No abstract available.
Ambulatory Surgical Procedures*

No Abstracts Available.
Bronchoscopy*

No abstract available.
Bleomycin* ; Warts*

BACKGROUND: The main function of melanocyte is known to proiect the skin from hazardous sun-light. But, some investigators have claimed lately that melanocytes are also related to the immunologic role in the epidermis becauase these cells produce IL-1 activity and IL-lb convertase activity, in vitro. OBJECTIVE: Our purposee were to investigate the effects of rIFN-b on the proliferation of melanocytes, melanin content, and the expression of HLA-DR aritign on melanocytes after a rIFN-y exposure. MEHTODS: The number of melanocytes, the melanin content, and the expression of HLA-DR antigen were evaluated on culturect human melanocytes according to a time sequence and various concentrations of rIFN-y. RESULTS: Antiproliferative activity on melanocytes was dependent on the exposure time and the concentration of rIFN-r. According to the exposure time and the concentration of rIFN-r, melanogenic activity was inhibited or stimulated, Normal melanocytes didnt express HLA-DR antigen, but when normal melanocytes were exposed to rIFN-r, the expression of HLA-DR antigen increased in a timeand concentration-dependent fashion. After the removal of rIFN-r fiom the culture media the expression of HLA-DR antigen on melanocytes also disappeared. CONCLUSION: In our study, melanocytes seem to be related to the irnmunologic role in the epidermis because these cells expressed HLA-DR antigen after rIFN-r exposue and we think that study could help to investigate between melanocytes and immunalogic mechanisms in various inflammatory skin diseases.
Culture Media ; Epidermis ; HLA-DR Antigens ; Humans* ; Interleukin-1 ; Melanins ; Melanocytes ; Research Personnel ; Skin ; Skin Diseases

We investigated the distribution of S-100 protein positive dendritic cells in the skin lesions with tuberculoid sturcture. For this study, we selected the paraffin blocks of biopsied specimens with the characteristic histopathology of lupus vulgaris (5cases), tubereulosis verrucosa cutis (1 case), lupus milaris disseminatus faciei (4 cases), and erythema induratum (7 cases). The cells were identified by immunohistochemical demonstration in paraffin sections. The results were as follows: 1. S-100 protein positive dendritic cells were regularly visualized in all lesions examined. 2. S-100 protein positive dendritic cells appeared usually between the lymphohistiocytic infiltrates around the tuberculoid granulomas in contrast to the cells of monocyte-macrophage system which were within the granulomas. And they appeared occasionally (e.g. in a case of lupus vulgaris) between epitheloid cells in the granulomas. 3. S-100 protein positive dendritic cells were more numerous in the granulomatous lesions which showed the well-formed tuberculoid sturcture. From these results, we suggested the S-100 protein positive dendritic cells act as accessory cells in the pathogenesis of the granulomatous lesions by the delayed type hypersensitivity.
Dendritic Cells* ; Erythema Induratum ; Granuloma ; Hypersensitivity ; Lupus Vulgaris ; Paraffin ; S100 Proteins ; Skin*

