Objective To predict the pharmacological effect and targets of main chemical components of Lindera aggregata, and construct the multi-target network. Methods The potential targets and pathways of linderene acetate, isocembrol, laurolitsine, β-humulene, chamazulene, laurotetanine, and lindestrenolide, selected as the representative compounds of oils, alkaloids, and furan sesquiterpene lactones from Linderae Radix, were predicted by methods of network pharmacology. The pharmacodynamic effects of main chemical constituents of L. aggregata was analyzed by data integration. Results The in silico prediction results showed that seven compounds of L. aggregata affected 20 related pathways through 40 potential targets. The pathways were involved in several links including inflammatory, analgesic, gastrointestinal movement regulation, anti-oxidation, antitumor, liver injury protection, and immunoregulation. The various components showed common targets, pathways, and pharmacodynamic effects and had different emphases. Conclusion The pathways related to L. aggregata oils, alkaloids, and furan sesquiterpene lactones were connected by the common targets, showing the synergistic effect of different compounds by acting on multi-targets and multi-pathways. This study provides references for systematic exploration on the pharmacological actions and mechanisms of L. aggregata.

Objective To investigate the variation of morbidity and clinical features of Henoch-Seh(o)nlein purpura (HSP) in childhood in recent years.Methods The clinical data of 901 cases with HSP admitted to our hospital from January 1,1995 to December 31,2005 were retrospectively analyzed.The constitute rate of admission,the initial clinical presentations,specific manifestations such as multi-system 23/2165(1.06%),29/2098(1.38%),24/1973(1.22%),39/2008(1.94%),54/2433(2.22%),86/2611(3.29%),94/2724(3.45%),99/3014(3;28%),138/2900(4.76%),143/3177(4.50%)and 172/3500(4.91%),resp-sixty-five of 901 HSP children (1 8.3%) had no palpable purpura at onset, 90 cases initially manifested as abdominal pain and (or) gastrointestinal bleeding,14 of them was diagnosed by gastroendoscopy which demonstrated mucous membrane vasculitis.Sixty-three cases manifested as arthritis/arthralgias,6 cases presented as renal involvement,1 case with neurological symptoms and 5 cases with other symptoms at their pancreatic involvement was present in 3 cases,cardiac involvement in 47 Cases and one case had lung hemorrhage.Conclusion The morbidity of HSP has increased in recent years.The diagnosis in patients who do not have palpable purpura at onset and patients who present with the cerebral,pulmonary,cardiac and pancreatic involvement as the initial manifestations is difficult.Special attention should be paid to this group of patients.Gastrointestinal endoscope is valuable in diagnosing HSP in patients whose initial symptoms are abdominal pain and (or) gastrointestinal bleeding.

Objective To investigate the role and intracellular signal transduction mechanism in the injury of renal tubular cells induced by postasphyxial-serum in neonate.Methods Human renal proximal tubular cell(HK-2 cell) was used as target cell. The experiment was designed as:control group, asphyxia group ,and pyrrolidine dithiocarbamate (PDTC)blocking group. The attacking concentration of serum was 20%, and the apoptosis rate of HK-2 cells was detected by flow cytometer.Results Compared with controls[(13.3?1.70)%],after being stimulated with postasphyxial-serum, the apoptosis rate of HK-2 cells of asphyxia group [(46.73?3.68)%] and PDTC blocking group [(31.19?2.79)%]were significantly increased(P

Objective To investigate the role of postasphyxial-serum of neonate in inducing injury of human renal proximal tubular cells(HK-2 cells).Methods HK-2 cells were used as target cell.The neonatal different concentration postasphyxial-serum of 1,3,7 days after asphyxia were used as attacking means.The experimental groups were divided into 15 groups:the 2.5%,5.0%,10.0%,(20.0%) attacking concertration groups of 1,3,7 day after asphyxia and control group of each concertration.The culture medium and concertration of the control group and the experimental groups were the same.The changes of morphology were observed under inverted microscope,the cell viability was measured by 3-(4,5-dimethyl-2-thiazoly1)-2,5-diphenyl-2H-tetrazolium bromide(MTT) method and the leakage rate of lactate dehydrogenase(LDH) was determined by biochemical methods.Results Compared with control group,the changes in morphology of HK-2 were most serious and obvious,the cell viability were obviously decreased(all P

