Objective; To construct a promoter identifying plasmid with GFP as reporter gene, and then identify the promoter activity of HCV 5'- UTR with this construct. Methods: In order to construct the promoter identifying plasmid with GFP as reporter gene, the fragment of EGFP was obtained from the plasmid pEGFP - N1 by restrict enzymes digestion. And this fragment was combined with the larger fragment of plasmid PGL3 enhancer digested by the same enzymes. The fragment of HCV 5'- UTR was obtained by PCR amplification and inserted into the promoter identifying plasmid. The structure of constructed plasmid was confirmed by electrophoresis analysis and DNA sequencing. The function of construct was confirmed by lipofectamine - mediated transient expression in HepG2 cells. Results: DNA sequencing showed that the inserted fragment of the constructed plasmid was the same as the template HCV genome. The HepG2 cells transfected with promoter indentifying plasmid nearly didn' t express the reporter gene of GFP while the plasmid with HCV 5'- UTR could express the GFP gene. Conclusions; The results showed that the author successfully constructed the promoter identifying plasmid with GFP as reporter gene. The fragment of HCV 5'- UTR could behaviour as an eurakocyte promoter in HepG2 cells.

Objective To study the change and its correlation between plasma concentration of glutathione peroxidase and polymorphisms of the glutathione peroxidase(GPx-3) promoter gene in patients with acute cerebral infarction(ACI).Methods 94 patients with ACI and 80 normal controls were detected the concentration of plasma glutathione peroxidas.The patients with ACI were undertaken neural function deficient scale(NDS) after 1 d onset.GPx-3 gene polymorphism were detected using polymerase chain reaction and ligase detection reaction(PCR-LDR) in patients with ACI.Results Plasma glutathione peroxidase concentration in ACI group were lower than that in the normal control group in first day onset(P0.05).The plasma concentration of glutathione peroxidase and NDS in patients with mutation of GPx-3 promoter gene were obviously lower than those in the patients without mutation(P

A new target in cancer treatment involves tumor-associated macrophages (TAMs) which are infiltrated in microenvi-ronment. By secreting a wide range of cancer-promoting cytokines, such as vascular endothelial growth factor, interleukins, and matrix metalloproteinase, TAMs can promote the proliferation, invasion, and metastasis of cancer cells. Cyclooxygenase-2 (COX-2), an inflam-matory factor that is significant for angiogenesis and immunoregulation within the local microenvironment, may also contribute to can-cer progression and act as a novel target for breast cancer therapy. Several COX-2 inhibitors, such as celecoxib, have shown potential as suppressors of TAMs and the microenvironment. Hence, the current study discusses the crosstalk between TAMs-delivered important cytokines and COX-2 in the breast cancer microenvironment, and then analyzes the value of homologous antagonists alone or in combi-nation with COX-2 inhibitors. This paper aims to provide the theoretical principle of multi-target selection in TAMs blockage, and offer a new direction for biological targeted therapy in breast cancer treatment.

Tumor markers can reflect tumor existence,and open an entrance to diagnose tumor at early stage.Recent researches reveal that gastric cancer related tumor markers such as microRNAs,enzymes,cytokines and antibodies-antigens are significant for the diagnosis,treatment,relapse surveillance,prognosis evaluation of gastric cancer.

Oxygen free radical, an important risk factor for cerebral infarction, plays an important role in the formation of atherosclerosis, and it is one of the major factors of cerebral isehemia-reperfusion injury after cerebral infarction. Glutathione peroxidase (GPx) is a crucial antioxidant enzyme, its main role is to scavenge the excessive oxygen free radicals produced from metabolism or during the oxidative stress. The deficiency of GPx will increase the risk of cerebral infarction. This article reviews the biological characteristics of GPx and its correlation with cerebral infarction.

Objective To investigate the effect of progesterone pretreatment of focal cerebral ischemic and reperfusion injury (fCIRI) and underlying molecular mechanisms.Methods A single intraperitoneal injection of progesterone (8 mg/kg) given 1 h,48 h and 96 h before fCIRI was established in male Sprague-Dawley rats.The number of survival of neurons in hippocampal CA1 region of the ischemiaside,as well as spatial memory function,was detected on days 3-8 after fCIRI.Extracellular-signalregulated kinase 1/2 phosphorylation (p-ERK1/2) and nuclear translocation of p-ERK1/2 in hippocampal CA1 region were examined using western blot.Results The number of survival of neuronal cells was significantly increased in ischemic groups treated with progesterone at 1 h and 48 h pre-fCIRI (164.3 ± 11.0,218.5 ± 9.1 and 142.7 ± 12.1,F =29.4,P ＜ 0.01) compared with fCIRI group treated with vehicle.Likewise,the escape-latency to reach the hidden-platform recorded in day 5 of Morris water maze test was reduced markedly in fCIRI-treatment groups compared with the vehicle group(10.3 ± 11.1,19.2 ±9.6 and 32.4 ± 14.3 ;F =35.8,P ＜0.01).The level of p-ERK1/2 was elevated notably during 24 h to 48 h postprogesterone by western blot,while restored to the baseline at 96 h post-progesterone.Improved nuclear translocation of p-ERK1/2 was observed from 2 h to 48 h post-progesterone.The progesterone receptor antagonist RU486 blocked the exaltation of either intracellular level or nuclear translocation of p-ERK1/2,which was induced by progesterone.Conclusions The pretreatment with progesterone exerts a neuroprotective effect against the ischemia-induced neuronal death and ameliorates the deficits in spatial memory through enhancing the activation of ERK1/2.The neuroprotection derived from pretreatment with progesterone achieves a time window of not less than 48 h,which is progesterone receptor-mediated ERK1/2 signaling pathway-dependent.

