BACKGROUND: It is known that there is a pronounced circardian periodicity for the time of onset of acute myocardial infarction(AMI), with prominent increase in incidence of onset in the morning hours. However, the characteristic circardian variability in AMI is blunted in patients receiving beta-blockers or aspirin therapy before their presentation with AMI. These findings are attributed to the increase in platelet aggregability, blood coagulability, and plasma catecholamine that change coronary tone and myocardial oxygen demand. We hypothesize that, in addition to above physiologic and biochemical parameters, morphologic patterns of the coronary artery lesions are related to the development of circardian variation in AMI. METHOD: Subjects were 160 patients with AMI(male 92, female 68, mean age 56.9 +/-10.5 years old). Patients were classified by the time of onset of typical chest pain(AMI) by 6-hour interval from mid-night. Circardian variability of onset of AMI was compared with clinical findings and coronary angiographic findings. RESULTS: Incidence of onset of AMI was most frequent in the morning hours(6AM-noon,42.5%). There was no difference in degree of stenosis, lesion length, incidence of intraluminal thrombus, among 3 subgroups of AMI according to time of attack. Morning hour group had more frequent ulceration of coronary lesion than that of other groups(22.4% vs. 5.4%, p<0.01), and less frequent calcified lesion than that of other groups(3.0% vs 5.4%, p<0.05). Normal or minimal coronary artery lesion, that is Iess than 25% stenosis, was more frequent in the morning hour group comparing to that of other groups(11.9% vs. 9.78%). Eccentric stenosis(15.7% vs, 11,1%) and diffuse irregular lesion(25.5% vs. 16.7%) tended to be more frequent in the morning hour group. There were no differences in sex, age, incidence of hypertension, cigarette smoking, diabetes, degree of alcohol ingestion, ejection fraction, maximal CK value, preinfarction angina duration, past history of MI, and in incidence of arrhythmia. CONCLUSIONS: There were more ulcerative coronary atherosclerotic lesions, but fewer calcified coronary lesions in the morning group than in afternoon and night group. These findings indicate that morphology of coronary artery lesions may play a role in causing circardian variation in AMI.
Angina, Unstable ; Arrhythmias, Cardiac ; Aspirin ; Blood Platelets ; Constriction, Pathologic ; Coronary Vessels* ; Eating ; Female ; Humans ; Hypertension ; Incidence ; Myocardial Infarction* ; Oxygen ; Periodicity ; Plasma ; Smoking ; Thorax ; Thrombosis ; Ulcer

BACKGROUND: It is known that there is a pronounced circardian periodicity for the time of onset of acute myocardial infarction(AMI), with prominent increase in incidence of onset in the morning hours. However, the characteristic circardian variability in AMI is blunted in patients receiving beta-blockers or aspirin therapy before their presentation with AMI. These findings are attributed to the increase in platelet aggregability, blood coagulability, and plasma catecholamine that change coronary tone and myocardial oxygen demand. We hypothesize that, in addition to above physiologic and biochemical parameters, morphologic patterns of the coronary artery lesions are related to the development of circardian variation in AMI. METHOD: Subjects were 160 patients with AMI(male 92, female 68, mean age 56.9 +/-10.5 years old). Patients were classified by the time of onset of typical chest pain(AMI) by 6-hour interval from mid-night. Circardian variability of onset of AMI was compared with clinical findings and coronary angiographic findings. RESULTS: Incidence of onset of AMI was most frequent in the morning hours(6AM-noon,42.5%). There was no difference in degree of stenosis, lesion length, incidence of intraluminal thrombus, among 3 subgroups of AMI according to time of attack. Morning hour group had more frequent ulceration of coronary lesion than that of other groups(22.4% vs. 5.4%, p<0.01), and less frequent calcified lesion than that of other groups(3.0% vs 5.4%, p<0.05). Normal or minimal coronary artery lesion, that is Iess than 25% stenosis, was more frequent in the morning hour group comparing to that of other groups(11.9% vs. 9.78%). Eccentric stenosis(15.7% vs, 11,1%) and diffuse irregular lesion(25.5% vs. 16.7%) tended to be more frequent in the morning hour group. There were no differences in sex, age, incidence of hypertension, cigarette smoking, diabetes, degree of alcohol ingestion, ejection fraction, maximal CK value, preinfarction angina duration, past history of MI, and in incidence of arrhythmia. CONCLUSIONS: There were more ulcerative coronary atherosclerotic lesions, but fewer calcified coronary lesions in the morning group than in afternoon and night group. These findings indicate that morphology of coronary artery lesions may play a role in causing circardian variation in AMI.
Angina, Unstable ; Arrhythmias, Cardiac ; Aspirin ; Blood Platelets ; Constriction, Pathologic ; Coronary Vessels* ; Eating ; Female ; Humans ; Hypertension ; Incidence ; Myocardial Infarction* ; Oxygen ; Periodicity ; Plasma ; Smoking ; Thorax ; Thrombosis ; Ulcer

