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Maxwell’s demon is an imaginary entity that reduces the entropy of a system and generates free energy in the system. About 150 years after its proposal, theoretical studies explained the physical validity of Maxwell’s demon in the context of information thermodynamics, and there have been successful experimental demonstrations of energy generation by the demon. The demon’s next task is to convert the generated free energy to work that acts on the surroundings. Here, we demonstrate that Maxwell’s demon can generate and output electric current and power with individual randomly moving electrons in small transistors. Real-time monitoring of electron motion shows that two transistors functioning as gates that control an electron’s trajectory so that an electron moves directionally. A numerical calculation reveals that power generation is increased by miniaturizing the room in which the electrons are partitioned. These results suggest that evolving transistor-miniaturization technology can increase the demon’s power output. The study of Maxwell's demon provides a link between information thermodynamics and modern electronics. Using integrated nanometer-scale transistors in a single electron box configuration, Chida et al ., demonstrate the extraction of electrical power by Maxwell’s demon.

Patients with primary aldosteronism have a higher risk of chronic kidney disease. Visceral fat tissue is hypothesized to stimulate the adrenal glands to overproduce aldosterone, and aldosterone promotes visceral fat tissue to produce inflammatory cytokines. However, it is unclear whether the volume of accumulated visceral fat tissue is associated with renal impairment among patients with hyperaldosteronism. We conducted a single-center cross-sectional study to assess the association between the estimated glomerular filtration rate and the ratio of the visceral-to-subcutaneous fat volume calculated by computed tomography. One hundred eighty patients with primary aldosteronism were enrolled. The mean ± SD age was 52.7 ± 11.0 years, and 60.0% were women. The ratio of visceral-to-subcutaneous fat volume was highly correlated with the estimated glomerular filtration rate ( r  = 0.49, p  < 0.001). In multiple linear regression models, the ratio of visceral-to-subcutaneous fat tissue volume was significantly associated with the estimated glomerular filtration rate (estimates: −4.56 mL/min/1.73 m² per 1-SD), and there was an interaction effect between the plasma aldosterone concentration and the ratio of visceral-to-subcutaneous fat volume ( p  < 0.05). The group with a higher plasma aldosterone concentration exhibited a steeper decline in eGFR than the lower plasma aldosterone concentration group when the ratio increased. The ratio of visceral-to-subcutaneous fat tissue volume was an independent risk factor for renal dysfunction. This association increased in the presence of a high plasma aldosterone concentration. Clinicians should pay attention to the ratio of visceral-to-subcutaneous fat tissue volume and encourage primary aldosteronism patients to improve their lifestyle in addition to treating renin-aldosterone activity.

The efficacy and safety of blood pressure lowering in patients with heart failure with preserved ejection fraction (HFpEF) remain unknown. We systematically searched PubMed/Medline, ICHUSHI, EMBASE, and the Cochrane Central Library database for randomized controlled trials (RCTs) assessing the efficacy and safety of blood pressure lowering in patients with HFpEF that were published from January 1996 to July 2017. Our study included a total of 10 RCTs involving 13,091 patients with HFpEF that compared all-cause mortality, cardiovascular mortality, heart failure hospitalization, renal dysfunction, and/or hypotension between drug intervention and control groups. Then, we analyzed systolic blood pressure (SBP) before and during trials using the SBP from the RCTs data. SBP decreased in the intervention group (134.7-130.2 mmHg) more than that in the control group (134.4-133.3 mmHg), and heart failure hospitalization was reduced in the intervention group compared to that in the control group [RR 0.89 (0.82-0.97), P = 0.006]. There was no effect of treatment on all-cause mortality, cardiovascular mortality, and hypotension. However, in the studies that compared renal function, SBP decreased in the intervention group (134.3-129.6 mmHg) more than that in the control group (134.0-132.8 mmHg), and the occurrence of renal dysfunction increased in the intervention group compared to that in the control group [RR 1.52 (1.31-1.76), P < 0.00001)]. Blood pressure lowering that achieves SBP levels of ~130 mmHg may be related to the reduction in heart failure hospitalization in patients with HFpEF, but it also possibly leads to an increased risk of renal dysfunction.

BackgroundChronic kidney disease–mineral and bone disorder (CKD–MBD), nutritional status, and uremia management have been emphasized for bone management in hemodialysis patients. Nevertheless, valuable data on the importance of muscle mass in bone management are limited, including whether conventional management alone can prevent osteoporosis. Thus, the importance of muscle mass and strength, independent of the conventional management in osteoporosis prevention among hemodialysis patients, was evaluated.MethodsPatients with a history of hemodialysis 6 months or longer were selected. We assessed the risk for osteoporosis associated with calf circumference or grip strength using multivariable adjustment for indices of CKD–MBD, nutrition, and dialysis adequacy. Moreover, the associations between bone mineral density (BMD), calf circumference, grip strength, and bone metabolic markers were also evaluated.ResultsA total of 136 patients were included. The odds ratios (95% confidence interval) for osteoporosis at the femoral neck were 1.25 (1.04–1.54, P < 0.05) and 1.08 (1.00–1.18, P < 0.05) per 1 cm shorter calf circumference or 1 kg weaker grip strength, respectively. Shorter calf circumference was significantly associated with a lower BMD at the femoral neck and lumbar spine (P < 0.001). Weaker grip strength was also associated with lower BMD at the femoral neck (P < 0.01). Calf circumference or grip strength was negatively correlated with bone metabolic marker values.ConclusionShorter calf circumference or weaker grip strength was associated with osteoporosis risk and lower BMD among hemodialysis patients, independent of the conventional therapies.

