OBJECTIVETo compare therapeutic effects of clavicular hook-plate fixation and modified Weaver-Dunn surgery combined with clavicular hook-plate fixation in treating Tossy type III acromioclavicular joint dislocation.

METHODSForty-one patients with Tossy type III acromioclavicular dislocation treated by operation were retrospectively analysis from January 2012 to January 2014. The patients were divided into clavicular hook-plate fixation group (group A) and modified Weaver-Dunn surgery combined with clavicular hook-plate fixation (group B) according to surgical procedures. In group A, there were 15 males and 6 females aged from 17 to 51 years old with an average of (31.60 ± 12.58) years old, preoperative Constant-Murley score was 40.25 ± 9.80, and treated with clavicular hook-plate fixation. In group B, there were 13 males and 7 females aged from 18 to 48 years old with an average of (29.40 ± 11.27) years old, preoperative Constant-Murley score was 41.45 ± 8.81, and treated with modified Weaver-Dunn surgery combined with clavicular hook-plate fixation. Operative time, blood loss, imaging changes before and after operation, postoperative complications were compared; Constant-Murley score at 3, 6 and 12 months after operation were evaluated.

RESULTSIn group A, operative time was 40.50 ± 24.36) min, blood loss was (75.30 ± 30.36) ml; In group B, operative time was (60.10 ± 23.55) min, blood loss was (100.70 ± 40.12) ml. Twenty-one patients in group A were followed-up from 12 to 18 months with an average of (14.8 ± 3.1) months; 20 patients in group B were followed-up from 12 to 14 months with an average of (13.6 ± 1.5) months. There were no significant differences in operative time, blood loss and follow-up time between two groups. Complications were in six patients of group A and 3 patients of group B, and there were no significant meaning between two groups. At 6 months after operation, Constant-Murley score in group A was 88.85 ± 4.23, 92.15 ± 3.82 in group B; and had significant meaning between two groups (t = -2.56, P = 0.022 < 0.05). While there were no differences in Constant-Murley score in other times.

CONCLUSIONBoth of clavicular hook-plate fixation and modified Weaver-Dunn surgery combined with clavicular hook-plate fixation are effective operative methods for the treatment of Tossy type III acromioclavicular dislocation. Clavicular hook-plate fixation has advantage of less trauma, while modified Weaver-Dunn surgery combined with clavicular hook-plate fixation could reconstruct coracoclavicular ligament more stronger, clavicular hook plate could take out earlier, also improve shoulder joint function earlier.

Acromioclavicular Joint ; injuries ; Adolescent ; Adult ; Bone Plates ; Case-Control Studies ; Female ; Fracture Fixation, Internal ; methods ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Shoulder Dislocation ; surgery

OBJECTIVETo elucidate whether the plasma concentration of NT-proBNP in patients with acute coronary syndrome (ACS) correlated with severity of the diseases and whether NT-proBNP is a reliable biochemical marker correctly indicates the severity of ACS.

METHODSEighty-nine subjects came from CCU of Cardiology Department of People's Hospital Beijing University from October 2003 to June 2004 and aged 34-85 y (66.89 +/- 11.12 y). In this study the spectrum of ACS only included unstable angina pectoris (UA) and acute myocardial infarction (AMI). Patients with UA were separated into 3 groups by Braunwald classes and those with AMI were separated into 4 groups by Killip classes when their venous blood samples were collected. Plasma concentration of NT-proBNP was measured by enzyme linked immunoabsorbent assay. Data was estimated by SPSS.

RESULTSThe concentration of NT-proBNP in patients with ACS was dramatically correlative with the severity of the diseases: with the upgrading of Braunwald classes, the concentration of NT-proBNP in patients with UA increased gradually; in patients with AMI it also raised gradually with the upgrading of killip classes; furthermore, the plasma concentration of NT-proBNP in patients with AIM increased much more than that in patients with UA when they are at the similar NYHA functional class.

CONCLUSIONPlasma concentration of NT-proBNP in patients with ACS might be a reliable biochemical marker which can objectively indicate the degree of this diseases.

