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Pediatric liver transplantation is an important modality for treating biliary atresia. The overall survival (OS) rate of pediatric liver transplantation has significantly improved compared with that of 20 years ago, but it is still unsatisfactory. The anesthesia strategy of maintaining low central venous pressure (CVP) has shown a positive effect on prognosis in adult liver transplantation. However, this relationship remains unclear in pediatric liver transplantation. Thus, this study was conducted to review the data of pediatric living-donor liver transplantation to analyze the associations of different CVP levels with the prognosis of recipients.This was a retrospective study and the patients were divided into two groups according to CVP levels after abdominal closure: low CVP (LCVP) (≤ 10 cmHIn the study, 712 patients, including 470 in the LCVP group and 242 in the HCVP group, were enrolled. After propensity score matching, 212 pairs remained in the group. The LCVP group showed a higher overall survival rate than the HCVP group in the Kaplan-Meier curves and multivariate Cox regression analyses (P = 0.018), and the HCVP group had a hazard ratio of 2.445 (95% confidence interval, 1.163-5.140).This study confirmed that a low-CVP level at the end of surgery is associated with improved overall survival and a shorter length of hospital stay.

Hepatocytes are the main cell components of the liver and perform metabolic, detoxification, and endocrine functions. Functional hepatocytes are of great value in drug development, toxicity evaluation, and cell therapy for liver diseases. In recent years, an increasing number of in vitro models have been developed to screen drugs and test their toxicity. However, maintaining hepatocyte function in vitro for a long time is a serious challenge. Even freshly isolated liver cells cultured for a short time may lose function via spontaneous dedifferentiation. Thus, novel cell culture systems allowing extended hepatocyte maintenance and more predictive long-term in vitro studies are required. In this study, we developed a conditioned culture system composed of a small-molecule combination that can maintain hepatocyte morphology and functions over the long term. Two-month culture of primary human hepatocytes showed that the conditioned medium was able to stably preserve hepatic functions such as albumin and α-antitrypsin secretion, hepatic transport activity, urea synthesis, and ammonia elimination. Furthermore, this culture model can be used to assess drug-induced hepatotoxicity in vitro. In summary, our work suggests a feasible approach to maintain hepatocyte function in vitro and proposes a promising model for long-term toxicological studies and drug development.

Rationale: The idiosyncratic drug-induced liver injury (iDILI) is a major cause of acute liver injury and a key challenge in late-stage drug development. Individual heterogeneity is considered to be an essential factor of iDILI. However, few in vitro model can predict heterogeneity in iDILI. We have previously shown that mouse and human hepatocytes can be converted to expandable liver progenitor-like cells in vitro (HepLPCs). However, the limited proliferation potential of human HepLPCs confines its industrial application. Here, we reported the generation of a novel hepatocyte model not only to provide unlimited cell sources for human hepatocytes but also to establish a tool for studying iDILI in vitro. Methods: Human primary hepatocytes were isolated by modified two-step perfusion technique. The chemical reprogramming culture condition together with gene-transfer were then used to generate the immortalized HepLPC cell lines (iHepLPCs). Growth curve, doubling time, and karyotype were analyzed to evaluate the proliferation characteristics of iHepLPCs. Modified Hepatocyte Maturation Medium and 3D spheroid culture were applied to re-differentiate iHepLPCs. Results: iHepLPCs exhibited efficient expansion for at least 40 population doublings, with a stable proliferative ability. They could easily differentiate back into metabolically functional hepatocytes in vitro within 10 days. Furthermore, under three-dimensional culture conditions, the formed hepatic spheroids showed multiple liver functions and toxicity profiles close to those of primary human hepatocytes. Importantly, we established a hepatocyte bank by generating a specific number of such cell lines. Screening for population heterogeneity allowed us to analyze the in vitro heterogeneous responses to hepatotoxicity induced by molecular targeted drugs. Conclusions: In light of the proliferative capacity and the heterogeneity they represented, these iHepLPCs cell lines may offer assistance in studying xenobiotic metabolism as well as liver diseases in vitro.

