Adolescent ; Adult ; Child ; Cholesteatoma, Middle Ear ; surgery ; Ear, Middle ; Female ; Humans ; Male ; Middle Aged ; Young Adult

Objective To explore the sensitivity and specificity of colposcopy directed biopsy (CDB) and the value of loop electrosurgical excision procedure (LEEP) for the diagnosis and treatment of microinvasive cervical cancer (MCC). Methods One hundred and thirty five patients with MCC were diagnosed with LEEP in Obstetrics and Gynecology Hospital, Fudan University from April 2008 to November 2010, and were retrospectively analyzed on CDB diagnoses and following treatment after LEEP. According to patient′s desire for preservation of fertility and cone margin status, following strategies after LEEP included follow-up, second LEEP, hysterectomy, modified radical hysterectomy and radical hysterectomy. Single and multiple factors related to residual lesions after LEEP were analysed with Pearson Chi-square test and logistic regression model, respectively. Results CDB diagnosed MCC with a sensitivity of 4.4%(6/135), specificity of 100.0%(4 680/4 680), and false negative rate of 95.6%(129/135). Among the 135 patients, 29 did not receive further treatment in our hospital and lost contact. One hundred and six patients had secondary treatment or follow-up in our hospital, 4 of among which were closely followed up;one hundred and two received further treatment, which included 6 cases with second LEEP (3 received extrafascial hysterectomy after repeat LEEP), 59 cases hysterectomy, 14 cases modified radical hysterectomy and 26 cases radical hysterectomy. For factors related to residual lesions after LEEP, single factor analysis showed that the ratio of residual lesion in patients aged 27-39, 40-49 and 50-65 years were respectively 19.0%(11/58), 15.4%(10/65) and 5/12 (χ2=4.505, P=0.105). Residual lesions occurred in 24.7%(23/93) of patients with positive LEEP margins, which was more than that 7.1%(3/42) of patients with negative LEEP margins (χ2=5.756, P=0.016). The ratio of residual lesions in patients with positive endocervical, ectocervical and deep stromal margins were respectively 29.6%(8/27), 17.1%(7/41)and 30.6%(11/36;χ2=2.275, P=0.321). Residual lesions in patients with or without lymph vascular space invasion (LVSI) were 2/7 and 18.8%(24/128), respectively (χ2=0.412, P=0.521). The ratio of residual lesions in patients with invasion depth of<1 mm was 17.1%(7/41), 1-<3 mm was 19.0%(16/84), and 3-5 mm was 3/10, with no significant difference among three groups (χ2=0.870, P=0.647). Logistic regression analysis showed positive cone margin (OR=5.069, P=0.014) and age (OR=1.080, P=0.024) were the independent risk factors of residual lesions after LEEP conization. Conclusions CDB alone is not adequate for the diagnosis of MCC. For young patients who desire to preserve fertility with a negative cone margin, close follow-up is acceptable. Cone margin status and age are two independent risk factors for residual lesions after LEEP.

Adult ; Cochlear Implantation ; Female ; Hearing Loss, Sensorineural ; etiology ; surgery ; Humans ; Meniere Disease ; complications ; surgery

Administration, Sublingual ; Bacterial Vaccines ; administration & dosage ; immunology ; Child ; Child, Preschool ; Double-Blind Method ; Female ; Humans ; Immunoglobulin A ; blood ; Immunoglobulin A, Secretory ; analysis ; Male ; Pseudomonas Vaccines ; Recurrence ; Respiratory Tract Infections ; immunology ; prevention & control ; Treatment Outcome

OBJECTIVETo study the effects of acitretin on the expression of signaling pathway-related genes in an epidermal squamous-cell carcinoma cell line.

METHODSThe mRNA expression levels of STAT3, cyclin D1 and p42/44MAPK were detected in a human epidermal carcinoma cell line A431 by RT-PCR. Their expressions at protein level were studied by Western blot. The expression levels were studied in cells treated with or without 10(-5) mol/L acitretin at different time intervals.

RESULTS(1) Acitretin could significantly inhibit the expression of STAT3 and cyclin D1 mRNA in a time-dependent manner (P < 0.05). The STAT3 and cyclin D1 protein expression levels were down-regulated. Acitretin could also down-regulate the p42/4MAPK mRNA expression. (2) After incubation with acitretin, the mRNA level of cyclin D1 cells was positively correlated with that of STAT3 (P < 0.05). The cyclin D1 protein level was also positively correlated with that of STAT3 (P < 0.05). However there was no correlation of mRNA levels between cyclin D1 and p42/44MAPK.

