Nuclear factor erythroid-2 related factor 2 ( Nrf2 ) is an important nuclear transcription factor which protects cells a-gainst oxidative stress injury. Upon exposure to reactive oxygen species ( ROS) or electrophilic stress, Nrf2 can translocate into the nucleus, and then bind to the antioxidant response element ( ARE) , regulating the expression of several antioxidant enzymes and phase Ⅱ detoxifying enzymes which aimed at the detoxifica-tion and elimination of harmful exogenous chemicals, resulting in the facilitation of hepatoprotection. Oxidative stress is the com-mon pathogenesis of many liver diseases, while the Nrf2-ARE signaling pathway is extremely important in the prevention and progression of many liver diseases. Nrf2 has more recently been implicated as a new therapeutic target in treating liver diseases. Here, we focus on the most common liver diseases and the devel-opment of these conditions where activation of Nrf2 may alleviate disease progression, so as to provide reference for related re-search in the future.

The Medical Healthcare Service Center,located at the Youxian District,Mianyang City of Sichuan Province,successfully rescued the people affected by the Wenchuan earthquake and the Tangjiashan barrier lake with great help from the senior hospitals.We suggest that the community healthcare service center could play an important role in emergency response system.

AIM: To explore the regulatory effects of cytokines such as EGF, bFGF on expression of neural-specific molecules in mononuclear cells (MNCs) cultured in H-DMEM medium. METHODS: The umbilical cord blood samples were collected from health puerperal natural delivery. The mononuclear cells were isolated by centrifugation over Lymphoprep and planted in T-75 flasks containing H-DMEM medium with or without addition of EGF, bFGF or EGF plus bFGF at a final concentration of 20 ?g/L, respectively. Phenotypic changes were monitored by inverse phase-contrast microscopy. Tau and MAP2 mRNA were determined by reverse-transcript polymerase chain reaction (RT-PCR). Tau and MAP2-positive cell were determined by immunocytochemistry. RESULTS: The expression of tau protein mRNA was negative in uncultured cells, but MAP2 mRNA was positive. In cultured cells, tau protein mRNA expressed positively, MAP2 mRNA expression was upregulated by EGF+bFGF, EGF or bFGF compared with control group (no cytokines). The upregulatory capability of EGF+bFGF to MAP2 mRNA expression was stronger than that of EGF or bFGF alone. The same upregulatory tendency was noted in tau mRNA expression. In the group of control, bFGF, EGF, EGF+bFGF, the rate of MAP2-positive cells was 14.4%, 19.6%, 25.6%, 33.5%, respectively. Tau protein-positive cells were 13.5%, 15.3%, 21.4%, 29.8%, respectively. Under inverse microscopy, the freshly isolated MNCs were small and round, after culturing, the cells became larger with some big, long cytodenrites in the EGF+bFGF group, with 1 or 2 threadlike cytodenrites in the EGF group, or with some short multi-dendron like-astrocyte in the bFGF group and control group, but the number of astrocyte-like cells in the control group was less than that in bFGF group. CONCLUSION: MNCs derived from human umbilical cord blood cells express some neural specific molecules and are upregulated by cytokines, especially EGF and bFGF, which have the synergetic action. [

