Objective To evaluate the epidemiological characteristics of brucellosis in Jinan city and to identify its cause in order to provide evidence for development of specific preventive strategies in the future.Methods Epidemic information of the disease and survey data of brucellosis cases from 2002 to 2008 in the Infectious and Endemic Disease Control Jinan Centre for Disease Control and Prevention were analyzed statistically.Results From 2002 to 2008, 52 cases were diagnosed as brucellosis, among which 39 cases from Zhangqiu city.The incidence rate ranged from 0.02 to 0.10 hundred thousandth from 2002 to 2006, and 0.25 and 0.26 hundred thousandth in 2007 and 2008, respectively. The disease was found each mouth throughout the year, marked with summer peak[38.46%(20/52)]. Patients increased year after year in summer and spring seasons(r = 0.92, P ＜ 0.01) .The disease was most commonly found in 30 - 59 age group[69.23%(36/52)];men women incidence ratio was 1.67: 1.00;farmers accounting for 94.23%(49/52). There were 5 clusters of family outbreak brucellosis, involving 12 cases. Forty five patients contacted with sheep, accounting for 86.54% (45/52). Conclusions Brucellosis epidemic in Jinan is in an upward trend, mainly in summer and spring, elderly and middle-aged men farmers are the majority of patients. Zhangqiu of Jinan city is a key place for prevention and control of brucellosis;source of infection is not completely eliminated, exotic livestock have not been effectively quarantined, practitioners with weak sense of self-protection is the main reason of the epidemic rise.

Adult ; Dapsone ; adverse effects ; Humans ; Infectious Mononucleosis ; chemically induced ; Male ; Pemphigus ; drug therapy ; Syndrome

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

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

BACKGROUNDDermal papilla cells (DPC) are a group of mesenchyme-derived cells at the base of the hair follicle, where they regulate and control hair follicle growth through the expression and secretion of cytokines. Nevertheless, the role of DPC derived chemokines and other cytokines in the hair follicle biology remain speculative. In this study, we investigated the expression of basic fibroblast growth factor (bFGF), endothelin-1 (ET-1) and stem cell factor (SCF) in different passages of cultured DPC and their effects on the biological behaviour of DPC.

METHODSThe expression of bFGF, ET-1 and SCF in different passages of cultured DPC and their possible effects on the biological behavior of DPC are investigated using in situ hybridization and immunochemistry. In addition, we performed transplantation of hair follicle cells into nude mice. The cultured DPC, dermal sheath cells and fibroblast of human scalp, respectively, were mixed with cells of the hair follicle epithelium in different ratios, and then were cultured in hair follicle organotypic cultures or implanted into the subcutis of nude mice.

RESULTSThe expression of ET-1 and SCF in early passages of cultured DPC became stronger, but turned weaker and even negative in late passages (> 6 passages). Hair follicle-like structures were formed after DPC combined with the cells of hair follicle epithelium cells in hair follicle organotypic cultures. When hair follicle organotypic cultures were implanted into the subcutis of nude mice, the relative intact hair follicles were formed. After the transplantation of hair follicle cells into the nude mice, the hair follicle-like structure was formed in the group that contained DPC mixed with hair follicle epithelium cells. However, no hair follicles were formed in the other two groups. It was found that the higher the expression of ET-1 and SCF in DPC, the stronger the ability of DPC to induce hair follicle regeneration.

CONCLUSIONSThe cultured DPC can induce hair follicle regeneration and sustain hair growth in vivo and in vitro. Moreover, the expression of ET-1 and SCF is correlated with the ability of DPC inducing hair follicle regeneration.

Animals ; Cells, Cultured ; Endothelin-1 ; analysis ; Fibroblast Growth Factor 2 ; analysis ; Hair Follicle ; physiology ; Humans ; Immunohistochemistry ; In Situ Hybridization ; Mice ; Mice, Nude ; Regeneration ; Skin ; chemistry ; cytology ; Stem Cell Factor ; analysis

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 investigate the effect of fetal bovine serum (FBS) on expression of pigment epithelium-derived factor (PEDF) in normal epidermal keratinocytes and dermal fibroblasts.

METHODSKeratinocytes and fibroblasts were incubated with 10% FBS. PEDF protein level in the cells was determined by immunofluorescence and Western blot.

