Sepsis is essentially a result from immunological dissonance provoked by severe insults such as fulminant infection,severe trauma and extensive burns.It originates from excessive inflammatory responses and develops into immune paralysis or immunosupression.It has been demonstrated that cellular immune response plays a vital role in the pathogenesis of sepsis.In the stage of excessive inflammation,several kinds of immune cells are activated by pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs) and subsequently produce a vast number of pro-inflammatory cytokines,while during the stage of immune paralysis,excessive apoptosis could result in decrease of immune cells with functional compromise.Inhibitory or regulatory immune cell subsets eventually dominate the direction of immune response and the production of inhibitory cytokines is enhanced.For clinical practice,surveillance of changes and shift in overall immune function is a basis for immunotherapy,especially to immunomodulation therapy.However,there is still a lack of adequate indexes or markers for integral evaluation of host immune state in the development of sepsis.

Objective:To investigate the risk factors for refeeding syndrome (RFS) in patients with severe stroke.Methods:Patients with stroke admitted to the Neuro Intensive Care Unit, Nanfang Hospital, Southern Medical University and received enteral nutrition support >72 h from January 2013 to July 2019 were enrolled retrospectively. RFS was defined as a new onset of hypophosphatemia within 72 h after the start of nutritional support, that is, blood phosphorus <0.65 mmol/L and a decrease of >0.16 mmol/L from the baseline value. The independent risk factors for RFS were identified by multivariate logistic regression model. Results:A total of 209 patients with severe stroke were included, with a median age of 65 years (interquartile range [ IQR] 53 to 72 years), and 154 were males (73.7%); 136 patients had cerebral infarction (65.1%), 73 had intracerebral hemorrhage (34.9%). The baseline median National Institutes of Health Stroke Scale (NIHSS) score was 15 ( IQR, 11-20), the median Glasgow Coma Scale score was 9 ( IQR, 6-12), the median Acute Physiology and Chronic Health Score was 16 ( IQR, 11-20), the median Nutrition Risk in Critically Ill (NUTRIC) score was 3 ( IQR 2-5), and the median Sequential Organ Failure Assessment (SOFA) score was 4 ( IQR, 3-6); the baseline median serum phosphorus was 1.05 mmol/L ( IQR, 0.90-1.19 mmol/L). A total of 34 patients (16.3%) developed RFS. Multivariate logistic regression analysis showed that male (odds ratio 3.565, 95% confidence interval 1.150-11.053; P=0.028) and patients with higher SOFA score (odds ratio 1.246, 95% confidence interval 1.077-1.442; P=0.032) were more likely to develop RFS. Conclusions:RFS is not rare in patients with severe stroke. Males and patients with severe disease are more likely to develop RFS.

To observe the effect and its potential mechanism of monoclonal antibody to tumor necrosis factor-alpha(TNF? MoAb)on systemic hemodynamics and survival rate after intestinal ischemia/reperfusion (Ⅱ/R). Method: SD rats were subjected to 75 rain of superior mesenteric artery occlusion followed by 6 hours of reperfusion. The animals were treated intravenously with either TNF? MoAb(20mg/kg)or the control protein(albumin, 20mg/kg) 30 min prior to the onset of ischemia. Result: Pretreatment with TNF? MoAb significantly attenuated the decrease in blood pressure and cardiac index compared to controls throughout the 6-hour period of observation(P

Objective To study the relationship between Epstein-Barr virus(EBV) and Hapatocellular carcinoma (HCC). Methods Polymerase chain reaction (PCR) and immunohistochemical staining were applied to detect EBV in paraffin tissue sections from 78 HCC patients. Results EBV DNA was detected in 22 patients (28 2%) by PCR. Immunohistochemical staining of EBV LMP1 revealed that the positive signals were mainly localized in the tumor cells. Conclusions These observations suggest that EBV may pay a role in the development of HCC.

Although endovascular therapy improves the recanalization rate of acute large vessel occlusive ischemic stroke, about half of the patients still have poor functional outcome at 90 d, which is called " futile recanalization" . This article reviews and summarizes the predictive factors of futile recanalization after endovascular therapy in acute anterior circulation ischemic stroke, in order to provide help for clinical work and scientific research in the future.

