Abstract Introduction: Diffuse coronary artery disease (CAD) has a poor prognosis and many patients are ineligible for conventional coronary artery bypass grafting (CABG). This study evaluated the 12-month outcomes of coronary artery reconstruction and surgical patch angioplasty of the coronary artery for diffuse CAD. Methods: A retrospective cohort study of patients who underwent CABG with surgical patch angioplasty of the coronary artery (reconstruction group) or standard CABG alone (standard group) at the Cardiovascular Surgery Department of the local Hospital between January 2014 and January 2016. Follow-up was censored at 12 months after surgery. Results: Cardiopulmonary bypass and aortic cross-clamping durations were longer in the reconstruction group (n=32) than in the standard group (n=125) (P<0.05). There were no differences in graft blood flow and postoperative levels of cardiac markers between the two groups (P>0.05). In the reconstruction group, one patient died; a vein graft showed occlusion. In the standard group, two patients died; one left internal mammary artery graft and three vein grafts showed occlusion. There were no significant differences in mortality, major adverse cardiovascular and cerebrovascular events, and patency between the two groups (P>0.05). Conclusion: Coronary artery reconstruction and surgical patch angioplasty of the coronary artery can be performed for diffuse CAD. Patient outcomes were not significantly different from those of patients who underwent standard CABG.

Abstract Purpose Patients with diabetes are vulnerable to myocardial I/R (ischaemia/reperfusion) injury, but are not responsive to IPO (ischaemic post-conditioning). We hypothesized that decreased cardiac Adiponectin (APN) is responsible for the loss of diabetic heart sensitivity to IPO cardioprotecton. Methods Diabetic rats were subjected to I/R injury (30 min of LAD occlusion followed by 120 min of reperfusion). Myocardial infarct area was determined by TTC staining. Cardiac function was monitored by a microcatheter. ANP, 15-F2t-isoprostane, nitrotyrosine and MDA were measured by assay kits. Levels of p-Akt, total-Akt and GAPDH were determined by Western Blot. Results Diabetic rats subjected to myocardial IR exhibited severe myocardial infarction and oxidative stress injury, lower APN in the plasma and cardiac p-Akt expression ( P <0.05). IPO significantly attenuated myocardial injury and up-regulated plasma APN content and cardiac p-Akt expression in non-diabetic rats but not in diabetic rats. Linear correlation analysis showed that the expression of adiponectin was positively correlated with p-Akt and negatively correlated with myocardial infarction area ( P <0.01). Conclusion Protective effect of IPO was tightly correlated with the expression of adiponectin, exacerbation of I/R injury and ineffectiveness of IPO was partially due to the decline of adiponectin and inactivation of Akt in diabetes mellitus.

Abstract Purpose: To investigate whether the neuroprotective effect of TSA on cerebral ischemia reperfusion injury is mediated by the activation of Akt/GSK-3β signaling pathway. Methods: Mice were randomly divided into four groups (n=15): sham group (S); ischemia reperfusion group (IR); ischemia reperfusion and pretreated with TSA group (IR+T); ischemia reperfusion and pretreated with TSA and LY294002 group (IR+T+L). The model of cerebral ischemia reperfusion was established by 1h of MCAO following 24h of reperfusion. TSA (5mg/kg) was intraperitoneally given for 3 days before MCAO, Akt inhibitor, LY294002 (15 nmol/kg) was injected by tail vein 30 min before the MCAO. Results: TSA significantly increased the expression of p-Akt, p-GSK-3β proteins and the levels of SOD, Bcl-2, reduced the infarct volume and the levels of MDA, ROS, TNF-α, IL-1β, Bax, Caspase-3, TUNEL and attenuated neurological deficit in mice with transient MCAO, LY294002 weakened such effect of TSA dramatically. Conclusions: TSA could significantly decrease the neurological deficit and reduce the cerebral infarct volume, oxidative stress, inflammation, as well as apoptosis during cerebral ischemia reperfusion injury, which was achieved by activation of the Akt/GSK-3β signaling pathway.

