ABSTRACT
OBJECTIVE: To establish a model for predicting the outcome according to the clinical and computed tomography(CT) image data of patients with intracerebral hemorrhage(ICH). METHODS: The clinical and CT image data of the patients with ICH in Qinghai Provincial People's Hospital and Xuzhou Central Hospital were collected. The risk factors related to the poor outcome of the patients were determined by univariate and multivariate logistic regression analysis. To determine the effect of factors related to poor outcome, the nomogram model was made by software of R 3.5.2 and the support vector machine operation was completed by software of SPSS Modelor. RESULTS: A total of 8265 patients were collected and 1186 patients met the criteria of the study. Age, hospitalization days, blend sign, intraventricular extension, subarachnoid hemorrhage, midline shift, diabetes and baseline hematoma volume were independent predictors of poor outcome. Among these factors, baseline hematoma volume๥20ml (odds ratio:13.706, 95% confidence interval:9.070-20.709, p < 0.001) was the most significant factor for poor outcome, followed by the volume among 10ml-20ml (odds ratio:11.834, 95% confidence interval:7.909-17.707, p < 0.001). It was concluded that the highest percentage of weight in outcome was baseline hematoma volume (25.0%), followed by intraventricular hemorrhage (23.0%). CONCLUSION: This predictive model might accurately predict the outcome of patients with ICH. It might have a wide range of application prospects in clinical.
Subject(s)
Cerebral Hemorrhage/diagnostic imaging , Decision Support Techniques , Nomograms , Support Vector Machine , Tomography, X-Ray Computed , Cerebral Hemorrhage/physiopathology , Cerebral Hemorrhage/therapy , China , Female , Humans , Male , Middle Aged , Predictive Value of Tests , Prognosis , Retrospective Studies , Risk Assessment , Risk Factors , Time FactorsABSTRACT
Mitochondrial dysfunction contributes to brain injury following global cerebral ischemia after cardiac arrest. Carbon monoxide treatment has shown potent cytoprotective effects in ischemia/reperfusion injury. This study aimed to investigate the effects of carbon monoxide-releasing molecules on brain mitochondrial dysfunction and brain injury following resuscitation after cardiac arrest in rats. A rat model of cardiac arrest was established by asphyxia. The animals were randomly divided into the following 3 groups: cardiac arrest and resuscitation group, cardiac arrest and resuscitation plus carbon monoxide intervention group, and sham control group (no cardiac arrest). After the return of spontaneous circulation, neurologic deficit scores (NDS) and S-100B levels were significantly decreased at 24, 48, and 72 h, but carbon monoxide treatment improved the NDS and S-100B levels at 24 h and the 3-day survival rates of the rats. This treatment also decreased the number of damaged neurons in the hippocampus CA1 area and increased the brain mitochondrial activity. In addition, it increased mitochondrial biogenesis by increasing the expression of biogenesis factors including peroxisome proliferator-activated receptor-γ coactivator-1α, nuclear respiratory factor-1, nuclear respiratory factor-2 and mitochondrial transcription factor A. Thus, this study showed that carbon monoxide treatment alleviated brain injury after cardiac arrest in rats by increased brain mitochondrial biogenesis.
Subject(s)
Brain Ischemia/drug therapy , Brain Ischemia/metabolism , Carbon Monoxide/therapeutic use , Heart Arrest/drug therapy , Heart Arrest/metabolism , Mitochondria/metabolism , Organelle Biogenesis , Animals , Brain/drug effects , Brain/metabolism , Brain Ischemia/etiology , DNA-Binding Proteins/metabolism , GA-Binding Protein Transcription Factor/metabolism , Heart Arrest/complications , Male , Mitochondria/drug effects , Mitochondrial Proteins/metabolism , Nuclear Respiratory Factor 1/metabolism , PPAR alpha/metabolism , Rats , Transcription Factors/metabolismABSTRACT
OBJECTIVE: To observe the expression of Bcl-2 and Bax proteins in rat's myocardial cells after Macleaya cordata alkaloids poisoning, and to provide certain molecular biology references for the detection of Macleaya cordata alkaloids poisoning. METHODS: Experimental model of Macleaya cordata alkaloids poisoning was established, the expression levels of Bcl-2 and Bax proteins in these cells were detected by immunohistochemistry, and the results were analyzed by computer image system. RESULTS: The expression levels of Bcl-2 and Bax proteins in myocardial cells in poisoning groups were much greater than those in the control groups (P<0.05). CONCLUSION: If the clinical symptoms may not be obvious, the detection of Bcl-2 and Bax proteins level by immunohistochemistry still could be ancillary method.
