Brain edema could be secondary to cerebral lesion caused by a variety of reasons, severe cases may result in brain herniation or even death. Accurate real-time monitoring of cerebral edema, rational application of dehydrating drugs, and timely treatment of cerebral edema were very important for patients. However, there were defects in the monitoring methods commonly used in clinical practice. Noninvasive brain-edema monitoring was a new method, which can quantify the degree of brain edema by electromagnetic disturbance and directly reflect the state of brain edema. This article reviews the application of noninvasive brain-edema monitoring in the treatment of in critically ill patients with traumatic brain injury.

Objective:To evaluate the role of small ubiquitin-associated modifier (SUMO) E3 ligase (PIAS)-regulated SUMOylation of peroxisome proliferator-activated receptor γ (PPARγ) in the endogenous protective mechanism against endotoxin-induced acute lung injury (ALI) in mice.Methods:Experiment Ⅰ Twenty-four clean-grade wild type male C57BL/6 mice, aged 6-8 weeks, weighing 18-22 g, were divided into 4 groups ( n=6 each) using a random number table method: control group (C group), ALI group, ALI+ PPARγ inducer TZD group (ALI+ T group) and ALI+ TZD+ SUMOylation inhibitor anacardic acid group (ALI+ T+ A group). Lipopolysaccharide (LPS) 15 mg/kg was injected into the tail vein to develop the ALI model. In ALI+ T+ A group, anacardic acid 5 mg/kg was intraperitoneally injected at 1 h before LPS administration. In ALI+ T group and ALI+ T+ A group, TZD 50 mg/kg was intraperitoneally injected at 30 min before LPS administration. The mice were sacrificed at 12 h after LPS administration, and the lung tissues were obtained to examine the pathological changes which were scored and to determine the wet/dry (W/D) weight ratio, and expression of PIAS1, PIAS2, PIAS3 and PIASy protein and mRNA (by Western blot or polymerase chain reaction). Experiment Ⅱ Mouse alveolar macrophages (MH-S cells) were cultured in vitro and divided into 4 groups ( n=5 each) using a random number table method: control group (C group), LPS group, LPS+ PIAS2 siRNA group (L+ P group) and LPS+ Con siRNA group (L+ C group). Cells were routinely cultured in group C. Cells were stimulated with 10 μg/ml LPS to develop the model of endotoxin challenge. PIAS2 siRNA 50 nmol/L and Con siRNA 50 nmol/L were transfected at 48 h before LPS was added in L+ P group and L+ C group, respectively. The cells were collected at 24 h of incubation with LPS to determine the cell viability, levels of M1 and M2 alveolar macrophages (by flow cytometry), expression of PIAS2 and PPARγ (by Western blot), co-expression of PPARγ-SUMO1 (by immunoprecipitation) and expression of tumor necrosis factor-alpha (TNF-α) and interleukin-10 (IL-10) mRNA (by polymerase chain reaction). The ratio of M1/M2 was calculated. Results:Experiment Ⅰ Compared with C group, the lung injury scores and W/D ratio were significantly increased, and the expression of PIAS2 protein and mRNA was up-regulated in the other three groups ( P<0.05). Compared with ALI group, the lung injury scores and W/D ratio were significantly decreased, and the expression of PIAS2 protein and mRNA was up-regulated in ALI+ T group and ALI+ T+ A group ( P<0.05). Compared with ALI+ T group, the lung injury scores and W/D ratio were significantly increased, and the expression of PIAS2 protein and mRNA was down-regulated in ALI+ T+ A group ( P<0.05). There was no significant difference in the expression of PIAS1, PIAS3 and PIASy protein and mRNA in lung tissues among the four groups ( P>0.05). Experiment Ⅱ Compared with C group, the cell viability was significantly decreased, the expression of PPARγ and co-expression of PPARγ-SUMO1 was up-regulated, the levels of M1 and M2 macrophages and M1/M2 ratio were increased, the expression of TNF-α mRNA was up-regulated, and the expression of IL-10 mRNA was down-regulated in the other three groups, and PIAS2 expression was significantly up-regulated in L group and L+ C group ( P<0.05). Compared with L group, the cell viability was significantly decreased, the expression of PIAS2 and PPARγ and PPARγ-SUMO1 co-expression were down-regulated, the M1 macrophage level and M1/M2 ratio were increased, TNF-α mRNA expression was up-regulated, and the expression of IL-10 mRNA was down-regulated in L+ P group ( P<0.05), and no significant change was found in the parameters mentioned above in L+ C group ( P>0.05). Compared with L+ C group, the cell viability was significantly decreased, the expression of PIAS2 and PPARγ and co-expression of PPARγ-SUMO1 were down-regulated, the level of M1 alveolar macrophages and M1/M2 ratio were increased, the expression of TNF-α mRNA was down-regulated, and the expression of IL-10 mRNA was up-regulated in L+ P group ( P<0.05). Conclusions:PIAS2-regulated SUMOylation of PPARγ is the endogenous protective mechanism against endotoxin-induced ALI in mice, which may be related to inhibition of macrophage polarization into M1 type and alleviation of inflammatory responses.

