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Background and Aims. Endotoxemia (ET) is a common critical illness in patients receiving intensive care and is associated with high mortality and prolonged hospital stay. The intestinal epithelial cell dysfunction is regarded as the “engine” of deteriorated ET. Although electroacupuncture (EA) can mitigate endotoxin-induced intestinal epithelial cell dysfunction in ET, the mechanism through which EA improves endotoxin-induced intestinal injury for preventing ET deterioration needs further investigation. Methods. An in vivo ET model was developed by injecting lipopolysaccharide (LPS) in wild-type and PINK1-knockout mice. An in vitro model was also established by incubating epithelial cells in the serum samples obtained from both groups of mice. Hemin and zinc protoporphyrin IX (ZnPP) were applied to activate or inhibit heme oxygenase 1 (HO-1) production. EA treatment was performed for 30 min consecutively for 5 days before LPS injection, and on the day of the experiment, EA was performed throughout the process. Samples were harvested at 6 h after LPS induction for analyzing tissue injury, oxidative stress, ATP production, activity of diamine oxidase (DAO), and changes in the levels of HO-1, PTEN-induced putative kinase 1 (PINK1), mitochondrial fusion and fission marker gene, caspase-1, and interleukin 1 beta (IL-1β). Results. In the wild-type models (both in vivo and vitro), EA alleviated LPS-induced intestinal injury and mitochondrial dysfunction, as indicated by decreased reactive oxygen species (ROS) production and oxygen consumption rate (OCR) and reduced levels of mitochondrial fission proteins. EA treatment also boosted histopathological morphology, ATP levels, DAO activity, and levels of mitochondrial fusion proteins in vivo and vitro. The effect of EA was enhanced by hemin but suppressed by Znpp. However, EA + AP, Znpp, or hemin had no effects on the LPS-induced, PINK1-knocked out mouse models. Conclusion. EA may improve the HO-1/PINK1 pathway-mediated mitochondrial dynamic balance to protect the intestinal barrier in patients with ET.

Yanfang Zhang, Lirong Gong, Yuan Zhang, Shuan Dong, Jia Shi, Xiangyun Li, Yan Guo, Simeng He, Xiaoyang Wu, Shasha Liu, Huayang Liu, Lantian Zhang, Jianbo Yu Department of Anesthesiology and Critical Care Medicine, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, People’s Republic of ChinaCorrespondence: Jianbo Yu, Department of Anesthesiology and Critical Care Medicine, Tianjin Nankai Hospital, 6 Changjiang Road, Tianjin, 300100, People’s Republic of China, Tel +86-22-23475289, Email 30717008@nankai.edu.cnPurpose: To investigate the effect of transcutaneous electrical acupoint stimulation (TEAS) on urinary retention after laparoscopic cholecystectomy in elderly patients, and to explore the relationship between TEAS and urinary ATP.Patients and Methods: The TEAS group was administered active TEAS at specific acupuncture points prior to induction of anesthesia and continued for 45 mins after surgery. In the control group, participants received sham stimulus at the same acupoints and no output current was delivered by disconnecting the device’s output line. Urine samples were collected and evaluated in the first spontaneous voiding after surgery. In this study, postoperative urinary retention (POUR) was the primary outcome, which was diagnosed based on clinical symptoms, ultrasound assessments, and the need for bladder catheterization. Secondary outcomes include urinary ATP, postoperative spontaneous urination, urination symptoms, catheter-related bladder discomfort (CRBD), delirium, duration and hospitalization costs.Results: The study involved 598 patients recruited and randomized between August 2018 and June 2020. Among these patients, 547 (91.5%) completed the study and were analyzed. There were 64 cases of POUR, including 23 (8.4%, 95% confidence interval [CI]: 6.4– 9.9%) in the TEAS group and 41 (15.0%, 95% CI: 9.3– 13.4%) in the control group (p = 0.017). A significant difference was observed between the TEAS and control groups for urinary ATP concentration in the first spontaneous urine postoperatively (344 nmol/L versus 233 nmol/L, p=0.001). There was a shorter spontaneous voiding recovery time, smaller voiding threshold, less postoperative catheterization, less CRBD, and lower hospitalization costs in TEAS group compared with control group.Conclusion: TEAS reduces the incidence of POUR in elderly patients undergoing laparoscopic cholecystectomy, which may be related to an increase in bladder ATP release.Keywords: transcutaneous electrical acupoint stimulation, urinary retention, ATP, catheterization, laparoscopic surgery, catheter-related bladder discomfort

