Sequence variations in GATA4 and CITED2 gene among patients with cardiac septation defects from Xinjiang, China.

Studies have shown that genetic factors play an important role in CHD's development. The mutations in GATA4 and CITED2 genes result in the failure of the heart to develop normally, thereby leading to septal defects. The present study investigated the underlying molecular aetiology of patients with cardiac septation defects from Xinjiang. We investigated variants of the GATA4 and CITED2 gene coding regions in 172 patients with cardiac septation defects by sequencing. Healthy controls (n = 200) were included. Three heterozygous variations (p.V380M, p.P394T, and p.P407Q) of the GATA4 gene were identified in three patients. p.V380M was discovered in a patient with atrial septal defect. p.P394T was noted in a patient with atrial septal defect. p.V380M and p.P407Q of the GATA4 gene were detected in one patient with ventricular septal defect. A novel homozygous variation (p. Sl92G) of the CITED2 gene was found in one patient with ventricular septal defect. Other patients and healthy individuals were normal. The limited prevalence of genetic variations observed in individuals with cardiac septal defects from Xinjiang provides evidence in favour of the hypothesis that CHD is a polygenic hereditary disorder. It is plausible that mutations in the GATA4 and CITED2 genes could potentially underlie the occurrence of idiopathic CHD in affected patients.

Analysis of clinical effects, inflammatory stress and immune cell levels in patients with acute aortic dissection after TEVAR / 中国医师杂志

Objective:To investigate the clinical effects, inflammatory stress and immune cell levels of patients with acute aortic dissection (AD) after thoracic aortic endovascular repair (TEVAR).Methods:A retrospective analysis of 60 patients with acute aortic dissection admitted to our hospital from April 2014 to January 2016 were divided into conservative group ( n=30) and TEVAR group ( n=30) according to different treatment methods. The conservative group was given drug therapy, and the TEVAR group was given a thoracic aortic endovascular repair therapy. The inflammatory cytokines and immune cell levels of the two groups were measured before and after treatment. The therapeutic effects and the long-term effects of the two groups were analyzed. Results:Before treatment, there was no significant difference in serum interleukin (IL)-6, IL-8 and tumor necrosis factor-α (TNF-α) levels between the two groups ( P>0.05). After treatment, the levels of inflammatory cytokines in the two groups were significantly lower than those before treatment ( P<0.05); The levels of IL-6, IL-8 and TNF-α in the TEVAR group were significantly lower than those in the conservative group ( P<0.05). Before treatment, there was no significant difference in white blood cell count, neutrophil count, lymphocyte count and monocyte count between the two groups ( P>0.05). After treatment, the number of white blood cells and neutrophils decreased significantly in the two groups; and the number of lymphocytes in the two groups was significantly increased ( P<0.05). The number of white blood cells and neutrophils in the TEVAR group was significantly lower than that in the control group, and the number of lymphocytes was significantly higher than that in the conservative group ( P<0.05). The effective rate of the TEVAR group was significantly higher than that of the conservative group ( P<0.05). There was no significant difference in hospital mortality, hospitalization time and hospitalization complication between the two groups ( P>0.05). The 2-year survival rate of the TEVAR group was significantly higher than that of the conservative group. The postoperative complication rate was significantly lower than the conservative group ( P<0.05). There was no significant difference in the 1-year survival rate and secondary intervention rate between the two groups ( P>0.05). Conclusions:TEVAR has a better therapeutic effect, and improve survival rate to some extent.

Changes of coagulation / fibrinolysis factors in patients with type A aortic dissection after operation / 中国医师杂志

Objective:To investigate the changes of coagulation/fibrinolysis factors in patients with type A aortic dissection (AD) at early and middle stages after ascending aorta replacement+ total arch replacement+ elephant nose stenting.Methods:According to the inclusion and exclusion criteria, patients with type A AD who underwent cardiac surgery in Xinjiang Uygur Autonomous Region People′s Hospital from August 2017 to August 2018 were selected as the study group. According to the duration of onset, patients were divided into acute AD group (course <2 weeks) and chronic AD group (course ≥2 weeks). Both groups were treated with ascending aorta replacement + total arch replacement + elephant nose stenting. Fasting venous blood was drawn from the two groups, and the blood indexes [prothrombin time (PT), activated partial thrombo plastin time (APTT), fibrinogen (Fib), bone morphogenetic proteins (BMP)] and fibrinolysis indexes [D-dimer, tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor (PAI)] were detected by enzyme-linked immunosorbent assay (ELISA).Results:The ELISA result showed that changes of PT, APTT, Fib, BMP, D-dimer, and PAI in patients with acute and chronic AD at 12 months after operation were significantly lower than those before operation ( P<0.05). The changes of t-PA in patients with acute and chronic AD at 12 months after operation were significantly higher than those before operation ( P<0.05). There was no significant difference in postoperative effective rate, in-hospital mortality, length of stay, incidence of complications and early and mid-term survival rate between the two groups ( P>0.05). Conclusions:Ascending aorta replacement+ total arch replacement+ elephant nose stent is effective in the treatment type A AD, and can significantly improve the expression of coagulation/ fibrinolysis markers in early and middle period after operation.

