Analysis of mental health status and related factors in patients with acute cerebral infarction

BACKGROUND Acute cerebral infarction(ACI)is characterized by a high incidence of morbidity,disability,recurrence,death and heavy economic burden,and has become a disease of concern in global researchers.As ACI has serious effects on patients’physical status,life and economy,often causing anxiety,depression and other psychological problems,these problems can lead to the aggravation of physical symptoms;thus,it is very important to understand the factors affecting the mental health of these patients.AIM To understand the elements that affect the mental health of patients who have suffered an ACI.METHODS A questionnaire survey was conducted among patients with ACI admitted to three tertiary hospitals(Quanzhou First Hospital,Fuqing City Hospital Affiliated to Fujian Medical University,and the 900 Hospital of the Joint Service Support Force of the People’s Liberation Army of China)in Fujian Province from January 2022 to December 2022 using the convenience sampling method.ACI inpatients who met the inclusion criteria were selected.Informed consent was obtained from the patients before the investigation,and a face-to-face questionnaire survey was conducted using a unified scale.The questionnaire included a general situation questionnaire,Zung’s self-rating depression scale and Zung’s self-rating anxiety scale.All questionnaires were checked by two researchers and then the data were input and sorted using Excel software.The general situation of patients with ACI was analyzed by descriptive statistics,the influence of variables on mental health by the independent sample t test and variance analysis,and the influencing factors on psychological distress were analyzed by multiple stepwise regression.RESULTS The average age of the 220 patients with ACI was 68.64±10.74 years,including 142 males and 78 females.Most of the patients were between 60 and 74 years old,the majority had high school or technical secondary school education,most lived with their spouse,and most lived in cities.The majority of patients had a personal income of 3001 to 5000 RMB yuan per month.The new rural cooperative medical insurance system had the largest number of participants.Most stroke patients were cared for by their spouses and of these patients,52.3%had previously smoked.Univariate analysis showed that gender,age,residence,course of disease,number of previous chronic diseases and smoking history were the main factors affecting the anxiety scores of patients with ACI.Age,living conditions,monthly income,course of disease and knowledge of disease were the primary variables influencing the depression score in patients with ACI.The findings of multivariate analysis revealed that the course of disease and gender were the most important factors influencing patients’anxiety scores,and the course of disease was also the most important factor influencing patients’depression scores.CONCLUSION Long disease course and female patients with ACI were more likely to have psychological problems such as a high incidence of emotional disorders.These groups require more attention and counseling.

Responses of serum inflammatory factor high-sensitivity C-reactive protein, interleukin-6, and tumor necrosis factor-alpha in elderly males with cerebral infarction Non-randomized concurrent control

BACKGROUND： Cerebral infarction is poorly treated due to neuronal necrosis and secondary pathophysiological changes; for example, free radical production and inflammatory reactions. OBJECTIVE： To detect the levels of high-sensitivity C-reactive protein （hs-CRP）, interleukin-6 （IL-6）, and tumor necrosis factor- a （TNF- α ） in elderly males with cerebral infarction. DESIGN： Non-randomized current control study. SETTING： Cadre Medical Department, Guizhou Provincial People＇s Hospital. PARTICIPANTS： Forty elderly males （65-89 years old） with cerebral infarction were selected from Cadre Medical Department, Guizhou Provincial People＇s Hospital from February 2004 to December 2006. All patients met the diagnostic criteria of cerebral infarction modified at the 4th National Cerebrovascular Disease Academic Meeting, and were diagnosed on the basis of CT or MRI tests. Furthermore, 35 elderly male inpatients （65-87 years old） without cerebral infarction were selected as the control group. Included subjects provided confirmed consent and did not have heart disease, diabetes mellitus, lipid disorder, acute trauma, infection, rheumatism, or other inflammatory diseases. The study was approved by the local ethics committee. There were no significant differences in age, blood pressure, and lipid levels between the cerebral infarction group and the control group （P 〉 0.05）, and this suggested that the baseline data of both groups were comparable. METHODS： Fasting venous blood was drawn from cerebral infarction patients 24 hours after cerebral infarction attack and from control subjects 24 hours after hospitalization. A latex-enhanced immunoturbidimetric assay and an enzyme-linked immunosorbent assay were used to detect the levels of hs-CRP, IL-6, and TNF- α in the serum. MAIN OUTCOME MEASURES： The levels of hs-CRP, 1L-6, and TNF- α in the serum in both groups. RESULTS： Forty cerebral infarction patients and thirty-five control subjects were included in the final analysis without any loss. Levels of hs-CRP, IL-6, and TNF-α in the cerebral infarction group were significantly higher than those in the control group （P 〈 0.01 ）. CONCLUSION： Levels of serum inflammatory reactive factors are increased in elderly males with cerebral infarction.

