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 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.;

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.

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 investigate the expression of brain-derived neurotrophic factor (BDNF) mRNA and immunoreactivity in experimental acute inflammatory brain injury.

METHODSTen rats were inoculated with pneumococcus to establish the model of bacterial inflammatory brain injury and other 6 rats were used as normal controls. At 24 h after inoculating, the expression of BDNF mRNA and BDNF protein in brain tissue was detected by in situ hybridization and immunohistochemical methods, respectively.

RESULTThe necrosis of neuron in cerebral cortex and hippocampus was observed after infection. The increase of BDNF mRNA expression in the cerebral cortex and hippocampus of experimental animals was demonstrated at 24 h after inoculation: (0.1194 +/- 0.02941 compared with 0.0662 +/- 0.01176)A and (0.1608 +/-0.01854 compared with 0.0680 +/- 0.00946)A (P<0.01), respectively. Compared with controls the expression of BDNF protein in the cerebral cortex and hippocampus was enhanced at 24 h of inoculation:(177.04+/-43.66 compared with 79.79+/-7.23)mm(2) (P<0.01) and (81.78 +/-37.47 compared with 42.98 +/-20.44)mm(2) (P<0.01), respectively. Strong positive hybridization and immunoreactivity were observed in the infiltrated inflammatory cell in leptomeninges, subarachnoid cavity, ventricles and brain parenchyma in the brain from the experimental rats.

CONCLUSIONThe expression of BDNF mRNA and BDNF protein increases following brain inflammatory injury, which supports the hypothesis that BDNF may constitute intrinsic neuroprotective mechanism as a part of the inflammatory response.

Acute Disease ; Animals ; Brain-Derived Neurotrophic Factor ; analysis ; genetics ; Calcium ; metabolism ; Female ; Immunohistochemistry ; Male ; Meningitis, Pneumococcal ; metabolism ; RNA, Messenger ; analysis ; Rats ; Rats, Sprague-Dawley