An ultrafast piezoelectric Z-scanner with a resonance frequency above 1.1 MHz for high-speed atomic force microscopy.

The Z-scanner is the major component limiting the speed performance of all current high-speed atomic force microscopy systems. Here, we present an ultrafast piezoelectric Z-scanner with a resonance frequency above 1.1 MHz, achieving a record response time of ∼0.14 µs, approximately twice as fast as conventional piezoelectric-based Z-scanners. In the mechanical design, a small piezo-stack is supported at its bottom four vertices on a cone-like hollow, allowing the resonance frequency of the Z-scanner to remain as high as that of the piezo in free vibration. Its maximum displacement, ∼190 nm at 50 V, is large enough for imaging bio-molecules. For imaging bio-molecules in a buffer solution, the upper half of the Z-scanner is wrapped in a thin film resistant to water and chemicals, providing an excellent waterproof and mechanical durability without lowering the resonance frequency. We demonstrate that this Z-scanner can observe actin filaments, fragile biological polymers, for more than five times longer than the conventional Z-scanner at a tip velocity of 800 µm/s.

Effects of a lifestyle development program designed to reduce the risk factors for cognitive decline on the mental health of elderly individuals.

BACKGROUND: The incidence of Alzheimer's disease (AD) along with depression is high in the elderly. In the present study, a program that allows the elderly individuals to voluntarily manage and develop lifestyles that may reduce the risk factors for cognitive decline was applied to the participants to evaluate its effect on the mental health of these individuals. METHODS: The participants were randomly assigned to an intervention group and a control group. The program was conducted during 7 months in the intervention group, and it had seven times of group activities, performed once a month for about 1 h, and individual activities to reduce the risk factors for cognitive decline, performed every day. To evaluate the effects of the program on the mental health of the participants, the Geriatric Depression Scale (GDS) and Philadelphia Geriatric Center Morale Scale (PGC) were used. These two scales were applied twice to the intervention and control groups. RESULTS: The GDS score revealed no change in the score in the intervention group before and after the 7-month program implementation; however, in the control group, the score was significantly higher after program implementation than that before. The PGC score revealed no change in the intervention group before and after 7-month program implementation; however, in the control group, the score was significantly lower after program implementation than that before. Additionally, it revealed no change in the GDS score in the depression-prone control group before and after 7-month program implementation; however, in the depression-prone intervention group, the GDS score was significantly lower after program implementation than that before. CONCLUSIONS: The intervention program that allows the elderly individuals to voluntarily manage and develop lifestyles that may reduce the risk factors for cognitive decline is expected to maintain mental health in elderly individuals.

Azilsartan attenuates cardiac damage caused by high salt intake through the downregulation of the cardiac (pro)renin receptor and its downstream signals in spontaneously hypertensive rats.

We examined whether the stimulation of the angiotensin II AT1 receptor increases the expression of the cardiac (pro)renin receptor ((P)RR) and its downstream signals and whether the blockade of the angiotensin II AT1 receptor by azilsartan decreases the expression of the cardiac (P)RR and its signaling in spontaneously hypertensive rats (SHRs) with a high-salt intake. Rats received normal-salt (0.9%) chow, high-salt (8.9%) chow, normal-salt chow with 1 mg/day of azilsartan, and high-salt chow with 1 mg/day of azilsartan from 6 to 12 weeks of age. Rats with normal-salt chow were administered 100 ng/kg/min of angiotensin II by osmotic minipump from 6 to 12 weeks of age. A high-salt diet and angiotensin II significantly increased the systolic blood pressure; overexpressed cardiac (P)RR, phosphorylated (p)-ERK1/2, p-p38MAPK, p-HSP27, and TGF-ß1; enhanced cardiac interstitial and perivascular fibrosis, cardiomyocyte size, interventricular septum (IVS) thickness, and left ventricular (LV) end-diastolic dimension; and decreased LV fractional shortening. Azilsartan decreased systolic blood pressure, cardiac expressions of (P)RR, p-ERK1/2, p-p38MAPK, p-HSP27, and TGF-ß1, cardiac interstitial and perivascular fibrosis, cardiomyocyte size, and LV diastolic dimension, and improved LV fractional shortening. In conclusion, azilsartan attenuates cardiac damage caused by high salt intake through the downregulation of the cardiac (pro)renin receptor and its downstream signals in SHRs.