Changes in tumor necrosis factor alpha and myeloper-oxidase in mouse models of local cerebral infarction induced by photochemical method

BACKGROUND： Lots of evidences have demonstrated that acute inflammatory reaction plays an important role in cerebral ischemia and cerebral ischemia/reperfusion injury. Tumor necrosis factor （TNF）, as one of important inflammatory cytokines, also participates in the injury. OBJECTIVE： To observe the changes in TNF-α expression and myeloperoxidase （MPO） activity of mouse models of local cerebral infarction induced by photochemical method, and analyze the correlation of TNF-α expression and MPO activity. DESIGN： Randomized controlled experiment. SETTING： Laboratory of Cerebral Microcirculation, Taishan Medical College. MATERIALS： Sixty involved male adult Kunming mice were provided by the Experimental Animal Center of Shandong University. TNF-α primary antibody, kits for enzyme-linked immunosorbent assay（ELISA） and streptavidin-biotin complex immunohistochemical dyeing kit were purchased from Boster Company（Wuhan）. MPO kit was purchased from Jiancheng Bioengineering Institute （Nanjing）. Cold light source was developed by Hengfa Co.,Ltd.（ LG-150, Xuzhou）. METHODS： This experiment was carried out in the Laboratory of Cerebral Microcirculation of Taishan Medical College between July 2004 and July 2005. The involved 60 Kumning mice were randomized into 3 groups： normal control group （n =6）, sham-operation group （n =6） and model group （n =48）. Mice in the model group were observed at 30 minutes, 1, 3, 6, 12, 24, 48 and 72 hours after illumination, separately, 6 mice at each time point. In the model group, mice models of local cerebral infarction were developed as follows： The mice were anesthetized to expose left skulls. Taking 2 mm left to sagittal suture and 2 mm posterior to coronal suture as center, a field with diameter of 3 mm for illumination was set. The optical fiber detecting head of cold light source was vertically close to exposed skull. The mice were injected with rose Bengal for 5 minutes, and then cold light source was open for 10 minutes, Illumination was omitted in the sham-operation group. Mice in the control group were not modeled. At postoperative 6 hours, TNF-α expression in infracted-side cortex was detected with immunohistochemical method and ELISA, and MPO activity in infracted-side cortex with chromatometry. MPO activity could reflect the infiltration degree of neutrophils in tissue. Stronger activity indicated severer infiltration. Single-factor analysis of variance was used for comparison among groups, q test for pairwise comparison and correlative analysis for detecting the inter-parameter correlation. MAIN OUTCOME MEASURES： Changes in TNF-α expression and MPO activity of left cortex of mice in each group. RESULTS： Sixty mice were involved in the final analysis. After cerebral infarction, TNF-α positive cells were neurons and glial cells mainly, distributing in and around the infarct region. TNF-α expression in cortex of mice of sham-operation group was （615.7 ±16.1 ） ng/L, and that of model group increased to （792.2± 17.8） ng/L at 3 hours after illumination, and reached peak [ （921.9±23.9） ng/L] at 6 hours after illumination, and decreased to （848.0±30.6） ng/L at 12 hours after illumination and recovered to the normal level [ （625.3 ± 14.3） ng/L] at 72 hours after illumination. MPO activity of sham-operation group was （7.151±0.433） nkat/g, and that of model group increased to （10.469±0.600） nkat/g at 3 hours after illumination, reached the peak [ （ 15.486 ± 0.650） nkat/g] at 12 hours after illumination, decreased to （11.052 ± 0,617） nkat/g at 24 hours after illumination and recovered to the normal level [ （7.418 ± 0.617） nkat/g] at 72 hours after illumination. Change of MPO activity lagged behind that of TNF-α, and correlative analysis showed that the both were positively correlated （r =0.953, P 〈 0.01 ） . CONCLUSION： In the acute stage of cerebral infarction of mice induced by photochemical method, TNF-α expression in infarcted-side cortex is closely related with infiltration of neutrophils. TNF-α induces inflammatory cells to intrude into ischemic brain tissue, and participates in the inflammatory reaction process at the early stage of cerebral ischemia.

