Objective To review the important points in the preoperative assessment and the surgical technique in precise hepatic pedicle dissection in anatomical hepatic segmentectomy.Methods 104 patients who underwent anatomical hepatic segmentectomy were divided into two groups according to the different surgical approaches adopted in a prospective and non-randomized manner:the precise hepatic pedicle dissection group (the precise group,n=44) and the conventional hepatectomy group (the conventional group,n=60).The perioperative and follow-up data were analyzed.Patients who had primary liver cancer,including hepatocellular carcinoma and intrahepatic cholangiocellular carcinoma,were analyzed separately.Results (1) There was no perioperative death in the two groups.There was no significant differences in blood loss and transfusion between the 2 groups of patients (P=0.069,0.208; t=1.844,1.266).There was a significantly higher rate of vascular inflow occlusion (P=0.001).There were significantly longer periods of vascular inflow occlusion and operative time (P=0.001,0.001; t=3.849,3.574) in the precise group.There was no significant difference in postoperative complications (P=0.988) and the duration of postoperative hospital stay (P=0.509;t=0.662) between the two groups.(2) In patients with primary liver cancer,there were no significant differences between the precise group (n=29) and the conventional group (n=41) in tumor margin positivity,vascular invasion and pathological staging (P=0.985,0.630,0.769).(3) All patients were followed up for two years.When compared with the conventional group,the disease-free survival (P=0.012),overall survival (P =0.006),and median survival (16.5 ± 4.5mo vs.7.8 ± 3.8mo)were significantly longer in the precise group.Conclusion Precise hepatic pedicle dissection had the same safety and efficacy as conventional method in partial hepatectomy.For primary liver cancer,precise hepatic pedicle dissection had better survival compared to the conventional method when the surgical margin was negative.

Objective: To study the microbial transformation of ursolic acid using Penicillium melinii. Methods: Ursolic acid was put into the fluid medium inoculated with fungius (P. melinii AS3.4774) and cultured in the shaker at 28 °C and 140 r/min for 5 d. The crude extract was separated by chromatography. The structures of transformed products were elucidated based on the extentive NMR studies. Results: Ursolic acid was transformed by P. melinii AS3.4774 and three major derivatives were isolated and elucidated. They were 3-carbonyl ursolic acid, ursolic acid-28-O-β-D-glucopyranosyl ester, and ursolic acid-3-O-β-D-glucopyranoside. Conclusion: It is the first time that the three major derivatives could be microbial synthesized from ursolic acid by P. melinii AS3.4774.

OBJECTIVETo explore the effect of Tongfu Jinghua Decoction (TJD) on hemodynamics and tissue oxygen metabolism in patients with post-traumatic sepsis shock.

METHODSTotally 60 patients were randomly assigned to the treatment group and the control group, 30 in each group. Patients in the treatment group took TJD or were administered with TJD by nasal feeding in combined with conventional Western medical treatment, while patients in the control group only received conventional Western medical treatment. Changes of each index in hemodynamics and tissue oxygen metabolism were observed before treatment, and at 6, 12, 24, and 48 h after treatment.

RESULTSCompared with before treatment in the same group, hemodynamic changes were significantly improved at each time point in the two groups. All indices of tissue oxygen metabolism at each time point of the two groups were significantly improved, except changes of O2 extraction ratio (ER) after treatment in the control group (P < 0.05, P < 0.01). Compared with the control group in the same period, heart rate (HR), systemic vascular resist- ance (SVR), and cardiac output (CO) were significantly improved with statistical difference (P < 0.05, P < 0.01). Mean arterial pressure (MAP), central venous pressure (CVP), and cardiac index (CI) were significantly improved at 6, 12, and 24 h after treatment with statistical difference (P < 0.05, P < 0.01). Each index of tissue oxygen metabolism in the treatment group were all improved at each time point with statistical difference (P < 0.05, P < 0.01).

CONCLUSIONTJD combined with conventional Western medical treatment could quickly improve hemodynamics and tissue oxygen metabolism disorder in patients with septic shock, and its curative effect was superior to that of conventional Western medical treatment alone.

Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Heart Rate ; Hemodynamics ; drug effects ; Humans ; Oxygen ; metabolism ; Sepsis ; Shock, Septic ; drug therapy ; metabolism

Blood Chemical Analysis ; methods ; Humans ; Metronidazole ; blood ; Spectrophotometry, Ultraviolet

OBJECTIVETo observe the protection of Qingyuan Shenghua Decoction (QSD) on multiple organs of sepsis patients after bone trauma, and to preliminarily explore its mechanism.