No abstract available.
Adipose Tissue* ; Apoptosis ; Lipodystrophy*

No abstract available.
Epidermal Cyst

No abstract available.
Gastric Mucosa* ; Meckel Diverticulum* ; Ulcer*

BACKGROUND: Although actinic keratosis and Bowens disease ar considered as carcinoma in situ, most of them are biologically benign and dont progress to invasive squamous cell carcinoma. It is little known why they take the benign courses and which factors are involved in the tumorigenesis. Keratoacanthoma, self-regresi;ing benign tumor, may be sometimes or fused morphologically with well-differentiated squamous cell carcinoma. So it is necessary to find a useful marker to help us distinguish them. OBJECTIVES: We performed this study to gain a better understani ling of biologic behaviour and tumerigenesis of epidermal keiatinocytic neoplasms. METHODS: We investigated the expression of p53 protein and priliferating cell nuclear antigen (PCNA) by an immunohistochemical method on the formalin-fixed, araffinembedded tissue specimens of epidermal keratinocytic neoplasms. RESULTS: Fourteen out of 20 cases of squamous cell carcinoma(70.0%), 14 out of 22 cases of actinic keratosis(63.6%), and 13 out of 20 cases of Bowens disease(65.0%) showed p53 protein expression, but keratoacanthoma was negative. All the tumors studied sho ved significantly increased numbers of PCNA-positive eells when compared with normal epidermis and characteristic distribution pattern. of PCNA-positive cells. Most cases of actinic keratosis exhibited the basal dysplastic pattern, but Bo wenoid variants showed diffuse dysplastic pattern. Karatoacanthoma revealed the marginal pattern and Bowens disease showed the diffuse dysplastic pattern. Well-differentiated squamous cell carcinoria showed the basal dysplastic pattern, while poorly differentiated squamous cell carcinoma revealed d ffuse dysplastic pattern. CONCLUSION: Our results suggest that p53 mutation is a common and early genetic change in the epidermal tumorigenesis and may be used as a good marker for malignan transformation, but it does not seem to correlate with the biollagic behavior or prognosis of epidermal neoplasms. PCNA, which is considered as a proliferation-relaited marker, was expressed with chavaceristic distribution patterns according to the type of tumors, but the frequency of PCNA expression is unlikely to reflct the malignant potential of epidermal neoplasms.
Actins ; Bowen's Disease ; Carcinogenesis ; Carcinoma in Situ ; Carcinoma, Squamous Cell ; Epidermis ; Keratoacanthoma ; Keratosis, Actinic ; Prognosis ; Proliferating Cell Nuclear Antigen*

BACKGROUND: Although actinic keratosis and Bowens disease ar considered as carcinoma in situ, most of them are biologically benign and dont progress to invasive squamous cell carcinoma. It is little known why they take the benign courses and which factors are involved in the tumorigenesis. Keratoacanthoma, self-regresi;ing benign tumor, may be sometimes or fused morphologically with well-differentiated squamous cell carcinoma. So it is necessary to find a useful marker to help us distinguish them. OBJECTIVES: We performed this study to gain a better understani ling of biologic behaviour and tumerigenesis of epidermal keiatinocytic neoplasms. METHODS: We investigated the expression of p53 protein and priliferating cell nuclear antigen (PCNA) by an immunohistochemical method on the formalin-fixed, araffinembedded tissue specimens of epidermal keratinocytic neoplasms. RESULTS: Fourteen out of 20 cases of squamous cell carcinoma(70.0%), 14 out of 22 cases of actinic keratosis(63.6%), and 13 out of 20 cases of Bowens disease(65.0%) showed p53 protein expression, but keratoacanthoma was negative. All the tumors studied sho ved significantly increased numbers of PCNA-positive eells when compared with normal epidermis and characteristic distribution pattern. of PCNA-positive cells. Most cases of actinic keratosis exhibited the basal dysplastic pattern, but Bo wenoid variants showed diffuse dysplastic pattern. Karatoacanthoma revealed the marginal pattern and Bowens disease showed the diffuse dysplastic pattern. Well-differentiated squamous cell carcinoria showed the basal dysplastic pattern, while poorly differentiated squamous cell carcinoma revealed d ffuse dysplastic pattern. CONCLUSION: Our results suggest that p53 mutation is a common and early genetic change in the epidermal tumorigenesis and may be used as a good marker for malignan transformation, but it does not seem to correlate with the biollagic behavior or prognosis of epidermal neoplasms. PCNA, which is considered as a proliferation-relaited marker, was expressed with chavaceristic distribution patterns according to the type of tumors, but the frequency of PCNA expression is unlikely to reflct the malignant potential of epidermal neoplasms.
Actins ; Bowen's Disease ; Carcinogenesis ; Carcinoma in Situ ; Carcinoma, Squamous Cell ; Epidermis ; Keratoacanthoma ; Keratosis, Actinic ; Prognosis ; Proliferating Cell Nuclear Antigen*