recorded and APC PCI, Troponin I and Creatine kinase-MB concentrations were repeatedly measured 3 times at 6 h interval. Results: The 74 patients who were eventually diagnosed with myocardial infarction had a higher median level of APC-PCI complex than those Without myocardial damage; 0.27 vs. 0.20 mu g/L (p = 0.001). In a multivariate regression model, APC-PCI level in the fourth quartile (> 0.32 mu g/L) independently predicted myocardial infarction with an odds ratio of 3.7 (95% CI 1.4-9.6, p < 0.01). Conclusion: Early APC-PCI elevation can be detected among patients with a normal first Troponin I and non-ST-elevation myocardial infarction and provides additional risk assessment in acute coronary syndrome. (c) 2005 Published by Elsevier Ltd.
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4.
  • James, Stefan, 1964-, et al. (author)
  • Bivalirudin Versus Heparin Monotherapy in ST-Segment-Elevation Myocardial Infarction
  • 2021
  • In: Circulation. Cardiovascular Interventions. - : Lippincott Williams & Wilkins. - 1941-7640 .- 1941-7632. ; 14:12
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Bivalirudin was not superior to unfractionated heparin in patients with myocardial infarction (MI) treated with percutaneous coronary intervention and no planned use of GPI (glycoprotein IIb/IIIa inhibitors) in contemporary clinical practice of radial access and potent P2Y12-inhibitors in the VALIDATE-SWEDEHEART randomized clinical trial (Bivalirudin Versus Heparin in STEMI and NSTEMI Patients on Modern Antiplatelet Therapy-Swedish Web-System for Enhancement and Development of Evidence-Based Care in Heart Disease Evaluated According to Recommended Therapies Registry).METHODS: In this prespecified separately powered subgroup analysis, we included patients with ST-segment-elevation MI undergoing primary percutaneous coronary intervention with the primary composite end point of all-cause death, MI, or major bleeding event within 180 days.RESULTS: Among the 6006 patients enrolled in the trial, 3005 patients with ST-segment-elevation MI were randomized to receive bivalirudin or heparin. The mean age was 66.8 years. According to protocol recommendations, 87% were treated with potent oral P2Y12-inhibitors before start of angiography and radial access was used in 90%. GPI was used in 51 (3.4%) and 74 (4.9%) of patients randomized to receive bivalirudin and heparin, respectively. The primary end point occurred in 12.5% (187 of 1501) and 13.0% (196 of 1504; hazard ratio [HR], 0.95 [95% CI, 0.78-1.17], P=0.64) with consistent results in all major subgroups. All-cause death occurred in 3.9% versus 3.9% (HR, 1.00 [0.70-1.45], P=0.98), MI in 1.7% versus 2.2% (HR, 0.76 [0.45-1.28], P=0.30), major bleeding in 8.3% versus 8.0% (HR, 1.04 [0.81-1.33], P=0.78), and definite stent thrombosis in 0.5% versus 1.3% (HR, 0.42 [0.18-0.96], P=0.04).CONCLUSIONS: In patients with ST-segment-elevation MI undergoing primary percutaneous coronary intervention with radial access and receiving current recommended treatments with potent P2Y12-inhibitors rate of the composite of all-cause death, MI, or major bleeding was not lower in those randomized to receive bivalirudin as compared with heparin.REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02311231.
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5.
  • Khoshnood, Ardavan, et al. (author)
  • Effect of oxygen therapy on chest pain in patients with ST elevation myocardial infarction : results from the randomized SOCCER trial
  • 2018
  • In: Scandinavian Cardiovascular Journal. - : Informa UK Limited. - 1401-7431 .- 1651-2006. ; 52:2, s. 69-73
  • Journal article (peer-reviewed)abstract
    • Objective. Oxygen (O2) have been a cornerstone in the treatment of acute myocardial infarction. Studies have been inconclusive regarding the cardiovascular and analgesic effects of oxygen in these patients. In the SOCCER trial, we compared the effects of oxygen treatment versus room air in patients with ST-elevation myocardial infarction (STEMI). There was no difference in myocardial salvage index or infarct size assessed with cardiac magnetic resonance imaging. In the present subanalysis, we wanted to evaluate the effect of O2 on chest pain in patients with STEMI. Design. Normoxic patients with first time STEMI were randomized in the ambulance to standard care with 10 l/min O2 or room air until the end of the percutaneous coronary intervention (PCI). The ambulance personnel noted the patients´ chest pain on a visual analog scale (VAS; 1-10) before randomization and after the transport but before the start of the PCI, and also registered the amount of morphine given. Results. 160 patients were randomized to O2 (n = 85) or room air (n = 75). The O2 group had a higher median VAS at randomization than the air group (7.0 ± 2.3 vs 6.0 ± 2.9; p = .02) and also received a higher median total dose of morphine (5.0 mg ± 4.4 vs 4.0 mg ± 3.7; p = .02). There was no difference between the O2 and air groups in VAS at the start of the PCI (4.0 ± 2.4 vs 3.0 ± 2.5; p = .05) or in the median VAS decrease from randomization to the start of the PCI (−2.0 ± 2.2 vs −1.0 ± 2.9; p = .18). Conclusion. Taken together with previously published data, these results do not support a significant analgesic effect of oxygen in patients with STEMI. European Clinical Trials Database (EudraCT): 2011-001452-11. ClinicalTrials.gov Identifier: NCT01423929
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6.
