Objective:To get the message ofthe cardiac dysfunction arises from the cerebral hemorrhage in CH patients by investigate the relationship among the Electrocardiographic abnormalities、the hemorrhagic location、the cerebral lesion degree and the outcome.Methods:Analysis the ECG of the 304 acute hemorrhagic stroke patients who made the final diagnosis by CT,without the history of heart disease.Results:There are evident change of the ECG in acute hemorrhagic stroke patients,the total incidence rate reach up to 67.1%(204/304),and these change keep close tothe cerebral lesion location that different fromthe relation between themand the cerebral lesion degree and link with the prognosis with the cerebral lesion degree,P

Objective To investigate the inhibitory effect of ester catechin monomers-EGCG, GCG on the growth of human colon carcinoma cell line SW480 and its potential mechanism. Methods MTT assay, soft-agar colony formation test, Hoechst 33258 stain and flow cytometry analysis were used to determine the inhibitory effect of theasinesin(TS), and its monomers-EGCG, GCG on SW480 growth. Results EGCG, GCG and TS significantly inhibited the growth of human colon carcinoma cell line SW480 in dose-dependent manner, and their half inhibitory concentration (IC 50 ) was 108.88, 183.21, and 83.36?g?ml -1 , respectively. 24 hours after treatment with IC 50 of EGCG, GCG and TS, the colony formation rate of SW480 cells in the experimental group was obviously lower than that in the control group. Hoechst 33258 staining showed typical apoptotic features such as cell shrinkage, nuclear condensation and cell splinter in the experimental group. A subdiploid peak before G 0/G 1 phase in the experimental group was observed by flow cytometry. Conclusion In accord with TS, EGCG and GCG could inhibit the growth of colon carcinoma cell line SW480 cells, the mechanism of which may be related to inducing cell apoptosis.

Objective To evaluate the efficacy of intra-articular dexmedetomidine mixed with ropivacaine for postoperative analgesia after arthroscopic knee surgery.Methods Sixty ASA physical status Ⅰ or Ⅱ patients,aged 20-64 yr,weighing 50-90 kg,with body height 160-180cm,scheduled for elective arthroscopic knee surgery,were randomly assigned into 2 equal groups using a random number table:ropivacaine group (group R) and dexmedetomidine mixed with ropivacaine group (group RD).In group R,the mixture of noraml saline 1 ml and 19 ml of 0.25％ ropivacaine was injected intra-articularly at the end of surgery.In group RD,the mixture of dexmedetomidine 1 μg/kg and 19 ml of 0.25％ ropivacaine was injected intra-articularly at the end of surgery.VAS scores at rest and during activity were observed and recorded at 1,2,4,8,12,20 and 24 h after surgery.The duration of analgesia after sugery (from the time immediately after intra-articular administration to the time of first administration of fentanyl as an adjunct to analgesia) and consumption of fentanyl at 24 h after surgery were recorded.Results Compared with group R,VAS scores were significantly decreased at 1,2,4 and 8 h after surgery,the duration of analgesia after sugery was prolonged,and the consumption of fentanyl at 24 h after surgery was reduced in group RD (P ＜ 0.05 or 0.01).There was no significant difference in VAS scores at 12-24 h after surgery between the two groups (P ＞ 0.05).Conclusion Intra-articular dexmedetomidine can significantly improve the efficacy of ropivacaine for postoperative analgesia after arthroscopic knee surgery.

BACKGROUND:There is no clear conclusion on whether the lung cancer stem cels can induce to spheroid formation and have tumorigenicity. OBJECTIVE: To observe the spheroid formation induced by human lung adenocarcinoma cel line SPC-A1 and the tumorigenic ability of lung cancer stem cels. METHODS:SPC-A1 at proliferating phase was cultured in serum-free DF12 culture medium, and then recombinant human insulin-like growth factor-1, recombinant human epidermal growth factor, and recombinant human fibroblast growth factor-10 were added to induce spheroid cels. Immune fluorescence detection and PCR amplification were done to understand the expression of stem cel associated markers. NOD-SCID immunodeficient mice were subcutaneously implanted with lung spheroid cels to observe the tumor growth.In vivo fluorescence imager was used for radiography. RESULTS AND CONCLUSION:After 5-10 days, lung spheroid cels were harvested. RT-PCR results showed that lung spheroid cels were positive for CD24, CD221, CCSP and SP-C. In addition, the lung spheroid cels and purified CD24+, CD221+ lung cancer stem cels were both positive for TTF-1 of lung stem cels, OCT4 and Nanog of embryonic stem cels and TTF-1 of Bmi-1 lung stem cels. The fluorescence detection showed that over 80% lung spheroid cels expressed CCSP and OCT4; SPC-A1 cels had the characteristics of alveolar type II cels, and also expressed SP-C protein, but only about 5% of the cels expressed CCSP and OCT4. At 50 days after subcutaneous implantation of lung spheroid cels, in vivo fluorescence imaging showed that the diameter of tumor in mice was 1 cm, indicating human lung adenocarcinoma cel line SPC-A1 can induce the spheroid formation, and lung cancer stem cels rich in the cel spheres have the tumorigenic ability.

