Objective To observe the serum B-type natriuretic peptide(BNP)changes in patients with acute coronary syndrome during percutaneous coronary intervention(PCI).Method The serum BNP level was determined and the heart function was assessed in 236 consecutive patients with acute coronary syndrome(ACS) admitted to CCU and in 54 normal normal suvjects as control from January 2005 to December 2006 in Tongji Hospital.The ACS patients were further divided into various subgroups according to the involved arteries and performance of PCI.Serum BNP,hypersensitive c respose protein(HsCRP)level,amd heart comstitution and function were analyzed.Results The serum BNP and HsCRP level were significantly increased in patients with ACS [(332.06?483.17)ng/L and(31.06?52.15)mg/L]more than those in normal subjects [(81.44?195.55)ng/L and(11.15?20.78)mg/L,respectively,P

Objective To study the effects of oxymatrine as inhibitor of hemorrhagic fever with renal syndrome virus (HFRSV) infection in vitro and in vivo.Methods In vitro studies,a dose of oxymatrine without cytotoxicity and 76-118 strain of HFRSV was taken to treat Vero cells in three ways:①After treated with oxymatrine for 48 h,Vero cells were attacked by HFRSV at dilution of 10-1 ～ 10-6,respectively for 24 h before changing to maintenance medium; ②Vero cells were first attacked by HFRSV of 10-1 ～ 10-6 dilution respectively,then oxymatrine was used for 48 h before changing to maintenance medium; ③Vero cells were attacked by HFRSV at dilution of 10-1 ～ 10-6 respectively,and meanwhile treated with oxymatrine for 48 h before changing to maintenance mcdium.Each dilution handled four porocytes,and four positive controls were set up at the same time.Indirect immunofluorescence assay (IFA) was performed to determine the inhibitory effect of oxymatrine in experimental group and positive control.In vivo studies,thirty 2-week-old hamsters,weighing about 30-40 g,were divided into experimental and control groups according to body weight,n =15.These aninals were inoculated intraperitoneally with HFRSV in 100TCID50(0.1 ml each); on days 4-13,0.1 ml of oxymatrine 1:100 were given to each hamster in experimental group daily by intraperitoneal injection,while the same amount of saline was given to the control ones.Lung tissue of hamsters was then dissected out to slice to be identified by immunofluorcscence stain.Results It was demonstrated that oxymatrine with the diluted fractions of 1:8 was safe in vitro.When the virus dilution of HFRSV was l0-4,compared with control groups,the differences were statistically significant in method 2 and 3 (z =-2.53,-2.53,all P ＜ 0.05),while no statistical significance in method 1 (z＝5.36,P＞ 0.05).When the virus dilution of HFRSV was 10-1 ～ 10-3,10-5,10-6,the differences were not statistically significant (z--0.00,-0.32,-0.19,4.21,4.21,all P ＞ 0.05).In vivo studies,compared with control group,the differences were statistically significant in experimental group (z =-3.85,P ＜ 0.05).Conclusion Oxymatrine significantly inhibites HFRSV.

Objective To study the protective effect of Irisin in doxorubicin(Dox)induced-Cardiomyopathy and its possible mechanism.Methods AC 16 cells were used to construct Dox injury model and divided into control group(AC 16 cells were cultured with complete medium),Irisin group(AC16 cells were treated with 10 ng·L-1 Irisin for 24 h),Dox group(AC 16 cells were treated with 4 μmol·L-1 Dox for 24 h),Dox+Irisin group(AC 16 cells were pretreated with 10 ng·L-1 Irisin for 2 h,and then treated with 4 pmol·L-1 Dox for 24 h).Cell counting kit-8(CCK-8),terminal deoxynucleotidyl transferase-mediated nick end labeling(TUNEL)and lactate dehydrogenase(LDH)were used to detect the proliferation,apoptosis and mortality of AC 16 cells.Western blot was used to detect the expression levels of nuclear factor-κB(NF-κB)signaling pathway and apoptotic factors B-cell lymphoma-2(Bcl-2),Bcl-2-associated X protein(Bax)and caspase-9 protein.Mito-Tracker Red CMXRos probe was used to detect mitochondrial membrane potential.Results In the contrl group,Irisin group,Dox group,Dox+Irisin group,the rate of apoptosis were(0.97±0.09)％,0,(42.80±6.70)％,(11.74±1.79)％;the expression of Bax protein were 0.85±0.01,0.36±0.02,1.15±0.07,0.37±0.11;the expression of caspase-9 protein were 0.52±0.02,0.59±0.03,1.11±0.02,0.67±0.08;the expression of Bcl-2 protein were 1.01±0.04,1.05±0.25,0.43±0.02 and 0.99±0.30;the probability of mitochondrial damage were(0.02±0.01)％,(0.5±0.15)％,(38.6±2.39)％,(1.58±0.54)％.The difference of the above indexes between the contrl group and the Dox group were statistically significant(all P＜0.05);the difference between Dox group and Dox+Irisin group were statisically significant(all P＜0.05).Conclusion Irisin could reduce the expression level of Bax,caspase-9,p-NF-κB,and p-mTOR caused by Dox,increase the expression level of Bcl-2,ameliorate the myocardial damage caused by Dox,and reduce cardiotoxicity.

