Objective To investigate the possibility of the involvement of RhoA/mDia1 pathway to cause the expression of phosphorylate ezrin-radixin-moesin (p-ERM) in rat pulmonary micro-vascular endothelial cell (PMVEC) after the stimulation of lipopolysaccharide (LPS).Methods The specimens of lung tissue were taken from healthy male SPF grade SD rat with 100-120 g body weight which was purchased from the laboratory animal center of Anhui province.After culture,the PMVECs were randomly divided into dose-dependent groups (0,0.1,1,10 μg/mL LPS added in PMVECs and cultured for30 min,n =8 in each),time-dependent groups (10 μg/mL LPS added to PMVECs cultured for 0,15,30,60,120 min,n =8 in each) and intervention group (n =8).In the intervention group,PMVECs were cultured with 1 μg/mL C3 transferase in serum free media for 240 min,followed by treatment with 10 μg/mL LPS for 30 min.Meanwhile,two control groups in serum-free DMEM medium were made by adding 10.μg/mL LPS to PMVECs and 1 μg/mL C3 transferase to PMVECs respectively cultured for 30 min (n =8 in each).Western blot was used to detect the level of p-ERM,ERM and mDia1.Data were analyzed with SPSS 16.0 software,while one way analysis of variance (ANOVA) was used to compare multiple sets of variables,the intergroup comparisons were analyzed by the least-significant-difference (LSD) tests,with P ＜0.05 for the statistically significant difference.Results ERM,p-ERM and mDia1 were presented in rat PMVEC.Stimulation with LPS up-regulated p-ERM,mDia1 in a dose-dependent manner:LPS [0 μg/mL LPS group:(0.520±0.101),0.1 μg/mL LPS group:(0.657 ±0.092),1 μg/mL LPS group:(0.891 ±0.167),10 μg/mL LPS group:(1.227 ±0.106);0 μg/mL group vs.0.1 μg/mL group,P ＞0.05;the rest P ＜0.01];and mDia1 [0 μg/mL LPS group:(0.200 ±0.102),0.1 μg/mL LPS group:(0.430 ±0.121),1 μg/mL LPS group:(0.603 ±0.154),10 μg/mL LPS group:(0.887 ±0.204);0.1 μg/mL group vs.1 μg/mL group,P ＞ 0.05;the rest P ＜ 0.05].In time-dependent group,the level of p-ERM protein increased at 15 min (0.670 ±0.149),peaked at 30 min (1.175 ±0.103),then decreased,at 60 min (0.959 ±0.189),90 min (0.842 ±0.129),but kept at higher level at 120 min (0.767 ±0.097) than that in control group (0.471 ±0.157,15 min group vs.120 min group,60 min group vs.90 min group and 90 min group vs.120 min group,P ＞ 0.05;the rest P ＜ 0.05);and the level of mDia1 increased at 15 min (0.779 ±0.035),peaked at 30 min (0.889 ±0.036) then decreased at 60 min (0.648 ±0.019),90 min (0.582 ±0.068),but kept at higher level at 120 min (0.526 ±0.059) than that in control group (0.284±0.118,all P ＜ 0.01).C3 transferase caused a marked attenuation of LPS induced p-ERM expression [control group:(0.339 ± 0.069);C3 + LPS group:(0.438 ± 0.07);C3 control group:(0.352 ± 0.071);LPS control group:(0.634 ± 0.191),C3 + LPS group vs.LPS control group,P =0.01],as the same in mDia1 [control group:(0.449 ±0.122);C3 + LPS group:(0.380 ±0.148);C3 control group:(0.404 ±0.164);LPS control group:(0.622 ±0.174),C3 + LPS group vs.LPS control group,P ＜ 0.01].Conclusions LPS could up-regulated the expression of p-ERM protein,and inhibition of RhoA/mDia1 signal pathway by C3 transferase could down-regulated the p-ERM levels.