RESULTSPEDF was localized mostly in the cytoplasm,while some in the nuclei. The distribution of PEDF in cytoplasm was in a granular pattern. 10% FBS increased the expression of PEDF both in keratinocytes and fibroblasts,but histamine and Phorbol 12-myristate 13-acetate (PMA) did not interfere the distribution of PEDF in cells.

CONCLUSION10% FBS can upregulate expression of PEDF in epidermal keratinocytes and dermal fibroblasts.

Animals ; Cattle ; Cells, Cultured ; Epidermis ; cytology ; metabolism ; Eye Proteins ; genetics ; metabolism ; Fetus ; Fibroblasts ; cytology ; metabolism ; Keratinocytes ; cytology ; metabolism ; Nerve Growth Factors ; genetics ; metabolism ; Serpins ; genetics ; metabolism ; Serum ; physiology ; Skin ; cytology ; metabolism ; Up-Regulation

OBJECTIVETo determine the autocrine effect of vascular endothelial growth factor (VEGF) on epidermal keratinocytes HaCaT cells.

METHODSCultured HaCaT cells were treated with various concentrations of VEGF(165) (0,1,5,10,25,50,100 ng/ml) or Avastin (0,0.063,0.125,0.25,0.50,1.0,2.0 mg/ml) in vitro. HaCaT cell proliferation was determined by MTT assay and the cell migration was measured by migration assay. The effect of VEGF(165) (10 ng/ml) on phosphorylation of ERK1/2 was detected in HaCaT cells pretreated or not pretreated with Avastin (0.5 mg/ml).

RESULTSVEGF enhanced the proliferation and migration of HaCaT cells in a dose-dependent manner, while Avastin inhibited the effects of VEGF also in a dose-dependent manner. VEGF(165) (10 ng/ml) induced the phosphorylation of ERK1/2 in HaCaT cells,but which was blocked by Avastin (0.5 mg/ml).

CONCLUSIONVEGF enhanced the proliferation and migration of HaCaT cells in a dose-dependent manner, while Avastin inhibited the effects of VEGF also in a dose-dependent manner. VEGF(165) (10 ng/ml) induced the phosphorylation of ERK1/2 in HaCaT cells,but which was blocked by Avastin (0.5 mg/ml).

Autocrine Communication ; Cell Line ; Cell Proliferation ; drug effects ; Dose-Response Relationship, Drug ; Epidermis ; cytology ; Humans ; Keratinocytes ; cytology ; Skin ; cytology ; Vascular Endothelial Growth Factor A ; pharmacology

OBJECTIVETo investigate the anti-tumor effect and the mechanism of down-regulation of HER - 2 by cabamazepine in SKBR - 3 cells , a breast cancer cell line with HER - 2 over - expression.

METHODSWestern blotting was performed to evaluate the Her-2 expression level. The mRNA level of HER-2 was detected by RT-PCR. Immunoprecipitation was applied to detect the chaperon function and acetylation level of HSP90. The viability of cells was tested by MTT assay.

RESULTSCabamazepine treatment down-regulated HER-2 expression. Only HER-2 protein level decrease was observed with 10 micromol/L cabamazepine treatment, but both protein and mRNA expressions were inhibited by 100 micromol/L cabamazepine. Cabamazepine treatment could induce a higher acetylation level of HSP90 and destroy its chaperon function. Cabamazepine exerted synergism with Herceptin in promoting HER-2 protein degradation and synergism or potentiation with Herceptin or 17-AAG in inhibition of proliferation.

CONCLUSIONCabamazepine can reduce the expression of HER-2 and show a synergistic effect with Herceptin or 17-AAG. There may be potential benefits of carbamazepine for cancer therapy in future. HER-2;

Acetylation ; drug effects ; Antibodies, Monoclonal ; pharmacology ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents ; pharmacology ; Benzoquinones ; pharmacology ; Blotting, Western ; Breast Neoplasms ; metabolism ; pathology ; Carbamazepine ; pharmacology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Down-Regulation ; drug effects ; Drug Synergism ; Female ; Gene Expression Regulation, Neoplastic ; drug effects ; HSP90 Heat-Shock Proteins ; antagonists & inhibitors ; genetics ; metabolism ; Histone Deacetylase Inhibitors ; Humans ; Lactams, Macrocyclic ; pharmacology ; RNA, Messenger ; genetics ; metabolism ; Receptor, ErbB-2 ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Trastuzumab