Objective To investigate the safety and therapeutic effect of intra-carotid infusion with cold sa line in rats with acute focal cerebral ischemia-reperfusion injury.Methods 60 rats were randomly divided into six groups:sham operated group,normal infusion group,stroke group,local hypothermic group,local normothermic group,and systemic infusion group.Brain infarct volume and cerebral water content were analyzed 48 h after ischemia.Neurological deficits were assessed using the mNSS 24 h and 48 h after infarction.Results In the local hypothermic group,brain temperature was reduced to 33 to 34 ℃ within 5 to 10 minutes,and this significantly low temperature maintained to nearly 60 minutes after infusion continued.Physiological variables were not significantly different among each time point (P ＞ 0.05).No significant morphological abnormality was found in brain sections stained with TTC and HE.Animals receiving local cold infusion significantly decreased infarct volume and brain water content compared to stroke group (P ＜ 0.05).Both 24 h and 48 h mNSS in local hypothermic group was significantly lower than those in other groups (P ＜ 0.05).Conclusions Intra-carotid infusion with cold saline can quickly and effectively reduce brain temperature and is a relatively safe cooling method.Local hypothermia significantly reduced brain infarct volume,decreased brain water content and improved neurological functional outcomes after brain ischemia.

Objective To investigate the expression of matrix metalloproteinase-2 (MMP-2)and matrix metalloproteinase-9(MMP-9) in MIA PaCa-2 cells blocked by AS-ODN cultured in hypoxia.Methods Heparanase(Hpa) expression of MIA PaCa-2 cells was blocked by AS-ODN and cultured in hypoxia.The expression of MMP-2 and MMP-9 mRNA and proteins in cell lysate was evaluated by RT-PCR and Western blot respectively,and the enzymatic activities of MMP-2 and MMP-9 in supernatants were detected by gelatinase activity assay.Results Hypoxia stimulated mRNA and protein expression of MMP-9 in cultured MIA PaCa-2 cells and elevated at 6h,12 h(P ＜0.05)and 24 h(P ＜ 0.01).When Hpa expression was inhibited by AS-ODN,the expression of MMP-9 mRNA and protein as well as the gelatinase activity in supernatant decreased dramatically at 12 h and 24 h,especially at 24h(P ＜0.01),however,no significant difference of MMP-2 expression and gelatinase activity was observed after AS-ODN transfection.(P ＞ 0.05).Conclusion In hypoxia,MMP-9 expression,either mRNA or protein in cultured MIA PaCa-2 cells,increased gradually accompanied with elevated gelatinase activities.When the heparanase expression was inhibited,the MMP-9 mRNA and protein,as well as the gelatinase B activity in supernatant,were decreased dramatically at 12h and 24h,however,no significantly differences of MMP-2 expression and gelatinase A activity were observed after the AS-ODN transfection.

Objective To evaluate the pathogenesis and disease progression by detecting the expression of Serum High mobility group protein 1 (HMGB1) and TLR2 in monocytes of patients with systemic lupus erythematosus (SLE).Methods Forty patients with SLE were selected randomly,20 patients were in active disease group and others were in stable disease group.The expression of HMGB1 in the serum of these cases were detected by enzyme linked immunosorbent assay (ELISA) and TLR2 on CD14+ monocytes in the peripheral blood were detected by FCM.The correlation between these indexes and clinical,laboratory indexes about SLE were analyzed using one-way ANOVA,and Kruskal-Wallis test.Results The expression levels of HMGB-1 in serum was [(48.9±11.3) μg/L] in the active group,while that was [(14.8±1.9) μg/L] in the stable group was,and [(13.5±3.6) μg/L] in the control group.HMGB1 in the active SLE group was significantly higher (P＜0.05) when compared with that of the stable and control group.The expression of TLR2 in the peripheral blood mononuclear cells was [(96.7±1.3)％] in the active group,[(83.5±9.1)％] in the stable group,and [(83.3±9.9)％] in the control group TLR2 in the active SLE group was up-regulated when compared with the stable and control groups (P＞0.05).There were positive correlation between the serum levels of HMGB1and TLR2 in the peripheral blood mononuclear cells (r=0.551,P＜0.05).Conclusion The expression levels of HMGB-1 in serum and the expression of TLR2 in peripheral blood mononuclear cells may participate in the pathological processes of SLE.