Background This study attempted to investigate the impact of hepatopulmonary syndrome (HPS) on postoperative outcomes in hepatitis B virus-induced hepatocellular carcinoma (HBV-HCC) patients. Methods HBV-HCC patients undergoing primary curative hepatectomy for HCC in our hospital were diagnosed with HPS by contrast-enhanced echocardiography (CEE) and arterial blood gas analysis. Patients were divided into HPS, intrapulmonary vascular dilation (IPVD) (patients with positive CEE results and normal oxygenation) and control (patients with negative CEE results) groups. Baseline information, perioperative clinical data and postoperative pulmonary complications (PPCs) were compared among all groups. Cytokines in patient serums from each group (n = 8) were also assessed. Results Eighty-seven patients undergoing hepatectomy from October 2019 to January 2020 were analyzed. The average time in the postanaesthesia care unit (112.10 ± 38.57 min) and oxygen absorption after extubation [34.0 (14.5-54.5) min] in the HPS group was longer than in IPVD [81.81 ± 26.18 min and 16.0 (12.3-24.0) min] and control [93.70 ± 34.06 min and 20.5 (13.8-37.0) min] groups. There were no significant differences in oxygen absorption time after extubation between HPS and control groups. The incidence of PPCs, especially bi-lateral pleural effusions in the HPS group (61.9%), was higher than in IPVD (12.5%) and control (30.0%) groups. Increased serum levels of the growth-regulated oncogene, monocyte chemoattractant protein, soluble CD40 ligand and interleukin 8 might be related to delayed recovery in HPS patients. Conclusions HPS patients with HBV-HCC suffer delayed postoperative recovery and are at higher risk for PPCs, especially bi-lateral pleural effusions, which might be associated with changes in certain cytokines.

Neonatal jaundice is a common symptom that occurs in neonates during the first month of their life and is generally divided into physiological and pathological subtypes. In serious cases, pathological neonatal jaundice frequently shows complications including seizures, cerebral palsy, and kernicterus. However, due to the unclear pathogenesis of pathological neonatal jaundice, effective drugs for this disease remain unsatisfied. In the present study, we first estimated the protective effects of folic acid (FA) on phenylhydrazine (PHA) or homocysteine (Hcy)-injected neonatal rats (2-3 days aged). Intriguingly, we found that FA significantly decreased the elevated total bilirubin (TBIL) and direct bilirubin (DBIL) concentration, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) activity in PHA- or Hcy-injected rats, indicating that FA improves liver functions. Meanwhile, our results also showed that the plasma Hcy level and N-homocysteinylation (N-Hcy) modification of albumin were significantly elevated in the jaundice rats, which were obviously reversed after FA administration. Furthermore, we identified a novel N-Hcy modification site K

Clinical advancement of the bioartificial liver is hampered by the lack of expandable human hepatocytes and appropriate bioreactors and carriers to encourage hepatic cells to function during extracorporeal circulation. We have recently developed an efficient approach for derivation of expandable liver progenitor-like cells from human primary hepatocytes (HepLPCs). Here, we generated immortalized and functionally enhanced HepLPCs by introducing FOXA3, a hepatocyte nuclear factor that enables potentially complete hepatic function. When cultured on macroporous carriers in an air-liquid interactive bioartificial liver (Ali-BAL) support device, the integrated cells were alternately exposed to aeration and nutrition and grew to form high-density three-dimensional constructs. This led to highly efficient mass transfer and supported liver functions such as albumin biosynthesis and ammonia detoxification via ureagenesis. In a porcine model of drug overdose-induced acute liver failure (ALF), extracorporeal Ali-BAL treatment for 3 hours prevented hepatic encephalopathy and led to markedly improved survival (83%, n = 6) compared to ALF control (17%, n = 6, P = 0.02) and device-only (no-cell) therapy (0%, n = 6, P = 0.003). The blood ammonia concentrations, as well as the biochemical and coagulation indices, were reduced in Ali-BAL-treated pigs. Ali-BAL treatment attenuated liver damage, ameliorated inflammation, and enhanced liver regeneration in the ALF porcine model and could be considered as a potential therapeutic avenue for patients with ALF.

