Disease relevance of Skin Ulcer

• Disease states developing selectively in SOCS-1(-/-) IFN-gamma(-/-) mice were polycystic kidneys, pneumonia, chronic skin ulcers, and chronic granulomas in the gut and various other organs [1].
• Gene therapy approaches involving vascular endothelial growth factor (VEGF) to promote therapeutic angiogenesis are under consideration for conditions ranging from ischemic heart disease to nonhealing skin ulcers [2].
• Discontinuation of amantadine resulted in resolution of trophic skin ulcers, paresthesias, and distal weakness [3].
• To elucidate some of the factors responsible for the induction of VEGF in chronic skin ulcers, cultured fibroblasts were exposed to hypoxia and/or growth factors [4].
• Wild type and a control vaccinia recombinant produced large (greater than 5000 mm2) skin ulcers in this species, but the IL-2 expressing recombinant produced no ulceration [5].

Psychiatry related information on Skin Ulcer

• Mutations at the PEPD locus cause prolidase deficiency (McKusick 170100), a rare autosomal recessive disorder characterized by iminodipeptiduria, skin ulcers, mental retardation, and recurrent infections [6].

High impact information on Skin Ulcer

• Tretinoin tocoferil is an alpha-tocopherol ester of all-trans retinoic acid (RA) and safely used in the treatment of skin ulcer [7].
• Chemotherapeutic agents such as doxorubicin, which bind to DNA, are especially prone to cause severe extravasation skin ulcers [8].
• These results show that experimental MMC-induced skin ulcers in mice can be ameliorated with an immediate application of topical DMSO [9].
• Biopsy samples of re-epithelizing epidermis from patients with skin ulcers were collected, and HBD3 mRNA level measured in the epidermis [10].
• CR also extended life span in p53(+/-) mice, but 50% of p53(+/-) mice subjected to CR still developed skin ulcers and mean life span was shorter than that seen in WT mice [11].

Chemical compound and disease context of Skin Ulcer

• Ultrastructure of doxorubicin (adriamycin)-induced skin ulcers in rats [12].
• All of the patients had a history of both intravenous and subcutaneous cocaine and heroin use with chronic suppurative skin ulcers [13].
• Assessment of skin ulcer healing capability by technetium-99m phosphate angiogram and blood-pool images [14].
• These findings give experimental support for the clinical use of CO2 bathing in the treatment of disturbances of skin circulation as well as skin ulcers and wounds [15].
• It also produced skin ulcers on id administration, but they were less severe than those caused by bisantrene [16].

Biological context of Skin Ulcer

• The skin ulcers continued to deteriorate despite a swift reduction of the IL-5 gene expression and peripheral eosinophil count following systemic corticosteroid treatment [17].
• These results suggest that SM-10902 ointment promotes wound healing through the stimulation of angiogenesis and the improvement of blood flow in neovascularization of repairing wound and may be useful in the treatment of skin ulcers caused by peripheral circulatory insufficiency [18].

Anatomical context of Skin Ulcer

• Age younger than 40 years, no skin ulcers, no tumor invasion in the superficial dermis, and CD8+, TcRbetaF1 +, CD95 (Fas)-, and CD56- tumor cells were significantly better prognostic factors (P < .01) [19].
• The proportion of methicillin resistance was highest among S. aureus isolates associated with upper respiratory specimens (42.8%); the proportion of methicillin resistance was 39.3% among skin ulcer isolates, 10.7% among urinary tract infection isolates, and lowest among isolates associated with blood and prostate discharge (3.6% each) [20].
• The aim of this study was to examine immunohistochemically the expression of beta-defensin-2 (hBD2), GM-CSF, VEGF growth factors and accumulation of CD1a+ Langerhans cells (LC) in epidermis from chronic skin ulcers and to compare it to normal skin from the corresponding areas [21].

Gene context of Skin Ulcer

• We examined these proteins by immunohistochemical methods in 12 cases of skin ulcer, using seven anti-keratin antibodies, anti-filaggrin, and anti-p63 antibody [22].
• Although keratinocyte-specific Stat3-disrupted mice were born normal with intact skin and the first hair cycle, they exhibited retardation of wound healing and absence of the second hair cycle onward, leading to development of spontaneous skin ulcers and alopecia as they aged [23].
• Expression of telomerase reverse transcriptase in radiation-induced chronic human skin ulcer [24].
• Overexpression of MDM2, p53, and NCAM proteins in human radiation-induced skin ulcers [25].
• It has been hypothesized that excessive activity of matrix metalloproteinases (MMPs), in particular the gelatinases MMP-9 and MMP-2, contributes to poor healing of chronic skin ulcers [26].

Analytical, diagnostic and therapeutic context of Skin Ulcer

• The anthracycline antibiotics DAUNO and ESO produced the largest skin ulcers when administered intradermally at clinically relevant doses (adjusted on the basis of comparable body surface areas) [27].
• Prolidase deficiency is a rare hereditary disorder with a wide spectrum of clinical manifestations including skin ulcers, eczematous eruptions, characteristic facies, mental retardation, splenomegaly, and susceptibility to infections [28].
• An experimental skin ulcer was developed by intradermal injection of acetic acid [29].
• Previous antibiotic therapy and transfer from long-term care facilities or nursing homes are associated with bacteraemia caused by methicillin-resistant coagulase-negative staphylococci, while skin ulcer and cellulites are independent risk-factors for MRSA bacteraemia [30].
• We studied the overexpression of c-erbB-2 and p21 oncoproteins in human radiation-induced skin ulcers using immunohistochemistry [31].

References