Objective To investigate the role of erythropoietin(EPO)in relieving the injury of human renal tubular cells (HK-2) induced by postasphyxial-serum of neonates.Methods Human renal proximal tubular cell(HK-2) was used as the target cell.The experiment was designed as control group, asphyxia group,and group of pretreatment with EPO. The attacking concentration of serum was 200 mL/L,then the changes of morphology were observed under inverted microscope,and the cell viability was measured by 3-(4,5-dimethy lthiazcl-2-yl)-2,5-diphenyl-tetazolium bromide(MTT) methods,and the leakage rate of lactate dehydrogenase(LDH) was determined by biochemical methods.Results Compared with control group,the change in morphology of HK-2 was most serious and obvious,and the leakage rate of LDH increased significantly,and the cell viability decreased obviously in asphyxia group.But compared with asphyxia group,the change in morphology of HK-2 was obviously improved,and the leakage rate of LDH decreased and the cell viability increased in group of pretreatment with EPO in a dose-dependent manner except the group of 1 IU/mL.Conclusion EPO can play the role in relieving the injury of renal tubular cells induced by postasphyxial-serum in neonates.

Objective To explore the effect of postasphyxial-serum in neonate on the expressions of Bcl-2-antagonist of cell death(BAD)and Bcl-2-associated X protein(BAX)in renal tubular cells(HK-2).Methods HK-2 cells were used as target cells.The experiment were divided into control group,asphyxia group and pyrrolodine dithiocarbamate(PDTC)blocking group.Control group:DMEM culture fluid was not contained asphyxia blood serum in every group;asphxia group:DMEM culture fluid contained 20 mL/L asphyxia blood serum in every group;PDTC blocking group:DMEM culture fluid contained 20 mL/L asphyxia blood serum and 40 ?mol/L PDTC in every group.The expressions of both BAD and BAX on cytoplast were detected by immunohistochemical method.Results Calculated Points according to HSCORE,compared with controls group[(1.97?0.26)and(1.77?0.11)],after stimulated with postasphyxial-serum,the expressions of both BAD and BAX of HK-2 cells of asphyxia group[(2.73?0.20)and(2.44?0.13)] and PDTC blocking group[(2.38?0.13)and(2.17?0.08)] significantly increased[F(BAD)=28.61,F(BAX)=15.51 Pa

Objective To explore the effect of postasphyxial-serum in neonate on expression of serine protease Omi/HtrA2 in renal tubular cells(HK-2).Methods Human renal proximal tubular cell line HK-2 cell was used as target cell.The cultural cells in orifice were divided into control group and asphyxia-serum attacking group.Blood was cowected from asphyxia newborns by means of femoral venous puncture,then the serum was garthered,anticoagulated by liquemie,3 000 r/min centrifuged 20 min,abstracted serum,thermostatic waterbathed the serum at 56 ℃,so that to inactivate addiment,filtered germ by micropore filte,the attacking concentrtion of serum was 200 mL/L,the cells of the asphyxia-serum attacking group were attacked by asphyxia-serum,and the cells of control group were cultivated with normal nutritive medium when the cells was needed.After 24 hours,the cells were tixed,then the expression of Omi/HtrA2 in cytoplast was detected by the use of immunohistochemical method.Results Omi/HtrA2 was inaurate or yellow brown and localized to the cytoplast.The rate of the cell expressed Omi/HtrA2 was(9.0?2.5)% in control group,after stimulated with postasphyxial-serum,in asphyxia group the rate of the cell expressed Omi/HtrA2 was(25.15?3.5)%,there was significant difference between 2 groups(t=-15.322 P

OBJECTIVETo investigate the association of p53 codon 72 polymorphism with susceptibility to esophageal cancer and lung cancer in the northern Chinese population.

METHODSp53 codon 72 genotyping was performed by amplifying DNA fragments with sequence specific primers among 173 patients with esophageal squamous cell carcinoma, 98 with non-small cell lung carcinoma as well as 136 healthy controls.

