papillon-lefevre disease/opuch

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Revealing anti-inflammation mechanism of water-extract and oil of forsythiae fructus on carrageenan-Induced edema rats by serum metabolomics.

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Forsythiae Fructus is an important Chinese medicine which shows a significant effect against inflammation. This study aimed to investigate the preventive anti-inflammation mechanism of Forsythiae Fructus by serum metabolomics strategy and compare the difference of the metabolism pathways between

Characterization of three edema-inducing phospholipase A2 enzymes from habu (Trimeresurus flavoviridis) venom and their interaction with the alkaloid aristolochic acid.

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A basic phospholipase A2 (PLA2) enzyme, TFV PL-X (pI 9.2) and two acidic PLA2 enzymes, TFV PL-Ia (pI 4.9) and TFV PL-Ib (pI 4.5) were purified from Trimeresurus flavoviridis venom on CM-Sephadex C-25 and QAE-Sephadex A-25 columns, respectively. The basic enzyme exists as a monomer, whereas the

Molecular mechanism of lung hemorrhage induction by VRV-PL-VIIIa from Russell's viper (Vipera russelli) venom.

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The basic phospholipase A(2) (VRV-PL-VIIIa) from Vipera russelli venom induces multiple toxic effects including neurotoxicity, myotoxicity, edema and hemorrhage. This phospholipase A(2) has been extensively characterized for its pharmacological properties except for hemorrhagic activity. In the

Analysis of Vipera russelli venom using polyclonal antibodies prepared against its purified toxic phospholipase A2 VRV PL-V.

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Vipera russelli venom induces predominantly neurotoxic, myotoxic necrotic and hemorrhagic symptoms in experimental animals and has several hydrolytic enzyme activities. In this study, V. russelli venom is characterized both as a PLA2 and as a toxin. Anti PL-V Ig (antibodies to a toxic phospholipase

Association of Urinary Plasminogen-Plasmin with Edema and Epithelial Sodium Channel Activation in Patients with Nephrotic Syndrome.

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Previous animal experiments and small human studies suggest that urinary plasmin can activate the epithelial sodium channel (ENaC) and contribute to sodium retention in nephrotic syndrome (NS), but this however is not well studied in clinical settings, and its relevance to edema

Identification of Pulmonary Edema in Forensic Autopsy Cases of Sudden Cardiac Death Using Fourier Transform Infrared Microspectroscopy: A Pilot Study.

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Many studies have proven the usefulness of biofluid-based infrared spectroscopy in the clinical domain for diagnosis and monitoring the progression of diseases. Here we present a state-of-the-art study in the forensic field that employed Fourier transform infrared microspectroscopy for postmortem

Monoclonal antibodies to VRV-PL-VIIIa, a basic multitoxic phospholipase A2 from Vipera russelli venom.

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VRV-PL-VIIIa, the most basic phospholipase A2 (PLA2) from the venom of Vipera russelli, induces multiple toxic effects, including neurotoxicity, myotoxicity, edema and hemorrhage. Rabbit polyclonal anti-serum was raised against VRV-PL-VIIIa. The antiserum cross-reacted in enzyme-linked immunosorbant

Characterization, amino acid sequence and evolution of edema-inducing, basic phospholipase A2 from Trimeresurus flavoviridis venom.

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Two phospholipases A2 (PLA2s) were purified from the venom of Trimeresurus flavoviridis (Crotalinae) inhabiting Tokunoshima island, Japan, and named PLA-A and PLA-B in the order of elution on a cation-exchange column. Lipolytic activities of PLA-A and PLA-B toward mixed micelles and liposomes were

Role of Rho-kinase in reexpansion pulmonary edema in rabbits.

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Reexpansion of a collapsed lung increases the microvascular permeability and causes reexpansion pulmonary edema. Neutrophils and their products have been implicated in the development of this phenomenon. The small GTP-binding proteins Rho and its target Rho-kinase (ROCK) regulate endothelial

Sepsis in the baboon: factors affecting resuscitation and pulmonary edema in animals resuscitated with Ringer's lactate versus Plasmanate.

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Septic shock and the formation of pulmonary edema were studied in 19 baboons. Four animals served as controls. Four were subjected to deep septic shock by infusion of live E. coli and then deliberately killed while in deep shock. Four were subjected to septic shock, resuscitated with Ringer's

Identification of pulmonary edema in forensic autopsy cases of fatal anaphylactic shock using Fourier transform infrared microspectroscopy.

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Anaphylaxis is a rapid allergic reaction that may cause sudden death. Currently, postmortem diagnosis of anaphylactic shock is sometimes difficult and often achieved through exclusion. The aim of our study was to investigate whether Fourier transform infrared (FTIR) microspectroscopy combined with

Increased pulmonary vascular permeability as a cause of re-expansion edema in rabbits.

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In order to study the mechanism(s) underlying re-expansion edema, we measured the concentration of labeled albumin (RISA) in the extravascular, extracellular water (EVECW) of the lung as a measure of pulmonary vascular permeability. Re-expansion edema was first induced by rapid re-expansion of

Polyunsaturated Fatty Acid Composition of Surgically Removed Hard Exudates in Diabetic Macular Edema.

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Three eyes of 2 patients with diabetic macular edema underwent a vitrectomy to remove subfoveal hard exudates. Fatty acid compositions of hard exudates and plasma phospholipids (PL) as an objective estimation of dietary intake were analyzed. Polyunsaturated fatty acids (PUFA) were relatively

Purification and partial biochemical characterization of an edema inducing phospholipase A2 from Vipera russelli (Russell's viper) snake venom.

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A phospholipase A2 (VRV PL-VI) from Vipera russelli venom was purified to homogeneity in a single step on CM-Sephadex C-25 column. VRV PL-VI is a basic protein with a mol. wt of about 12,000 and showed a basic pH optimum and a high temperature maximum. It hydrolysed purified phospholipids in the

Inhibition of secretary PLA₂--VRV-PL-VIIIa of Russell's viper venom by standard aqueous stem bark extract of Mangifera indica L.

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The aqueous extract of Mangifera indica is known to possess anti-snake venom activities. However, its inhibitory potency and mechanism of action on multi-toxic phospholipases A2s, which are the most toxic and lethal component of snake venom is still unknown. Therefore, this study was carried out to

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