CONCLUSIONRegulation of the Jak/STAT3 signaling pathway may play an important role in the effect of acitretin on epidermal squamous-cell carcinoma cells. The abnormal expression of STAT3 can be regarded as a prerequisite for acitretin treatment effect.

Acitretin ; pharmacology ; Antineoplastic Agents ; pharmacology ; Carcinoma, Squamous Cell ; metabolism ; pathology ; Cell Line, Tumor ; Cyclin D1 ; biosynthesis ; genetics ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Humans ; Mitogen-Activated Protein Kinase 1 ; biosynthesis ; genetics ; Mitogen-Activated Protein Kinase 3 ; biosynthesis ; genetics ; RNA, Messenger ; biosynthesis ; genetics ; STAT3 Transcription Factor ; biosynthesis ; genetics ; Signal Transduction

OBJECTIVE To investigate how MLKL functions on the membrane and explore its electrophysiological characters and structure. METHODS The full-length human MLKL were expressed in SF21 cells and purified using glutathione-sepharose affinity chromatography. The currents of purified MLKL proteins were recorded in avoltage-clamp mode using a Warner BC-535 bilayer clamp amplifier. The currents were digitized using pCLAMP 10.2 software. HEK293 cells were cultured and transfected with MLKL plasmid. Cell viability was examined using the CellTiter- Glo Luminescent Cell Viability Assay kit. RESULT MLKL forms cation channels that are permeable preferentially to Mg2+ rather than Ca2+ in the presence of Na+ and K+. Moreover,each MLKL monomer contains five transmembrane helices:H1, H2, H3 , H5 and H6 of the N-terminal domain which is sufficient to form channels. Finally, MLKL-induced membrane depolarization and cell death exhibit a positive correlation to its channel activity.

OBJECTIVETo investigate the clinical value of osseointegration for repairing auricular defects and deformity.

METHODSTwenty cases (21 ears) including congenital and non-congenital auricular defects and deformity, were treated with osseointegrated prostheses according to the manual of Branemark implanting system. The first-stage operation was for osseointegration of implants, and the second-stage was for anchoring the prostheses. All cases were followed up for six months to three years.

RESULTSOne-time success rate is 100%. Satisfactory rate of appearance recovery is 90.47%. The infection rate between osseointegrated implants and surrounding tissue is 14.28%. The stability rate of prostheses is 100%.

CONCLUSIONSIt has a good result to apply osseointegrated prostheses for repairing auricular defects and deformity.

Adolescent ; Adult ; Child ; Ear Auricle ; abnormalities ; injuries ; surgery ; Female ; Humans ; Male ; Osseointegration ; Prosthesis Implantation ; Reconstructive Surgical Procedures ; methods ; Treatment Outcome ; Young Adult

OBJECTIVETo study the effects of Acitretin on growth inhibition and apoptosis of epidermoid carcinoma cell line A431 and its molecular mechanisms.

METHODSA431 cells were treated with Acitretin at the concentration of 10(-5)mol/L in different time intervals. The inhibition of cell growth was determined by MTT method, morphological changes were observed by electron microscopy, apoptosis was assessed by flow cytometry and Annexin-V staining. The mRNA expression levels of STAT3, cyclinD1 and p42/44MAPK were detected by reverse transcriptase polymerase chain reaction (RT-PCR). The protein expression levels of P-STAT3 and CyclinD1 were observed by Western blot in A431 cells.

RESULT(1)Acitretin inhibited the growth of A431 cells in vitro in a dose-and time-dependent manner. Morphological changes revealed characteristics of cell apoptosis. Flow cytometry showed more sub-G(1) phase in A431 cells and more cells positively stained with Annexin-V. (2)Acitretin significantly inhibited the expression of STAT3 and CyclinD1 mRNA in A431 cells in vitro in a time-dependent manner(P<0.05). The p-STAT3 and CyclinD1 protein levels were down regulated. The Acitretin could also down regulate the p42/4MAPK mRNA in A431 cells. (3) After incubation with Acitretin, the mRNA level of CyclinD1 in A431 cells was positively correlated with that of STAT3(p<0.05). The protein level of CyclinD1 was also positively correlated with that of p-STAT3(p<0.05). However, there was no correlation between Mrna levels of CyclinD1 and p42/44MAPK.

CONCLUSION(1)Acitretin plays an inhibitory role in the tumor cell growth and induces the cell apoptosis in A431 cells. (2)The regulation of the Jak/STAT3 signaling pathway may play an important role in inducing growth inhibition and apoptosis by Acitretin in A431 cells.