Cellular fibronectin (cFn) is a type of bioactive non-collagen glycoprotein regarded as the main substance used to maintain periodontal attachment. The content of cFn in some specific sites can reflect the progress of periodontitis or peri-implantitis. This study aims to evaluate the expression of cFn messenger RNA (mRNA) in tissues of adult periodontitis and peri-implantitis by real-time fluorescent quantitative polymerase chain reaction (PCR) and to determine its clinical significance. A total of 30 patients were divided into three groups of 10: healthy, adult periodontitis and peri-implantitis. Periodontal tissue biopsies (1 mm×1 mm×1 mm) from each patient were frozen in liquid nitrogen. Total RNA was extracted from these tissues, and the content, purity and integrity were detected. Specific primers were designed according to the sequence, and the mRNA expression levels of cellular fibronectin were detected by real-time PCR. The purity and integrity of the extracted total RNA were both high, and the specificity of amplified genes was very high with no other pollution. The mRNA expression of cFn in the adult periodontitis group (1.526±0.441) was lower than that in the healthy group (3.253±0.736). However, the mRNA expression of cFn in the peri-implantitis group (3.965±0.537) was significantly higher than that in the healthy group. The difference revealed that although both processes were destructive inflammatory reactions in the periodontium, the pathomechanisms were different and the variation started from the transcription level of the cFn gene.
Adult ; Alveolar Bone Loss ; metabolism ; Female ; Fibronectins ; analysis ; genetics ; Gingiva ; metabolism ; Humans ; Male ; Middle Aged ; Peri-Implantitis ; metabolism ; Periodontal Attachment Loss ; metabolism ; Periodontal Index ; Periodontal Pocket ; metabolism ; Periodontitis ; metabolism ; Periodontium ; metabolism ; RNA, Messenger ; analysis ; Real-Time Polymerase Chain Reaction ; Transcription, Genetic ; genetics ; Young Adult

Objective To explore the role of potassium channel in cardiomyocyte apoptosis induced by ischemia/reperfusion process. Methods Cell viability,caspase-3 activity,intracellular reactive oxygen species(ROS)levels and cell membrane integrity were observed in apoptotic model of mouse cardiomyocytes induced by ischemia/reperfusion(I/R).Experiment groups included negative control,positive control(I/R)and drug treatment group(I/R + potassium channel blocker).Results (1)Potassium channel blockers potently inhibited cardiomyocyte apoptosis induced by I/R.Cell viability in Quinine(81.1%)and BaCl2(82.3%)groups were higher than in positive group (52.1%)(all P＜0.01).(2)Compared with positive control group(482.3%),potassium channel blockers(188.3% in Quinine group and 191.4% in BaCl2 group)inhibited caspase-3 activity significantly 24 hours after reperfusion(P＜0.01).(3)In both positive control and drug groups,the cell lactate dehydrogenase(LDH)leakage was less than 10% at 96 hours after reperfusion.Conclusions Potassium channel blockers can protect injured cardiomyocyte by inhibiting caspase-3 activity and ROS production in I/R process.

ObjectiveTo evaluate the role of p38MAPK signaling pathway in the up-regulation of heme oxygenase-1 (HO-1) expression in the lung tissue in rats with acute lung injury (AL1) induced by endotoxic shock.MethodsForty-eight male SD rats,aged 8 weeks,weighing 180-200 g,were randomly divided into 4 groups ( n =12 each):control group ( group C ) ; endotoxic shock group ( group LS );endotoxic shock +SB203580 (a specific p38MAPK inhibitor) group (group LSS) and SB203580 group (group SB).Normal saline 0.5ml was injected via the femoral vein in groups C and SB,while LPS 10 mg/kg (in 0.5 ml normal saline) was injected via the femoral vein in groups LS and LSS.When MAP was decreased to 75％ of baseline value,10％ dimethyl sulfoxide (DMSO) 0.1 ml was infused via the femoral vein in groups C and LS,while SB203580 5 mol/kg (in 10％ DMSO 0.1 ml) was infused via the femoral vein at a rate of 0.01 ml/min in groups LSS and SB.Arterial blood samples were obtained at 6 h after LPS or normal saline was given for blood gas analysis and oxygenation index (PaO2/FiO2) was calculated.Then the rats were sacrificed and the lungs were removed for microscopic examination.The pathological changes of the lung were scored.The lung water content was calculated.The MDA content,SOD activity,and expression of HO-1 mRNA and protein,p38MAPK protein and phospharylated p38MAPK (p-p38MAPK) protein were determined.ResultsCompared with group C,the oxygenation index and SOD activity were significantly decreased,the pathological score,lung water content and MDA content were significantly increased,and the expression of HO-1 mRNA and protein and p-p38MAPK protein was significantly up-regulated ( P＜0.05),while no significant change was found in p38MAPK protein expression in groups LS and LSS,and no significant change was found in the indexes mentioned above in group SB (P＞0.05).Compared with group LS,the oxygenation index and SOD activity were significantly increased,the pathological score,lung water content and MDA content were significantly decreased,the expression of HO-1 mRNA and protein was significantly up-regulated,and p-p38MAPK protein expression was down-regulated ( P＜0.05),and no significant change was found in p38MAPK protein expression in group LSS ( P＞0.05).ConclusionThe inhibition of p38MAPK signaling pathway can lead to the up-regulation of HO-1 expression in lung tissues in rats with ALI induced by endotoxic shock.

