Biomedical subjects

H M Sheu

Publications and source records attributed to H M Sheu.

36 records · Page 2Linked to original sources

PubMed1994

Establishment and characterization of a continuous human basal cell carcinoma cell line from facial skin (I) cytological behavior of early passages.

Basal cell carcinomas (BCCs) are one of the most common skin malignant diseases of human beings in the course of a lifetime. BCC is a slow growing tumor of epithelial origin. Most of the BCC tumors have a normal diploid DNA configuration and have been successfully passaged for a short-term only. We now report a long-term culture (BCC-1/KMC) of human BCC derived from the undifferentiated type of facial BCC tumor on the thermal traumatic scar, which was aneuploidy and subculture for more than 100 passages. The population doubling time of BCC-1/KMC cells at the third passage was 38.86 hours. This immortalized and tumorigenic cell line expresses epithelial markers of keratin filaments and desmosomes. The genetic markers of this cell line have HLA-A2, A24, B27, B35, Cw3, DR2 and DR12. The BCC-1/KMC cells have successfully adapted to grow in a cheaper commercial medium (RPMI 1640) and at a moderate concentration of calcium (0.4 mM).

Animals↗

PubMed1992

Alterations of skin-associated lymphoid tissue in the carcinogenesis of arsenical skin cancer.

We investigated the skin-associated lymphoid tissue in arsenical skin cancers, including 14 Bowen's disease, 6 basal cell carcinoma and 6 squamous cell carcinoma patients from an endemic area by immunohistochemical and morphometric methods. There was a progressive decrease of Langerhans cells in the order of normal skin, normal appearing edge and arsenical cancers. A disruption of the uniform Langerhans cell dendrites was also noticed. The Langerhans cell density in arsenical tumors did not correlate with the peritumoral infiltrates. The prominent infiltrated cells in the peritumoral area had T cell markers. The number of peritumoral T lymphocytes in squamous cell carcinoma was significantly less than that of Bowen's disease and basal cell carcinoma. Peritumoral mononuclear infiltrates in Bowen's disease and squamous cell carcinoma showed a higher helper/suppressor T cell ratio than that in basal cell carcinoma. This may be accounted for by a selective increased recruitment of helper T cells to the tumor infiltrates in Bowen's disease and squamous cell carcinoma.

Arsenic Poisoning↗

PubMed1992

[Schizophrenia and factitious cheilitis: a case report].

Factitious Cheilitis is a rare skin disorder which has been seen in patients with emotional disturbances, particularly in cases with neurotic and personality disorders. However, there have been no reports of factitious cheilitis seen in cases of schizophrenia. This study reports on a case of schizophrenic disorder, where the patient was observed to develop factitious cheilitis whilst subject to unstable psychiatric conditions. The case reported here is of a 59 year-old female widow, who has experienced the delusion of being controlled, the delusion of being possessed. Been subject to auditory hallucination and vague somatic pain for eight years and had a very poor psychotropic drug compliance. Observation revealed frequent licking of the lips unrelated to drug-induced dyskinesia, but as a possibly linked response to hallucination whilst subject to an intense unstable emotional and painful state. Factitious cheilitis was proved with biopsy of the lips and pathological findings of acanthosis, hyperkeratosis and parakeratosis. After psychiatric and dermatologic care, her cheilitic condition improved. This study demonstrates that factitious cheilitis can be seen in a schizophrenic patient, specifically where hallucination and emotional instability coupled with long-term licking of the lips can result in factitious cheilitis. The relationship of skin disorder and psychiatric illness is discussed.

Cheilitis↗

PubMed1991

Modulation of epidermal terminal differentiation in patients after long-term topical corticosteroids.

The expression of the various markers for terminal epidermal differentiation in atrophic skin of patients after long-term topical corticosteroids (TCS) was studied by electron microscopy, immunofluorescence using antibody to profilaggrin/filaggrin (PF/FG), immunoperoxidase staining using antibody to involucrin, and oil red O stain for neural lipids of the stratum corneum. Thirty-nine patients were subdivided into two groups: (A) 19 patients suffering from rebound phenomenon after stopping TCS and (B) 20 patients without rebound phenomenon. Biopsy specimens were taken before ending the use of TCS in both groups. In group A, both the morphological markers (including the different epidermal strata, keratohyalin granules, lamellar granules, and cornified cell envelopes) and the molecular markers (including involucrin, PF/FG, and neutral lipids) of terminal epidermal differentiation were significantly suppressed. On the other hand, the differentiational markers in the atrophic skin of patients without rebound phenomena were only slightly altered. These results suggest that potent TCS not only has antiproliferative actions but also inhibits the differentiation of epidermis, resulting in structural defects in the epidermis, especially the stratum corneum.