Resumo Fundamentos: A denervação simpática renal por radiofrequência (DSR) mostra redução eficaz da pressão arterial (PA) de pacientes hipertensos, ainda que os mecanismos específicos permaneçam obscuros. Objetivo: Fizemos a hipótese de que níveis alterados de noradrenalina (NA) e mudanças nas enzimas relacionadas à NA e enzima conversora de angiotensina 2 (ECA-2), angiotensina (Ang)-(1-7) e receptor Mas são mediadores dos efeitos antihipertensivos da DSR. Métodos: Foram avaliados os valores médios de pressão arterial sistólica (PAS), pressão arterial diastólica (PAD) e pressão arterial média (PAM) no início e durante o seguimento. Foram medidas as concentrações plasmática e renal de noradrenalina (NA) por cromatografia líquida de alta eficiência com detecção eletroquímica, e os níveis de enzima relacionada à NA e ECA2-Ang-(1-7)-Mas através de PCR em tempo real, Western blot e imunohistoquímica ou Elisa em um modelo canino de hipertensão que recebeu ração rica em gordura e foi tratado com DSR. Os parâmetros também foram determinados em um grupo de cirurgia simulada submetido à arteriografia renal e em um grupo controle que recebeu dieta normal. Resultados: DSR causou diminuição da PAS, PAD, PAM e das concentrações plasmática e renal de NA. Em comparação ao grupo placebo, a expressão da tirosina hidroxilase (TH) renal foi menor e a da renalase foi maior no grupo DSR. Em comparação ao grupo controle, os níveis de TH renal e de catecol-o-metil-transferase (COMT) foram maiores e os de renalase foram menores no grupo cirurgia simulada. Além disso, os níveis renais de ECA2, Ang-(1-7) e Mas foram maiores no grupo DSR do que no grupo cirurgia simulada, que, por sua vez, foram menores do que no grupo controle. Conclusões: A DSR mostra efeitos anti-hipertensivos com redução da NA e ativação da ECA2-Ang-(1-7)-Mas, o que indica que pode contribuir com o efeito anti-hipertensivo da DSR.

Abstract Background: Radiofrequency ablation of renal sympathetic nerve (RDN) shows effective BP reduction in hypertensive patients while the specific mechanisms remain unclear. Objective: We hypothesized that abnormal levels of norepinephrine (NE) and changes in NE-related enzymes and angiotensinconverting enzyme 2 (ACE2), angiotensin (Ang)-(1-7) and Mas receptor mediate the anti-hypertensive effects of RDN. Methods: Mean values of systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) were assessed at baseline and follow-up. Plasma and renal norepinephrine (NE) concentrations were determined using highperformance liquid chromatography with electrochemical detection, and levels of NE-related enzyme and ACE2-Ang(1-7)- Mas were measured using real time PCR, Western blot and immunohistochemistry or Elisa in a hypertensive canine model fed with high-fat diet and treated with RDN. The parameters were also determined in a sham group treated with renal arteriography and a control group fed with normal diet. Results: RDN decreased SBP, DBP, MAP, plasma and renal NE. Compared with the sham group, renal tyrosine hydroxylase (TH) expression was lower and renalase expression was higher in the RDN group. Compared with the control group, renal TH and catechol-o-methyl transferase (COMT) were higher and renalase was lower in the sham group. Moreover, renal ACE2, Ang-(1-7) and Mas levels of the RDN group were higher than those of the sham group, which were lower than those of the control group. Conclusion: RDN shows anti-hypertensive effect with reduced NE and activation of ACE2-Ang(1-7)-Mas, indicating that it may contribute to the anti-hypertensive effect of RDN.

Gas phase heats of formation (HOF) of 18 kinds of 390 organic compounds were calculated by quantum chemical calculation using semi-empirical PM3, PDDG and PM6 methods. The calculated HOFs were compared with the experimental data to illustrate the accuracy for different kinds of organics. Furthermore, the calculated values were linearly fitted with experimental values using the least square method, and were afterward substituted into the fitted regression equations to obtain the calibrated ones. The results show that, for 10 kinds of the selected organics, PM6 is more accurate, and PDDG is more accurate for 7 kinds of organics, while PM3 is only good for amino acid. As a whole, PM6 predicts the HOFs more accurately, with its weighted total mean average deviation (WTMAD) being 0.4 kJ/mol and 2.4 kJ/mol smaller than those of PM3 and PDDG, respectively. On the other hand, our results show that PDDG is the best to differentiate the isomers, with its mean average deviation (MAD) for isomerization energy being 7.8 kJ/mol and 11.0 kJ/mol smaller than PM6 and PM3, respectively. After the calibration, the values of MADs from the PM3, PDDG and PM6 results for most organics are reduced by 0.1 to 18.2 kJ/mol, with exceptions of the PM3 for amines, PDDG for carboxylic acids, and PM6 for ethers.

