AIM:To investigate the mechanisms and protective effects of recombinant human tumor necrosis factor receptor :Fc fusion protein(rhTNFR:Fc)on the acute lung injury induced by lipopo1ysaccharide(LPS)in rats.METHODS:The rat model of acute lung injury was established with LPS and the rats were randomly divided into four groups:control group,rhTNFR:Fc group,LPS group and rhTNFR:Fc+LPS group.After administration,the rats' death was recorded,the pulmonary wet/dry weight ratios were determined,the changes of lung histopathology were observed by HE dyeing,the levels of TNF-? and the bioactivity in serum were detected.RESULTS:Compared with control group the rats' mortality rate and pulmonary wet/dry weight ratio were significantly higher in the LPS group(P

Objective To investigate the protective effects of recombinant human tumor necrosis factor receptor:Fc fusion protein (rhuTNFR:Ice)on the acute renal injury induced by lipepelysaccharide(LPS)in rats.Methods Models ofacute renal injury in rats were constructed by intravenous injection of LPS 10 m/kg.Forty-eight SD rats weighing 180～240g were randomly divided into 4 groups with 12 animals each group,including control group,rhuTNFR:Fc group,LPS groupand rhuTNFR:Fc+LPS group.Mean arterial pressure(MAP)wKs continuously monitored for 6 h.The levels of blood tLrea nitrogen(BUN)。Creatinine(Cr),TNF-αas well as TNF-α bioactivity were assessed.The myeloperoxinse(MPO)and superoxide dismutase(SOD)activity,content ofmalondialdehyde(MDA)were also measured.Pathologic changes of lung tissue in each group were observed by HE staining.Results Compared with LPS group,the status of hypotension and pathological manifestation in kidneys were ameliorated,and MPO activity significantly decreased in rhuTNFR:Fc+LPS group(P<0.05).Conclusion These data suggest that rhuTNFR:Fc can ablate the rise in serum TNF-α bioactivity that occurs in response to LPS,and rhuTNFR:Fc could in part protect rats from the acute renal injury induced by LPS.

Objective To investigate the protective effects and the undedying mechanism of recombinant human tumor necrosis factor receptor: Fc fusion protein (Yisaipu, rhu TNFR: Fc) on the lipopolysaccharide (LPS) induced acute liver injury of rats. Method Totally48 SD rats were randondy divided into four groups , in-cluding control gronp (n = 12), Yisaipu group(n = 12), LPS gronp(n = 12) and Yisaipu + IPS group(n = 12). The models of acute liver injury were produced by injection of LPS intravenously. Being fasted for 12 h, the rats were anaesthetized (60 mg/kg pentobarbital sodium, i.p.) and cannulated into carotid arteries. The cannula was connected with the multi-channel creature signal analysis system. The rata in control group and LPS group were injected with normal saline or LPS in dose of 5 mg/kg through rats' sublingual vein respectively. While the rats in Yisaipu group and Yisaipu + LPS group was pretreated with Yisaipu in dose of 0.4 mg/kg subcutaneously 24 h be-fore normal saline or LPS infusion. Six rats of each goup were randomly selected and mean arterial pressure (MAP) were monitored for 6 h via multi-channel creature signal analysis system, and rats' survival rate was calcu-lated. The rats whose MAP less than 10 mmHg were considered to die and the alive rats during period of observa-tion sacrificed by exsanguination. The liver tissue at the same site was removed, fixing in 10% formalin or stored at -80 ℃. To detect serum TNF-α, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) level, 0.2 mL blood samples were collected from the carotid artery 2 and 3 h after the injection of saline or LPS. The serum was collected from centrifuged blood samples and stored at -80 ℃. Enzyme-linked immunosorbent assay (ELISA) and flow cytometry were used to assess serum TNF-α level and bioactivity respectively. We also measured the serum ALT and AST levels, the myeloperoxiase (MPO) and superexide dismutase (SOD) activity, and malon-dialdehyde (MDA) content in liver tissue The pathology of hepatic tissue was evaluated by HE staining. Statistical-ly,the data of TNF-α level and bioactivity, ALT and AST release, and MDA content were analyzed by ANOVA, and rat survival rate were analyzed by Chi-square Tests. Results The rats in control group and Yisaipu group were all survived. Rat survival rate was significantly higher in Yisaipu + LPS group (67%) than in LPS group (17%) (P < 0.05). Serum TNF-α bioactivity was significantly lower in Yisaipu + LPS group than in LPS group [(7.3±2.8)% vs.(51.3±6.4)%, P <0.05]. Compared with IPS group, Yisaipu pretreatment decreased MDA content [(1.40±0.10)vs. (2.81±0.11) nmol/mgprot, P <0.05]and MPO acticity [(0.38±0.04) vs. (0.54±0.02) U/g, P <0.05]in hepatic tissue, while SOD activity [(188.4±20.2) vs. (142.5 ± 18.3) U/mgprot, P <0.05]was increased. The serum AST level, ALT level and the pathology in the liver were also ameliorated correspondingly. Conclusions These data suggest that Yisaipu could protect rats from LPsinduced a-cute liver injury by inhibiting TNF-α bioactivity and by enhancing anti-oxidation.