Scheduled maintenance and condition-based online monitoring are among the focal points of recent research to enhance nuclear plant safety. One of the most effective ways to monitor plant conditions is by implementing a full-scope, plant-wide fault diagnostic system. However, most of the proposed diagnostic techniques are perceived as unreliable by operators because they lack an explanation module, their implementation is complex, and their decision/inference path is unclear. Graphical formalism has been considered for fault diagnosis because of its clear decision and inference modules, and its ability to display the complex causal relationships between plant variables and reveal the propagation path used for fault localization in complex systems. However, in a graph-based approach, decision-making is slow because of rule explosion. In this paper, we present an enhanced signed directed graph that utilizes qualitative trend evaluation and a granular computing algorithm to improve the decision speed and increase the resolution of the graphical method. We integrate the attribute reduction capability of granular computing with the causal/fault propagation reasoning capability of the signed directed graph and comprehensive rules in a decision table to diagnose faults in a nuclear power plant. Qualitative trend analysis is used to solve the problems of fault diagnostic threshold selection and signed directed graph node state determination. The similarity reasoning and detection ability of the granular computing algorithm ensure a compact decision table and improve the decision result. The performance of the proposed enhanced system was evaluated on selected faults of the Chinese Fuqing 2 nuclear reactor. The proposed method offers improved diagnostic speed and efficient data processing. In addition, the result shows a considerable reduction in false positives, indicating that the method provides a reliable diagnostic system to support further intervention by operators.

Background: In this study, the effects of sevoflurane or propofol on immune function in patients undergoing partial hepatectomy were investigated during general anesthesia and after surgery.Methods: Seventy-two patients undergoing hepatectomy were randomized into sevoflurane group or propofol group. Sevoflurane or target-controlled infusion (TCI) of propofol was separately used to anesthesia induction and maintenance of two groups. Venous blood samples were taken before induction, 2 hours after anesthesia and 2 hours after surgery for measurement of the percentages of T lymphocyte (CD3+, CD4+, CD8+) and NK cells.Results: Compared with that before anesthesia induction, percentage change in CD3+ and CD4+ T cells to baseline was -0.7% and 3.8% in sevoflurane group, 10.2% and 20.2% in propofol group 2 hours after anesthesia (P=0.002 for CD3+ T cells and P=0.029 for CD4+ T cells ). Percentage change in NK cells was 17.6% in sevoflurane and -12.2% in propofol group 2 hours after anesthesia respectively (P=0.03). There was no significant difference in percentage change 2 hours after surgery of T cells and NK cells to baseline between two groups.Conclusions: Our study indicates that use of propofol during general anesthesia tend to increase the percentages of peripheral CD3+ and CD4+ cells, while sevoflurane increase the peripheral NK cells. Citation: Hao Gao, Jin-Chao Song, Jin-Min Zhang, Ying-Fu Jiao, Zhi-Jie Lu,Tian-Zhu Tao, et al. Effects of sevoflurane or propofol on immune function in patients undergoing hepatectomy. J Anesth Perioper Med 2017; 4: 1-6. doi: 10.24015/JAPM.2017.0001This is an open-access article, published by Evidence Based Communications (EBC). This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium or format for any lawful purpose. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