Changes of Tumor Necrosis Factor-α and the Effects of Ulinastatin Injection during Cardiopulmonary Cerebral Resuscitation

Summary: The changes of tumor necrosis factor-α (TNF-α) and brain ultrastructure during cardiopulmonary resuscitation and the effects of ulinastation injection were observed, and the mechanism was investigated. Twenty-four adult healthy Sprague-Dawley rats were randomly divided into control group (8 rats), resuscitation group (8 rats) and ulinastatin (UTI) group (8 rats). Rats in control group underwent tracheotomy without clipping the trachea to induce circulatory and respiratory standstill. Rats in resuscitation and ulinastatin group were subjected to the procedure of establishing the model of cardiopulmonary cerebral resuscitation (CPCR). Rats in ulinastatin group were given with UTI 104 U/kg once after CPCR. In the control group, the plasma was collected immediate, 30 min, 2 h, 4 h, and 6 h after tracheotomy. In resuscitation group and UTI group, plasma was collected immediate after tracheotomy, 30 min, 2 h, 4 h and 6 h after successful resuscitation. The plasma levels of TNF-α were determined by radioimmunoassay (RIA). At the end of the experiment, 2 rats were randomly selected from each group and were decapitated. The cortex of the brain was taken out immediately to observe the ultrastructure changes. In control group, there were no significant differences in the level of TNF-α among different time points (P>0.05). In resuscitation group, the level of TNF-α was increased obviously after resuscitation (P<0.01) and reached its peak 2 h later after resuscitation. An increasing trend of TNF-α showed in UTI group. There were no differences in TNF-α among each sample taken after successful resuscitation and that after tracheotomy. The utrastructure of brains showed the injury in UTI group was ameliorated as compared with that in resuscitation group. In early period of CPCR, TNF-α was expressed rapidly and kept increasing. It indicated that TNF-α might take part in the tissue injury after CPCR. The administration of UTI during CACR could depress TNF-α and ameliorate brain injury. By regulating the expression of damaging mediator, UTI might provide a protective effect on the tissue injury after CPCR.

Effects of Intravenous Thrombolytic Therapy with Alteplase on Neurological Function,Coagulation Function and Serum Inflammatory Factors in Patients with Acute Cerebral Infarction

Objective:To investigate the effects of intravenous thrombolysis therapy with alteplase on neurological function,coagulation function and serum inflammatory factors in patients with acute cerebral infarction.Methods:A total of 96 patients with acute cerebral infarction admitted to our hospital from September 2017 to October 2019 were randomly divided into two groups,with 48 patients in each group.The control group(n=48)received routine treatment,and the observation group received intravenous thrombolysis therapy with alteplase on the basis of routine treatment.The neurological deficit score,prothrombin time(PT),activated partial thromboplastin time(APTT),tumor necrosis factor-a level(TNF-α),and high-sensitivity C-reactive protein(hs-CRP)were compared between the two groups after 15 days of treatment.Results:After treatment,NIHSS scores in both groups were lower than those before treatment;PT levels were increased,while APTT,TNF-αand hs-CRP levels were all decreased in both groups,and the changes in the observation group were greater than those in the control group,with statistically significant difference(P<0.05).Conclusions:Intravenous thrombolysis therapy with alteplase can improve the neurological function,coagulation function and serum levels of inflammatory factors in patients with acute cerebral infarction,which is worthy of clinical application.

Effect of butylphthalide injection on inflammatory factors, neurological factors and hemorheology in patients with acute cerebral infarction

Objective: To investigate the effects of butylphthalide injection on inflammatory factors, neurological factors and hemorheology in patients with acute cerebral infarction. Methods:The patients in the observation group were treated with intravenous infusion of butyphthalide on the basis of the control group, 120 cases of acute cerebral infarction patients are randomly divided into control group (n=60) and observation group (n=60), patients in the control group were given conventional thraphy, on the basis of the thraphy of the control group, the observation group were treated with intravenous infusion of butyphthalide. Both groups were given sustainable treatment for 14 d, the levels of inflammatory factors, neurological factors and hemorheologywere compared before and after the treatment. Results: The levels of serum hs-CRP, TNF-α, NSE, MBP, S100B, whole blood viscosity, plasma specific viscosity, hematocrit and platelet aggregation rate in the two groups before treatment were no significant difference. After treatment, the levels of hs-CRP, TNF-α in the observation group and observation group were (4.98±1.14) mg/L, (5.54±1.29) ng/L and (7.54±0.93) mg/L, (8.32±1.31) ng/L, which were significantly lower than those in the same group before treatment, and the level of hs-CRP, TNF-α in the observation group were significantly lower than those in the control group;the levels of NSE, MBP, S100B in the observation group and observation group were (6.38±2.39) μg/L, (10.19±3.28) μg/L, (0.96±0.09) ng/L and (11.73±2.43) μg/L, (17.43±4.51) μg/L, (1.65±0.12) ng/L, which were significantly lower than those in the same group before treatment, and the observation group levels were significantly lower than those in the control group;the levels of whole blood viscosity, plasma specific viscosity, hematocrit and platelet aggregation rate in the observation group and observation group were(5.17±0.89) mPa?s,(1.32±0.22) mPa?s, (0.35±0.13)%, (0.32±0.08)% and (5.68±0.91) mPa?s, (1.63±0.24) mPa?s, (0.41±0.14)%, (0.40±0.11)%, which were significantly lower than those in the same group before treatment, and the observation group levels were significantly lower than those in the control group. Conclusion: On the basis of conventional treatment, the addition of butyphthalide can effectively reduce the level of serum inflammatory factors, promote the repair of nerve function, improve the level of hemorheology, which has important clinical value.