RESULTSNo significant difference of p53 allelotype and genotype distribution was observed between esophageal cancer and lung cancer patients. The Pro allele frequency was significantly higher among esophageal cancer and lung cancer patients than among healthy controls (P value was 0.024 and 0.027 respectively). There were no significant differences in Pro/Arg and Arg/Arg genotype frequency among cancer patients and healthy controls (P > 0.05). However, the Pro/Pro genotype frequency was significantly higher among esophageal cancer and lung cancer patients than among healthy controls (P value was 0.041 and 0.026 respectively). The risk of Pro homozygotes for both esophageal cancer and lung cancer was about 2 times against Arg homozygotes with adjusted odds ratio of 2.12 (95% CI = 1.13 - 4.01) and 2.30 (95% CI = 1.13 - 4.93), respectively. There was no interaction between p53 Pro/Pro genotype and smoking status to the risk for esophageal cancer and lung cancer.

CONCLUSIONIn the northern Chinese population, p53 Pro/Pro genotype is an independent risk factor for both esophageal cancer and lung cancer. The possible common genetic basis of the development of these two cancers is suggested by this study.

Alleles ; Asian Continental Ancestry Group ; Carcinoma, Non-Small-Cell Lung ; ethnology ; genetics ; Carcinoma, Squamous Cell ; ethnology ; genetics ; China ; Codon ; genetics ; Esophageal Neoplasms ; ethnology ; genetics ; Genetic Predisposition to Disease ; Genotype ; Humans ; Lung Neoplasms ; ethnology ; genetics ; Odds Ratio ; Polymorphism, Genetic ; Tumor Suppressor Protein p53 ; genetics

OBJECTIVETo study the role of serum from asphyxiated neonates in the inducement of human renal proximal tubular epithelial cells (HK-2) adhesion to neutrophils and possible mechanisms.

METHODSHK-2 cells were cultured randomly with 20% serum from neonates (1, 3, and 7 days after asphyxia), pyrrolidine dithiocarbamate (PDTC) or placebo. The activity of myeloperoxidase (MPO), an indicator of adhesion ability of HK-2 cells to neutrophils in suspensions, was detected by the biochemistry assay. Intercellular adhesion molecule-1 (ICAM-1) and nuclear factor-kappaB (NF-kappaB) of HK-2 cells were examined with the immunohistochemical staining.

RESULTSThe expression of MPO in the post-asphyxial 1-day serum treatment group were significantly higher than that in the PDTC treatment and the control groups as well as the post-asphyxial 3 and 7-day serum treatment groups (P<0.01). The expression of ICAM-1 and NF-kappaB in the post-asphyxial 1-day serum treatment group was also significantly higher than that in the other groups (P<0.01).

CONCLUSIONSSerum from asphyxiated neonates can induce HK-2 cell adhesion to neutrophils, possibly through activating NF-kappaB and increasing the synthesis and expression of ICAM-1 on the surface of renal tubular epithelial cells.

Asphyxia Neonatorum ; blood ; complications ; Cell Adhesion ; Cells, Cultured ; Humans ; Infant, Newborn ; Intercellular Adhesion Molecule-1 ; analysis ; biosynthesis ; Kidney Tubules ; pathology ; NF-kappa B ; analysis ; metabolism ; Neutrophils ; physiology

OBJECTIVETo investigate whether human L02 hepatocytes could survive after implanting them into normal, immunocompetent rats.

METHODSHuman L02 hepatocytes were injected through the uterine walls into the intraperitoneal cavities of fetal Sprague-Dawley rats to induce immune tolerance to human L02 hepatocytes. Human L02 hepatocytes stained with DiI were implanted into the spleens of the 2-week old rats. Immuno-fluorescent staining, SP immunohistochemistry, and DiI staining were used to detect human albumin and specific proliferating cell nuclear antigen (PCNA) in the rat livers. The distribution of human L02 hepatocytes was observed under the fluorescent microscope.

RESULTSDynamic distribution of human L02 hepatocytes in the rat livers was observed from the 1st to the 10th week after the implantation. Human albumin was detected at 2, 4, 6 and 8 weeks, and at the 4th week it had the highest level. Specific human PCNA was detected in the rat livers from the 2nd to the 6th week after implantation. The PCNA positive cells were most abundant at the 4th week.

CONCLUSIONHuman L02 hepatocytes can survive and proliferate for 10 weeks after implanting them into genetically normal immunocompetent rats.

Animals ; Cell Transplantation ; Cells, Cultured ; Disease Models, Animal ; Female ; Graft Survival ; Hepatocytes ; cytology ; Humans ; Pregnancy ; Rats ; Rats, Sprague-Dawley