Buschke-Lowenstein tumor is a rare disease in the category of designated as verrucous carcinoma characterized by its invasive downward penetration of underlying tissues in the perineum and perianal regions. Viruses, unclean sanitation and cytotoxic immune reaction have been proposed as the etiology of the tumor. However, among all the causes, recent studies have emphasized on the associaton of the tumor and human papilloma virus (HPV). Expecially, HPV also has been discovered in several cutaneous and anogenital lesions of solid organ transplant recipients. We herein report a case of Buschke-Lowenstein tumor in a renal transplant recipient with HPV 6 and 16 coinfection proved by HPV genotyping of DNA extracted from the biopsy specimen of the tumor.
Biopsy ; Buschke-Lowenstein Tumor* ; Carcinoma, Verrucous ; Coinfection ; DNA ; Human papillomavirus 6 ; Humans ; Papilloma ; Perineum ; Rare Diseases ; Sanitation ; Transplantation* ; Transplants

CTLA-4 (=CD152), a T cell activation antigen, has been known to be homologous to CD28 in its molecular and genomic structure. Both of these two molecules are sharing their counterreceptors, B7 (CDSO) and B7-2 (CD86) and are known to play a crucial role in T cell activation. In previous our study it was reported that there are 2 forms of CTLA-4 antigen in activated human T cells, 30 kD membrane-bound form and 34 kD cytosolic-sequestered form and the former was less than 5 % of total of this antigen induced. Aims of this study are to confirm previous finding by using flow cytometry and to characterize the cytoplasmic form of human CTLA-4 by using ultrafiltration and immunoprecipitation techniques. In PHA stimulated peripheral blood lymphocyte surface expression of CTLA-4 was less than 2.1% of any of CD4+, CD8+ and CD56+ subsets. And the 34 kD form of CTLA-4 was detected in CDS+ subset only. This discrepancy confirms that 34 kD antigen is the cytoplasmic form of human CTLA-4. In ultrafiltration and subsequent Western blot analysis study this 34 kD antigen was detected in >100 kD fraction only. And in non-reducing condition this antigen formed high molecular weght complex (MW > 350 kD). In immunoprecipitation study using anti-peptide A antibody it was found that this high molecular weight complex consists of the 34 kD cytoplasmic form of CTLA-4 and previously unknown 54 kD antigen and 46 kD antigen at 1:1:8-10 ratio. And none of these 3 molecules were identified in membrane fraction of activated human T cell. The result of this study implies that CTLA-4 molecule induced upon T cell activation mainly sequestered in cytoplasrn and another signal is necessary to target this antigen on the activated T cell surface.
Antigens, CD27 ; Blotting, Western ; CTLA-4 Antigen ; Cytoplasm* ; Flow Cytometry ; Humans* ; Immunoprecipitation ; Lymphocytes ; Membranes ; Molecular Weight ; T-Lymphocytes ; Ultrafiltration

No abstract available.
Animals ; Asian Continental Ancestry Group* ; Cricetinae ; Cricetulus* ; Female ; Humans* ; Ovary*

No abstract available.
Antigen-Antibody Complex* ; Humans ; Interleukin-2* ; Ovarian Neoplasms*

No abstract available.
Humans ; Methacholine Chloride* ; Rhinitis*

Actinomycosis, in which the principal causative agent in man is known to Actinomyces israelii, is a chronic, suppurative diseases characterized by extensive fibrosis, multiple abscesses, and formation of sinus tracts that drain suppurative exudates. On the basis of the anatomical sites involved; it can be subclassified into the cervicofacial form, which is the most common form, pulmonary form and abdominal form. Kidneys are rarely affected. Clinically, radiologically, and at operation it is difficult to differentiate the renal actinomycosis from renal tuberculosis and renal carcinoma. The prognosis is excellent after nephrectomy followed by appropriate antibiotic therapy. We presented a case of renal actinomycosis with a brief review of the literatures.
Male ; Humans

BACKGROUND: We have previously demonstrated that phorbol myristate acetate (PMA)-induced increases in melanoma cell binding to endothelial cells derived from human dermis (HDMEC) are not mediated via known cell adhesion molecules and may be affected through microvessel-specific novel proteins not previously described on endothelial cells. OBJECTIVE: This study was performed to identify new molecules which may play a role in HDMEC-melanoma cells binding. METHODS: We have generated a monoclonal antibody(Mab) against PMA-stimulated HDMEC. A Mab was evaluated functionally through melanoma cell-endothelial cell adherence assay and characterized by Western immunoblot. RESULTS: Mab EM-71 recognized a molecule with expression levels in vitro that could be upregulated by PMA(EM-71 molecule). The expression of EM-71 molecule on HDMEC was increased in a dose-dependent manner by PMA only, but not affected by interleukin 1 alpha(IL-lα) or tumor necrosis factor alpha(TNFα) PMA augmented melanoma cell adherence to HDMEC, which is coincident with an increase in EM-71 molecule expression on HDMEC by PMA. Mab EM-71 partially inhibited up to 59% of the increased melanoma cell binding to PMA-stimulated HDMEC and failed to block melanoma cell binding to IL-lα or TNFα-stimulated HDMEC. Western immunoblots of lysates of HDMEC demonstrated a 200 kDa protein on HDMEC. CONCLUSION: This study demonstrates that EM-71 molecule may play a partial role in melanoma binding to PMA-stimulated HDMEC.
Blotting, Western ; Cell Adhesion Molecules ; Dermis ; Endothelial Cells* ; Humans* ; In Vitro Techniques ; Interleukin-1 ; Melanoma* ; Tetradecanoylphorbol Acetate ; Tumor Necrosis Factor-alpha

