Sevoflurane provided quicker emergence and early recovery compared with halothane, but the incidence of delirium was greater in preschool boys after sevoflurane.
Two-phase contrast-enhanced CT proved useful in predicting LV functional recovery and WT in patients who had experienced acute MI and undergone successful angioplasty.
The boys who were anxious before anesthesia showed a significantly greater incidence of problematic behavior on emergence from halothane anesthesia, compared with the boys who were calm before anesthesia.
Perivascular adipose tissue exhibits characteristics of active local inflammation, which contributes to the development of atherosclerotic disease as a complication of obesity/metabolic syndrome. However, the precise role of perivascular adipose tissue in the progression of abdominal aortic aneurysm remains unclear. To test the hypothesis that genetic deletion of angiotensin II type 1a (AT) receptor in perivascular visceral adipose tissue (VAT) can attenuate aortic aneurysm formation in apolipoprotein E-deficient (ApoE) mice, we performed adipose tissue transplantation experiments by using an angiotensin II-induced aneurysm murine model, in which we transplanted VAT from ApoE or ApoE AT donor mice onto the abdominal aorta of ApoE recipient mice. Compared with ApoE VAT transplantation, ApoE AT VAT transplantation markedly attenuated aortic aneurysm formation, macrophage infiltration, and gelatinolytic activity in the abdominal aorta. AT receptor activation led to the polarization of macrophages in perivascular VAT toward the proinflammatory phenotype. Moreover, osteopontin expression and gelatinolytic activity were considerably lower in ApoE AT perivascular VAT than in ApoE perivascular VAT, and angiotensin II-induced osteopontin secretion from adipocytes was eliminated after deletion of AT receptor in adipocytes. Notably, induction of macrophage migration by conditioned medium from angiotensin II-stimulated wild-type adipocytes was suppressed by treatment with an osteopontin-neutralizing antibody, and ApoE OPN VAT transplantation more potently attenuated aortic aneurysm formation than ApoE VAT transplantation. Our findings indicate a previously unrecognized effect of AT receptor in perivascular VAT on the pathogenesis of abdominal aortic aneurysm.
Objective
The NR4A orphan nuclear receptor NOR1 functions as a constitutively active transcription factor regulating cellular inflammation and proliferation. In the present study, we employed bone marrow transplantation to determine the selective contribution of NOR1 expression in hematopoietic stem cells to the development of atherosclerosis.
Methods and Results
Reconstitution of lethally irradiated apoE−/− mice with NOR1-deficient hematopoietic stem cells accelerated atherosclerosis formation and macrophage recruitment following feeding a diet enriched in saturated fat. NOR1 deficiency in hematopoietic stem cells induced splenomegaly and monocytosis, specifically the abundance of inflammatory Ly6C+ monocytes. Bone marrow transplantation studies further confirmed that NOR1 suppresses the proliferation of macrophage and dendritic progenitor (MDP) cells. Expression analysis identified RUNX1, a critical regulator of hematopoietic stem cell expansion, as a target gene suppressed by NOR1 in MDP cells. Finally, in addition to inducing Ly6C+ monocytosis, NOR1 deletion increased the replicative rate of lesional macrophages and induced local foam cell formation within the atherosclerotic plaque.
Conclusion
Collectively, our studies demonstrate that NOR1 deletion in hematopoietic stem cells accelerates atherosclerosis formation by promoting myelopoiesis in the stem cell compartment and by inducing local pro-atherogenic activities in the macrophage, including lesional macrophage proliferation and foam cell formation.
here are 2 types of hypertrophic obstructive cardiomyopathy (HOCM): obstruction at the subaorta, called idiopathic hypertrophic subaortic stenosis (IHSS), 1 and obstruction at the mid left ventricle. 2 In contrast to the many studies of IHSS, only a few studies, other than case reports, have focused on midventricular obstruction (MVO). Two patients with MVO were reported for the first time in 1976 by Falicov et al, 2 one of whom suddenly died shortly after unsuccessful myectomy. Maron et al elucidated that the left ventricular pressure gradient (LVPG) was related to even prognosis in patients with hypertrophic cardiomyopathy (HCM). 3 Thus, attenuation of the LVPG has recently become an important strategy in the management of patients with HOCM.In the clinical setting, patients with MVO may often be overlooked. Very recently we reported that there are 2 specific patterns of carotid pulse tracing in these patients, 4 by which they may be diagnosed with ease. As to the treatment of patients with MVO, Hintringer et al reported the usefulness of permanent DDD pacing to alleviate LVPG and symptoms in an 85-year-old woman with MVO who did not respond to pharmacological therapy. 5 In patients with MVO, unlike those with IHSS, therapies involving myotomy or myectomy and alcohol septal ablation require great caution to prevent the induction or deterioration of mitral regurgitation. Both -blockers and calcium antagonists are often insufficient for attenuating LVPG. In 1982, Pollick reported the usefulness of the antiarrhythmic drug disopyramide in attenuating LVPG in IHSS. 6 Unfortunately sustained use of disopyramide is difficult owing to the thirst, dysuria and so on related to its strong anticholinergic action. We previously reported the usefulness of the antiarrhythmic drug, cibenzoline, the anticholinergic action of which is very weak, 7 to attenuate LVPG in IHSS. 8 In the present study, therefore, we examined the acute and chronic effect of cibenzoline on LVPG and left ventricular (LV) diastolic dysfunction in patients with MVO.
Methods
Study SubjectsTwenty-three patients with MVO participated in this study after giving written informed consent. Twenty healthy control subjects served as the comparison of the hemo-
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