Objecfive To explore pathological mechanism and treatment of central hyponatrem-ia. Methods Synchronous assay was made to detect changes of atrial natriuretic peptide(ANP),brain natriuretic peptide(BNP),endogenous digitalis-like substance(EDLS),antideuretic hormone (ADH),Na+ concentrations in blood and urine as well as osmotic pressure of plasma and urine in 68 pa-tients with traumatic brain injury(TBI). Results Of all,there were 27 patients with hyponatremia,mostly in patients with severe or critical TBI.There found syndrome of inappropriate secretion of antidi-uretic hormone(SIADH)in 7 patients and cerebral salt wasting syndrome(CSWS)in 20. Conclu-sions The central hyponatremia in patients with TBI may be related to the increased secretion of EDLS and ADH.The decrease of ANP and BNP in blood has no direct effect on Na+ concentration in blood.In-travenous injection of extrinsic thyrotropin releasing hormone(TRH)may inhibit dilutional hyponatremia resulted from increased secretion of ADH in TBI patients.

Objective To investigate the role of calcitonin gene-related peptide(CGRP)and IP3 signal pathway in ischemic preconditioning(IPC)in the isolated perfused hearts of rats with type 1 diabetes mellitus. Methods Type 1 diabetes mellitus rat models were established in 80 SD rats,and were randomly divided into 4 week(D-4w)group and 8 week (D-8w)group.These two groups were randomly subdivided into model control(D-Cont)group,type 1 diabetes mellitus ischemia-reperfusion(IR)group,IPC group,CGRP(IPC+CGRP)group and IP3 inhibitor wortmanin(IPC+WMN) group.Another 16 rats were served as normal control(N-Cont)group.In vitro perfusion models of isolated hearts were established by Langendorff methods,and CGRP or wortmanin(WMN)were administered during perfusion.The left ventricle function of isolated heart in each group was monitored by multichannel biosignal analysis system,and coronary artery flow was recorded.The serum CGRP levels were detected by ELISA.The activity of lactate dehydrogenase(LDH)and creatine kinase(CK)in effluent of coronary artery was detected by biochemical method.The size of myocardial infarction was determined by NBT staining,and apoptosis of cadiocytes was detected by TUNEL method. Results Compared with N- Cont group,the CGRP level in serum of rats with type 1 diabetes mellitus decreased with time,the basic left ventricle function decreased,while the activity of LDH and CK in effluent of coronary artery,size of myocardial infarction and cardiomyocyte apoptosis index increased(P<0.05).Compared with N-Cont group,the left ventricle function was significantly lower in IR group,and more severe myocardial damage was observed.IPC improved myocardial damage of D-4w IR group,while had no protection on D-8w IR group.Compared with IPC group,the left ventricle function was significantly improved in IPC+CGRP group.IPC+WMN blocked the myocardial protection of D-4w group from IPC.Conclusion CGRP and IP3 signal pathway are involved in the protection provided by IPC in isolated hearts of rats with type 1 diabetes mellitus.

Three kinds of biomedical materials of stomatology were introduced,including metal materials,polymers and non-metal bio composites.The literatures related to stomatology biomedical materials from 2008 to 2015 were collected in PubMed medical literature retrieval service system,and then statistical method was used to analyze the literature number,the numbers of literatures on different materials as well as the nations distribution.Composite,intelligent and functional materials were pointed out to be taking the place of metal materials,and thus might extend their clinical application in the future.

Objective·To observe mitochondria permeability transition pore (mPTP) opening and apoptosis of H9c2 myocardial cell stimulated by lipopolysaccharide (LPS),and to explore the anti-apoptotic effect of combined application of cyclosporine A (CsA) and ryanodine (Rya).Methods·The H9c2 cells were divided into Control group,LPS group,LPS+CsA group,LPS+Rya group,and LPS+CsA+Rya group.The mPTP opening state,Ca2+ concentration within cell and mitochondrial,mitochondrial membrane potential (AΦm),cell apoptosis,expression of Bax and Bcl-2 at mRNA and protein levels,and activity of caspase 3 were determined respectively.Results·mPTP opened after being stimulated by LPS for 24 h,which increased the fluorescence intensity for Ca2+in cytosolic and mitochondria by 298％ and 231％ respectively,induced about 1/3 cell apoptosis,improved the activity of caspase 3 approximately twice,and enhanced expression ofBax mRNA (P=0.008).The combined use of CsA and Rya effectively inhibited mPTP opening,increased the enhancement of fluorescence intensity for Ca2+in both cytosolic and mitochondria,maintained normal AΦrn,reduced LPS-induced apoptosis,inhibited the activity of caspase 3,and decreased Bax mRNA expression level induced by LPS in the myocardial cells.Conclusion·mPTP plays an important role in in LPS-induced myocardial apoptosis,whereas the combination of CsA and Rya can alleviate it effectively.

