thymidine/infarction

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Cell proliferation after ischemic infarction in gerbil brain.

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In order to study cell proliferation after ischemic infarction, a model of bilateral common carotid artery occlusion in the gerbil was developed. A comparison of survival rates after 15, 30, 45 and 60 min of occlusion revealed that 45 min was the maximum duration of ischemia after which most (72%)

Streptokinase immunogenicity in thrombolytic therapy for acute myocardial infarction.

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The major drawback in implementing thrombolytic therapy with streptokinase in cases of acute myocardial infarction (AMI) stems from its antigenicity. To evaluate the dimensions of this problem, the immune response following thrombolytic therapy with streptokinase was prospectively studied in 16

[Metabolic pool of purine and pyrimidine compounds in the venous blood of patients with myocardial infarction and stenocardia].

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Venous blood acid-soluble fraction was investigated by means of high-efficiency liquid chromatography in patients with myocardial infarction and angina pectoris. Myocardial ischemia is shown to result in marked changes of purine and pyrimidine metabolism. A rise in intermediate and end products of

[Autoradiographic study of DNA synthesis in rats with experimental myocardial infarct].

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Rats with experimental myocardial infarction were injected with 3H-thymidine; DNA-synthesizing nuclei were counted in different parts of the heart. Myocardial infarction enhanced insignificantly the DNA synthesis in the nuclei of myocytes located at the periphery of the injured zone. However the

[Activation of rat heart atrial and auricular cells after left ventricular infarct].

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The number of the DNA-synthesizing nuclei in the connective tissue cells of the auricle and the auricula atril rose from the 1st to the 15th day after the experimental induction of left ventricular infarction in rats. In the myocytes of the auricula atril the amount of the labeled nuclei peaked on

Dexamethasone treatment of post-MI rats attenuates sympathetic innervation of the infarct region.

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Sympathetic fiber innervation of the damaged region following injury represents a conserved event of wound healing. The present study tested the hypothesis that impaired scar healing in post-myocardial infarction (post-MI) rats was associated with a reduction of sympathetic fibers innervating the

[Proliferative processes in the myocardium in different parts of the heart during the creation of experimental myocardial infarct of the left ventricle in 2- and 3-week-old rats].

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As a result of 30 times repeated injections of 3H-thymidine (3HTdr) to neonate rats, beginning from days 13 or 21 post partum, ca. 20 and 10% of myonuclei in the left and right atria were labeled, respectively, while in both ventricles cumulative labeling of myocytes was nearly ten times lower. In

[DNA synthesis in myocytes of the heart conduction system in myocardial infarction induced in young rats].

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The myocardial infarction was induced in 13- and 21-day-old rats. The extent of the DNA synthesis activation in myocytes of conduction system compartments compared with atrial and ventricular myocytes was evaluated by cumulative indices of labeled nuclei after 30-times-repeated 2H-thymidine

The effect of exercise on cell proliferation in the non-ischemic heart after myocardial infarction.

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The influence of physical training (180 hours, 3 hours per day) on the 3H-thymidine incorporation into the connective tissue cell nuclei and into the myocardial cell nuclei of the non-ischemic heart after myocardial infarction was studied in 38 untrained and trained male Wistar rats. In the

Suicide gene-mediated sequencing ablation revealed the potential therapeutic mechanism of induced pluripotent stem cell-derived cardiovascular cell patch post-myocardial infarction.

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OBJECTIVE This study is designed to assess the protective cardiac effects after myocardial infarction (MI) of (i) cardiovascular progenitor cells (PC) differentiated directly into cardiomyocytes (CM) and endothelial cells (ECs) at the injury site, as separable from the effects of (ii) paracrine

DNA synthesis in myocytes from different myocardial compartments of young rats in norm, after experimental infarction and in vitro.

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Following 30 repeated 3H-thymidine (3HTdr) injections to rats beginning from days 13 and 21 after birth ca. 20 and 10% of labeled nuclei were observed in the left and right atria, respectively, while in both ventricles cumulative labeling of myocytes was nearly ten times lower. In rats of the same

Thymidine kinase (TK) activity as a prognostic parameter of survival in lymphoma patients.

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ATP-thymidine 5'-phosphotransferase (TK) is a cellular enzyme involved in DNA synthesis, activated during the G1/S phase of the cell cycle. Elevated TK serum levels can be found in cancer patients due to the active proliferation of tumor cells. TK serum activity was tested by a radioenzymatic

[DNA biosynthesis in the muscular and connective tissue cells of the heart in experimental myocardial infarct].

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In 60 rabbits with experimental myocardial infarction induces by ligation of the anterior branch of the left coronary artery, DNA synthesis was studied by means of H3-thymidine in muscular and connective tissue cells depending on the period of myocardial infarction. The development of myocardial

DNA synthesis in rat atrial myocytes as a response to left ventricular infarction. An autoradiographic study of enzymatically dissociated myocytes.

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An autoradiographic study was performed on enzymatically isolated atrial muscle cells to examine the DNA synthetic response of atria to left ventricular infarction. DNA synthesis was studied in left and right atrial myocytes and nonmyocytes of: young Sprague-Dawley rats 11 days after ligation of the

[Cells containing smooth-muscle myosin during healing of myocardial infarction in rats].

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Immunoperoxidase and autoradiographic techniques were used to examine smooth muscle myosin-containing cells in the injured zone during rat myocardial infarction healing. It was discovered that smooth muscle myosin-containing cells occurred on the 3d day of myocardial infarction and persisted during

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