OBJECTIVETo study the clinicopathological characteristics of papillary cystadenoma of the epididymis.

METHODSUsing routine pathology and immunohistochemistry, we observed the surgically obtained samples from 2 cases of papillary cystadenoma of the epididymis, analyzed their pathological features and clinical presentations, and reviewed the related literature.

RESULTSThe 2 patients were both adult males. The tumors typically manifested as painless swelling in the epididymis, with occasionally dull pain and tenesmus in 1 of the cases. Pathologically, the lesions exhibited three morphological features, i. e., dilated ducts and small cysts surrounded by fibrous connective tissue, adenoid papillary hyperplasia into the cysts embraced by fibrovascular stroma, and acidophil substance present in the cysts. Immunohistochemistry showed that the tumors were strongly positive for CK8/18, CK7, and EMA, but negative for CK20, CEA, MC, Calretenin, P53, P63, SMA, VHL, and CD10, with the positive rate of Ki-67 <1%. Follow-up visits revealed good prognosis in both cases.

CONCLUSIONPapillary cystadenoma of the epididymis is a rare benign tumor in the male urogenital system, which may be accompanied by the VHL syndrome. Surgery is the first choice for its treatment.

Adult ; Cystadenoma, Papillary ; chemistry ; pathology ; Epididymis ; Genital Neoplasms, Male ; chemistry ; pathology ; Humans ; Immunohistochemistry ; Male ; von Hippel-Lindau Disease

Adolescent ; Adult ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Hepatitis B virus ; genetics ; Hepatitis B, Chronic ; drug therapy ; virology ; Humans ; Lamivudine ; therapeutic use ; Male ; Middle Aged ; Mutation ; Phytotherapy

OBJECTIVETo investigate the relation between transdifferentiation of the airway myofibroblasts and the expression level of (trypsinogen16, TG16) in vitro and explore the mechanism of airway basement membrane thickening.

METHODSThe total lung proteins were extracted from normal and OVA-induced asthmatic mice and the protein expression profiles were analyzed with SDS-PAGE. The differentially expressed proteins were isolated for analysis with liquid chromatography-mass spectrometry. TG16 was cloned from mouse lung tissue and subcloned into the expression vector pcDNA3.0 to generate a pcDNA3-TG16 plasmid. The vectors were transfected into mouse embryonic fibroblast 3T3 cells and cultured in MEM in the presence of transforming growth factor-beta1 (TGF-beta1). The mRNA levels of alpha-actin and the housekeeping GAPDH gene were analyzed with RT-PCR. Using RNA interference, TG16 expression was suppressed and the resultant alpha-actin or GAPDH protein levels were analyzed using Western blotting.

RESULTSIn the total lung proteins from OVA-induced mice, a 25 000 Da protein was significantly enhanced in comparison with the protein profiles of normal mice. The protein band was identified to represent the protein of TG16. With TGF-beta1 stimulation, transfection with the plasmid pcDNA3-TG16 significantly suppressed the mRNA expression of alpha-actin (alpha-actin/GAPDH=1.78-/+0.50) in 3T3 cells as compared with the expression in cells transfected with pcDNA3.0 (3.20-/+1.36); transfection of the cells with TG16 stealth RNAi oligonucleotide to decrease TG16 mRNA level upregulated the protein level of alpha-actin (3.60-/+0.44) as compared with the alpha-actin protein level in 3T3 cells transfected with control oligonucleotide (2.78-/+0.50).

CONCLUSIONTG16 can inhibit the expression of alpha-actin in fibroblasts, which might be a protective mechanism in the progression of airway remodeling in asthma.

3T3 Cells ; Actins ; biosynthesis ; genetics ; Animals ; Cell Transdifferentiation ; drug effects ; genetics ; physiology ; Chromatography, Liquid ; Fibroblasts ; cytology ; drug effects ; metabolism ; Lung ; cytology ; metabolism ; Male ; Mass Spectrometry ; Mice ; Mice, Inbred BALB C ; Myoblasts ; cytology ; drug effects ; metabolism ; Proteomics ; methods ; RNA, Messenger ; biosynthesis ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection ; Transforming Growth Factor beta1 ; pharmacology ; Trypsinogen ; genetics ; metabolism

OBJECTIVETo explore the mechanism of signal transduction in respiratory syncytial virus (RSV)-induced expression of thymic stromal lymphopoietin (TSLP) in bronchial epithelial cells.

