Objective To establish the radiolabeling method for peptide K237 with 131I and investigate the biodistribution and therapeutic efficacy of 131I-K237 on nude mice bearing human lung cancer.Methods Iodogen method was used for labeling K237. The bioactivity of 131I-K237 was tested by human umbilical vein endothelial cell ( HUVEC ) proliferation inhibitory assay and the affinity of 131I-K237 was examined by competition binding studies. Twenty-five mice were divided into five groups randomly, including physiologic saline (group 1), K237 (40 μg) (group 2), 131I ( 11. 1 MBq) (group 3), 131I-K237 (K237 40 μg, 11. 1 MBq) intravenously ( group 4), and 131I-K237 ( K237 40 μg, 11.1 MBq) intratumorally (group 5). Injections were repeated at 15 d after the first injection. The tumor growth inhibition rate was calculated. Student's t-test and analysis of variance (ANOVA) were used for testing significant differences of data. Results The inhibition rate of HUVEC proliferation had no significant difference between radiolabeled K237 and unlabeled K237 ( (73.69 ± 5.36) % vs ( 62.68 ± 3.83 ) %, t = 1.67, P ＞ 0.05 ). The growth of transplanted lung cancer was inhibited by 75. 01 % in group 4, 78.99% in group 5, 31.15% in group 2 and 12.61% in group 3, respectively. The average tumor volume of groups 4 and 5 were significantly smaller than that of groups 1,2, and 3 ( F = 15. 233 and 13.611, respectively, P ＜0. 01 ). Conclusion 131I-K237 can be readily radiolabeled and it can effectively inhibit the growth of tumor in nude mice bearing human lung cancer.

OBJECTIVETo search for an optimum method for testicular prothesis implantation in the treatment of testis loss.

METHODSWe retrospectively analyzed the surgical methods and outcomes of 53 cases of terminal prostate cancer and 4 cases of unilateral testicular torsion treated by implantation of testicular prothesis with the polypropylene mesh.

RESULTSThe 57 male patients all received testicular prothesis with the polypropylene mesh. All the patients were satisfied with the appearance and size of the scrotum after surgery. No scrotal hematoma, prosthesis infection, or autoimmune disease occurred postoperatively.

CONCLUSIONTestis loss is not a rare condition clinically, for the treatment of which surgical implantation of testicular prothesis with the polypropylene mesh can achieve both a fine tissue compatibility and a desirable scrotal appearance.

Humans ; Male ; Polypropylenes ; Prostatic Neoplasms ; surgery ; Prostheses and Implants ; Retrospective Studies ; Scrotum ; Spermatic Cord Torsion ; surgery ; Surgical Mesh ; Testis

Objective To construct recombinant Mycobacterium smegmatis vaccine expressing Cysticercus cellulosae cC1 anti-gen. Methods The recombinant pET28a-cC1 plasmid was extracted and double digested by Xho I and BamH I restriction en-zymes,and shuttle plasmid pMV261 was extracted and double digested by Hind III and BamH I restriction enzymes. Both frag-ments were modified by Klenow fragment to form blunt end,then the large fragments of cC1 and pMV261 plasmid were purified and ligated by T4 ligase enzyme. The recombinant pMV261-cC1 plasmid was constructed and sequenced. Then the pMV261-cC1 plasmid was transformed into Mycobacterium smegmatis by the electrotransformation method. The recombinant cC1-Mycobacterium smegmatis was induced by heat and identified by the Western blotting method with the sera of cysticercosis patients. In addition, the growth states of the Mycobacterium smegmatis and the recombinant cC1-Mycobacterium smegmatis were compared and the growth curves were drawn. Results The restriction enzyme and sequencing results showed that the recombinant pMV261-cC1 plasmid was successfully constructed. After heat induction,a 40 kD band was showed by PAGE analysis of cC1-Mycobacterium smegmatis. The Western blotting results showed that the sera of cysticercosis patients could recognize the 40 kDa band,which sug-gested that cC1 protein was expressed in Mycobacterium smegmatis. Compared with the Mycobacterium smegmatis,the recombi-nant cC1-Mycobacterium smegmatis showed no significant difference in proliferation characteristics. Conclusion The recombi-nant cC1-Mycobacterium smegmatis vaccine has been successfully constructed.

