Objective To evaluate the application of transcatheter closure of patent ductus arteriosus (PDA) with severe pulmonary hypertention using the Amplatzer occluder device.Methods Fifty-one cases of PDA with severe pulmonary hypertention were treated by transcatheter closure with Amplatzer occluder. Patients mean age was 9.4 years (ranging 3 months to 60 years) and the mean weight was (18.7?13.8) kg (ranging 5.0 to 65.0 kg). The mean PDA diameter at its narrowest segment was (7.0?2.4) (ranging 3.0 to 15.0) mm. The achievement of permanent transcatheter closure was decided according to the change of the pulmonary arterial pressure, aortic pressure and oxygen saturation. Results The devices were successfully placed in all patients except one failure owing to the resistance of pulmonary hypertention. The systolic pulmonary pressure decreased from (84.7?13.5) (range 70 to 137) to mmHg to (46.1?14.9) (24 to 109)mmHg, and the mean pulmonary pressure decreased from (65.0?11.5) (42 to 97) mmHg to (31.3?11.6) (14 to 69) mmHg. Complete angiographic closure was seen 10 minutes after the device deployment in 30 out of 50 patients (60%), while trivial to small leak was present in 20 (40%). Complete echocardiographic closure was demonstrated in 49 out of 50 patients (98%) at 10 min, and 100% at 6-month follow-up in all patients. There were no PDA recanalization and migration of devices after the complete occlusion during following up.Conclusion Transcatheter closure of patent ductus arteriosus with severe pulmonary hypertention by using the Amplatzer occluder is a safe and effective interventional method with excellent short-term and middle-term results.

Assess retrospectively 75 cases of double chambered right ventricle confirmed by clinical examination and operation. The diagnosis and differential diagnosis were made by physical signs, chest X rays, electrocardiograph, echocardiogram, catheterization and right ventricular cardiograph features. Results showed that there were only 9 cases of simple form among 57 (76 %) cases with double chambered right ventricle before operative confirmation,and in 48 (64 %) cases it was accompanied by other intracardiac malformation. Eighteen (24%) cases were not diagnosed preoperatively. In order to raise the diagnotic rate, it was important to measure the pressure gradient between the pulmonary artery and the inflow tract of right ventricle, and evaluate carefully the right ventricular size and morphology by angiocardiography.

Objective To prepare in-house calibrator of apolipoprotein A1 and apolipoprotein B with the values are traceable to the WHO-International reference materials SP1-01 and SP3-07.Methods We participated in the Northwest lipid research laboratory (NWLRL) protocol for target value transfer of WHO-IFCC apo A1 and apoB reference materials, and evaluated of comparability of the measurement.The analyses were performed on a Olympus AU 400, apo A1 and apoB were determined by immunoturbidimetric endpoint method.Results Through 3-step study, the precision and accuracy of apo A1 and apoB determination of our company met the NWLRL criteria.Correlation coefficients between obtained and assigned values of NWLRL on 40 individual serum samples were 0.983 for apo A1, 0.987 for apoB, the average absolute bias were 2.7 % for apo A1, 3.0 % for apoB, respectively.Conclusion NWLRL issued the certificate to Zhongsheng Beikong Bio-Technology and Science Inc.for the in-house apo A1 and apoB calibrator values are traceable to the WHO- International reference materials.

Abstract: Objective To study the effect and mechanism of Huaxian Sanjie compound granule on silicosis fibrosis in rats. Methods The specific pathogen free male SD rats were randomly divided into control group, silicosis model group and - interventiongroup,withsixratsineachgroup.Disposableventilatorcombinedwithnon exposedintratrachealdripwasused,the ratsinthesilicosismodelgroupandinterventiongroupweretreatedwith 1.0mLsilica suspensionwithamassconcentrationof 50.0 g/L to establish silicon dust rat model, while the rats in the control group were treated with equal volume of 0.9% sodium chloride solution. After 24 hours of dust exposure, the rats in the intervention group were given 10 mL/kg body weight of Huaxian Sanjie compound granule suspension with a mass concentration of 212.5 g/L by gavage, while the rats in the control group and silicosis model group were given the same amount of 0.9% sodium chloride solution, once a day. Three rats in each groupweresacrificedonthe14thand28thday,respectively,andtheirlungtissueswereseparatedforpathologicalexamination.----Thelevelsofinterleukin6(IL6)andtransforminggrowthfactorβ

Objective To study binocular rivalry (BR)objectively and the correlation between fusiform face area (FFA)and visual cortex.Methods Six subjects participated in this study,with one eye presented a normal face expres-sion picture flickered at 8.57 Hz,while the other presented a fearful face flickered at 12 Hz or 15 Hz,respectively.Electro-encephalogram(EEG)was recorded during this process.Steady state visual evoked potential(SSVEP)evoked by two flick-ering rates was analyzed by time-frequency analysis of short time fourier transformation(STFT).The time index of BR was estimated and the correlation coefficient between FFA and visual cortex compared.Results The total average time was (411.6 ±73.8)ms for the left eye and (547.6 ±126.7)ms for the right eye.The switch rate of the two groups was not different,but the left FFA was more sensitive than the right FFA in process of the fearful face.Neither side of FFA had any frequency preference to the flickered fearful face.Conclusion SSVEP can be used as a frequency tag of BR or as a tool to evaluate visual sensation under BR objectively.SSVEP combined with BR can be used in research of neural mechanisms of visual awareness.

