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Objective To disscuss and analyze the clinical effects of whole body mild hypothermia on MODS caused by cerebral hemorrhage.Methods One hundred and eighty patients with MODS caused by cerebral hemorrhage during the period of hospitalized from January 2013 to December 2015 in ICU of our hospital were divided into two groups (observation group and control group) randomly,90 cases patients in each group.Patients in control group were treated with conventional treatment intervention,patients in control group were treated with whole body mild hypothermia on the base of conventional treatment intervention,the score of MODS,the ratio of,VO2 and DO2,the time during the period of hospitalized in ICU,the time of mechanical ventilation,epilepsy incidence and mortality,NIHSS score and PADL score of the patients in these two group after treatment were compared.Results After the comparion,the score of MODS and the state of oxygen consumption and oxygen supply of the patients in observation group were better than the patients in control group,there was significant differences,and had statistical significance (P＜0.05);the time during the period of hospitalized in ICU and the time of mechanical ventilation of the patients in observation group were shorter than the patients in control group,there was significant difference,and had statistical significance (P＜0.05);the mortality were reduce significantly of the patients in observation group than the patients in control group,there was significant difference,and had statistical significance (P＜0.05);the epilepsy incidence of the patients in observation group and control has no significant difference,has no statistical significance (P＞0.05);the NIHSS score and PADL score of the patients in observation group were higher than the patients in control group,there was significant difference,and has statistical significance (P＜0.05).Conclusion The clinical effects of whole body mild hypothermia on MODS caused by cerebral hemorrhage have important significance,can effectively improve the balance of multiple organ dysfunction syndrome patients,can delay the progression of multiple organ dysfunction syndrome patients,improve the prognosis,it is worthy of clinical application and promotion.
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Objective To study the risky factors related to postoperative mortality after surgical intervention for intra-ventricular hemorrhage (IVH).Methods The clinical data of 142 IVH patients aged from 19 to 86 years with 77 male and 65 female were collected from 2007 to 2010 for retrospective analysis with SPSS version 13.0 package.Multi-factorial Logistic regression analysis and mono-factorial x2 analysis were used to find out the risk factors related to post-operative death. Results Of 142 patients,48 (33.8％) died.Mono-factorial analysis demonstrated that the risk factors of death after surgical intervention to IVH were elderly age ( ＞ 65 years),history of hypertension,low GGS score,intra-ventricular diffuse bleeding,preoperative obstructive hydrocephalus and coagulation abnormality,postoperative central high pyrexia and central diabetes insipidus,postoperative hemorrhage of alimentary tract,pulmonary infection,and drainage after operation ≥7 days ( P ＜ 0.05 or P ＜ 0.01 ).Multi-factorial Logistic regression analysis,on the other hand,revealed the independent factors associated with postoperative IVH mortality were postoperative central high fever,preoperative obstructive hydrocephalus (P ＜ 0.01 ); drainage after operation ≥7 days,postoperative pulmonary infection,elderly age,low GCS score,intra-ventricular diffuse bleeding and history of hypertension ( P ＜ 0.05 ). Conclusions General condition of patients with IVH and CT findings are likely related to mortality,and active prevention against various complications is the crucial approach to lowering postoperative mortality and improving prognosis.
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Objective To study the variables of behavioral function and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) figure in Bcl-2 transgenic (TG) mice and control mice after spinal cord injury (SCI), thus to find new ideas and ways for diagnosing and treating SCI. Method The genesis of Bcl-2 overexpression transgenic (TG) mice were produced by injection of Bcl-2 plasmid into the fertilized ova of mice.Nine Bcl-2 TG mice and nine control mice were subjected to SCI of moderate severity at T10, with the use of weight dropping (WD) method (impact force 2.5～3.0 g·cm). Up to 1 day , 7 days, and 14 days after SCI,functional deficits were evaluated with BBB scales, and the apoptosis of neurons was investigated by using TUNEL method. Another three mice of control group were only treated with laminectomy without SCI for comparison. Results The mean functional scores in the control mice were lower than those in the Bcl-2 TG mice, although the unpaired T -test revealed no significant differences. On the other hand, the number of TUNEL positive neurons and IOD(Integrated Optical Density)score in the Bcl-2 TG mice were both significantly lower than those in the control mice. Conclusions This experiment suggests that overexpression of Bcl-2 may suppress neuronal apoptosis after SCI. The Bcl-2 may be an important factor in relieving the damage within CNS after trauma.
