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infarction/l tyrosine
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Enhanced efferocytosis of apoptotic cardiomyocytes through myeloid-epithelial-reproductive tyrosine kinase links acute inflammation resolution to cardiac repair after infarction.
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BACKGROUND
Efficient clearance of apoptotic cells (efferocytosis) is a prerequisite for inflammation resolution and tissue repair. After myocardial infarction, phagocytes are recruited to the heart and promote clearance of dying cardiomyocytes. The molecular mechanisms of efferocytosis of
[A case of recurrent cerebral infarction during treatment with oral tyrosine kinase inhibitors for chronic myelogenous leukemia].
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A 76-year-old man, diagnosed with chronic myeloid leukemia in 2010, had been on nilotinib for 7 years. He presented with right hemiparesis in September 2017. He had no history of hypertension, diabetes, hyperlipidemia, heart disease, or smoking. Brain MRI revealed a border-zone infarction of the
Atorvastatin increases plasma soluble Fms-like tyrosine kinase-1 and decreases vascular endothelial growth factor and placental growth factor in association with improvement of ventricular function in acute myocardial infarction.
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OBJECTIVE
This study examined whether atorvastatin increases plasma levels of soluble Fms-like tyrosine kinase 1 (sFlt-1) and reciprocally decreases vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) levels in patients with acute myocardial infarction
Striatal infarction in the rat causes a transient reduction of tyrosine hydroxylase immunoreactivity in the ipsilateral substantia nigra.
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Dopaminergic neurons of the substantia nigra pars compacta were examined in the rat brain following striatal infarction subsequent to transient focal cerebral ischemia. Rats had the middle cerebral artery occluded for 2 h or were sham-operated, and tyrosine hydroxylase immunoreactivity was evaluated
Protein tyrosine kinase is not involved in the infarct size-limiting effect of ischemic preconditioning in canine hearts.
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Protein kinase C (PKC) plays an important role in ischemic preconditioning (IP). Because (1) tyrosine kinase is located at the downstream of PKC for IP in the rabbit hearts and (2) we have reported that ecto-5'-nucleotidase is the substrate for PKC and plays a crucial role for the infarct
Protein tyrosine kinase is downstream of protein kinase C for ischemic preconditioning's anti-infarct effect in the rabbit heart.
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The present study tested the hypothesis that one or more tyrosine kinase(s) are downstream of protein kinase C (PKC) in the signal transduction pathway responsible for the cardioprotective effect of ischemic preconditioning (PC). Isolated rabbit hearts were subjected to 30 min of regional ischemia
[Tryptophan and tyrosine in blood and cerebrospinal fluid in patients with recent cerebral infarct].
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The determinations were carried out in the blood and cerebrospinal fluid of 40 patients with recent cerebral infarction and 30 controls. Tryptophan concentration was determined by the fluorimetric method of Denckla and Dewey, and tyrosine concentration by the method of Waalkes and Udenfried. A
Role of Src protein tyrosine kinases in late preconditioning against myocardial infarction.
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Although Src protein tyrosine kinases (PTKs) have been shown to be essential in late preconditioning (PC) against myocardial stunning, their role in triggering versus mediating late PC against myocardial infarction remains unclear. Four groups of conscious rabbits were subjected to a 30-min coronary
[Level of tyrosine in the blood of patients with acute myocardial infarction during the assessment of corticosteroid hormone production].
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Variations of blood 11-HOCS and tyrosine suggested as an indicator of tissue glucocorticoid provision were investigated in 54 patients with acute myocardial infarction (AMI). Where AMI takes a favourable course, the adrenocortical activity meets bodily requirements in about 25% of patients, whereas
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
Impact of soluble fms-like tyrosine kinase-1 and placental growth factor serum levels for risk stratification and early diagnosis in patients with suspected acute myocardial infarction.
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OBJECTIVE
Angiogenic factors play an important role in the development of atherosclerosis and show pronounced changes during acute myocardial infarction (AMI). We analysed the impact of placental growth factor (PlGF) and its endogen opponent, soluble fms-like tyrosine kinase-1 (sFlt-1), on clinical
DNA polymorphisms in the tyrosine hydroxylase and GNB3 genes: association with unexpected death from acute myocardial infarction and increased heart weight.
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Sudden and unexpected death from myocardial infarction (MI) is one of the most commonly observed findings in forensic medicine. To investigate the biochemical and genetic background of this disease we investigated the genotypes for two polymorphisms associated with hypertension: TH01, a tetrameric
Aberrant distribution of tyrosine hydroxylase and substance P in infants with brain-stem infarction.
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The distribution of tyrosine hydroxylase (TH) and substance P (SP) was examined in the brain-stem of 4 infants with respiratory abnormalities associated with remote brain-stem or cerebellar infarction utilizing immunohistochemical methods. TH-immunoreactive cells and SP-immunoreactive fibers were
TH01, a tetrameric short tandem repeat locus in the tyrosine hydroxylase gene: association with myocardial hypertrophy and death from myocardial infarction?
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TH01 is a tetrameric short tandem repeat locus located in intron 01 of the tyrosine hydroxylase gene. The tyrosine hydroxylase catalyzes the hydroxylation of L-tyrosine to L-DOPA and is the rate limiting enzyme in the synthesis of catecholamines like noradrenaline or adrenaline, which are pivotal in
Decreases in repetitive extrasystole threshold in the conscious pig with myocardial infarct were reversed by tyrosine.
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Reports indicate that the administration of tyrosine, the precursor amino acid for catecholaminergic neurotransmitters, may be beneficial under conditions of physiologic stress. We studied the effects of tyrosine on vulnerability to ventricular arrhythmia in conscious pigs with healing myocardial
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