Sepsis caused acute lung injury (ALI) is a kind of serious disease in critically ill patients with very high morbidity and mortality. Recently, it has been demonstrated that Golgi is involved in the process of oxidative stress. However, whether Golgi stress is associated with oxidative stress in septic induced acute lung injury has not been elucidated. In this research, we found that lipopolysaccharide (LPS) induced oxidative stress, apoptosis, inflammation and Golgi morphology changes in acute lung injury both in vivo and in vitro. The knockout of heme oxygenase-1(HO-1) aggravated oxidative stress, inflammation, apoptosis and reduced the expression of Golgi matrix protein 130 (GM130), mannosidase Ⅱ, Golgi-associated protein golgin A1 (Golgin 97), and increased the expression of Golgi phosphoprotein 3 (GOLPH3), which caused the fragmentation of Golgi. Furtherly, the activation of hypoxia inducible factor-1α (HIF-1α)/HO-1 pathway, attenuates Golgi stress and oxidative stress by increasing the levels of GM130, mannosidase Ⅱ, Golgin 97, and decreasing the expression of GOLPH3 both in vivo and in vitro. Therefore, the activation of HO-1 plays a crucial role in alleviating sepsis-induced acute lung injury by regulating Golgi stress, oxidative stress, which may provide a therapeutic target for the treatment of acute lung injury., Graphical abstract Image 1

This paper proposes a self-synchronizing synchronverter controller design that leverages the addition of a virtual resistance (along with a suitable coordinate transformation) to compute feedback signals during self synchronization prior to grid connection. With respect to analysis, we exploit separation-of-time-scales arguments and develop appropriate reduced-order models, which are well-suited for studying phase-angle and voltage-magnitude self-synchronization dynamics independently. Our work provides analytical justification for the effects of pertinent controller parameters and system initial conditions on self-synchronization dynamics observed empirically in time-domain simulations. As such, it offers practical guidance on favourable parameter-value settings to achieve fast self synchronization, and it yields accurate estimates for self-synchronization times with well-tuned parameters. Through numerical simulations and experiments, we illustrate the efficacy of the proposed controller design and verify the validity of subsequent analyses.

Endotoxin-induced acute lung injury (ALI) has a high mortality rate, and there are limited effective treatment options available. The aim of the present study was to identify if dexmedetomidine could regulate mitochondrial fusion and fission through the protein kinase C (PKC)-α/haem oxygenase (HO)-1 pathway to protect against endotoxin-induced ALI.Dexmedetomidine was administered by intraperitoneal injection once daily for three days prior to induction of lung injury to mice. Mice in the PKC-α inhibitor group received dexmedetomidine by intraperitoneal injection 1 h after each chelerythrine injection, and lipopolysaccharide was injected 1 h after the last dose of dexmedetomidine. The lung wet/dry weight ratio, oxidative stress, inflammatory response, and expression levels of PKC-α, Nrf2, HO-1, Mfn1, Mfn2, OPA1, Drp1, and Fis1 were determined.Dexmedetomidine administration attenuated lung oxidative stress, decreased inflammatory cytokines secretion, and downregulated the expression levels of Drp1 and Fis1. Moreover, dexmedetomidine increased levels of Mfn1, Mfn2, and OPA1, and alleviated endotoxin-induced lung injury. Administration of chelerythrine partially reversed the pneumoprotective effects of dexmedetomidine.Dexmedetomidine may activate the PKC-ɑ/HO-1 pathway to increase the expression of Mfn1, Mfn2, and OPA1, while decreasing Drp1 and Fis1 expression, thereby reduce endotoxin-induced acute lung injury.

This paper identifies the importance of considering the full-order virtual synchronous machine (VSM) dynamics while tuning parameters in its cascaded voltage and current control loops. Via a numerical example, we highlight that the conventional tuning method of the voltage and current loops may not ensure system stability. This is because the tuning method does not consider full-order system dynamics. Thus, we improve the tuning method for the VSM voltage and current loops using small-signal analysis of the full-order VSM model. The proposed tuning method ensures system stability in the small-signal sense, and it is computationally inexpensive. We verify the effectiveness of the proposed tuning method via numerical simulations.

Increasing lines of evidence identified that dexmedetomidine (DEX) exerted protective effects against sepsis-stimulated acute lung injury via anti-inflammation, anti-oxidation and anti-apoptosis. However, the mechanisms remain unclear. Herein, we investigated whether DEX afforded lung protection by regulating the process of mitochondrial dynamics through the HIF-1a/HO-1 pathway in vivo and in vitro. Using C57BL/6J mice exposed to lipopolysaccharide, it was initially observed that preemptive administration of DEX (50μg/kg) alleviated lung pathologic injury, reduced oxidative stress indices (OSI), improved mitochondrial dysfunction, upregulated the expression of HIF-1α and HO-1, accompanied by shifting the dynamic course of mitochondria into fusion. Moreover, HO-1-knockout mice or HO-1 siRNA transfected NR8383 cells were pretreated with HIF-1α stabilizer DMOG and DEX to validate the effect of HIF-1a/HO-1 pathway on DEX-mediated mitochondrial dynamics in a model of endotoxin-induced lung injury. We found that pretreatment with DEX and DMOG distinctly relieved lung injury, decreased the levels of mitochondrial ROS and mtDNA, reduced OSI, increased nuclear accumulation of HIF-1a and HO-1 protein in wild type mice but not HO-1 KO mice. Similar observations were recapitulated in NC siRNA transfected NR8383 cells after LPS stimulation but not HO-1 siRNA transfected cells. Concertedly, DEX reversed the impaired mitochondrial morphology in LPS stimulated-wild type mice or NC siRNA transfected NR8383 cells, upregulated the expression of mitochondrial fusion protein, while downregulated the expression of fission protein in HIF-1a/HO-1 dependent pathway. Altogether, our data both in vivo and in vitro certified that DEX treatment ameliorated endotoxin-induced acute lung injury by preserving the dynamic equilibrium of mitochondrial fusion/fission through the regulation of HIF-1a/HO-1 signaling pathway.