Backgroud: To investigate the effects and their mechanisms of emulsified sevoflurane and ulinastatin on liver and lung injury induced by obstructive jaundice in rats.Methods: For the in vivo study, male Sprague-Dawley rats were randomized into two parts. Part 1: Sham group, bile duct ligation (BDL) group, BDL and lipid vehicle infusion (BDL+V) group, BDL+ulinastatin (BDL+U) group, BDL+emulsified sevoflurane (BDL+E) group; Liver and lung function was examined by the concentrations of Total Bilirubin (TBIL), Alanine Transaminase (ALT), and lung arterial blood gas analysis. Liver and lung damage was estimated histologically with haematoxylin and eosin (HE) staining in liver and lung samples. F4/80, the molecular marker of activated macrophages, was assessed by immunohistochemistry (IHC). Part 2: Sham+Gadolinium chloride (GdCl3)group, BDL+GdCl3 group, BDL+U+GdCl3 group, BDL+E+GdCl3 group. After the deletion of macrophages, liver and lung examinations were evaluated histologically with HE staining in GdCl3 treated rats. For the in vitro study, the RAW264.7 cell line was stimulated by the different treatments, then terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL staining), Hoechst 33342 staining and the expressions of apoptotic related genes were evaluated to further determine the protective effects of ulinastatin and emulsified sevoflurane.Results: Emulsified sevoflurane and ulinastatin therapies alleviated cholestatic liver and lung damage, inhibited the activation of macrophages in the liver and lung tissues, and improved the liver and lung functions. And they were also found to inhibit apoptosis pathways.Conclusions: Emulsified sevoflurane and ulinastatin treatments were proved to ameliorate BDL-induced cholestatic liver and lung injuries, which were related to the inactivation of the macrophages and the regulation of apoptosis pathways. The above-mentioned mechanisms show new promising approach for the multi-organs injuries in the perioperative management. Citation: Cai-Yang Chen, Ming Zhu, Long Wang, Fei-Xiang Wu, Li-Qun Yang, Wei-Feng Yu. Effects of emulsified sevoflurane and ulinastatin on liver and lung injury induced by bile duct ligation in rats. J Anesth Perioper Med 2017; 4: 7-16. doi: 10.24015/JAPM.2017.0002This is an open-access article, published by Evidence Based Communications (EBC). This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium or format for any lawful purpose. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

Front cover: The cover image, by Yu‐Xi Zhou et al., is based on the Original Article IL‐2mAb reduces demyelination after focal cerebral ischemia by suppressing CD8+ T cells. DOI: https://doi.org/10.1111/cns.13084. [Image: see text]

The study of pathophysiological mechanisms in human liver disease has been constrained by the inability to expand primary hepatocytes in vitro while maintaining proliferative capacity and metabolic function. We and others have previously shown that mouse mature hepatocytes can be converted to liver progenitor-like cells in vitro with defined chemical factors. Here we describe a protocol achieving efficient conversion of human primary hepatocytes into liver progenitor-like cells (HepLPCs) through delivery of developmentally relevant cues, including NAD + -dependent deacetylase SIRT1 signaling. These HepLPCs could be expanded significantly during in vitro passage. The expanded cells can readily be converted back into metabolically functional hepatocytes in vitro and upon transplantation in vivo. Under three-dimensional culture conditions, differentiated cells generated from HepLPCs regained the ability to support infection or reactivation of hepatitis B virus (HBV). Our work demonstrates the utility of the conversion between hepatocyte and liver progenitor-like cells for studying HBV biology and antiviral therapies. These findings will facilitate the study of liver diseases and regenerative medicine.

The (2+1)-dimensional Konopelchenko—Dubrovsky equation is an important prototypic model in nonlinear physics, which can be applied to many fields. Various nonlinear excitations of the (2+1)-dimensional Konopelchenko—Dubrovsky equation have been found by many methods. However, it is very difficult to find interaction solutions among different types of nonlinear excitations. In this paper, with the help of the Riccati equation, the (2+1)-dimensional Konopelchenko—Dubrovsky equation is solved by the consistent Riccati expansion (CRE). Furthermore, we obtain the soliton-cnoidal wave interaction solution of the (2+1)-dimensional Konopelchenko—Dubrovsky equation.

