BACKGROUND:In the whole world, spinal cord injuries caused by trauma lead to more than 180 000 people presenting with permanent impairment annualy. A large number of experiments have confirmed in recent years, under physiological conditions, microRNA has specific expression and plays an important role in the nervous system. OBJECTIVE: To discuss the changes in microRNA expression induced by injuries as wel as the pathophysiological significance in spinal cord injury, and to explore the development potential of microRNA in tissue-engineered and clinical repair of spinal cord injury. METHODS:A computer-based search of PubMed and Chinese Journal Database was performed for related articles published from January 2000 to December 2014 using the keywords of “SCI, microRNA, transcriptional control, clinical research progress” in English and Chinese. Finaly, 38 articles were included for result analysis. RESULTS AND CONCLUSION: Mechanical injury initialy triggers a series of complex secondary damages, including nervous, vascular and immune systems, which can influence the severity of spinal cord injury to a great extent. Secondary damage to the spinal cord is mainly attributed to the activation and deactivation of some specific genes associated with celular and biochemical mechanisms, such as cysteine aspartate specific protease (caspase) gene family, apoptosis related protein Fas and its ligand Fasl system, P53 gene, apoptosis related gene Bcl-2 family. Recent studies have proved that the functional activation of microRNA expression is the key to spinal cord injury. With the development of biological information engineering, studies and controling technologies associated with microRNA expression have been gradualy dominated, some clinical application based on microRNA technology has entered the clinical trial stage. It is believed that with the continuous development of technology and decrease of cost, permanent dysfunction due to spinal cord injury can be regulated and repaired through the microRNA technology at gene level in the future.

Objective Previous studies have found that micheliolide(MCL) could improve the sensitivity of breast cancer cells to chemotherapeutic drugs such as cisplatin and induce the apoptosis of breast cancer cells.This article aims to study the proliferation inhibition effect of micheliolide on lung cancer cells H460 and its underlying mechanism.Methods Human lung cancer cell line H460 was treated with different concentrations of micheliolide(30,60,90μmol/L).Then the cell proliferation was measured by-CCK8 and plate colony formation assays.The apoptosis and the cell cycle were detected by flow cytometry.Western blot was used to determine the mechanism of how MCL affecting cancer cell H460.Results Compared with the control (275.00±7.21), the clone numbers after 30μmol/L,60μmol/L and 90μmol/L MCL treatment(199.00±5.66,166.00±1.41, 90.00±7.81) were significantly decreased (P<0.05).Meanwhile, the CCK-8 results showed that compared to the control group, A value was significantly increased after 30μmol/L MCL treatment for 72h and 96h, and 60μmol/L or 90μmol/L MCL treatment for 48h,72h and 96 h (P<0.05).Compared with the control apoptotic ratio [(2.90±0.03)％], the ratio of early and late apoptotic cells after 30μmol/L, 60μmol/L and 90μmol/L MCL treatment [(5.23±0.76)％, (9.06±0.47)％, (19.00±0.64)％] were significantly increased (P<0.05).Compared with the control group, the ratio of G2/M phase cells[(12.52±0.88) ％ ,(17.22±0.43)％, (19.84±0.31)％] was gradually increased after 30μmol/L, 60μmol/L and 90μmol/L MCL treatment, and there was statistically significant difference after 60μmol/L and 90μmol/L MCL treatment (P<0.05).The ratio of S+G1/G0 phase cells[(87.53±1.06)％ ,(82.94±0.67)％ ,(79.79±0.21)％] was gradually decreased after 30μmol/L, 60μmol/L and 90μmol/L MCL treatment, and there was statistically significant difference after 60μmol/L and 90μmol/L MCL treatment (P<0.05).The expression level of notch4 was significantly decreased after 30μmol/L, 60μmol/L and 90μmol/L MCL treatment (P<0.05), while the expression level of cleaved caspase3 was significantly upregulated (P<0.05).Conclusion MCL exerted an inhibitory effect on lung cancer cell H460.

Objective To observe the curative effect of Weifuchun combined with Shenqifuzheng pills in the treatment of chronic atrophic gastritis.Methods 85 cases patients were divided into the control group of 42 cases and the treatment group of 43 cases.The control group were treated with omeprazole enteric -coated capsules and colloidal bismmth pectin,while the treatment group were treated with Weifuchun and Shenqifuzheng pills.The course of treatment was two months.The patients were treated by endoscopy and pathological review after the treatment,then the datas were comparedwith that before treatment.Results The total effective rate of the treatment group was 67.44%,which of the control group was 40.48%,the was statistically significant difference between the two groups (χ2 =6.22,P <0.05).The symptom scores of stomach tingling,stomach fullness,facial darkness,anorexia and melena in the two groups had statistically significant differences (t =6.14,P <0.05).Conclusion Weifuchun combined with Shenqi-fuzheng pills have good curative effect in the treatment of chronic atrophic gastritis.It should be popularized in clinic.

