Disaster Planning ; organization & administration ; Emergencies ; Emergency Medical Services ; organization & administration ; Humans ; Public Health ; methods

AIM: To investigate the effects of Scutellaria barbata flavonoids (SBF) on neurofibrillary tangle (NFT) aggregation, tau protein phosphorylation and the regulated mechanism of glycogen synthase kinase (GSK) 3βand protein phosphatase (PP) 2A in the rats induced by amyloid βprotein 25-35 (Aβ25-35) in combination with AlCl3 and re-combinant human transforming growth factor ( RHTGF)-β1( composited Aβ) .METHODS:The male SD rats were used to establish the simulated Alzheimer disease ( AD) model by intracerebroventricular injection of composited Aβ.The Morris water maze was applied for screening the successful model rats with learning and memory deficits .The successful model rats were daily and orally administrated with SBF at doses of 35, 70 and 140 mg/kg or positive control drug Ginkgo biloba leaves flavonoids ( GLF) at 140 mg/kg for 37 d.The silver nitrate staining was used to determine the cortical NFT .The protein levels of total tau, phosphorylated protein of tau at Ser199 and Ser214 sites, GSK3βand PP2A in hippocampus and cortex were determined by Western blot .The mRNA expression of GSK3βand PP2A in the hippocampus and cortex was detected by RT-PCR.RESULTS:Compared with sham group , the cell number of positive NFT with silver nitrate staining in model rat cerebral cortex was significantly increased .The protein levels of phosphorylated tau protein at Ser 199 and Ser214 sites, GSK3βin the hippocampus and cerebral cortex in the model rats dramatically elevated , and PP2A was marked decreased as compared with the sham group rats.Meanwhile, the mRNA expression of GSK-3βsignificantly increased but PP2A was de-creased.However, these above abnormalities were differently attenuated by treating with SBF at different doses or GLF at 140 mg/kg for 37 d.CONCLUSION: SBF suppresses the NFT aggregation by inhibition of the regulatory functions of GSK-3βand PP2A, thus reducing the phosphorylation of tau protein .

In order to test the equilibrium solubility of puerarin in different solvents and solubilizer,cilia toxicity and irritation of these excipient, the balance method, toad in the ciliary body toxicity and rat nasal mucosa irritation were used respectively. Results showed that puerarin solubility was 56.44 g x L(-1) in combined solvent of 30% PEG200 and 10% Kolliphor HS 15. With normal saline solution as negative control and sodium deoxycholate as positive control, the effects of 30% PEG200, 30% PEG 400, 10% Kolliphor HS 15 and combination of 30% of PEG200 and 10% Kolliphor HS 15 on toad palate cilium were observed and cilia movement duration was recorded. The results indicated that there was no significant difference in cilia movement duration among 30% PEG200, 10% Kolliphor HS 15 and normal saline group. The rats long-term nasal mucous membrane irritation of 30% PEG 400, 10% Kolliphor HS 15, which had no cilia toxicity, was studied, with normal saline solution as negative control. There were no significant difference revealed on rat nasal mucosa epithelial thickness among 30% PEG 400, 10% Kolliphor HS 15 and normal saline. Above researches showed 30% PEG 400, 10% Kolliphor HS 15 was ideal for solubility of puerarin nasal drops and showed a lower cilia toxicity and irritation, and can be used as the solvent and solubilizer of puerarin nasal drops.
Administration, Intranasal ; methods ; Animals ; Anura ; Cilia ; chemistry ; Female ; Isoflavones ; chemistry ; Male ; Nasal Mucosa ; Polyethylene Glycols ; chemistry ; Rats ; Rats, Sprague-Dawley ; Solubility ; Solvents ; chemistry

Using sustained release tablets of gardenia extract as model drug and DPPH radical scavenging capacity as antioxidant index, the feasibility of using pharmacodynamics index was explored to evaluate sustained release tablets. Applying the established quantifiable method of DPPH radical scavenging to the dissolved liquid of model drug, release profiles and biological effects profiles were drawn, and their correlation was discussed. A good correlation was observed by linear regression and f2 actor, suggesting that the indicator could be used to evaluate sustained release tabletsofextracts of gardenia in which iridoids were mainly involved.
Antioxidants ; metabolism ; pharmacology ; Biphenyl Compounds ; metabolism ; Delayed-Action Preparations ; metabolism ; pharmacokinetics ; Free Radicals ; metabolism ; Gardenia ; chemistry ; Kinetics ; Linear Models ; Oxidation-Reduction ; drug effects ; Picrates ; metabolism ; Plant Extracts ; metabolism ; pharmacokinetics ; Tablets