ObjectiveTo acquire the basic information of trainees and analyze the training results and it' s influence factors in the training of rural health appropriate technology in Jiangsu.MethodsWe used the questionnaire to collect data of the trainees' personal information and training results after training.Results A total of 2284 valid questionnaires were collected. There were 73.6％ trainees came from township hospitals,95.1 ％ of them under 45 years old,62.9％ for females,79.2％ have been working for 8 years,3％ with senior professional titles,only 0.4％ had acquire the master's degree or above.Multiple regression analysis showed that the different level of hospitals,the training needs, suitable degree,knowledge familiarity before the training,expert instruction and learning were the main influence factors for the master of the technology; The influence factors for the wish to be re-training were working age,education,the demand for training technology,ease of learning,expert instruction,grasp of this time,appliance of the technology.Conclusionlong-term mechanism for trainning and continue education should be established,and medical workers in rural areas should be strengthen to take the technical training to further improve the rural medical services.

Objective To evaluate the role of activator protein-1 (AP-1 ) in electro-acupuncture (EA )-induced up-regulation of heme oxygenase-1 (HO-1 ) expression in lung tissues in a rabbit model of endotoxic shock .Methods Seventy healthy male New Zealand white rabbits ,aged 2 months ,weighing 1.5-2.0 kg ,were randomly divided into 7 groups ( n=10 each ) using a random number table :normal control group (group C ) , endotoxic shock-induced acute lung injury (ALI ) group (group ALI ) , EA + ALI group (group EL ) , non-acupoint+EA+ ALI group (group NEL ) , curcumin (HO-1 inhibitor ) group (group Cur ) , dimethyl sulfoxide group (group D ) ,and EA+ALI+curcumin group (group ELC ) .Bilateral 15 min EA stimulation of Zusanli and Feishu (according to atlas of animals acupoints ) was performed (frequency 15Hz ) once a day for 5 consecutive days before lipopolysaccharide (LPS ) administration in EL and ELC groups ,while in group NEL ,EA stimulation was performed at non-acupoints located 0.5 cm lateral to Zusanli and Feishu acupoints with the same parameters . The animals were anesthetized with urethane and tracheostomized .The animals kept spontaneous breathing .Right internal carotid artery was cannulated for blood pressure monitoring . Ear vein was cannulated for drug administration .At 5 days after EA stimulation ,curcumin 25 mg/kg (in 0.5 ml of 0.1% dimethyl sulfoxide ) was injected in Cur and ELC groups ,0.1% dimethyl sulfoxide 0.5 ml was injected in D group ,and the equal volume of normal saline was given in the other groups .LPS 5 mg/kg (in 2 ml of 0.9% normal saline ) was injected intravenously at 30 min after administration in ALI ,EL ,NEL and ELC groups ,while the equal volume of normal saline was given in the other three groups .Endotoxic shock was confirmed by decrease in mean arterial pressure to 75% of the baseline value within 2 h after LPS injection .Blood samples were collected from the common carotid artery at 6 h after LPS or normal saline administration and the rabbits were then sacrificed .The lungs were removed for microscopic examination and the pathological changes were scored .The wet/dry lung weight ratio (W/D ratio ) was calculated .The malondialdehyde (MDA ) content and superoxide dismutase (SOD ) activity in lung tissues were detected ,and the expression of HO-1 mRNA ,HO-1 ,c-Jun mRNA and c-Jun in lung tissues was determined by Western blot .Results Compared with group C ,the pathological score ,W/D ratio and MDA content were significantly increased ,and the SOD activity was decreased in ALI ,EL ,NEL and ELC groups ,the expression of HO-1 mRNA ,HO-1 ,c-Jun mRNA and c-Jun was up-regulated in groups ALI ,EL and NEL ( P<0.05 ) ,while no significant change was found in the expression of c-Jun mRNA and c-Jun in group ELC ( P>0.05) .There was no significant difference in the parameters mentioned above between Cur and D groups ( P>0.05 ) .Compared with group ALI ,the pathological score ,W/D ratio and MDA content were significantly decreased ,and SOD activity was increased ,and the expression of HO-1 mRNA and HO-1 was up-regulated in EL and ELC groups ( P<0.05) ,the expression of c-Jun mRNA and c-Jun was up-regulated in group EL ,while down-regulated in group ELC ( P<0.05) ,and no significant change was found in the parameters mentioned above in group NEL ( P>0.05) .The pathological score ,W/D ratio and MDA content were significantly higher ,and the SOD activity and expression of HO-1 mRNA ,HO-1 ,c-Jun mRNA and c-Jun were lower in group ELC than in group EL ( P<0.05) .Conclusion EA up-regulates HO-1 expression through activating AP-1 during endotoxic shock-induced ALI in rabbits ,thus protecting the lung .