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Objective To observe the relationship between high-mobility group box-1 protein HMGB-1 andthe prognosis of systemic inflammatory response syndrome (SIRS) patients after multiple trauma. Method Sixtypatients with SIRS after multiple trauma in the emergency trauma center were divided into multiple organ dysfunc-tion syndrome (MODS) group and non-MODS group according to the MODS diagnostic criteria, and were followedup for 28 days and then assigned to survival group and fatal group, respectively. Another 20 healthy people wereera-oiled in the conrtol group. The levels of HMGB-1 were measured by ELISA at 24 hours, 3 days, 5 days and 7days after admission. APACHE Ⅱ scores were calculated. Results The concentrations of HMGB- 1 in the patientswith SIRS after trauma at every time point were higher than those in control group (P<0.01). The concentrationsof HMGB-1 and APACHEⅡ scores in the MODS group and the fatal group were higher than those in non-MODSgroup and the survival group (P<0.05 and P<0.01 separately). There was positive correlation between theconcentrations of HMGB-1 and APACHE Ⅱ scores (r=0.7938, P<0.05). Conclusions As an importantpro-inflammatory cytokine in sepsis, HMGB-1 may play a role in the development of SIRS after multiple trauma andcan be used to assess the severity of illness and prognosis.
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OBJECTIVE: To probe into the progression of biochemical study on caspase-3 and its functions in disorders of center nerve system.DATA SOURCES:The relevant papers were looked up on Medline database from January 1995 to February 2005 with the retrieved words as"caspase-3", "apoptosis", "center nerve system" and "emergency diseases" in combination, limited in English version.STUDY SELECTION: By initial checking,the papers on caspase-3 in molecular biology and randomized control experiments on caspase-3 and the disorders in center nerve system were collected.DATA EXTRACTION: Totally 156 papers were collected directly related to caspase-3 and center nerve system, of which, 25 papers were in conformity with the criteria and 131 papers were exuded because of repeated contents and indirect relation with this paper.DATA SYNTHESIS: To synthesize the relevant information from the retrieved papers and sum up that the activity of caspase-3 is increased after acute cerebral injury, acute spinal injury, cerebral ischemia and cerebral hemorrhage and broadspectrum caspase-3 inhibitor, Z-VAD-fmk can reduce significantly the activity of caspase-3.CONCLUSION: Caspase-3 is the most important protease in cell apoptosis, it is the component in downstream effect of coordination of various apoptotic approaches and is the only way in protease cascade of cell apoptosis. The activated caspase-3 can split the essential and protective enzymes in cell and result in the alternations of apeptosis in morphology and biochemistry. DNA segmentation is the important biochemical property of nerve cell apoptosis at early stage in acute cerebral injury and the formation of it is necessary.
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OBJECTIVE: Controversy over the presence of neuronal apoptosis in acute brain injuries has not been resolved due to the lack of direct evidence. In this article, the authors briefly review the current research progress of apoptosis and discuss the relationship between acute brain injuries and neuronal apoptosis.DATA SOURCES: A computer-based retrieval for relevant papers with abstracts indexed in Medline database published in English full text between January 1995 and February 2005 was conducted using the key words of "acute brain injuries" and "Neuronal apoptosis". Related articles in Chinese full text published between January 2000 and December 2004 were also searched in Chinese periodical full text database, Wanfang databases with key words of "acute traumatic brain injury, neuronal apoptosis".STUDY SELECTION: The retrieved articles were first examined to exclude review articles and repetitions, and only randomized and non-randomized controlled experiments or clinical trials on acute traumatic brain injury and neuronal apoptosis were included.DATA EXTRACTION: Altogether 136 articles directly related to acute traumatic brain injury and neuronal apoptosis were collected, among which 19 met the inclusion criteria with the other 117 removed for repetition or irrelevancy.DATA SYNTHESIS: The valid articles were reviewed to identify the factors related to neuronal apoptosis, apoptotic network theory, detection methods of apoptosis, and the relationship between acute traumatic brain injury and neuronal apoptosis as well as the possible mechanisms.CONCLUSION: Neuronal apoptosis occurs after acute traumatic brain injury, which induces intrinsic and extrinsic neuronal environment changes including increased extracellular excitatory amino acid content, massive free radical production and abnormal gene expression. These factors interact with each other and modulate neuronal apoptosis through multiple pathways.