Objective To investigate the effect of selective phosphatase inhibitors Salubrinal on autophagy and apoptosis in the lung tissue of rats with acute paraquat (PQ) poisoning,and to explore its mechanism.Methods 200 Wistar rats were randomly divided into four groups by randomized arrangement table formed by computer,with 50 rats in each group.PQ poisoning model was reproduced by one time gastric lavage with 1 mL of 40 mg/kg PQ solution followed by intraperitoneal injection of 1 mL normal saline (NS) once a day.The rats in control group were lavaged once with 1 mL of NS followed by intraperitoneal injection of 1 mL NS twice a day.The rats in Sal 0.5 and Sal 1.0 groups were intraperitoneal injected with 1 mL Salubrinal 0.5 mg/kg or 1.0 mg/kg on the 1st,3rd,and 5th day after PQ poisoning once a day.The lung tissue was harvested on the 7th day after poisoning,and the changes in histomorphology were observed using hematoxylin and eosin (HE) staining.The positive expression of autophagy-related protein LC3-Ⅱ in lung tissue was observed after immunohistochemistry staining,and LC3-Ⅱ and caspase-3 protein expressions were determined by Western Blot.Results HE staining results showed partial abnormal pulmonary structure in the PQ poisoning group:collapse of pulmonary alveoli,enlargement of the cavity,local infiltration of inflammatory cells,increasing thickness in the alveoli wall and obvious bleeding in the local lung tissue.Compared with the PQ poisoning group,the above changes in Sal 0.5 and Sal 1.0 groups were obviously relieved.It was shown by immunohistochemistry staining that compared with control group,the positive expression of LC3-Ⅱ was obviously decreased in the PQ poisoning group,Sal 0.5,and Sal 1.0 groups (A value:78.34 ± 10.71,76.52 ± 8.21,77.48 ± 9.11 vs.117.58 ± 15.26,all P＜0.05).There was no significant difference in positive expression of LC3-Ⅱ between each of the later three groups (all P＞0.05).Western Blot results showed:compared with the control group,the protein expressions of LC3-Ⅱ and caspase-3 were significantly increased in PQ poisoning group [LC3-Ⅱ (A value):0.22 ±0.05 vs.0.14 ±0.03,caspase-3 (A value):0.115 ± 0.013 vs.0.023 ± 0.006,both P＜0.05].Compared with PQ poisoning group,the protein expressions of LC3-Ⅱ and caspase-3 were obviously decreased in the Sal 0.5 and Sal 1.0 groups [LC3-Ⅱ (A value):0.19 ±0.05,0.18 ±0.04 vs.0.22 ±0.05; caspase-3 (A value):0.078 ±0.012,0.076 ±0.010 vs.0.115 ±0.013,all P＜0.05].Conclusions The endoplasmic reticulum stress-autophagy is activated in the pulmonary cell of acute PQ poisoning rats.Salubrinal can decrease the autophagy and apoptosis in the lung of rats with acute PQ poisoning,which play a role in the treatment.

