Adult ; Dust ; analysis ; Female ; Humans ; Male ; Middle Aged ; Neural Networks (Computer) ; Occupational Exposure ; Silicosis ; diagnosis ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; methods

to common antifungal drugs.

Objective:To investigate the efficiency of Agrobacterium tumefaciensmediated transfor-mation of Aspergillus fumigatus by using pyrG as a recessive selectable marker.Methods: FAP1 and SHO1 genes target sequences,composed of a selectable marker pyrG and the flanking sequences of the FAP1 and the SHO1 genes,were cloned into a binary plasmid pDHt/sk,respectively.The produced plasmids were transformed into A.tumefaciens.The A.tumefaciens and uracil auxotroph A.fumigatus were cocultured in induction medium without uricil and uridine at 24 ℃ for 48 h.To inhibit growth of A.tumefaciens and to select transformants,the cultures were transferred to 37 ℃ and incubated for another 48 h.Results: In this study,A.tumefaciens-medidated transformation of A.fumigatus produced high homologous recombination rates,which was 44%(7 of 16) for FAP1 and 35%(7 of 20) for SHO1.Conclusion: Our study showed that A.tumefaciens-medidated transformation by using pyrG as a recessive selectable marker is an efficient tool for target gene deletion of A.fumigatus.

Objective To evaluate the effect of NGX6 combined with cisplatin on the inhibition rate of A549 cells and NCI-H1975 cells and antitumor effects in vivo.Methods The NGX6 was loaded in the LPD, and prepare Liposome protamine DNA complexes.A549 cells and NCI-H1975 cells were seperately divided into NGX6 group ( 30 μg/mL NGX6 concentration ) , cisplatin group, NGX6 +cisplatin group, PBS as negative control group.The effect of cytotoxicity of four group on A549 cells and NCI-H1975 cell were evaluated by MTT assay.the clone forming rate and the inhibition rate were determined by Cell colony count.lung transplantation tumor model were successfully established, then nude mice were divided into four groups as abeve, each group of 10, tumor size and survival period were determined tumor cell apoptosis were observed.Results The cell viability of A549 cells and NCI-H1975 cells of (NGX6 +cisplatin) were lower than that of NGX6 group, cisplatin group and saline group, respectively(P<0.01).The cloning efficiency of A549 cells and NCI-H1975 cells of ( NGX6 +cisplatin) were lower than that of NGX6 group, cisplatin group and saline group, respectively(P<0.01).The tumor inhibitory rate was in vivo for (NGX6 +cisplatin) was higher than other group(P<0.01).The median survival of nude mice in (NGX6 +cisplatin), NGX6, cisplatin and saline group were 43,31,29 and 15 days.Conclusion NGX6 combination with cisplatin can inhibit the cell proliferate of lung cancer cells and inhibit the tumor growth and the combination of NGX6 and cisplatin may be a potentially effective treatment for lung cancer.

Objective To explore the methods of cerebral palsy registration. Methods The operation of cerebral palsy registration in Jiamusi was introduced, including the development of the management system, and contents, steps and notices of registration. Results 51 cases with cerebral palsy in Jiamusi were registered from Januaray 1st, 2002 to December 31st, 2011. Conclusion Less children with cerebral palsy had registered, and received insufficient rehabilitation.

OBJECTIVETo observe the expression of P-selectin (Ps), intercellular adhesion molecule-1 (ICAM-1) and nuclear factor-kappa B (NF-kappaB) in lung tissues of acute lung injury (ALI) rat model induced by oleic acid (OA) and to explore the protective effects of melatonin (MT) in lung tissues in rats.

METHODSAll rats were randomly divided into four groups: control group, OA group, MT + OA group and SB203580 + OA group. Rat model of ALI was established by intravenous injection of oleic acid (OA). Lung coefficient was measured, lung tissues were imbedded by paraffin to observe morphological changes and the expression of Ps, ICAM-1 and NF-kappaB in lung tissues by means of immunohistochemistry staining.

RESULTSCompared with control group, the lung coefficient increased significantly in OA group (P < 0.05). Alveolar septum thickened significantly in OA group, there had many infiltrated inflammatory cells and collapsed alveoli of lung; positive expression of Ps, ICAM-1 and NF-kappaB were very obvious (P < 0.05); the administration of MT and SB203580 mitigated above changes significantly (P < 0.05).

CONCLUSIONMT possesses obviously protective effect on lung tissues during ALI, its protective mechanism might be related to the inhibition of the expression of Ps, ICAM-1 and NF-kappaB.