Study on risk factors of hemorrhagic transformation in patients with acute cerebral infarction after non thrombolysis

Objective:To study the risk factors of hemorrhagic transformation in patients with acute cerebral infarction and to analyze the risk factors.Methods: A total of 96 patients with acute cerebral infarction after the thrombolysis in our hospital from June 2016 to December 2017 were selected as the research object. And they were divided into bleeding group 48 cases and hemorrhage transformation group 48 cases according to whether with hemorrhage occurs transformation. Then the lipid metabolism, atrial fibrillation, history of smoking and drinking, history of hypertension and diabetes, blood pressure, treatment time after onset and infarction area of two groups were compared, and the relationship between those factors and the disease were analyzed by the multi-factor Logistic regression analysis.Results: The atrial fibrillation, history of smoking and drinking of two groups had significant differences;The hospital fasting plasma glucose and LDL-C level of two groups had significant differences;the treatment time after onset and infarction area of two groups had significant differences;The multi-factor Logistic regression analysis showed that atrial fibrillation, blood glucose on admission, LDL-C and large area of infarction are the factors affecting the risk of bleeding in patients with acute cerebral infarction transformation.Conclusion:Atrial fibrillation, blood glucose on admission, LDL-C, treatment time after onset and large area of infarction belongs to the patients with acute cerebral infarction after the thrombolysis transformation of bleeding risk factors.

Effect of atorvastatin and clopidogrel on inflammatory factors, blood coagulation and platelet activation in patients with acute cerebral infarction

Objective: To investigate the effects of atorvastatin combined with clopidogrel on inflammatory factors, coagulation and platelet activation in patients with acute cerebral infarction. Methods: A total of 140 cases patients with acute cerebral infarction who were confirmed by clinical and imaging diagnoses were randomly divided into treatment group (70 cases) and control group (70 cases). Both groups were treated routinely before treatment. The observation group was treated with clopidogrel and atorvastatin, while the control group was treated with aspirin and atorvastatin. The changes of inflammatory factors, coagulation function and platelet activation index before and after treatment were compared between the two groups. Result: Before treatment, the levels of serum soluble intercellular adhesion molecule-1 (sICAM-1), transforming growth factor-β (TGF-β), coagulation parameters prothrombin time(PT), activated partial thromboplastin time (APTT), fibrinogen (FIB), coagulation index of platelets platelet -membrane glycoprotein (CD62p), lysosomal granular membrane glycoprotein (CD63), platelet-monocyte aggregates (PMA), coagulation parameters were not statistically significant. After treatment, the levels of sICAM-1, CD62p, CD63, PMA and FIB in both groups decreased and the levels of TGF-β, PT and APTT increased. The levels of sICAM-1, FIB, CD62p, CD63 and PMA in the observation group were (370.32±37.13) ng/mL, (1.97±0.21) g/L, (1.38±0.14)%, (0.22±0.02)%, and (18.47+1.85)% respectively, which were lower than those in the control group ((410.47±42.32) ng/mL, (2.58±0.26) s, (2.67±0.27)%, (0.35±0.03)% and (22.87±2.91)%)While the levels of TGF-β, PT and APPT were (231.53±23.52) ng/mL, (15.42±1.53) s, (37.31±3.54) s were higher than the control group ((218.56±22.17) ng/mL, (12.32±1.27) s and (29.89±3.01)s)And the differences were significant. Conclusion: Atorvastatin combined with clopidogrel treatment can effectively relieve the inflammatory response, reduce the release of inflammatory cytokines, improve blood coagulation and inhibit platelet aggregation in patients with acute cerebral infarction. So it deserves further clinical promotion.