Objective To evaluate the relationship and screening value of percentage of body fat (BF%) and waist height ratio (WHtR) for hyperlipidemia in physical examination people. Methods A total of 2 668 objects taking physical examination in Henan Province People′s Hospital from September to December 2014 were included in this study. Values of height, body mass index (BMI), waist circumference, body composition and blood lipid level were detected. The receiver oper?ating characteristic curve (ROC) was used to analyze the screening rate of WHtR and BF%on hyperlipidemia with sensitivi?ty, specific and area under the curve (AUC). After stratified by age, waist circumference and BMI, multivariable logistic re?gression analysis was used to investigate the association between hyperlipidemia risk, BF% and WHtR. Results The screening accuracy rate on hyperlipidemia was higher for BF%, AUC was 0.79 in both female and male people. Among wom?en with BMI<18.5 kg/m2 and 18.5~<24 kg/m2, the risk of hyperlipidemia was higher in superfatted group than that of normal group. There was no correlation between WHtR and hyperlipidemia. Among men older than 40 y or with abnormal waist cir?cumference (≥85 cm), the risk of hyperlipidemia was higher in superfatted group than that of normal group, but not associat?ed with WHtR. Conclusion The BF%is a better screening indicator for hyperlipidemia compared with that of WHtR and BMI. Women with BMI<18.5 kg/m2 and 18.5~<24 kg/m2 and men older than 40 y or with waist circumference over 85 cm are suggested to do body composition tests to improve screening accuracy for hyperlipidemia.

Objective To explore the effect of hospital-community-family integrated care on the physical and mental function of discharged stroke patients. Methods Sixty stroke patients discharged from the third people′s hospital of Bengbu were recruited from January 1, 2014 to April 30, 2015. The patients were divided into intervention group and control group by random number table, and 30 patients in each group. Rehabilitated nursing intervention including feeding, language, physical and psychological and psychological trainings were conducted in intervention group, while participants in control group only received routing nursing service. Then, the Barthel index scores, Fugl-Meyer motor function scores and Hanmilton Depression Scale (HAMD) scores were assessed in both two groups pre-intervention and six months after intervention. Results Intervened before and 6 months after the intervention group of patients with Barthel index score respectively (44.17 ± 11.21) points, (72.47 ± 15.36) points, Fugl-Meyer motor function scores were respectively (43.47±16.22) points, (62.39 ±15.41) points, HAMD scores were (26.81 ± 8.24) points, (17.42 ± 6.29). The difference was statistically significant (t=8.16, 4.64, 4.97, P <0.01). In contrast, the control group of patients with Barthel index score changes showed statistical significance (t=1.94, P=0.03), HAMD score also had differences (t=1.86, P=0.04) and the change was far less than the intervention group. Between the two groups after the intervention compared with Barthel index score, Fugl-Meyer motor function score and HAMD also had statistical significance (t=5.81, 3.55, 2.35, P = 0.00). Conclusions The rehabilitated nursing intervention has evident effects onliving environment,daily life, physical and mental function in discharged stroke patients, and the intervention approaches we used have certain clinical practice value.

Purpose To investigate the effects of chemotactic factor CCR4 on the abi1ity of pro1iferation,ce11 cyc1e,invasion,and mi-gration of human ga11b1adder cancer ce11. Methods Western b1ot was used to detect the expression 1eve1 of CCR4 in ga11b1adder carci-noma ce11s. Ga11b1adder carcinoma ce11s was infected by means of s1ow virus,the CCR4 gene si1encing was conducted using siRNA-CCR4 interference techno1ogy. Ga11b1adder carcinoma ce11s GBC-SD were divided into three groups( GBC-SD,GBC-SD/CCR4-RNAi and GBC-SD/contro1). CCL17,a 1igand of CCR4,was used to act on these three groups of ce11s. CCK8 method was used to detect the ce11 pro1iferation abi1ity of three groups. F1ow cytometry was used to test ce11 cyc1e. Tanswe11 assay was app1ied to detect ce11 migration and invasion abi1ity. Western b1ot was performed to detect the expression of its corresponding 1igands CCL17 and CCL22 proteins. Re-sults CCR4 gene si1ence did not inf1uence ce11 cyc1e and pro1iferation of ga11b1adder ce11 GBC-SD,but can significant1y inhibit GBC-SD ce11 invasion and movement abi1ity,CCR4 gene si1ence had no inf1uence on the expression of CCL17 and CCL22 gene in tumor ce11s. Conclusion Ga11b1adder carcinoma ce11s GBC-SD express chemokine receptor CCR4,chemokine receptor CCR4 can promote the invasion and metastasis of GBC-SD ce11s.

