Objective To assess the safety and efficacy of domestic sirolimus-eluting stent(SES)compared with bare metal stent(BMS)in the primary percutaneous coronary intervention(PCI)for patients with ST-segment elevation AMI in a real-world scenario.Method From January 2005 to March 2006,a total of 143 patient with ST-segment elevation AMI were enrolled in this study,and all of them underwent primary percutaneous coronary intervention(PCI).Among the 143 patients,74 were treated with domestic SESs(Firebird stent)and 69 with BMSs.The incidence of major adverse cardiovascular events(MACE:death,reinfarction,and target vessel revascularization[TVR])was evaluated at 30 days and 180 days.Continuous variables were compared using Student's unpaired t test.Categorical variables were compared using Fisher's test.Cox proportional hazard survival models were used to assess risk reduction of adverse events.P value

In order to find highly active antidiabetic lead compound, sixteen 4-aminobenzoic acid derivatives were designed and synthesized directly through Mannich reaction in the solution of ethanol at 15-35 degrees C with facile method, mild reaction condition and high yield (45%-90%). Fifteen of them are new compounds. Their structures were confirmed by 1H NMR, 13C NMR, IR, ESI-MS and HR-MS. Alpha-glucosidase inhibitory activity of these compounds indicated that most of these compounds possess the activity with the order: 2c > 2b > 2h > 1a > 1f. The structure-activity relationship of these 4-aminobenzoic acid derivatives was also discussed.
4-Aminobenzoic Acid ; chemical synthesis ; pharmacology ; Drug Design ; Glycoside Hydrolase Inhibitors ; Hypoglycemic Agents ; chemical synthesis ; pharmacology ; Mannich Bases ; chemistry ; Molecular Structure ; Structure-Activity Relationship ; alpha-Glucosidases ; metabolism ; para-Aminobenzoates

Cryptosporidium andersoni ATP-binding cassette (CaABC) is an important membrane protein involved in substrate transport across the membrane. In this research, the nucleotide binding domain (NBD) of CaABC gene was amplified by PCR, and the eukaryotic expression vector of pEGFP-C1-CaNBD was reconstructed. Then, the recombinant plasmid of pEGFP-C1-CaNBD was transformed into the mouse intestinal epithelial cells (IECs) to study the iron transportation function of CaABC. The results indicated that NBD region of CaABC gene can significantly elevate the transport efficiency of Ca2+, Mg2+, K+, and HCO3 - in IECs (P<0.05). The significance of this study is to find the ATPase inhibitors for NBD region of CaABC gene and to inhibit ATP binding and nutrient transport of CaABC transporter. Thus, C. andersoni will be killed by inhibition of nutrient uptake. This will open up a new way for treatment of cryptosporidiosis.
ATP-Binding Cassette Transporters/*chemistry/*genetics/metabolism ; Adenosine Triphosphate/metabolism ; Amino Acid Sequence ; Animals ; Calcium/metabolism ; *Cloning, Molecular ; Cryptosporidiosis/parasitology ; Cryptosporidium/chemistry/genetics/*metabolism ; Humans ; Iron/metabolism ; Mice ; Molecular Sequence Data ; Protein Structure, Tertiary ; Protozoan Proteins/*chemistry/*genetics/metabolism ; Sequence Alignment

OBJECTIVETo investigate the changes of gene expression file in transitional cell carcinoma of bladder after hepatocyte cell adhesion molecule(hepaCAM) overexpression.

METHODSAffymetrix Human Genome U133 Plus 2.0 Array was used to investigate the changes of gene expression profile between adenovirus-green fluorescent protein(GFP) -hepaCAM group and GFP group in transitional cell carcinoma of bladder EJ cells.Significant Analysis of Microarray(SAM) was used to screen the differentially expressed genes, DAVID software was used to conduct gene ontology analysis and wikiPathway analysis based on the differentially expressed genes. Reverse transcription-polymerase chain reaction and Western blot were applied to verify microarray data.

RESULTSCompared with the GFP group, a total of 2469 genes were up-regulated or down-regulated by more than 2 times in the GFP-hepaCAM group. Among these genes, 1602 genes were up-regulated and 867 were down-regulated.Most of the differentially expressed genes were involved in the function of cell proliferation and cell cycle regulation. The mRNA expressions of nibrin, liver kinase B1, and cyclin D1 detected by reverse transcription-polymerase chain reaction in three different bladder cancer cell lines were consistent with the microarray data.The protein expressions of nibrin and liver kinase B1 in these three cell lines measured by Western blot were consistent with the mRNA expression.

CONCLUSIONSHepaCAM can alter the gene expression profile of bladder cancer EJ cells. The well-known anti-tumor effect of hepaCAM may be mediated by regulating the gene expression via multiple pathways.