Objective To investigate the protective effects of sulforaphen (SFN) on focal cerebral ischemia/reperfusion injuy (IRI) in rats in order to explore the mechanisms.Methods Twenty-four male SD rats were randomly (random number) divided into Sham-operated group (A group,n =8),IRI group (B group,n =12),sulforaphen group (C group,n =8).SD rats were made to be transient focal cerebral IRI models.SFN 5 mg/kg was injected intraperitoneally to rats 15 minutes after IRI in C group,and rats of group A and group B received equal volume PBS instead.Infarct volume was measured by TTC staining and morphologic changes were observed with HE staining.Neuronal cell apoptosis index was detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) assay.Rats were sacrificed at 24 h after IRI.The protein levels of NF-κB p65 and iNOS were detected by using western bloting and the mRNA expressions of NF-κB p65 and iNOS were detected by using RT-PCR.Results Compared with the group B,infarct volume was significantly smaller in group C,the number of neuronal cell apoptosis in brain tissue were decreased significantly in group C [(96.34 ±3.72) vs.(124.65 ±3.85),P ＜ 0.01],the levels of NF-κB and iNOS in brain tissue of rats were decreased in the SFN group (P ＜ 0.01).SFN reduced neuronal cell apoptosis,injury,and infarct volume [(0.26 ± 0.018) vs.(0.43 ±0.031),P ＜0.01].The mRNA expression and protein level of NF-κBp65 were decreased in the group C.And the mRNA expression and protein level of induced nitric oxide synthase (iNOS) in IRI affected brain tissue were decreased in the group C [(0.67 ± 0.042) vs.(0.56 ± 0.032),P ＜ 0.01].Conclusions SFN might decrease the neuronal cell apoptosis caused by ischemia/repeffusion injury,and this protective effect is mediated by decreasing the level of NF-κB and iNOS.

Objective To investigate the sedative effects and the adverse reactions in the elderly patients received different speed of dexmedetomidine (Dex) intravenous infusion. Methods Eighty elderly cases were randomly divided into four groups. Group D0 was the control group, while the group D1, D2 and D3 were the trial groups. The heart rates, blood pressure, SpO2, Ramsay sedation score and Narcotrend value were recorded. Results The sedation onset time of the D2, D3 group was faster than those in the D0 and D1 groups (P <0.05, respectively), and the duration of sedation in groups D2 and D3 were significantly longer than that in the D0 and D1 groups (P < 0.05). Among the four groups, no significant differences in the incidence of hypotension or bradycardia needed vasopressors or atropine to treat and oxygen saturation were shown (P > 0.05). Conclusion Intravenous infusion of Dex by doses of 0.75 ~ 1.0 μg/(kg·h) during hip surgery in the elderly patients under spinal anesthesia could lead to a safe and effective sedation.

Objective To assess the effect of surgical repair of medial orbital wall combined with orbital floor fracture via lower lid subciliary approach. Design Retrospective case series. Participants 18 cases of medial orbital wall combined with orbital floor fracture. Methods All patients underwent the reconstruction of orbital wall via lower lid subciliary approach. The composite hydroxyapatite was implanted into the surface of medial orbital wall and orbital floor after lacriminal cyst was completely dissected and protected during the operation. Orbital axial and coronal CT, three-dimension CT scan have been used in all the cases preoperalively and postoperatively. Preoperative CT was compared with postoperative CT. Main Outcome Measures Clinical symptoms and complications. Results All patients were followed up for 3 to 18 months. The postoperative scar of infracillary skin was not obvious. The composite hydroxyapatite was not rejected and dislocated in all cases postoperatively. No postoperative epiphora was found in either case. Preoperative diplopia and enophthalmos were corrected. Conclusion The treatment of medial orbital wall combined with orbital floor fracture via an isolated lower lid subciliary approach was feasible. But the incision was only used in the treatment of inferior medial orbital wall combined with orbital floor fracture, especially the transition area fracture between the orbital floor and medial orbital wall.

Objective To analyze the statistical correlation between 25-hydroxyl vitamin D and bone metabolism parameters in-cluding parathyroid hormone(PTH),N-terminal osteocalcin (N-MID),calcitonin(CT),bone alkaline phosphatase(BALP),and dis-cuss the significance in clinical diagnosis,prevention and treatment.Methods 411 cases of hospitalized patients were collected from January to September in 2014,including 316 women,95 men,age arranged from 37 to 96,the average age was(69.29±12.21).Use electro chemiluminescence immunoassay(ECLIA)method to detect the levels of 25-hydroxyl vitamin D,PTH,N-MID,CT,and BALP in hospitalized patients and explore the relationship of 25-hydroxyl vitamin D and serum bone markers in osteoporosis pa-tients.Results It was showed that vitamin D and PTH,BALP were negative correlation(P <0.05);There was no significant corre-lation between calcitonin and N-terminal osteocalcin(N-MID)(P >0.05 ).Regression analysis showed that regression equation for vitamin D and blood bone markers was:Y =19.02-0.066PTH-0.09BALP.Conclusion There was some correlation between 25-hydroxyl vitamin D and PTH,BALP in patients with osteoporosis.By taking a combination test of these markers,it can provide some basic data for clinical osteoporosis diagnosis,prevention and control.