Objective To observe the expression of PAX-2 and PTEN in different types of endometrial lesions, and to study their relationship with endometrial intraepithelial neoplasia (EIN). Methods 60 cases of endometrial hyperplasic lesions and 70 cases of endometrial carcinoma were enrolled. All cases were reclassified by using the diagnostic criteria of EIN, and PAX-2 and PTEN were stained to compare the difference among them. Results The deletion rates of PAX-2 in benign hyperplasia, EIN and endometrial carcinoma were 39.5 % (15/38), 72.7 % (16/22) and 78.6 % (55/70), respectively, and there was a statistical difference (χ2= 21.664, P= 0.000). The deletion rates of PTEN in benign hyperplasia, EIN and endometrial carcinoma were 47.4%(18/38), 54.5%(12/22) and 75.7%(53/70), respectively, and there was no statistical difference (χ2=2.878, P=0.411). Conclusion The staining of PAX-2 could be considered as a reliable adjuvant diagnostic method in the diagnostic criteria of EIN, however, the loss of PTEN just should be regarded as a suggestion of EIN, not a confirmed diagnostic basis.

Prostate-specific membrane antigen (PSMA), the research of which has flourished in recent years, is a specific prostate cancer marker. PSMA plays a more and more important role in the early diagnosis, gene treatment and prognosis of the disease course of prostate cancer. This review focuses on the progress in researches of the structure, function, expression traits and gene expression of the PSMA protein, prostate cancer radioimmunoimaging, DNA vaccines and suicide gene therapy based on PSMA, as well as the role of PSMA in the clinical diagnosis and treatment of prostate cancer.
Antigens, Surface ; genetics ; Gene Expression Regulation, Neoplastic ; Glutamate Carboxypeptidase II ; genetics ; Humans ; Male ; Prostate-Specific Antigen ; genetics ; Prostatic Neoplasms ; diagnosis ; genetics ; therapy ; RNA, Messenger ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVETo assess the effect of the maximal androgen blockade(MAB) and MAB combined with 125I brachytherapy on prostatic cancer.

METHODSForty-four patients with prostatic cancer (from 1993 to 2002), 28 at pathologic stage C and 16 at stage D, were analyzed retrospectively. Thirty-five of them were treated by bilateral orchidectomy and anti-androgen drugs, i.e. MAB, and 9 treated by MAB combined with 125I brachytherapy. The survival rates and the variation of serum prostate-specific antigen (PSA) levels between pre- and post-treatment were compared.

RESULTSThe level of PSA decreased from 60.3 micrograms/L to 12.1 micrograms/L in 35 patients treated by MAB, and from 72.1 micrograms/L to 3.6 micrograms/L in 9 patients treated by MAB combined with 125I brachytherapy after 6 months. The post-treatment survival rates were 81.3% (26/32, excluding 3 deaths by other diseases) for patients treated by MAB after a mean follow-up of 39.2 (9-84) months and 100% for patients by MAB combined with 125I brachytherapy after a mean follow-up of 13(7-24) months.

CONCLUSIONMAB and MAB combined with 125I brachytherapy are effective for patients with prostatic cancer.

Aged ; Aged, 80 and over ; Androgen Antagonists ; therapeutic use ; Brachytherapy ; Combined Modality Therapy ; Humans ; Iodine Radioisotopes ; therapeutic use ; Male ; Middle Aged ; Prostatic Neoplasms ; mortality ; therapy ; Retrospective Studies ; Survival Rate

BACKGROUNDInterleukin-13 (IL-13) is recognized to be a key modulator in the pathogenesis of Th2-induced allergic inflammation. Transcription factors GATA3 and NFAT1 have been both implicated in the regulation of Th2 cytokines. We previously demonstrated the GATA3-NFAT1 association during human T cell activation. However, the function of the GATA3-NFAT1 complex in Th2 cytokines regulation is still unknown. Small interference RNA (siRNA) was constructed to knock down GATA3 expression in Hut-78 cells to investigate the possible role of GATA3-NFAT1 complex in IL-13 transcription.

METHODSCells were stimulated with anti-CD3 plus anti-CD28 antibodies to mimic in vivo antigen-mediated co-stimulation; the expression of IL-13 mRNA was determined by real-time PCR; chromation immunoprecipitation (CHIP) assay was employed to investigate the NFAT1 binding to IL-13 promoter.

RESULTSGATA3 siRNA suppressed the expression of GATA3 both in mRNA and protein levels in Hut-78 cells. The binding of NFAT1 to IL-13 promoter was inhibited by GATA3 siRNA in activated T cells, which was followed by the reduction of IL-13 transcription.

CONCLUSIONGATA3-NFAT1 complex may play an important role in the regulation of IL-13 transcription in human T cells.