Various pharmacological agents and protective methods have been shown to reverse pneumoperitoneum-related lung injury, but identifying the best strategy is challenging. Herein, we employed lung tissues and blood samples from C57BL/6 mice with pneumoperitoneum-induced lung injury and blood samples from patients who received laparoscopic gynecological surgery to investigate the therapeutic role of hydromorphone in pneumoperitoneum-induced lung injury along with the underlying mechanism. We found that pretreatment with hydromorphone alleviated lung injury in mice that underwent CO2 insufflation, decreased the levels of myeloperoxidase (MPO), total oxidant status (TOS), and oxidative stress index (OSI), and increased total antioxidant status (TAS). In addition, after pretreatment with hydromorphone, upregulated HO-1 protein expression, reduced mitochondrial DNA content, and improved mitochondrial morphology and dynamics were observed in mice subjected to pneumoperitoneum. Immunohistochemical staining also verified that hydromorphone could increase the expression of HO-1 in lung tissues in mice subjected to CO2 pneumoperitoneum. Notably, in mice treated with HO-1-siRNA, the protective effects of hydromorphone against pneumoperitoneum-induced lung injury were abolished, and hydromorphone did not have additional protective effects on mitochondria. Additionally, in clinical patients who received laparoscopic gynecological surgery, pretreatment with hydromorphone resulted in lower serum levels of club cell secretory protein-16 (CC-16) and intercellular adhesion molecule-1 (ICAM-1), a lower prooxidant-antioxidant balance (PAB), and higher heme oxygenase-1 (HO-1) activity than morphine pretreatment. Collectively, our results suggest that hydromorphone protects against CO2 pneumoperitoneum-induced lung injury via HO-1-regulated mitochondrial dynamics and may be a promising strategy to treat CO2 pneumoperitoneum-induced lung injury.

Background The protective effects of carbon monoxide against the lipopolysaccharide (LPS)-induced lung injury were attributed to maintenance of mitochondrial dynamics, but the mechanisms remain unexplored. Materials and methods Using a rat model of acute lung injury induced by LPS and the LPS attacking cell model, we investigated the effects of pretreatment of carbon monoxide molecule-2 (CORM-2) on the acute lung injury and expressions of mitofusin proteins that play a critical role in mitochondrial dynamics. Results We found that preadministration of CORM-2, not the inactive form of CORM-2, significantly reduced the lung injury, levels of inflammatory cytokines, and the degree of oxidative stress caused by LPS. What was more, it increased the expressions of mitofusin proteins. Similar findings were also found in LPS-stimulating cell model. However, when the cells were treated in combination with LPS, CORM-2, and SB203580, it completely abolished the protection of CORM-2, reflected by increased levels of inflammatory cytokines and malonaldehyde, decreased activities of superoxide dismutase, along with the lower expressions of mitofusin proteins and the ratio of p-p38 mitogen activated protein kinase to p38 mitogen activated protein kinase. Conclusions Our observations suggest that pretreatment with CORM-2 could attenuate LPS-induced lung injury by inducing the expressions of mitofusin proteins via p38 mitogen activated protein kinase pathway.

This paper proposes a method to directly compute controller parameter values in a synchronverter augmented with a so-called damping correction loop, and in so doing, achieve desired transient and steady-state response. The proposed approach is grounded in a reduced third-order system model that captures pertinent dynamic characteristics of the synchronverter active-power loop (APL), particularly those of the dominant mode. This reduced-order model helps to identify and explain a shortcoming in a previous parameter tuning method. Central to the proposed parameter computation method is to express APL parameters of the original system as closed- form functions of the poles of the reduced-order system. Since the reduced-order model retains dominant-mode dynamic behaviours of the original system, APL parameters can be directly computed according to specified APL dominant mode. Time-domain simulations are provided to validate the accuracy of the reduced-order model and the proposed direct-computation parameter tuning method.