METHODSThe eukaryotic expression vector of RSV F protein, pcDNA3-F, was constructed and transfected into in vitro cultured human bronchial epithelial cell line CRL-9483, which was also transfected with Smad7 expression vector pcDNA3/Smad7 or exposed to p38, ERK1/2, JNK, and JAK/STAT1 inhibitors. The mRNA levels of TSLP and the housekeeping GAPDH gene were analyzed 24 h later with semi-quantitative RT-PCR. In cells with downregulated TSLP mRNA expression due to the addition of the signal inhibitors, cytoplasm TSLP or GAPDH protein levels were further analyzed using Western blotting.

RESULTSVirtually no TSLP mRNA expression was detected by RT-PCR in cultured CRL-9483 cells transfected with pcDNA3 exclusively (TSLP/GAPDH relative total gray scale of 0.10-/+0.03), while cell transfection with pcDNA3-F resulted in significantly increased TSLP mRNA level (0.42-/+0.20, P=0.024). In the presence of F protein expression, both p38 and JNK inhibitors could downregulate TSLP mRNA levels (0.14-/+0.04, P=0.036; 0.23-/+0.07, P=0.048, respectively), while TGF-beta-Smad inhibiting protein Smad7 (0.60-/+0.25), ERK 1/2 inhibitor (0.45-/+0.23), and JAK/STAT1inhibitor (0.44-/+0.25) failed to block TSLP expression (P>0.05). Western blotting showed that p38 inhibitor (TSLP/GAPDH relative total gray scale=3.67-/+1.18, P=0.018) and JNK inhibitor (1.48-/+0.77, P=0.004) also downregulated the protein levels of TSLP as compared with pcDNA3-F transfection group (8.13-/+2.20).

CONCLUSIONRSV F protein can stimulate TSLP expression in human bronchial epithelial cells mediated partially by p38 and JNK signal pathways.

Bronchi ; cytology ; metabolism ; virology ; Cell Line ; Cytokines ; genetics ; metabolism ; Epithelial Cells ; metabolism ; virology ; Gene Expression ; Humans ; MAP Kinase Kinase 4 ; genetics ; metabolism ; Respiratory Syncytial Virus Infections ; genetics ; metabolism ; virology ; Respiratory Syncytial Viruses ; genetics ; physiology ; Signal Transduction ; Viral Fusion Proteins ; genetics ; metabolism ; p38 Mitogen-Activated Protein Kinases ; genetics ; metabolism

This study was aimed to investigate the cytotoxic effect of the Naja Naja Actra Venom Component (NNAVC) combined with activated immune cells on human acute myeloblastic leukemia line KG1a cells. The cytotoxic effects of NNAVC at different concentrations on KG1a cells were measured by CCK-8 method. LDH releasing assay was used to detect the cytotoxic effects of activated immune cells, NNAVC combined with activated immune cells on KG1a cells and the sensitivity of KG1a treated with NNAVC to activated immune cells. The results showed that the inhibitory rate of NNAVC on KG1a cells increased with the concentration enhancement, the cytotoxicity of activated immune cells at the different effector to target (E:T) ratios(6.25:1, 12.5:1, 25:1) on KG1a cells were 12.30%, 24.85% and 52.26%. The cytotoxicity of NNAVC combined with activated immune cells at the different E:T cell ratios (10:1, 20: 1) on KG1a cells were 56.21% and 85.59%, which were higher than that of NNAVC or activated immune cells alone. The cytotoxicity of activated immune cells at the E: T cell ratio of 10:1 on KG1a cells treated with NNAVC at different concentrations were 25.65%, 31.33%, 28.63% and 16.78%, respectively, and that at the E:T cell ratio of 20: 1 were 40.62%, 44.70%, 44.62% and 40.72%. It is concluded that:both of NNAVC and activated immune cells have lethal effect on KG1a cells, and the combination of NNAVC and activated immune cells can strengthen their effect on KG1a.
Animals ; Cell Line, Tumor ; drug effects ; Cytotoxicity, Immunologic ; Elapidae ; Humans ; Immunocompetence ; Leukemia, Myeloid, Acute ; immunology ; pathology ; Venoms ; pharmacology