Objective To investigate the effects of pulsed electromagnetic fields(PEMFs)on proliferation and differentiation of endothelial progenitor cells(EPCs).Methods EPCs were isolated from rat bone marrow by density gradient centrifugation.EPCs were exposed to PEMFs from the 5th day to the end of culture.MTT was used to measure the proliferation of EPCs.The expression ofⅧ-related antigen and NOS_3 was evaluated by flow cytometry. Results Compared with the control,the proliferating ability of EPCs exposed to PEMFs was stronger;the number ofⅧ-related antigen and NOS_3 positive cells increased significantly in EPCs exposed in PEMFs.Conclusion PEMFs promotes the proliferation and differentiation of rat bone marrow EPCs.

Objective To explore the prognostic value of biomarkers in type 2 diabetic patients with acute myocardial infarction (AMI), this study was to investigate the associations between the neutrophil to lymphocyte ratio (NLR), the Global Registry of Acute Coronary Events (GRACE) score and in-hospital mortality. MethodsSeven hundred and seven consecutive AMI patients were divided into diabetic group (DM-AMI group), impaired glucose tolerance group (IGT-AMI group), and normal glycemic group (NGT-AMI group). The laboratory and clinical characteristics were assessed retrospectively from the medical records. The NLR and GRACE score were calculated. Results In AMI patients, the DM-AMI group had significantly higher NLR and GRACE scores compared with those from the IGT-AMI group and NGT-AMI group (P<0.01 or P<0.05). In DM-AMI group, the NLR and GRACE score were considerably elevated in the elderly DM-AMI group compared with their younger counterparts (both P<0.01). Furthermore, the NLR was considerably higher in the high-risk group than those in both the low- and medium-risk groups based on the GRACE score (both P<0.01). The NLR was positively correlated with the GRACE score in DM-AMI group(r=0.425, P<0.01). The NLR level and GRACE score were higher in the death group than those in surviving patients (both P<0.01). The optimal cut-off levels of 9.36 for NLR and 166 for GRACE score seem to predicte death in-hospital. Based on the receiver operating characteristic curve, when to predict death in-hospital, the best cutoff value of NLR was 9.36 (sensitivity 80.8%, specificity 69.6%; area under curve 0.787), and the best cutoff value of GRACE score was 166 (sensitivity 76.9%, specificity 76.4%; area under curve 0.778). Conclusion An elevated NLR is a potential predictor of in-hospital mortality in type 2 diabetic patients with AMI, which could help clinicians indentify high-risk patients and determine appropriate treatment strategies. <英文关鍵词>>=Neutrophil to lymphocyte ratio; In-hospital mortality; Acute myocardial infarction; Diabetes mellitus, type 2

Objective To explore the mechanism that gold nanorods trigger apoptosis in cancer cells.Methods Gold nanorods was synthesized by gold seed growing method, and its characterization was detected; gold nanorods on cell proliferation-toxicity were evaluated by CCK-8 Kit and apoptosis were detected by flow; mitochondrial membrane potential were tested by JC-1 and activation of Caspase 9 and Caspase 3 were detected by western blot. Results The results found that gold nanorods had nontoxic to normal cells, but highly toxic to tumor cells; and with the increasing of gold nanorods’ working time, the percentage of apoptotic cancer cells was increasing; in addition to, normal cells’ mitochondrial membrane potential did not change, but cancer cells had a significant reduction in mitochondrial membrane potential.Conclusion This study proves that gold nanorods induce apoptosis through the mitochondrial apoptosis pathway.

