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Heat stroke is a life-threatening disorder triggered by thermoregulatory failure. Hyperthermia-induced splanchnic hypoperfusion has been reported to induce intestinal barrier dysfunction and systemic immune response that ultimately cause multiple-organ failure and death. Intestinal goblet cells contribute greatly to the formation of mucus barrier, which hinders translocation of gut microorganisms. Studies have reported that misoprostol can not only alleviate ischemic injury but also protect GI mucosal layer. Therefore, we evaluated the effects of misoprostol on intestinal goblet cells after heat stress and on multiple-organ dysfunction in heat stroke rats.Heat stress was established in the heating chamber and followed by misoprostol treatment. Changes in hemodynamics, organ function indices, inflammation, oxidative stress, and survival rate were analyzed. Furthermore, ilea and LS174T cells were used to examine intestinal functions.Heat stress caused dysfunction of intestinal goblet cells and damage to ilea by increasing oxidative stress and apoptosis. Increased nitrosative stress and inflammation accompanied by hypotension, hypoperfusion, tachycardia, multiple-organ dysfunction, and death were observed in the heat stroke rat model. Treatment of LS174T cells with misoprostol not only decreased oxidative stress and apoptosis but also reduced cytotoxicity caused by heat stress. Moreover, misoprostol prevented disruption of the enteric barrier, multiple-organ injury, and death in rats with heat stroke.This study indicates that misoprostol could alleviate intestinal damage and organ injury caused by heat stress and be a potential therapy for heat-related illnesses.

OBJECTIVES Robotic mitral valve replacement (MVR) emerged in the late 1990s as an alternative approach to conventional sternotomy. With the increased use of bioprosthetic valves worldwide and strong patient desire for minimally invasive procedures, the safety and feasibility of robotic MVRs with bioprosthetic valves require investigation. METHODS Between January 2013 and May 2017, 52 consecutive patients underwent robotic MVRs using the da Vinci Si surgical system (Intuitive Surgical Inc., Sunnyvale, CA, USA). Their mean age was 55.1 ± 13.8 years, and mean EuroSCORE II was 2.25% ± 1.25%. Among the enrolled patients, 32 (61.5%) patients presented with preoperative atrial fibrillation, 6 (11.5%) patients had experienced embolic stroke and 5 (9.6%) patients had undergone previous cardiac surgery. The operations were performed using cardiopulmonary bypass (CPB) under an arrested heart status. RESULTS Five porcine valves and 47 bovine valves were implanted. A total of 38 (73.1%) patients received concomitant cardiac procedures, including 26 Cox-maze IV procedures, 12 tricuspid valve repairs and 5 atrial septal defect repairs. The mean aortic cross-clamp and CPB times were 141.3 ± 34.3 min and 217.1 ± 42.0 min, respectively. There was no operative mortality. During the mean follow-up of 29 ± 15 months, no prosthesis degeneration was noted. The average left atrial dimension exhibited a significant decrease from 51.4 ± 11.5 mm to 42.6 ± 10.1 mm. CONCLUSIONS Robotic MVR with bioprosthetic valves is safe, feasible and reproducible. Mid-term results are encouraging. Both aortic cross-clamp and CPB times can be improved with experience.

Human parvovirus B19 (B19) and human bocavirus 1 (HBoV) are the only known pathogenic parvoviruses, and are responsible for a variety of diseases in human beings. Mounting evidence indicates a strong association between B19 infection and cardiac disorders including myocarditis, dilated cardiomyopathy and heart failure. However, very limited information about the role of HBoV in cardiac disorders is known. To elucidate the effects of B19 and HBoV on cardiac disorders, we expressed EGFP‑conjugate constructs of B19‑VP1 unique region (VP1u) and HBoV‑VP1u, along with the mutants EGFP‑B19‑VP1uD175A and EGFP‑HBoV‑VP1uV12A, in H9c2 cells by stable transfection. The protein expression levels of EGFP, EGFP‑B19‑VP1u, EGFP‑B19‑VP1uD175A, EGFP‑HBoV‑VP1u and EGFP‑HBoV‑VP1uV12A in H9c2 cells were observed under a fluorescence microscope and confirmed by western blotting. Secreted phospholipase A2 (sPLA2) activity was detected in B19‑VP1u and HBoV‑VP1u but not B19‑VP1uD175A and HBoV‑VP1uV12A recombinant proteins. Significantly higher expression levels of MCP2 and IP‑10 mRNA were detected in H9c2 cells that were transfected with pEGFP‑B19‑VP1u, compared with in those cells transfected with pEGFP‑HBoV‑VP1u, pEGFP‑B19‑VP1uD175A or pEGFP‑HBoV‑VP1uV12A. Significantly higher protein levels of IL‑1β and IL‑6 were detected in H9c2 cells transfected with pEGFP‑B19‑VP1u or pEGFP‑HBoV‑VP1u, compared with in those cells transfected with pEGFP‑B19‑VP1uD175A or pEGFP‑HBoV‑VP1uV12A. Notably, significantly higher expression of both TNF‑α and NF‑κB was observed only in H9c2 cells transfected with pEGFP‑B19‑VP1u, but not in those cells transfected with pEGFP‑HBoV‑VP1u, pEGFP‑B19‑VP1uD175A or pEGFP‑HBoV‑VP1uV12A. These findings, to our knowledge for the first time, reveal the difference between B19‑VP1u and HBoV‑VP1u in H9c2 cells and provide insight into the roles of B19‑VP1u and HBoV‑VP1u in the pathogenesis of cardiac inflammation.

