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

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

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.
Antigen-Antibody Complex* ; Humans ; Interleukin-2* ; Ovarian Neoplasms*

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

BACKGROUND: Unplanned extubation (UE) of patients requiring mechanical ventilation in an intensive care unit (ICU) is associated with poor outcomes for patients and organizations. This study was conducted to assess the clinical features of patients who experienced UE and to determine the risk factors affecting reintubation after UE in an ICU. METHODS: Among all adult patients admitted to the ICU in our institution who required mechanical ventilation between January 2011 and December 2013, those in whom UE was noted were included in the study. Data were categorized according to noninvasive or invasive management after UE. RESULTS: The rate of UE was 0.78% (the number of UEs per 100 days of mechanical ventilation). The incidence of self-extubation was 97.2%, while extubation was accidental in the remaining patients. Two cases of cardiac arrest combined with respiratory arrest after UE were noted. Of the 214 incidents, 54.7% required invasive management after UE. Long duration of mechanical ventilation (odds ratio [OR] 1.52; 95% confidence interval [CI] 1.32-1.75; p = 0.000) and high ICU mortality (OR 4.39; 95% CI 1.33-14.50; p = 0.015) showed the most significant association with invasive management after UE. In multivariate analysis, younger age (OR 0.96; 95% CI 0.93-0.99; p = 0.005), medical patients (OR 4.36; 95% CI 1.95-9.75; p = 0.000), use of sedative medication (OR 4.95; 95% CI 1.97-12.41; p = 0.001), large amount of secretion (OR 2.66; 95% CI 1.01-7.02; p = 0.049), and low PaO2/FiO2 ratio (OR 0.99; 95% CI 0.98-0.99; p = 0.000) were independent risk factors of invasive management after UE. CONCLUSIONS: To prevent unfavorable clinical outcomes, close attention and proper ventilatory support are required for patients with risk factors who require invasive management after UE.
Adult ; Heart Arrest ; Humans ; Incidence ; Intensive Care Units* ; Critical Care* ; Mortality ; Multivariate Analysis ; Respiration, Artificial ; Risk Factors

No abstract available.
Humans*

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.
Glioblastoma* ; Keratosis, Seborrheic

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