  • Khoshnood, Ardavan, et al. (author)
  • Effect of oxygen therapy on myocardial salvage in ST elevation myocardial infarction : the randomized SOCCER trial
  • 2018
  • In: European Journal of Emergency Medicine. - 0969-9546. ; 25:2, s. 78-84
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: Recent studies suggest that administration of O2 in patients with acute myocardial infarction may have negative effects. With the use of cardiac MRI (CMR), we evaluated the effects of supplemental O2 in patients with ST elevation myocardial infarction (STEMI) accepted for acute percutaneous coronary intervention (PCI).MATERIALS AND METHODS: This study was a randomized-controlled trial conducted at two university hospitals in Sweden. Normoxic STEMI patients were randomized in the ambulance to either supplemental O2 (10 l/min) or room air until the conclusion of the PCI. CMR was performed 2-6 days after the inclusion. The primary endpoint was the myocardial salvage index assessed by CMR. The secondary endpoints included infarct size and myocardium at risk.RESULTS: At inclusion, the O2 (n=46) and air (n=49) patient groups had similar patient characteristics. There were no significant differences in myocardial salvage index [53.9±25.1 vs. 49.3±24.0%; 95% confidence interval (CI): -5.4 to 14.6], myocardium at risk (31.9±10.0% of the left ventricle in the O2 group vs. 30.0±11.8% in the air group; 95% CI: -2.6 to 6.3), or infarct size (15.6±10.4% of the left ventricle vs. 16.0±11.0%; 95% CI: -4.7 to 4.1).CONCLUSION: In STEMI patients undergoing acute PCI, we found no effect of high-flow oxygen compared with room air on the size of ischemia before PCI, myocardial salvage, or the resulting infarct size. These results support the safety of withholding supplemental oxygen in normoxic STEMI patients.
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7.
  • Khoshnood, Ardavan, et al. (author)
  • Effects of oxygen therapy on wall-motion score index in patients with ST elevation myocardial infarction-the randomized SOCCER trial
  • 2017
  • In: Echocardiography. - : Wiley. - 0742-2822. ; 34:8, s. 1130-1137
  • Journal article (peer-reviewed)abstract
    • Background: Although oxygen (O2) is routinely used in patients with acute myocardial infarction (AMI), it may have negative effects. In this substudy of the SOCCER trial, we aimed to evaluate the effects of O2-treatment on myocardial function in patients with ST elevation myocardial infarction (STEMI). Methods: Normoxic (≥94%) STEMI patients were randomized in the ambulance to either supplemental O2 or room air until the end of the percutaneous coronary intervention (PCI). The patients underwent echocardiography on day 2-3 after the PCI and once again after 6 months. The study endpoints were wall-motion score index (WMSI) and left ventricular ejection fraction (LVEF). Results: Forty-six patients in the O2 group and 41 in the air group were included in the analysis. The index echocardiography showed no significant differences between the groups in WMSI (1.32±0.27 for O2 group vs 1.28±0.28 for air group) or LVEF (47.0±8.5% vs 49.2±8.1%). Nor were there differences at 6 months in WMSI (1.16±0.25 vs 1.14±0.24) or LVEF (53.5±5.8% vs 53.5±6.9%). Conclusion: The present findings indicate no harm or benefit of supplemental O2 on myocardial function in STEMI patients. Our results support that it is safe to withhold supplemental O2 in normoxic STEMI patients.
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