This paper studied the diagnosis and embryology of 20 cases lacking one pulmonary artery out of 2040 patients operated for tetralogy of Fallot. History of severe cyanosis syncope and hemoptysis was usually present in the majority of these patients. The important diagnosis characteristic was asymmetry of plumonary vascularity on X-ray film and the decrease of pulmonary cascular markings on the side without plumonary artery. A right ventricular cardiogram can confirm the absence of one pulmonary artery or the blind-end like change.

Objective:To investigate the effect of oleanolic acid (OA) on Sirtuin1 (SIRT1)-mediated high-mobility group box 1(HMGB1) deacetylation in the early brain injury after subarachnoid hemorrhage (SAH).Methods:A total of 176 male Sprague-Dawley rats were randomly divided into Sham operation (Sham group) ( n=48), SAH group ( n=48), OA group ( n=48) and Sirtinol group ( n=32). Rats in the SAH group, OA group and the Sirtinol group all adopted internal carotid artery puncture to construct SAH model, while rats in the sham group did not adopt puncture. One hour after modeling, the rats in the OA group were given intraperitoneal injection of OA (20 mg/kg), and the rats in the Sirtinol group were given intracerebroventricular injection of Sirtinol (2 mmol/L, 30 μL/kg). The rats in the sham group and SAH group were injected with equal volumes of sodium chloride injection. The SAH score and neurological score were performed 24 h after SAH, and the water content in the brain tissue and Evans blue exudation rate were measured. The expressions of HMGB1, SIRT1 and acetylated HMGB1 proteins in the brain tissue of rats were detected by Western Blot. The expression of HMGB1 mRNA in the brain of the rats was detected by quantitative real-time PCR. The distribution of HMGB1 protein in the brain of the rats was observed by immunofluorescence staining. TUNEL staining was used to observe the neuronal apoptosis in the brain tissue of the rats. Results:Compared with the SAH group, the SAH score of the OA group was significantly reduced ( P<0.001), the Garcia score was increased ( P<0.01), and the brain water content and Evans blue exudation rate were both reduced (all P<0.01). Compared with the OA group, the SAH score of the Sirtinol group was increased ( P<0.01), the Garcia score was significantly decreased ( P<0.001), and the brain water content and Evans blue exudation rate were both increased (all P<0.01). The results of Western Blot and real-time fluorescent quantitative PCR showed that, compared with the SAH group, the protein level ( P<0.01) and mRNA level ( P<0.05) of HMGB1 in the OA group were decreased, the expression of SIRT1 protein was significantly increased ( P<0.001), and the expression of acetylated HMGB1 protein was decreased ( P<0.01). Immunofluorescence staining showed that OA inhibited the migration of HMGB1 protein from the nucleus to the cytoplasm. TUNEL staining showed that OA could effectively reduce the number of TUNEL-positive cells. Compared with the OA group, Sirtinol significantly increased the number of TUNEL-positive cells. Conclusions:OA can reduce the release of HMGB1 through the SIRT1/HMGB1 pathway, thereby protecting the early brain injury after SAH.

Objective:To investigate the effect of Sirtuin 1 (SIRT1) on subarachnoid hemorrhage (SAH) and its possible mechanism.Methods:A mouse model of SAH was constructed by internal carotid artery puncture. The protein and mRNA expression levels of SIRT1 at 0, 3, 6, 12, 24, 48, and 72 h were detected by Western Blot and qRT-PCR. A Western Blot assay was used to examine SIRT1 and the expression levels of endoplasmic reticulum stress-related markers GRP78, p-PERK/PERK, p-eIF2α/eIF2α, and CHOP after administration of a SIRT1 inhibitor or SIRT1 si-RNA. At 24 h after SAH, subarachnoid hemorrhage volume, neurological function score, brain water content, and blood-brain barrier integrity were measured.Results:The highest expression of SIRT1 protein and mRNA was observed at 24 h compared with other time points, and the differences were statistically significant (all P < 0.001). Inhibition of SIRT1 expression leads to increased expression of endoplasmic reticulum stress-related proteins GRP78, p-PERK/PERK, p-eIF2α/eIF2α, and CHOP, exacerbating hemorrhage and brain water content, disrupting blood-brain barrier integrity, and significantly reducing neurological function scores. Conclusions:Inhibition of SIRT1 expression significantly increased the endoplasmic reticulum response to excitation and exacerbated early brain injury after SAH.