The Hokkaido Eastern Iburi Earthquake (M = 6.7) occurred on Sep. 6, 2018 in the southern part of Central Hokkaido, Japan. Since Paleogene, this region has experienced the dextral oblique transpression between the Eurasia and North American (Okhotsk) Plates and the subsequent collision between the Northeast Japan Arc and the Kuril Arc due to the oblique subduction of the Pacific Plate. This earthquake occurred beneath the foreland fold-and-thrust belt of the Hidaka Collision zone developed by the collision process, and is characterized by its deep focal depth (~ 37 km) and complicated rupture process. The reanalyses of controlled source seismic data collected in the 1998–2000 Hokkaido Transect Project revealed the detailed structure beneath the fold-and-thrust belt, and its relationship with the aftershock activity of this earthquake. Our reflection processing using the CRS/MDRS stacking method imaged for the first time the lower crust and uppermost mantle structures of the Northeast Japan Arc underthrust beneath a thick (~ 5–10 km) sedimentary package of the fold-and-thrust belt. Based on the analysis of the refraction/wide-angle reflection data, the total thickness of this Northeast Japan Arc crust is only 16–22 km. The Moho is at depths of 26–28 km in the source region of the Hokkaido Eastern Iburi Earthquake. Our hypocenter determination using a 3D structure model shows that most of the aftershocks are distributed in a depth range of 7–45 km with steep geometry facing to the east. The seismic activity is quite low within the thick sediments of the fold–thrust belt, from which we find no indication on the relationship of this event with the shallow (< 10–15 km) and rather flat active faults developed in the fold-and-thrust belt. On the other hand, a number of aftershocks are distributed below the Moho. This high activity may be caused by the cold crust delaminated from the Kuril Arc side by the arc–arc collision, which prevents the thermal circulation and cools the forearc uppermost mantle to generate an environment more favorable for brittle fracture.

Manipulation of single electrons is the key to developing ultimate electronics such as single-electron-based information processors and electrical standards in metrology. Especially, high-frequency and high-accuracy single-electron pumps are essential to realize practical current standards. While electrically defined quantum dots are widely used to build single-electron pumps, a localized state in semiconductors is also a potential candidate for accurate pumps because it can have a large activation energy for the captured electron. However, the transfer mechanism of such localized-state-mediated single-electron pumps for high-accuracy operation at a high frequency has not been well examined. Here we demonstrate a single-electron pump using a single-trap level with an activation energy of a few ten millielectron volts in Si nanotransistors. By means of gate control of capture and emission rates, the pump operates at a frequency of 3 GHz with an accuracy of better than 10 −3 at 17 K, indicating that an electric field at the trap level lowers the capture and emission time to less than 25 ps. Devices that generate single electrons are crucial for a precise definition of the ampere—the SI unit for electrical current. Yamahata et al . now demonstrate a silicon-based transistor that can accurately emit lone electrons at a rate of over 3 billion per second.

ATP2B1 is a gene associated with hypertension. We reported previously that mice lacking ATP2B1 in vascular smooth muscle cells (VSMC ATP2B1 KO mice) exhibited high blood pressure and increased intracellular calcium concentration. The present study was designed to investigate whether lack of the ATP2B1 gene causes a higher response to calcium channel blockers (CCBs) than to other types of anti-hypertensive drugs. Both VSMC ATP2B1 KO and control mice were administered anti-hypertensive drugs while monitoring blood pressure shifts. We also examined the association of nitric oxide synthase (NOS) activity in those mice to investigate whether another mechanism of hypertension existed. VSMC ATP2B1 KO mice exhibited significantly greater anti-hypertensive effects with a single injection of nicardipine, but the effects of an angiotensin II receptor blocker (ARB), an α-blocker and amlodipine on blood pressure were all similar to control mice. However, long-term treatment with amlodipine, but not an ARB, significantly decreased the blood pressure of KO mice compared with control mice. Both mRNA and protein expression levels of the L-type calcium channel were significantly upregulated in KO VSMCs. There were no alterations in neural NOS protein expression of VSMCs or in urinary NO production between the two groups. VSMC ATP2B1 KO mice had a higher response to CCBs for blood pressure-lowering effects than other anti-hypertensive drugs. These results mean that increased intracellular calcium concentration in VSMCs due to lack of ATP2B1 and subsequent activation of L-type calcium channels mainly affects blood pressure and suggests increased susceptibility to CCBs in this type of hypertension.

The ATP2B1 gene is associated with hypertension. We previously reported that systemic heterozygous ATP2B1-null (ATP2B1 ) mice exhibited hypertension due to impaired endothelial nitric oxide synthase (eNOS) activity and decreased nitric oxide (NO) production. The ATP2B1 gene encodes plasma membrane calcium ATPase 1 (PMCA1), which has been thought to regulate only intracellular Ca concentration. However, recently, it has been suggested that ATP2B1 works not only at cellular levels, but also throughout the entire body, including in the calcium metabolism, using small intestine-specific ATP2B1 knockout mice. To clarify the roles of ATP2B1 in the entire body and the effects of ATP2B1 on blood pressure, we examined the alterations of calcium related factors in ATP2B1 mice. ATP2B1 mice exhibited hypocalcemia. The expression of ATP2B1 in the kidney and small intestine decreased, and hypercalciuria was confirmed in ATP2B1 mice. The intact-PTH levels were lower, and bone mineral density was increased in these mice. These results suggest that hypocalcemia is mainly a result of inhibited bone resorption without compensation by PTH secretion in the case of ATP2B1 knockout. Moreover, NO production may be affected by reduced PTH secretion, which may cause the increase in vascular contractility in these mice. The ATP2B1 gene is important for not only intra-cellular calcium regulation but also for calcium homeostasis and blood pressure control.

In the original publication of this article (Iwasaki et al. 2019), the author name ‘Matsubara Makoto’ in author list is not correct. The correct name should be ‘Makoto Matsubara’.