Objective The objective of this study was to explore the expression of miRNA-124(miR-124)and its correlation with E-cadherin and androgen receptor(AR)in triple-negative breast cancer(TNBC).Methods The expression of miR-124 was detected by RT-PCR in TNBC tissues and adjacent normal breast tissues.The expression of E-cadherin and AR in TNBC was detected by immunohistochemistry.Results The expression of miR-124 in TNBC tissues was significantly correlated with histological grade and the expression of E-cadherin(P<0.05),and the expression of miR-124 in TNBC tissues was significantly lower than that in adjacent normal breast tissues.No correlation was found between miR-124 and AR in TNBC tissues(P>0.05).Conclusion In TNBC,miR-124 may play an anti-tumor effect by modulating the expression of E-cadherin.

Objective:To investigate the preventive efficacy of pirfenidone in esophageal stent-related restenosis and the related underlying mechanisms.Methods:Twenty-four rats underwent esophageal stent placement were included in this study. The rats were randomly assigned to three groups, with 8 rats in each group. The three groups were set to receive placebo, 150 mg/kg pirfenidone and 300 mg/kg pirfenidone daily by oral administration for 28 days, respectively. Twenty-eight days after stent placement, the stented esophagi were harvested for histological examinations. The number of epithelial layers, the thickness of submucosal fibrosis, the percentage of granulation tissue area, the degree of inflammatory cell infiltration, the degree of collagen deposition, and the α-SMA staining scores were evaluated. One-way ANOVA was performed for the statistical comparison of the number of epithelial layers, the degree of inflammatory cell infiltration, the degree of collagen deposition and the α-SMA staining scores among these three groups. The Kruskal-Wallis H test was used for comparison of the thickness of submucosal fibrosis and the percentage of granulation tissue area among the three groups. Results:Gross pathological findings showed that both pirfenidone groups had significantly less luminal fibrotic tissue formation and restenosis than placebo group. The percentage of granulation tissue areas in placebo group, 150 mg/kg and 300 mg/kg pirfenidone groups were 57.23%±25.68%, 21.80%±6.65% and 12.18%±6.37%, respectively. Both pirfenidone groups showed significantly less granulation tissue areas than placebo group ( P<0.01). The degree of inflammatory cell infiltration, the degree of collagen deposition and the α-SMA staining scores were 3.28±0.55, 3.38±0.63 and 2.75±0.38 in placebo group, 2.30±0.46, 2.36±0.58 and 2.00±0.42 in 150 mg/kg pirfenidone group, and 1.86±0.38, 1.91±0.41 and 1.57±0.28 in 300 mg/kg pirfenidone group, respectively. Both pirfenidone groups showed significantly less inflammatory cell infiltration, collagen deposition and α-SMA staining scores than placebo group ( P<0.01). Conclusion:Pirfenidone can suppress esophageal stent-related restenosis in rats by significantly inhibiting inflammation, myofibroblast activation and proliferation, and fibrotic tissue formation.