Objective To observe the effect of ginsenoside Rb1,the most abundant ginsenoside in ginseng root,on differentiation and lipolysis of 3T3-L1 cells and to explore its anti-diabetic mechanism.Methods 3T3-L1 preadipoeytes were induced under standard differentiation process in the presence of 0.1,1,10,100?mol/L ginsenoside Rb_1 for 6 days.Oil red O staining,measurement of triglyceride contents and glucose uptake assay were performed.The expressions of mRNA and protein of PPAR?2,C/EBP?,ap2,glucose transporter (Glut) 1,and Glut4 were analysed with quantitative real time-PCR and Western blot.The binding affinity of Rb_1 to PPAR?-LBD was evaluated by Surface Plasmon Resonance (SPR).Lipolysis of adipocytes was examined by the measurement of glycerol released from adipoeytes treated with Rb_1 for 1 h.Results Ginsenoside Rb_1 facilitated differentiation of 3T3-L1 preadipoeytes in a dose-depondent manner.10?mol/L ginsenoside Rb_1 increased lipid accumulation by about 56%.Treatment of differentiating adipocytes with 10?mol/L ginsenoside Rb_1 increased the expressions of PPAR?2 and C/EBP?mRNA and protein,as well as mRNA expression of ap2,one of their target genes.After treatment of differentiating adipoeytes with Rb_1,basal and insulin-mediated glucose transport augmented significantly accompanied by up-regulations of mRNA and protein level of Glut4,but not of Glutl.SPR showed Rb_1 could bind to PPAR?which suggested Rb_1 was a ligand of PPAR?.Ginsenoside Rb_1 inhibited basal lipolysis in adipoeytos in a dose-dependent manner.However,it did not affect isoproterenol-stimulated lipolysis.Conclusion As a PPAR?ligand,ginsenoside Rb_1 promotes adipogenesis,inhibitas basal lipolysis and inereasos basal and insulin-mediated glucose transport in cultured adipoeytes.Therefore,anti-diabetic and insulin-sensitizing activity of ginsenosides is,at least in part,involved in the enhancing effect on PPAR?2 and C/EBP?expressions,hence promoting adipogenesis and glucose uptake,and inhibiting lipolysis in adipocytes.

OBJECTIVETo reconstruct a penis with sensation and erectile function maintained by corpora cavernosa lengthening and skin flap transferring in the penis defect cases.

METHODSThe procedure was based on the use of releasing the suspensory ligaments and part of crus, various flaps were designed as coverage material. Penis residual stump was advanced to anterior portion of the newly reconstruction penile body as "glans".

RESULTS40 patients with penis defect have been operated by the above methods. In the cases, length of the penis varied from 0.5-4.0 cm in the flaccid, 1.5-5.0 cm in erect state before operation. And after operation, it turned to 5.0-8.5 cm in the flaccid, 7.0-12.5 cm in erect state. Most of the patients recovered gross tactile sensation and had satisfactory erectile function.

CONCLUSIONWith this method, the reconstructed penis tends to have a better appearance and function. It's a more optimal method compared with the conventional operation.

Adult ; Humans ; Male ; Penile Erection ; Penis ; injuries ; innervation ; surgery ; Reconstructive Surgical Procedures ; methods ; Sensation

OBJECTIVE: To investigate the effect of lidocaine on LPS induced apoptosis of cultured adult rat alveolar Type II (AT-II) cells. METHODS: Cultured cells were exposed to LPS and lidocaine for 24 hours. Apoptosis and necrosis rates of cells were detected by flow cytometry and electron microscope. The activity of lactic dehydrogenase (LDH) was analyzed by using LDH kits. RESULTS: LPS induced the AT-II cell injuries by increasing not only the necrosis and apoptosis rates but also the LDH release of cultured AT-II in vitro. Lidocaine decreased the necrosis and apoptosis rates of AT-II cells. CONCLUSION Lidocaine can directly inhibit the apoptosis and necrosis induced by LPS in cultured AT-II cells.
Animals ; Apoptosis ; drug effects ; Cells, Cultured ; Epithelial Cells ; pathology ; Flow Cytometry ; Lactate Dehydrogenases ; metabolism ; Lidocaine ; pharmacology ; Lipopolysaccharides ; Necrosis ; Protective Agents ; pharmacology ; Pulmonary Alveoli ; pathology ; Rats ; Rats, Sprague-Dawley