The objective of this study was to investigate the effect of cyclooxygenase-2 (COX-2) in the angiogenesis of bone marrow in leukemia patients. 51 patients with newly diagnosed acute leukemia were taken as study objects, 18 healthy volunteers were enrolled in the control group. Bone marrow microvessel density (MVD) in bone marrow biopsy tissue section was determined with immunohistochemistry method, the vascular endothelial growth factor level in serum was detected with ELISA method and the expression of cyclooxygenase-2 in bone marrow cells was assayed by flow cytometry. The results showed that the MVD, VEGF level, positive rate of COX-2 expression in leukemia group all obviously increased as compared with the control group (p < 0.05). The correlative coefficients of MVD, VEGF level and COX-2 expression rate were 0.614, 0.423 and 0.577 respectively (p < 0.05). In conclusion, as well as solid tumors, leukemia may be also a angiogenesis-dependent malignant tumor. Coordination of COX-2 with VEGF may promote angiogenesis in bone marrow.
Adolescent ; Adult ; Aged ; Bone Marrow Cells ; metabolism ; pathology ; Case-Control Studies ; Child ; Child, Preschool ; Cyclooxygenase 2 ; metabolism ; Female ; Humans ; Infant ; Leukemia ; metabolism ; pathology ; Male ; Middle Aged ; Neovascularization, Pathologic ; metabolism ; pathology ; Vascular Endothelial Growth Factor A ; metabolism ; Young Adult

OBJECTIVEThe aim of this study was to evaluate the association between Chlamydia pneumoniae (CP) infection and primary biliary cirrhosis (PBC).

METHODSChlamydia pneumoniae IgG and IgM were determined by enzyme-linked immunosorbent assay (ELISA) in 41 well-established PBC patients and two race-matched control groups, PHC, n = 70; healthy controls, HC, n =57).

RESULTSThe mean levels and seroprevalence of CP IgG in PBC group and PHC group were significantly higher than in the HC [(46.8 +/- 43.4) RU/ml, (49.5 +/- 45.2) RU/ml vs (28.3 +/- 32.7) RU/ml, P = 0.042 and P < 0.001 respectively; 68.3%, 71.4% vs 42.1%, chi2 values were 5.389 and 11.110 respectively]. There was a markedly elevated seroprevalence of CP IgM in patients with PBC (22.0%) compared with the PHC and HC groups. The odds ratios (ORs) for the presence of CP IgG and IgM for the PBC patients versus the HC were 2.7 (95% CI 0.9 to 6.1) and 5.1 (95% CI 1.4 to 18.5). Though there was no correlation in the level of CP IgG with total IgG in sera of patients with PBC (r=-0.857, p=0.344), CP IgM was related with the abnormally high concentrations of total IgM in the PBC group.

CONCLUSIONSThe results of this study do not support the hypothesis that infection with Chlamydia pneumoniae may be a triggering agent for PBC, but suggest that Chlamydia pneumoniae infection probably contributes to the high level of IgM presented in most of the patients with PBC

Adult ; Aged ; Aged, 80 and over ; Antibodies, Bacterial ; blood ; Chlamydophila Infections ; complications ; Chlamydophila pneumoniae ; isolation & purification ; Female ; Humans ; Immunoglobulin M ; blood ; Liver Cirrhosis, Biliary ; complications ; microbiology ; Male ; Middle Aged