Restoration of lower extremity function is one of the important goals for rehabilitation of stroke patients. As a non-invasive brain stimulation technique, transcranial magnetic stimulation can regulate neuronal excitability and promote neuroplasticity, which has great potential in the field of neurorehabilitation. Repetitive transcranial magnetic stimulation has been widely used to treat upper extremity and hand motor function after stroke. Recent studies have shown that repetitive transcranial magnetic stimulation can improve the motor function of lower limbs after stroke. This article explores the clinical progress of repetitive transcranial magnetic stimulation in lower extremity motor function after stroke, and investigates the mechanism hypothesis of motor function system dysfunction after stroke and possible mechanism of reorganization of lower extremity motor function after stroke, in order to provide new ideas for future research and clinical application.

Objective:To evaluate the relationship between heme oxygenase-1 (HO-1) and peroxisome proliferator-activated receptor γ (PPARγ) during alveolar macrophage polarization in a mouse model of endotoxin-induced acute lung injury (ALI).Methods:Thirty clean-grade male C57BL/6 mice (24 wide-type mice and 6 HO-1 knockout mice), aged 6-8 weeks, weighing 18-22 g, were studied.Wide-type mice were divided into 4 groups ( n=6 each) using a random number table method: control group (C group), ALI group, ALI+ HO-1 agonist hemin group (ALI+ H group), and ALI+ hemin+ PPARγ antagonist T0070907 group (ALI+ H+ T group).HO-1 knockout mice in which the ALI model was developed served as ALI+ HO-1 -/- group.ALI model was developed by injecting lipopolysaccharide (LPS) 15 mg/kg via the tail vein in anesthetized animals.T0070907 1.5 mg/kg was intraperitoneally injected at 1 h before LPS administration in ALI+ H+ T group, and hemin 50 mg/kg was intraperitoneally injected at 30 min before LPS administration in ALI+ H group and ALI+ H+ T group.Mice were sacrificed at 12 h after LPS administration, and lung tissues were obtained to measure the wet to dry weight ratio (W/D ratio), to observe pathological changes which were scored, and to determine the F4/80+ /CD86+ labeled M1 alveolar macrophages and the F4/80+ /CD206+ labeled M2 alveolar macrophages (by flow cytometry), contents of M1 macrophage-related genes inducible nitric oxide synthase (iNOS) and M2 macrophage-related genes Arginase-1 (Arg-1) (by enzyme-linked immunosorbent assay), and the expression of HO-1 and PPARγ (by Western blot). Results:Compared with C group, the lung injury score, W/D ratio, levels of CD86 and CD206, and contents of iNOS and Arg-1 were significantly increased, and PPARγ expression was up-regulated in the other four groups ( P<0.05), and HO-1 protein expression was up-regulated in ALI, ALI+ H and ALI+ H+ T groups ( P<0.05).Compared with ALI group, the lung injury score, W/D ratio, and levels of CD86 and iNOS were significantly increased, the levels of CD206 and Arg-1 were decreased, and the expression of HO-1 and PPARγ was down-regulated in ALI+ HO-1 -/- group, the lung injury score, W/D ratio and levels of CD86 and iNOS were significantly decreased, the levels of CD206 and Arg-1 were increased, and the expression of HO-1 and PPARγ was up-regulated in ALI+ H group ( P<0.05), and no significant change was found in the parameters mentioned above in ALI+ H+ T group ( P>0.05).Compared with ALI+ H group, the lung injury score, W/D ratio and levels of CD86 and iNOS were significantly increased, the levels of CD206 and Arg-1 were decreased, the expression of PPARγ was down-regulated ( P<0.05), and no significant change was found in the expression of HO-1 in ALI+ H+ T group ( P>0.05). Conclusions:HO-1 can up-regulate the expression of PPARγ, inhibit the polarization of alveolar macrophages toward M1 phenotype and promote the polarization toward M2 phenotype, thus playing an endogenous protective role in endotoxin-induced ALI in mice.

