Background The optimal time window for the administration of hypothermia following cerebral ischemia has been studied for decades, with disparity outcomes. In this study, the efficacy of mild brain hypothermia beginni...Background The optimal time window for the administration of hypothermia following cerebral ischemia has been studied for decades, with disparity outcomes. In this study, the efficacy of mild brain hypothermia beginning at different time intervals on brain endogenous antioxidant enzyme and energy metabolites was investigated in a model of global cerebral ischemia. Methods Forty-eight male Sprague-Dawley rats were divided into a sham-operated group, a normothermia （37℃-38℃） ischemic group and a mild hypothermic （31℃-32℃） ischemia groups. Rats in the last group were subdivided into four groups： 240 minutes of hypothermia, 30 minutes of normothermia plus 210 minutes of hypothermia, 60 minutes of normothermia plus 180 minutes of hypothermia and 90 minutes of normothermia plus 150 minutes of hypothermia （n=8）. Global cerebral ischemia was established using the Pulsinelli four-vessel occlusion model for 20 minutes and mild hypothermia was applied after 20 minutes of ischemia. Brain.tissue was collected following 20 minutes of cerebral ischemia and 240 minutes of reperfusion, and used to measure the levels of superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px）, reduced glutathione （GSH） and adenosine triphosphate （ATP）. Results Mild hypothermia that was started within 0 to 60 minutes delayed the consumption of SOD, GSH-Px, GSH, and ATP （P 〈0.05 or P 〈0.01） in ischemic tissue, as compared to a normothermic ischemia group. In contrast, mild hypothermia beginning at 90 minutes had little effect on the levels of SOD, GSH-Px, GSH, and ATP （P〉0.05）. Conclusions Postischemic mild brain hypothermia can significantly delay the consumption of endogenous antioxidant enzymes and energy metabolites, which are critical to the process of cerebral protection by mild hypothermia. These results show that mild hypothermia limits ischemic injury if started within 60 minutes, but loses its protective effects when delayed until 90 minutes following cerebral ischemia.展开更多
Therapeutic strategies for destroying cancer cells by making its death programs run again. The normal cell passes through several stages (Accumulation stage, Detoxification stage, Formation of free radical stage and A...Therapeutic strategies for destroying cancer cells by making its death programs run again. The normal cell passes through several stages (Accumulation stage, Detoxification stage, Formation of free radical stage and Activation of nuclear factor kappa B stage and the shutting down of programs of cell death stage) to become a cancerous cell. The success of the therapeutic strategy to treat cancer depends on making either one or both programs of cell death run again. Shutting down one stage completely will be sufficient to stop the transformation of the natural cell into a cancerous cell, which eliminates the production of hydrogen peroxide, thus the activity of the NF-Kb will be inhibited. However, shutting down all stages is the most comprehensive therapeutic strategy and guarantees treatment success.展开更多
Cancer is cell fleeing from death by blocking the intrinsic and extrinsic pathways of cell death programs. In the present work, the experimental formula was designed to remove these blockers. It was applied on 120 Swi...Cancer is cell fleeing from death by blocking the intrinsic and extrinsic pathways of cell death programs. In the present work, the experimental formula was designed to remove these blockers. It was applied on 120 Swiss albino mice which were inoculated intraperitoneally and subcutaneously with Ehrlich Ascites Carcinoma cells;1 × (106) cell/mouse. The activity of the cell death programs of the tumor was detected by measuring the volume of Ascites fluid, counting the number of dead cancer cells, measuring the size of the tumor, detecting the positive reaction of caspase enzyme in cancer cells and presence of macrophages and apoptotic bodies in tumor tissue. The experimental formula succeeded in removing the blockers of the cell death program in cancer cells returning the cell death program to work again.展开更多
Congestive heart failure is a disease in which initially compensatory changes in cardiac , vascular, and renal functions become detrimental over time. The changes are mediated by a large number of neurohormones and cy...Congestive heart failure is a disease in which initially compensatory changes in cardiac , vascular, and renal functions become detrimental over time. The changes are mediated by a large number of neurohormones and cytokines. Counter-regulatory hormones also play a role, but are generally insufficient to offset the adverse effects of the neurohormones or progression of the disease. Symptoms of heart failure occurs in the 'presence of systolic dysfunction, usually documented by a decrease in ejection fraction, or can present with impaired diastolic function occasionally labeled as heart failure with preserved systolic function of the left ventricle. Heart failure and its treatment represent a medical problem of significant importance because of the high mortality associated with it despite the current therapy , which has substantial evidence of reduction in mortality and morbidity. Prevention or slowing of the progressive deterioration in function of the heart and other organs involved through utilizing new agents that affect more or different neurohormonal pathways may be beneficial and forms the focus of heart failure research and drug development. However , the multiplicity of hormonal effects mandate the use of complex therapy in the management of congestive heart failure(CHF). The new agents in addition to the conventional therapy used in the management of heart failure are; Human B-type nalriuretic peptide (in the treatment of decompensated CHF) , endothelin receptor antagonists, calcium sensitizers, neutral endopeptidase (NEP) and vasopeptidase inhibitors, vasopressin antagonists and cytokine inhibitors.展开更多