The liver injury induced by Polygonum multiflorum Thunb. (PM) was investigated based on idiosyncratic hepatotoxicity model co-treated with lipopolysaccharide (LPS) at a non-hepatotoxic dose. Sprague-Dawley (SD) rats were intragastrically administered with three doses (18.9, 37.8, 75.6 g crude drug per kg body weight) of 50% alcohol extracts of PM alone or co-treated with non-toxic dose of LPS (2.8 mg·kg(-1)) via tail vein injection. The plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were assayed and the isolated livers were evaluated for histopathological changes. The dose-toxicity relationships of single treatment of PM or co-treatment of LPS were investigated comparatively to elucidate the idiosyncratic hepatotoxicity of PM. The results showed that no significant alterations of plasma ALT and AST activities were observed in the groups of solo-administration of LPS (2.8 mg·kg(-1), i.v.) or different dosage (18.9, 37.8 and 75.6 g·kg(-1), i.g.) of PM, compared to normal control group (P > 0.05); while significant elevations were observed in the co-administration groups of PM and LPS. Treatment with LPS alone caused slight infiltration of inflammatory cells in portal area but no evident hepatocytes injury. Co-treatment with LPS and PM (75.6 g·kg(-1), i.g.) caused hepatocyte focal necrosis, loss of central vein intima and a large number of inflammatory cell infiltration in portal areas. When further reduce the dosage of PM, significant increases of plasma ALT and AST activities (P < 0.05) were still observed in co-administration groups of LPS and PM (1.08 or 2.16 g·kg(-1)), but not in LPS or PM solo-administration groups. Nevertheless, the co-treatment of low dosage of PM (0.54 g·kg(-1)) with LPS did not induce any alteration of plasma ALT and AST. In conclusion, intragastric administration with 75.6 g·kg(-1) of PM did not induce liver injury in normal rats model; while the 2 folds of clinical equivalent dose of PM (1.08 g·kg(-1)) could result in liver injury in the LPS-based idiosyncratic hepatotoxicity model, which could be used to evaluate the idiosyncratic hepatotoxicity of PM.
Alanine Transaminase ; blood ; Animals ; Aspartate Aminotransferases ; blood ; Chemical and Drug Induced Liver Injury ; pathology ; Hepatocytes ; pathology ; Lipopolysaccharides ; Polygonum ; toxicity ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo study aberrant expression of cell cycle control genes in patients with myelodysplastic syndromes (MDS).

METHODSReverse transcription polymerase chain reaction (RT-PCR) was used to investigate the expression of cell cycle control genes (cyclin D2, cyclin D3, cyclin A1, cyclin E, CDK2, CDK4, CDK6, p21, p27, p57, Rb and E2F1) in bone marrow mononuclear cells (BMMNCs) from 29 normal control, 27 MDS and 19 de novo acute myeloid leukemia (AML).

RESULTSThe expression levels of cyclin D3 (0.65 +/- 0.17, P < 0.05) and cyclin A1 (0.48 +/- 0.04, P < 0.05) in MDS were higher than those in normal control and significantly lower than those in AML. The expression rates and levels of cyclin D2 (40.7% and 0.78 +/- 0.21) and cyclin E (51.9% and 0.52 +/- 0.10) in MDS were statistically higher than those in normal control and AML. The expression level of CDK2 in MDS (0.66 +/- 0.19, P < 0.01) was higher than that in normal control (0.42 +/- 0.04) and the expression rate of CDK6 in MDS (25.9%) higher than in normal control (3.4%, P < 0.05). There was no significant difference of the expression rates and levels of CDK4 in MDS, AML and normal control. The expression rates and levels of p21 (77.8% and 1.18 +/- 0.21) and p27 (48.1% and 1.14 +/- 0.40) in MDS were statistically higher than those in normal control and AML. The expression level of p57 in MDS (0.69 +/- 0.06) was higher than that (0.53 +/- 0.05, P < 0.01) in normal control but lower than in AML (0.96 +/- 0.16, P < 0.01). The expression rate (55.6%) and level (0.85 +/- 0.17) of Rb in MDS were significantly higher than those in normal control and AML. The expression rate (7.4%) and level (0.39 +/- 0.04) of E2F1 in MDS were comparable to those in normal control but lower than those in AML.

CONCLUSIONMDS clones have aberrant mechanism of cell cycle control: high expressions of cyclin family members, CDK2 and CDK6 may lead to high proliferation; high expression of p21 and p27 may cause the G1 phase arrest.

Adolescent ; Adult ; Cell Cycle Proteins ; genetics ; Child ; Cyclin-Dependent Kinase Inhibitor Proteins ; genetics ; Cyclin-Dependent Kinases ; genetics ; E2F1 Transcription Factor ; genetics ; Female ; Gene Expression Profiling ; Humans ; Male ; Middle Aged ; Myelodysplastic Syndromes ; genetics ; pathology ; Retinoblastoma Protein ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Young Adult