Background and aims One central factor in hepatopulmonary syndrome (HPS) pathogenesis is intravascular accumulation of activated macrophages in small pulmonary arteries. However, molecular mechanism underlying the macrophage accumulation in HPS is unknown. In this study, we aimed to explore whether elevated COX-2 induces the Bone morphogenic protein-2 (BMP-2)/Crossveinless-2 (CV-2) imbalance and then activation of BMP signaling pathway promotes the macrophage accumulation in Common Bile Duct Ligation (CBDL) rat lung. Methods The COX-2/PGE2 signaling activation, the BMP-2/CV-2 imbalance and the activation of Smad1 were evaluated in CBDL rat lung and in cultured pulmonary microvascular endothelial cells (PMVECs) under the HPS serum stimulation. The effects of Parecoxib (COX-2 inhibitor), BMP-2 and CV-2 recombinant proteins on 4-week CBDL rat lung were determined, respectively. Results The COX-2/PGE2 signaling pathway was activated in CBDL rat lung in vivo and PMVECs in vitro , which was due to the activation of NF-κB P65. The inhibition of COX-2 by Parecoxib reduced macrophage accumulation, decreased lung angiogenesis and improved HPS. Meanwhile, the CBDL rat lung secreted more BMP-2 but less CV-2, and the imbalance between BMP-2 and CV-2 exacerbated the BMP signaling activation thus promoting the macrophage accumulation and lung angiogenesis. The BMP-2/CV-2 imbalance is dependent on the COX-2/PGE2 signaling pathway, and thus the effects of this imbalance can be reversed by adminstration of Parecoxib. Conclusion Our findings indicate that inhibition of COX-2 by parecoxib can improve the HPS through the repression of BMP signaling and macrophage accumulation.

Aim of review: Firstly brought up by Bedford in 1955, postoperative cognitive dysfunction (POCD) has been given increasing attention due to the increase of the elderly population. Although many researches have been conducted on POCD, the understanding of this clinical syndrome is still limited. There are currently many disputes regarding almost every aspects of POCD, even the term itself has not been included in the MeSH Database. This review aims to discuss the major disputes about POCD that hinder research consistency and provide possible perspectives for future research.Method: Recent articles and literatures about POCD were searched and reviewed. First, basic knowledge of POCD, including characteristics and incidence, risk factors, mechanisms, prevention and intervention are introduced. Second, the major obstacles of investigating POCD are discussed. Then two major problems are proposed: 1) Does the POCD in patients really start postoperatively? 2) Is POCD only related to old age? Finally, the never-ending argument regarding the role of anesthesia on POCD is discussed.Recent findings: Recent researches regarding POCD focused on the surgery-related neuroinflammation mechanism, and efforts have been made to find some biomarkers of POCD. In terms of POCD, there are many fundamental concepts and in urgent need of consensus. First, unifying the terms used among studies will benefit the communication of knowledge. Second, questions like whether POCD should be defined as a general cognitive decline that include other forms such as postoperative delirium, or they should be considered as separate unique illnesses, and whether or not young patients should be included when POCD is discussed, need to be answered. Only after answering these questions, will the study of POCD be less disputable. Third but not the least, efforts should be made trying to make "golden-standard" in regard of the testing methods of POCD both clinically and pre-clinically.Summary: Although lots of researches have been conducted on POCD, the understanding of this clinical syndrome is still very limited. There are currently many disputes regarding almost every aspect of POCD. It's time for clinicians and scholars to strike some fundamental consensus for the better investigation of POCD. How to find a way to increase the rigor of experimental design is an important question that still seeks answers. Citation: Ni An, Wei-Feng Yu. Difficulties in understanding postoperative cognitive dysfunction. J Anesth Perioper Med 2017; 4: 87-94. doi: 10.24015/JAPM.2017.0010This is an open-access article, published by Evidence Based Communications (EBC). This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium or format for any lawful purpose. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

