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Rare earth (RE)-doped BaTiO3 materials are promising dielectric materials for base-metal electrode multilayer ceramic capacitors (BME-MLCCs). Thus, the fundamental understanding of their effect on dielectric properties and reliability is crucial for further improvement of its performance. Herein, according to Preisach model, the dielectric stability of Dy and Y-doped BaTiO3 MLCCs with different particle sizes was investigated in this study. First order reversal curve (FORC) analysis showed that the reversible and irreversible domain wall motion of Dy-doped samples was weaker than that of Y-doped samples. Results also showed that the higher "shell" proportion of "core-shell" structure in Dy-doping was beneficial for improving the dielectric stability and insulation resistance degradation. The findings provide a comprehensive understanding and illustrate the significant role of the "core-shell" volume ratio in the tetragonality and domain wall motion in RE-doped BaTiO3 materials, and consequently laying an important ground work to obtain high dielectric stability and reliability in BME-MLCCs. [ABSTRACT FROM AUTHOR]

In rats, both central and systemic ANG II type 1 ([AT.sub.1]) receptor blockade attenuate sympathetic hyperactivity, but central blockade more effectively attenuates left ventricular (LV) dysfunction post-myocardial infarction (MI). In protocol 1, we examined whether functional effects on cardiac load may play a role and different cardiac effects disappear after withdrawal of the blockade. Wistar rats were infused for 4 wk post-MI intracerebroventricularly (1 mg x [kg.sup.-1] x [day.sup.-1]) or injected subcutaneously daily (100 mg x [kg.sup.-1] x [day.sup.-1]) with losartan. LV dimensions and function were assessed at 4 wk and at 6 wk post-MI, i.e., 2 wk after discontinuing treatments. At 4 and 6 wk post-MI, LV dimensions were increased and ejection fraction was decreased. Intracerebroventricular but not subcutaneous losartan significantly improved these parameters. At 6 wk, LV peak systolic pressure (LVPSP) and maximal or minimal first derivative of change in pressure over time (dP/[dt.sub.max/min]) were decreased and LV end-diastolic pressure (LVEDP) was increased. All four indexes were improved by previous intracerebroventricular losartan, whereas subcutaneous losartan improved LVEDP only. In protocol H, we evaluated effects of oral instead of subcutaneous administration of losartan for 4 wk post-MI. Losartan (~200 mg x [kg.sup.-1] x [day.sup.-1]) either via drinking water or by gavage similarly decreased [AT.sub.1] receptor binding densities in brain nuclei and improved LVEDP but further decreased LVPSP and dP/[dt.sub.max]. These results indicate that effects on cardiac load by peripheral [AT.sub.1] receptor blockade or the pharmacokinetic profile of subcutaneous versus oral dosing do not contribute to the different cardiac effects of central versus systemic [AT.sub.1] receptor blockade post-MI. losartan; cardiac remodeling; echocardiography; Millar catheter; brain; ANG II type 1