Cells, Cultured ; GATA3 Transcription Factor ; antagonists & inhibitors ; genetics ; Humans ; Interleukin-13 ; genetics ; NFATC Transcription Factors ; metabolism ; Promoter Regions, Genetic ; RNA, Small Interfering ; genetics ; T-Lymphocytes ; metabolism ; Transfection

OBJECTIVETo investigate the post-operative complications and preventative strategies of them in transurethral electrovaporization of the prostate(TVP).

METHODSNine hundred and twenty patients with symptomatic benign prostatic hyperplasia (BPH) were treated by TVP.

RESULTSPost-operative complications included severe Hemorrhage in 30 cases (3.3%), transurethral resection syndrome (TURS) in 6 cases (0.7%), acute lower urinary tract infection in 16 cases (1.7), acute epididymitis in 11 cases (1.2%), acute urinary retention in 34 cases (3.7%), incontinence in 35 cases (3.8%), urethral stricture in 26 cases (2.8%), recurrence in 22 cases (2.4%). There were retrograde ejaculation in 54.5% (24/44) and impotence in 9.1% (4/44).

CONCLUSIONAlthough TVP is more effective than standard TURP in the treatment of lower urinary tract symptoms caused by BPH, complications during TVP procedures require special consideration.

Aged ; Aged, 80 and over ; Electrosurgery ; adverse effects ; Humans ; Male ; Middle Aged ; Postoperative Complications ; prevention & control ; Prostatic Hyperplasia ; surgery ; Transurethral Resection of Prostate ; adverse effects

OBJECTIVETo assess the radioactive damage induced by interstitial 125I seed implantation to the rabbit urethra.

METHODSWe implanted 24 rabbits with 125I seeds 1.0 cm to the urethra at the radiation dose of 14.8 MBq (Group A), 29.6 MBq (Group B) and 44.4 MBq (Group C), while a non-radioactive seed was implanted near the urethra of the controls (Group D). Four weeks later, we detected the radiation-induced pathological and morphological changes in the urethra by H&E, light microscopy and electron microscopy.

RESULTSFour weeks after the implantation, no obvious histopathological and ultrastructural changes were observed in the urethral tissues of the experimental rabbits as compared with the control group. The scores on the radioactive damages to the urethra obtained by light microscopy were (2.20 +/- 0.18), (2.23 +/- 0.15), (2.27 +/- 0.10) and (2.10 +/- 0.17) respectively in Group A, B, C and D, with no significant differences between the first three groups and the control (P > 0.05). And the scores on the FlaMeng semi- quantitative analysis of mitochondria in the experimental groups were (1.23 +/- 0.13), (1.34 +/- 0.25) and (1.41 +/- 0.30) respectively, not significantly different from (1.12 +/- 0.13) the control (P > 0. 05).

CONCLUSIONThe radioactive damage induced by 125I seeds to the urethra increases with the enhanced radiation dose. Intraoperative implantation of 125I seeds at the prescription dose has no obvious adverse effect on the rabbit urethra.

Animals ; Dose-Response Relationship, Radiation ; Iodine Radioisotopes ; adverse effects ; Male ; Microscopy, Electron ; Rabbits ; Radiation Injuries, Experimental ; etiology ; pathology ; Urethra ; pathology ; radiation effects ; ultrastructure

BACKGROUNDTyrosine kinase signaling cascades play a critical role in the pathogenesis of allergic airway inflammation. Sunitinib, a multitargeted receptor tyrosine kinase inhibitor, has been reported to exert potent immunoregulatory, anti-inflammatory and anti-fibrosis effects. We investigated whether sunitinib could suppress the progression of airway inflammation, airway hyperresponsiveness (AHR), and airway remodeling in a murine model of chronic asthma.

METHODSOvalbumin (OVA)-sensitized mice were chronically challenged with aerosolized OVA for 8 weeks. Some mice were intragastrically administered with sunitinib (40 mg/kg) daily during the period of OVA challenge. Twelve hours after the last OVA challenge, mice were evaluated for the development of airway inflammation, AHR and airway remodeling. The levels of total serum immunoglobulin E (IgE) and Th2 cytokines (interleukin (IL)-4 and IL-13) in bronchoalveolar lavage fluid (BALF) were measured by ELISA. The expression of phosphorylated c-kit protein in the lungs was detected by immunoprecipitation/Western blotting (IP/WB) analysis.

RESULTSSunitinib significantly inhibited eosinophilic airway inflammation, persistent AHR and airway remodeling in chronic experimental asthma. It reduced levels of total serum IgE and BALF Th2 cytokines and also lowered the expression of phosphorylated c-kit protein in remodelled airways.

CONCLUSIONSSunitinib may inhibit the development of airway inflammation, AHR and airway remodeling. It is potentially beneficial to the prevention or treatment of asthma.