Objective To study the role of hydrogen sulfide (H2S) in the effect of SB203580 on proliferation and apoptosis of hepatic stellate cells and the effects of H2S on expressions of collagenⅠand collagenⅢmRNA in hepatic stel-late cells. Methods There were five groups of HSC-T6 cells in this study including control group (DMEM medium contain-ing10%fetal bovine serum), dimethyl sulfoxide (DMSO) group, sodium hydrosulfide (NaHS)group,SB203580 (SB)group and SB+NaHS group. MTT method was used to detect the cell proliferation and inhibition rate of HSC-T6 cells treated by SB203580 and H2S. The apoptotic rate of HSC-T6 cells was detected by flow cytometry with annexin V-FITC/PI double staining. RT-PCR was used to detect the expressions of collagenⅠand collagenⅢmRNA in HSC-T6. Results The apop-totic rate of HSC-T6 cells was significantly higher in SB group and SB+NaHS group than that of control group, and the rate was significantly higher in SB+NaHS group than that of SB group (P＜0.05). There was no significant difference in the apop-totic rate of HSC-T6 cells between DMSO and NaHS groups than that of control group. The expressions of collagenⅠand col-lagenⅢmRNA were found in five groups of cells. There was a higher expression of collagenⅠand collagenⅢmRNA in NaHS group than that of control group (P＜0.05). The expressions of collagenⅠand collagenⅢmRNA were significantly lower in SB group and SB+NaHS group than those of control group and NaHS group (P＜0.05). Conclusion H2S activated P38MAPK signal pathway. And P38MAPK was specifically blocked by SB203580 in HSC-T6 cells, which inhibited the cell proliferation stimulated by H2S and promoted the apoptosis.

This study investigated the effect of arctigenin (Arc) on the cell activation, cytokines expression, proliferation, and cell-cycle distribution of mouse T lymphocytes. Mouse lymphocytes were prepared from lymph node and treated with Phorbol-12-myristate-13-acetate (PMA)/Ionimycin (Ion) and/or Arc. CD69, CD25, cytokines, proliferation and cell cycle were assayed by flow cytometry. The results showed that, at concentrations of less than 1.00 micromol x L(-1), Arc expressed non-obvious cell damage to cultured lymphocytes, however, it could significantly down-regulate the expression of CD69 and CD25, as well as TNF-alpha, IFN-gamma, IL-2, IL-4, IL-6 and IL-10 on PMA/Ion stimulated lymphocytes. At the same time, Arc could also inhibit the proliferation of PMA/Ion-activated lymphocytes and exhibited lymphocyte G 0/G1 phase cycle arrest. These results suggest that Arc possesses significant anti-inflammatory effects that may be mediated through the regulation of cell activation, cytokines expression and cell proliferation.
Animals ; Anti-Inflammatory Agents ; isolation & purification ; pharmacology ; Antigens, CD ; metabolism ; Antigens, Differentiation, T-Lymphocyte ; metabolism ; Arctium ; chemistry ; Cell Cycle Checkpoints ; drug effects ; Cell Proliferation ; drug effects ; Cytokines ; metabolism ; Female ; Furans ; isolation & purification ; pharmacology ; Interferon-gamma ; metabolism ; Interleukin-10 ; metabolism ; Interleukin-2 ; metabolism ; Interleukin-2 Receptor alpha Subunit ; metabolism ; Interleukin-4 ; metabolism ; Interleukin-6 ; metabolism ; Ionomycin ; pharmacology ; Lectins, C-Type ; metabolism ; Lignans ; isolation & purification ; pharmacology ; Lymphocyte Activation ; drug effects ; Mice ; Mice, Inbred BALB C ; Plants, Medicinal ; chemistry ; T-Lymphocytes ; cytology ; drug effects ; immunology ; Tetradecanoylphorbol Acetate ; pharmacology ; Tumor Necrosis Factor-alpha ; metabolism

Adult ; Burkitt Lymphoma ; metabolism ; pathology ; CD3 Complex ; metabolism ; DNA Nucleotidylexotransferase ; metabolism ; Diagnosis, Differential ; Female ; Granulosa Cell Tumor ; metabolism ; pathology ; Humans ; Ki-67 Antigen ; metabolism ; Leukocyte Common Antigens ; metabolism ; Ovarian Neoplasms ; metabolism ; pathology ; surgery ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma ; metabolism ; pathology ; surgery ; Sarcoma, Myeloid ; metabolism ; pathology

OBJECTIVETo evaluate the therapeutic effect of overactive bladder after transurethral resection of prostate (TURP) preventively treated with electroacupuncture and Tolterodine.

