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Background-Previous studies have suggested that systematic ablation of ganglionated plexi (GP) could increase the shortterm success rate of radiofrequency ablation for atrial fibrillation, but the long-term efficacy of this approach is not fully established. Methods and Results-Twenty-four mongrel dogs were divided into 3 groups: epicardial GP ablation group 1 (n=8), epicardial GP ablation group 2 (n=8), and a sham operation group (n=8). In the 2 epicardial GP ablation groups, the 4 major GP and the ligament of Marshall were systematically ablated. The effective refractory period and inducibility of tachyarrhythmias were measured before and immediately after GP ablation in epicardial GP ablation group 1 and 8 weeks later in the other 2 groups. Tyrosine hydroxylase and choline acetyltransferase expressions were also determined immunohistochemically 8 weeks later in the latter groups. Compared with epicardial GP ablation group 1 and the sham operation group, epicardial GP ablation group 2 had the shortest atrial and ventricular effective refractory period and the highest inducibility of atrial tachyarrhythmias. The inducibility of ventricular tachyarrhythmias among the 3 groups was comparable. The density of tyrosine hydroxylase-and choline acetyltransferase-positive nerves in the atrium was the highest in epicardial GP group 2, whereas there were no significant intergroup differences in the densities of these 2 types of nerves in the ventricle. Conclusions-After 8 weeks of healing, epicardial GP ablation without additional atrial ablation was potentially proarrhythmic, which may be attributable to decreased atrial effective refractory period and hyper-reinnervation involving both sympathetic and parasympathetic nerves. Methods Animal PreparationAll animal studies were reviewed and approved by the Institutional Animal Care and Use Committee at our institution. Twenty-four adult mongrel dogs (18-25 kg) were divided into 3 groups: epicardial GP ablation group 1 (n=8), epicardial GP ablation group 2 (n=8), and a sham operation group (n=8). All dogs were anesthetized with 5% sodium pentobarbital (2-3 mL/kg) given intravenously, followed by an additional dose of 1 mL/kg at the end of each hour. A tracheal cannula was inserted, and intermittent positive pressure ventilation with room air was delivered by a respirator. A 6-lead frontal ECG was recorded continuously during the procedure (filter, 0.05-30 Hz). After left thoracotomy at the fourth intercostal space, the heart was exposed in a pericardial cradle. GP AblationIn the 2 epicardial GP ablation groups, the LOM and the fat pads that contain the superior left GP and inferior left GP were exposed by left thoracotomy. After the superior left GP, inferior left GP, and LOM were ablated, the fat pads that contain the anterior right GP and inferior right GP were exposed by lifting up the pericardium, and the anterior right GP and inferior right GP were ablated sequentially through the left incision. The GP was localized by applying high-frequency stimulation (HFS; 20 Hz; ...

The CT genotype of NFE2L2-ins1 + C11108T and the TT genotype of GST01-C428T are susceptible factors for CHD. The AG, GG and (AG + GG) genotypes of DHFR-c594 + 59del19 are protective genotypes for CHD. Compound mutants for (MTHFD-G1958A, MTHFR-C677T and MTR-A2756G) and (MTHFD-G1958A, RFC1-G80A and MTR-A2756G) may increase the risk of CHD.

Uroguanylin (UGN) is a peptide hormone that binds to and activates the intestinal epithelial cell (IEC) transmembrane receptor guanylate cyclase C (GC-C), which in turn increases intracellular cGMP. Gene targeting of murine UGN or GC-C results in significantly lower levels of cGMP in IECs. On the basis of effects of cGMP in nonintestinal systems, we hypothesized that loss of GC-C activation would increase intestinal epithelial apoptosis following radiation-induced injury. We first compared apoptosis from the proximal jejunum of C57BL/6 wild-type (WT) and GC-C knockout (KO) mice 3 h after they received 5 Gy of gamma-irradiation. We then investigated whether supplementation via intraperitoneal injection of 1 mM 8BrcGMP would mitigate radiation-induced apoptosis in these experimental animals. Identical experiments were performed in BALB/c UGN WT and KO mice. Apoptosis was assessed by quantitating morphological indications of cell death, terminal dUTP nick-end labeling, and cleaved caspase 3 immunohistochemistry. Both UGN KO and GC-C KO mice were more susceptible than their WT littermates in this in vivo model of apoptotic injury. Furthermore, cGMP supplementation in both GC-C and UGN KO animals ameliorated radiation-induced apoptosis. Neither WT strain demonstrated significant alteration in apoptotic susceptibility as a result of cGMP supplementation before radiation injury. These in vivo findings demonstrate increased radiosensitivity of IECs in UGN and GC-C KO mice and a role for cGMP as a primary downstream mediator of GC-C activation in the protection of these IECs from radiation-induced apoptosis.