METHODSTotally 60 sepsis patients after bone trauma were randomly assigned to the treatment group and the control group according to random digit table, 30 in each group. All patients received routine Western medical treatment. Patients in the treatment group additionally took QSD or were nasally fed with QSD, one dose per day for 1 week. Changes of WBC, oxygenation index (PaO2/FiO2), serum creatinine (SCr), total bilirubin (TBIL), aspartate aminotransferase (AST), fibrinogen (FIB), D-dimer (DD), activated partial thromboplastin time (APTT), pro-calcitonin (PCT), C-reactive protein (CRP), heart rate (HR), mean arterial pressure (MAP), intra-abdominal pressure, scores for Acute Physiology and Chronic Health Evaluation II (APACHE II), sequential organ failure assessment (SOFA) scores were observed before treatment and on day 1, 3 and 7 after treatment.

RESULTSCompared with the control group at the same time point, MAP increased at post-treatment day 1 and 3; CRP, APTT, HR, SCr, TBIL, AST, intra-abdominal pressure at post-treatment day 3 obviously decreased in the treatment group (P < 0.05, P < 0.01). WBC, SOFA scores, PCT, CRP, APACHE II, APTT, D-D, HR, SCr, TBIL, AST and intra-abdominal pressure significantly decreased; FIB, MAP and PaO2/FiO2 obviously increased at post-treatment day 7 (P < 0.05, P < 0.01).

CONCLUSIONQSD had good protective effect on multiple organ function in sepsis patients after bone trauma, and its mechanism might be related with effectively clearing endotoxin, alleviating inflammatory reactions, and fighting against coagulation dysfunction.

APACHE ; Blood Coagulation ; Bone Diseases ; complications ; C-Reactive Protein ; metabolism ; Calcitonin ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Fibrin Fibrinogen Degradation Products ; metabolism ; Humans ; Inflammation ; Partial Thromboplastin Time ; Protein Precursors ; metabolism ; Sepsis ; drug therapy ; etiology

OBJECTIVETo explore the effects of naloxone on the expression of c-kit receptor (c-kit R) and its ligand stem cell factor (SCF) in human embryo neuronal hypoxic injury.

METHODSSerum-free cerebral cortical cultures prepared from embryonic human brains were deprived of both oxygen and glucose which would set up an environment more likely with that of in vivo ischemic injury. Neurons in 24-well culture plates were randomly divided into four groups: control group, hypoxia group, naloxone 0.5 microg/ml group and naloxone 10 microg/ml group. MTT assay and biological analysis were performed to study the cell death and the changes of extracellular concentrations of lactate dehydrogenase (LDH) after combined oxygen-glucose deprivation. Neurons in 25 ml culture flasks were also randomly allocated into four groups as previously described. Intracellular total RNA were extracted at different time points: pre-hypoxia, immediately after hypoxia, and 3, 6, 12, and 24 hours after reoxygenation. The changes of SCF/c-kit R mRNA expression in hypoxic neurons treated with different concentrations of naloxone pre and post oxygen-glucose deprivation were determined with RT-PCR.

RESULTSThe cell vitality detected by MTT assay decreased significantly in hypoxia group and naloxone 0.5 microg/ml group when compared with control group (P<0.01), while no significant difference was found between naloxone 0.5 microg/ml group and hypoxia group or between naloxone 10 microg/ml group and control group. Extracellular concentration of LDH significantly increased in hypoxia group (P<0.05), while no difference was found between naloxone 0.5 microg/ml group and control group, between naloxone 0.5 microg/ml and hypoxia group, or between naloxone 10 microg/ml and control group (all P>0.05). Immediately after oxygen-glucose deprivation, the expression of SCF/c-kit R mRNA increased significantly (P<0.01). Among those the expression of SCF presented a distribution of double-peak value within 24 hours. After treated with different concentrations of naloxone, the peak value of each group were delayed to appear and went down with the increasing of naloxone concentration. The peak values in all treated groups were significantly different from that in control group (P<0.01).

CONCLUSIONSThe expression of SCF/c-kit R mRNA increases at the early stage after combined oxygen-glucose deprivation. Naloxone 0.5 microg/ml can attenuate cell injuries and regulate the expression of SCF/c-kit R. Naloxone may protect neurons by modulating the expressions of some cytokines.

Cell Hypoxia ; drug effects ; physiology ; Cells, Cultured ; Cerebral Cortex ; cytology ; Humans ; Naloxone ; pharmacology ; Neurons ; drug effects ; metabolism ; pathology ; Proto-Oncogene Proteins c-kit ; genetics ; metabolism ; RNA, Messenger ; genetics ; Stem Cell Factor ; genetics ; metabolism

Coal ; Dust ; analysis ; Gases ; adverse effects ; Humans ; Male ; Middle Aged ; Occupational Exposure ; analysis ; Pulmonary Alveolar Proteinosis ; etiology

OBJECTIVETo investigate the effects of naloxone on glutamate release in combined oxygen-glucose deprivation of primary cultured human embryo neurons.