The proliferation and migration of vascular smooth muscle cells (VSMCs) are key contributors to the development of atherosclerosis and restenosis. We investigated the impact of rosuvastatin (RSV) on platelet-derived growth factor (PDGF)-BB-induced proliferation and migration of VSMCs, with a focus on the Akt/mTORautophagy signaling pathways. The cytotoxicity of RSV was assessed using MTT and annexin V staining, while the proliferation and migration capabilities of PDGF-BBinduced VSMCs were evaluated using MTT and cell migration assays. Confocal microscopy was employed to examine autophagic cell images, and protein expressions were analyzed via Western blotting. Our key findings revealed that RSV inhibited PDGF-BB-induced proliferation and migration of VSMCs, significantly reducing the expression of proliferating cell nuclear antigen and matrix metalloproteinase-2, which are crucial for these processes. RSV also enhanced autophagy in PDGF-BBstimulated cells by inducing the maturation of microtubule-associated protein light chain 3 and increasing the expression of Beclin-1, autophagy related (Atg)3, Atg5, and Atg7. The regulatory effects of RSV on PDGF-BB-induced autophagy, proliferation, and migration were associated with the suppression of the Akt/mTOR signaling pathway. These findings suggest that RSV may have potential therapeutic benefits in preventing and treating vascular diseases by targeting the Akt/mTOR pathway and inducing autophagy.

The proliferation and migration of vascular smooth muscle cells (VSMCs) are key contributors to the development of atherosclerosis and restenosis. We investigated the impact of rosuvastatin (RSV) on platelet-derived growth factor (PDGF)-BB-induced proliferation and migration of VSMCs, with a focus on the Akt/mTORautophagy signaling pathways. The cytotoxicity of RSV was assessed using MTT and annexin V staining, while the proliferation and migration capabilities of PDGF-BBinduced VSMCs were evaluated using MTT and cell migration assays. Confocal microscopy was employed to examine autophagic cell images, and protein expressions were analyzed via Western blotting. Our key findings revealed that RSV inhibited PDGF-BB-induced proliferation and migration of VSMCs, significantly reducing the expression of proliferating cell nuclear antigen and matrix metalloproteinase-2, which are crucial for these processes. RSV also enhanced autophagy in PDGF-BBstimulated cells by inducing the maturation of microtubule-associated protein light chain 3 and increasing the expression of Beclin-1, autophagy related (Atg)3, Atg5, and Atg7. The regulatory effects of RSV on PDGF-BB-induced autophagy, proliferation, and migration were associated with the suppression of the Akt/mTOR signaling pathway. These findings suggest that RSV may have potential therapeutic benefits in preventing and treating vascular diseases by targeting the Akt/mTOR pathway and inducing autophagy.

The proliferation and migration of vascular smooth muscle cells (VSMCs) are key contributors to the development of atherosclerosis and restenosis. We investigated the impact of rosuvastatin (RSV) on platelet-derived growth factor (PDGF)-BB-induced proliferation and migration of VSMCs, with a focus on the Akt/mTORautophagy signaling pathways. The cytotoxicity of RSV was assessed using MTT and annexin V staining, while the proliferation and migration capabilities of PDGF-BBinduced VSMCs were evaluated using MTT and cell migration assays. Confocal microscopy was employed to examine autophagic cell images, and protein expressions were analyzed via Western blotting. Our key findings revealed that RSV inhibited PDGF-BB-induced proliferation and migration of VSMCs, significantly reducing the expression of proliferating cell nuclear antigen and matrix metalloproteinase-2, which are crucial for these processes. RSV also enhanced autophagy in PDGF-BBstimulated cells by inducing the maturation of microtubule-associated protein light chain 3 and increasing the expression of Beclin-1, autophagy related (Atg)3, Atg5, and Atg7. The regulatory effects of RSV on PDGF-BB-induced autophagy, proliferation, and migration were associated with the suppression of the Akt/mTOR signaling pathway. These findings suggest that RSV may have potential therapeutic benefits in preventing and treating vascular diseases by targeting the Akt/mTOR pathway and inducing autophagy.