Background: The pathogenesis of inflammatory bowel disease (IBD) is linked to an intricate association of environmental, microbial, and host-related factors. Polysaccharide affects host immunity by regulating the composition and metabolism of gut microbiota is the common mechanism of disease resistance. However, the efficacy and mechanism of Schisandra chinensis polysaccharide (SCP) in the treatment of inflammatory bowel disease have not been studied. Objective: To explore the effect and mechanism of SCP on dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) in mice. Materials/Methods: In this study, we established a mouse model of UC, and used SCP for treatment intervention. The biochemical indexes related to inflammation were determined by ELISA kit, and the therapeutic effect of SCP on UC was clarified. Then, 16S rDNA sequencing was used to study the effect of SCP on the composition and diversity of gut microbiota. At the same time, GC-MS was used to determine the content of short chain fatty acids in intestinal contents. Finally, the relationship among gut microbiota, short chain fatty acids and inflammatory factors was analyzed, and to comprehensively explain the effect and mechanism of SCP on UC. Results: The results showed that SCP could significantly improve the physiological state of UC mice and regulate the level of inflammatory factors to normal levels. Meanwhile, SCP could significantly regulate the imbalance of gut microbiota and increase the content of SCFAs. In addition, the results of the correlation between gut microbiota and SCFAs showed that butyric acid, isobutyric acid and valeric acid had the highest correlation with gut microbiota. Su et al. Schisandra chinensis Polysaccharide Anti-colitis Conclusion: In conclusion, this research showed that SCP can inhibit inflammatory bowel disease by regulating the composition and metabolism of gut microbiota, and indicating that SCP may be used as adjuvant therapy for IBD patients.

A Gram-stain-positive, endospore-forming, rod-shaped bacterium, designated XJ259T , was isolated from a cold spring sample from Xinjiang Uyghur Autonomous Region, China. The isolate grew optimally at 20-30 6C and pH 7.3-7.8. Comparative analysis of the 16S rRNA gene sequence showed that isolate XJ259 T belonged phylogenetically to the genus Paenibacillus, and was most closely related to Paenibacillus xinjiangensis B538 T (with 96.6 % sequence similarity),Paenibacillus glycanilyticus DS-1 T (96.3 %) and Paenibacillus castaneae Ch-32 T (96.1 %), sharing less than 96.0 % sequence similarity with all other members of the genus Paenibacillus. Chemotaxonomic analysis revealing menaquinone-7 (MK-7) as the major isoprenoid quinone, diphosphatidylglycerol, phosphatidylethanolamine and two unknown phosphoglycolipids as the major cellular polar lipids, a DNA G+C content of 47.0 mol%, and anteiso-C 15 : 0 and C 16 : 0 as the major fatty acids supported affiliation of the new isolate to the genus Paenibacillus. Based on these data, isolate XJ259

Vasostatin-1 suppresses AF inducibility, likely by inhibiting GP function. These data may provide new insights into the role of peptide neuromodulators for AF therapy.

Skeletal muscle cells are exposed to mechanical stretch during embryogenesis. Increased stretch may contribute to cell death, and the molecular regulation by stretch remains incompletely understood. The aim of this study was to investigate the effects of cyclic stretch on cell death and apoptosis in myoblast using a Flexercell Strain Unit. Apoptosis was studied by annexin V binding and PI staining, DNA size analysis, electron microphotograph, and caspase assays. Fas/FasL expression was determined by Western blot. When myoblasts were cultured on a flexible membrane and subjected to cyclic strain stress, apoptosis was observed in a time-dependent manner. We also determined that stretch induced cleavage of caspase-3 and increased caspase-3 activity. Caspase-3 inhibition reduced stretch-induced apoptosis. Protein levels of Fas and FasL remained unchanged. Our findings implicated that stretch-induced cell death is an apoptotic event, and that the activation of caspase cascades is required in stretch-induced cell apoptosis. Furthermore, we had provided evidence that caspase-3 mediated cyclic stretch-induced myoblast apoptosis. Mechanical forces induced activation of caspase-3 via signaling pathways independent of Fas/FasL system.