IntroductionPrevious studies have shown that a single sub-anesthetic dose of ketamine exerts fast-acting antidepressant effects in patients and in animal models of depression. However, the underlying mechanisms are not totally understood. This study aims to investigate the effects of acute administration of different doses of ketamine on the immobility time of rats in the forced swimming test (FST) and to determine levels of hippocampal brain-derived neurotrophic factor (BDNF) and mammalian target of rapamycin (mTOR).MethodsForty male Wistar rats weighing 180–220 g were randomly divided into four groups (n = 10 each): group saline and groups ketamine 5, 10, and 15 mg/kg. On the first day, all animals were forced to swim for 15 min. On the second day ketamine (5, 10, and 15 mg/kg, respectively) was given intraperitoneally, at 30 min before the second episode of the forced swimming test. Immobility times of the rats during the forced swimming test were recorded. The animals were then decapitated. The hippocampus was harvested for determination of BDNF and mTOR levels.ResultsCompared with group saline, administration of ketamine at a dose of 5, 10, and 15 mg/kg decreased the duration of immobility (P < 0.05 for all doses). Ketamine at doses of both 10 and 15 mg/kg showed a significant increase in the expression of hippocampal BDNF (P < 0.05 for both doses). Ketamine given at doses of 5, 10, and 15 mg/kg showed significant increases in relative levels of hippocampal p-mTOR (P < 0.05 for all doses)ConclusionThe antidepressant effect of ketamine might be related to the increased expression of BDNF and mTOR in the hippocampus of rats.

BackgroundExtra-Corporeal Membrane Oxygenation (ECMO) therapy is associated with high risk of neurologic injury. But the mechanism of neurologic injury during and/or after ECMO therapy is still unclear. Recent animal experiments confirmed that ECMO treatment increases the immune inflammatory response. The aim of this study is to investigate the effect of VV- ECMO on immune inflammatory response of cerebral tissues and neurological impairment.Methods18 porcine were randomly divided into control, sham and ECMO group (n = 6/group). ECMO was run 24 h in the ECMO group, and serum collected at 0, 2, 6, 12 and 24 h during ECMO treatment for the analysis of cytokine (IL-1β, IL-6, IL-10, TNF-a) and cerebral injury specific biomarker S100B and NSE. After 24 h ECMO treatment, all animals were euthanized and cerebral tissues (hypothalamus, hippocampus and cortex) were collected for measure of mRNA and protein levels of cytokine (IL-1β, IL-6, IL-10, TNF-a).ResultsThe results during ECMO treatment showed that all the pro-inflammation cytokines were increased significantly after 2 h, and anti-inflammation IL-10 showed transient hoist in the first 2 h in serum. After 24 h ECMO therapy, the mRNA levels of pro-inflammation cytokines and anti-inflammation IL-10 were simultaneously up-regulated in cerebral tissues (hypothalamus, hippocampus and cortex). And protein concentrations also showed different increasing levels in cerebral tissues. However, during the ECMO treatment, S100B and NSE protein in serum did not change significantly.ConclusionThese findings suggest VV-ECMO treatment can not only lead to immune inflammatory response in blood, but can also produce immune and inflammatory response in cerebral tissues. However the extent of immune inflammation was not sufficient to cause significant neurological impairment in this study. But the correlation between cerebral inflammatory response and cerebral impairment need to further explore.

The first total synthesis of (+)-frondosin A was accomplished in 19 longest linear and 21 total steps from commercially available materials. The key features of the synthesis include a Ru-catalyzed [5+2] cycloaddition, a Claisen rearrangement, and a ring expansion to construct the core of the frondosin A in a diastereoselective and regioselective fashion. This is the first application of a Ru-catalyzed [5+2] cycloaddition in the total synthesis of a natural product. Through this synthesis, the absolute configuration of (+)-frondosin A was established.