Objective To investigate the effects of ulinastatin on autophagy and apoptosis of lung cells in rats with acute paraquat poisoning.Methods A total of 150 Wistar rats were randomly (random number) divided into three groups.The rats in control group had stomach lavaged once with 1 mL of normal saline followed by intraperitoneal injection of 1 mL normal saline twice a day.PQ poisoning model was produced by stomach lavaged once with 1 mL of 40 mg/kg PQ solution followed by intraperitoneal injection of 1 mL normal saline once a day.In PQ + ulinastatin (PU) group,UTI in dose of 12 000 U/kg was intraperitoneally injected in rats twice a day.The lung tissue was obtained on the 7th day after modeling,and the histopathological changes were observed under microscope after hematoxylin and eosin (HE) staining.The positive expressions of autophagy-related LC3 protein LC3 and Bcl-2 pretein in lung tissue were observed after immunohistochemistry staining,and the levels of LC3、Bax 、Bcl-2 proteins were determined by Western blot.Results HE staining Results showed:it was observed from the PQ poisoning group that the abnormal cellular structure,enlargement in the pulmonary alveoli,leaking a lot of inflammatory cells,increased thickness of the alveoli wall and bleeding in the local area of lung tissue.Compared with the PQ poisoning group,the above changes in ulinastatin groups were relieved.Western blot Results showed:compared with the control group,the protein expressions of LC3-A/B were significantly increased in PQ poisoning group [LC3-A/B expression (A scale):0.22 ± 0.05 vs.0.14 ± 0.03,F =22.48,P ＜ 0.01].compared with PQ group,the expression of LC3 A/B obviously increased in the group of PU [LC3-A/B expression (A scale):0.36 ± 0.08 vs.0.22 ± 0.05,F =22.78,P ＜ 0.01].compared with Con group,the expression of Bcl-2/Bax obviously decreased in the group of PQ [Bcl-2/Bax expression (A scale),0.11 ±0.04 vs.0.83 ± 0.09,F =154.43,P ＜ 0.01].Compared with PQ poisoning group,the protein expressions of Bcl-2/Bax were obviously increased in PU groups [Bcl-2/Bax expression (A scale):(0.63 ± 018) vs.(0.11 ±0.04),F =154.43,P ＜0.01].Immunohistochemistry result:compared with Con group,the expression of LC3 and Bcl-2 obviously decreased in the group of PQ [LC3expression (A scale):(78.34±10.71) vs.(117.58±15.26),F=31.63,P＜0.01) (Bcl-2 expression (A scale):(62.54±9.74)vs.(130.52 ± 9.86,F =118.44,P ＜ 0.01).Compared with PQ poisoning group,the protein expressions of LC3 and Bcl-2 were obviously increased in PU groups [LC3expression (A scale):(162.58 ± 25.76) vs.(78.34 ± 10.71),F=31.63,P＜0.01]; [Bcl-2 expression (A scale):(145.56±10.26) vs.(62.54±9.74),F=118.44,P ＜ 0.01].Conclusions Theendoplasmic reticulum stress-autophagy is activated in the lung cells of rats with acute PQ poisoning.UTI can adjust endoplasmic reticul um stress,increased the expression of Bcl-2 and enhance the proportion of Bcl-2/Bax to protect the lungs of rats from acute PQ poisoning.

AIM:To investigate the effects of microRNA-29a and 133a expression in the atrium on atrial fibril-lation (AF) and fibrosis.METHODS:Chronic rapid atrial pacing was used to establish the persistent AF dog model , and the sham group was also set up .The cardiac ultrasound measurement was used for determining the cardiac structure size . The Masson 3 color staining were used to evaluate the stage of fibrosis .The expression of microRNA-29a and 133a in the left atrium ( LA) was detected by real-time transcriptase polymerase chain reaction .RESULTS: Compared with before modeling , no statistical difference of atrial dilatation and decreased ejection fraction in the model dogs with persistent AF was observed (P>0.05).Compared with sham group, the degree of fibrosis and collagen volume fraction (CVF) in per-sistent AF model group were increased obviously (P<0.05).The expression of microRNA-29a and 133a were decreased obviously (P<0.01, P<0.05).CONCLUSION:Structural remodeling of the atrium and atrial fibrosis are the essential for development and maintenance of atrial fibrillation .Down-regulation of microRNA-29a and 133a expression may be very important molecular mechanism for atrial structural remodeling in the persistent AF model dogs .

Objective: To study the relationship between dilated cardiomyopathy and nuclear lamina protein (LMNA) gene mutation in Kazak ethnics at Xinjiang area.
Methods: A Kazak familial dilated cardiomyopathy (FDCM) with 31 members was studied. In addition, 160 patients with idiopathic dilated cardiomyopathy (IDCM) with 160 healthy controls were enrolled in our study, and they were divided into 4 groups: IDCM-Kazak, IDCM-Han and Control-Kazak, Control-Han.n=80 in each group. Peripheral blood DNA were extracted, 12 exons with nearby introns of LMNA gene were detected by PCR and the ampliifed products were sequenced and compared with the standard template of CHROMAS and BLAST software to identify mutation sites. LMNA mutation in both Kazak and Han IDCM patients were investigated.
Results: A novel LMNA mutation (insC, CGG→CCG) at exon 7 was identiifed in a FDCM proband, it caused an amino acid substitution as Arg to Pro, and a known LMNA polymorphism loci rs4641 (c.1362C>T His454His) was fund at exon 10. In addition, LMNA polymorphism loci rs4641 genotype distribution (χ2=5.16,P=0.036) and allele frequency (χ2=4.50,P=0.034) were statistically different between IDCM-Kazak group and Control-Kazak group; while such differences were no statistic meaning between IDCM-Han group and Control-Han group. Logistic regression analysis indicated that LMNA polymorphism loci rs4641 was related to IDCM occurrence in Kazak ethnics (P=0.025, OR=0.412, 95% CI 0.189-0.896).
Conclusion: LMNA polymorphism loci rs4641 was related to IDCM in Kazak ethnics at Xinjiang area, which might be susceptible loci for IDCM occurrence.