Chronic restraint stress induces esophageal fibrosis with enhanced oxidative stress in a murine model.

Although the underlying mechanism of stress remains unknown, it has been associated with the pathophysiology of gastroesophageal reflux diseases, the development of which appear to be accelerated by oxidative stress and fibrosis. The aim of the current study was to investigate the effect of chronic restraint stress on esophageal oxidative stress and fibrosis, as well as the impact of oxidative stress in a murine model whereby 8-week old C57BL/6J male mice were subjected to intermittent chronic restraint stress for a two-week period. The current study demonstrated that chronic restraint stress significantly reduced the body weight of mice compared with the control group. Although chronic restraint stress did not significantly alter the levels of triglycerides or cholesterol, free fatty acid concentration was significantly increased compared with the control group. Furthermore, chronic restraint stress significantly upregulated the expression levels of several fibrotic biomarkers including collagen type I, transforming growth factor ß-1, α-smooth muscle actin and SMAD-3 compared with the control group. In addition, the expression levels of the reactive oxygen species (ROS) NADPH oxidase-4 and malondialdehyde were significantly increased, while the expression levels of nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 were significantly decreased in esophageal tissue from mice in the chronic restraint stress group compared with the control group. In conclusion, chronic restraint stress may induce esophageal fibrosis by accumulating ROS and increasing fibrotic gene expression in a murine model.

Chronic stress augments esophageal inflammation, and alters the expression of transient receptor potential vanilloid 1 and protease­activated receptor 2 in a murine model.

Stress is a pivotal factor for inflammation, reactive oxygen species (ROS) production and formation of visceral hypersensitivity (VH) in the process of gastroesophageal reflux disease (GERD). In the present study, the effects of stress on esophageal inflammation, oxidative stress and VH were investigated in a chronic restraint stress mouse model. C57BL/6J male mice were subjected to 2 weeks of intermittent restraint stress, and histopathological analysis revealed that stress induced esophageal inflammation and fibrosis, while no distinct changes were detected in non­stressed control mice. In addition, increased NADPH oxidase 4 expression was observed in the plasma and esophagus of stressed mice, indicating accumulation of ROS. The expression levels of antioxidants, including Mn­superoxide dismutase (MnSOD), Cu/Zn­SOD, catalase and glutathione peroxidase, were also analyzed using reverse transcription­quantitative polymerase chain reaction (RT­qPCR). In addition, transient receptor potential vanilloid 1 (TRPV­1) and protease­activated receptor 2 (PAR­2), which are crucial receptors for VH, were measured by immunohistochemistry and RT­qPCR. The results demonstrated that stress markedly reduced antioxidant expression, while it significantly upregulated TRPV­1 and PAR­2 expression levels in the mouse esophagus. Finally, 2 weeks of restraint stress significantly increased the esophageal and plasma levels of inflammatory cytokines, including interleukin (IL)­6, IL­8, interferon­Î³ and tumor necrosis factor­α. Taken together, the present study results indicated that stress­induced esophageal inflammation and ROS generation involves VH.

Left ventricular remodeling in patients with acute type B aortic dissection after thoracic endovascular aortic repair: Short- and mid-term outcomes.

BACKGROUND: Left ventricular (LV) remodeling remains unknown in patients with acute Type B aortic dissection (aTBAD) after thoracic endovascular aortic repair (TEVAR) during follow-up. METHODS: Between May 2004 and January 2016, 163 consecutive patients (136 males, mean preoperative age: 51.06 ±â€¯10.79 years) with aTBAD underwent TEVAR. A linear mixed model was used to evaluate risk factor influencing on LV remodeling and investigate longitudinal changes in LV thickness, diameter, volume, function and mass at preoperation, postoperation, short- and mid-term follow-up. RESULTS: Median follow-up time was 48.0 months (quartiles 1-3, 31-84 months, maximum 147 months). LV thickness and mass followed a continuous downward trend over time. Interventricular septal thickness at end-diastole significantly decreased at mid-term follow-up (time, p < 0.001: preoperative 11.59 ±â€¯0.14 mm vs mid-term 10.82 ±â€¯0.15 mm, p < 0.001; postoperative 11.40 ±â€¯0.14 mm vs mid-term 10.82 ±â€¯0.15 mm, p = 0.006). LV posterior wall thickness at end-diastole was markedly reduced at mid-term follow-up (time, p < 0.001: preoperative 10.89 ±â€¯0.11 mm vs mid-term 10.02 ±â€¯0.11 mm, p < 0.001; postoperative 10.78 ±â€¯0.13 mm vs mid-term 10.02 ±â€¯0.11 mm, p < 0.001; short-term 10.56 ±â€¯0.15 mm vs mid-term 10.02 ±â€¯0.11 mm, p = 0.021). LV mass index markedly decreased during follow-up (time, p = 0.001: preoperative 129.60 ±â€¯3.55 g/m2 vs short-term 119.26 ±â€¯3.19 g/m2, p = 0.009; preoperative 129.60 ±â€¯3.55 g/m2 vs mid-term 115.79 ±â€¯3.62 g/m2, p = 0.003). LV function was improved, but not significantly so, during follow-up. Strict blood pressure control had no influence on LV remodeling. True lumen followed a continuous enlargement trend in terms of proximal thoracic aorta and celiac trunk level during follow-up. CONCLUSIONS: TEVAR can reverse LV remodeling and LV hypertrophy in patients with aTBAD during follow-up.