Objective The TLR4 signaling pathway may be involved in the development and progression of hepatocarcinoma . This study aimed to investigate the effect of inhibiting the TLR 4 signaling pathway on the orthotopic implanted liver tumor (OILT) in mice. Methods A TLR4-silencing siRNA lentiviral vector was constructed and transfected into mouse hepatoma H 22 cells.Mouse hepatoma H22 cells were divided into groups A (blank control), B (empty vector) and C (siRNA lentiviral vector), those in group A left untreated and those in groups B and C infected with an empty vector and the TLR 4-silencing siRNA lentiviral vector , respectively. The volumes of the OILTs in different groups measured and the expressions of TLR 4, MyD88, NF-κB and TRAM in the tumor cells de-termined by immunohistochemistry and Western blot . Results The OILT volume was significantly reduced in group C than in A and B ([568.3±90.3] vs [1303.0±194.1] and [1385.0±137.0] mm3 , P<0.05), and so were the expressions of TLR4, MyD88, NF-κB and TRAM in the tumor cells (P<0.05). Conclusion Down-regula-ting the TLR4 signaling pathway can suppress the growth of the ortho -topic implanted liver tumor in mice, which may be associated with the activation of NF-κB by the MyD88-dependent signaling pathway and that of TRAM by the MyD88-independent signaling pathway .

OBJECTIVETo analyze the clinical features of facial nerve neuroma about its diagnosis and management.

METHODSTen patients with facial nerve neuroma were analyzed retrospectively from February 1993 to August 2005. The period of follow-up varied from 1.5 years to 10 years (mean 5 years). Facial nerve function was evaluated with House-Brackmann grading system.

RESULTSThe patients complained of facial paralysis in 7 cases, otitis media in 1 case, a mass in parotid gland in 1 case and a mass on the side of the orbital on face in 1 case. Seven patients were undergone either CT scan or MRI or both. Image studies revealed mass located along the facial nerve course from the nerve endings to the intracranial parts. All the patients accepted the surgery. Intraoperative findings showed that the tumor location matched the image findings. Postoperative pathological diagnosis demonstrated 8 Schwannoma, 2 neurofibroma. There was partial tumor resection in 1 patient accepted and his nerve function was unchanged. Four patients were undergone facial nerve graft but 1 case failed while facial nerve function was improved in 3 other patients. Two patients underwent tumor resection while the continuity of facial nerve was preserved as result their facial nerve function improved respectively. No facial nerve reconstruction was done on other 2 patients.

CONCLUSIONSMultiple origins of facial nerve neuroma were noted and the most common system was facial nerve palsy. The decision on how to treat these patients should be individualized and based on initial facial function, growth rate, surgical experience and informed patient consent. The more effective methods need being seeked for the management of facial nerve neuroma.

Adolescent ; Adult ; Cranial Nerve Neoplasms ; diagnosis ; surgery ; Facial Nerve ; physiopathology ; Facial Paralysis ; diagnosis ; etiology ; Female ; Humans ; Male ; Middle Aged ; Neoplasms, Multiple Primary ; diagnosis ; surgery ; Retrospective Studies ; Young Adult

OBJECTIVETo study the role of herpes simplex virus type 1 ( HSV-1 ) in facial paralysis by developing an experimental animal model of viral facial paralysis.

METHODSBoth sides of posterior auricular branch of facial nerve were anatomies and incised in 66 mice. The HSV-1 was inoculated into right ear branch and fetal bovine serum was inoculated into left ear branch as control. The symmetry of mouse face was observed and scored. The temporal bones were serially sectioned and stained with hematoxylin and eosin. The extratemporal facial nerves were stained with osmium tetroxide. HSV-1 DNA in bilateral facial nerve, brain stem, trigeminal ganglion and spinal cord was detected by the polymerase chain reaction.