METHODSOne hundred and twenty cases of benign prostate hyperplasia of TURP were randomly divided into an electroacupuncture and medicine group, an electroacupuncture group, a medicine group and a control group, 30 cases in each group. All the patients were treated with TURP under the continuous epidural anesthesia, and the catheter was retained for 5-7 days. In electroacupuncture group, before the surgery of the same day, Huiyang (BL 35), Ciliao (BL 32), Qugu (CV 2) and Huiyin (CV 1) were acupunctured with electroacupuncture for 30 min, once a day, 5-7 days' treatment was applied. In medicine group, Tolterodine Tartrate tablet was taken for 2 mg in the morning of surgery day, twice a day and treatment was applied for 5-7 days. In electroacupuncture and medicine group, the comprehensive therapies above in both electroacupuncture group and medicine group were applied. In control group, Pethidine of 50 mg was given by intramuscular injection when bladder was overactive, combined with Anisodamine injection of 10 mg according to the symptoms. The frequency and lasting time of bladder overactivity were compared within 72 hours after TURP in each group.

RESULTSAfter TURP, the frequency of bladder overactivity were 2-4 times a day, and lasted for 5-15 min each time in control group. The frequency and lasting time of bladder overactivity in treatment groups at different time were less than those in control group (P < 0.01, P < 0.001). There was no significant difference in comparison of frequency and lasting time of bladder overactivity between electroacupuncture and medicine group (all P > 0.05). The frequency and lasting time of bladder hyperactivity in electroacupuncture and medicine group were less than those in the electroacupuncture group and the medicine group at 24 hours, 24-48 hours, 48-72 hours after TUPR (P < 0.05, P < 0.01, P < 0.001).

CONCLUSIONAfter TURP, early prevention of combined therapy of electroacupuncture and Tolterodine with oral administration is superior to that of electroacupuncture therapy or Tolterodine for overactive bladder treatment, and it is the safe and effective method to treat overactive bladder.

Aged ; Aged, 80 and over ; Benzhydryl Compounds ; therapeutic use ; Combined Modality Therapy ; Cresols ; therapeutic use ; Electroacupuncture ; Humans ; Male ; Middle Aged ; Phenylpropanolamine ; therapeutic use ; Postoperative Complications ; drug therapy ; etiology ; physiopathology ; therapy ; Prostate ; surgery ; Tolterodine Tartrate ; Transurethral Resection of Prostate ; adverse effects ; Urinary Bladder, Overactive ; drug therapy ; etiology ; physiopathology ; therapy