Administration, Topical↗

PubMed1991

Mast cell degranulation and elastolysis in the early stage of striae distensae.

The lesions of nine patients with early striae distensae (SD) during puberty were examined by light and electron microscopy. Specific changes were seen in very early stage SD, and in clinically uninvolved skin 0.5 to 3 cm remote from the edge of the long axis of the SD lesions. Sequential changes of elastolysis accompanied by mast cell degranulation appeared first, followed by an influx of activated macrophages that enveloped fragmented elastic fibers. The relationships among elastic fibers, mast cells, and macrophages seen in the present work suggest their critical roles in the process of SD formation, especially in the early stage. Our results also indicate that the elastic fiber is the primary target of the pathological process, and the abnormalities extend as far as 3 cm beyond the lesion into normal skin.

Adolescent↗

PubMed1991

Alterations in water content of the stratum corneum following long-term topical corticosteroids.

The water content of the stratum corneum (SC), profilaggrin/filaggrin (PF/FG) and stratum corneum neutral lipids were examined in 23 patients following use of long-term topical corticosteroids (TCS). All patients showed the rebound phenomenon after stopping TCS. Biopsy specimens were taken from the atrophic skin and from the peripheral normal skin of patients. The histopathological examination showed a thinning of the horny layer and the epidermis, along with a decrease in or the absence of the granular layer in the patient's lesional skin. Oil red 0 staining for SC neutral lipids revealed that the intensity of the lipid staining was markedly reduced. Ultrastructural observation also revealed an obvious decrease in both the formation of keratohyalin granules and in the membrane-coating granules of steroid-treated skin. Furthermore, indirect immunofluorescence for PF/FG demonstrated markedly reduced immunofluorescence. In agreement with the above results, the mean water content of the SC in lesional skin was also significantly decreased when compared with that of controls. Since the water content of SC is suggested to be dependent on both the keratohyalin-derived natural moisturizing agents of the SC and the SC intercellular lipids, the present results suggest that the diminution in SC lipids and PF/FG in steroid-treated skin may play an important role in the low hydration state of the SC and the clinical manifestations of scaling and dryness of the skin in patients suffering from the rebound phenomenon after stopping TCS.

Administration, Topical↗

PubMed1991

[Necrolytic migratory erythema as the first manifestation of glucagonoma].

A 49-year-old woman suffered from recurrent episodes of necrolytic migratory erythema over the lower legs, lower abdomen, and buttocks for more than two years. Stomatitis, glossitis and vaginitis were the accompanying symptoms and signs during each episode. The result of skin biopsy revealed superficial necrosis in the upper half of the epidermis. Laboratory examinations revealed mild glucose intolerance and hypoaminoacidemia. Fasting plasma glucagon level measured by radioimmunoassay was 890 pg/mL. Oral glucose loading test showed a paradoxical increase in plasma glucagon level up to 1,500 pg/mL. Abdominal echo, computerized axial tomography, and celiac angiography demonstrated a hypervascular tumor, 4 cm in diameters, located at the pancreatic head. Glucagonoma syndrome was confirmed and diagnosed. The patient underwent surgical resection of the tumor mass. Necrolytic migratory erythema disappeared thereafter, and the plasma glucagon level declined to 120 pg/mL. Histologically, the tumor revealed an islet cell carcinoma composed of moderately uniform cells with a few mitosis, arranged in cords and nests. Abundant characteristic secretory granules of the pancreatic A cell were found within the tumor cells by electron microscopic examination.

Erythema↗

PubMed1991

[Expression of keratin 16 in normal and lesional skin of solitary and multiple Bowen's disease using monoclonal antibody Ks 8.12 staining].

