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 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.

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 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.

Objective To explore therapeutic effects of combinative artificial kidney treatment on renal osteopathy.Methods HD + HP Group composed by 30 urinaemia was treated with hemodialysis and hemoperfusion,and the HD Group was treated only with hemodialysis.Clinical symptoms and lab indicators including osteodynia,itch of skin,blood pressure,appetite,sleep,as well as BUN,SCr,Hb,BPC,Ca,P and iPTH,were compared between the two groups.Results Osteodynia decreased by 67.7% (21/31),and itch of skin by 71.0% (22/31)in HD group.Osteodynia decreased by 96.7% (29/30) ,and itch of skin by 96.7% (29/30) in HD + HP group (P ＜0.01 ).iPTH were (65.5 ± 34.4) pmol/L before treatment and (57.1 ± 21.4) pmol/L after treatment in HD group,and (73.5 ± 44.4)pmol/L and (19.1 ± 17.4)pmol/L in HD + HP group.HD Group eliminated less iPTH (P ＞0.05).HD + HP Group removed more serum poison molecules than HD Group ( P ＜ 0.05 ).Conclusions For patients in maintenance-dialysis stage but with higher iPTH,hemodialysis combined with hemoperfusion removes more poison molecules,consequently decreases incidence of renal osteopathy.

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 investigate the diagnostic significance of the relative band power(RBP) of EEG in acute focal cerebral ischemia (AFCI). Methods EEG monitoring was performed in 20 patients with AFCI (51 lesions) in neurological intensive care unit (NICU) and 20 patients with normal EEG (control group) in NICU. The changes of bilateral RBP were observed and analyzed comparatively. RBP in the infarction group was compared with that in the control group. The diagnostic capabilities of all wave-band RBPs were assessed with the receiver operating characteristic (ROC) analysis. Results AFCI shoved asymmetry on all the wave-band RBPs. The RBP of of δwave on the lesion side was significantly higher than that on the normal side (P <0.01). RBPs of α, β and θ waves were decreased significantly (P <0.05). RBP of δ wave in the infarction group was increased significantly compared to the control group (P < 0.01 ). RBPs of α and β waves were decreased significantly (P <0.01). The diagnostic accuracy of the RBP of α was the highest, and both β and δ waves also had significance for the diagnosis of AFCI. Conclusions RBP had an important significance for the early diagnosis of AFCI. Conclusions RBP had an important significance for the early diagnosis of AFCI.

This study is to investigate the effects of aqueous extract of Schisandra chinensis Baill (WWZ), kadsurin, schisandrin A, schisandrin B and schisandrol B on rat hepatic CYP3A. Rats received a daily gavage of aqueous extract of WWZ for different times. The livers were harvested after gavage and subjected to microsome preparation. Microsomal CYP3A activity was determined by measuring the amount of the metabolite of testosterone (6 beta-hydroxytestosterone) with HPLC. Aqueous extract of WWZ, kadsurin and schisandrin A were incubated with microsomes obtained from rat. Microsomal CYP3A activity was determined by HPLC. Primary hepatocytes were separated and extracted from rat, then were treated with aqueous extract of WWZ, schisandrin A, schisandrin B and schisandrol B. Then, the expression of CYP3A1 mRNA was analyzed by RT-PCR. As for the in vivo assay, aqueous extract of WWZ significantly inhibited the enzyme activity of CYP3A after 12 h gavage. The inhibitory effect was converted to inductive effect after 3-day gavage. Aqueous extract of WWZ could induce the enzyme activity of CYP3A after 6-day gavage. Aqueous extract of WWZ and kadsurin showed a dose-dependent inhibition of CYP3A (IC50 of 487.8 microg mL(-1) and 6.2 micromol L(-1), separately). In rat primary hepatocytes, aqueous extract of WWZ (2.5 mg mL(-1)), schisandrin A (0.1 micromol L(-1)), schisandrin B (0.1 micromol L(-1)) and schisandrol B (10 micromol L(-1)) increased significantly the expression of CYP3A1 mRNA by 23%, 55%, 42% and 27%, respectively. Aqueous extract of WWZ could show dual effect on the enzyme activity of CYP3A in rat in vivo. Meanwhile, kadsurin showed a dose-dependent inhibition of the enzyme activity of hepatic CYP3A in vitro. And schisandrin A, schisandrin B and schisandrol B showed significant inductive effect on the expression of rat CYP3A1 mRNA.

0.05),and the levels of Fib and D-dimer were obviously higher but AT-Ⅲ was obviously lower in 2 NS groups than those in normal control group(P