Pathogenesis of Parkinson's disease (PD),a common neurodegenerative disease,is not well established.Immune-inflammatory responses are considered to be important in the development and progression of PD,including over-activated microglia,increased inflammatory cytokines,changes in compositions and phenotypes of T lymphocytes,increased antibodies produced by B lymphocytes.Recent studies have found that T cells in PD patients can recognize α-synuclein peptides and become a research hotspot.In this review,we summarize the research progress in innate and adaptive immune-inflammatory responses in pathogenesis of PD.

OBJECTIVETo research the pharmacological action of curcumin solid dispersions (SDs, curcumin and polyvinylpyrrolidone (PVP) k30 in the ratio of 1:8) was investigated on experimental gastric ulcer in rats and mice.

METHODAnimals were randomly divided into several experimental groups. Each group consisted of 10 animals. The control group received PVP vehicle (720 mg x kg(-1), po) throughout the course of the experiments. The treatment groups received different doses of curcumin SDs (equivalent to curcumin 10, 30 and 90 mg x kg(-1), po), and ranitidine (27 mg x kg(-1), po) was used as the positive control. In acetic acid-induced gastric ulcers model, serum NO, plasma ET and gastric ulcer indexes of rats were measured after oral administration for 14 d. In rat ulcer model induced by pylorus-ligature, gastric volume pepsin and gastric ulcer indexes of rats were measured after oral administration for 3 d and pylorus-ligature inducement for 16 h. Gastric ulcer indexes of mice were measurement after oral administration for 3 d and subcutaneous injection reserpine 10 mg x kg(-1).

RESULTThe results showed that curcumin SDs (equivalent to curcumin 30, and 90 mg x kg(-1), po) could reduce the ulcer indexes 4.59 +/- 0.96 and 3.33 +/- 0.93 (P < 0.01), and increase serum NO level (29.75 +/- 5.90) mmol x L(-1) (P < 0.05) and (39.63 +/- 12.73) mmol x L(-1) (P < 0.01), compared to gastric index 5.87 +/- 0.48 and NO level (23.63 +/- 5.73) mmol x L(-1) in control group. Compared to plasma ET (163.65 +/- 63.84) ng x L(-1) in control group, curcumin SDs (equivalent to 90 mg x kg(-1), po) could decrease plasma ET level (104.22 +/- 63.84) ng x L(-1) (P < 0.05). Compared to gastric ulcer indexes 4.25 +/- 0.71 of control group in rat pylorus-ligature model, curcumin SDs (equivalent to curcumin 90 mg x kg(-1)) could reduce gastric ulcer to 2.38 +/- 0.74 (P < 0.01). Compared to gastric volume (14.61 +/- 1.80) mL, acidity of gastric juice (87.70 +/- 9.84) mmol x L(-1), and the activity of pepsin (408.63 +/- 41.75) U x mL(-1), curcumin SDs (equivalent to curcumin 30, 90 mg x kg(-1)) could reduce gastric volume to (12.68 +/- 1.46) mL (P < 0.05) and (9.99 +/- 0.79) mL (P < 0.01), reduce acidity of gastric juice to (77.62 +/- 8.34) mmol x L(-1) (P < 0.05) and (65.77 +/- 8.19) mmol x L(-1) (P < 0.01), inhibit the activity of pepsin to (358.13 +/- 37.44) U x mL(-1) (P < 0.05) and (292.13 +/- 41.93) U x mL(-1) (P < 0.01). In reserpine-induce gastric ulcer model, curcumin SDs (equivalent to curcumin 30, 90 mg x kg(-1)) could reduce gastric ulcer indexes to 3.88 +/- 0.40 and 3.03 +/- 0.64 (P < 0.01), compared to that of control group 5.13 +/- 0.59.