Acitretin ; pharmacology ; Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Carcinoma, Squamous Cell ; pathology ; Cell Line, Tumor ; Humans ; Signal Transduction ; drug effects ; Skin Neoplasms ; pathology

OBJECTIVETo search for genes related to cisplatin (DDP) sensitivity in small-cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC) cell lines.

METHODSThe sensitivity of 4 SCLC lines and 6 NSCLC lines to DDP was evaluated by MTT assay. The expression of 1291 genes related to DDP-sensitivity in the 10 cell lines was measured by cDNA macroarray and the relationship between genes and DDP-sensitivity was analyzed.

RESULTS20 genes were negatively related to DDP-sensitivity in the SCLC and NSCLC cell lines, including Metallothionein, Cathepsin B, TIMP1, TNF-R1, TGF beta-induced 68 000, Cathepsin L, Galectin-1, Annexin 11, PAI-1, IGFBP4, UPAR, Jagged, CD13, alpha 1 A-AR, EphA2 (Eck), APC, RhoC, Fibromodulin, GATA-6 and HSC 70, while only procoagula and MDM2 were positively related to DDP-sensitivity in the SCLC and NSCLC cell lines. 10 genes were negatively related to DDP-sensitivity in the SCLC cell lines, including VHL, MMP-7, Elongin A, GSK-3 beta, SLC, Galectin-3, integrin beta 5, moesin, IKK beta, and ETV 1, while only AT2 was positively related to DDP-sensitivity in the SCLC cell lines. 10 genes were negatively related to DDP-sensitivity in the NSCLC cell lines, including Clusterin, FG FR-2, Thrombospondin 1, HSP 32, Lactate dehydrogenase A, P300, Thymosin beta l0, CD81, C/EBP gamma, Rak, while only CaMKK and TPA were positively related to DDP-sensitivity in the NSCLC cell lines.

CONCLUSIONThere were 45 genes related to DDP-sensitivity in 10 lung cancer cell lines. There were 22 co-expressed genes in both SCLC and NSCLC cell lines, and only 11 and 12 genes expressed in the SCLC and NSCLC cell lines, respectively.

Antineoplastic Agents ; pharmacology ; Carcinoma, Non-Small-Cell Lung ; genetics ; metabolism ; pathology ; Cell Line, Tumor ; Cisplatin ; pharmacology ; Drug Resistance, Neoplasm ; Gene Expression Profiling ; methods ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms ; genetics ; metabolism ; pathology ; Oligonucleotide Array Sequence Analysis ; methods ; Small Cell Lung Carcinoma ; genetics ; metabolism ; pathology

OBJECTIVETo evaluate the radiation induced parotid dysfunction in nasopharyngeal carcinoma (NPC) patients who had received different methods of radiotherapy.

METHODSFrom January 1996 to January 2000, 380 NPC patients were divided into conventional fraction (CF-175 patients), late-course accelerated hyperfractionation (LCAF-63 patients) and intensity modulated radiation therapy (IMRT-142 patients) groups. Conventional radiotherapy was given with a total dose of 70 Gy. Patients in the LCAF group were treated with the same fractionation as CF group until the dose of 36 - 40 Gy, then followed by LCAF radiotherapy to a total dose of 75 Gy. IMRT in the form of full-course was given to a total dose of 72 Gy. Acute parotiditis was observed during the treatment. The parotid secretory function was examined 2 years after radiotherapy.

RESULTSThe dose of parotid in IMRT was much lower than those in the other 2 groups. Extreme damage rates of parotid secretory function in CF, LCAF and IMRT groups were 81.7%, 81.0% and 69.7% (P < 0.05); acute parotiditis rates were 23.4%, 20.4% and 41.3% respectively, with the differences among the 3 groups significant (P < 0.05).

CONCLUSIONThe radiation parotid functional damage differs in the various methods of radiotherapy. IMRT, being able to improve the tumor target coverage and spare the adjacent critical structures, is indicated for NPC.

Adolescent ; Adult ; Carcinoma, Squamous Cell ; radiotherapy ; Dose Fractionation ; Female ; Humans ; Male ; Middle Aged ; Nasopharyngeal Neoplasms ; radiotherapy ; Parotid Gland ; physiopathology ; radiation effects ; Parotitis ; etiology ; Radiation Injuries ; physiopathology ; Radiotherapy, Intensity-Modulated ; methods