The role of chronic restrain stress induced Nox-4 expression and its significances in adipose inflammation / 中华内分泌代谢杂志

Objective To investigate stress induced Nox-4 expression and to explore its role in adipose inflammation. Methods Twenty male Kunming mice were randomly divided into two groups ( n=10 each) , chronic restraint stress group and control group. Stress mice were restrained in self-made restraint device for 2 hours per day for 14 days. HE staining, immunohistochemistry, RT-PCR, and ELISA were used to analyze the expression of Nox-4, CD11b, antioxidant protein ( Mn SOD, GSH-Px, Catalase), adipocytokines ( adiponectin, MCP-1, IL-6, TNF-a). Results White adipose tissue (WAT) of stress mice inguinal fat pad significantly shrank compared to control group. HE staining showed that there were a large number of mononuclear cells, neutrophils, eosinophils, and cell infiltration reactions and inflammatory changes in WAT of stress mice. The stress significantly increased CD11b-positive cells and the expression of mF4/80, CD68. The concentration of serum FFA in stress group increased significantly, nearly twice of the control group ( P<0.01) . Nox-4 positive staining cells in stress WAT were deeper and more abundant. The level of Nox-4 in stress WAT was significantly higher than that of control group(P<0.01). The levels of antioxidant proteins such as Mn-SOD, GSH-Px, and catalase in stress WAT were significantly lower than those of control group (P<0.01). The expression levels of adiponectin in stress WAT were significantly reduced as compared to control group ( P<0.01) . The levels of MCP-1, IL-6 and TNF-α in stress WAT were significantly higher than those in control group (P<0.01). Conclusion Stress may lead to imbalance of adipose oxidation/antioxidant system and abnormal expression of adipocytokines, which may result in adipose inflammation.

Multiple factor analysis of preoperative myocardial enzymes in stanford type B aortic dissection / 国际外科学杂志

Objective To investigate preoperative myocardial enzymes and realative influencing factors in Stanford B type aortic dissection.Methods From Jan.2004 to Sep.2013,151 consecutive patients with Stanford type B aortic dissection were admitted to hospital,aged from 31 to 76 average:(51.51 ± 10.90)year sold.Ninty-five healthy people with similar age and sex were taken as the control group.Fasting venous blood collected more than 12h was collected,myocardial enzymes indexes such as CK,CKMB,LDH,HBDH were measured by Roche modular automatic biochemical analysis system.Primary entry tear and extent of aortic dissection was measured by Toshiba Aquilion ONE 320 slice CT.Degree of aortic valve insufficiency was measured by Philips Sonos 5500 Color Doppler ultrasonic diagnostic apparatus.Results Compared with control group,the level of myocardial enzymes (LDH,HBDH) of aortic dissection group increased significantly(P ＜ 0.01).part myocardial enzymes indexes(CK,LDH,HBDH) of acute stage group existed difference(P ＜ 0.05).Myocardial enzymes indexes only CK existed difference between acute stage group and subacute stage group and chronic stage group(F =18.72,P =0.000),no difference between subacute stage group and chronic stage group.LDH,HBDH of each sub group of aortic dissection group were higher than that of control group,P ＜ 0.01.Trough correlation analysis,CK negatively correlated with disease course of aortic dissection and patients sex [(r =-0.446 ; P =0.000) ; (r =-0.303 ; P =0.000)],CKMB negatively correlated patients sex [(r=-0.203;P=0.020)],LDH negatively correlated with patients sex [(r =-0.171 ;P =0.049)],positively with left ventricular end-diastolic diameter and left ventricular end-systolic diameter [(r =0.202 ; P =0.022) ; (r =0.271 ; P =0.002)].HBDH positively correlated with left ventricular enddiastolic diameter and left ventricular end-systolic diameter [(r =0.385 ;P =0.002) ; (r =0.515 ; P =0.000)],negatively with degree of aortic insufficiency [(r =-0.528 ;P =0.006)].Conclusions Myocardial enzymes rise in preoperative Stanford B aortic dissection,more representing skeletal muscle injury.Be affected by stage of aortic dissection,lower limb skeletal muscle injury aggravates more seriously in acute stage group persists entering the sub acute stage.