The importance of the Ni catalyst in achieving catalytic asymmetric Ni/Cr-mediated coupling reactions effectively is demonstrated. Six phenanthroline-NiCl(2) complexes 1a-c and 2a-c and five types of alkenyl iodides A-E were chosen for the study, thereby demonstrating that these Ni catalysts display a wide range of overall reactivity profiles in terms of the degree of asymmetric induction, geometrical isomerization, and coupling rate. For three types of alkenyl iodides A-C, a satisfactory Ni catalyst(s) was found within 1a-c and 2a-c. For disubstituted (Z)-alkenyl iodide D, 2c was identified as an acceptable Ni catalyst in terms of the absence of Z → E isomerization and the degree of asymmetric induction but not in terms of the coupling rate. Two phosphine-based Ni catalysts, [(Me)(3)P](2)·NiCl(2) and [(cy)(3)P](2)·NiCl(2), were found to meet all three criteria for D. The bond-forming reaction at the C16-C17 position of palytoxin was used to demonstrate the usefulness of the Ni catalysts thus identified.

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BackgroundVasopressin is widely used to treat various type of hypotension, but the effect of vasopressin on coronary artery bypass grafting surgery (CABG) patients is not clear. This study was to investigate the effect of vasopressin on the hemodynamics in CABG patients.MethodsTwenty coronary artery disease (CAD) patients were randomly divided into two groups: norepinephrine group and vasopressin group. During the anesthesia and the operation, the central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) were maintained to 8-10cmH2O, and the hemocrit was maintained above 30% through lactate ringer’s mixture, artifact colloid and red blood cells. The invasive artery blood pressure (IBP) was maintained by appropriate anesthetic depth and norepinephrine or vasopressin respectively. The target IBP was 70 mmHg, and heart rate (HR) was 60 bpm. The MAP (mean artery pressure), HR, ST-T, CVP, PAP (pulmonary artery pressure), PCWP, SVR (systemic vascular resistance), PVR (pulmonary vascular resistance), CO (cardiac output), urine output, blood gas analysis, surgery duration and blood loss were monitored.ResultsThe MAP, HR, and ST-T were stable in either group during the operation. CVP, PCWP and SVR increased but CI deceased during the posterior descending artery (PDA) was grafted in both groups and without any significant difference between them. PAP increased during PDA was grafted in either group and there was significant difference between the two groups. PVR increased during ADA and PDA being grafted in norepinephrine group but not in vasopressin group. Metoprolol usage was 11.2 mg and 5.9 mg in norepinephrine group and vasopressin group respectively.ConclusionVasopressin was better than norepinephrine.to keep the hemodynamics stability of patients undergoing CABG surgery.

Benzo[b]fluorenols were prepared by a new palladium-catalyzed one-pot reaction of enone-ynes with 3-bromoprop-1-yne through intramolecular dehydroaromatization and carbonyl reduction.

Extracorporeal membrane oxygenation (ECMO) therapy can result in systemic immune inflammation and trigger a hemolytic response, both of which can lead to oxidative stress injury. However, currently, there are few studies about whether ECMO can lead to oxidative stress injury. The objective of this study was to determine the effect of ECMO therapy on systemic oxidative stress. Twelve pigs were randomly divided into control and ECMO treatment groups. Blood samples were collected at -1, 0, 2, 6, 12, and 24 h during ECMO therapy in order to measure the levels of various oxidative stress markers in plasma. All animals included in the study were euthanized after 24 h of ECMO treatment. Malondialdehyde (MDA) was used as a marker of oxidation, and superoxide dismutase (SOD), glutathione (GSH), and total antioxidant capacity (T-AOC) were used as indices for antioxidant activity. The plasma levels of each molecule were similar when measured at -1 and 0 h (P > 0.05). In the control group, MDA, SOD, GSH, and T-AOC remained relatively constant throughout the study period. However, when ECMO was administered for 2 h, plasma levels of MDA increased significantly; conversely, levels of SOD, GSH, and T-AOC decreased. Maximum MDA levels and minimal SOD, GSH, and T-AOC levels were observed after 6 h of ECMO treatment. MDA and SOD levels had returned to baseline at 24 h. At this time-point, levels of MDA and T-AOC in samples from the right frontal cortex and jejunum differed significantly between the control and ECMO treatment groups. These results show that early ECMO treatment can induce significant oxidative stress injury in plasma. However, in the latter stage of the treatment, the oxidative stress injury can be repaired gradually. ECMO treatment can also result in mild oxidative stress injury in the jejunum and brain tissue.