RESULTSTwenty-eight (42. 42%) mice developed right facial paralysis between 2 and 5 days after inoculation. Continuing 3-6 days, the facial paralysis recovered spontaneously. Thirty-eight mice had no signs of facial paralysis. Compared with the left, nerve swelling, inflammatory cell infiltration were manifested in right temporal facial nerve of paralyzed mice. The ratio of the cross-sectional area of the facial nerve to the facial canal ( FN/FC ) was significantly higher than that on the control side (P < 0.01). Demyelinated nerve fibers were seen in the right extratemporal facial nerve. Not only in paralyzed mice, but also in non-paralyzed mice, HSV DNA was detected in some nerve tissues.

CONCLUSIONSInoculating HSV-1 into posterior auricular branch of facial nerve can produce an acute and transient facial paralysis in mice. The possible pathophysiologic mechanism of the facial paralysis is viral invasion and transportation from distal branch to main trunk. Then the viral facial neuritis causes facial paralysis.

Animals ; Disease Models, Animal ; Facial Nerve ; virology ; Facial Nerve Diseases ; virology ; Female ; Herpes Simplex ; physiopathology ; Herpesvirus 1, Human ; Mice ; Mice, Inbred BALB C

This study was purposed to investigate the effect of multiple myeloma patients' sera on hepcidin mRNA expression of Hep-3b hepatoma cell line and effect of human interleukin-6 (IL-6) antibody or recombinant human erythropoietin (rhEPO) on hepcidin mRNA expression. The clinical information and serum of multiple myeloma patients were collected. Their sera of a final concentration of 10% were added into Hep-3b cell medium. The mRNA from Hep-3b cells was extracted, and hepcidin mRNA expression was detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). A final concentration of 10 ng/ml human IL-6 antibody and 2 U/ml rhEPO were added into the medium respectively. The results showed that the sera of untreated multiple myeloma patients elevated hepcidin mRNA expression of Hep-3b cells, compared with healthy controls and iron deficiency anemia patients. This effect was fully neutralized by human IL-6 antibody or rhEPO. The hemoglobin (Hb) level was stable during the follow up of regularly treated multiple myeloma patients and the effect of MM patient serum on Hep-3b cell hepcidin mRNA expression was reduced. It is concluded that the hepcidin mRNA expression of Hep-3b cell can be increased by untreated multiple myeloma patient serum. This promotive effect can be antagonised by IL-6, which suggests that IL-6 may be possible to elevate expression level of hepcidin in Hep-3b cells and results in anemia of chronic disease (ACD). The above mentioned promotive effects also can be suppressed by rhEPO, which indicates that the rhEPO may possess curative effect for ACD disease. During short-term follow-up of treated patients with multiple myeloma the Hb level is stable, the influence of patients serum on hepcidin mRNA of Hep-3b cells decreases, which shows the stabilization of disease and amelioration of ACD patient status.
Adult ; Aged ; Antibodies, Monoclonal ; pharmacology ; Antimicrobial Cationic Peptides ; genetics ; Cell Line, Tumor ; Erythropoietin ; blood ; pharmacology ; Female ; Hepcidins ; Humans ; Interleukin-6 ; immunology ; Male ; Middle Aged ; Multiple Myeloma ; genetics ; metabolism ; RNA, Messenger ; genetics

OBJECTIVETo prepare ITP plasma IgG and its F(ab')2 fragments and investigate their immunoreactivity to platelet GPIIb/IIIa and/or GPIb/IX and their effects on platelet aggregation function.

METHODSThe ITP patients having inhibitory autoantibody to the platelet aggregation were selected by modified MAIPA and platelet aggregation test with turbidimetry. Plasma IgG and its F(ab')2 fragments were prepared by streptococcal protein A affinity column and pepsin digestion. The immunoreactivity and the effects on platelet aggregation function of the whole antibody and its fragments were detected by modified MAIPA and platelet aggregation test, respectively.