Functional studies indicate that the sympathoexcitatory and pressor responses to an increase in cerebrospinal fluid (CSF) [[Na.sup.+]] by central infusion of [Na.sup.+]-rich artificial cerebrospinal fluid (aCSF) in Wistar rats are mediated in the brain by mineralocorticoid receptor (MR) activation, ouabain-like compounds (OLC), and A[T.sub.1]receptor stimulation. In the present study, we examined whether increasing CSF [[Na.sup.+]] by intracerebroventricular infusion of [Na.sup.+]-rich aCSF activates MR and thereby increases OLC and components of the renin-angiotensin system in the brain. Male Wistar rats received via osmotic minipump an intracerebroventricular infusion of aCSF or [Na.sup.+]-rich aCSF, in some groups combined with intracerebroventricular infusion of spironolactone (100 ng/h), antibody Fab fragments (to bind OLC), or as control [gamma]-globulins. After 2 wk of infusion, resting blood pressure and heart rate were recorded, OLC and aldosterone content in the hypothalamus were assessed by a specific ELISA or radioimmunoassay, and angiotensin-converting enzyme (ACE) and A[T.sub.1]-receptor binding densities in various brain nuclei were measured by autoradiography using [sup.125]I-labeled 351 A and [sup.125]I-labeled ANG II. When compared with intracerebroventricular aCSF, intracerebroventricular [Na.sup.+]-rich aCSF increased CSF [[Na.sup.+]] by ~5 mmol/l, mean arterial pressure by ~20 mmHg, heart rate by ~65 beats/min, and hypothalamic content of OLC by 50% and of aldosterone by 33%. Intracerebroventricular spironolactone did not affect CSF [[Na.sup.+]] but blocked the [Na.sup.+]-rich aCSF-induced increases in blood pressure and heart rate and OLC content. Intracerebroventricular [Na.sup.+]-rich aCSF increased ACE and A[T.sub.1]-receptor-binding densities in several brain nuclei, and Fab fragments blocked these increases. These data indicate that in Wistar rats, a chronic increase in CSF [[Na.sup.+]] may increase hypothalamic aldosterone and activate CNS pathways involving MR, and OLC, leading to increases in A[T.sub.1]-receptor and ACE densities in brain areas involved in cardiovascular regulation and hypertension. brain mineralocorticoid receptor; ouabain; angiotensin-converting enzyme; A[T.sub.1]-receptor doi:10.1152/ajpheart.00024.2006

Chronic subcutaneous infusion of ouabain causes hypertension via central pathways involving angiotensin type 1 (A[T.sub.1]) receptor stimulation. The present study assessed plasma and tissue ANG I and II levels as well as A[T.sub.1] receptor and angiotensin-converting enzyme (ACE) mRNA levels and binding densities by real-time PCR and in vitro autoradiography in relevant brain nuclei and peripheral tissues (heart and kidney) in rats at 1 and/or 2 wk after start of ouabain infusion at 50 [micro]g/day. After 2 wk (but not after 1 wk), blood pressures significantly increased (+ 15 mmHg). At 2 wk, plasma ANG I and II levels were markedly suppressed by ouabain. In contrast, in the heart and kidneys, ANG I levels were not affected, and ANG II levels tended to decrease, whereas in the hypothalamus ANG II content clearly increased. At 1 wk, no changes in ACE and A[T.sub.1] receptor densities were seen. After 2 wk, there were significant decreases in AT~ receptor mRNA and densities in the organum vasculosum of the lamina terminalis (OVLT), subfornical organ (SFO), and paraventricular nucleus (PVN). ACE densities decreased only in the OVLT and SFO, but ACE mRNA showed more variable responses (decrease in OVLT vs. increase in PVN). In the kidneys, at 2 wk both A[T.sub.1] receptor and ACE densities were decreased, but mRNA abundance did not change. The heart showed no significant changes. The increase in hypothalamic ANG II content and associated decreases in central A[T.sub.1] receptor and ACE densities support the involvement of the brain renin-angiotensin system in the central hypertensive mechanism of action of ouabain. angiotensin II; angiotensin type 1 receptors; angiotensin-converting enzyme; brain; kidneys doi:10.1152/ajpheart.01148.2005