The proliferation and migration of vascular smooth muscle cells (VSMCs) are key contributors to the development of atherosclerosis and restenosis. We investigated the impact of rosuvastatin (RSV) on platelet-derived growth factor (PDGF)-BB-induced proliferation and migration of VSMCs, with a focus on the Akt/mTORautophagy signaling pathways. The cytotoxicity of RSV was assessed using MTT and annexin V staining, while the proliferation and migration capabilities of PDGF-BBinduced VSMCs were evaluated using MTT and cell migration assays. Confocal microscopy was employed to examine autophagic cell images, and protein expressions were analyzed via Western blotting. Our key findings revealed that RSV inhibited PDGF-BB-induced proliferation and migration of VSMCs, significantly reducing the expression of proliferating cell nuclear antigen and matrix metalloproteinase-2, which are crucial for these processes. RSV also enhanced autophagy in PDGF-BBstimulated cells by inducing the maturation of microtubule-associated protein light chain 3 and increasing the expression of Beclin-1, autophagy related (Atg)3, Atg5, and Atg7. The regulatory effects of RSV on PDGF-BB-induced autophagy, proliferation, and migration were associated with the suppression of the Akt/mTOR signaling pathway. These findings suggest that RSV may have potential therapeutic benefits in preventing and treating vascular diseases by targeting the Akt/mTOR pathway and inducing autophagy.

The proliferation and migration of vascular smooth muscle cells (VSMCs) are key contributors to the development of atherosclerosis and restenosis. We investigated the impact of rosuvastatin (RSV) on platelet-derived growth factor (PDGF)-BB-induced proliferation and migration of VSMCs, with a focus on the Akt/mTORautophagy signaling pathways. The cytotoxicity of RSV was assessed using MTT and annexin V staining, while the proliferation and migration capabilities of PDGF-BBinduced VSMCs were evaluated using MTT and cell migration assays. Confocal microscopy was employed to examine autophagic cell images, and protein expressions were analyzed via Western blotting. Our key findings revealed that RSV inhibited PDGF-BB-induced proliferation and migration of VSMCs, significantly reducing the expression of proliferating cell nuclear antigen and matrix metalloproteinase-2, which are crucial for these processes. RSV also enhanced autophagy in PDGF-BBstimulated cells by inducing the maturation of microtubule-associated protein light chain 3 and increasing the expression of Beclin-1, autophagy related (Atg)3, Atg5, and Atg7. The regulatory effects of RSV on PDGF-BB-induced autophagy, proliferation, and migration were associated with the suppression of the Akt/mTOR signaling pathway. These findings suggest that RSV may have potential therapeutic benefits in preventing and treating vascular diseases by targeting the Akt/mTOR pathway and inducing autophagy.

In the originally published version of this article, the last line of footnotes was omitted in Table 2.

OBJECTIVE: This study was conducted to elucidate neuroprotective effect of carnosine in early stage of stroke. METHODS: Early stage of rodent stroke model and neuroblastoma chemical hypoxia model was established by middle cerebral artery occlusion and antimycin A. Neuroprotective effect of carnosine was investigated with 100, 250, and 500 mg of carnosine treatment. And antioxidant expression was analyzed by enzyme linked immunosorbent assay (ELISA) and western blot in brain and blood. RESULTS: Intraperitoneal injection of 500 mg carnosine induced significant decrease of infarct volume and expansion of penumbra (p<0.05). The expression of superoxide dismutase (SOD) showed significant increase than in saline group in blood and brain (p<0.05). In the analysis of chemical hypoxia, carnosine induced increase of neuronal cell viability and decrease of reactive oxygen species (ROS) production. CONCLUSION: Carnosine has neuroprotective property which was related to antioxidant capacity in early stage of stroke. And, the oxidative stress should be considered one of major factor in early ischemic stroke.
Anoxia ; Antimycin A ; Blotting, Western ; Brain ; Carnosine* ; Cell Survival ; Enzyme-Linked Immunosorbent Assay ; Infarction, Middle Cerebral Artery ; Injections, Intraperitoneal ; Ischemia* ; Neuroblastoma ; Neurons ; Neuroprotective Agents* ; Oxidative Stress ; Reactive Oxygen Species ; Rodentia* ; Stroke ; Superoxide Dismutase

No abstract available.
Histiocytosis ; Histiocytosis, Non-Langerhans-Cell ; Stomach* ; Xanthomatosis*