It is now well established that inflammation plays an important role in the development of numerous chronic metabolic diseases including insulin resistance (IR) and type 2 diabetes (T2DM). Skeletal muscle is responsible for 75% of total insulin-dependent glucose uptake; consequently, skeletal muscle IR is considered to be the primary defect of systemic IR development. Our pre- vious study has shown that rutaecarpine (Rut) can benefit blood lipid profile, mitigate inflammation, and improve kidney, liver, pan- creas pathology status of T2DM rats. However, the effects of Rut on inflammatory cytokines in the development of IR-skeletal muscle cells have not been studied. Thus, our objective was to investigate effects of Rut on inflammatory cytokines interleukiri (IL)-1, IL-6 and tumor necrosis factor (TNF)-α in insulin resistant primary skeletal muscle cells (IR-PSMC). Primary cultures of skeletal muscle cells were prepared from 5 neonate SD rats, and the primary rat skeletal muscle cells were identified by cell morphology, effect of ru- taecarpine on cell proliferation by MTT assay. IR-PSMC cells were induced by palmitic acid (PA), the glucose concentration was measured by glucose oxidase and peroxidase (GOD-POD) method. The effects of Rut on inflammatory cytokines IL-1, IL-6 and TNF-α in IR-PSMC cells were tested by enzyme-linked immunosorbent assay (ELISA) kit. The results show that the primary skeletal muscle cells from neonatal rat cultured for 2-4 days, parallel alignment regularly, and cultured for 7 days, cells fused and myotube formed. It was shown that Rut in concentration 0-180. 0 μmol x L(-1) possessed no cytotoxic effect towards cultured primary skeletal muscle cells. However, after 24 h exposure to 0.6 mmol x L(-1) PA, primary skeletal muscle cells were able to induce a state of insulin resistance. The results obtained indicated significant decrease (P < 0.05 to P < 0.001) IL-1, IL-6 and TNF-α production by cultured IR-PSMC cells when incubating 24 hours with Rut, beginning from 20 to 180.0 μmol x L(-1). IL-1, IL-6 and TNF-α in the Rut treated groups were dose-dependently decreased compared with that in the IR-PSMC control group. Our results demonstrated that the Rut promoted glucose consumption and improved insulin resistance possibly through suppression of inflammatory cytokines in the IR-PSMC cells.
Animals ; Cell Proliferation ; drug effects ; Cytokines ; metabolism ; Female ; Glucose ; metabolism ; Indole Alkaloids ; pharmacology ; Inflammation ; metabolism ; Insulin Resistance ; Male ; Muscle, Skeletal ; cytology ; drug effects ; metabolism ; Quinazolines ; pharmacology ; Rats

AIM:To investigate the effect of over-expression of peroxisome proliferator-activated receptor γ co-activator-1α (PGC-1α) on mitochondrial morphology and cell apoptosis in the cortical neurons with oxygen glucose depriva-tion/reoxygenation(OGD/R). METHODS:The whole gene sequence of PGC-1α was obtained from the cerebral cortex of C57BL/6 mice by RT-PCR and cloned into the eukaryotic expression vector pEGFP-N1. The pEGFP-N1-PGC-1α was iden-tified by PCR,and transfected into cortical neurons. The level of PGC-1α expression was identified by Western blot. The cortical neurons transfected with pEGFP-N1 and pEGFP-N1-PGC-1α vectors were treated with OGD/R. The mitochondrial mass,reactive oxygen species (ROS) and ATP production,cell apoptosis and changes of cleaved caspase-3 were detected by MitoTracker Red staining,flow cytometry,ATP metabolic assay kit and TUNEL. RESULTS:Over-expression of PGC-1α inhibited the decrease in mitochondrial biogenesis capacity and the ROS formation of OGD/R neurons(P<0.05),en-hanced the ability of ATP synthesis (P<0.01),inhibited neuronal apoptosis (P<0.01) and decreased the activation of caspase-3 (P<0.01). CONCLUSION:PGC-1α over-expression inhibits neuronal apoptosis with OGD/R treatment by promoting mitochondrial biogenesis,inhibiting the production of ROS and maintaining mitochondrial function. PGC-1α may be used as a target for the development of cerebral ischemia/reperfusion injury drugs.

Objective To build a foundation for determination of C reaction protein,C reaction protein was expressed and purified,and the immune reactivity of the purified protein was identified.Methods The CRP cDNA was amplified by RT-PCR from human liver cDNA library and inserted into expression vector pCRTT/NT.The recombined plasmid CRP-pCRTT/NT which expressed the fusion protein of CRP was then transferred into lysogenic host strain E coli.BL21 (DE3).The target protein was identified using SDS- polyacrylamide gel electrophoresis (SDS-PAGE).Affinity chromatography was used for protein purification.The immune reactivity of purified CRP was identified by Western blot using anti-CRP specific antibody.Results Recombiant human CRP was expressed in inclusion bodies of E.coli with a six histamine tag.The purify of recombinant protein was detected by SDS-PAGE as a single band at 30 000 and was identified by Western blot.Conclusions A plasmid expressed CRP protein is constructed and the purification system of CRP protein is established.The immune reactivity of the purified protein is identified by Western blot,which makes a good base for the preparation of CRP test kit.