Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Necrotizing dermatitis in patients being treated with cancer chemotherapeutic agents can be of several types. Microbial causes can include a variety of bacteria and fungi, the most common being Pseudomonas aeruginosa. Gangrene from occlusive causes is not uncommon among cancer patients with coexisting atheromatous, thromboembolic, or obliterative vascular disease. Toxic gangrene is most commonly caused by extravasation of intravenously administered cytotoxic antineoplastic drugs but has also been associated with the use of coumarin congeners and the bite of the brown recluse spider. Pyoderma gangrenosum is an idiopathic condition that has been reported in association with myeloproliferative disorders. Finally, necrosis can be caused by the neoplasm itself, when its growth is so great that blood vessels are compressed and ischemia of the surrounding tissue results.
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PMID:Necrotizing dermatitis in patients receiving cancer chemotherapy. 346 38

Porcine necrotic ear syndrome is a disease of swine characterized by large erosive lesions at the margin of the pinna(e). The gross and microscopic characteristics of the lesions were studied in 38 pigs selected from eight affected swine herds. The progression of the lesions was examined in a herd of 174 weaned pigs in a total confinement nursery. The lesions began as a superficial vesicular dermatitis associated with superficial auricular trauma and progressed to become exudative and encrusted. Localized lesions slowly healed or sporadically progressed to deep necrotic ulcers. The early lesions resembled the epidermal changes produced by Staphylococcus hyicus. Deep ulceration and necrosis was attributed to the invasion of streptococci into the dermis resulting in cellulitis, vasculitis, thrombosis, ischemia, and necrosis.
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PMID:Lesions of porcine necrotic ear syndrome. 673 Jan 99

The histologic studies of the decubitus ulcer spectrum, which include blanchable erythema, nonblanchable erythema, decubitus dermatitis, decubitus ulcer, and the black eschar/gangrene reveal a dynamic process. The initial change occurs in the vessels of the papillary dermis. This is followed by necrosis of skin structures. The eschar/gangrene represents a full-thickness defect due either to prolonged ischemia and anoxemia or a sudden large vessel occlusion caused by shearing injury.
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PMID:Histopathology of the decubitus ulcer. 709 63

A wide spectrum of diseases of the skin are manifested as a blistering process. Blistering may occur as a secondary event associated with viral or bacterial infections of the skin, eg, herpes simplex and impetigo, or with local injury of the skin, eg, burns, ischemia, and dermatitis. In other diseases, blistering of the skin occurs as a primary event and is associated with tissue injury and fluid accumulation within a specific layer of the skin: intraepidermal, dermal-epidermal junction, or subepidermal. Blister formation in this latter group of diseases is due to either genetic mutation or an autoimmune response. Genodermatoses associated with blisters are typically manifested in the neonate, whereas the autoimmune blistering disorders are acquired and usually expressed later in life. Recent advances have uncovered the relevance of the keratinocyte cytoskeleton, the desmosome, the hemidesmosome, and extracellular matrix proteins in blister formation. A pathogenetic classification of blistering diseases is presented.
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PMID:End of the century overview of skin blisters. 1063 12

We report the first case of a 33-year-old woman with multiple sclerosis, who developed a livedo-like dermatitis after injection of Copolymere-1. This disease is characterized by the development of acute violent pain during or immediately after injection, and a livedo-like plaque followed by necrosis corresponding to an arterial ischemia by vasospasm or thrombosis. Early treatment with vasoactive and anticoagulation agents is required. Surgery may be necessary.
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PMID:[Livedo-like dermatitis (Nicolau's syndrome) after injection of Copolymer-1 (Glatiramer acetate)]. 1277 3

1. Lipoxins (LX) and aspirin-triggered 15-epi-lipoxins (ATL) exert potent anti-inflammatory actions. In the present study, we determined the anti-inflammatory efficacy of endogenous LXA(4) and LXB(4), the stable ATL analog ATLa2, and a series of novel 3-oxa-ATL analogs (ZK-996, ZK-990, ZK-994, and ZK-142) after intravenous, oral, and topical administration in mice. 2. LXA(4), LXB(4), ATLa2, and ZK-994 were orally active, exhibiting potent systemic inhibition of zymosan A-induced peritonitis at very low doses (50 ng kg(-1)-50 microg kg(-1)). 3. Intravenous ZK-994 and ZK-142 (500 microg kg(-1)) potently attenuated hind limb ischemia/reperfusion-induced lung injury, with 32+/-12 and 53+/-5% inhibition (P<0.05), respectively, of neutrophil accumulation in lungs. The same dose of ATLa2 had no significant protective action. 4. Topical application of ATLa2, ZK-994, and ZK-142 ( approximately 20 microg cm(-2)) prevented vascular leakage and neutrophil infiltration in LTB(4)/PGE(2)-stimulated ear skin inflammation. While ATLa2 and ZK-142 displayed approximately equal anti-inflammatory efficacy in this model, ZK-994 displayed a slower onset of action. 5. In summary, native LXA(4) and LXB(4), and analogs ATLa2, ZK-142, and ZK-994 retain broad anti-inflammatory effects after intravenous, oral, and topical administration. The 3-oxa-ATL analogs, which have enhanced metabolic and chemical stability and a superior pharmacokinetic profile, provide new opportunities to explore the actions and therapeutic potential for LX and ATL.
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PMID:Lipoxins and novel 15-epi-lipoxin analogs display potent anti-inflammatory actions after oral administration. 1530 82