Angiogenesis Inhibitors ; pharmacology ; Animals ; Asthma ; chemically induced ; drug therapy ; immunology ; Blotting, Western ; Bronchial Hyperreactivity ; chemically induced ; immunology ; Bronchoalveolar Lavage Fluid ; chemistry ; Female ; Immunoglobulin E ; blood ; Immunohistochemistry ; Immunoprecipitation ; In Vitro Techniques ; Indoles ; pharmacology ; Inflammation ; chemically induced ; immunology ; Interleukin-13 ; metabolism ; Interleukin-4 ; metabolism ; Lung ; drug effects ; immunology ; metabolism ; Mice ; Mice, Inbred BALB C ; Ovalbumin ; pharmacology ; Proto-Oncogene Proteins c-kit ; metabolism ; Pyrroles ; pharmacology

BACKGROUNDNuclear factor kappaB (NF-kappaB) overactivation, requiring phosphorylation and degradation of its inhibitor IkappaBalpha, is the basis for chronicity of airway inflammation in asthma. Based on our previous plasmid pShuttle-IkappaBalpha, carrying an IkappaBalpha gene from human placenta, we optimized a novel IkappaBalpha mutant (IkappaBalphaM) gene, constructed and characterized its replication-deficient recombinant adenovirus (AdIkappaBalphaM), and tested whether AdIkappaBalphaM-mediated overexpression of IkappaBalphaM could inhibit the NF-kappaB activation in endothelial cells.

METHODSIkappaBalphaM gene (203 - 1003 bp) encoding 267 amino acids, acquired by site-directed deleting N-terminal phosphorylation sites of serine 32/36, was subcloned into the pShuttle and pGEM-T vectors for further polymerase chain reaction (PCR), restriction digestion, deoxyribonucleic acid (DNA) sequencing and homology analyses. Subsequent to inserting the expression unit of pShuttle-IkappaBalphaM, containing cytomegalovirus (CMV) promoter, IkappaBalphaM complementary DNA (cDNA) and polyadenylic acid (PolyA) signals, into the type 5 adenovirus (Ad5) vector, the resultant AdIkappaBalphaM was packaged in human embryonic kidney (HEK) 293 cells by cotransfection with lipofectamine. Western blot analysis and electrophoretic mobility shift assay were utilized to detect the AdIkappaBalphaM-mediated overexpression of IkappaBalphaM in HEK293 cells and its suppressive effect on phorbol 12-myristate 13-acetate (PMA)-induced NF-kappaB activation in human umbilical vein endothelial (ECV304) cells, respectively.

RESULTSThe relevant nucleotides and deduced amino acids of 801 bp IkappaBalphaM gene were consistent with those of IkappaBalpha gene (GenBank accession number: M69043). The titer of the prepared AdIkappaBalphaM was 4.0 x 10 (12) plaque-forming units (pfu)/L. Moreover, the IkappaBalphaM gene was overexpressed in HEK293 cells, and potently inhibited the PMA-induced NF-kappaB activation in ECV304 cells dose-dependently.

CONCLUSIONSAdIkappaBalphaM is a novel vector for both efficient transfer and specific overexpression of IkappaBalphaM gene, as well as potent inhibition of NF-kappaB activity, providing a promising strategy for gene therapy of asthma.

Adenoviridae ; genetics ; Cell Line ; Endothelial Cells ; metabolism ; Genetic Therapy ; Humans ; I-kappa B Proteins ; genetics ; Mutation ; NF-KappaB Inhibitor alpha ; NF-kappa B ; antagonists & inhibitors ; Tetradecanoylphorbol Acetate ; pharmacology

OBJECTIVETo investigate a new operation method for the treatment of benign prostate hyperplasia(BPH).

METHODSOne hundred and seventy-nine patients with BPH were treated by the combined use of transurethral electrovaporization ablation of the prostate(TUVP) and transurethral resection of the prostate(TURP).

RESULTSThe procedure was successful and the results were satisfactory, with little bleeding and no serious complication. IPSS decreased from 29.0 preoperatively to 7.6 postoperatively (P < 0.05) and Qmax increased from 5.8 ml/s preoperatively to 14.8 ml/s postoperatively(P < 0.05).

CONCLUSIONSThe combined use of TUVP and TURP is a safe, effective and ideal method for the treatment of BPH.

Aged ; Aged, 80 and over ; Electrosurgery ; Humans ; Male ; Middle Aged ; Prostatic Hyperplasia ; surgery ; Transurethral Resection of Prostate ; methods

Animals ; Arsenicals ; pharmacology ; Cell Line, Tumor ; Chromatin Immunoprecipitation ; GATA3 Transcription Factor ; metabolism ; Gene Expression ; drug effects ; Humans ; Immunoprecipitation ; Interleukin-13 ; genetics ; metabolism ; Mice ; Oxides ; pharmacology ; Promoter Regions, Genetic ; genetics ; Protein Binding ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; drug effects ; T-Lymphocytes ; drug effects ; metabolism