Effects of Xuefu Zhuyu Decoction combined with conventional therapy on inflammatory response, oxidative stress, endothelium and related factors in patients with acute cerebral infarction

Objective: To explore the effects of Xuefu Zhuyu Decoction combined with conventional therapy on inflammatory response, oxidative stress, endothelium and related factors in patients with acute cerebral infarction. Methods: A total of 162 patients with acute cerebral infarction admitted to our hospital from November 2016 to January 1818 were selected as subjects. According to the random sampling method, the subjects were divided into 81 cases in the control group and 81 cases in the observation group. The control group was treated with conventional intracranial pressure, anticoagulation, anti-oxidation and lipid-lowering treatment. The observation group was treated with Xuefu Zhuyu Decoction on the basis of the control group. The changes of inflammatory response, oxidative stress, endothelium and related factors were compared and analyzed. Results:Before treatment, the levels of TNF-α, CRP, SOD, MDA, AOPPS, NO, ET-1, MMP-9, PAF and IGF-1 in the two groups were not significantly different, and there was no statistical significance. After treatment, the levels of TNF-α and CRP in the two groups were significantly lower than those before treatment, and the levels of TNF-α and CRP in the observation group were significantly lower than control group;the levels of MDA and AOPPS in the two groups were significantly lower than those before treatment, while the level of SOD was significantly higher than before treatment, and the levels of MDA and AOPPS in the observation group were significantly lower than control group, while the level of SOD was significantly higher. In the control group;the level of ET-1 in the two groups was significantly lower than that before treatment, while the level of NO was significantly higher than that before the treatment, and in the observation group the level of ET-1 was significantly lower than the control group, while the level of NO was significantly higher. In the control group;the levels of MMP-9 and PAF in the two groups were significantly lower than those before treatment, while the level of IGF-1 was significantly higher than before treatment, and the levels of MMP-9 and PAF in the observation group were significantly lower than control group, while the level of IGF-1 was significantly higher than control group. Conclusions: Xuefu Zhuyu Decoction combined with conventional treatment of acute cerebral infarction can effectively reduce inflammation and oxidative stress, improve vascular endothelial function and nerve function, and significantly reduce the degree of brain injury, which has clinical significance.

Brain edema and tumor necrosis factor-like weak inducer of apoptosis in rats with cerebral ischemia

BACKGROUND： Recent studies have demonstrated that tumor necrosis factor-like weak inducer of apoptosis （TWEAK） participates in brain edema. However, it is unclear whether blood-brain barrier （BBB） disruption is associated with TWEAK during the process of brain edema OBJECTIVE： To investigate the effects of TWEAK on BBB permeability in brain edema. DESIGN, TIME AND SETTING： An immunohistochemical observation, randomized, controlled animal experiment was performed at the Laboratory of Neurosurgical Anatomy, Xiangya Medical College, Central South University ＆ Central Laboratory, Third Xiangya Hospital, Central South University between January 2006 and December 2007. MATERIALS： A total of 48 adult Wistar rats were randomly divided into three groups： normal control （n = 8）, sham-operated （n = 8）, and ischemia/reperfusion （n = 32）. Rats from the ischemia/reperfusion group were randomly assigned to four subgroups according to different time points, i.e., 2 hours of ischemia followed by 6 hours （n = 8）, 12 hours （n = 8）, 1 day （n = 8）, or 12 days （n = 8） of reperfusion. METHODS： Focal cerebral ischemia/reperfusion injury was induced by middle cerebral artery occlusion （MCAO） using the suture method in rats from the ischemia/reperfusion group. Thread was introduced at a depth of 17-19 mm. Rats in the sham-operated group were subjected to experimental procedures similar to the ischemia/reperfusion group; however, the introducing depth of thread was 10 mm. The normal control group was not given any intervention. MAIN OUTCOME MEASURES： TWEAK expression was examined by immunohistochemistry; brain water content on the ischemic side was calculated as the ratio of dry to wet tissue weight; BBB permeability was measured by Evans blue extravasation. RESULTS： A total of eight rats died prior to and after surgery and an additional eight rats were randomly entered into the study. Thus 48 rats were included in the final analysis. In the ischemia/reperfusion group, TWEAK-positive cells were present in the ischemic penumbra surrounding the lamellar necrotic region in the fight cerebral hemisphere at 6 hours reperfusion and increased thereafter; by 2 days reperfusion they had reached a peak level, which was significantly higher than the sham-operated and normal control groups （P 〈 0.05）. At 6 hours reperfusion, both brain water content and Evans blue extravasation showed the same tendency for change as TWEAK expression. Pearson correlation analysis results revealed that the degree of TWEAK expression was positively correlated with brain water content （r = 0.892, P 〈 0.05）. CONCLUSION： The present results confirmed that TWEAK was involved in BBB disruption and participated in brain edema following cerebral ischemia.