Bowen's disease is an intraepidermal squamous cell carcinoma usually consisting of a solitary lesion. However, multiple Bowen's lesions are one of the characteristics of arsenicalism in endemic areas where people drink deep well water containing high concentrations of arsenic along the southwest coast of Taiwan. This work seeks to clarify the differences between multiple Bowen's disease in the blackfoot disease endemic area, and solitary Bowen's disease in a non-endemic area by means of Ks 8.12 monoclonal cytokeratin antibody staining. Ks 8.12 may be regarded as a specific antibody for Keratin 16 in the skin and is used as a marker for hyperproliferation. Our results show that Ks 8.12 staining of normal skin in patients with a solitary Bowen's lesion is patchy and always restricted to the basal cell layer. By contrast, the normal skin of patients with multiple Bowen's lesions shows diffuse Ks 8.12 staining of the basal cell layer and various degrees of staining of the suprabasal layers. Similar results were observed in both solitary and multiple Bowen's lesions showing diffuse Ks 8.12 staining of the epidermis. Our results revealed clear differences in keratin expression between the clinically normal skin of patients with solitary Bowen's disease and that of patients with chronic arsenicalism. Finally the clinically normal skin of patients with multipole Bowen's disease showed characteristic changes in the expression of Keratin 16 in the suprabasal layers.

Aged↗

PubMed1990

[A study of changes in the ratio of collagen types in skin after long-term treatment with topical glucocorticoids].

The topical glucocorticoids, widely used in the treatment of a variety of skin disorders, usually induce skin atrophy after long-term administration. In this study, the skin from a 30-year-old female patient was used, and the changes in the ratio of collagen types in atrophic skin derived from the treatment with glucocorticoid were investigated in comparison with that of normal human skin. By transmission electron microscopy, the collagen fibrils in the papillary dermis of normal skin were loose and fine, their diameters ranging from 30 to 40 nm; while those in the atrophic skin appeared tightly compact, their diameters increasing to 50-60 nm. The collagen chains, alpha 1 (I), alpha 2 and alpha 2 (III), from peptic digest of skin were separated by interrupted gel electrophoresis. The ratios of collagen type III to type I as calculated from the normal skins of a 21- and a 39-week fetus and a 36-year-old human were 49.45, 45.51 and 43.65%, respectively, while that of the atrophic skin was 12.89%. Therefore, the persistent treatment of skin with topical glucocorticoids results in a decrease in the ratio of collagen type III to type I.

Administration, Topical↗

PubMed1989

Involvement of protein kinase C in translocation of desmoplakins from cytosol to plasma membrane during desmosome formation in human squamous cell carcinoma cells grown in low to normal calcium concentration.

The intracellular signal transduction mechanism leading to desmosome formation in low-calcium-grown keratinocytes after addition of calcium to the medium was studied by immunofluorescence using antibodies to desmoplakins I and II (cytoplasmic desmosomal proteins) and by electron microscopy before and after addition of calcium; protein kinase C (PKC) activators 12-O-tetradecanoylphorbol-13-acetate (TPA), phorbol-12,13-dibutyrate (PDBu), and 1,2-dioctanoylglycerol (DOG); calcium ionophore A23187; selective PKC inhibitors 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) and staurosporine; and a Ca2+/calmodulin-dependent kinase inhibitor, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7). In previous studies using a low-calcium-grown human epidermal squamous cell carcinoma, we have shown that an increase in extracellular Ca2+ caused a four-fold increase in PKC activity and addition of TPA (10 ng/ml) induced a transient increase in membrane-bound PKC activity in association with cell-cell contact formation. The present study showed that TPA (10 ng/ml). PDBu (10 ng/ml), and DOG (1 mg/ml) induced a rapid cell-cell contact and redistribution of desmoplakins from cytoplasm to the plasma membrane with desmosome formation within 60-120 min, which was similar, although less marked, to the effect of increased Ca2+. The TPA-induced desmosome formation was inhibited by selective PKC inhibitors, H-7 (20 microM) or staurosporine (100 nM). On the other hand, calcium ionophore A23187 induced only a temporary increase in the number of desmoplakin-containing fluorescent spots in the cytoplasm and a temporary cell-cell attachment without desmosome formation. The calcium-induced desmosome formation was partially inhibited by 20-100 microM H-7 or 100 nM staurosporine; however, it was not inhibited by W-7 at a concentration of 25 microM, at which this agent selectively inhibits calmodulin-dependent protein kinase. These results suggest that PKC activation plays an important role in desmoplakin translocation from the cytoplasm to the plasma membrane as one of the processes of calcium-induced desmosome formation.

Calcimycin↗

PubMed1987