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Assessment of serum phenylalanine and tyrosine isomers in patients with ST-segment elevation vs non-ST-segment elevation myocardial infarction

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Background: Under conditions of oxidative stress, hydroxyl radicals can oxidize phenylalanine (Phe) into various tyrosine (Tyr) isomers (meta-, ortho-, and para-tyrosine; m-, o-, and p-Tyr), depending on the location of the hydroxyl group

[Plasma amino acid concentrations and isoleucine-phenylalanine quotient in patients with acute myocardial infarct during amino acid infusion].

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OBJECTIVE The influence of substitution with two different amino acid solutions on changes in plasma amino acids were studied in patients with acute myocardial infarction. METHODS Thirty consecutive patients admitted to an intensive care unit were included in this open, nonrandomized study. The

Neuroprotective action of halogenated derivatives of L-phenylalanine.

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OBJECTIVE The aromatic amino acid L-Phenylalanine (L-Phe) significantly and reversibly depresses excitatory glutamatergic synaptic transmission (GST) via a unique set of presynaptic and postsynaptic mechanisms. Therefore, we hypothesized that endogenous derivatives of L-Phe, which display potent

Amino acid concentrations in cerebrospinal fluid in presenile and senile dementia of Alzheimer type and multi-infarct dementia.

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Free amino acid levels were measured in cerebrospinal fluid (CSF) from demented patients (D, n = 30) suffering from presenile and senile dementia of Alzheimer type (PDAT, n = 7; SDAT, n = 9), multi-infarct dementia (MID, n = 14) and a reference sample group consisting of young neurotic patients (R,

Reduced oxidative activity of circulating neutrophils in patients after myocardial infarction.

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Circulating neutrophils isolated from patients 3-4 h after a myocardial infarction produced less O2-. compared with controls, when stimulated with phorbol myristate acetate or formyl-methionine-leucine-phenylalanine. Three days after the infarction the O2-. generation elicited by both stimuli

Transcardiac alteration of neutrophil function before and after coronary thrombolysis in human myocardial infarction.

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We examined function of isolated neutrophils taken from aorta and coronary sinus before and after thrombolytic reperfusion in 17 patients whose infarct-related coronary arteries were totally occluded. Before reperfusion in left coronary artery disease, free radical generation by activated

Polymorphonuclear leukocyte membrane fluidity and cytosolic Ca(2+) content in young adults with acute myocardial infarction. Evaluation at the initial stage and after 12 months.

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Our aim was to examine two aspects of polymorphonuclear leukocyte (PMN) rheology (membrane fluidity and cytosolic Ca2+ content), at baseline and after in vitro activation, in a group of young adults with acute myocardial infarction (AMI) at the initial stage and after 12 months. We enrolled 21 AMI

A new prostacyclin analog, KP-10614, inhibits platelet-polymorphonuclear leukocyte interaction and limits experimental infarct size in rat heart.

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A chemically stable prostacyclin analog, KP-10614 [(4Z,16S)-4, 5, 18, 18, 19, 19-hexadehydro-16,20-dimethyl-delta 6(9 alpha)-9(O)-methano-prostaglandin I1], was synthesized to increase the cytoprotective activity and to decrease the hypotensive activity. We have reported that KP-10614, infused i.v.

Effects of endogenously produced leukotrienes, thromboxane, and prostaglandins on coronary vascular resistance in rabbit myocardial infarction.

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In an effort to evaluate the synthesis and function of eicosanoids in myocardial infarction, we have developed a technique of in vivo myocardial infarction in rabbits followed by ex vivo cardiac perfusion. Isolated Langendorff perfused infarcted hearts (removed 1 or 4 d after infarction) responded

The effect of six prostaglandins, prostacyclin and iloprost on generation of superoxide anions by human polymorphonuclear leukocytes stimulated by zymosan or formyl-methionyl-leucyl-phenylalanine.

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Prostaglandins (PG) E2,E1,6-keto-E1 and D2 at concentrations of 0.15-0.80 microM inhibited by 25% the generation of superoxide anions (O2-) in human polymorphonuclear leukocytes (PMNs) stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP). The potency of that inhibition by either PGD2 or PGE1

Exaggerated atrial arachidonate metabolism in rabbit left ventricular myocardial infarction.

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Isolated perfused rabbit hearts that have previously been subjected to in vivo left ventricular myocardial infarction respond to N-formylmethionyl-leucyl-phenylalanine (fMLP) or bradykinin (BK) administration with the synthesis of large quantities of eicosanoids. To anatomically localize these

fMet-Leu-Phe receptor expression by an interstitial cell in rabbit right atrium following left ventricular myocardial infarction.

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Previous studies have shown that rabbit hearts subjected to in vivo left ventricular myocardial infarction and subsequent ex vivo perfusion respond to N-formylmethionyl-leucyl-phenylalanine (fMLP) with enhanced eicosanoid synthesis. This synthetic response occurs primarily in the right cardiac

Hydrophilic interaction and reversed-phase ultraperformance liquid chromatography TOF-MS for serum metabonomic analysis of myocardial infarction in rats and its applications.

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An ultra performance liquid chromatography coupled to mass spectrometry-based metabonomic approach, which utilizes both reversed-performance (RP) chromatography and hydrophilic interaction chromatography (HILIC) separations, has been developed to characterize the global serum metabolic profile

Distinguishing Intracerebral Hemorrhage from Acute Cerebral Infarction through Metabolomics.

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UNASSIGNED Acute cerebral infarction (ACI) and intracerebral hemorrhage (ICH) are potentially lethal cerebrovascular diseases that seriously impact public health. ACI and ICH share several common clinical manifestations but have totally divergent therapeutic strategies. A poor diagnosis can affect

Inhibition of neutrophil migration by a protein kinase inhibitor for the treatment of ischemic brain infarction.

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This study investigated the therapeutic potential of agents that inhibited neutrophil infiltration in cerebral ischemic infarction. The migration of neutrophils elicited by N-formyl-methionyl-leucyl-phenylalanine, tumor necrosis factor, C5a or platelet-activating factor was potently inhibited by

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