High surface laser-induced damage threshold of SrB4O7 single crystals under 266-nm (DUV) laser irradiation.

Under 266-nm (deep ultraviolet, DUV) laser irradiation, an SrB4O7 (SBO) single crystal has been found to exhibit a surface laser-induced damage threshold (LIDT) of ∼ 16.4 J/cm2, which is higher than those of a synthetic silica glass (4.8 J/cm2) and a calcium fluoride (CaF2) crystal (11.4 J/cm2). By catalyst-referred etching (CARE), the LIDT of an SBO crystal can also be improved to around 24.1 J/cm2, which is 1.4 and 6.0 times higher compared to an unetched crystal and a silica glass, respectively. With high surface LIDTs, SBO single crystals can then be used as optical window materials for high-power DUV laser systems.

Antiferromagnetism in perfectly ordered L10-MnAl with stoichiometric composition and its mechanism.

Manganese (Mn)-based strong magnets have long been a challenge because their 3d half-filled nature, owing to the close proximity of Mn atoms, results in antiferromagnetic ordering. Among various Mn magnetic materials, L10-MnAl (τ-phase) has received much attention since it shows ferromagnetism at a high Curie temperature despite the very short Mn-Mn distance. However, because of the difficult synthesis of the stoichiometric and perfectly ordered τ-phase, its intrinsic magnetic properties and mechanism are unclear. Here, we show the first observation of antiferromagnetism, having sixfold magnetic superstructure along the c-axis, in stoichiometric and chemically ordered τ-phase. Moreover, we found that super-exchange interaction between Mn atoms via p-electrons of Al atoms causes antiferromagnetism in τ-phase. The ferromagnetism in the conventional Mn-rich τ-phase results from the suppression of the super-exchange interaction due to the substitution the excess Mn atoms for the Al atoms. The current study of Mn-based magnetic materials mainly focuses on the lattice constant engineering based on the simple Beth-Slater picture of direct exchange. These findings present effective ways to obtain high magnetization without antiferromagnetic ordering.

[Carfilzomib-induced renal impairment with albuminuria in a patient with relapsed/refractory multiple myeloma].

A 70-year-old woman was diagnosed with multiple myeloma in 2014. She achieved complete remission (CR) after bortezomib, cyclophosphamide, dexamethasone (VCD) therapy and lenalidomide, dexamethasone (Rd) therapy; however, she relapsed in 2017. Although she achieved second CR by carfilzomib, dexamethasone (Kd) therapy, serum creatinine levels increased with urinary protein after 17 courses of Kd therapy. Urinary protein test revealed albuminuria, whereas M-protein was undetectable. Carfilzomib-induced renal impairment was suspected due to absence of other causes, such as progression of myeloma or autoimmune disease. On discontinuation of Kd therapy, urinary protein decreased rapidly with improvement of serum creatinine levels within a month. Carfilzomib-induced nephrotoxicity is a rare but important adverse event.

Impact of local strain on Ti-L2,3 electron energy-loss near-edge structures of BaTiO3: a first-principles multiplet study.

Identification of local strains is crucial because the local strains largely influence the ferroelectric property of BaTiO3. The effects of local strains induced by external pressures on the Ti-L2,3 electron energy-loss near-edge structure (ELNES) of BaTiO3 were theoretically investigated using first-principles multiplet calculations. We revealed that the effects appear in the position of the spectral threshold, namely the spectrum shifts to lower and higher energy sides by the tensile and compressive pressures, respectively. We concluded that conventional ELNES observations can identify only large strains induced by -10 GPa, and 0.1 eV energy resolution is required to identify ±2% of strains.

Morning blood pressure hyper-reactivity is an independent predictor for hypertensive cardiac hypertrophy in a community-dwelling population.

BACKGROUND: Morning blood pressure (BP) surge seems to be a risk factor for cardiovascular events. Although physical activity after arising significantly affects morning BP surge, it has remained unclear whether morning BP surge after controlling for physical activity (morning BP reactivity) is associated with target organ damage. METHODS: We performed ambulatory BP monitoring with simultaneous actigraphy and echocardiography in 120 community-dwelling Japanese subjects. We determined the waking time by actigraphy, and defined morning BP surge (MBPS) as the average of systolic BP during the 2 h after awakening minus the average of systolic BPs during the 1 h that included the lowest sleep BP. The ratio of MBPS/(sum of the 2-h physical activity after the arising time)0.5 was calculated as the morning BP reactivity (MBPR). RESULTS: In all the subjects studied (n = 120), MBPR was positively associated with left ventricular (LV) mass index (r = 0.30, P = .001). The MBPR had a positive association with both 24-h BP variability (SD) (r = 0.373, P < .001) and awake BP variability (r = 0.20, P < .05). The MBP hyper-reactive group (the highest quartile [Q4] of MBPR: n = 30) had significantly higher LV mass index than the nonreactive group (the other quartiles [Q1 to 3]: n = 90) (140 v 113 g/m(2), P < .001). Even after controlling for age, body mass index, gender, and 24-h systolic BP, the MBP hyper-reactive status still remained a strong predictor for LV hypertrophy. CONCLUSIONS: Exaggerated MBPS, adjusted for physical activity, is associated with cardiac hypertrophy independent of ambulatory BP level in a community-dwelling population.