Animals ; Disease Models, Animal ; Liver ; pathology ; Liver Failure, Acute ; metabolism ; pathology ; Male ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley ; Transcription Factor RelA ; metabolism

Shikonin, the main active ingredient of Lithospermum, and its derivatives have been proved to have antitumor effects, and the anti-tumor mechanisms involve multiple targets. Based on recent literatures, this review focuses on the antitumor effects and its mechanisms. More emphases are given on the aspects of induction of apoptosis, induction of necrosis, acting on matrix metalloproteinase, acting on the protein tyrosine kinase and antiangiogenesis. The current status and problems of shikonin derivatives in antitumor effects are simply summarized and lookout for the development of antitumor drugs with shikonin as leading compounds.
Antineoplastic Agents, Phytogenic ; isolation & purification ; pharmacology ; therapeutic use ; Apoptosis ; drug effects ; Cell Line, Tumor ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; therapeutic use ; Humans ; Lithospermum ; chemistry ; Matrix Metalloproteinase 9 ; metabolism ; Naphthoquinones ; isolation & purification ; pharmacology ; therapeutic use ; Necrosis ; Neoplasms ; drug therapy ; metabolism ; pathology ; Neovascularization, Pathologic ; prevention & control ; Plants, Medicinal ; chemistry ; Protein-Tyrosine Kinases ; metabolism ; Reactive Oxygen Species ; metabolism

AIM: The study was undertaken to investigate the effort of Dexamethasone (DEX) on cultured rabbit corneal epithelial (RCE) cells and rabbit corneal epithelial wound healing.METHODS: For the in vitro experiments, primary cultures of RCE cells were used. DEX in different concentrations was added to cultured RCE cells. The effects were measured with tetrazolium salt (MTT)method and flow cytometry. For the in vivo wound-healing experiments, a central corneal deepithelialization was created and were treated with 0.1g/L DEX eyedrop randomly explain how randomly. Epithelial wound healing was evaluated clinically and analyzed histopathologically using light microscopy along with immunohistochemical staning and electronic microscopy.RESULTS: Less than 0.1g/L DEX didn't influence survival rate in cell culture conditions by MTT assay. Flow cytometric studies revealed that 0.1g/L DFX had no effect on cellular growth phase in cultured rabbit corneal epithelial cells. The mean time of the epithelial healing was significantly shorter in the DEX-treated group than in the control group at 24h. There were strong proliferative-cell-nuclear-antigen(PCNA) expressions in newly generated epithelial cells of both groups. The Dex-treated group had a more regular architecture of stromal lamella and significantly less inflammatory response than the control group under electronic microscopy.CONCLUSION: Less than 0.1g/L DEX had no inhibiting effect on cultured rabbit corneal epithelial cell growth.0.1g/L DEX eye drops can effectively promote epithelial growth and reduce inflammatory response, which may have useful clinical application at the early stage of corneal wound healing process.