Acute Coronary Syndrome ; blood ; physiopathology ; Adult ; Aged ; Aged, 80 and over ; Humans ; Middle Aged ; Natriuretic Peptide, Brain ; blood ; Peptide Fragments ; blood

AIM: To investigate the mechanism of the AP-1 signal transduction pathway inhibited by JIP in nasopharyngeal carcinoma cells. METHODS: AP-1 activity was triggered by Dox-induced LMP1 expression in Tet-on-LMP1-HNE 2 cells (L7). The retention of phospho-JNK in the cytoplasm caused by JIP was examined with immunofluroscence assay. RESULTS: 24 h after transfection of L7 cells with the JIP expression plasmid, the translocation of activated JNK was inhibited, which resulted in the retention of phospho-JNK in the cytoplasm and down-regulation of the AP-1 activity. CONCLUSION: JIP down-regulates the activity of AP-1 through the inhibition of the translocation of JNK.

Abstract:Objective To elucidate the mechanisms by which Epstein-Barr virus-encoded latent membrane protein 1 activates NF-κB in nasopharyngeal carcinoma cells.Methods A tetracycline-regulated LMP1-expressing nasopharyngeal carcinoma cell line, Tet-on-LMP1-HNE2, was used as the cell model. The kinetics of the expression of proteins, including LMP1, IκBα and IκBβ, was analyzed by Western blotting. The subcellular localization of NF-κB (p65) was detected by indirect immunofluorescence assay. The NF-κB transactivity was studied by transient transfection and reporter gene assay. Results IκBα was phosphorylated and degraded after the inducible expression of LMP1, although the total protein levels remained stable. The steady-state level of total IκBβ protein may have resulted from the initiation of an autoregulation loop after the activation of NF-κB. No change in the IκBβ level was detected. NF-κB (p65) was translocated from the cytoplasm to the nucleus following degradation of IκBα. After the introduction of the dominant-negative mutant of IκBα (Del 71) into Tet-on-LMP1-HNE2 cells, both nuclear translocation and transactivation of NF-κB induced by LMP1 was significantly inhibited. Conclusions The results indicated that in nasopharyngeal carcinoma cells, LMP1 activated NF-κB via phosphorylation and degradation of IκBα, but not IκBβ. The dominant-negative mutant of IκBα (Del 71) could completely inhibit both the nuclear translocation and transactivation of NF-κB induced by LMP1.

BACKGROUNDThe over increase of sympathetic drive in chronic heart failure (CHF) is with main responsibility for the deterioration and mortality of the disease. Myocardial (123)I-metaiodobenzylganidine (MIBG) scintigraphy is a non-invasive convenient method to assess sympathetic dysfunction in patients with CHF. The aim of the study was to detect if sympathetic antidrive analysed through myocardial MIBG scintigraphy plays a crucial role in long-term prognosis in CHF.

METHODSSixty-four enrolled patients underwent myocardial MIBG scintigraphy, and their plasma concentration of brain natriuretic peptide (BNP), myocardial contractile reserve (MCR), rest left ventricular ejection fraction (rest LVEF) and New York Heart Association (NYHA) function class were assessed. They were separated into groups according to median of above parameters. Endpoint was cardiac death and it was recorded in each group during average 54 months' follow-up.

RESULTSAt the end of follow-up, group with lower ratio of heart/mediastinum (H/M) had more death events (P = 0.001), and its BNP level was higher and MCR level was lower (P = 0.003 and 0.001, respectively); but its rest LVEF and NYHA function class were not significantly different. H/M, MCR and BNP correlated closely with death (P = 0.000, 0.000 and 0.001, respectively). Among the three indicators the death risk ratio (RR) of H/M was 4.66, more than MCR and BNP (1.88 and 2.56, respectively). However, rest LVEF and NYHA function class did not correlate with death (P = 0.652 and 0.384, respectively). The group with lower H/M and MCR, higher BNP had much more death than that with higher H/M and MCR, lower BNP, the RR being 12.8.

CONCLUSIONSMyocardial MIBG scintigraphy is a long-term prognostic marker in CHF. BNP, MCR are also excellent predictors of long-term prognosis in CHF, but not stronger than myocardial MIBG scintigraphy. If the three indicators were joined together, the prediction would become most powerful. Rest LVEF and NYHA have no significance in long-term prediction of CHF.