The virtual synchronous generator (VSG) is a power-electronic controller that mimics the dynamic behaviour of synchronous generators. It is a promising technology to enable integration of renewable energy conversion systems under weak-grid conditions. By providing virtual inertia, the VSG improves system stability. However, under weak-grid conditions, system stability may also be adversely affected by the VSG exceeding its active-power transfer capacity, leading to a phenomenon known as voltage instability. In this paper, we highlight this problem via simulations conducted for a microgrid test system. Then, we offer analytical justification for the mechanism and root cause of the observed voltage instability. We further propose two countermeasures to improve the active-power transfer capacity. The first is based on existing VSG capabilities so that no new components are needed in the controller, and the second requires additional components but enables full use of the VSG capacity.

Acute respiratory distress syndrome (ARDS) is one of the most devastating complications of sepsis lacking of effective therapy. Mitochondrial dynamics undergoing continuous fusion and fission play a crucial role in mitochondrial structure and function. Fis1, as a small protein located on the outer membrane of mitochondria, has been thought to be an important protein mediated mitochondrial fission. During ARDS, alveolar macrophages suffer from increased oxidative stress and apoptosis, and also accompanied by disrupted mitochondrial dynamics. In addition, as one of the products of heme degradation catalyzed by heme oxygenase, carbon monoxide (CO) possesses powerful protective properties in vivo or in vitro models, such as anti-inflammatory, antioxidant and anti-apoptosis function. However, there is little evidence that CO alleviates oxidative stress damage through altering mitochondrial fission in alveolar macrophages. In the present study, our results showed that CO increased cell vitality, improved mitochondrial SOD activity, reduced reactive oxygen species (ROS) production and inhibited cell apoptosis in NR8383 exposed to LPS. Meanwhile, CO decreased the expression of Fis1, increased mitochondrial membrane potential and sustained elongation of mitochondria in LPS-incubated NR8383. Overall, our study underscored a critical role of CO in suppressing the expression of Fis1 and alleviating LPS- induced oxidative stress damage in alveolar macrophages.

In this paper, we propose an idea to integrate more renewable energy into the existing China power grid and to provide remote islands with a reliable power supply. The idea is to expand the existing point-to-point line-commutated converter (LCC) HVDC transmission link into a hybrid multiterminal HVDC (hybrid MTDC) system, which contains LCC stations and voltage-source converter (VSC) stations. Accordingly, this paper proposes a novel control strategy for this system called active voltage feedback control, which does not need any high-speed communication system under various disturbances, such as wind speed variations, load fluctuations, faults, etc. This paper also adds secondary frequency regulation to the synchronverter, which is one way of combining the VSC converter with synchronous machine behavior. Then, this paper applies an approach to limit its current under fault conditions. Finally, the entire hybrid MTDC system is modeled in PSCAD/EMTDC. Simulation results show that the improved synchronverter is able to achieve secondary frequency control, and the presented active voltage feedback control works very well when exposed to various disturbances.

Sepsis-related acute lung injury (ALI) remains a major cause of mortality in critically ill patients and lacks specific therapy. Mitochondrial dysfunction is involved in the progression of septic lung injury. Mitochondrial dynamics, mitophagy, and biogenesis converge to constitute the assiduous quality control of mitochondria (MQC). Heme oxygenase-1 (HO-1) protects against sepsis-induced ALI through the modulation of mitochondrial dynamics. However, the causal relationship between HO-1 and the general processes of MQC, and their associated cellular pathways in sepsis-related ALI remain ill-defined. Herein, lipopolysaccharide (LPS)-induced ALI in Sprague-Dawley rats together with LPS-induced oxidative injury in RAW264.7 macrophages were used to investigate whether the PI3K/Akt pathway-mediated induction of HO-1 preserves MQC and alleviates septic lung injury. After pretreatment with hemin, a potent inducer of HO-1, LPS-induced cell apoptosis, enhanced mitochondrial fragmentation, and mitochondrial membrane potential damage were significantly reduced in macrophages. In rats, these effects were accompanied by a higher survival rate, less damage to lung tissue, a 28.5% elevation in lung mitochondria MnSOD activity, and a 39.2% increase in respiratory control ratios. Concomitantly, HO-1 induction preserved the dynamic process of mitochondrial fusion/fission (Mfn2, OPA1, Drp1), promoted mitochondrial biogenesis (NRF1, PGC1α, Tfam), and facilitated the key mediators of mitochondrial mitophagy (Parkin, PINK1) at mRNA and protein levels. Notably, LY294002, a PI3K inhibitor, or knockdown of PI3K by small interfering RNA significantly suppressed Akt phosphorylation, attenuated HO-1 induction, and further reversed these beneficial effects evoked by hemin pretreatment in RAW264.7 cells or rats received LPS, indicating a direct involvement of PI3K/Akt pathway. Taken together, our results indicated that HO-1 activation, through PI3K/Akt pathway, plays a critical role in protecting lung from oxidative injury in the setting of sepsis by regulating MQC. HO-1 may therefore be a therapeutic target for the prevention sepsis-related lung injury.