Objective:To discuss the antioxidant and anti-apoptosis effects of 3-hydroxy-olea- 12-en-28-oic acid (OA) on subarachnoid hemorrhage (SAH) and their mechanisms in rat models.Methods:In experiment one: 144 SD rats were divided into sham-operated group, SAH group and SAH+20 mg/kg OA group by random number table method ( n=48); SAH models were established by standard endovascular puncture method; rats in the SAH+20 mg/kg OA group received intraperitoneal injection of OA one h after modeling, while rats in the sham-operated group received the same operation without perforation; brain edema, destruction of blood-brain barrier, SAH severity degrees (Sugawa scale scores), neurological function scale scores and other early brain injury-related indicators were detected in rats from the three groups; the levels of malondialdehyde (MDA), superoxide dismutase (SOD) were investigated; the activation of nuclear factor related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) axis and neuronal apoptosis after SAH were detected. In experiment two: another 36 rats were divided into sham-operated group, SAH model group, sham operated+negative control siRNA group, SAH+negative control siRNA group, sham operated+Nrf siRNA group and SAH+Nrf siRNA group according to random number table method ( n=6); treatment methods in the sham-operated group and SAH modeling methods were the same as experiment one; negative control siRNA or Nrf siRNA were injected into the lateral ventricle of rats in the later 4 groups 24 h before SAH modeling; expressions of apoptosis-related factors in the downstream of Nrf2/HO-1 axis were detected in rats from the 6 groups. Results:In experiment one: (1) as compared with rats in the SAH group, rats in the SAH+20 mg/kg OA group had significantly decreased Sugawa scale scores, statistically increased neurological function scale scores and balance beam scale scores, significantly decreased brain moisture content and Evans blue exhalation rate ( P<0.05); (2) as compared with SAH group, SAH+20 mg/kg OA group had significantly decreased MDA level, and significantly increased SOD, glutathione peroxudase and catalase levels ( P<0.05); (3) the expressions of Nrf2, HO-1 and B-cell lymphoma-2(Bcl-2) were significantly increased, the expressions of apoptosis-related factors cytochrome-C, caspase-3 and activated caspase 3 were signficantly decreased, and the number of apoptotic neurons was significantly samller in the SAH+20 mg/kg OA group as compared with those in the SAH group ( P<0.05). In experiment two: as compared with those in the SAH+negative control siRNA group, the protein expressions of HO-1 and Bcl-2 in the SAH+Nrf siRNA group were significantly decreased, while the expression levels of cytochrome C, caspase-3 and activated caspase 3 were statistically increased ( P<0.05). Conclusion:OA can reduce the occurrence of oxidative stress and neuronal apoptosis by activating Nrf2/HO-1 axis.

OBJECTIVE: To assess the association of CYP2C19 and CYP3A5 gene polymorphisms with the risk of myocardial infarction. METHODS: Five hundred patients with myocardial infarction and 500 healthy controls were randomly selected. Fluorescent PCR and Sanger sequencing were used to detect the CYP2C19 and CYP3A5 gene polymorphisms. Logistic regression was used to analyze the correlation between the polymorphisms and myocardial infarction. Quanto software was used to evaluate the statistical power. RESULTS: The two groups had significant difference in the frequency of AG, GG genotypes and A allele of the CYP2C19 gene rs4986893 locus and the AA, AG, GG genotypes and G allele of the CYP3A5 gene rs776746 locus ( P<0.05), but not in the frequency of genotypes and alleles of CYP2C19 gene rs4244285 and rs12248560 loci, and the AA genotype of the rs4986893 locus. After correction for age, gender, and body mass index, Logistic regression indicated that the AG genotype and A allele of the CYP2C19 gene rs4986893 locus, and the GG genotype and G allele of CYP3A5 gene rs776746 locus are associated with susceptibility of myocardial infarction, while rs4986893 GG genotype and AA and AG genotypes of rs776746 may confer a protective effect. Based on the sample size and allele frequency, analysis with Quanto software suggested that the result of this study has a statistical power of 99%. CONCLUSION CYP2C19 and CYP3A5 gene polymorphisms may increase the risk for myocardial infarction.
Cytochrome P-450 CYP2C19/genetics* ; Cytochrome P-450 CYP3A/genetics* ; Gene Frequency ; Genotype ; Humans ; Myocardial Infarction/genetics* ; Polymorphism, Genetic ; Polymorphism, Single Nucleotide