The causes of obstructive jaundice are varied, but it is most commonly due to choledocholithiasis; benign strictures of the biliary tract; pancreaticobiliary malignancies; and metastatic disease. Surgery in patients with obstructive jaundice is generally considered to be associated with a higher incidence of complications and mortality. Therefore, it poses a considerable challenge to the anesthesiologist, surgeons, and the intensive care team. However, appropriate preoperative evaluation and optimization can greatly contribute to a favorable outcome for perioperative jaundiced patients. This article outlines the association between obstructive jaundice and perioperative management, and reviews the clinical and experimental studies that have contributed to our knowledge of the underlying pathophysiologic mechanisms. Pathophysiology caused by obstructive jaundice involving coagulopathies, infection, renal dysfunction, and other adverse events should be fully assessed and reversed preoperatively. The depressed cardiovascular effects of obstructive jaundice are worth noticing because it has complicated mechanisms and needs to be further explored. Alterations of anesthesia-related drugs induced by obstructive jaundice are varied and clinicians should be aware of the possible need for a decrease in the anesthetic dose. Recommendations concerning the perioperative management of the patients with obstructive jaundice including preoperative biliary drainage, anti-infection, nutrition support, coagulation reversal, cardiovascular evaluation, perioperative fluid therapy, and hemodynamic optimization should be taken.

Two copper (II) complexes L1Cu and L2Cu (H2L1 = 4,9-dimethyl-2,11-dioxy-5,8-diazacycldode-2,4,8,10-tetraene; H2L2 = diethyl-3,8-dimethyl-4,7-diazadeca-2,8-diene-1,10-dioat) were prepared and displayed good catalytic efficiency for the oxidations of Mandelic acid (MA), 4-hydroxymandelic acid (4-HMA) and 4-methoxymandelic acid (4-MMA) by H2O2 in aqueous solution at 35 °C. The apparent first-order rate constants kobs of oxidations of MA, 4-HMA and 4-MMA were obtained in the range of pH 2.5–4.5. It was great interesting that the complexes LCu displayed excellent catalytic ability for the selective oxidation of Mandelic acids into aromatic aldehydes (S > 98%). The active species generated by reacting copper (II) complexes LCu with H2O2 was characterized by UV–vis, electrospray ionization mass spectrometry (ESI-MS) and cyclic voltammetry (CV). The LCuI- OOH species was suggested as the possible active species. The geometric configurations of LCu and the LCuI- OOH species were calculated with Density Functional Theory (DFT) method. The LCuI- OOH species is stable and possesses relatively high oxidation potential in aqueous solution at ambient temperature. This study also provides a new insight for the degradation of lignin.

The Boussinesq equation is one of important prototypic models in nonlinear physics. Various nonlinear excitations of the Boussinesq equation have been found by many methods. However, it is very difficult to find interaction solutions among different types of nonlinear excitations. In this peper, two equivalent very simple methods, the truncated Painleve analysis and the generalized tanh function expansion approaches, are developed to find interaction solutions between solitons and any other types of Boussinesq waves.

A scheme is proposed for fabricating single wall carbon nanocones standing on metal surfaces with controlled sizes and cone angles by tailoring graphene sheets. A statistical model to examine the feasibility and stability of the cones has been developed. Combined with classical molecular dynamics simulations and ab initio calculations, the results show that cones with five different cone angles can be obtained, and the cone consisting of only 70 atoms can exist for 1011 years at room temperature.

Objective: To investigate whether emulsified isoflurane preconditioning could reduce lung injury induced by hepatic I/R in rats and its mechanism.Materials and methods: 32 pentobarbital-anesthetized Sprague-Dawley rats were equally randomized into four groups: laparotomy group (Sham group), hepatic I/R and normal saline infusion group (I/R+S group), I/R and lipid vehicle infusion (I/R+V group), or I/R and 8% emulsified isoflurane infusion (I/R+E group) at the rate of 8 ml·kg-1·h-1 for 30 min. Blood supply of the hepatic artery and portal vein to the left and the median liver lobes was occluded for 90 min after 30-min washout time. Reperfusion was allowed to proceed for 4 h before sacrifice of the animals. Lung injury was observed histologically. Neutrophil infiltration and TNF-α concentration in serum and lung were measured. Changes of wet-to-dry weight ratios in lung tissue, ICAM-1 expression and NF-κB activity in lung after hepatic I/R were determined.Results: Compared with I/R+S or I/R+V group, emulsified isoflurane preconditioning reduced hepatic I/R-induced lung histologic injury and inhibited the increase of myeloperoxidase (MPO) activity in the lung tissue markedly (5.5±1.37 and 5.22±1.33 vs 3.81±1.62 U/g, Pvs 72.44±17.28 pg/ml, Pvs 292.62±74.56 pg/ml, Pvs 0.62±0.21, Pvs 4.01±0.86, PConclusions: Emulsified isoflurane preconditioning markedly attenuated hepatic I/R-induced lung injury in rats, which may be hopefully applied to the clinical treatment of organ injury caused by hepatic surgery, transplantation or hemorrhagic shock.