3-Iodobenzylguanidine ; Adult ; Aged ; Aprotinin ; chemistry ; Brain ; metabolism ; Echocardiography ; Edetic Acid ; chemistry ; Female ; Heart Failure ; metabolism ; pathology ; Humans ; Male ; Middle Aged ; Myocardial Perfusion Imaging ; methods ; Natriuretic Peptides ; metabolism ; Prognosis ; Prospective Studies

OBJECTIVETo elucidate the interference effect of Epigallocatechin-3-Gallate (EGCG) on targets of Activator Protein-1 (AP-1) signal transduction pathway activated by EB virus encoded latent membrane protein 1 in nasopharyngeal carcinoma (NPC) cell lines.

METHODSSurvival rate of cells was determined by MTT assay. AP-1 and CyclinD1 activation were analyzed by promoter luciferase reporter system. Nuclear translocation of JNK was analyzed by indirect immunofluorescence. Protein expression and phosphorylation were observed by Western blot.

RESULTSEGCG inhibited the survival of CNE1 and CNE-LMP1 cells and the activity of AP-1 caused by LMP1 in CNE-LMP1 cells. EGCG also inhibited the nuclear translocation of JNK and the phosphorylation of c-Jun. It also inhibited cyclinD1 promoter activity and cyclinD1 expression.

CONCLUSIONEGCG inhibits AP-1, JNK, c-Jun and cyclinD1 which are key targets on AP-1 signal transduction pathway. The results may explain the molecular mechanism of action of EGCG against nasopharyngeal carcinoma.

Carcinoma, Squamous Cell ; metabolism ; pathology ; virology ; Catechin ; analogs & derivatives ; pharmacology ; Cell Line, Tumor ; Cell Survival ; drug effects ; Herpesvirus 4, Human ; Humans ; JNK Mitogen-Activated Protein Kinases ; metabolism ; MAP Kinase Kinase 4 ; Mitogen-Activated Protein Kinase Kinases ; metabolism ; Nasopharyngeal Neoplasms ; metabolism ; pathology ; virology ; Phosphorylation ; drug effects ; Protein Transport ; drug effects ; Proto-Oncogene Proteins c-jun ; metabolism ; Signal Transduction ; drug effects ; Transcription Factor AP-1 ; metabolism ; Viral Matrix Proteins ; genetics ; metabolism ; physiology

This paper introduces the significance, the present development situation and some suggestions of the medical measurements.
Diagnostic Equipment ; standards ; Equipment and Supplies ; standards ; Magnetic Resonance Imaging ; instrumentation ; standards ; Medical Staff ; education ; Research Design ; standards ; Tomography, X-Ray Computed ; standards

OBJECTIVETo identify factors associated with YMDD mutation in patients with chronic hepatitis B before and after lamivudine treatment in Zunyi region.

METHODS53 patients with chronic hepatitis B were enrolled in this study, HBV DNA,HBV markers, ALT, AST, TBil, albumin in the serum were examined at 0, 3, 6, 12, 18 and 24 months after lamivudine treatment. HBV genotype and YMDD mutation were determined by sequencing before lamivudine treatment. YMDD mutation was checked again if serum HBV DNA rebound to more than 1 x 10(4) copies/ml after the initial decrease.

RESULTSHBV genotype in Zunyi region is constitute of B, C and B+C genotype. YMDD mutation occurred in 18 cases after lamivudine treatment, the rate of YMDD mutation was 15.1%, and 34.0% after 1 year and 2 years treatment. There are four types of mutation: rtL180M/M204V, rtL180M/M204I, rtM204I, rtL180M. rtM204V mutation in C gene was always accompanied by rtL180M mutation (100%). The rate of rtL180M/M204V mutation in genotype C group was significantly higher than that in genotype B group (77.8% to 25.0%), the same was true for the rtL180M/ M204I mutation (22.2% to 12.5%). There was no point mutation in genotype C group. The point mutation of rtM204I and rtL180M appeared only in genotype B group. Gender, nation, family history of hepatitis B and HBeAg were not associated with YMDD mutation (P more than 0.05), while the mutation rate was associated with the disease course and severity of disease. YMDD mutation did not occur in patients with low HBV DNA level (less than 10(5) copies/ml).

CONCLUSIONYMDD mutation after lamivudine therapy is associated with HBV genotype and P gene mutation type, and prolonged treatment increases the the mutation rate. In order to reduce the incidence of YMDD mutation, patients with shorter disease course, lower HBV DNA level, more serious liver damage should be treated with lamivudine.