[Summary] Robotic totally endoscopic coronary artery bypass on beating heart (BH-TECAB), a minimally invasive surgical approach with rapid postoperative recovery , is becoming the future trend of minimally invasive coronary surgery , which demands a higher standard for anesthetic management . It comprises pressured pneumothorax , unilateral lung ventilation , transesophageal echocardiography monitoring , hemodynamics maintaining , preparation for cardiopulmonary bypass and conversion to sternotomy , and ventricular fibrillation treatment , which require anesthesiologists to achieve more refined perioperative management and pathophysiological regulation .

Objective To investigate the effect of high mobility group box-1 protein (HMGB1) on inter-leukin-2 (1L-2) and interleukin-2 receptor α (IL-2α) expressions in human T lymphocytes and its potential regulat-ing mechanism in vitro. Method Human T lymphocytes were isolated and suspended, the cells were cultured with 20 μg/mL phytohemagglutinin (PHA) in 5% CO_2 at 37 ℃, recombinant human HMGB1 (rhHMGB1, 0, 10, 100, 1000 ng/mL) was added with the PHA and cultures were centrifuged at 12 and 48 hours for cell collect-ing. Reverse transcription polymerase chain reaction (RT-PCR) amplification was perfomed to determine gene ex-pressions of IL-2, IL-2Rα. IL-2, sIL-2R protein levels in cell culture supematants were measured by ELIZA. Re-sults After coincubated with rhHMGB1 (10, 100, and 1000 ng/mL) for 12 hours, IL-2 levels in cell culture su-pernatants respectively were 0 . 064 ± 0. 017 μg/L, 0.076±0.033 μg/L, and 0.061 ±0.02 μg/L, which were significantly higher compared with the untreated cells (0.045±0.011 μg/L, P < 0.05 or P < 0.01). Mean-while, IL-2 mRNA expression was markedly up-regulated following rhHMGB1 stimulation in various doses (F = 4.6872, P < 0.01). At 48 bourn, however, both IL-2 mRNA expression and protein production tended to de-crease along with an increased dose of dd-IMGB1 stimulationn. IL-2/sIL-2R ratio in 1000 ng/mL rhHMGB1 was markedly lower than that in 10 ng/ml rhHMGB1 (0.036±0.015 vs.0.055±0.017, P <0.05), together with down-regulation of IL-2Rα mRNA expression(P <0.01). Conclusions These data indieated that HMGBI could marked influence the IL-2/IL-2R expression in human T lymphocytes. With the increase in stimulating doses and prolongation of time, HMGBI might down-regulate T cell-mediated immune response of human lymphocytes.

OBJECTIVEThe purpose of this study is to investigate the influence of cryogenic treatment and age-hardening heat treatment on the corrosion behavior of a dental casting Ag-Pd alloy.

METHODSA low gold content dental casting alloy composed of Ag-Pd-Cu-Au was prepared for this study. Corrosion test was performed according to ISO 10271:2001 dental metallie-corrosion test methods. Experimental specimens were casted according to a standard dental lost-wax casting procedure, treated with solution by heating the specimens to 900 degrees C, and immediately quenched in ice water. The specimens were then divided into four groups and subjected to heat treatment, cryogenic treatment, and heat treatment combined with cryogenic treatment. The specimens after the solution treatment were taken as control. The metallographic structures of the specimens were observed. The electrochemical parameters and the quantity of non-precious metallic ions released were evaluated via electrochemical and static immersion tests.

RESULTSMetallographic observation revealed that all the treatments resulted in a change in the microstructure of the alloy. The treatments were effective in improving the electrochemical parameters, such as an increase in Eocp and Ecorr and a decrease in Icorr (P < 0.05). The amount of non-noble metal ions released showed no difference compared with the control group (P > 0.05).

CONCLUSIONAfter different treatments, the antierosion properties of the alloy satisfied the ISO requirements. Age-hardening heat treatment and cryogenic treatment improved the corrosion resistance of the alloy.

Alloys ; Copper ; Corrosion ; Dental Alloys ; Gold Alloys ; Hot Temperature ; Palladium ; Silver

Anticoagulants ; classification ; therapeutic use ; Child ; Humans ; Sepsis ; drug therapy ; physiopathology ; Treatment Outcome

OBJECTIVETo investigate the functions of human periodontal myofibroblast (MFB) in vitro.