OBJECTIVEPrevious studies have clarified that calcitonin gene-related peptide (CGRP) can promote the biologi- cal activity of osteoblasts. To further reveal the role of CGRP in bone repair, we studied its influence on osteogenic differentia- tion of mouse bone marrow stromal cells (BMSCs) and initially explored the effect of the Hippo signaling pathway with this process.

METHODSBMSCs were induced to osteogenic differentiate osteoblasts by different concentrations of CGRP for a screening of the optimal concentration. CGRP was added in BMSCs, then the activity of alkaline phosphatase (ALP) and the number of mineralized nodules were examined by specific ALP kits after 48 hours and alizarin red staining fluid after 7 days, respectively. The protein expression of p-Mst1/2 was measured by Western blot. Verteporfin was used to block the downstream Yap signaling. The mRNA expression of collagen type I (Col I) and runt-related transcription factor 2 (Runx2) were detected by reverse transcription-polymerase chain reaction.

RESULTSCompared to the blank group, different concentrations of CGRP (10⁻⁹, 10⁻⁸, 10⁻⁷ mol · L⁻¹), especially 10⁻⁸ mol · L⁻¹, significantly increased the ALP activity of BMSCs (P < 0.05). Alizarin red staining also showed more mineralized nodules in 10⁻⁸ mol · L⁻¹ group. The expression of p-Mst1/2 increased in the CGRP group (P < 0.05). Verteporfin treatment effectively decreased the mRNA expression of Runx2 and Col I (P < 0.05).

CONCLUSIONThe Hippo signaling pathway plays a role in CGRP-induced osteogenic differentiation in mouse BMSCs.

Alkaline Phosphatase ; Animals ; Calcitonin ; genetics ; metabolism ; Calcitonin Gene-Related Peptide ; metabolism ; Cell Differentiation ; Cells, Cultured ; Collagen Type I ; Core Binding Factor Alpha 1 Subunit ; Mesenchymal Stromal Cells ; physiology ; Mice ; Osteoblasts ; Osteogenesis ; physiology ; Signal Transduction

Objective To discover radioresistance-associated proteins by performing comparative proteomic analysis on nasopharyngeal carcinoma cell lines.Methods The total proteins were extracted from radioresistant human nasopharyngeal carcinoma cell line CNE-2R and its parental cell line CNE-2,respectively.These proteins were separated by high quality two-dimensional polyacrylamide gel electrophoresis (2-DE) and then the 2-DE profiles were screened for differentially expressed protein spots by the Image Master 5.0 software.Those spots were identified by a matrix-assisted laser desorption/ionization time-of-flight tandem mass spectrometry.Results 32 significantly differentially expressed protein spots were screened in two different radiosensitivity cell lines and 11 proteins were identified by tandem mass spectrometry,among which 3 proteins were up-regulated in radioresistant human nasopharyngcal carcinoma cell line CNE-2R and the other 8 proteins were down-regulated.Conclusions The differentially expressed proteins of nasopharyegeal carcinoma cells with different radiosensitivity were mainly involved in apoptosis regulation,DNA damage and repair,cell cycle regulation,RNA transcription,cell signaling,cytoskeleton formation and radiation stress responses.

Objective To investigate the expression of CD133 mRNA in tissues of gastric cancer,and explore its relationship with clinicopathological features. Methods The tissues of gastric cancer and normal tissues adjacent to gastric cancer were obtained from 31 patients.The expression of CD133 mRNA was detected by semi-quantitative RT-PCR,and its relationship with clinicopathological features such as sex,age,tumor diameter,infiltration depth,TNM staging,tumor differentiation,lymph node metastasis and Ki-67 proliferation index was analysed. Results The relative gray scale values of CD133 mRNA in tissues of gastric cancer and normal tissues adjacent to gastric cancer were 0.378 3±0.141 1 and 0.038 1 ±0.091 9,respectively(P=0.000).The relative gray scale values of CD133 mRNA in tissues of gastric cancer with tumor diameter>5 cm were significantly higher than those with tumor diameter≤5 cm[(0.439 3±0.148 4)vs(0.334 3±0.121 2)](P=0.041),and those in tissues with lymph node metastasis were significantly higher than those without lymph node metastasis[(0.426 6±0.132 0)vs(0.239 5±0.030 9)](P=0.004).The rate of lymph node metastasis and the number of metastatic lymph nodes were positively related to relative gray scale values of CD133 mRNA(r=0.466,P=0.008;r=0.464,P=0.009).The relative gray scale values of CD133 mRNA in those with low expression of Ki-67 were significantly higher than those with high expression of Ki-67[(0.436 4±0.139 8)vs(0.316 4±0.117 4)](P=0.02),and expression of Ki-67 were negatively related to relative gray scale values of CD133 mRNA(r=-0.461,P=0.009).Conclusion The expression of CD133 mRNA in tissues of gastric cancer was associated with the rate of lymph node metastasis,number of metastatic lymph nodes and expression of Ki-67,which reflect the status of lymph node metastasis and proliferation of gastric cancer.