Objective To investigate the clinical features and current therapy of atrial fibrillation (AF) of inpatients in Urumqi,China.Methods The clinical data of inpatients diagnosed with AF from January,2008 to December,2012,in 12 hospitals in Urumqi were retrospectively analyzed.Results Totally 1 310 AF inpatients were enrolled in this study with the age of (64.8 ±3.3) years old and a men to women ratio of 1.39.Most patients were in age groups of 61-70 years (26.5％) and 71-80 years (27.6％).More patients with paroxysmal AF were at cardiac function class Ⅰ-Ⅱ (75.2％),while more patients with persistent AF were at cardiac function class Ⅲ-Ⅳ (31.0％) (both P values ＜ 0.05).The most common co-morbidities of AF were hypertension (49.2％),coronary heart disease (38.5％),diabetes mellitus (20.1％).Compared with patients of chronic AF,the patients of paroxysmal AF had higher success rates in amiodarone conversation and sinus rhythm maintenance after ablation (44.8％ vs 29.9％,87.5％ vs 68.9％,P values ＜ 0.05).Among the 1 310 inpatients,992 patients (75.7％) received antithrombotic therapy.There were statistically significant differences in CHA2DS2 score and incidence rate of cerebral infarction among patients receiving aspirin,warfarin or rivaroxaban/other anticoagulation drugs [2 (1,3) vs 3 (2,4) vs 3 (2,5) and 6.3％ vs 23.8％ vs 30.2％,both P values ＜0.05].Conclusion Our results of AF inpatients' age,gender,related disease distribution,AF types,incidence of stoke,therapeutic and epidemiological features are in accordance with the domestic and abroad reports.

Objective To explore the value of distinguishment of hepatocellular carcinoma (HCC), cirrhosis nodules and normal liver based on neural networks in the ~(31)P-MR spectroscopy. MethodsA total of 66 data of ~(31)P-MRS were analysed using back-propagation neural network, including 37 samples of liver cirrhosis, 13 samples of HCC and 16 samples of normal liver. ResultsThe cross-valiation experiments showed that diagnostic accuracy rate of HCC increased from 85.47% to 92.31% with neural network model based on the ~(31)P-MR spectroscopy data analysis. Conclusion ~(31) P-MRS data analysis based on neural network model provides a valuable diagnostic tool of HCC in vivo.

Objective: To observe the clinical characteristics and current treatment status in patients with chronic heart failure (CHF) at different grade hospitals in Xinjiang Area.
Methods: A total of 5357 patients with CHF diagnosis discharged from 20 different grade hospitals in Xinjiang area from 2011-01 to 2012-02 were enrolled. The age, gender, nationality, etiology of CHF, cardiac function, complications and current medication status in all patients were systemically studied.
Results:①There were 2295/5357 (42.8%) patients with Han nationality, 2255 (42.1%) with Uyghur nationality and 8.07 (15.1%) with other nationalities. The average age of patients was at (64.60 ± 12.77) years.②The etiology of CHF were, in turn, as: coronary artery disease (CAD) 50.8%, hypertension (31.8%), dilated cardiomyopathy (7.2%).③ The ratios of patients with NYHA III-IV in county hospital 440/682 (64.5%), in regional hospital 1180/1557 (75.8%) were higher than that that in grade A class 3 hospital 967/3118 (31.0%), ( =1390.362,P=0.000).④The patients in county hospital, regional hospital showed increased left atrial diameter (44.7 ± 8.8) mm, (39.5 ± 8.1) mm and left ventricular end-diastolic diameter (60.6 ± 11.1) mm, (56.9 ± 11.1) mm than those in grade A class 3 hospital (37.3 ± 7.1) mm and (53.8 ± 9.7) mm; while decreased LVEF (41.9 ± 10.5) %, (42.3 ± 13.0) % than that in grade A class 3 hospital (46.5 ± 12.8), allP<0.001.⑤The medication status in different grade hospitals as ACEI/ARB, β-blocker, aldosterone antagonist, diuretics, digitalis were at 72.8%, 66.8%, 46.6% , 45.5% and 26.8% respectively. The application of ACEI/ARB and β-blocker in county hospital (61.4% and 51.5%) and in regional hospital (72.3% and 58.3%) were lower than those in grade A class 3 hospital (75.6% and 74.3%); while the application of aldosterone antagonist in county hospitals (57.9%) and in regional hospital (73.8%) were higher than that in grade A class 3 hospital (30.6%), allP<0.001.
Conclusion: The etiology of CHF were mainly as CAD and hypertension in Xinjiang area, the patients in county and regional hospitals had more severe conditions than that in grade A class 3 hospital, which implying the distance between the guideline standard and real practice especially in basic level hospitals.

