Effects of methylmercury on DNA synthesis of human fetal astrocytes: a radioautographic study.
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Biomedical subjects
Publications and source records attributed to K H Cho.
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Porokeratosis is a genodermatosis characterized by abnormal epidermal keratinization with the histologic finding of cornoid lamella. To date, five clinical variants have been identified. However, the coexistence of these variants in a single patient has been described only rarely. We report a 5-year-old girl with the simultaneous occurrence of porokeratotic lesions in linear and disseminated patterns. Linear lesions were detected at birth and the disseminated lesions developed at the age of 3 years. Histologically the lesions had cornoid lamella, which is typical of this condition.
Rickets or osteomalacia secondary to tumor in either bone or soft tissue is rare and interesting in that it can be cured after removal of the tumor. The majority of the reported cases occurred in adults older than 30 years, and the most commonly associated types were vascular and fibrous tumors. We present a new case of aggressive osteoblastoma in the ilium, which induced vitamin D-resistant rickets in an 8-year, 9-month-old boy. Radiographs and blood chemistry findings on admission showed typical features of active hypophosphatemic ricketts. He underwent three local excisions of the tumor. At 10-year follow-up, the patient was symptom free but short. When a child has symptoms of rickets that develop relatively later than ordinary vitamin D-resistant rickets, every effort should be made to search out a tumorous lesion before attributing it to a renal origin.
Oral mucosal keratinocytes represent the cells that first encounter tobacco components. Therefore, tobacco-induced abnormal alteration of the mucosal keratinocytes may contribute to the development of oral white lesions. Nicotine is an ingredient of all tobacco products and pharmacologically the most active component of tobacco smoke. To clarify the effects of nicotine on the keratinization of oral mucosal and epidermal keratinocytes, we reconstructed artificial buccal mucosal and skin equivalents using keratinocytes and fibroblasts from noncornifying buccal mucosa and adult foreskin, respectively. The effect of nicotine on keratinization was assessed with morphology, immunohistochemistry and immunoblotting. Long-term treatment with nicotine for 2 weeks enhanced in a dose-dependent manner the expression of differentiation-specific proteins of oral mucosal keratinocytes on living oral mucosal equivalent and epidermal keratinocytes on living skin equivalent, respectively. The effect of nicotine on the cell viability was measured by the 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay. Oral mucosal keratinocytes showed a higher resistance to nicotine toxicity than epidermal keratinocytes. Our results suggest that nicotine stimulates differentiation of both mucosal and epidermal keratinocytes, and this nicotine-induced abnormal differentiation may be associated with the development of oral white lesions.
The distribution and density of gastric endocrine cells in Balb/c mice bearing CT-26 carcinoma cells were studied immunohistochemically employing specific antisera against serotonin, somatostatin, glucagon, gastrin, cholecystokinin (CCK)-8 and human pancreatic polypeptide (hPP). The animals were divided into two groups, a non-implanted sham group and a CT-26 carcinoma cell-implanted group. Samples were collected from two regions of the stomach (fundus and pylorus) at 28 days after implantation of the medium or the CT-26 cells (1x10(5) cells/mouse). Five of the 6 types of immunoreactive (IR) cells were identified, with only the hPP IR cells not being detected. The regional distribution of the gastric endocrine cells in the CT-26 implanted group was similar to that of the non-implanted sham group. However, the endocrine cells were significantly decreased in the CT-26-implanted group as compared to those of the non-implanted sham group. Serotonin- and somatostatin-IR cells in the fundus and pylorus , and gastrin- and CCK-8-IR cells in the pylorus of the CT-26 implanted groups were significantly decreased compared to those of the sham group. In addition, glucagon-IR cells were restricted only to the fundus of the sham animals. hPP-IR cells were not detected in either the T-26 implanted- or the non-implanted group. Since endocrine cells are the anatomical units responsible for the production of gut hormones, a change in their density may reflect a change in their capacity to produce such hormones. Implantation of the tumor cell mass induced severe quantitative changes in gastric endocrine cell density, an abnormality which may contribute to the development of gastrointestinal symptoms, such as anorexia and indigestion, frequently encountered in cancer patients.
We investigated whether calcipotriol, a synthetic derivative of vitamin D3 has the ability to correct defects in the control of proliferation and differentiation of human squamous carcinoma cells using the raft culture of SCC 13 cell line. Calcipotriol treatment at concentrations of 10(-8)-10(-6) M considerably enhanced terminal differentiation of SCC 13 cells, as shown by the appearance of enucleated-eosinophilic cells as well as granular cells in their upper cell layers. Immunohistochemical staining showed marked increases in the differentiation of marker proteins such as keratin 1, involucrin, or filaggrin expressing cells in their upper layers. The elevated expression at protein level was confirmed by immunoblotting analysis. Furthermore, calcipotriol also stimulated basal cell marker proteins such as keratin 14 and EGF receptor. However, the numbers of basal marker expressing cells within the architecture of SCC 13 raft culture were markedly reduced upon calcipotriol treatment, and their localization was mainly restricted in the innermost cell layer. In addition, calcipotriol stimulated EGF receptor biosynthesis for the first 16 hours post treatment and subsequently inhibited [3H]-thymidine incorporation of SCC 13 cells at 24 hours. In this study, we have clearly demonstrated that the long term application of calcipotriol considerably improves the complex defects in the regulation of proliferation and differentiation of SCC 13 cells, as supported by morphological and biochemical observations. This provides an evidence that calcipotriol can be applied clinically as a potent differentiation inducer in the treatment of human squamous cell carcinoma.