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phenylalanine/edema
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Relationship between airway microvascular leakage, edema, and baseline airway functions.
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This study was designed to examine the relationship among microvascular leakage, edema, and baseline airway function. Microvascular leakage was induced in the airways of anesthetized, tracheostomized New Zealand White rabbits (n = 22) by using nebulized N-formyl-methionyl-leucyl-phenylalanine (10
Studies on human plasma C1 inactivator-enzyme interactions. II. Structural features of an abnormal C1 inactivator from a kindred with hereditary angioneurotic edema.
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The function and several of the structural features of the C1 inactivator protein isolated from the plasma of a mother and daughter with the variant form of hereditary angioneurotic edema have been examined. These abnormal inhibitors shared immunologic identity with the normal C1 inactivator
Inhibitory Effects of Medium Molecular Weight Heparinyl Amino Acid Derivatives on Ischemic Paw Edema in Mice.
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We investigated the radical-scavenging effects of heparin (HE), medium molecular weight heparinyl phenylalanine (MHF), and medium molecular weight heparinyl leucine (MHL) using ischemic paw edema in mice. We also examined the activated partial thromboplastin time (APTT) of mice that were
Pertussis toxin from Bordetella pertussis blocks neutrophil migration and neutrophil-dependent edema in response to inflammation.
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Pertussis toxin (Ptx) is a hexameric protein with classical AB architecture produced by Bordetella pertussis. The aim of this study was to investigate the effect of Ptx on migration of polymorphonuclear leukocytes to site of inflammation and on cell-dependent edema. Ptx was purified from the
Tumor necrosis factor-alpha primes pulmonary hemodynamic response to N-formyl-L-methionyl-L-leucyl-L-phenylalanine.
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We tested the hypothesis that tumor necrosis factor-alpha (TNF-alpha) primes the hemodynamic response to the neutrophil agonist N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP) in lungs isolated from guinea pigs. Lungs were isolated from animals 18 h after injection of TNF-alpha (3.20 x 10(5)
Regional isolated perfusion of extremities for melanoma: a 20-year experience with drugs other than L-phenylalanine mustard.
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Recurrent melanoma of the extremities can lead to bulky symptomatic lesions that become difficult management problems. Treatment of these tumors with isolated limb perfusion with high dose chemotherapy may offer palliation in a number of patients. Unfortunately, the most commonly used drug,
Alpha1-acid glycoprotein suppresses rat acute inflammatory paw edema through the inhibition of neutrophils activation and prostaglandin E2 generation.
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Alpha(1)-acid glycoprotein (AGP) is an acute phase protein. Whereas the expression of AGP in an inflammatory state is enhanced by inflammatory cytokines including interleukin-1, 6 (IL-1 and IL-6), and tumor necrosis factor-alpha (TNF-alpha), the biological significance of AGP remains unclear. In the
Inhibition by nilvadipine of ischemic and carrageenan paw edema as well as of superoxide radical production from neutrophils and xanthine oxidase.
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1. Nilvadipine (FK 235, FR 34235) suppressed ischemia (20 min)-reflow (20 min)-induced paw edema of mice (ED30:0.4 mg/kg i.v. and 2 mg/kg p.o.). Other calcium entry blockers of dihydropyridine-type also suppressed the edema, but 30-fold higher doses were required. 2. Oral dosing of nilvadipine
Characterization of the Systemic Findings of Patients Undergoing Initiation of Anti-Vascular Endothelial Growth Factor Therapy for Diabetic Macular Edema in Routine Clinical Practice.
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An assessment of progression of brain edema with amino acid levels in cerebrospinal fluid and changes in electroencephalogram in an adult cat model of cold brain injury.
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We investigated the relationship between the changes of the electroencephalogram (EEG) and concentration of amino acids (AAs) in cerebrospinal fluid (CSF) using a model of cold brain injury. A cold injury was made over the motor area of anesthetized adult cats (n = 45). The AAs in CSF from cisterna
New biological properties of pyrroloquinoline quinone and its related compounds: inhibition of chemiluminescence, lipid peroxidation and rat paw edema.
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Pyrroloquinoline quinone (PQQ) inhibited the chemiluminescence (CL) from mouse peritoneal cells initiated by zymosan, carrageenin and N-formyl-methionyl-leucyl-phenylalanine and CL generated by the xanthine-xanthine oxidase reaction and the lipid peroxidation in the rat brain homogenate. The
Structural requirements for the edema-inducing and hemolytic activities of mastoparan B isolated from the hornet (Vespa basalis) venom.
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Mastoparan B (MP-B) is a cationic tetradecapeptide isolated from the black-bellied hornet (Vespa basalis) venom. It has a primary structure (LKLKSIVSWAKKVL-CONH2) distinct from other vespine mastoparans. The peptide caused a dose-dependent swelling in rat hind paw and showed a potent hemolytic
Clinical Review Report: Nitisinone (Nitisinone Tablets): (Cycle Pharmaceuticals Ltd.): Indication: For the treatment of patients with hereditary tyrosinemia type 1 in combination with dietary restriction of tyrosine and phenylalanine
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Hereditary tyrosinemia type 1 (HT-1) is a rare, autosomal recessive disorder of amino acid metabolism. The deficiency of fumarylacetoacetate hydrolase (FAH), which is the last enzyme in the pathway of tyrosine catabolism, results in the accumulation of toxic metabolites in the FAH-deficient
Suppressed Vascular Leakage and Myocardial Edema Improve Outcome From Myocardial Infarction
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Aim: The acute phase of myocardial infarction (MI) is accompanied by edema contributing to tissue damage and disease outcome. Here, we aimed to identify the mechanism whereby vascular endothelial growth factor (VEGF)-A induces myocardial
Dynamic Phenylalanine Clamp Interactions Define Single-Channel Polypeptide Translocation through the Anthrax Toxin Protective Antigen Channel.
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Anthrax toxin is an intracellularly acting toxin where sufficient detail is known about the structure of its channel, allowing for molecular investigations of translocation. The toxin is composed of three proteins, protective antigen (PA), lethal factor (LF), and edema factor (EF). The toxin's
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