Animals ; Antibodies ; immunology ; therapeutic use ; Female ; Graves Disease ; immunology ; prevention & control ; Immune Tolerance ; immunology ; Mice ; Mice, Inbred BALB C ; Receptors, Thyrotropin ; immunology

OBJECTIVETo investigate serum level and gene polymorphisms of matrix metalloproteinase 9 (MMP-9), and platelet glycoprotein VI (GPVI) in patients with acute coronary syndrome (ACS).

METHODSIn a prospective study of 179 patients with documented ACS and 164 controls, we measured baseline serum MMP-9 levels using ELISA and determined the MMP-9/C-1562T and MMP-9/G5564A genotypes using PCR-restriction fragment length polymorphism. Fib serum level was measured by Clauss assay. We also analyzed the Fib/Bbeta-148C/T and GPVI/T13254C polymorphisms.

RESULTSSerum levels of MMP-9 and Fib in ACS patients were significantly higher than in controls (P < 0.001), and serum level of Fib in the acute myocardial infarction group was higher than in patients with unstable angina (P < 0.05). No significant difference between ACS patients and controls was found in frequencies of MMP-9/C-1562T, MMP-9/G5564A, Fib/Bbeta-148C/T, and GPVI/T13254C genotypes and alleles (P > 0.05). The T allele of the Fib/Bbeta-148T polymorphism was associated with increased plasma Fib level (P < 0.05). There was a strong positive correlation between serum level of MMP-9 and Fib (r = 0.289, P < 0.01).

CONCLUSIONSerum levels of MMP-9 and Fib were independent risk factors of ACS. There was an obvious relationship between the Bbeta-148C/T mutation and high Fib level. No significant difference between controls and ACS patients was found in the frequencies of MMP-9 C-1562T and G5564A, Fib Bbeta-148C/T and GPVI T13254C genotypes and alleles (P > 0.05).

Acute Coronary Syndrome ; genetics ; Adult ; Aged ; Case-Control Studies ; Female ; Humans ; Male ; Matrix Metalloproteinase 9 ; blood ; genetics ; Middle Aged ; Platelet Membrane Glycoproteins ; genetics ; Polymorphism, Single Nucleotide

OBJECTIVEDisruptive behavior disorder (DBD) is one of the main comorbidity of attention deficit hyperactivity disorder (ADHD). Previous studies showed significantly different serotonin function between ADHD children with and without the comorbidity of DBD. Therefore, it is needed to compare these two groups in terms of serotonin receptor gene polymorphisms, which may provide further evidence for the previous studies. The current study aimed to investigate the relationship between two serotonin receptor 2C (HTR2C) gene polymorphisms, that are C-759T and G-697C polymorphisms, and ADHD with or without concomitant DBD.

METHODBlood samples were taken from 237 trios with probands of ADHD with DBD comorbidity and 251 trios with probands of ADHD without comorbidity of DBD. All the subjects were from the ADHD clinic of Peking University Sixth Hospital. DNA was extracted and PCR was performed to amplify the fragments containing both C-759T and G-697C polymorphisms. AciI was used to detect different alleles of the two polymorphisms. Both allele-based and haplotype-based TDT analyses were used to test the association of the two polymorphisms of HTR2C gene and ADHD with or without comorbidity of DBD.

RESULTSThe haplotypes -759C (chi(2) = 4.25, P = 0.04), -697G(chi(2) = 3.21, P = 0.07), as well as -759C/-697G were over-transmitted (chi(2) = 4.31, P = 0.04) to the probands of ADHD without DBD. No biased transmission of any allele and haplotype were found in families with probands of ADHD with DBD.

CONCLUSIONADHD with or without the comorbidity DBD was different at the level of HTR2C gene polymorphisms of C-759T and G-697C. HTR2C is related to ADHD without DBD, while not related to ADHD with DBD. The results suggested that the two groups may have different genetic background, at least in HTR2C.

Alleles ; Attention Deficit Disorder with Hyperactivity ; complications ; genetics ; Attention Deficit and Disruptive Behavior Disorders ; complications ; genetics ; Child ; Comorbidity ; Gene Frequency ; Genetic Predisposition to Disease ; Genetic Testing ; Genotype ; Haplotypes ; Humans ; Linkage Disequilibrium ; Polymorphism, Genetic ; Receptor, Serotonin, 5-HT2C ; genetics ; Receptors, Serotonin ; Serotonin ; genetics