Objective To investigate the association of red cell distribution width (RDW) with all-cause and cardiovascular disease (CVD)-related mortality in patients undergoing continuous ambulatory peritoneal dialysis (CAPD).Methods A retrospective analysis was performed on 207 patients who initiated CAPD for more than 3 months between July 2005 and March 2016 in the First Hospital Affiliated to Zhengzhou University.Baseline data on demographic,clinical and biochemical variables as well as comorbidities were obtained;medications and clinic outcomes were recorded.According to receiver operator characteristic curve (ROC) analysis,patients were divided into high RDW (RDW ＞ 15.1％) and low RDW (RDW≤ 15.1％) groups.The data of two groups were compared and Spearman's correlation analysis was used to explore the association of RDW with clinical and biochemical parameters.Survival curves were calculated using Kaplan-Meier method.Cox regression model was employed to analyze risk factors of all-cause and CVD-related mortality.Results In this study,207 CAPD patients were enrolled.The overall median survival time was 80 months.And the median survival time of high RDW group (68 patients) and low RDW group (139 patients) were 59 months and 96 months,respectively.There were statistical differences in diastole pressure,hemoglobin,hematocrit,serum albumin,intact parathyroid hormone (iPTH),eGFR,cholesterol,lipoprotein a,4-hour dialysate-to-plasma ratio for creatinine (4hD/Pcr),total Ccr (P ＜ 0.05,respectively);the two groups also varied in the proportion of chronic obstructive pulmonary disease,cardiovascular disease and hyperlipidemia,as well as in the use of iron supplements,angiotensin-converting enzyme (ACE) inhibitors or angiotensin Ⅱ receptor blockers (ARB),and beta-receptor blockers (P＜0.05,respectively).Cardiovascular event was a leading cause of mortality.Kaplan-Meier survival curves showed that the high RDW group had higher all-cause and CVD-related mortality compared with the low RDW group (P ＜ 0.01).The 1-year,3-year,and 5-year patient survivals of the high RDW and low RDW group were 87.97％ vs 97.01％,58.02％ vs 81.53％,and 41.62％ vs 67.96％,respectively,demonstrating significant differences (P=0.001).Multivariate Cox regression analysis showed that high RDW was independent risk factor for all-cause mortality (HR=1.212,95％CI:1.007-1.458,P=0.042) and CVD-related mortality (HR=1.697,95％ CI:1.030-2.795,P=0.038).Conclusion RDW is associated with mortality risks in CAPD patients and can be stratified as a valuable indicator for the risk of death.