Objective To investigate the risk factors for hospital-acquired pneumonia (HAP) in a neurological intensive care unit (NICU).Methods The patients aged ≥ 18 years admitted in NICU of Nanfang Hospital for ≥ 48 hours from May 2010 to April 2011 were enrolled.The possible risk factors,including the general information,the worst Glasgow Coma Scale (GCS) score,as well as Acute Physiology and Chronic Health Evaluation (APACHE) Ⅱ scores within 24 hours in NICU,whether the occurrence of HAP,whether with some underlying disease or symptoms within the time of study and using specific drug therapy or invasive procedures were investigated retrospectively.The duration of continuous medical interventions was recorded at the same time,and the continuous variables were quantified and stratified.Results A total of 243 patients were enrolled,and 50 (20.6％) of them developed HAP.Univariate analysis showed that the proportions of coma (44.0％ vs.29.0％ ;x2 =4.091,P =0.043) and APACHE Ⅱ score ≥ 15 (60.0％ vs.38.9％ ;x2 =7.232,P =0.007) in the HAP group were significantly higher than those in the non-HAP group.There were significant differences in using antacids (＜ 6 d: 38.0％ vs.19.7％ ; ≥ 6 d: 18.0％ vs.25.9％ ; x2 =7.521,P =0.023),sedatives (＜2 d: 30.0％ vs.37.3％ ; ≥2 d: 46.0％ vs.28.0％ ;x2 =6.064,P =0.048),blood products (＜3 d: 24.0％ vs.9.8％ ; ≥ 3 d: 6.0％ vs.7.3％ ; x2 =7.150,P =0.028),endotracheal intubation (＜ 5 d:24.0％ vs.10.9％ ; ≥ 5d: 26.0％ vs.15.5％ ; x2 =10.698,P =0.005),mechanical ventilation (＜ 4 d:6.0％ vs.7.8％ ; ≥ 4 d: 30.0％ vs.7.8％ ; x2=,P =0.000) and indwelling nasogastric tube (＜ 7 d:56.0％vs.37.3％ ; ≥7d: 42.0％ vs.44.6％ ;x2 =10.410,P =0.005) between the two groups.Multivariate logistic regression analysis showed that mechanical ventilation ≥ 4 d (odds ratio [OR] 6.481,95％ confidence interval [CI] 2.522-16.654; P=0.000),indwelling nasogastric tube ＜7 d (OR 12.504,95％ CI 1.614-96.869; P =0.016) and using antacids ＜ 6 d (OR 2.271,95％ CI 1.042-4.949; P =0.039) were the independent risk factors for HAP in NICU patients.Conclusions Mechanical ventilation,indwelling nasogastric tube and using antacids are the independent risk factors for HAP in NICU patients,and thus it needs to take targeted measures.

Objective To extract alkaloids from Corydalis decumbens (AsCD) by supercritical CO2 fluid extraction (SFE) and to evaluate protective effects of AsCD against hydrogen peroxide (H2O2)-induced apoptosis in rat PC12 cells.Methods AsCD were extracted by SFE and oxidative damage PC12 cells model was induced by H2O2.The survival rate of the cells was determined by MTT assay; Lactate dehydrogenase release was determined by ultraviolet spectrophotometry; Flow cytometry was used to detect apoptosis; Caspase-3 mRNA and protein were determined by real-time PCR and Western blotting assay,respectively.Results AsCD remarkably reduced the cytotoxicity,prevented membrane damage,and inhibited cell apoptosis.AsCD inhibited Caspase-3 mRNA and protein expression induced by H2O2 in PC12 cells.Conclusion AsCD possess protective effects against H2O2-induced apoptosis in PC12 cells,and the mechanism of AsCD responsible to the inhibition of apoptosis is possibly attributed to thedown-regulating Caspase-3 expression.AsCD might be useful in the treatment of oxidative stress-related neurodegenerative diseases.