Determinants of exaggerated difference in morning and evening blood pressure measured by self-measured blood pressure monitoring in medicated hypertensive patients: Jichi Morning Hypertension Research (J-MORE) Study.

BACKGROUND: Morning blood pressure (BP) surge in ambulatory BP monitoring was a risk factor for stroke in our previous study. We studied the determinants of the morning minus evening systolic BP difference (ME difference) in self-measured BP monitoring, as a possible risk factor for stroke in medicated hypertensive patients. METHODS: Nine hundred sixty-nine hypertensive outpatients receiving stable antihypertensive drug treatment were studied using self-measured BP monitoring in the morning and evening. RESULTS: The ME difference ranged from -37.3 to 53.3 mm Hg (mean 7.9 mm Hg). The highest quartile (Q4) of the ME difference group (>15.0 mm Hg) had older age (68.0+/-9.8 years v 66.2+/-10.3 years, P=.01) and higher prevalence of men (48.3% v 39.9%, P=.02), regular alcohol drinkers (34.7% v 26.0%, P=.01) and beta-blocker use (26.9% v 19.9%, P=.03) than the other quartile groups (Q1 to Q3), whereas there was no significant difference in the average of morning and evening (ME average) BP. In logistic regression analysis controlling for ME average and other confounding factors, independent risks for Q4 of ME difference were older age (10 years older: odds ratio [OR] 1.21, P=.01, 95% confidence interval (CI) 1.04-1.42), regular alcohol drinker (OR 1.51, P=.04, 95% CI 1.01-2.26), and beta-blocker use (OR 1.50, P=.02, 95% CI 1.06-2.12). CONCLUSIONS: Older age, beta-blocker use, and regular alcohol drinking were significant determinants of the exaggerated ME difference in medicated hypertensive patients.

Smart intramedullary rod for correction of pediatric bone deformity: a preliminary study.

We were interested in determining if a smart intramedullary rod made of nitinol shape-memory alloy is capable of correcting deformed immature long bones. Because of limitations in our study design the process was reversed in that we examined the smart rod's ability to create a deformity rather than to correct one. Smart rods of different lengths and diameters were heat-treated to resume a radius of curvature of 30 to 110 mm. The low and high temperature phases of the smart rods were set, respectively, at 0 degrees C to 4 degrees C and 36 degrees C to 38 degrees C. The preshaped smart intramedullary rods were implanted in the cooled martensite phase in the medullary canal of the tibia in eight rabbits, where they restored their austenite form, causing a continuous bending force. On a weekly basis anteroposterior and lateral radiographs of the surgically treated tibia and the contralateral tibia were obtained for comparison. Rabbits were euthanized 6 weeks after surgery and computed tomography scans of both tibias were used for image analysis. Smart rods with a larger radius of curvature showed only minimal signs of remodeling; however, rods with a radius of curvature of 50 and 70 mm generated enough force history to create bone remodeling and deformation. The amount of bone deformation was highly magnified when unicortical corticotomy on the tension side was done. Based on this preliminary study the technology of the smart intramedullary rod may provide a valuable alternative method to correct pediatric skeletal deformities.

Associations between nondipping of nocturnal blood pressure decrease and cardiovascular target organ damage in strictly selected community-dwelling normotensives.