This paper proposes a fast self-synchronizing synchronverter controller design, which synchronizes the synchronverter inner voltage to the grid-side voltage without needing to measure its phase angle, prior to physical connection to the grid. The proposed design centres on the addition of a virtual resistance branch (along with a suitable coordinate transformation), which provides the controller with virtual active- and reactive-power output feedback signals during self synchronization, even though the actual outputs are zero before grid connection. The virtual resistance branch enables fast self synchronization by avoiding inductance dynamics in prevailing methods that use a virtual impedance branch. At the same time, the parameter tuning process is simplified as fewer parameters require tuning. Moreover, the effects of these parameters on synchronization dynamics are well defined. Time-domain simulations are provided to validate that the proposed controller design self synchronizes quickly and that its parameters are easily tuneable.

This paper proposes to augment the conventional synchronverter control scheme with an auxiliary loop to freely adjust the dynamic response speed. This loop is dubbed as a damping correction loop since its form and function are reminiscent of the damping component in the classical synchronous generator model. Central to the proposed auxiliary loop is the creation of an additional tuneable parameter that allows for unrestricted adjustment of the system damping ratio without affecting the steady-state frequency droop characteristic, which is an improvement over the conventional synchronverter design. In the proposed method, relevant parameters are analytically tuned and active- and reactive-power coupling effects are reduced when operating with increased response speed. The dynamic response and robustness of the approach are verified via extensive small-signal analysis. Furthermore, time-domain simulations highlight the advantages of the proposed method over existing ones.

Sepsis-related acute respiratory distress syndrome is characterized by marked oxidative stress and mitochondrial dysfunction lacking of specific therapy. Heme oxygenase (HO)-1 followed by endogenous carbon monoxide (CO) exerted a cytoprotective effect against multi-organ damage during sepsis. Additionally, the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway, which serves as an upstream regulator of HO-1, was associated with inflammation and oxidative stress. Therefore, the purpose of the present study was to investigate whether the PI3K/Akt pathway was involved in the effects of HO-1/CO on the expression of mitochondrial fission 1 protein (Fis1). In the present study, CO releasing molecule-2 (CORM2), as the exogenous source of CO, plus LY294002, as a specific PI3K inhibitor, were pre-incubated in lipopolysaccharide (LPS)-simulated rat NR8383 alveolar macrophages. The results demonstrated that CORM2 improved cell viability, inhibited tumor necrosis factor-α levels, malondialdehyde contents, while elevating interleukin-10 levels and superoxide dismutase activities. In addition, pretreatment with CORM2 suppressed the fragmentation of mitochondria, upregulated the expressions of phosphorylated-Akt and HO-1 but downregulated the levels of Fis1 mRNA and protein in LPS-exposed cells. However, pretreatment with LY294002 significantly inhibited the phosphorylation of Akt, decreased HO-1 levels, aggravated mitochondrial fragmentation, increased Fis1 mRNA and protein levels, and reversed the above protective effects of CORM2. Collectively, the results of the present study indicated that the PI3K/Akt pathway mediated the cytoprotective effects of HO-1/CO on the transcription and translational levels of Fis1, and alleviated LPS-induced oxidative injury in alveolar macrophages.

To investigate the impact of professional physician-coordinated intensive follow-up on long-term expenditures after percutaneous coronary intervention (PCI) in unstable angina (UA) patients.In this study, there were 669 UA patients who underwent successful PCI and followed up for 3 years, then divided into the intensive follow-up group (N = 337), and the usual follow-up group (N = 332). Patients were provided with detailed discharge information and individualized follow-up schedules. The intensive group received the extra follow-up times and medical consultations, and all patients were followed up for approximately 3 years.At the 3-year mark after PCI, the cumulative major adverse cardiac events (MACE), recurrence of myocardial ischemia, cardiac death, all-cause death and revascularization in the intensive group were lower than in the usual group. Additionally, the proportion of good medication adherence was significantly higher than in the usual group (56.4% vs. 46.1%, p0.001). The hospitalization daytime, total hospitalization cost and total medical cost in the intensive group were lower. Multiple linear regression showed that diabetes, hypertension, intensive follow-up and good medication adherence were associated with emergency and regular clinical cost (p0.05), the re-hospitalization cost (p0.05) and the total medical cost (p0.05) of patient care. Intensive follow-up and good adherence were negatively correlated with the cost of re-hospitalization (standardized coefficients = -0.132, -0.128, p0.05) and total medical costs (standardized coefficients = -0.072, -0.086, p0.05).Intensive follow-up can reduce MACE, improve medication adherence and save long-term total medical costs, just by increasing the emergency and regular clinical visits cost in UA patients after PCI.