Ubiquitin Reduces Expression of Intercellular Adhesion Molecules and Tumor Necrosis Factor-α in Lung Tissue of Experimental Acute Lung Injury

Background Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are two important cytokines in inflammatory response, which may induce rolling and adhesion of both leukocytes and lymphocytes, while modulating vascular permeability at the same time. These adhesion molecules usually serve as surrogate markers of activation and injury of vascular endothelial cells. Tumor necrosis factor-α (TNF-α) is a key factor to induce the expression and production of the above cell adhesion molecules. However, it remains to be elucidated whether exogenous ubiquitin exerts any effect on the cytokines in sepsis-induced ALI. Methods Sixty mice were devided randomly into five groups with twelve mice in each group, i.e. CLP group, SHAM group, UB1 group (10 mg/kg), UB2 group (5 mg/kg) and UB3 group(1 mg/kg). Mice of SHAM group underwent sham operation, and other four groups underwent CLP. Six hours after surgery, mice of three UB groups received ubiquitin by caudal vein injection while CLP and SHAM group received vehicle. Seven hours after surgery, blood and lungs of all mice were collected. ICAM-1, VCAM-1 and TNF-α level of 9% lung homogenate and serum TNF-α level were measured by ELISA. Results Pulmonary ICAM-1, VCAM-1 and TNF-α level of three UB groups were lower than CLP and SHAM group, and there were several comparisons with a statistically significant difference. Serum TNF-α level of three UB groups were slightly lower than CLP group, but far higher than SHAM group. Pulmonary ICAM-1 level, VCAM-1 level and serum TNF-α level of UB3 group were lower than UB1 and UB2 group, and there was a significant difference in VCAM-1 between UB3 and UB1 group. Pulmonary TNF-α level of UB3 group was slightly higher than UB1 and UB2 group.

Hypoxic preconditioning stimulates angiogenesis in ischemic penumbra after acute cerebral infarction

Previous studies have demonstrated the protective effect of hypoxic preconditioning on acute cerebral infarction, but the mechanisms underlying this protection remain unclear. To investigate the protective mechanisms of hypoxic preconditioning in relation to its effects on angiogenesis, we in- duced a photochemical model of cerebral infarction in an inbred line of mice （BALB/c）. Mice were then exposed to hypoxic preconditioning 30 minutes prior to model establishment. Results showed significantly increased vascular endothelial growth factor and CD31 expression in the ischemic penumbra at 24 and 72 hours post infarction, mainly in neurons and vascular endothelial cells. Hypoxic preconditioning increased vascular endothelial growth factor and CD31 expression in the ischemic penumbra and the expression of vascular endothelial growth factor was positively related to that of CD31. Moreover, hypoxic preconditioning reduced the infarct volume and improved neu- rological function in mice. These findings indicate that the protective role of hypoxic preconditioning in acute cerebral infarction may possibly be due to an increase in expression of vascular endothelial growth factor and CD31 in the ischemic penumbra, which promoted angiogenesis.

Research of expression quantity of serum miR-146a and miR-146b in patients with acute cerebral infarction before and after the intervention of rosuvastatin