Objective To evaluate the effect of bone marrow-derived mesenchymal stem cells (BMSCs) on mammalian target of rapamycin (mTOR) signaling pathways in lung tissues of rats with acute lung injury (ALI).Methods Healthy pathogen-free adult male Sprague-Dawley rats were selected,and the BMSCs were obtained and cultured in vitro.One hundred and five healthy clean adult male SpragueDawley rats,weighing 170-190 g,were divided into 5 groups (n=21 each) using a random number table:control group (group C),PBS group,group ALI,ALI plus BMSC group (group ALI+BMSCs),and ALI plus phosphate buffer solution (PBS) group (group ALI+PBS).Group C received no treatment.PBS 0.5 ml was injected via the tail vein in group PBS.Lipopolysaccharide (LPS,0.5 ml) 5 mg/kg was intraperitoneally injected to establish the model of ALI in group ALI.BMSCs (0.5 ml) 1×104 cells/ml were injected via the tail vein after intraperitoneal injection of LPS in group ALI+ BMSCs.PBS 0.5 ml was injected via the tail vein after intraperitoneal injection of LPS in group ALI+PBS.Arterial blood samples were collected for blood gas analysis at 6,24 and 48 h after injection of BMSCs.Lungs were then removed for determination of wet/dry weight ratio (W/D ratio) and expression of mTOR,nuclear factor kappa B (NF-κB) and tumor necrosis factor-alpha (TNF-o) in lung tissues (by Western blot) and for examination of the pathologic changes of lungs tissues (using haematoxylin and eosin staining).Results Compared with group C,pH value and PaO2 were significantly decreased,PaCO2 and W/D ratio were increased,and the expression of mTOR,NF-κB and TNF-α was up-regulated at each time point in ALI,ALI+BMSCs and ALI+PBS groups (P＜0.05).Compared with group ALI,pH value and PaO2 were significantly increased,PaCO2 and W/D ratio were decreased,the expression of mTOR,NF-κB and TNF-α was down-regulated at each time point (P＜0.05),and the pathologic changes of lungs tissues were significantly attenuated in group ALI+BMSCs.Conclusion The mechanism by which BMSCs reduce ALI may be associated with inhibiting mTOR signaling pathways in lung tissues of rats.

Objective To evaluate the effect of bone marrow-derived mesenchymal stem cells (BMSCs) on transforming growth factor-β1 (TGF-β1)/Smad signaling pathway during acute lung injury (ALI) in rats.Methods Healthy clean-grade adult male Sprague-Dawley rats,aged 4-5 weeks,weighing 100-120 g,were selected,and BMSCs were prepared and cultured in vitro.Eighty-four healthy clean-grade adult male Sprague-Dawley rats,aged 4 weeks,weighing 170-190 g,were selected and divided into 4 groups (n=21 each) using a random number table method:control group (group C),group ALI,ALI plus BMSCs group (group ALI + BMSCs),and ALI plus phosphate buffer solution (PBS)group (group ALI+PBS).ALI was induced by intraperitoneally injecting 5 mg/kg lipopolysaccharide 0.5 ml in anesthetized rats.In group ALI+BMSCs,1×104 cells/ml BMSCs 0.5 ml (in PBS) was injected via the tail vein after intraperitoneal injection of lipopolysaccharide.PBS 0.5 ml was injected via the tail vein after intraperitoneal injection of lipopolysaccharide in group ALI+PBS.Arterial blood samples were collected at 6,24 and 48 h after injecting BMSCs for blood gas analysis and for determination of wet to dry weight ratio (W/D ratio),pathological changes (using haematoxylin and eosin staining),and expression of TGF-β1,Smad2 and Smad3 in lung tissues (by Western blot).Results Compared with group C,PaO2 was significantly decreased,PaCO2 and W/D ratio were increased,the expression of TGF-β1,Smad2 and Smad3 in lung tissues was up-regulated (P＜0.05),and the pathological changes of lung tissues were accentuated in ALI,ALI+BMSCs and ALI+PBS groups.Compared with group ALI,PaO2 was significantly increased,PaCO2and W/D ratio were decreased,the expression of TGF-β1,Smad2 and Smad3 in lung tissues was down-regulated (P＜0.05),and the pathological changes of lung tissues were significantly reduced in group ALI+BMSCs.Conclusion The mechanism by which BMSCs mitigates ALI may be associated with inhibiting TGF-β1/Smad signaling pathway in rats.

OBJECTIVETo identify the genetic mutation underlying congenital hypofibrinogenamia in a Chinese pedigree.

