Background： Chronic stress contributes to increased risks ofatherosclerotic diseases including heart disease, stroke, and transient ischemic attack. However, its underline mechanisms are poorly understood. This study...Background： Chronic stress contributes to increased risks ofatherosclerotic diseases including heart disease, stroke, and transient ischemic attack. However, its underline mechanisms are poorly understood. This study aimed to elucidate the mechanism via which chronic stress exerts its effect on atherosclerosis （AS）. Methods： Fifty male New Zealand white rabbits were used. Aortic balloon-injury model was applied. Both social stress and physical stress methods were adopted to establish chronic stress models. The lumen stenotic degree, intimal and medial areas, maximum fibrous cap thickness, and plaque contents were measured with histological sections. Proteomic methods were applied to detect protein changes in abdominal aortas to identify the specialized mediators. Real-time reverse transcription-polymerase chain reaction was used for further verification and investigation. Results： The stress rabbits exhibited lower body weight, worse fur state, more inactivity behavior, and higher serum cortisol level. Chronic stress was significantly associated with the decreased medial area and increased plaque instability, which was manifested by thinner fibrous caps, larger lipid cores, more macrophages, and new vessels but fewer smooth muscle cells and elastic fibers. After chronic stress, the apoptosis-related genes UBE2K, BAX, b）~S, Ca.v^ase 3, Caspase 9, and P53 were upregulated, and B^Z-2/BAX was down-regulated; the angiogenesis-related genes ANG and VEGF-A were also highly expressed in atherosclerotic arteries. Conclusions： Rabbit models of chronic stress were successfully established by applying both social stress and physical stress for 8 weeks. Chronic stress can reduce AS tunica media and accelerate plaque instability by promoting apoptosis and neovascularization.展开更多
To the Editor： A 63-year-old man was transferred to the Department of Neurology for changes in personality and social withdrawal on March 03, 2015. He appeared to be unwilling to talk to his family, whereas he had pr...To the Editor： A 63-year-old man was transferred to the Department of Neurology for changes in personality and social withdrawal on March 03, 2015. He appeared to be unwilling to talk to his family, whereas he had previously been social and caring. He exhibited unusual behavior, dressing his clothes inside out, and impulsively eating foods. He also had excessive daytime sleepiness. However, the patient himself was unaware of this behavior. He was suspected as having herpes simplex encephalitis in the local hospital and was then administered acyclovir intravenously for 21 days. The patient＇s condition did not improve.展开更多
文摘Background： Chronic stress contributes to increased risks ofatherosclerotic diseases including heart disease, stroke, and transient ischemic attack. However, its underline mechanisms are poorly understood. This study aimed to elucidate the mechanism via which chronic stress exerts its effect on atherosclerosis （AS）. Methods： Fifty male New Zealand white rabbits were used. Aortic balloon-injury model was applied. Both social stress and physical stress methods were adopted to establish chronic stress models. The lumen stenotic degree, intimal and medial areas, maximum fibrous cap thickness, and plaque contents were measured with histological sections. Proteomic methods were applied to detect protein changes in abdominal aortas to identify the specialized mediators. Real-time reverse transcription-polymerase chain reaction was used for further verification and investigation. Results： The stress rabbits exhibited lower body weight, worse fur state, more inactivity behavior, and higher serum cortisol level. Chronic stress was significantly associated with the decreased medial area and increased plaque instability, which was manifested by thinner fibrous caps, larger lipid cores, more macrophages, and new vessels but fewer smooth muscle cells and elastic fibers. After chronic stress, the apoptosis-related genes UBE2K, BAX, b）~S, Ca.v^ase 3, Caspase 9, and P53 were upregulated, and B^Z-2/BAX was down-regulated; the angiogenesis-related genes ANG and VEGF-A were also highly expressed in atherosclerotic arteries. Conclusions： Rabbit models of chronic stress were successfully established by applying both social stress and physical stress for 8 weeks. Chronic stress can reduce AS tunica media and accelerate plaque instability by promoting apoptosis and neovascularization.
文摘To the Editor： A 63-year-old man was transferred to the Department of Neurology for changes in personality and social withdrawal on March 03, 2015. He appeared to be unwilling to talk to his family, whereas he had previously been social and caring. He exhibited unusual behavior, dressing his clothes inside out, and impulsively eating foods. He also had excessive daytime sleepiness. However, the patient himself was unaware of this behavior. He was suspected as having herpes simplex encephalitis in the local hospital and was then administered acyclovir intravenously for 21 days. The patient＇s condition did not improve.