Objective: To explore the relationship between atrial MMP-9 with its inhibitor (TIMP-1), anti-apoptosis gene (BCL-2) with apoptosis gene (BAX) and the aging with atrial remodeling in experimental dog model during atrial ifbrillation (AF), in order to better deal with the aging caused AF.
Methods: The experimental dogs were divided into 4 groups: ①Adult with sinus rhythm (ASR) group, ②Elder with sinus rhythm (ESR) group and③Adult with AF (AAF) group,④Elder with AF (EAF) group. n=7 in each group. Chronic AF model was induced by rapid and persistent atrial pacing. The mRNA and protein expressions of MMP-9, TIMP-1 and BCL-2, BAX were measured by real time quantitative RT-PCR and Western blot analysis. The cellular ultra structural remodeling was examined by optical/electron microscopy, and the apoptosis index was determined by TUNEL method,
Results: Compared with adult dogs, the elder dogs showed obviously increased expressions of MMP-9, BAX, and decreased expressions of TIMP-1, BCL-2, all P<0.05. Compared with SR gods, the AF dogs presented up-regulated expressions
of MMP-9, BAX, all P<0.05, and down-regulated expressions of TIMP-1, BCL-2, all P<0.05, such changes were most obvious in elder AF dogs. Accompanying with the aging and AF, the degree of atrial ifbrosis, cellular ultra structure and the apoptosis index were changed with the statistic meaning.
Conclusion: The abnormal expressions of MMP-9/TIMP-1 and BCL-2/BAX might be one of the molecular mechanisms for aging caused AF in experimental dog model.

Objective To evaluate the association between LDL-C and ischemic stroke in patients with nonvalvular atrial fibrillation (AF).Method A total of 2 470 patients with nonvalvular AF were included in the present study.The clinical data and laboratory examination results of the patients in the hospital were collected.The subjects were either divided into the ischemic stroke history (n =560),and non-ischemic stroke history groups (n =1 910),or divided into the low-middle risk (n =566) and high risk groups (n =1 904) based on CHA2 DS2-VASc score.Results There were significant differences in the proportion of Han,the ratio of gender,age,hemoglobin,hematocrit,ALT,serum uric acid,HDL-C and LDL-C between the patients with ischemic stroke history and without (all P ＜ 0.05).Similarly,there were significant differences in the proportion of Han,the ratio of gender,age,white blood cell count,hemoglobin,hematocrit,platelet count,ALT,albumin,TG and LDL-C between subjects in the low-middle risk group and those in the high risk group (all P ＜ 0.05).A logistical regression analysis showed that LDL-C was an independent risk factor for both the ischemic stroke history (OR 2.089,95％ CI 1.860-2.347,P ＜0.05),and future ischemic stroke risk (OR 1.270,95％ CI 1.079-1.494,P ＜ 0.05) in patients with nonvalvular AF.Conclusion LDL-C is associated with ischemic stroke in patients with nonvalvular AF,and it is also an independent risk factor for future ischemic stroke in these patients.

Objective: Present study analyzed the association betwen the postassium voltage-gated channel KQT-like subfamily member 1 gene (KCNQ1) mutation and the clinical and the electrocardiographic features in 2 pedigrees with congenital long QT syndrome type 1 (LQT1) in Xinjiang Uygur Autonomous Region. Methods: Three family members were diagnosed as LQT1 patients in 2 Uygur congenital LQT1 families, these 3 LQT1 patients served as long QT group, 24 Uygur healthy volunteers served as control group. Electrocardiogram (ECG) and the gene detection were applied to compare the ECG and molecular genetic features between the long QT group and control group, and to explore the relationship between the KCNQ1 gene mutation and the clinical and the electrocardiographic features in these 2 families with congenital long QT syndrome type 1. Results: The LQT1 was diagnosed in 3 cases of the 2 pedigrees. The common features of ECG were QTc>480 ms, prolonged ST segment, and delayed T wave. The gene test evidenced a polymorphism of KCNQ1 gene exon 13:47G➝A(R16R). The mutation of 133G➝A9(G45S) of exon 16 resulted in the change of the original glycine (G) to serine (s). The ECG of the control group were normal, and there were no KCNQ1 gene mutations in control group. Conclusion The exon sequencing results of KCNQ1 gene in 2 Xinjiang Uygur congenital long LQT1 families showed that exon16 missense changes (133G to A (G45S)) can lead to amino acid mutation, this mutation may be a pathogenic mutation. Subsequent validation of the expanded sample will provide a reference for revealing the relationship between the KCNQ1 gene and the pathogenesis of LQT1.