Excessively low salt diet damages the heart through activation of cardiac (pro) renin receptor, renin-angiotensin-aldosterone, and sympatho-adrenal systems in spontaneously hypertensive rats.

OBJECTIVE: A high salt intake causes hypertension and leads to cardiovascular disease. Therefore, a low salt diet is now recommended to prevent hypertension and cardiovascular disease. However, it is still unknown whether an excessively low salt diet is beneficial or harmful for the heart. METHODS: Wistar Kyoto rats (WKYs) and spontaneously hypertensive rats (SHRs) received normal salt chow (0.9% salt diet) and excessively low salt chow (0.01% salt diet referred to as saltless diet) for 8 weeks from 8 to 16 weeks of age. The effects of the excessively low salt diet on the cardiac (pro) renin receptor, renin-angiotensin-aldosterone, and sympatho-adrenal systems were investigated. RESULTS: The excessively low salt diet did not affect the systolic blood pressure but significantly increased the heart rate both in WKYs and SHRs. The excessively low salt diet significantly elevated plasma renin activity, plasma angiotensin I, II and aldosterone concentrations, and plasma noradrenaline and adrenaline concentrations both in WKYs and SHRs. Cardiac expressions of renin, prorenin, (P)RR, angiotensinogen, and angiotensin II AT1 receptor and phosphorylated (p)-ERK1/2, p-HSP27, p-38MAPK, and TGF-ß1 were significantly enhanced by the excessively low salt diet in both WKYs and SHRs. The excessively low salt diet accelerated cardiac interstitial and perivascular fibrosis and increased the cardiomyocyte size and interventricular septum thickness in WKYs and SHRs but the extent was greater in SHRs. CONCLUSION: An excessively low salt diet damages the heart through activation of plasma renin-angiotensin-aldosterone and sympatho-adrenal systems and activation of cardiac (P)RR and angiotensin II AT1 receptor and their downstream signals both in WKYs and SHRs.

High salt intake damages the heart through activation of cardiac (pro) renin receptors even at an early stage of hypertension.

OBJECTIVE: It has not yet been fully elucidated whether cardiac tissue levels of prorenin, renin and (P)RR are activated in hypertension with a high salt intake. We hypothesized that a high salt intake activates the cardiac tissue renin angiotensin system and prorenin-(pro)renin receptor system, and damages the heart at an early stage of hypertension. METHODS: Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) received regular (normal-salt diet, 0.9%) and high-salt (8.9%) chow for 6 weeks from 6 to 12 weeks of age. The systolic blood pressure, plasma renin activity (PRA) and plasma angiotensin II concentration were measured, and the protein expressions of prorenin, (pro)renin receptor, angiotensinogen, angiotensin II AT1 receptor, ERK1/2, TGF-ß, p38MAPK and HSP27 in the myocardium were investigated. The cardiac function was assessed by echocardiography, and histological analysis of the myocardium was performed. RESULTS: The high-salt diet significantly increased the systolic blood pressure, and significantly reduced the PRA and plasma angiotensin II concentration both in the WKYs and SHRs. Cardiac expressions of prorenin, renin, (P)RR, angiotensinogen, angiotensin II AT1 receptor, phosphorylated (p)-ERK1/2, p-p38MAPK, TGF-ß and p-HSP27 were significantly increased by the high salt diet both in the WKYs and SHRs. The high-salt diet significantly increased the interventricular septum thickness and cardiomyocyte size, and accelerated cardiac interstitial and perivascular fibrosis both in the WKYs and SHRs. On the other hand, dilatation of left ventricular end-diastolic dimension and impairment of left ventricular fractional shortening was shown only in salt loaded SHRs. CONCLUSION: The high-salt diet markedly accelerated cardiac damage through the stimulation of cardiac (P)RR and angiotensin II AT1 receptor by increasing tissue prorenin, renin and angiotensinogen and the activation of ERK1/2, TGF-ß, p38MAPK and HSP27 under higher blood pressure.