The present study tested the hypothesis that 17[beta]-estradiol ([E.sub.2]) inhibits increases in angiotensin-converting enzyme (ACE) and ANG II type 1 receptor (A[T.sub.1]R) in the brain and heart after myocardial infarction (MI) and, thereby, inhibits development of left ventricular (LV) dysfunction after MI. Agematched female Wistar rats were treated as follows: 1) no surgery (ovary intact), 2) ovariectomy + subcutaneous vehicle treatment (OVX + Veh), or 3) OVX + subcutaneous administration of a high dose of [E.sub.2] (OVX + high-[E.sub.2]). After 2 wk, rats were randomly assigned to coronary artery ligation (MI) and sham operation groups and studied after 3 wk. [E.sub.2] status did not affect LV function in sham rats. At 2-3 wk after MI, impairment of LV function was similar across MI groups, as measured by echocardiography and direct LV catheterization. LV ACE mRNA abundance and activity were increased severalfold in all MI groups compared with respective sham animals and to similar levels across MI groups. In most brain nuclei, ACE and A[T.sub.1]R densities increased after MI. Unexpectedly, compared with the respective sham groups the relative increase was clearest (20-40%) in OVX + high-[E.sub.2] MI rats, somewhat less (10-15%) in ovary-intact MI rats, and least (< 10-15%) in OVX + Veh MI rats. However, because in the sham group brain ACE and A[T.sub.1]R densities increased in the OVX + Veh rats and decreased in the OVX + high-[E.sub.2] rats compared with the ovary-intact rats, actual ACE and A[T.sub.1]R densities in most brain nuclei were modestly higher ( ovariectomy; heart failure; estrogens

In the brain, ouabain-like compounds (OLC) and the reninangiotensin system (RAS) contribute to sympathetic hyperactivity in rats after myocardial infarction (MI). This study aimed to evaluate changes in components of the central vs. the peripheral RAS. Angiotensin-converting enzyme (ACE) and angiotensin type 1 (A[T.sub.1]) receptor binding densities were determined by measuring [sup.125]I-labeled 351A and [sup.125]I-labeled ANG II binding 4 and 8 wk after MI. In the brain, ACE and A[T.sub.1] receptor binding increased 8-15% in the subfornical organ, 14-22% in the organum vasculosum laminae terminalis, 20-34% in the paraventricular nucleus, and 13-15% in the median preoptic nucleus. In the heart, the greatest increase in ACE and A[T.sub.1] receptor binding occurred at the infarct scar (~10-fold) and the least in the right ventricle (2-fold). In kidneys, ACE and A[T.sub.1] receptor binding decreased 10-15%. After intracerebroventricular infusion of Fab fragments to block brain OLC from 0.5 to 4 wk after MI, increases in ACE and A[T.sub.1] receptors in the subfornical organ, organum vasculosum laminae terminalis, paraventricular nucleus, and medial preoptic nucleus were markedly inhibited, and ACE and A[T.sub.1] receptor densities in the heart increased less (6-fold in the infarct scar). In kidneys, decreases in ACE and A[T.sub.1] receptor binding were absent after treatment with Fab fragments. These results demonstrate that ACE and A[T.sub.1] receptor binding densities increase not only in the heart but also in relevant areas of the brain of rats after MI. Brain OLC appears to play a major role in activation of brain RAS in rats after MI and, to a modest degree, in activation of the cardiac RAS. renin-angiotensin system; autoradiography; heart failure

Wang, Jun Ming, Shereeni J. Veerasingham, Junhui Tan, and Frans H.H. Leenen. Effects of high salt intake on brain A[T.sub.1] receptor densities in Dahl rats. Am J Physiol Heart Circ Physiol 285: H1949-H1955, 2003. First published July 3, 2003; 10.1152/ajpheart.00744.2002.--To assess effects of dietary salt on brain A[T.sub.1] receptor densities, 4-wk-old Dahl salt-sensitive (Dahl S) and salt-resistant (Dahl R) rats were fed a regular (101 [micro]mol Na/g) or high (1,370 [micro]mol Na/g)-salt diet for 1, 2, or 4 wk. A[T.sub.1] receptors were assessed by quantitative in vitro autoradiography. A[T.sub.1] receptor densities did not differ significantly between strains on the regular salt diet. The high-salt diet for 1 or 2 wk increased A[T.sub.1] receptor binding by 21-64% in the Dahl S rats in the subfornical organ, median preoptic nucleus, paraventricular nucleus, and suprachiasmatic nucleus. No changes were noted in the Dahl R rats. After 4 wk on a high-salt diet, increases in A[T.sub.1] receptor binding persisted in Dahl S rats but were now also noted in the paraventricular nucleus, median preoptic nucleus, and suprachiasmatic nucleus of Dahl R rats. At 4 wk on the diet, intracerebroventricular captopril caused clear decreases in blood pressure only in the Dahl S on the highsalt diet but caused largely similar relative increases in brain A[T.sub.1] receptor densities in Dahl S and R on the high-salt diet versus regular salt diet. These data demonstrate that high salt intake rapidly (within 1 wk) increases A[T.sub.1] receptor densities in specific brain nuclei in Dahl S and later (by 4 wk) also in Dahl R rats. Because the brain renin-angiotensin system only contributes to salt-induced hypertension in Dahl S rats, further studies are needed to determine which of the salt-induced increases in brain A[T.sub.1] receptor densities contribute to the hypertension and which to other aspects of body homeostasis. brain renin-angiotensin system; salt-induced hypertension; angiotensin II; autoradiography