ObjectiveTo investigate the effect of rhPTH (1-34) and elcatonin on bone metabolism and serum secreted protein acidic and rich in cysteine ( SPARC ) in postmenopausal women with osteoporosis.Methods One hundred and twenty-four postmenopausal women with osteoporosis were randomly divided into 2 groups:One group was treated with recombinant human parathyroid hormone ( 1-34 ) [ rhPTH ( 1-34 ) ] 200 U/d by subcutaneous injection (PTH group,n =89 )and another group was treated with elcatonin 20 U/week by intramuscular injection (CT group,n =35 ) for 12 months.All patients received a basic therapy with oral calcium ( Ca 600 mg+ Vit D3125 U,q..d.).The bone mineral density ( BMD ) of lumbar spine( L2-4 ),the left femoral neck,greater trochanter,and Ward's triangle,serum calcium and phosphate were measured by baseline,6 months' and 12 months.Levels of serum bone-specific alkaline phosphatase( BSAP),serum secreted protein acidic and rich in cysteine (SPARC)were determined by an ELISA assay.ResultsBy 12 months,rhPTH ( 1-34 ) treatment significantly increased the lumbar spine L2-4 BMD 7.9％ (P＜0.05),serum calcium 8.3 ％ ( P＜ 0.05 ),serum BSAP 93.4％ ( P＜ 0.05 ),serum SPARC by 12.6％[ ( 195.68±59.57 vs 173.81 ±81.33 ) pμg/L,P＜0.05 ].Elcatonin therapy increased the lumbar spine L2-4 BMD by 3.2％ (P＜0.05) at the end of 12 months,but elcatonin did not influence serum calcium,BSAP and SPARC.The rhPTH( 1-34 ) increased lumbar spine L2-4 BMD more than elcatonin did at 12 months( P＜0.05 ).ConclusionrhPTH (1-34) could promote the bone anabolism more effectively than elcatonin did.Serum SPARC may play an important role in promoting osteogenesis by rhPTH.

Background Intravitreal injection with triamcinolone acetonide (TA) may cause complications,including increase of intraoculapressure (IOP),cataracand endophthalmitis.Ketorolatromethamine (Ketorolac) inew,lesadverse reactionof non-steroidal anti-inflammatory drug.The action mechanism of Ketorolaisimilato TA.Therefore,Ketorolamay be completely opartly replace Tin the treatmenof retinal edema.Objective The purpose of thistudy wato investigate the effectof Tand Ketorolaon the expressionof aquaporin-4 (AQP4) and vasculaendothelial growth facto(VEGF) in hypoxiretinal Müllecellin vitro and to explore the mechanism of treating retinal edemwith Tand Ketorolac.MethodThe propose of research and use of the animalwere approved by Animal ExperimenResearch Review Committee of Hubei University of Medicine.Twenty eyeof New Zealand albino rabbitwere extracted and the retinal tissue waisolated.The Müllecellwere cultured and passaged using the enzymatidigestion method and Müllecellwere identified using glial fibrillary acidiprotein (GFAP),vimentin and α-smooth muscle actin (α-SMA) by immunofluorescence staining.The hypoxicell modelwere established by culturing the cellin DMEM with 500 μmol/L CoCl2 fo0,6,12,24 hours.The cellof hypoxifo24 hourwere divided into normal control group,hypoxicontrol group,hypoxia+50,100,200 mg/L To50,100,200 mg/L Ketorolagroups.Corresponding drugwere added into the medium in the differengroups.The expressionof AQP4 mRNand VEGF mRNin Müllecellwere detected by semi-quantitative reverse transcription PC(RT-PCR).ResultThe cellgrew well and reached 80％ confluence with the irregulashape and ovoid nuclei 14-15 dayaftecultured.More than 95％ primary cellshowed positive reaction to GFAP,vimentin and α-SMA.The expressing levelof AQP4 mRNand VEGF mRNin Müllecell(values) were significantly differenin varioutime point(AQP4 mRNA:F=18.70,P＜0.01 ; VEGF mRNA:F =53.20,P＜0.01),and those of 6,12 and 24 houraftecultured with CoCl2were increased than those withouCoCl2 (P＜0.05).The expressing levelof AQP4 mRNand VEGF mRNin Müllecell(values) were significandifferenamong the normal control group,hypoxicontrol group,hypoxia+50,100,200 mg/L ToKetorolagroup(AQP4 mRNA:F =27.98,P ＜ 0.01 ; VEGF mRNA:F =10.03,P ＜0.01).Compared with the hypoxicontrol group,the expressing levelof AQP4 mRNand VEGF mRNin the Müllecellwere declined in the hypoxia+ 100,200 mg/L Tgroup and the hypoxia+100,200 mg/L Ketorolagroup (P＜0.05).The expressing levelof AQP4 mRNand VEGF mRNwere found statistically insignificandifference between hypoxia+ 100 mg/L Tgroup and hypoxia+ 100 mg/L Ketorolagroup,obetween hypoxia+ 200 mg/L Tgroup and hypoxi+200 mg/L Ketorolagroup (P＞ 0.05).ConclusionTand Ketorolacan downregulate the expressionof AQP4 and VEGF in Müllecellundehypoxiconditions,inferring thathey have similamechanism in the impacon AQP4 function in retinal edematoueye.