CONCLUSIONSeveral animal gastric ulcer models prove that curcumin SDs has anti-gastric ulcer effects by inhibiting gastric acid secretion, reducing gastric juice acidity, inhibiting the activity of pepsin and promoting healing of ulcer. These findings show a potential application of curcumin SDs as an anti-ulcerogenic drug.

Animals ; Anti-Ulcer Agents ; administration & dosage ; chemistry ; Curcumin ; administration & dosage ; chemistry ; Disease Models, Animal ; Female ; Humans ; Male ; Plant Extracts ; administration & dosage ; chemistry ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Stomach Ulcer ; drug therapy

The causes of primary adrenal insufficiency(PAI) are varying, however, anti-phospholipid syndrome (APS) is a relatively rare one. PAI lacks unique clinical manifestations, so the confirmation of PAI was easily to be neglected by physicians. We report a case with abdominal pain as the first complaint, followed by multiple infections, thrombotic events, and aggravating fatigue. Through a series of the laboratory examination, medical imaging, and pathology examination, this patient was diagnosed as PAI caused by APS. Combining this report with literature review, we aim to raise awareness of the disease and avoid misdiagnosis and missed diagnosis.

Objective To investigate the effect of galectin-1 preconditioning on pyroptosis of venti-lator-induced lung injury(VILI)in mice.Methods Thirty clean grade healthy male C57BL/6 mice,aged 6-8 weeks,weighing 22-30 g,were divided into three groups by random number table method:control group(group C),VILI group(group V),and galectin-1+VILI group(group G),10 mice in each group.After endotracheal intubation,group C kept spontaneous breathing for 4 hours,groups V and G kept me-chanical ventilation for 4 hours.One hour before endotracheal intubation,groups C and V were intraperito-neally injected with normal saline 0.75 ml,and group G was intraperitoneally injected with galectin-1 3 μg.Arterial blood was collected before endotracheal intubation and after spontaneous respiration or ventilation to detect PaO2.Then mice were sacrificed and bronchoalveolar lavage fluid(BALF)was collected.Concentra-tions of IL-1β and IL-18 in BALF were detected by ELISA.Lung tissue was collected for determination of the wet weight/dry weight ratio(W/D).The expression of GSDMD,caspase-1,and caspase-11 mRNA and protein in lung tissues were detected by qRT-PCR and Western blot.Pathological changes of the lungs were observed and scored by HE staining.Results Compared with group C,PaO2 were significantly decreased,W/D,concentrations of IL-1β and IL-18 in BALF,mRNA and protein expressions of GSDMD,caspase-1 and caspase-11,and lung injury score were significantly increased in groups V and G(P＜0.05).Com-pared with group V,PaO2 was significantly increased,W/D,concentrations of IL-1β and IL-18 in BALF,mRNA and protein expressions of GSDMD,caspase-1,and caspase-11,and lung injury score were signifi-cantly decreased in group G(P＜0.05).Conclusion Galectin-1 can increase PaO2 in mice and reduce IL-1β and IL-18 concentration,mRNA expression and protein content of classical non-classical pyroptosis pathway related genes,and reduce VILI in mice.