Objective: To study the expression quantity of serum miR-146a and miR-146b in patients with acute cerebral infarction before and after the intervention of rosuvastatin and its correlation with toll-like receptor 2 (TLR2) and TLR4 signaling pathways. Methods:A total of 65 patients with acute cerebral infarction treated in our hospital from December 2015 to August 2016 were selected for prospective study. They were treated with lipid-lowering rosuvastatin, and peripheral blood samples were collected at 8th week before and after treatment, respectively. Serum was separated and expression quantity of miR-146a and miR-146b and contents of TNF-α, interleukin (IL)-1β, IL-6 and IL-17 were determined. Peripheral blood mononuclear cells were isolated and fluorescence intensities of TLR2, TLR4, myeloid differentiation primary response gene 88 (MyD88), interleukin-1 receptor-associated kinase 1 (IRAK-1) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) were measured. Results:At 8th week of intervention of rosuvastatin, expression quantity of serum miR-146a [(0.762 ± 0.092)vs. (0.346 ± 0.053)] and miR-146b [(0.714 ± 0.088)vs. (0.317 ± 0.047)] in patients with acute cerebral infarction was significantly higher than those before the intervention. Fluorescence intensities of peripheral blood mononuclear cells such as TLR2 [(10.34 ± 1.27)vs. (16.94 ± 1.94)], TLR4 [(11.37 ± 1.54)vs. (24.35 ± 3.26)], IRAK [(9.34 ± 0.92)vs. (15.32 ± 1.82)], MyD88 [(4.42 ± 0.56) vs. (9.41 ± 1.03)] and NF-kB [(6.65 ± 0.78) vs. (13.49 ± 1.76)] and contents of inflammatory factors such as TNF-α [(64.26 ± 8.29) μg/L vs. (106.39 ± 13.84) μg/L], IL-1β [(37.91 ± 5.24) μg/Lvs. (64.23 ± 8.33) μg/L], IL-6 [(34.28 ± 4.85) ng/Lvs. (82.46 ± 11.97) ng/L] and IL-17 [(56.75 ± 7.49) ng/Lvs. (98.31 ± 11.36) ng/L] of serum were all significantly lower than those before the intervention. Expression quantity of serum miR-146a and miR-146b had a negative correlation with fluorescence intensities of TLR2, TLR4, IRAK, MyD88 and NF-kB. Fluorescence intensities of TLR2 and TLR4 in peripheral blood mononuclear cells had a positive correlation with contents of TNF-α, IL-1β, IL-6 and IL-17 in serum. Conclusions: Treatment with rosuvastatin can up-regulate the expression quantity of serum miR-146a and miR-146b in patients with acute cerebral infarction and further inhibit the secretion of IRAK, MyD88, NF-kB, TNF-α, IL-1β, IL-6 and IL-17 mediated by TLR2 and TLR4.

Effects of Remifentanil Pretreatment on Inflammatory Response in Rats with Acute Cerebral Ischemia Injury

[Objectives]This study was conducted to investigate the effects of remifentanil pretreatment on inflammatory factors in rats with acute cerebral ischemia.[Methods]Sixty SD rats were randomly divided into the normal control group,sham operation group,ischemic brain injury group,and remifentanil pretreatment group.Except the normal control group,each group was divided into three subgroups(six in each group)according to the sampling time points of 6,12 and 24 h after execution.After modeling,the rats were scored for neurological deficit,and observed for pathological changes of neurons in the brain tissue by HE staining and the brain infarct volume by TTC staining,and the expression levels of TNF-α,IL-6 and IL-8 were detected by RT-PCR.[Results]HE staining:No significant changes were observed in the pathological morphology of the brain tissue in the blank group and sham operation group;and the neuronal structure of rats in the acute cerebral ischemia group was obviously damaged,and the neuronal damage in the remifentanil pretreatment group was less than that in the acute cerebral ischemia group at each time point.TTC staining:The gray brain infarct area in the remifentanil pretreatment group was significantly smaller than that in the cerebral ischemia group(P<0.05).RT-PCR detection results:The expression levels of TNF-α,IL-6 and IL-8 in the blank group and sham surgery group did not show significant changes at different times(P>0.05);and compared with the cerebral ischemia group,the expression levels of TNF-α,IL-6,and IL-8 in the remifentanil pretreatment group were significantly reduced at all time points(P<0.05).[Conclusions]Remifentanil pretreatment could protect the brain by reducing the expression of inflammatory factors after cerebral ischemia injury.

Effects of Xingnaojing Injection on Cerebral Neurological Function and ET-1, hs-CRP and TNF-α Levels in Elderly Patients with Acute Cerebral Infarction

