No abstract available.
Diabetic Nephropathies*

No abstract available.
Erythrocytes* ; Humans ; Kidney Failure, Chronic*

Lung cancer is the most common malignant tumor worldwide and its incidence continues to rise each year. Recent development of molecular biologic method has led to advances in determining the etiologic factors of lung cancer and the establishment of cell lines has provided a lot of information on the through chemosensitivity, radiation biology studies, cytogenetics, and molecular biologic studies, which permits improved treatment for lung cancer. We established a small cell lung cancer cell line, designated JePa-1, obtained from malignant pericardial effusion of small cell lung cancer patient and characterized its morphologic and molecular biologic features. the JePa-1 cell line grew relatively slowly (doubling time 45hrs) as very loosely adherent floating aggregates growing in small clumps with distinct cell outlines and intertwined cords. Also JePa-1 cell line secreted antidiuretic hormones. Electronmicroscopic examination revealed that JePa-1 cell line and xenografts contained electron dense core granules, characteristic of being of neuroendocrine origin. To investigate the tumorigenic capacity, the JePa-1 cell line was injected into SCID and nude mice. Tumors taken from xenografts were observed in 3 out of 4 of the SCID mice and 2 out of 4 of the nude mice. The histologic characteristics of the xenografts were similar to those of the cell line and the original cytologic finding of the pericardial fluid, suggesting small cell carcinoma. The results of immunohistochemical markers showed reactivity for Rb protein, c-myc, TGF-alpha, TGF-beta , EGFR, keratin, NSE, chromogranin, and EMA. The DNA ploidy and the index of the JePa-1 cells was tetraploid and 2.13, respectively. The positive rate for the Rb, c-myc and K-ras proteins of the JePa-1 cell line were 98.9%, 99.3%, and 99.7% respectively as determined by flow cytometry. Cytogenetic analysis using the G-banding technique showed 65 chromosomes with various numerical and structural abnormalities. On examination of the expression of TGF-alpha, TGF-beta , and EGFR by PCR, only the EGFR was positive Through the establishment of JePa-1 cell line, we report in this paper the characterization of a small cell lung cancer such as morphologic and immunocytochemical features, growth characteristics in culture, hormone production, expression of oncoprotein and several growth factors, tumorigenicity, chromosomal abnormalities, and DNA ploidy and index. The JePa-1 cell line will be valuable in vitro studies for the etiology, treatment and the prognostic factors in small cell lung cancer.
Animals ; Carcinoma, Small Cell ; Cell Line ; Chromosome Aberrations ; Cytogenetic Analysis ; Cytogenetics ; DNA ; Flow Cytometry ; Heterografts ; Humans ; Immunohistochemistry ; Incidence ; Intercellular Signaling Peptides and Proteins ; Lung Neoplasms ; Mice ; Mice, Nude ; Mice, SCID ; Pericardial Effusion ; Ploidies ; Polymerase Chain Reaction ; Radiobiology ; Retinoblastoma Protein ; Small Cell Lung Carcinoma* ; Tetraploidy ; Transforming Growth Factor alpha ; Transforming Growth Factor beta ; Vasopressins

No Abstract Available.

No abstract available.
Antioxidants* ; Glutathione* ; Humans

We reviewed 40 cases of femoral shaft fractures in children treated with split Russel traction and initial fracture angulation above 10 degree. The treatment of femoral shaft fractures in children is various according to age. Satisfactory results have been reported with split-Russel traction. At an average follow-up of 33 months, we obtained following results about remodelling of fracture site & physeal site, possible acceptable angulation of fracture. 1. The average time of traction was 18 days, and hip spica cast was applied for 28 days. 2. Malunion within 25degrees in flexion & 23degrees in valgus & 24degrees in varus was well corrected spontaneously. 3. Average correction of initial angular deformity was 86% at last follow up. 4. Anterior angulation was corrected at 83%, varus 87%, valgus 88%. 5. Remodelling according to direction of deformity was no statistical correlation (P>0.05), and then spontaneous correction of angular deformity was same without relation to direction of deformity. 6. Remodelling according to site was statistical correlation (P<0.05), fracture site 26%, physes 74%. And proximal physes 36%, distal physes 38%.
Child* ; Congenital Abnormalities* ; Follow-Up Studies ; Hip ; Humans ; Traction*

No abstract available.
Emphysema* ; Heart Septal Defects, Ventricular*

No abstract available.

BACKGROUND: CTLA4 (CD152), which is expressed on the surface of T cells following activation, has a much higher affinity for B7 molecules comparing to CD28, and is a negative regulator of T cell activation. In contrast to stimulating and agonistic capabilities of monoclonal antibodies specific to CTLA-4, CTLA4Ig fusion protein appears to act as CD28 antagonist and inhibits in vitro and in vivo T cell priming in variety of immunological conditions. We've set out to confirm whether inhibition of the CD28-B7 costimulatory response using a soluble form of human CTLA4Ig fusion protein would lead to persistent inhibition of alloreactive T cell activation. METHODS: We have used CHO-dhfr cell-line to produce CTLA4Ig fusion protein. After serum free culture of transfected cell line we purified this recombinant molecule by using protein A column. To confirm characterization of fusion protein, we carried out a series of Western blot, SDS-PAGE and silver staining analyses. We have also investigated the efficacy of CTLA4Ig in vitro such as mixed lymphocyte reaction (MLR) & cytotoxic T lymphocyte (CTL) response and in vivo such as experimental autoimmune encephalomyelitis (EAE), graft versus host disease (GVHD) and skin-graft whether this fusion protein could inhibit alloreactive T cell activation and lead to immunosuppression of activated T cell. RESULTS: In vitro assay, CTLA4Ig fusion protein inhibited immune response in T cell-specific manner: 1) Human CTLA4Ig inhibited allogeneic stimulation in murine MLR; 2) CTLA4Ig prevented the specific killing activity of CTL. In vivo assay, human CTLA4Ig revealed the capacities to induce alloantigen-specific hyporesponsiveness in mouse model: 1) GVHD was efficiently blocked by dose-dependent manner; 2) Clinical score of EAE was significantly decreased compared to nomal control; 3) The time of skin-graft rejection was not different between CTLA4Ig treated and control group. CONCLUSION: Human CTLA4Ig suppress the T cell-mediated immune response and efficiently inhibit the EAE, GVHD in mouse model. The mechanism of T cell suppression by human CTLA4Ig fusion protein may be originated from the suppression of activity of cytotoxic T cell. Human CTLA4Ig could not suppress the rejection in mouse skin-graft, this finding suggests that other mechanism except the suppression of cytotoxic T cell may exist on the suppression of graft rejection.
Animals ; Antibodies, Monoclonal ; B7 Antigens ; Blotting, Western ; Cell Line ; Electrophoresis, Polyacrylamide Gel ; Encephalomyelitis, Autoimmune, Experimental ; Graft Rejection ; Graft vs Host Disease ; Homicide ; Humans ; Immunosuppression ; Lymphocyte Culture Test, Mixed ; Lymphocytes ; Mice ; Silver Staining ; Staphylococcal Protein A ; T-Lymphocytes

No abstract available.
Diagnosis* ; Female ; Humans ; Polycystic Kidney Diseases*