Adult ; Aged ; Aged, 80 and over ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Male ; Middle Aged ; Phytotherapy ; Pulmonary Disease, Chronic Obstructive ; complications ; therapy ; Silicosis ; complications ; therapy

Adult ; Aged ; Cystostomy ; Drainage ; methods ; Humans ; Male ; Middle Aged ; Pneumothorax ; complications ; therapy ; Retrospective Studies ; Silicosis ; complications ; therapy

Calculi ; Humans ; Lung Diseases ; Male ; Middle Aged ; Pulmonary Alveoli ; pathology

Objective To investigate the effect of rosiglitazone on renal interstitial fibrosis in chronic cyclosporine nephropathy (CCN) rats.Methods Twenty-eight rats were randomly assigned to control group,rosiglitazone (RGZ,5 mg·kg-1·d-1) group,cyclosporine A(CsA,15 mg·kg-1·d-1) group,rosiglitazone (5 mg·kg-1·d-1) +CsA group.Real-time PCR and RT-PCR methods were used to investigate the expressions of OPN,RANTES on the 14th day and MMP-9,TIMP-1 on the 35th day in kidney of CCN respectively.Results In comparison with control group,the expressions of OPN,RANTES,MMP-9,TIMP-1 in CsA and RGZ+CsA groups were increased (P＜0.05).In comparison with the CsA group,the expressions of OPN,RANTES,MMP-9,TIMP-1 in CsA+RGZ group significantly decreased (P＜0.05).Conclusion Rosiglitazone may protect renal tissue after CCN by decreasing expressions of OPN,RANTES,MMP-9,TIPM-1.

Objective To study cutaneous ultrastructural changes and FERMT1 gene mutations in a patient with Kindler syndrome. Methods Clinical data were collected, and tissue samples obtained from the lesions of poikiloderma were observed by using transmission electron microscopy. Fifteen coding exons and their flanking sequences of the FERMT1 gene were amplified by PCR and DNA sequencing was followed.Results Reduplication of lamina densa was seen between the dermal-epidermal junctions of the lesional skin. The patient was found to be homozygous for a novel splice-site mutation (IVS9 + 1G ＞ A) in FERMT1 gene, and his parents were heterozygous for it. The mutation was undetected in fifty normal control individuals.Conclusions Transmission electron microscopy may serve as an ancillary examination for the diagnosis of Kindler syndrome. The IVS9+1G＞A mutation of FERMT1 gene may contribute to the clinical phenotype of Kindler syndrome in this patient.

Objective To explore the feasibility of artificial silastic framework(SF)in repair of large area of tracheal wall defects.Methods Twenty healthy adult dogs with tracheal defects for 2.5 cm?6.0 cm-3.0 cm?6.0cm were randomly and equally divided into experimental group(repaired with SF combined with sternohyoid fasciae)and control group(repaired with T-silastie tubule combined with sternohyoid fascial flap).After the operation,the animals were sacrificed at the 4th,8th,16th,24th, and 48th weeks respectively for harvesting the tracheae that were used for tracbeoscopically observing in- flammatory reaction of the repaired defect area and light microscopically observing epithelium healing on the repaired defect area.Results In the experiment group,the repaired trachea was smooth,without proliferation of granulation;and at the 8th week,the repaired defect area was covered with epithelial cells,with good functional recovery of respiration,phonation and deglutition.In the control group,there was obvious proliferation of granulation on the tracheal surface near anterior and posterior ends of T-silas tic tubule.The animals were under asphyxia to die with extraction of T-silastic tubule.Conclusions SF has excellent tracheal skeletal function.In the meantime,SF combined with sternohyoid fasciae is a simple but effective method for repair of large area of tracheal wall defects.

Objective The aim of this study was to investigate the effect of ultrasonically activated hematoporphyrin on ultrastructure of ehrlich ascites tumor(EAT) cells and to evaluate the potential mechanism of action inducing this cytotoxicity. Methods EAT cells in vitro were exposed to ultrasound at 2^0?MHz and 1^5?W/cm+2 for 3?min in the presence or absence of hematoporphyrin.The changes of ultrastructure of sample preparation for different time were observed by transmission electron microscope. Results The degree of destruction of treated EAT cells was enhanced with the increasing of time for the sample preparation.The sites destroyed mainly involved cell membrane,mitochondrion,endoplasmic reticulum and cell nuclei.Furthermore,morphoiogical characters of ultrasound-activated hematoporphyrin induced apoptosis were observed on EAT cells.Conclusion The killing of tumor cells was ascribed mainly to the damage of ultrastructure induced by ultrasound in combined with hematoporphyrin,apoptosis was also induced during ultrasound and hematoporphyrin killing process.;

OBJECTIVETo investigate the biological function of the hepatitis C virus (HCV)-encoded F protein in hepatocytes.