Carcinoma, Transitional Cell ; genetics ; pathology ; Cell Cycle Proteins ; metabolism ; Cell Line, Tumor ; Cyclin D1 ; metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; physiology ; Humans ; Nuclear Proteins ; metabolism ; Protein-Serine-Threonine Kinases ; metabolism ; Proteins ; genetics ; physiology ; Urinary Bladder Neoplasms ; genetics ; pathology

Twenty five new beta-aminoalcohols containing nabumetone moiety were prepared via the reduction of potassium borohydride with a convenient and efficient procedure, starting from beta-aminoketones that have been synthesized by our group. Their chemical structures were determined by IR, MS, 1H NMR, 13C NMR, HR-MS and antidiabetic activities were screened in vitro. Preliminary results revealed that the antidiabetic activity of most beta-aminoalcohols were better than that of the corresponding beta-aminoketones. Although most compounds showed weak antidiabetic activity, the alpha-glucosidase inhibitory activity of compounds 5hd(1) and 5id(2) reached 74.37% and 90.15%, respectively, which were superior to the positive control. The relative peroxisome proliferator-activated receptor response element (PPRE) activity of five compounds were more than 60%, among them compound 5ca possessed the highest activity (112.59%). As lead molecules of antidiabetic agents, compounds 5hd(1), 5id(2) and 5ca deserve further study.
Amino Alcohols ; chemical synthesis ; chemistry ; pharmacology ; Butanones ; chemical synthesis ; chemistry ; pharmacology ; Cyclooxygenase 2 Inhibitors ; chemical synthesis ; chemistry ; pharmacology ; Glycoside Hydrolase Inhibitors ; Hypoglycemic Agents ; chemical synthesis ; chemistry ; pharmacology ; Peroxisome Proliferator-Activated Receptors ; agonists ; metabolism ; Response Elements ; alpha-Glucosidases ; metabolism

OBJECTIVE: To determine the effects of sodiun aescinate on Bcl-2 and Caspase-3 protein expression and neuronal apoptosis after focal cerebral ischemia reperfusion injury in rats. METHODS: One hundred male Wistar rats were subjected to middle cerebral artery occlusion (MCAO) and reperfusion. The rats were divided randomly into 4 groups: sham-operated group and MCAO and reperfusion model groups which were randomly divided into control group, saline group, and sodium aescinate group. The immunohistochemistry staining and microscope image were used to observe the dynamic Bcl-2 and Caspase-3 protein expression in the ischemic penumbra after the reperfusion. Terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining was performed for the detection of apoptosis. RESULTS: Bcl-2 protein expression in the sodium aescinate group was significantly higher than that of the saline group and control group (P < 0.05). While Caspase-3 protein expression in the sodium aescinate group was then compared with those of the saline group and control group, and showed the difference was significant (P < 0.05). Compared with the saline group and control group, the number of apoptotic cells in the sodium aescinate group was significantly reduced (P < 0.01). CONCLUSION Sodium aescinate increases Bcl-2 protein expression and decreases Caspase-3 protein expression,through which it can protect the ischemia brain on reperfusion injury.
Alginates ; pharmacology ; Animals ; Apoptosis ; drug effects ; Brain Ischemia ; metabolism ; pathology ; Caspase 3 ; Caspases ; biosynthesis ; genetics ; Glucuronic Acid ; pharmacology ; Hexuronic Acids ; pharmacology ; Male ; Plants, Medicinal ; chemistry ; Proto-Oncogene Proteins c-bcl-2 ; biosynthesis ; genetics ; Random Allocation ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism ; pathology ; Saponins ; pharmacology

OBJECTIVETo investigate the autophagy of effector cells in lung tissue at different time points when rats were exposed to free SiO2 dust.

METHODSSixty Wistar rats (220∼230 g) were selected and allocated to experimental group (n = 30) and control group (n = 30). In the experimental group, a rat silicosis model was established by infusing SiO2 suspension into the trachea of rats. Six rats in each group were sacrificed on days 1, 7, 14, 21, or 28 of dust exposure. Lung tissue samples were collected to prepare lung tissue sections. The pulmonary inflammation and fibrosis were observed by HE staining. The proautophagosome, autophagosome, and autophagolysosome in lung tissue sections were observed under a transmission electron microscope.

RESULTSOn day 1 of dust exposure, many proautophagosomes and autophagosomes were seen in both experimental group and control group. On day 7 of dust exposure, the experimental group had more autophagosomes in lung tissue than the control group. On day 14 of dust exposure, the experimental group had fewer autophagosomes than the control group. On days 21 and 28, autophagolysosomes were seen in macrophage plasma in both experimental group and control group; the autophagolysosomes in experimental group showed cloudy swelling and expansion, and some were vacuolated, and these changes were more significant on day 28.

CONCLUSIONFree SiO2 dust can induce autophagy in the lung tissue of rats, with varying degrees at different time points of dust exposure.