Se calcularon los calores de formación en fase gaseosa (HOF) de 390 compuestos orgánicos agrupados en 18 familias de compuestos con química cuántica, utilizando los métodos semiempíricos PM3, PDDG y PM6. Los valores calculados de HOFs fueron comparados con los valores experimentales correspondientes, con el fin de evaluar la precisión de los métodos para describir cada una de las diferentes familias de compuestos. Para esto, los valores calculados y experimentales de HOF fueron ajustados a una línea recta por el método de mínimos cuadrados, las ecuaciones de ajuste fueron utilizadas como curvas de calibración. Estas curvas muestran que para 10 familias de compuestos, el método PM6 es el mejor; mientras que el PDDG es mejor para 7 familias de compuestos orgánicos y, el PM3 es bueno sólo para los aminoácidos. De manera general, el método PM6 predice con mejor aproximación los valores de HOF con un desviación media promedio (WTMAD) de 0.4 kJ/mol, un valor 2.4 kJ/mol menor que el que presentan los métodos PM3 y PDDG. Por otra parte, se muestra que el PDDG es el mejor método para diferenciar los isómeros, con un desviación media promedio (MAD) más pequeña para la energía de isomerización en 7.8 kJ/mol y 11.0 kJ/mol, con respecto a PM3 and PDDG, respectivamente. A través de la calibración, los valores de MADs obtenidos para PM3, PDDG y PM6 para la mayoría de los compuestos estudiados disminuyeron de 0.1 a 18.2 kJ/mol, con excepción para el PM3 de las aminas, PDDG para los ácidos carboxílicos y el PM6 para los éteres.

A Malária é responsavel por mais de 1.5 milhões de mortes anualmente, especialmente entre crianças (Snow et al. 2005). Apesar da gravidade da situação e grande esforço para o desenvolvimento de novas drogas (Yuan et al. 2011), os investimentos em drogas antimaláricas ainda é relativamente baixo. Brevemente, os alvos antimaláricos atualmente testados incluem: quinases, proteases, canais iônicos para GPCR, receptores nucleares entre outros (Gamo et al. 2010). No presente trabalho nós revisamos as vias de transdução de sinal em eritrócitos assim como eritrócitos infectados e interações com células endoteliais, denominada citoaderência. Este processo é conhecido por sua importante função na patogenicidade da malária severa. As moléculas expressas na superfície dos eritrócitos infectados (IE) e células endoteliais vasculares (EC) são importantes mediadores da citoaderência, não apenas induzindo mudanças estruturais e metabólicas nos dois lados, mas também desencadeiam diversos sinais do processo transducional, levando a alteração da expressão gênica, com o balanço entre a regulação positiva e negativa determinando a patologia endotelial durante a infecção malárica.

Malaria is responsible for more than 1.5 million deaths each year, especially among children (Snow et al. 2005). Despite of the severity of malaria situation and great effort to the development of new drug targets (Yuan et al. 2011) there is still a relative low investment toward antimalarial drugs. Briefly there are targets classes of antimalarial drugs currently being tested including: kinases, proteases, ion channel of GPCR, nuclear receptor, among others (Gamo et al. 2010). Here we review malaria signal transduction pathways in Red Blood Cells (RBC) as well as infected RBCs and endothelial cells interactions, namely cytoadherence. The last process is thought to play an important role in the pathogenesis of severe malaria. The molecules displayed on the surface of both infected erythrocytes (IE) and vascular endothelial cells (EC) exert themselves as important mediators in cytoadherence, in that they not only induce structural and metabolic changes on both sides, but also trigger multiple signal transduction processes, leading to alteration of gene expression, with the balance between positive and negative regulation determining endothelial pathology during a malaria infection.