METHODSThe full-length F gene was amplified by PCR from HCV genotype 1a and cloned into plasmid pSEB-3Flag by restriction enzyme digestion and ligation. Hepatoma cell lines, Huh7 and SMMC7721, were transfected with the resultant recombinant pSEB-3Flag-F or the original pSEB-3Flag (negative control) and screened with the selective antibiotic, blasticidin. Stable F gene and protein expression was verified by RT-PCR analysis. Analysis of cell growth and cell cycle was carried out by MTS assay, crystal violet staining and flow cytometry.

RESULTSHuh7 and SMMC7721 cells transfected with pSEB-3Flag-F plasmid (Huh7-F and SMMC7721-F, respectively) uniquely expressed the F gene and protein. The Huh7-F and SMMC7721-F cells showed significantly decreased proliferation rates, compared to the respective control groups. A similar HCV F-mediated growth-inhibiting activity was observed by the cell viability assay. Furthermore, cell cycle analysis revealed that the S-phase distribution was much lower in Huh7-F (47.12%) and SMMC7721-F (30.75%) cells than in the respective controls (55.35% and 33.23%, respectively) (P less than 0.05).

CONCLUSIONStable expression of the HCV F gene reduced the in vitro proliferation rate of hepatoma cell lines, indicating that the F protein may function as a growth inhibitor of infected cells.

Carcinoma, Hepatocellular ; metabolism ; pathology ; Cell Line, Tumor ; Cell Proliferation ; Hepacivirus ; genetics ; Humans ; Liver Neoplasms ; metabolism ; pathology ; Reverse Transcriptase Polymerase Chain Reaction ; Viral Core Proteins ; genetics ; metabolism

Adolescent ; Adult ; Female ; Follow-Up Studies ; Humans ; Male ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; drug therapy ; Treatment Outcome ; Young Adult

OBJECTIVETo explore the functional effects of MAPK pathway in the pathogenesis of human osteosarcoma.

METHODSGene microarray (Human Genome U133A, Affymetrix) was used to screen the differential expression of genes involved in MAPK pathway between osteosarcoma cell lines and 3 osteoblastic cell lines. KEGG metabolic pathway analysis was performed among significantly increased or decreased genes using the MATLAB software. Immunohistochemical technique was used to detect the expressions of ERK1/2, JNK and p38 proteins among 48 osteosarcoma and benign 24 osteoblastic tumor samples.

RESULTSUsing an entrance limit of > or = 2.0, 18 differentially expressed MAPK pathway-related genes were selected (10 up-regulated, 8 down-regulated) to mapped to the MAPK pathway of KEGG which are all important node genes. The positive rates of ERK1/2, JNK and p38 proteins were 83.3% (40/48), 72.9% (35/48) and 85.4% (41/48) in osteosarcomas,and 12.5% (3/24), 8.3% (2/24) and 16.7% (4/24) in the control group, respectively. The positive rates and expression intensities were statistically different between the 2 groups (P<0.01).

CONCLUSIONMAPK pathway plays an important role in the pathogenesis of osteosarcoma. ERK, JNK and p38 form an intercoordinating network and regulate the cell proliferation, differentiation, apoptosis, invasion and migration in osteosarcoma.

Adolescent ; Adult ; Aged ; Bone Neoplasms ; genetics ; metabolism ; pathology ; Cell Line, Tumor ; Child ; Female ; Gene Expression Profiling ; Humans ; JNK Mitogen-Activated Protein Kinases ; metabolism ; Male ; Middle Aged ; Mitogen-Activated Protein Kinase 1 ; metabolism ; Mitogen-Activated Protein Kinase 3 ; metabolism ; Mitogen-Activated Protein Kinases ; metabolism ; Oligonucleotide Array Sequence Analysis ; Osteoblastoma ; genetics ; metabolism ; pathology ; Osteosarcoma ; genetics ; metabolism ; pathology ; Signal Transduction ; Young Adult ; p38 Mitogen-Activated Protein Kinases ; metabolism