bromochloroacetic-acid and Skin-Ulcer

Topics: Actins; Adenoma; Adult; Biomarkers, Tumor; Biopsy; Breast Neoplasms; Carcinoembryonic Antigen; Cell Nucleus; Female; Glial Fibrillary Acidic Protein; Hemorrhage; Humans; Keratins; Neoplasms, Multiple Primary; Nipples; Skin Ulcer

Keratinocytes at wound margins undergo partial epithelial to mesenchymal transition (EMT). Based on previous in vitro and ex vivo findings, Slug (Snai2), a transcriptional regulator of EMT in development, may play an important role in this process.. This study was designed to validate an in vivo role for Slug in wound healing.. Excisional wounds in Slug null and wild type mice were examined histologically at 6, 24, 48, and 72h after wounding; reepithelialization was measured and immunohistochemistry for keratins 8, 10, 14, and 6 and E-cadherin was performed. In 20 Slug null and 20 wild type mice exposed three times weekly to two minimal erythemal doses of UVR, the development of non-healing cutaneous ulcers was documented. Ulcers were examined histologically and by immunohistochemistry.. The reepithelialization component of excisional wound healing was reduced 1.7-fold and expression of the Slug target genes keratin 8 and E-cadherin was increased at wound margins in Slug null compared to wild type mice. In contrast, no differences in expression of keratins 10 or 14 or in markers of proliferation K6 and Ki-67 were observed. Forty per cent of Slug null mice but no wild type mice developed non-healing cutaneous ulcers in response to chronic UVR. Keratinocytes at ulcer margins expressed high levels of keratin 8 and retained E-cadherin expression, thus resembling excisional wounds.. Slug is an important modulator of successful wound repair in adult tissue and may be critical for maintaining epidermal integrity in response to chronic injury.

Topics: Animals; Cadherins; Chronic Disease; Female; Keratinocytes; Keratins; Male; Mice; Mice, Knockout; Radiation Injuries, Experimental; Skin; Skin Ulcer; Snail Family Transcription Factors; Transcription Factors; Wound Healing

Cultured epidermal sheets were examined before and at various times after grafting on skin ulcer beds. Before grafting, the sheet consisted of four to five layers of keratinocytes with incomplete differentiation. Ten days after grafting, graft recipient sites showed compact hyperkeratosis, a normal-appearing epidermis, and a flat dermoepidermal junction. At 6 months, the stratum corneum had a basket-weave appearance but the dermoepidermal junction remained flat. Monoclonal antibodies to keratins 14 and 10 showed normal basal and suprabasal localization, respectively. Electron microscopy showed a normal basement membrane with anchoring fibrils. LH7:2, a monoclonal antibody that binds to the type VII collagen molecule, stained the dermoepidermal junction in all biopsy specimens. AE-1, an antibody that stains suprabasal cells in hyperproliferative skin, was expressed suprabasally for up to 12 weeks after healing (16 weeks after grafting), but expression was confined to the basal layer at 18 weeks after healing (6 months after grafting). Anti-involucrin staining was found in the deeper layers of the epidermis up to 12 weeks after healing (16 weeks after grafting) but had receded to a normal distribution in upper spinous and granular layers at 18 weeks (6 months after grafting). Overall, the histologic patterns observed in recipient sites during the first 4 months after grafting resembled those observed for 10 to 14 days in newly healed epidermis and in hyperproliferative states such as psoriasis. In four sex-mismatched graft sites, specimens were reacted with a biotinylated probe to the Y chromosome by in situ hybridization. Lack of Y chromosome-positive cells suggested that host keratinocytes had replaced the allografts. Multilocus DNA analysis in one patient confirmed this observation. Our data suggest that an altered state of epithelial maturation persists for several months after culture grafting, with restoration of the normal pattern by 6 months. No differences were detected between autografted and allografted sites.

Topics: Cells, Cultured; DNA; DNA Probes; Female; Graft Survival; Humans; Keratins; Keratosis; Skin; Skin Transplantation; Skin Ulcer; Wound Healing

Topics: Animals; Bandages; Bandages, Hydrocolloid; Biocompatible Materials; Cicatrix; Colloids; Epidermal Cells; Humans; Keratins; Polymers; Polysaccharides; Skin Transplantation; Skin Ulcer; Wound Healing

Topics: Burns; Epidermal Cells; Epidermis; Humans; Keratins; Skin Ulcer; Surgery, Plastic

Non-enzymatic glycosylation of keratin from the stratum corneum of the sole of the foot was measured by the thiobarbituric acid technique in thirty diabetic and thirty control subjects. A significant increase in the level of glycosylation was demonstrated in the diabetic subjects (P less than 0.001). HbA1 levels were measured in a further eighteen subjects at the same time as keratin was removed, and in this group a significant association between non-enzymatic glycosylation of that protein and diabetic control was demonstrated (P less than 0.01). In vitro incubation of keratin in the presence of free glucose produced increased non-enzymatic glycosylation (P less than 0.01) and this effect was blocked by incubation in the presence of increasing concentrations of aspirin (P less than 0.01). Measurement of non-enzymatic glycosylation of keratin in a further group of twenty diabetics with neuropathic ulceration showed a significant increase in levels when compared with a group of diabetics without ulcers (P less than 0.05). As keratin is the principle structural protein of the stratum corneum of the sole of the foot, it is possible that changes in this protein associated with non-enzymatic glycosylation may contribute to abnormalities seen in the skin of the feet of diabetics.

Topics: Adult; Aged; Aspirin; Diabetes Mellitus; Epidermis; Foot; Glucose; Glycated Hemoglobin; Humans; In Vitro Techniques; Keratins; Middle Aged; Skin Ulcer

Skin and serum zinc measurements have been made in patients with leprosy with and without trophic skin ulceration and in several other groups. Serum zinc concentrations were decreased in leprosy irrespective of the presence or absence of skin ulceration. Serum zinc concentrations in leprosy were also unrelated to smears positive for Mycobacterium leprae and to the clinical type of leprosy. Since a decrease of the serum zinc was also found in patients with dermatitis herpetiformis and pulmonary tuberculosis it seems likely that the decreased serum zinc in leprosy is a nonspecific metabolic consequence of chronic skin and internal disease. The mean skin zinc concentration in leprosy did not differ significantly from the corresponding value in control subjects, the lack of agreement between serum and skin concentrations being possibly related to the presence of nonexchangeable keratin-bound zinc in skin. Though the clinical significance of lowered serum zinc concentrations in leprosy is uncertain therapeutic trials of zinc treatment in leprosy with trophic skin ulceration seem justifiable.

Topics: Biopsy; Dapsone; Dermatitis Herpetiformis; Humans; Keratins; Leprosy; Mycobacterium leprae; Protein Binding; Serum Albumin; Skin; Skin Ulcer; Tuberculosis, Pulmonary; Zinc

Topics: Abscess; Aluminum; Animals; Hydrogen-Ion Concentration; Hyperplasia; Inflammation; Keratins; Mice; Permeability; Phospholipids; Protein Binding; Protein Denaturation; Skin; Skin Diseases; Skin Ulcer; Sulfhydryl Compounds; Swine

Topics: Aged; Biopsy; Blister; Connective Tissue Cells; Desmosomes; Female; Foot Dermatoses; Humans; Keratins; Lichen Planus; Nails; Recurrence; Skin Ulcer