The abnormal increase of iron content in the substantia nigra pars compacta of Parkinson's disease (PD) is closely related to dopaminergic neuron injury, which affects the occurrence and development of PD. MRI techniques, including iron concentration-sensitive R2*, Susceptibility Weighted Imaging (SWI) and Quantitative Susceptibility Mapping (QSM), have already applied in the quantification of iron load in brains. MRI techniques have wide application prospects in the early diagnosis, differential diagnosis, monitoring the disease progress and guiding treatment of PD. This article runs retrospective analysis on MRI quantitative research status of iron deposition in brains of patients with PD.

Objective:To evaluate the effect of panaxydol on ventilator-induced lung injury(VILI) in mice, and the relationship with Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor E2-related factor 2 (Nrf2) signaling pathway.Methods:Fifty healthy clean-grade male C57BL/6 mice, aged 6-8 weeks, weighing 20-25 g, were divided into 5 groups ( n=10 each) using a random number table method: control group (group C), VILI group, low-dose panaxydol group (L-PX group, 5 mg/kg), medium-dose panaxydol group (M-PX group, 10 mg/kg) and high-dose panaxydol group (H-PX group, 20 mg/kg). The corresponding doses of panaxydol were intraperitoneally injected for 7 consecutive days once a day in L-PX group, M-PX group and H-PX group. The equal volume of normal saline was given instead in C group and VILI group. Only tracheotomy was performed and animals kept spontaneous breathing for 4 h in group C, and the animals were mechanically ventilated (tidal volume 30 ml/kg, respiratory rate 70 breaths/min, inspiratory/expiratory ratio 1∶2, fraction of inspired oxygen 21%) for 4 h in VILI, L-PX, M-PX and H-PX groups. Blood samples from the femoral artery were collected for arterial blood gas analysis at 4 h of ventilation, and PaO 2 was recorded. The mice were then sacrificed under deep anesthesia, and bronchoalveolar lavage fluid (BALF), lung tissues and serum samples were collected. The concentrations of TNF-α and IL-1β in BALF and serum were measured by enzyme-linked immunosorbent assay. The wet/dry lung weight (W/D) ratio was measured, the protein concentrations in BALF were measured by bicinchoninic acid assay, the pathological changes of lung tissues were examined by HE staining, lung injury was scored, and the level of ROS in lung tissues was detected by DCFH-DA fluorescence probe.The expression of Keap1 and Nrf2 in lung tissues was detected by Western blot. Results:Compared with group C, the PaO 2 was significantly decreased, the lung injury score, W/D ratio, protein concentrations in BALF and concentrations of TNF-α and IL-1β in BALF and serum were increased, the expression of Keap1 and Nrf2 was up-regulated, and the fluorescence of ROS was enhanced in the other four groups ( P<0.05). Compared with group VILI, PaO 2 was significantly increased, the lung injury score was decreased, lung W/D ratio, protein concentrations in BALF, and concentrations of TNF-α and IL-1 β in BALF and serum were decreased, and the fluorescence of ROS was weakened in L-PX, M-PX, and H-PX groups, and the expression of Keap1 was down-regulated, the fluorescence of ROS was weakened, and the expression of Nrf2 was up-regulated in M-PX and H-PX groups ( P<0.05). Compared with group L-PX, PaO 2 was significantly increased, the lung injury score, W/D ratio, protein concentrations in BALF and concentrations of TNF-α and IL-1β in BALF were decreased, the expression of Keap1 was down-regulated, and the expression of Nrf2 was up-regulated and the fluorescence of ROS was weakened in M-PX and H-PX groups ( P<0.05). Compared with group M-PX, PaO 2 was significantly increased, the lung injury score, W/D ratio, protein concentrations in BALF and concentrations of TNF-α and IL-1β in BALF were decreased, the expression of Keap1 was down-regulated, the expression of Nrf2 was up-regulated, and the fluorescence of ROS was weakened in H-PX group( P<0.05). Conclusions:Panaxydol can reduce VILI in mice, and the mechanism may be related to activation of the Keap1/Nrf2 signaling pathway and inhibition of oxidative stress.