Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One of the most interesting glycosaminoglycans (GAGs) is heparansulphate, known as the physiological activator of antithrombin III and involved in the maintenance of the antithrombotic potential of uninjured endothelium. The aim of our study was to evaluate the tolerability and effectiveness of heparansulphate with respect to sulodexide, another GAG suitable for the treatment of venous diseases. The study was performed in a open-label, controlled, with parallel and randomized groups, design. Thirty patients (aged 32-72 years) suffering from superficial thrombophlebitis were treated for two weeks with heparansulphate 100 mg t.i.d. or sulodexide 250 LSU b.i.d., both given orally. Some coagulative and fibrinolytic parameters (PT; aPTT; fibrinogen; euglobulin lysis time; t-PA; PAI-1; ATIII; alpha 2-antiplasmin; D-Dimer and platelets count) were assayed at the beginning and at the end of the study. Moreover signs and symptoms of disease (skin trophism; local pain; itch and oedema) were assessed. Heparansulphate and sulodexide were able to reduce signs and symptoms with similar degree and to significantly modify t-PA, alpha 2-antiplasmin and ATIII levels without any difference between treatments. Our issues show that heparansulphate can be useful in superficial thrombophlebitis management.
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PMID:[Effectiveness and tolerability of heparan sulfate in the treatment of superficial thrombophlebitis. Controlled clinical study vs sulodexide]. 921 29

Histamine is known to excite a subset of C-fibers and cause itch sensation. Despite its well-defined excitatory action on sensory neurons, intracellular signaling mechanisms are not understood. Previously, we demonstrated that bradykinin excited sensory neurons by activating TRPV1 via the phospholipase A(2) (PLA(2)) and lipoxygenase (LO) pathway. We, thus, hypothesized that histamine excited sensory neurons via the PLA(2)/LO/TRPV1 pathway. Application of histamine elicited a rapid increase in intracellular Ca(2+) ([Ca(2+)](i)) that desensitized slowly in cultured dorsal root ganglion neurons. Histamine-induced [Ca(2+)](i) was dependent on extracellular Ca(2+) and inhibited by capsazepine and by SC0030, competitive antagonists of TRPV1. Quinacrine and nordihydroguaiaretic acid, a PLA(2) and an LO inhibitor, respectively, blocked the histamine-induced Ca(2+) influx in sensory neurons, while indomethacin (a cyclooxygenase inhibitor) did not. We thus conclude that histamine activates TRPV1 after stimulating the PLA(2)/LO pathway, leading to the excitation of sensory neurons. These results further provide an idea for potential use of TRPV1 antagonists as anti-itch drugs.
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PMID:Histamine-induced Ca(2+) influx via the PLA(2)/lipoxygenase/TRPV1 pathway in rat sensory neurons. 1513 18

The effect of the vesicating agent sulfur mustard (SM) has been investigated in vitro using murine peritoneal macrophages. The rationale for this study was three-fold: (1) the first symptoms after exposure to SM are mucous and cutaneous erythema, itching and oedema suggesting that inflammatory cells may represent an early target of SM toxicity; (2) it has been proposed that macrophages and their secretory products may participate in the degradation of the dermal-epidermal junction; and (3) macrophages are important components of the immune system and any alteration of their metabolism may be relevant in clarifying the immune impairments caused by SM. Cell viability, measured by LDH release and lysozyme production, was reduced in a concentration-dependent manner following exposure to SM at 10 mum or higher. A reduction of superoxide anion and hydrogen peroxide production was observed on exposure to concentrations greater than 10 and 1 mum, respectively. Cell-associated plasminogen activator activity was significanty increased (130% of the control) following exposure to 10 mum and a decrease occurred with exposures to 100 mum or more. The release of arachidonic acid equivalents was not significantly affected by SM treatment. These results demonstrate the cytotoxic effects of SM towards macrophages in culture. While activated macrophages may be present in the dermis after in vivo exposure to SM, no evidence was found of a direct stimulatory effect of SM on the production of macrophage inflammatory products.
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PMID:Effects of sulfur mustard on selected biochemical parameters of murine peritoneal macrophages in culture. 2069 97