BACKGROUND: In hypertensives, nondippers are more likely than dippers to suffer silent, as well as overt, hypertensive target organ damage. In this study, we investigated whether a nondipper status was associated with target organ damage in normotensives. METHODS: We performed ambulatory blood pressure (BP) monitoring, echocardiography, and carotid ultrasonography and measured natriuretic peptides and urinary albumin (UAE) in 74 normotensive subjects with the following criteria: 1) clinical BP <140/90 mm Hg; 2) average 24-h ambulatory BP <125/80 mm Hg. RESULTS: The left ventricular mass index (LVMI) and the relative wall thickness (RWT) measured by echocardiography were greater in nondippers than dippers (LVMI: 103 +/- 26 v 118 +/- 34 g/m(2), P <.05; RWT: 0.38 +/- 0.07 v 0.43 +/- 0.09, P <.01). Plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were higher in nondippers than dippers (ANP: 14 +/- 10 v 36 +/- 63 pg/mL, P <.01; BNP: 16 +/- 12 v 62 +/- 153 pg/mL, P <.05). There were no significant differences in UAE and intima-media thickness measured by carotid ultrasonography. CONCLUSIONS: Normotensive nondipping may not reflect renal damage, but may have a predominant effect on cardiac damage. Nondipping of nocturnal BP seems to be a determinant of cardiac hypertrophy and remodeling, and may result in a cardiovascular risk independent of ambulatory BP levels in normotensives.

Morning surge in blood pressure as a predictor of silent and clinical cerebrovascular disease in elderly hypertensives: a prospective study.

BACKGROUND: Cardiovascular events occur most frequently in the morning hours. We prospectively studied the association between the morning blood pressure (BP) surge and stroke in elderly hypertensives. METHODS AND RESULTS: We studied stroke prognosis in 519 older hypertensives in whom ambulatory BP monitoring was performed and silent cerebral infarct was assessed by brain MRI and who were followed up prospectively. The morning BP surge (MS) was calculated as follows: mean systolic BP during the 2 hours after awakening minus mean systolic BP during the 1 hour that included the lowest sleep BP. During an average duration of 41 months (range 1 to 68 months), 44 stroke events occurred. When the patients were divided into 2 groups according to MS, those in the top decile (MS group; MS > or =55 mm Hg, n=53) had a higher baseline prevalence of multiple infarcts (57% versus 33%, P=0.001) and a higher stroke incidence (19% versus 7.3%, P=0.004) during the follow-up period than the others (non-MS group; MS <55 mm Hg, n=466). After they were matched for age and 24-hour BP, the relative risk of the MS group versus the non-MS group remained significant (relative risk=2.7, P=0.04). The MS was associated with stroke events independently of 24-hour BP, nocturnal BP dipping status, and baseline prevalence of silent infarct (P=0.008). CONCLUSIONS: In older hypertensives, a higher morning BP surge is associated with stroke risk independently of ambulatory BP, nocturnal BP falls, and silent infarct. Reduction of the MS could thus be a new therapeutic target for preventing target organ damage and subsequent cardiovascular events in hypertensive patients.

U-curve relationship between orthostatic blood pressure change and silent cerebrovascular disease in elderly hypertensives: orthostatic hypertension as a new cardiovascular risk factor.

OBJECTIVES: The study investigated the clinical significance and mechanism of orthostatic blood pressure (BP) dysregulation in elderly hypertensive patients. BACKGROUND: Although orthostatic hypotension (OHYPO), often found in elderly hypertensive patients, has been recognized as a risk factor for syncope and cardiovascular disease, both the clinical significance and the mechanism of orthostatic hypertension (OHT) remain unclear. METHODS: We performed a head-up tilting test and brain magnetic resonance imaging (MRI) in 241 elderly subjects with sustained hypertension as indicated by ambulatory BP monitoring. We classified the patients into an OHT group with orthostatic increase of systolic blood pressure (SBP) of >or=20 mm Hg (n = 26), an OHYPO group with orthostatic SBP decrease of >or=20 mm Hg (n = 23), and a normal group with neither of these two patterns (n = 192). RESULTS: Silent cerebral infarcts were more common in the OHT (3.4/person, p < 0.0001) and OHYPO groups (2.7/person, p = 0.04) than in the normal group (1.4/person). Morning SBP was higher in the OHT group than in the normal group (159 vs. 149 mm Hg, p = 0.007), while there were no significant differences of these ambulatory BPs between the two groups during other periods. The OHT (21 mm Hg, p < 0.0001) and OHYPO (20 mm Hg, p = 0.01) groups had higher BP variability (standard deviation of awake SBP) than the normal group (17 mm Hg). The associations between orthostatic BP change and silent cerebrovascular disease remained significant after controlling for confounders, including ambulatory BP. The orthostatic BP increase was selectively abolished by alpha-adrenergic blocking, indicating that alpha-adrenergic activity is the predominant pathophysiologic mechanism of OHT. CONCLUSIONS: Silent cerebrovascular disease is advanced in elderly hypertensives having OHT. Elderly hypertensives with OHT or OHYPO may have an elevated risk of developing hypertensive cerebrovascular disease.