Purpose This study aimed to examine the application of intravascular ultrasound (IVUS) in ST-segment elevation myocardial infarction (STEMI) patients with high thrombus burden (thrombus grade ≥3) undergoing emergency diagnosis and primary percutaneous coronary intervention. Methods Eighty STEMI patients were enrolled and randomly assigned to the IVUS-guided group (38 patients) or non-IVUS group (42 patients). Stent implantation was performed in non-IVUS group patients. IVUS group patients were further divided into low-risk and high-risk patients on the basis of IVUS evaluation for determining whether stenting should be performed. Major adverse cardiac event (MACE) rates, changes in the left ventricular end-diastolic diameter (LVEDD) and ejection fraction (EF) values, and stent numbers were examined during hospitalization, and follow-up was performed at 1, 3, 6, and 12 months postoperatively. Results During hospitalization, there were no significant differences in the MACE rates, LVEDD, and EF values and in the follow-up outcomes at 1, 3, 6, and 12 months postoperatively among the patients in the 2 groups (P > 0.05). A significantly lower number of stents were implanted in the IVUS group than in the non-IVUS group patients (P

A new solvent extraction method recycling the acrylic acid (AA) from industrial waste fluid for producing acrylic acid was studied. The influencing factors of the species of diluents, concentration of extractant and temperature were investigated. The optimal process conditions were chosen that the 1-octanol as diluents, the concentration of tri-n-octylamine (TOA) 0.87mol/L, reaction temperature 298K after a series of experiments and analysis. The kinetics of extraction was studied by Lewis cell, the rate equation of extraction could be expressed as: RA=8.8×10-2[AA]1.5[TOA]2.1.

Extraction of citric acid from aqueous solutions with tertiary amine, dissolved in mixtures of kerosene and phase modifier have been studied as a function of exaction yield at different phase modifier volume fraction, temperatures, stirring speed and exaction time. The optimal experimental conditions of extraction were obtained: reaction temperature 303K, reaction time 3 min, the kerosene volume fraction 20%, and 45% 1−octanol as phase modifier, stirring speed 450rpm/min. Under these conditions, the extraction yield could reach 75%. The complex of citric acid and tertiary amine was a surfactant that makes surface tension decrease. The composition of the citric acid complex is (R3N) · (H3A). The formation of complex was exothermic reaction that the standard enthalpy change and standard entropy change are obtained: ΔHθ=-10.17kJ/mol, ΔSθ=-11.86J/(mol·K).

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a common and important oxidative stress in the lung. Mitochondrial fusion responds to the normal morphology and function of cells and is finely regulated by mitochondrial fusion proteins, such as mitofusin-1 protein (Mfn1), mitofusin-2 protein (Mfn2) and optical atrophy 1 (OPA1). Additionally, Mfn1 has been identified as the most important protein in mitochondrial fusion. Heme oxygenase-1 (HO-1) is a stress-inducible protein that plays a critical role in protecting against oxidative stress. However, whether the protection of HO-1 is related to mitochondrial fusion is still a question. Thus, our in vitro and in vivo experiments aimed to identify the relationship between HO-1 and Mfn1. Here, we used Hemin and ZnPP-IX as treatments in an in vivo experiment. Then, HO-1 and Mfn1 were measured using RT-PCR and Western blotting. Supernatants were analyzed for MDA, SOD, and ROS. Our results implied that HO-1 upregulation suppressed oxidative stress induced by LPS, and the possible mechanism could be associated with Mfn1 and the PI3K/Akt pathway.

Background Sepsis-associated acute lung injury remains the major cause of mortality in critically ill patients and is characterized by marked oxidative stress and mitochondrial dysfunction. Mitochondrial dynamics are indispensable for functional integrity. Additionally, heme oxygenase (HO)-1/carbon monoxide conferred cytoprotection against end-organ damage during endotoxic shock. Herein, we tested the hypothesis that HO-1/carbon monoxide played a critical role in maintaining the dynamic process of mitochondrial fusion/fission to mitigate lung injury in Sprague-Dawley rats or RAW 264.7 macrophages exposed to endotoxin. Methods The production of reactive oxygen species, the respiratory control ratio (RCR), and the expressions of HO-1 and mitochondrial dynamic markers were determined in macrophages. Concurrently, alterations in the pathology of lung tissue, lipid peroxidation, and the expressions of the crucial dynamic proteins were detected in rats. Results Endotoxin caused a 31% increase in reactive oxygen species and a 41% decrease in RCR levels (n = 5 per group). In parallel, the increased expression of HO-1 was observed in lipopolysaccharide-stimulated macrophages, concomitantly with excessive mitochondrial fission. Furthermore, carbon monoxide-releasing molecule-2 or hemin normalized mitochondrial dynamics, which were abrogated by zinc protoporphyrin IX. Additionally, impaired mitochondrial dynamic balance was shown in Sprague-Dawley rats that received lipopolysaccharide, accompanied by pathologic injury, elevated malondialdehyde contents, decreased manganese superoxide dismutase activities, and lowered RCR levels in rat lung mitochondria. However, the above parameters were augmented by zinc protoporphyrin IX and were in turn reversed by hemin. Conclusions The HO-1/carbon monoxide system modulated the imbalance of the dynamic mitochondrial fusion/fission process evoked by lipopolysaccharide and efficiently ameliorated endotoxin-induced lung injury in vivo and in vitro.