METHODSStandard coagulation tests including the prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), plasminogen activity (PLG:A), D-Dimer (DD) and fibrin degradation products (FDP) were tested with fresh plasma using a STA-R analyzer. The activity of fibrinogen (Fg:C) and fibrinogen antigen (Fg:Ag) were measured respectively with the Clauss method and immunoturbidimetry. All exons and exon-intron boundaries of the fibrinogen Aα-, Bβ-, and γ-chain genes (FGA, FGB and FGG) were amplified by PCR followed by direct sequencing. Suspected mutation was confirmed by reverse sequencing and analyzed with a Swiss-PdbViewer.

RESULTSThe PT level in the proband was normal, while the APTT and TT were slightly prolonged. The functional and antigen fibrinogen levels were both significantly reduced (0.91 g/L and 0.95 g/L, respectively). Similar abnormalities were also found in her father, elder sister, son and niece. The coagulant parameters of her mother were all within the normal range. Genetic analysis has reveled a heterozygous A>C change at nucleotide 5864 in exon 7 of γ gene in the proband, predicting a novel Lys232Thr mutation. The proband's father, elder sister, son and niece were all carriers of the same mutation. Protein model analysis indicated that the Lys232Thr mutation did not disrupt the native network of hydrogen bonds, but has changed the mutual electrostatic forces, resulting in increased instability of the protein.

CONCLUSIONThe heterozygous Lys232Thr mutation identified in the FGG gene probably underlies the hypofibrinogenemia in this pedigree.

Adult ; Afibrinogenemia ; congenital ; genetics ; Asian Continental Ancestry Group ; genetics ; Base Sequence ; China ; Female ; Fibrinogen ; genetics ; Humans ; Male ; Middle Aged ; Molecular Sequence Data ; Pedigree ; Peptide Fragments ; genetics ; Young Adult

The solute carrier family 12(SLC12)of cation-chloride cotransporters(CCCs)comprises potassium chlo-ride cotransporters(KCCs,e.g.KCC1,KCC2,KCC3,and KCC4)-mediated Cl-extrusion,and sodium po-tassium chloride cotransporters(N[K]CCs,NKCC1,NKCC2,and NCC)-mediated Cl-loading.The CCCs play vital roles in cell volume regulation and ion homeostasis.Gain-of-function or loss-of-function of these ion transporters can cause diseases in many tissues.In recent years,there have been considerable ad-vances in our understanding of CCCs'control mechanisms in cell volume regulations,with many tech-niques developed in studying the functions and activities of CCCs.Classic approaches to directly measure CCC activity involve assays that measure the transport of potassium substitutes through the CCCs.These techniques include the ammonium pulse technique,radioactive or nonradioactive rubidium ion uptake-assay,and thallium ion-uptake assay.CCCs'activity can also be indirectly observed by measuring y-aminobutyric acid(GABA)activity with patch-clamp electrophysiology and intracellular chloride con-centration with sensitive microelectrodes,radiotracer 36Cl-,and fluorescent dyes.Other techniques include directly looking at kinase regulatory sites phosphorylation,flame photometry,22Na+uptake assay,structural biology,molecular modeling,and high-throughput drug screening.This review sum-marizes the role of CCCs in genetic disorders and cell volume regulation,current methods applied in studying CCCs biology,and compounds developed that directly or indirectly target the CCCs for disease treatments.

Objective To study the effect of SLCO1B1 521 T>C and APOE gene polymorphisms on the clinical efficacy and safety of atorvastatin in ischemic stroke patients with dyslipidemia. Methods 210 cases of ischemic stroke with dyslipidemia were enrolled from April 2018 to December 2018 to determine SLCO1B1 521 T>C and APOE gene polymorphisms. Patients received atorvastatin 20 mg/d orally. TC, TG, HDL-C, LDL-C levels were measured to evaluate the efficacy 3 months pre-and post- treatment. TBil, ALT, AST, CK levels were assayed with following up adverse reactions to evaluate safety. Results SLCO1B1 521 T>C genotype distribution was TT79.05%, TC19.05%, CC1.90%. E2, E3, E4 allele frequencies of APOE genes were 14.28%, 67.62%, 18.10%. Each genotype conforms to the law of Hardy-Weinberg balance. After three months of medication, there were significant differences in TC, TG, LDL-C, HDL-C changes in patients with different APOE genotypes. No obvious abnormality was found in safety index. The incidence of myalgia in SLCO1B1521 T>C mutant group was significantly higher than that in the wild group (P<0.01). Conclusion Lipid regulation of atorvastatin was affected by APOE gene polymorphism. SLCO1B1521 T>C may be associated with myalgia, the adverse reaction of atorvastatin. The detection of SLCO1B1 and APOE genotyping is helpful for individualized treatment of blood lipids and provides basis for rational use of statins in patients for drug therapy management.

AIM: To investigate the effect of dapagliflozin on myocardial injury in type 1 diabetes mice and its mechanism. METHODS: Normal C57BL / 6J male mice were randomly divided into normal control group (Control), diabetes cardiomyopathy group (DCM) and dapagliflozin group (DAPA). The model of diabetes was induced by streptozotocin (STZ) and given maintenance feed. DAPA group was given 10 mg · kg