Animals ; Autophagy ; drug effects ; Dust ; Lung ; drug effects ; pathology ; Male ; Rats ; Rats, Wistar ; Silicon Dioxide ; toxicity

OBJECTIVEDuring progression of atherosclerosis, the vessel may develop either positive or negative remodeling. The pathophysiology of vascular remodeling is not fully understood. This study investigated the relationship between plaque characteristics and arterial remodeling using intravascular ultrasound imaging (IVUS).

METHODSA total of 77 patients (male 53, mean age 58 +/- 10 years) who underwent IVUS imaging (ClearView or Galaxy2, Boston Scientific, USA) of culprit vessel were enrolled in this study. Among the 77 patients, 31 presented with stable angina pectoris and 46 presented with acute coronary syndrome. Qualitative assessment of the lesion and quantitative measurement were performed in both stenotic and reference segments. The lesions were classified into soft plaque and hard plaque (including fibrous plaque, calcified plaque and mixed plaque) according to different ultrasound patterns of tissue reflection. The remodeling index (RI) was defined as the ratio of vessel cross sectional area (EEMcsa) of lesion segment to the mean reference EEMcsa. Positive remodeling was defined as RI > 1.0 and negative remodeling as RI < 1.0.

RESULTSOf 77 lesions, 45 (58%) had undergone positive remodeling, and 32 (42%) had negative remodeling. In comparison to the patients with negative remodeling, patients with positive remodeling presented with more acute coronary syndrome (74% vs. 43%, P = 0.006). Both the plaque area and the vessel area were significantly larger in the lesion with positive remodeling than in lesion with negative remodeling. The lesions with positive remodeling were predominantly soft (71% vs. 34%, P = 0.001) and had less calcification [21% vs. 54%, P = 0.003 and (18 +/- 37) degrees vs. (40 +/- 50) degrees, P = 0.027] compared with lesions with negative remodeling. The difference of clinical presentation and plaque characteristics between the patients with different patterns of remodeling is still significant with binary logistic analysis.

CONCLUSIONSCoronary arterial remodeling pattern is related to the clinical manifestation and the composition of plaque. Lesions presented with positive remodeling have a higher prevalence of soft plaque and less calcification.

Aged ; Coronary Disease ; diagnostic imaging ; physiopathology ; Coronary Vessels ; diagnostic imaging ; physiopathology ; Female ; Humans ; Male ; Middle Aged ; Ultrasonography, Interventional

Animals ; COS Cells ; Female ; Genetic Therapy ; Interleukin-12 ; genetics ; Liver Neoplasms, Experimental ; immunology ; therapy ; Mice ; Mice, Inbred BALB C ; T-Lymphocytes, Cytotoxic ; immunology

OBJECTIVETo ascertain whether connexin 26 (Cx26) gene was a nuclear modifier gene in an extensive family with matrilineal nonsyndromic deafness associated with A1555G mutation in Huaiyin, China.

METHODSFollowing PCR-restriction fragment length polymorphism (PCR-RFLP) with ApaI restriction enzyme, Cx26 genes from 26 cases, with A1555G mitochondrial mutations in this family, and 62 controls (including 2 patrilineal relatives, 10 spouse controls and 50 unrelated controls), were sequenced.

RESULTSCompared with the reference sequence of Cx26 gene, totally four kinds of nucleotide changes,79G -->A, 109G-->A, 341G-->A and 235delC, were detected in a heterozygous form. However, the former three were previously reported polymorphisms, and only the 235delC was a previously described recessive mutation associated with most autosomal nonsyndromic sensorineural hearing loss in Japan and China. Further study showed that the heterozygous 235delC mutation existed in both one individual with mild hearing loss and two individuals with normal hearing. Clinical characterization showed that 235delC mutation did not seem to modify the deafness phenotype due to the A1555G mutation. Moreover, this 235delC mutation was deduced to derive from a married-in control. Finally, there were no co-segregation between the phenotypes of hearing loss and the genotypes for Cx26 genes based on the four kinds of nucleotide changes.

CONCLUSIONSThe heterozygous 235delC mutation of the Cx26 gene may not modulate the severity of hearing loss associated with A1555G mutation and Cx26 gene is unlikely to be a modifier gene for hearing loss due to A1555G mitochondrial mutation in this Chinese family.

Adolescent ; Adult ; Case-Control Studies ; Child ; Child, Preschool ; China ; epidemiology ; Connexin 26 ; Connexins ; genetics ; Deafness ; epidemiology ; ethnology ; genetics ; Female ; Genotype ; Humans ; Infant ; Infant, Newborn ; Male ; Middle Aged ; Mutation ; Pedigree ; Phenotype ; Polymorphism, Restriction Fragment Length ; Sequence Analysis ; Young Adult