One characteristic of Chinese rivers is their high silt contents. The Yellow River is unique for its excessive suspended sediment of the world river. Its annual sediment discharge is 116 million tons and its average sediment concentration is about 37.5 kg/m. Hydropower stations on the Yellow River are all facing the erosion problems on hydraulic turbines. The main harms of hydraulic turbine erosion are as follows: shorten repair cycle time and increase repair workload, less efficient plant operation, high maintenance costs and high potential safety risks. For example, Sanmenxia Hydropower Station, which is in the midstream of the Yellow River, has multi-year average sediment concentration 37.5kg/m, the maximum sediment 91lkg/m. Its hydraulic turbine is Kaplan turbine. Because of high sediment content, its turbine erosion is very serious. After running 3630 hours, the most of the 3mm stainless steel plate welded in the back of blades has come off in 4# turbine. The gap size between the blades and the middle ring already was extended from 7～8mm to 20mm and the weight loss of the blades was 780kg. After running 7595 hours, the base material of the blade back was alveolate and the gap size was extended to 40～50mm. After 31000 hours, the triangle of the blade head has been rubbed off and the gap size was extended to 120mm. The turbine was almost scrapped. To reduce or eliminate the silt erosion, an effective way is to use surface coating to the through-flow parts of the hydraulic turbine.

Background: Neuropathic pain is characterized by hyperalgesia, allodynia and spontaneous pain. It often occurs as a result of injury to peripheral nerves, dorsal root ganglions (DRG), spinal cord, or brain. Recent studies have suggested that Toll-like receptor 4 (TLR4) might play a role in neuropathic pain. Methodology/Principal Findings: In this study, we investigated the role of TLR4 in a rat chronic constriction injury (CCI) model and explored the feasibility of treating neuropathic pain by inhibiting TLR4. Our results demonstrated that intrathecal siRNA-mediated suppression of TLR4 attenuated CCI-induced mechanical allodynia and thermal hyperalgesia through inhibiting the activation of NF-κB p65 and production of proinflammatory cytokines (e.g., TNF-α and IL-1β). Conclusions/Significance: These findings suggest that suppression of TLR4 mediated by intrathecally administered siRNA may be a new strategy for the treatment of neuropathic pain.

Objective To construct the recombinant adenovirus expressing small RNA of rats caspase-3 and observe the down-regulation effect of caspase-3 in neurons induced by lipopolysaccharide(LPS) in vitro. Methods pShuttleH1-siCas3 containing Oligo DNA of the targeting sequences and pEGFPC1-Cas3 containing caspase-3 and EGFP sequences were constructed respectively. pShuttleH1-siCas3 and pEGFPC1-Cas3 were co-transfected to the 293 cells by liposomes to determine interfering efficacy by flow cytometry. pShuttleH1-siCas3 was linearized and transformed into E. coli BJ5183 cells containing backbone plasmid pAdEasy-1. The recombinant plasmid was transfected into 293 cells to package the adenovirus Ad-siCas3. The titers of adenovirus were determined by the specific 50% tissue culture infection dosage method. After virus infected the cultured hippocampus neurons, LPS-induced apoptosis and caspase-3 mRNA expression were observed. Results It was identified that the sequence of target gene was correctly inserted into the genome of virus. The expression of green fluorescence protein was reduced by pShuttleH1-siCas3 in 293 cells. The titer of recombinant adenovirus was 1.06×1010 pfu/ml. After virus infection, caspase-3 mRNA was greatly reduced and neurons apoptosis was suppressed. Conclusion The recombinant adenovirus expressing rats caspase-3 siRNA were successfully constructed, which may probably be further used in pain therapy by its anti-apoptosis effect.