Adult ; Alanine Transaminase ; blood ; Antiviral Agents ; pharmacology ; therapeutic use ; Aspartate Aminotransferases ; blood ; China ; epidemiology ; DNA Mutational Analysis ; DNA Primers ; DNA, Viral ; blood ; genetics ; Drug Resistance, Viral ; Female ; Genotype ; Hepatitis B virus ; genetics ; Hepatitis B, Chronic ; blood ; drug therapy ; virology ; Humans ; Lamivudine ; pharmacology ; therapeutic use ; Male ; Mutation ; Polymerase Chain Reaction

OBJECTIVETo study the effects of sodium hydrosulfide (NaHS), hydrogen sulfide (H2S) donor, on LPS-induced polymorphonuclear neutrophil (PMN) accumulation and its mechanism.

METHODSThe animal model of acute lung injury (ALI) caused by intravenous injection of lipopolysaccharides (LPS). Adult male Spraguce-Dawley (SD) rats were randomly divided into four groups (n = 8 - 12 per group): Control group (0.5 ml/kg normal saline i.v.), LPS-treated group (1 mg/kg, i.v.), LPS plus NaHS (1 mg/kg i.v. and 28 micromol/kg i.p., respectively) and NaHS group (28 micromol/kg i.p.). Animals were sacrificed at 6 h after agent administration. Morphological changes of lung tissues were observed and polymorphonuclear neutrophil (PMN) number in alveolar septum was tested. The apoptosis of PMN in the bronchoalveolar lavage fluid (BALF) was examined with in situ TdT-mediated dUTP end labeling (TUNEL). Intercellular adhesion factor-1 (ICAM-1) and nuclear factor-kappaB (NF-kappaB) expressions in the lung tissue were analyzed by Western Blot.

RESULTSThe results showed that bleeding, edema, PMN accumulation and other pathological signs in the lung tissue emerged after LPS injection. Compared to control rats, the LPS-treated rats had increased PMN number, decreased PMN apoptotic percentages, and increased expressions of ICAM-1 and NF-kappaB. Administration of NaHS into LPS-treated rats reduced the PMN number and expressions of ICAM-1 and NF-kappaB but increased PMN apoptotic percentages. In addition, NaHS alleviated the degree of ALI. There were no significant differences of the above indicators between NaHS-treated rats and control rats.

CONCLUSIONNaHS can reduce the PMN accumulation in the lung, and its mechanism is related to down-regulation expression of ICAM-1 and promotion of PMN apoptosis induced by inhibition of NF-kappaB pathway.

Acute Lung Injury ; chemically induced ; metabolism ; pathology ; Animals ; Apoptosis ; Hydrogen Sulfide ; pharmacology ; Intercellular Adhesion Molecule-1 ; metabolism ; Lipopolysaccharides ; adverse effects ; Lung ; drug effects ; metabolism ; pathology ; Male ; NF-kappa B ; metabolism ; Neutrophils ; cytology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo observe the biological changes of primary human nasopharyngeal epithelial cells in the early stage of immortalization.

METHODSThe morphological changes of nasopharyngeal epithelial cells were observed by phase contrast microscopy, and the activity profile of senescence-associated beta-galactosidase (SA-beta-Gal) was detected by SA-beta-Gal staining. The expression of p16(INK4a) protein was tested by immunochemical assay, and the life span in vitro of nasopharyngeal epithelial cells was calculated as population doublings. In addition, the expression of Epstein-Barr (EB) virus latent membrane protein 1 (LMP1) was also detected by immunofluorescence staining.

RESULTSMorphologically, cells treated with EB virus and 12-o-tetradecanoyl-phorbol-13-acetate (TPA) formed multi-layer foci, and their cellular life span in vitro was extended (about 155 days of culture). A low percentage of cells (about 4.8%) expressed SA-beta-Gal activity at late primary culture, and did not always express p16(INK4a) protein in the progression of culture.

CONCLUSIONSNasopharyngeal epithelial cells treated with EB virus in cooperation with TPA can pass through the stage of senescence and enter the early stage of immortalization. Some changes of phenotype occur in these cells. Our results provide data for further studying the mechanism of immortalization and the establishment of a human nasopharyngeal epithelial cell line.

Cell Transformation, Viral ; Cellular Senescence ; Cyclin-Dependent Kinase Inhibitor p16 ; analysis ; Epithelial Cells ; physiology ; virology ; Herpesvirus 4, Human ; physiology ; Humans ; Nasopharynx ; cytology ; virology ; Tetradecanoylphorbol Acetate ; pharmacology