OBJECTIVE: To observe the effects of Xingnaojing Injection on the function of cranial nerves and the level of ET-1,hs-CRP and TNF-α in elderly patients with acute cerebral infarction. METHODS: A total of 86 elderly patients with acute cerebral infarction were randomly divided into observation group and control group. The 43 cases in the control group were treated by conventional Western medicine, and 43 cases in the observation group were treated by Xingnaojing injection on the basis of the treatment in control group. After 2 weeks' treatment in Xuancheng People's Hospital of Anhui Province, the neurological function(NIHSS score and MMSE score), daily living ability(BI Index score and ADL score),laboratory indicators(hs-CRP, ET-1, TNF-α) of the 2 groups before and after the treatment were observed and compared,the total clinical effectiveness of the 2 groups were compared. RESULTS: The total effective rate was 88.4% in the observation group, which was signi?cantly higher than that in the control group(62.8%)(P < 0.05). The NIHSS scores in the 2 groups were both signi?cantly increased after the treatment(P < 0.05) while the MMSE scores were signi?cantly decreased(P < 0.05) in the 2 groups, and the scores' improvement in the observation group was signi?cantly higher than that in the control group(P < 0.05). The BI score and ADL score were significantly increased in the 2 groups after the treatment(P < 0.05), and the improvements were obvious in the observation group. The levels of ET-1, hs-CRP and TNF-αin the 2 groups were signi?cantly decreased after the treatment(P < 0.05), and the indexes in the observation group were signi?cantly lower than that in the control group(P < 0.05). CONLUSIONS: Xingnaojing injection can reduce the levels of serum ET-1, hs-CRP and TNF-α, as well as the degree of neurological de?cit in the treatment of elderly patients with acute cerebral infarction. It is also helpful for the prognosis and outcomes of patients with cerebral infarction.

Mechanism of edaravone combined with urinary kallidinogenase for acute cerebral infarction patients

Objective:To observe the effects of edaravone combined with urinary kallidinogenase on serum ox-LDL, PCT, hs-CRP, TNF-α and T cell subsets in patients with acute cerebral infarction, so as to explore the mechanisms of combination therapy on patients with acute cerebral infarction. Methods:86 cases of patients with acute cerebral infarction in our hospital from March 2014 to May 2016 were randomly divided into two groups:control group and observation group, 43 cases in each group. All patients were given general treatment according to their own specific conditions, including hypoglycemic, pressure adjustment, prevention and treatment of complications, symptomatic support therapy, etc. The control group were given 30 mg Edaravone Injection on this basis with once per day for 14 d;The observation group was treated with 0. 15 PNA urinary kallidinogenase intravenous drip with once per day for 14 d on the basis of the control group. The levels of serum x-LDL, PCT, hs-CRP, TNF-αand CD3+, CD4+, CD8+, CD4+/CD8+were detected and compared between the two groups. Results:(1) Before treatment, there was no significant difference between the two groups on the levels of serum ox-LDL, PCT, hs-CRP, and TNF-α;after treatment, the serum levels of ox-LDL, PCT, hs-CRP and TNF-αin the two groups were significantly lower than that before treatment, and the difference was significant (P<0.05);(2) Before treatment, there was no significant difference between the two groups on the levels of serum CD3+, CD4+, CD8+, CD4+/CD8+;after treatment, the serum levels of CD3+, CD4+and CD4+/CD8+were significantly increased in the two groups, and the level of CD8+was significantly decreased compared with the same group before treatment, and the difference was significant (P<0.05);and the levels of serum CD3+, CD4+, CD8+and CD4+/CD8+in the observation group were significantly better than those in the control group, and the difference was significant (P<0.05). Conclusions:The treatment of combined application of urinary kallidinogenase and edaravone in patients with acute cerebral infarction, can significantly improve the serum levels of ox-LDL, PCT, hs-CRP, TNF-αand T cell subsets, further illustrates the synergistic effect of the combination, also shows that the two drugs for acute cerebral infarction can inhibit thrombosis to expand, reduce inflammation, relieve cerebral tissue damage, and improve neurological function.

Acute pancreatitis:The stress factor

Acute pancreatitis is an inflammatory disorder of the pancreas that may cause life-threatening complications.Etiologies of pancreatitis vary,with gallstones accounting for the majority of all cases,followed by alcohol.Other causes of pancreatitis include trauma,ischemia,mechanical obstruction,infections,autoimmune,hereditary,and drugs.The main events occurring in the pancreatic acinar cell that initiate and propagate acute pancreatitis include inhibition of secretion,intracellular activation of proteases,and generation of inflammatory mediators.Small cytokines known as chemokines are released from damaged pancreatic cells and attract inflammatory cells,whose systemic action ultimately determined the severity of the disease.Indeed,severe forms of pancreatitis may result in systemic inflammatory response syndrome and multiorgan dysfunction syndrome,characterized by a progressive physiologic failure of several interdependent organ systems.Stress occurs when homeostasis is threatened,and stressors can include physical or mental forces,or combinations of both.Depending on the timing and duration,stress can result in beneficial or harmful consequences.While it is well established that a previous acute-short-term stress decreases the severity of experimentally-induced pancreatitis,the worsening effects of chronic stress on the exocrine pancreas have received relatively little attention.This review will focus on the influence of both prior acute-short-term and chronic stress in acute pancreatitis.