METHODSThe primary cultured embryonic human cortical neurons were demonstrated by immunocytochemical stain of neural filament (NF). The neurons were randomly allocated into control group, hypoxic group, and experimental group. The experimental group was further divided into three subgroups pretreated with different concentrations of naloxone (0.25, 5, 10 microg/ml). The neurons of hypoxic group and experimental group were deprived both oxygen and glucose for 1 hours followed by 24 hours of reoxygenation. Meanwhile, we used 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, high performance liquid chromatography (HPLC), and biological analysis to study the survival rate of neurons and the changes of extracellular glutamate and lactate dehydrogenase (LDH) levels after 24 hours of reoxygenation.

RESULTSOne hour of oxygen-glucose deprivation followed by 24 hours of reoxygenation was associated with a large increase in extracellular LDH and glutamate and a significant decrease of cell vitality (P < 0.01). Naloxone exerted a concentration-dependent protection against neuronal injury provoked by combined oxygen-glucose deprivation. After reoxygenation, the extracellular concentrations of glutamate gradually decreased (P < 0.05, P < 0.01, respectively) and cell vitality increased (P < 0.01) with increase of the concentration of naloxone compared with control group. All of them returned to control level when naloxone was up to 10 microg/ml (P > 0.05).

CONCLUSIONNaloxone protects neurons from hypoxic injury by inhibiting the release of glutamate and therefore alleviating the exciting toxicity.

Cell Hypoxia ; Cells, Cultured ; Cerebral Cortex ; cytology ; Embryo, Mammalian ; Glutamic Acid ; metabolism ; Humans ; Naloxone ; pharmacology ; Neurons ; drug effects ; metabolism ; Neuroprotective Agents ; pharmacology

OBJECTIVETo determine the effect of neostigmine on antagonizing atracurium-induced neuromuscular blockage with sulfate magnesium pretreatment.

METHODSForty patients who undertook elective gynecologic laparoscopic examinations and treatments under general anesthesia were randomized into four groups (group A, B, C, and D, group A paired with group C, and group B paired with group D). Before induction of general anesthesia, patients in group A and group C received MgSO4 30 mg/kg in saline intravenously within 5 min, while patients in group B and group D received the same volume of saline. Anesthesia was induced with fentanyl and propofol; subsequently tracheal intubation was performed with 0.5 mg/kg atracurium after stabilization of the electromyography recording, and neostigmine (0.02 mg/kg) and atropine (0.01 mg/kg) were infused in group C and group D when neuromuscular recovery (T1/T(C)) reached 10%. T1/T(C) changes after neostigmine infusion as well as haemodynamic changes and other responses during induction and neostigmine and atropine infusion were recorded.

RESULTSThe neuromuscular recovery speed had no significant difference between group A and group B after the neuromuscular recovery reached 10%, but it was lower in group C than in group D (P < 0.05). Significant difference existed between group AC and group BD (P < 0.05). No haemodynamic changes and other responses were found during induction and neostigmine and atropine infusion.

CONCLUSIONNeostigmine-induced neuromuscular recovery can be attenuated in patients pretreated with magnesium sulfate.

Adolescent ; Adult ; Anesthesia, General ; Atracurium ; antagonists & inhibitors ; Cholinesterase Inhibitors ; pharmacology ; Female ; Humans ; Laparoscopy ; Magnesium Sulfate ; pharmacology ; Middle Aged ; Neostigmine ; pharmacology ; Neuromuscular Blockade ; Neuromuscular Nondepolarizing Agents ; antagonists & inhibitors

OBJECTIVETo promote stem cells differentiation into neurons and enhance neuromotor function after brain injury through brain-derived neurotrophic factor (BDNF) induction.

METHODSRecombinant adenovirus vector was applied to the transfection of BDNF into human-derived umbilical cord mesenchymal stem cells (UCMSCs). Enzyme linked immunosorbent assay (ELISA) was used to determine the secretion phase of BDNF. The brain injury model of athymic mice induced by hydraulic pressure percussion was established for transplantation of stem cells into the edge of injury site. Nerve function scores were obtained, and the expression level of transfected and non-transfected BDNF, proportion of neuron specific enolase (NSE) and glial fibrillary acidic protein (GFAP), and the number of apoptosis cells were compared respectively.

RESULTSThe BDNF expression achieved its stabilization at a high level 72 hours after gene transfection. The mouse obtained a better score of nerve function, and the proportion of the NSE-positive cells increased significantly (P<0.05), but GFAP-positive cells decreased in BDNF-UCMSCs group compared with the other two groups (P<0.05). At the site of high expression of BDNF, the number of apoptosis cells decreased markedly.

CONCLUSIONBDNF gene can promote the differentiation of the stem cells into neurons rather than glial cells, and enhance neuromotor function after brain injury.

Adenoviridae ; genetics ; Animals ; Apoptosis ; Brain Injuries ; physiopathology ; therapy ; Brain-Derived Neurotrophic Factor ; analysis ; genetics ; Cell Differentiation ; Glial Fibrillary Acidic Protein ; Humans ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stromal Cells ; cytology ; Mice ; Nerve Tissue Proteins ; analysis ; Neurons ; cytology ; Phosphopyruvate Hydratase ; analysis ; Transfection