Objective To investigate whether the JAK2/STAT3 signaling pathway is involved in the epithelial-mesenchymal transition (EMT) of peritoneal mesothelial cells in uremic peritoneal dialysis (PD) rats.Methods A total of 48 male Sprague-Dawley (SD) rats were randomly separated into six groups:normal control group (NC group,n=8),sham group (n=8),uremic group (n=8),PD group (n=8),S3I-201 control group (n=8) and S3I-201 group (n=8).Uremic model generated by 5/6 nephrectomy surgery in rats was established.The rats of PD group,S3I-201 control group and S3I-201 group received daily infusion of 4.25％ glucose-based peritoneal dialysate fluid (3 ml/100 g) from PD catheters for 28 days.Rats of S3I-201 group were injected with STAT3 inhibitor S3I-201 (2.5 mg/kg) solution from the catheters every other day;the same dose of the solvent of S3I-201 was simultaneously given to S3I-201 control group rats.After PD for 28 days,peritoneal function,pathologic changes,and microvessel density (MVD) were evaluated.Creatinine,urea nitrogen and interleukin-6 (IL-6) concentration in blood and dialysate,and protein and mRNA levels of phospho-JAK2 (p-JAK2),phospho-STAT3 (p-STAT3),E-cadherin,alpha-smooth muscle actin (α-SMA) and vascular endothelial growth factor (VEGF) in peritoneum were determined.Results Uremia and peritoneal dialysate could aggravate the peritoneal function and elevate peritoneal thickness and MVD.They could also increased the concentration of IL-6 in blood and dialysate and the expression levels of α-SMA,VEGF,p-JAK2 and p-STAT3 in peritoneum,while lowering E-cadherin expression in peritoneum.These manifestations were even more remarkable in PD group compared to those in uremic group.There was no statistical difference between the S3I-201 control group and the PD group as regards all the index (all P ＞ 0.05).Compared with the S3I-201 control group,the rats treated with S3I-201 showed better peritoneal function.S3I-201 could reduce peritoneal thickness (P＜0.05),MVD (P＜0.05),the concentration of IL-6 in blood and dialysate,the mRNA and protein expression of α-SMA,VEGF,p-JAK2 and p-STAT3 (all P ＜ 0.05),while enhance the mRNA and protein expression of E-cadherin (all P ＜ 0.05).Conclusions After STAT3 is inhibited,the peritoneal thickness,MVD and IL-6 concentration in PD rats are decreased,and EMT is also inhibited,while peritoneal function is improved.The JAK2/STAT3 signaling pathway may thus be involved in the process of EMT of peritoneum in uremic peritoneal dialysis rats by regulating the expression of IL-6.

A total of three hundred and fourteen patients with maxillofacial fracture under 14 years old were treated at Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Zhengzhou University from October 2010 to October 2017 were collected and retrospective analysis was conducted. Age, gender, injury factors, type of fracture, associated injuries and treatment has been analysed. There were 196 male and 118 female. The most common injury factor was fall (148 cases), accounting for 47.1% of all patients. The most common fracture type was mandible fracture (221 cases). Children are not very cooperative with clinical examination, which often leading to misdiagnosis. Age, gender, fracture injury factors, comorbidity and treatment were analyzed to provide the reference for the prevention, diagnosis and treatment.

Objective:To evaluate the changes of neurocognitive function in early stage in patients with first-episode schizophrenia.Methods:In this study,73 cases of patients with first-episode schizophrenia (research group) and 75 cases of health person (control group) were selected from January 2015 to January 2016 in our hospital.The neurocognitive function was evaluated by neuro-psychological testing tool and the data between two group were compared.Results:Scores of delayed recall,total recall,3 trial,2 trial and 1 trial of research group were lower than those of control group in BVMT-R test,and the difference was statistically significant (P＜0.05).In HVLT-R test,the scores of total delay,3 trial and 2 trial of research group were significantly lower than those of control group (P＜0.05).The consuming time of dominant hands and subdominant hands in pegboard tasks were significantly higher in research group than in control group (P＜0.05).Conpletion time of connection test A,color connection 1 and 2 in connection test of research group were significantly higher than those of control group (P＜0.05).Attempt number and correct number in research group in PASAT test were significantly lower than in control group (P＜0.05).Number of search errors in research group was higher than in control group,while number of search correct,search total score and digital sign score were significantly lower than in control group (P＜0.05).Total number of words,color and color / word count in research group were lower than in control group in Stroop color word test,and the difference was statistically significant (P＜0.05).WMS-Ⅲ test results between two group had no significant difference (P＞0.05).Conclusion:The neurocognitive function in early stage in patients with first-episode schizophrenia has been extensively damaged.