The presence of a local renin-angiotensin system has been established in organs that serve as angiotensin targets. In this study, the expression of angiotensinogen mRNA and subcellular localization of renin, angiotensin-converting enzyme, and angiotensin II were investigated in bovine adrenal medullary cells in primary culture. By light microscopy, expression of angiotensinogen mRNA, immunoreactive renin, angiotensin-converting enzyme, and angiotensin II were readily detectable only in the chromaffin cells. The density distribution of renin and angiotensin II in sucrose gradients suggested a concentration in chromaffin granules, a localization directly confirmed by immunoelectron microscopy. Reverse transcriptase-polymerase chain reaction and sequencing confirmed the expression of angiotensinogen in bovine chromaffin cells and the adrenal medulla. In addition, in vitro autoradiography indicated that both angiotensin-converting enzyme and angiotensin type I receptors were present in the adrenal medulla. These results provide the first direct evidence that chromaffin cells in the adrenal medulla are not only the target for angiotensin but should also be considered as potential local angiotensin-generating and -storing cells. in situ hybridization; immunocytochemistry; radioligand autoradiography; angiotensinogen

In order to achieve the composition optimization of eco-type UHPC and the improvement of the utilization rate of steel slag, using steel slag as auxiliary gelled material, the eco-type UHPC was prepared by D-optimal design method and establish the workability prediction model and the compressive strength prediction model to cany out multiple response analysis. With the help of the prediction model, the eco-type UHPC with low cement consumption and high steel slag utilization rate is designed to meet the requirements. The results show that the prediction model is reasonable and accurate. In the prediction model, superplasticizer and silica fume have a great influence on the workability, the interaction of cement, superplasticizer and steel slag have obvious influence on the workability and the addition of steel slag powder enhances the workability. The influences of silica fume and steel slag powder om compressive strength are significant, the interaction of cement and steel slag has little effect on compressive strength and the optimal value of compressive strength exists with the increase of steel slag powder. The optimal ratio of the eco-type UHPC realizes the substitution of steel slag for 30% (mass fraction) cement, and ensure the compressive strength above 130 MPa and the working performance above 260 mm. [ABSTRACT FROM AUTHOR]

In rats, both central and systemic ANG II type I (AT,) receptor blockade attenuate sympathetic hyperactivity, but central blockade more effectively attenuates left ventricular (LV) dysfunction post-myocardial infarction (MI). In protocol 1, we examined whether functional effects on cardiac load may play a role and different cardiac effects disappear after withdrawal of the blockade. Wistar rats were infused for 4 wk post-MI intracerebroventricularly (1 mg∙kg-1∙day-1) or injected subcutaneously daily (100 mg∙kg-1∙day-1) with losartan. LV dimensions and function were assessed at 4 wk and at 6 wk post-MI, i.e., 2 wk after discontinuing treatments. At 4 and 6 wk post-MI, LV dimensions were increased and ejection fraction was decreased. Intracerebroventricular but not subcutaneous losartan significantly improved these parameters. At 6 wk, LV peak systolic pressure (LVPSP) and maximal or minimal first derivative of change in pressure over time (dP/dtmax/min) were decreased and LV end-diastolic pressure (LVEDP) was increased. All four indexes were improved by previous intracerebroventricular losartan, whereas subcutaneous losartan improved LVEDP only. In protocol II, we evaluated effects of oral instead of subcutaneous administration of losartan for 4 wk post-MI. Losartan (∼200 mg∙kg-1∙day-1) either via drinking water or by gavage similarly decreased AT1 receptor binding densities in brain nuclei and improved LVEDP but further decreased LVPSP and dP/dtmax. These results indicate that effects on cardiac load by peripheral AT1 receptor blockade or the pharmacokinetic profile of subcutaneous versus oral dosing do not contribute to the different cardiac effects of central versus systemic AT, receptor blockade post-MI. [ABSTRACT FROM AUTHOR]