Patients with myocardial ischemia exhibit increased left ventricular end-diastolic pressure (LVEDP). The study was to evaluate the relationship between LVEDP measured by left cardiac catheterization and coronary artery disease (CAD) as well as its extent and severity evaluated by coronary angiography (CAG). 912 patients who underwent CAG and left cardiac catheterization were enrolled. There were 313 patients without CAD and 599 with CAD according to CAG. The extent and severity of coronary artery was evaluated by number of vessels and Gensini score. Analyze the correlation of LVEDP and CAD as well as its extent and severity. LVEDP was significantly higher in CAD patients than non-CAD (9.58±5.78 mmHg vs 10.9±5.46 mmHg, P

Electroacupuncture at select acupoints have been verified to protect against organ dysfunctions during endotoxic shock. And, heme oxygenase (HO)-1 as a phase II enzyme and antioxidant contributed to the protection of kidney in septic shock rats. The phosphatidylinositol 3-kinase (PI3K)-Akt pathway mediated the activation of NF-E2 related factor-2 (Nrf2), which was involved in HO-1 induction. To understand the efficacy of electroacupuncture stimulation in ameliorating acute kidney injury (AKI) through the PI3K/Akt/Nrf2 pathway and subsequent HO-1 upregulation, a dose of LPS 5mg/kg was administered intravenously to replicate the rabbit model of AKI induced by endotoxic shock. Electroacupuncture pretreatment was handled bilaterally at Zusanli and Neiguan acupoints for five consecutive days while sham electroacupuncture at non-acupoints as control. Results displayed that electroacupuncture stimulation significantly alleviated the morphologic renal damage, attenuated renal tubular apoptosis, suppressed the elevated biochemical indicators of AKI caused by LPS, enhanced the expressions of phospho-Akt, HO-1protein, Nrf2 total and nucleoprotein, and highlighted the proportions of Nrf2 nucleoprotein as a parallel. Furthermore, partial protective effects of elecroacupuncture were counteracted by preconditioning with wortmannin (the selective PI3K inhibitor), indicating a direct involvement of PI3K/Akt pathway. Inconsistently, wortmannin pretreatment made little difference to the expressions of HO-1, Nrf2 nucleoprotein and total protein, which indicated that PI3K/Akt may be not the only pathway responsible for electroacupuncture-afforded protection against LPS-induced AKI. These findings provide new insights into the potential future clinical applications of electroacupuncture for AKI induced by endotoxic shock instead of traditional remedies.

We report a systematic solid-state (17)O NMR study of free nucleic acid bases: thymine (T), uracil (U), cytosine (C), and guanine (G). Site-specifically (17)O-enriched samples were synthesized:[2-(17)O]thymine (1), [4-(17)O]thymine (2), [2-(17)O]uracil (3), [4-(17)O]uracil (4), [2-(17)O]cytosine (5), and [6-(17)O]guanine monohydrate (6). Magic-angle-spinning (MAS) and static (17)O NMR spectra were acquired at 11.75 T for compounds 1-6, from which information about the (17)O chemical shift and electric field gradient tensors was obtained. Extensive quantum chemical calculations were performed at the B3LYP/6-311++G(d,p) level of theory for (17)O NMR properties in various molecular models. The calculated (17)O NMR tensors are highly sensitive to the description of intermolecular hydrogen-bonding interactions at the target oxygen atom. A reasonably good agreement between experimental solid-state (17)O NMR data and B3LYP/6-311++G(d,p) calculations is achievable only in molecular cluster models where a complete hydrogen-bond network is considered. Using this theoretical approach, we also investigated the (17)O NMR tensors in two unusual structures: guanine- and uracil-quartets.