Programrned cell death (PCD), or apoptosis, is a process by which cells die in response to specific physiological and toxicological signals. This genetically programmed form of cellular suicide is intirnately involved in many biological processes including growth, metamorphosis, embryogenesis, and oncogenesis. Cells undergoing PCD in normal and neoplasmic tissues display the following biochemical and morphological features: internucleosomal DNA fragmentation, reduced cell volume, condensed chromatin in nucleus, zeiosis and generation of apoptotic bodies containing intact organelles and plasma rnembrane. Hybridoma cell production, resulting from the fusion of myeloma cells with antibody producing spleen cells, is widely used in various fields of life science. This technique requires hypoxanthine guanine phosphoribosyl transferase (HGPRT) deficient mutant myeloma cell line as a fusion partner. When these mutants cell is treated with aminopterin plus hypoxanthine-thymidine (HAT) after the cell fusion they are selectively and efficiently eliminated remaining fused hybridoma celis. But there hasn't been any report regarding the selective elimination mechanism of this HGPRT mutant myeloma cell. By using HGPRT myeloma P3-X 63-Ag8.653 (V653) as a model system, this study demonstrated that PCD was induced by aminopterin treatment of this V653 cell line. And the sequential ultrastructural changes during this death process were observed by using electron microscope. When V653 cells were incubated with 0.4 uM aminopterin, DNA fragmentation was detectable after 3 hours and peaked between 12 and 18 hours of aminopterin treatment and the cell viability decreased in a time dependant manner. V653 cells incubated with amiopterin showed following ultrastructural changes during the death process. Dilatation of rough endoplasmic reticulum (RER) and detachment of ribosomes were the earliest ultrastructural changes and first seen after 30 minute incubation. Dilatation of perinuclear cisternae began to appear after 1 hour and deformation of nucleoplasm such as decreased electron density of perinuclear heterochromatin and increased electron density of euchromatin were seen after 3 hours. Increased electron density of cytoplasm, decreased cell volume, condensation of chromatin and apoptotic bodies were observed in many cells after 9 hours but vacuolation by severe dilatation of RER was seen in some cells. 24 hours after incubation with aminopterin, many cells showed typical form of apoptosis characterized by cell shrinkage, increased electron density of cytoplasm and apoptotic bodies. On the contrary, some cells showed different type of cell death characterized by increased cell volume, decreased electron density of cytoplasm, severely dilated RER and apoptotic bodies. In both types of cells, mitochondrial cristae and limiting membrane of mitochondria are comparatively well preserved. In other cells, nuclei did not show significant changes but there were deformations of mitochondria such as markedly increased electron density and formation of lamella bodies. The death process of V653 cell was not synchronized among cells. The results of this study proved that aminopterin-induced selective elimination of fusion partner V653 myeloma cell is due to PCD. The earliest ultrastructural changes observed in this process were dilatation of RER and detachment of ribosomes. And there were two distinct morphological types in the PCD.
Aminopterin* ; Animals ; Apoptosis* ; Biological Processes ; Biological Science Disciplines ; Carcinogenesis ; Cell Death ; Cell Fusion ; Cell Line ; Cell Size ; Cell Survival ; Chromatin ; Cytoplasm ; Dilatation ; DNA Fragmentation ; Embryonic Development ; Endoplasmic Reticulum, Rough ; Euchromatin ; Female ; Guanine ; Heterochromatin ; Hybridomas ; Hypoxanthine ; Hypoxanthine Phosphoribosyltransferase ; Membranes ; Mice* ; Mitochondria ; Organelles ; Plasma ; Pregnancy ; Ribosomes ; Spleen ; Suicide ; Transferases

Antigen-specific T cell activation requires interaction of the T cell with specialized antigen-presenting cells. Signaling through the TCR is necessary but not sufficient to induce antigen-specific T cell activation and cytokine secretion. This first signal, termed signal 1, is both antigen-specific and MHC-restricted. Signal 2, which is neither antigen-specific nor MHC-restricted, is necessary to induce cytokine secretion, cellular proliferation, and effector function. Recently immunological studies in T cell activation area are mainly focused on biological and molecular biological characterization of TCR/CD3 complex and accessary molecules providing costimulatory signal (signal 2). If signal 2 is not delivered, T cell enter a state of long term un-responsiveness to specific antigen-termed anergy. Monoclonal antibody technique has been especially involved in recognizing novel inducible cell surface antigens on T cell activation. This study was aimed to develop monoclonal antibodies recognizing novel cytoplasmic proteins present in activated T cells. We make 6 monoclones involved in changing pattern of T cell activated cytoplasmic proteins. Using these 6 monoclonal antibodies analyze to find novel molecules involved in T cell activation associated response, apoptosis, and/or heat shock response of the T cells in early T cell activation.
Antibodies, Monoclonal* ; Antigen-Presenting Cells ; Antigens, Surface ; Apoptosis ; Cell Proliferation ; Cytoplasm* ; Heat-Shock Proteins ; Heat-Shock Response ; Humans* ; T-Lymphocytes*

No abstract available.
Humans*