Overt systemic inflammatory response is a predisposing mechanism for infection-induced skeletal muscle damage and rhabdomyolysis. Aberrant DNA methylation plays a crucial role in the pathophysiology of excessive inflammatory response. The antiarrhythmic drug procainamide is a non-nucleoside inhibitor of DNA methyltransferase 1 (DNMT1) used to alleviate DNA hypermethylation. Therefore, we evaluated the effects of procainamide on the syndromes and complications of rhabdomyolysis rats induced by lipopolysaccharide (LPS). Rhabdomyolysis animal model was established by intravenous infusion of LPS (5 mg/kg) accompanied by procainamide therapy (50 mg/kg). During the experimental period, the changes of hemodynamics, muscle injury index, kidney function, blood gas, blood electrolytes, blood glucose, and plasma interleukin-6 (IL-6) levels were examined. Kidneys and lungs were exercised to analyze superoxide production, neutrophil infiltration, and DNMTs expression. The rats in this model showed similar clinical syndromes and complications of rhabdomyolysis including high levels of plasma creatine kinase, acute kidney injury, hyperkalemia, hypocalcemia, metabolic acidosis, hypotension, tachycardia, and hypoglycemia. The increases of lung DNMT1 expression and plasma IL-6 concentration were also observed in rhabdomyolysis animals induced by LPS. Treatment with procainamide not only inhibited the overexpression of DNMT1 but also diminished the overproduction of IL-6 in rhabdomyolysis rats. In addition, procainamide improved muscle damage, renal dysfunction, electrolytes disturbance, metabolic acidosis, hypotension, and hypoglycemia in the rats with rhabdomyolysis. Moreover, another DNMT inhibitor hydralazine mitigated hypoglycemia, muscle damage, and renal dysfunction in rhabdomyolysis rats. These findings reveal that therapeutic effects of procainamide could be based on the suppression of DNMT1 and pro-inflammatory cytokine in endotoxin-induced rhabdomyolysis.

The aortovenous fistulas are rare, most of them are aortocaval fistula. The non-caval communication of the fistula is sparse. Herein we report a 47-year-old female diagnosed as traumatic aorto-superior mesenteric vein (Ao-SMV) fistula. The abdominal pain, fullness, and frank bruit on abdominal auscultation suggested the diagnosis of an intra-abdominal arteriovenous fistula. The diagnosis of Ao-SMV was further confirmed by the computed tomography (CT) and aortography. The fistula was successfully treated with transcatheter coil embolization. This is the first case of Ao-SMV fistula. It provides an alternative option of treatment other than conventional surgery.

Septic shock is a syndrome with severe hypotension and multiple organ dysfunction caused by an imbalance between pro-inflammatory and anti-inflammatory response. The most common risk factor of acute lung injury is severe sepsis. Patients with sepsis-related acute respiratory distress syndrome have higher mortality. Recent studies reveal regulatory roles of Wnt3a and Wnt5a signaling in inflammatory processes. Wnt3a signaling has been implicated in anti-inflammatory effects, whereas Wnt5a signaling has been postulated to have pro-inflammatory properties. However, the balance between Wnt3a and Wnt5a signaling pathway in the lung of rats with endotoxic shock has not been determined. Thus, we investigated the major components of Wnt3a and Wnt5a signaling pathway in the lung of endotoxemic rats. Male Wistar rats were intravenously infused with saline or lipopolysaccharide (LPS, 10 mg/kg). The changes of hemodynamics, biochemical variables, and arterial blood gas were examined during the experimental period. At 6 h after saline or LPS, animals were sacrificed, and lungs were obtained for analyzing superoxide production, water accumulation, histologic assessment, and protein expressions of Wnt3a and Wnt5a signaling pathway. Animals that received LPS showed circulatory failure, multiple organ dysfunction, metabolic acidosis, hyperventilation, lung edema, and high mortality. The lung from rats with endotoxic shock exhibited significant decreases in the levels of Wnt3a, Fzd1, Dsh1, phosphorylated GSK-3β at Ser9, and β-catenin. In contrast, the expressions of Wnt5a, Fzd5, and CaMKII were up-regulated in the lung of endotoxemic rats. These findings indicate the major components of Wnt3a and Wnt5a signaling in the lung are disturbed under endotoxic insult.