RESULTS(1) Anti-platelet GPIIb/IIIa and/or GPIb/IX autoantibodies were detected in 34 of 68 (53.6%) ITP patients' plasmas and that from 5 patients significantly inhibited the platelet aggregation induced by ADP or ristocetin. (2) By using protein A column combined with protease digestion, pure IgG and its F(ab')2 fragments were successfully obtained. (3) The purified IgG and its F(ab')2 fragments retained the ability to bind to their respective glycoproteins and inhibited the platelet aggregation function, whereas the IgG depleted plasma lost the ability of binding to the platelet GPs.

CONCLUSIONSF(ab')2 fragment of the IgG antibody is a functional fragment, which not only has the binding ability to the platelet GPs but also inhibits the platelet aggregation function in a dose-dependent manner.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Child ; Female ; Humans ; Immunoglobulin Fab Fragments ; immunology ; Immunoglobulin G ; immunology ; Integrin beta3 ; immunology ; Male ; Middle Aged ; Platelet Aggregation ; Platelet Membrane Glycoprotein IIb ; immunology ; Purpura, Thrombocytopenic, Idiopathic ; immunology ; physiopathology ; Young Adult

BACKGROUNDThe neonatal ventral hippocampal lesion (NVHL) rat model has been proposed as an experimental model for schizophrenia. NVHL rats display impaired central nervous system (CNS) inhibition, which may lead to a phenomenon similar to P50 sensory gating deficits observed in schizophrenic patients. In this study, we investigated whether sensory gating deficits occurred in the NVHL rat as a model for schizophrenia.

METHODSWe created the NVHL rat model using ibotenate. The P20 and N40 were measured to assess sensory response and gating in NVHL and sham rats. Epidural electrodes recorded evoked potentials (EPs), from which latencies, amplitudes, difference scores (S1-S2), and gating ratios (S2/S1) were assessed.

RESULTSCompared with sham controls, prolonged S1 N40 latency and decreased S2 N40 amplitude were detected in the NVHL group. In neither difference scores nor gating ratios, a significant difference was found between NVHL group and sham controls.

CONCLUSIONSNVHL rats may be a valid animal model for schizophrenia. This strategy will be useful in future neurobiological studies investigating the etiology of schizophrenia.

Animals ; Animals, Newborn ; Central Nervous System ; drug effects ; physiopathology ; Evoked Potentials, Auditory ; drug effects ; Hippocampus ; drug effects ; physiopathology ; Ibotenic Acid ; toxicity ; Rats ; Schizophrenia ; chemically induced ; physiopathology ; Sensory Gating ; drug effects

OBJECTIVETo evaluate the clinical efficacy of capecitabine combined with transcatheter arterial chemoembolization (TACE) for advanced liver cancer.

METHODSForty-nine patients with liver cancer were retrospectively divided into two groups: Treatment group, on the basis of TACE, 23 patients received oral capecitabine at 2500 mg/m(2), twice-daily for 14 days followed by 7-day rest period and repeated in every three week intervals for more than two cycles. Control group, 26 patients received TACE only at 2-month intervals for at least two cycles.

RESULTSIn capecitabine and TACE group: there were 1 CR, 14 PR, 5 SD and 3 PD; the overall response rate was 65.2%; the AFP and tumor reduction rates were 68.8% and 73.9%; the median survival time was 11.9 months. In the TACE only group: there were 0 CR, 7 PR, 12 SD and 7 PD; the overall response rate was 26.9%; the AFP and tumor reduction rates were 31.6 % and 30.8%; the median survival time was 8.3 months. The most common side-effects of capecitabine were hand-foot syndrome and diarrhea.

CONCLUSIONCapecitabine combined with TACE is safe and effective for advanced liver cancer.

Administration, Oral ; Adult ; Aged ; Antimetabolites, Antineoplastic ; administration & dosage ; Capecitabine ; Chemoembolization, Therapeutic ; Combined Modality Therapy ; Deoxycytidine ; administration & dosage ; analogs & derivatives ; Drug Administration Schedule ; Female ; Fluorouracil ; analogs & derivatives ; Humans ; Liver Neoplasms ; pathology ; therapy ; Male ; Middle Aged ; Mitomycin ; administration & dosage