文摘Background The optimal time window for the administration of hypothermia following cerebral ischemia has been studied for decades, with disparity outcomes. In this study, the efficacy of mild brain hypothermia beginning at different time intervals on brain endogenous antioxidant enzyme and energy metabolites was investigated in a model of global cerebral ischemia. Methods Forty-eight male Sprague-Dawley rats were divided into a sham-operated group, a normothermia （37℃-38℃） ischemic group and a mild hypothermic （31℃-32℃） ischemia groups. Rats in the last group were subdivided into four groups： 240 minutes of hypothermia, 30 minutes of normothermia plus 210 minutes of hypothermia, 60 minutes of normothermia plus 180 minutes of hypothermia and 90 minutes of normothermia plus 150 minutes of hypothermia （n=8）. Global cerebral ischemia was established using the Pulsinelli four-vessel occlusion model for 20 minutes and mild hypothermia was applied after 20 minutes of ischemia. Brain.tissue was collected following 20 minutes of cerebral ischemia and 240 minutes of reperfusion, and used to measure the levels of superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px）, reduced glutathione （GSH） and adenosine triphosphate （ATP）. Results Mild hypothermia that was started within 0 to 60 minutes delayed the consumption of SOD, GSH-Px, GSH, and ATP （P 〈0.05 or P 〈0.01） in ischemic tissue, as compared to a normothermic ischemia group. In contrast, mild hypothermia beginning at 90 minutes had little effect on the levels of SOD, GSH-Px, GSH, and ATP （P〉0.05）. Conclusions Postischemic mild brain hypothermia can significantly delay the consumption of endogenous antioxidant enzymes and energy metabolites, which are critical to the process of cerebral protection by mild hypothermia. These results show that mild hypothermia limits ischemic injury if started within 60 minutes, but loses its protective effects when delayed until 90 minutes following cerebral ischemia.
文摘Therapeutic strategies for destroying cancer cells by making its death programs run again. The normal cell passes through several stages (Accumulation stage, Detoxification stage, Formation of free radical stage and Activation of nuclear factor kappa B stage and the shutting down of programs of cell death stage) to become a cancerous cell. The success of the therapeutic strategy to treat cancer depends on making either one or both programs of cell death run again. Shutting down one stage completely will be sufficient to stop the transformation of the natural cell into a cancerous cell, which eliminates the production of hydrogen peroxide, thus the activity of the NF-Kb will be inhibited. However, shutting down all stages is the most comprehensive therapeutic strategy and guarantees treatment success.
文摘Cancer is cell fleeing from death by blocking the intrinsic and extrinsic pathways of cell death programs. In the present work, the experimental formula was designed to remove these blockers. It was applied on 120 Swiss albino mice which were inoculated intraperitoneally and subcutaneously with Ehrlich Ascites Carcinoma cells;1 × (106) cell/mouse. The activity of the cell death programs of the tumor was detected by measuring the volume of Ascites fluid, counting the number of dead cancer cells, measuring the size of the tumor, detecting the positive reaction of caspase enzyme in cancer cells and presence of macrophages and apoptotic bodies in tumor tissue. The experimental formula succeeded in removing the blockers of the cell death program in cancer cells returning the cell death program to work again.
文摘Congestive heart failure is a disease in which initially compensatory changes in cardiac , vascular, and renal functions become detrimental over time. The changes are mediated by a large number of neurohormones and cytokines. Counter-regulatory hormones also play a role, but are generally insufficient to offset the adverse effects of the neurohormones or progression of the disease. Symptoms of heart failure occurs in the 'presence of systolic dysfunction, usually documented by a decrease in ejection fraction, or can present with impaired diastolic function occasionally labeled as heart failure with preserved systolic function of the left ventricle. Heart failure and its treatment represent a medical problem of significant importance because of the high mortality associated with it despite the current therapy , which has substantial evidence of reduction in mortality and morbidity. Prevention or slowing of the progressive deterioration in function of the heart and other organs involved through utilizing new agents that affect more or different neurohormonal pathways may be beneficial and forms the focus of heart failure research and drug development. However , the multiplicity of hormonal effects mandate the use of complex therapy in the management of congestive heart failure(CHF). The new agents in addition to the conventional therapy used in the management of heart failure are; Human B-type nalriuretic peptide (in the treatment of decompensated CHF) , endothelin receptor antagonists, calcium sensitizers, neutral endopeptidase (NEP) and vasopeptidase inhibitors, vasopressin antagonists and cytokine inhibitors.