Objective To investigate the role of STAT3 transcription factor in IL-6 inducing epithelial mesenchymal transition (EMT) of human peritoneal mesothelial cells (HPMCs).Methods HPMCs were cultured in vitro and grouped.(1) According to the stimulation time with 50 μg/L IL-6,HPMCs were divided into 24,48,72 h groups.(2) HPMCs were grouped 50,100 μg/L according to IL-6 concentration.(3) HPMCs were respectively divided into control group,IL-6 group,empty vector group,empty vector+IL-6 group,virus infecting group and virus infecting+IL-6 group,as lenti-virus vector mediating RNA interference targeting STAT3 was applied.The mRNA expressions of E-cadherin,α-smooth muscle actin (α-SMA) and vascular endothelial growth factor (VEGF) were detected by real time PCR;their protein expressions and the phosphorylation of JAK2 and STAT3 were detected by Western blotting;the expressions and distribution of E-cadherin and α-SMA were observed by immunofluorescence.Results Compared with those in control group,the expression of E-cadherin decreased remarkably (P ＜ 0.05),while the expressions of VEGF and α-SMA and the ratio of phosphorylated (p)-JAK2/JAK2 and p-STAT3/STAT3 increased significantly in IL-6 concentration groups and stimulation time groups (all P ＜ 0.05),which had been dose and time dependent.Compared with empty vector+IL-6 group,virus infecting+IL-6 group had decreased expressions of VEGF and α-SMA,while increased expressions of E-cadherin (all P ＜ 0.05).Conclusions IL-6 can promote VEGF and α-SMA gene expression and prevent E-cadherin gene expression by STAT3,which involves in EMT of peritoneum fibrosis.While STAT3 gene is knocked-down,EMT is inhibited in HPMCs.

Objective To investigate the influence of left ventricular-arterial coupling(VAC) on clinical prognosis of elderly patients with septic shock.Methods A total of 56 elderly septic shoek patients were enrolled in this study,all of whom were admitted to Department of Intensive Care Unit in Zhejiang Hospital from August 2014 to October 2015.The patients were divided into two groups according to the status of left ventricular-arterial coupling when septic shock was diagnosed,which were left ventricular-arterial uncoupling group(UC group) and left ventricular-arterial coupling group(C group).Various parameters were recorded,including blood lactate level,central venous oxygen saturation(ScvO2),serum level of N-terminal pro-brain natriuretic peptide(NT-proBNP) and cardiac troponin Ⅰ (cTN Ⅰ),dose of vasoactive drugs,the total fluid volume and urine volume per hour within 24 hours.The 28-day survival rate was a key index of prognosis.Multivariate logistic regression was taken to analyze risk factors related to death within 28 day.Results Compared with C group,UC group had lower values of left ventricular ejection fraction[(42.43 ±4.76)％ vs (53.17±3.01)％;P＜0.01] and cardiac index[(2.36±0.68) L· min-1 · m 2vs (2.93±0.45)L · min-1 · m-2;P ＜0.01].Yet serum levels of NT-proBNP[lg NT-proBNP 3.93 ±0.53 vs 3.40 ±0.63;P =0.004] and cTN Ⅰ [lg cTN Ⅰ-0.16 ± 0.68 vs-1.03 ± 0.69;P ＜ 0.001] in UC group were higher than those in C group.Moreover,the total fluid volume within 24 hours [(3 806.3 ± 831.4) ml vs (3 142.0±770.0) ml;P =0.016],blood lactate level[(5.61 ±2.68) mmol/L vs (3.93 ± 1.59)mmol/L;P =0.043] and dose of norepinephrine[(0.630 ±0.300) μg · kg-1 · min-1 vs (0.292 ±0.234)μg · kg-1 · min-1;P =0.001] in UC group were greater than those in C group,while ScvO2 [(60.75 ±2.91)％ vs (64.42 ±2.19)％;P＜0.001] and urine volume per hour[(0.518 ±0.358) ml vs (0.926 ±0.678) ml;P =0.007] were less than those in C group.Compared with C group,UC group had a lower 28-day survival rate [43.2％ (19/44) vs 9/12;P =0.049].Ea/Ees ratio was negatively correlated with LVEF,ScvO2 (r =-0.686,P ＜ 0.001;r =-0.411,P =0.002),positively correlated with NT-proBNP,cTN Ⅰ (r =0.294,P =0.028;r =0.363,P =0.006),yet no obvious correlation was noticed with blood lactate level (r =0.170,P =0.21).Multiple logistic regression analysis showed that VAC(OR =11.187,95％ CI 2.489-50.285;P =0.002),lactate level (OR =1.727,95 ％ CI 1.164-2.563;P =0.007) and lg cTN Ⅰ (OR =0.247,95 ％ CI 0.079-0.779;P =0.017) were independent risk factors affecting 28-day mortality.Conclutions In elderly patients with septic shock,left ventricular-arterial uncoupling indicates a lower 28-day survival rate,worse cardiac function and tissue perfusion.Ea/Ees ratio might sever as a predictive indicator of 28-day mortality.