Acute Lung Injury ; chemically induced ; physiopathology ; prevention & control ; Animals ; Down-Regulation ; drug effects ; Intercellular Adhesion Molecule-1 ; metabolism ; Male ; Melatonin ; pharmacology ; therapeutic use ; NF-kappa B ; metabolism ; Oleic Acid ; adverse effects ; P-Selectin ; metabolism ; Protective Agents ; pharmacology ; Rats ; Rats, Sprague-Dawley

Objective To investigate the effect of amiloride on the invasion capacity of esophageal carcinoma EC9706 cell line in vitro and to elucidate its possible mechanism.Methods The invasion capacities of EC9706 cells pretreated with amiloride were measured by transwell chamber assay. The urokinase-type plasminogen activator (uPA) transcription were determined by RT-PCR.The protein expression of uPA were assessed by Western blot.Results After the EC9706 cells were pretreated with amiloride at different concentrations,the number of invaded cells was obviously less than those of control group with obvious dosage dependent pattern (96±7,78±6,57±6,33±4,15±3,F =43.46,P ＜ 0.01).The transcription levels of uPA mRNA and the protein expression levels of uPA in EC9706 cells decreased significantly compared with the control (mRNA:0.623±0.065,0.526±0.054,0.389±0.041,0.312±0.038,0.247±0.025,F =6.71,P ＜0.01; protein:0.732±0.064,0.644±0.057,0.533±0.058,0.391±0.036,0.267±0.043,F =6.71,P ＜0.01).Conclusion Amiloride inhibits the invasion capacity of esophageal carcinoma EC9706 cells.The mechanism might be associated with down-regulation of the expression of uPA.

Objective To investigate the expression and influence to tumor angiogenesis of urokinase-type plasminogen activator (uPA) and vascular endothelial growth factor (VEGF) in esophageal carcinoma. Methods The expression of uPA and VEGF in the tissue of normal (18 cases) and esophageal carcinoma (68 cases) were evaluated by SP immunohistochemistry, CD34 was detected as marking tumor microvessel density (MVD). uPA and VEGF expression were assessed as to the pathologically biological features of esophageal cancer and to the influence to tumor angiogenesis. Results The positive rates of uPA were 27.8 % (5/18) and 70.6 % (48/68) in the tissue of normal and esophageal carcinoma, respectively, there was significant difference in two tissues (x2 =11.63, P <0.05). The positive rates of VEGF were 22.2 % (4/18)and 63.2 % (43/68) in the tissue of normal and esophageal carcinoma, respectively, there was significant difference in two eissues (x2 =9.78, P <0.05). The expressions of uPA and VEGF in esophageal carcinoma were uniformity (x2 =9.72, P <0.05). The mean of MVD was 42.38±11.62. The positive rates of uPA and VEGF were higher in the high MVD group than those in the low MVD group (x2 =6.13, P <0.05, x2 =10.12, P <0.05,respectively). uPA and VEGF expressions in malignant tumors weren' t associated with age, gender and pathological types (P >0.05), but associated with clinical stage, histologic grading and lymph node metastasis (P <0.05). Conclusion Rising expression levels of uPA and VEGF are common in esophageal carcinoma. Altered expression of uPA and VEGF may contribute to tumor angiogenesis of esophageal carcinoma, whose overexpression indicate worse prognosis.

OBJECTIVETo evaluate the feasibility of the tissue engineered submandibular gland constructed in vivo based on submandibular gland cells and silk fibroin-chitosan (SFCS).

METHODSSubmandibular gland cells were obtained and purified. The second generation cells labeled by 5'-BrdU were seeded on SFCS(5 mm × 5 mm × 5 mm). Submandibular gland cells seeded on SFCS was implanted beneath the skin on the back. At 3, 7, 14 d post-implantation, implant sites were examined local and systemic responses. After paraffin embedding, serial sections 6 mm thick were cut and stained with either hematoxylin and eosin or brdu tissue stain for immunohistochemical studies and examined the responses of tissue. Scanning electron microscope was used to observe the growth behavior submandibular gland cells on SFCS scaffolds.

RESULTSGeneral observation: at the 3, 7, 14 d after in vivo implantation, capsule formed in the surface of insert. Histological observation: in experimental group, submandibular gland cells proliferate on the SFCS scaffold fused to form unit 14 d after implantation. Brdu immunohistochemical observation: the results of labelled cells were positive by immunohistochemical method at each time point. Cytokeratin-8 (CK-8) immunohistochemical observation: the results of labelled cells were positive by immunohistochemical method at each time point. With time, the positive cells gradually increased. Scanning electron microscope: the shape of the SFCS scaffold was mesh. At earlier, submandibular gland cells presence in disorder at attach to the SFCS. At the 14 d submandibular gland cells proliferate on the SFCS scaffold and form functional unit.

CONCLUSIONSSuch constructed tissue engineered submandibular gland based on submandibular gland cells and SFCS is promising.

Animals ; Cell Proliferation ; Cells, Cultured ; Chitosan ; chemistry ; Female ; Fibroins ; chemistry ; Keratin-8 ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Submandibular Gland ; cytology ; metabolism ; Tissue Engineering ; methods ; Tissue Scaffolds ; chemistry

Adolescent ; Astrocytoma ; classification ; metabolism ; pathology ; surgery ; Brain Neoplasms ; metabolism ; pathology ; surgery ; Child ; Child, Preschool ; Female ; Follow-Up Studies ; Glial Fibrillary Acidic Protein ; metabolism ; Humans ; Male ; Neoplasm Recurrence, Local ; Retrospective Studies ; S100 Proteins ; metabolism ; Vimentin ; metabolism