To assess effects of dietary salt on brain AT[sub 1] receptor densities, 4-wk-old Dahl salt-sensitive (Dahl S) and salt-resistant (Dahl R) rats were fed a regular (101 µmol Na/g) or high (1,370 µmol Na/g)-salt diet for 1, 2, or 4 wk. AT[sub 1] receptors were assessed by quantitative in vitro autoradiography. AT[sub 1] receptor densities did not differ significantly between strains on the regular salt diet. The high-salt diet for 1 or 2 wk increased AT[sub 1] receptor binding by 21-64% in the Dahl S rats in the subfornical organ, median preoptic nucleus, paraventricular nucleus, and suprachiasmatic nucleus. No changes were noted in the Dahl R rats. After 4 wk on a high-salt diet, increases in AT[sub 1] receptor binding persisted in Dahl S rats but were now also noted in the paraventricular nucleus, median preoptic nucleus, and suprachiasmatic nucleus of Dahl R rats. At 4 wk on the diet, intracerebroventricular captopril caused clear decreases in blood pressure only in the Dahl S on the highsalt diet but caused largely similar relative increases in brain AT[sub 1] receptor densities in Dahl S and R on the high-salt diet versus regular salt diet. These data demonstrate that high salt intake rapidly (within 1 wk) increases AT[sub 1] receptor densities in specific brain nuclei in Dahl S and later (by 4 wk) also in Dahl R rats. Because the brain renin-angiotensin system only contributes to salt-induced hypertension in Dahl S rats, further studies are needed to determine which of the salt-induced increases in brain AT[sub 1] receptor densities contribute to the hypertension and which to other aspects of body homeostasis. [ABSTRACT FROM AUTHOR]

Estrogens have been implicated in both worsening and protecting from cardiovascular disease. The effects of 17beta-estradiol (E2) on the cardiovascular system may be mediated, at least in part, by its modulation of local tissue renin-angiotensin systems (RAS). We assessed two critical components, angiotensin-converting enzyme (ACE) and ANG II type 1 receptor (AT(1)R), in the heart, lung, abdominal aorta, adrenal, kidney, and brain in four groups of female Wistar rats (n = 5-6/group): 1) sham ovariectomized, 2) ovariectomized (OVX) treated with subcutaneous vehicle, 3) OVX treated with 25 mug/day (regular) E2 subcutaneously, and 4) OVX treated with 250 mug/day (high) subcutaneous E2 for 2 or 5 wk. After 2 wk, plasma ACE activity was not altered by OVX, but it was 34-38% lower in OVX + regular E2 and OVX + high E2 rats compared with sham OVX rats, and these decreases were no longer present after 5 wk. After 5 wk, OVX alone increased ACE activity and binding densities, and AT(1)R binding densities by 15-100% in right ventricle, left ventricle (LV), kidney, lung, abdominal aorta, adrenal and several cardiovascular regulatory nuclei in the brain. These effects were, for the most part, prevented by regular E2 replacement and were reversed to decreases by high E2 treatment. This regulation of tissue ACE and AT(1)R is significant as the activity of these tissue RAS contributes to the pathogenesis and/or progression of hypertension, atherosclerosis, and LV remodeling after myocardial infarction.