METHODSHuman periodontal fibroblast (hPDLFs) was cultured and induced to MFB by transforming growth factor-β1 (TGF-β1). MFB was denoted as the experimental group, whereas the hPDLFs was the control group. The groups were continuously cultured and harvested at 0, 12, 24, 48, and 72 h. The MFB marker α-smooth muscle actin (α-SMA) was examined by immunocytochemistry. The expression of fibronectin (FN) between MFB was examined by immunocytochemistry to detect the MFB contact relationship. The mRNA expression levels of α-SMA, collagen (Col) I, and Col III were measured by reverse transcription-polymerase chain reaction (RT-PCT) to analyze extracellular matrix secretion. The protein expression levels of α-SMA and Col I were also assessed by Western blot.

RESULTSThe experimental group had significantly higher α-SMA expression than the control group at 0 h (P < 0.001). A positive expression of FN was found between MFB. The experimental group had significantly higher expression levels of Col I and Col III than the control group at 24 h (P < 0.001).

CONCLUSIONHuman periodontal MFB presents a continuous, high expression of α-SMA. MFB could interact through FN. MFB is significantly capable of extracellular matrix secretion.

Actins ; Epithelial Cells ; Extracellular Matrix ; Fibroblasts ; Fibronectins ; Humans ; Jaw ; metabolism ; Myofibroblasts ; Transforming Growth Factor beta1

Objective Up to now, the role of Brucea in early embryonic development of mice and its mechanism is still unclear.This paper aims to explore the role of Brusatol in mouse early embryonic development and its possible mechanism.Methods 100 kunming rats of clean grade(80 female rats and 20 male rats) were divided into 6 group: negative control group(no DMSO)、blank control group(culture in fresh CM with equal DMSO)、20nmol/L brusatol treated group、50nmol/L brusatol treated group、100nmol/L brusatol treated group、200nmol/L brusatol treated group(A solution of Brusatol was diluted in CM to concentrations of 20, 50, 100 or 200nmol/L.).Each group used an average of 20 embryos each time, repeated 4 times.Fertilized eggs after cultured 24h, 48h,72h, 96h were respectively 2-cell stage, 4-cell stage,morula and blastocyst stage..The embryo development rate was observed in the culture medium and the optimal concentration was selected, the embryos were collected to analysis the subcellular localization of the Nrf2 by immunofluorescence.The mRNA expression level of Cyclin B, CDK1 and the protein expression of Nrf2 were detected by Q-PCR and western blot respectively.Results In 4-cell stage, the embryo development rates of 20、50、100nmol/L brusatol treated groups[(75.0±2.8)%、(30.4±7.5)%、(4.2±5.9)%] significantly reduced compared with the negative control group[(93.0±2.8)%]、blank control group[(90.9±1.2)%].In morula stage, compared with blastocyst rates of negative control group、blank control group [(83.5±2.1)%、(84.2±1.2)%], 50nmol/L brusatol treated group[(19.3±13.1)%] decreased obviously [(79.00±0.06)% vs 100%, P<0.05].In the cellular immunofluorescence assay, the expression of Nrf2 protein in 50nmol/L brusatol treated group was lower than blank control group(P<0.05).We further found that 50nmol/L brusatol treated group decreased more mRNA levels of Cyclin B[(59.5±9.2)%] and CDK1[(56.0±1.4)%] than blank control group(100%) in G2/M phase(P<0.05).Conclusion In this study, Brusatol mainly affects the cell cycle transformation from G2 to M phase dependent on Cyclin B-CDK1, further inhibiting the development of the embryo through down-regulating Nrf2.

Objective To explore the preventive and protective effect of CGRP on focal cerebral infarction in rats.Methods Focal cerebral infarction model was made by photochemical reaction. The level of cerebral edema was assayed by measuring brain water content.Nervous system evaluation was scored by the method of Ohno, Bederson, LeWay standard. The volume of cerebral infarction and its location were determined by TTC staining.Results CGRP has significant preventive and protective effect to focal cerebral infarction which showed the nervous system scores took a favourable turn, brain edema descended and infarction volume reduced. This effect was related with the dose and the way of administration of CGRP. A single dose (1.33 BU/gBW) of CGRP didn't have significantly effective.It should be given for at least over 2 days. This protective effect did not increase when the dose increased to a certain level. As for the effect of the way of administration of CGRP, multiadministration of fewer doses CGRP was better while the total dose kept constantly.Conclusion CGRP has definite preventive and protective effect to focal cerebral infarction in rats.It has also better effective in inhibition of brain edema. However its dose should be confined in a proper level.