BACKGROUND The anti-oxidative and anti-inflammatory activities of electro-acupuncture (EA), a traditional clinical method, are widely accepted, but its mechanisms are not yet well defined. In this study, we investigated the role of extracellular signal-regulated kinases1/2 (ERK1/2) pathways on electro-acupuncture - mediated up-regulation of heme oxygenase-1 (HO-1) in rabbit lungs injured by LPS-induced endotoxic shock. MATERIAL/METHODS Seventy rabbits were randomly divided into 7 groups: group C, group M, group D, group SEAM, group EAM, group EAMPD, and group PD98059. Male New England white rabbits were given EA treatment on both sides once a day on days 1-5, and then received LPS to replicate the experimental model of injured lung induced by endotoxic shock. Then, they were killed by exsanguination at 6 h after LPS administration. The blood samples were collected for serum examination, and the lungs were removed for pathology examination, determination of wet-to-dry weight ratio, MDA content, SOD activity, serum tumor necrosis factor-α, determination of HO-1 protein and mRNA expression, and determination of ERK1/2 protein. RESULTS The results revealed that after EA treatment, expression of HO-1and ERK1/2 was slightly increased compared to those in other groups, accompanied with less severe lung injury as indicated by lower index of lung injury score, lower wet-to-dry weight ratio, MDA content, and serum tumor necrosis factor-α levels, and greater SOD activity (p

We report new solid-state 127 I NMR results for sheelite periodates, M IO 4 ( M = Na + , K + , Rb + , and NH + 4 ), and for pseudo-scheelite CsIO 4 and HIO 4 . The observed 127 I quadrupole coupling constants were between 1.0 and 43.0 MHz in agreement with previous NQR data. In contrast to an early 127 I NMR study (S. L. Segel and H. M. Vyas, 1980, J. Chem. Phys. 72 , 1406), we found that the 127 I chemical shift anisotropy is negligibly small in sheelite periodates. A small but definite 127 I chemical shift tensor was observed for pseudo-scheelite CsIO 4 .

We report two-dimensional (2D) (17)O multiple-quantum magic-angle spinning (MQMAS) NMR spectra for four (17)O-labeled organic compounds: [(17)O(2)]-D-alanine (1), potassium hydrogen [(17)O(4)]dibenzoate (2), [(17)O(4)]-D,L-glutamic acid.HCl (3) and [2,4-(17)O(2)]uracil (4). The high spectral resolution observed in the 2D (17)O MQMAS NMR spectra allows extraction of precise (17)O NMR parameters for all crystallographically distinct oxygen sites. We demonstrate that rotor synchronization is important in obtaining high-quality (17)O MQMAS spectra for organic compounds. Several issues related to the potential of (17)O MQMAS NMR for large biomolecular systems are also discussed.

We report a solid-state 17 O NMR study of [ α - 13 C , 17 O ] benzamide. The orientations of the 17 O electric-field-gradient and chemical shift tensors were determined from analysis of magic-angle spinning and stationary 17 O NMR spectra. The largest electric-field-gradient component lies in the amide plane and perpendicular to the 13 C– 17 O dipolar vector, whereas the intermediate electric-field-gradient component is along the CO bond. It is also found that the principal component of the 17 O chemical shift tensor with the least shielding, δ 11 , is approximately 18° off the CO bond and that the component with the most shielding, δ 33 , is perpendicular to the amide plane. The present study confirms our earlier results of quantum chemical calculations.

We have presented a systematic experimental and theoretical investigation of the carbonyl oxygen electric-field-gradient (EFG) tensor and chemical shielding (CS) tensor in crystalline amides. Three 17O-labled secondary amides, R1C[17O]-NHR2, have been synthesized: benzanilide (1), N-methylbenzamide (2), and acetanilide (3). Analysis of 17O magic-angle spinning (MAS) and stationary NMR spectra yields not only the magnitude but also the orientation of the carbonyl 17O EFG and CS tensors. For compounds 1−3, the carbonyl 17O quadrupolar coupling constant (QCC) and the span of the chemical shift tensor are found to be in the range of 8.5−8.97 MHz and 560−630 ppm, respectively. The largest 17O EFG component lies in the amide plane and is perpendicular to the CO bond, whereas the smallest component is perpendicular to the N−CO plane. For the carbonyl 17O CS tensor, the principal component with the largest shielding, δ33, is perpendicular to the amide plane, and the tensor component corresponding to the least sh...

We report the first experimental determination of the carbonyl 17O electric-field-gradient (EFG) tensor and chemical-shift (CS) tensor of a urea-type functional group, R1NHC(O)NHR2. Analysis of magic-angle spinning (MAS) and stationary 17O NMR spectra of crystalline [17O]urea yields not only the principal components of the carbonyl 17O EFG and CS tensors, but also their relative orientations. The carbonyl 17O quadrupole coupling constant (QCC) and the asymmetry parameter (η) in crystalline urea were found to be 7.24 ± 0.01 MHz and 0.92, respectively. The principal components of the 17O CS tensor were determined: δ11 = 300 ± 5, δ22 = 280 ± 5 and δ33 = 20 ± 5 ppm. The direction with the least shielding, δ11, is perpendicular to the CO bond and the principal component corresponding to the largest shielding, δ33, is perpendicular to the NC(O)N plane. The observed 17O CS tensor suggests that, in crystalline urea, the 17O paramagnetic shielding contributions from the σ → π* and π → σ* mixing are greater than t...