Electrochemical deposition method was employed to prepare CN x thin film from methanol-urea solution, and it was shown that adding a little acetic acid in the solution significantly affected the deposition process. After optimizing the experiment conditions, we obtained polycrystalline grains with sizes of about 3–7 μm on the faces of single crystal silicon. X-ray diffraction spectrua indicate that the grains are mainly composed of cubic phase mixed with a small amount of β and α phases.

The signal peptide is a critical component in the secretory expression of protein in eukaryotic cells. It has been verified that the signal peptide of mouse nerve growth factor could mediate the secretory expression of beta-endorphin in cultured non-neuronal cells. Although there is a counterpart of nerve growth factor in human genome, no research about the signal sequence from human genome has been reported. The function of mediating secretory expression is affected by many factors. We assumed that the counterpart from human genome could function as the signal peptide from mouse nerve growth factor does and these two signal sequences had different efficiency in mediating secretory expression of beta-endorphin, but we could not figure out which one had a better function. To validate our hypothesis and give an answer to the question, we constructed two eukaryotic vectors, pcDNA3.1-hEP and pcDNA3.1-mEP, containing human and mouse signal sequences in fusion genes, respectively. RT-PCR showed that the constructed fusion genes were expressed in NIH3T3 cells. We also found that the detected beta-endorphin by the immunofluorescent technique was mainly in the cytoplasm of NIH3T3 cells. The concentration of beta-endorphin in the culture medium by RIA is 280.33 ± 24.16 (pg/ml) and 191.04 ± 7.96 (pg/ml) from pcDNA3.1-hEP and pcDNA3.1-mEP, respectively, and there was a significant statistical difference between them (P < 0.05). A difference existed between them and that from blank vector individually (P < 0.01). These findings suggest that our constructed fusion gene containing the signal sequence of human nerve growth factor can be secretorily expressed and the efficiency of the signal peptide from human nerve growth factor is higher than that of mouse signal peptide.

Objective To explore the effect of cellular immunity in halothane hepatitis. Methods Hepatotoxicity model was established by exposing male Hartley guinea pigs to 1% halothane via inspiration for 4 h each time for 1 or 3 times within a 42-day interval. Then their hepatocytes and lymphocytes were collected and divided into 2 parts for different cultures. Hepatocytes were cultivated with or without 1% halothane for 4 h and lymphocytes were cultivated with or without 12.5 μg/ml trifluoroacetylated guinea pig serum albumin (TFA-GSA). Then the 2 kinds of hepatocytes were co-cultivated with lymphocytes (1:100) with or without TFA-GSA induction respectively and the supernatant fluid was taken after 24, 48 and 72 h to determine the concentration of alanine aminotransferase (ALT). The halothane cultivated hepatocytes were co-cultivated with various proportion of TFA-GSA antigen induced lymphocytes and ALT was determined after 48 h to determine the proper proportion of hepatocytes and lymphocyte. Results Lymphocytes of 3 times halothane induced guinea pigs caused a significant increase of ALT in hepatocytes with or without halothane induction. But the lymphocytes of 1 time halothane induced guinea pigs only caused a significant increase of ALT in hepatocytes with induction of halothane. The increase of ALT was only seen after 48-and 72-hour co-culture. The proper proportion of hepatocytes and lymphocytes was 1:100 for lymphocytes cytotoxicity. Conclusion Lymphocytes is sensitized after inhalation of halothane and generates cytotoxicity to hepatocytes. The immune response of lymphocytes to hepatocytes will be enhanced by repeated inhalation of halothane. The cellular immunity may be one of the mechanisms of halothane induced hepatotoxicity.