Heat shock proteins (Hsps) are molecular chaperones that assist intracellular folding, assembly and translocation of proteins in prokaryotic and eukaryotic cells. A variety of stresses including hyperthermia, radiation, heavy metals, ischemia, anoxia and reoxygenation have been shown to increase the expression of Hsps. Likewise, bacterial infection represents a stress for the host cell. In this study, expression of the constitutive (Hsp73) and inducible (Hsp72) isoforms of Hsp70 and Hsp90 was monitored in brain, heart, liver and skeletal muscle from the western painted turtle Chrysemys picta bellii diagnosed with Septicemic Cutaneous Ulcerative Dermatitis (SCUD). This disease is caused by a gram-negative bacterium probably belonging to the Citrobacter spp. The expression of Hsp73 increased 1.8-fold in brain and liver, 2.2-fold in heart but did not change in skeletal muscle; Hsp72 expression increased 5.5-fold in brain and 3-fold in liver but did not change in heart or skeletal muscle; Hsp90 expression increased 9-fold in brain, 2.7-fold in heart and 2.4-fold in skeletal muscle but did not change in liver. These results suggest a tissue-specific Hsp response during bacterial infection and a role for Hsps in immunopathological events in reptiles.
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PMID:Bacterial infection and tissue-specific Hsp72, -73 and -90 expression in western painted turtles. 1545 Aug 61

Lipoxin A4 (LXA4) and aspirin-triggered 15-epi-LXA4 are structurally and functionally distinct eicosanoids, with potent anti-inflammatory and immunomodulatory actions. Therapeutic use of LXA4 is greatly limited by its rapid metabolism in vivo and chemical instability. First-generation synthetic LXA4 analogs such as methyl (5R,6R,7E,9E,11Z,13E,15S)-16-(4-fluorophenoxy)-5,6,15-trihydroxy-7,9,11,13-hexadecatetraenoate (2, ATLa), were designed to minimize metabolism from the omega-end of the molecule. Pharmacokinetic analysis of ATLa revealed beta-oxidation as a novel route for LXA4 metabolism, prompting the development of second-generation 3-oxa-LXA4 analogs with improved pharmacokinetic disposition. Second-generation 3-oxa-LXA4 analogs such as (5R,6R,7E,9E,11Z,13E,15S)-16-(4-fluorophenoxy)-3-oxa-5,6,15-trihydroxy-7,9,11,13-hexadecatetraenoic acid (3), have shown potency and efficacy comparable to ATLa in diverse animal models after topical, intravenous or oral delivery. These include several acute (2-24 h) inflammatory reactions: calcium ionophore-induced skin edema and inflammation (topical), LTB4/PGE2-induced skin inflammation and vascular leak (topical), zymosan A-induced peritonitis (i.v. and oral) and ischemia-reperfusion-induced secondary organ injury (i.v.). Remarkably, 3-oxa-LXA4 analogs have potent once daily oral efficacy in preventing and promoting the resolution of established colitis induced by the hapten trinitrobenzene sulphonic acid (TNBS), an acute/chronic 7-14-day model of Crohn's disease. The second-generation 3-oxa-LXA4 analogs thus provide new stable pharmacophores with which to explore the emerging role of lipoxins as a new therapeutic principle for regulating inflammation, allergy and immune dysfunction in preclinical and clinical research.
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PMID:Second-generation beta-oxidation resistant 3-oxa-lipoxin A4 analogs. 1598 64

The formation of pressure ulcers is dependent on multiple factors including ischemia-reperfusion (IR). This study assessed the mechanism of a previously reported murine model of cutaneous IR injury. Three cycles of IR (days 1-3) by external application of two magnetic plates were performed to induce pressure ulcer formation. Increased infiltration of neutrophils and macrophages, and augmented expression of proinflammatory cytokines and inducible nitric oxide synthase (iNOS), were observed during IR cycles. In this model, monocyte chemoattractant protein-1 (MCP-1) was remarkably increased at day 1 in the skin followed by inflammatory cell infiltration. Therefore, IR cycles were performed in MCP-1-deficient (MCP-1(-/-)) mice to evaluate the role of this chemokine in pressure ulcer development. MCP-1(-/-) mice showed reduced macrophage infiltration and expression of tumor-necrosis factor-alpha (TNF)-alpha and iNOS during IR cycles leading to attenuated apoptosis and skin injury. Importantly, MCP-1 played a role in apoptosis and injury via inducing iNOS during the reperfusion rather than the ischemic period. These findings indicate that MCP-1 may be a critical factor for macrophage recruitment and subsequent skin inflammation and injury during IR cycles. We propose that this is a useful model for investigating the mechanism of pressure ulcer formation using various transgenic mice.
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PMID:The loss of MCP-1 attenuates cutaneous ischemia-reperfusion injury in a mouse model of pressure ulcer. 1821 77

In 1982, a third SOD enzyme was discovered by Marklund and co-workers and named SOD3 on extracellular superoxide dismutase (EC-SOD), as it was shown to be the predominant form in extracellular fluids such as lymph, synovial fluid, and plasma. Many studies have focused on the anti-oxidative effect of SOD3 in the lung and vascular wall where it is highly expressed. Thus, the roles of SOD3 as an anti-oxidative enzyme in ROS-mediated lung inflammation and vascular disease such as ischemia and atherosclerosis, and its mechanism have been extensively studied. However, our studies revealed that the role of SOD3 in inflammation is not simply due to radical scavenging; it affects immune responses and signal initiation. Further, we found that SOD3 is expressed throughout the epidermis and dermis, and its levels were altered upon the progression of inflammation. Considering that skin is the primarily contact with the exogenous environment, including UV, pathogens, and chemicals, it is necessary to understand the role of SOD3 in the prevention or suppression of skin inflammation. Here, we address the emerging role of SOD3 in the suppression of skin inflammation and immune response.
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PMID:Role of superoxide dismutase 3 in skin inflammation. 2276 88


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