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The basic and adaptive maximum power point tracking algorithms have been studied for distributed photovoltaic systems to maximize the energy production of a photovoltaic (PV) module. However, the basic maximum power point tracking algorithms using a fixed step size, such as perturb and observe and incremental conductance, suffer from a trade-off between tracking accuracy and tracking speed. Although the adaptive maximum power point tracking algorithms using a variable step size improve the maximum power point tracking efficiency and dynamic response of the basic algorithms, these algorithms still have the oscillations at the maximum power point, because the variable step size is sensitive to external factors. Therefore, this paper proposes an enhanced maximum power point tracking algorithm that can have fast dynamic response, low oscillations, and high maximum power point tracking efficiency. To achieve these advantages, the proposed maximum power point tracking algorithm uses two methods that can apply the optimal step size to each operating range. In the operating range near the maximum power point, a small fixed step size is used to minimize the oscillations at the maximum power point. In contrast, in the operating range far from the maximum power point, a variable step size proportional to the slope of the power-voltage curve of PV module is used to achieve fast tracking speed under dynamic weather conditions. As a result, the proposed algorithm can achieve higher maximum power point tracking efficiency, faster dynamic response, and lower oscillations than the basic and adaptive algorithms. The theoretical analysis and performance of the proposed algorithm were verified by experimental results. In addition, the comparative experimental results of the proposed algorithm with the other maximum power point tracking algorithms show the superiority of the proposed algorithm.

Macrophage inhibitory cytokine 1 (MIC-1), which is overproduced in various human cancers and associated with cachexia, acts on the hypothalamus to suppress appetite and reduce body weight. We investigated the mechanisms through which MIC-1 affects bile acid metabolism and gallstone formation, which are poorly understood. Over 6 weeks, male C57BL/6 mice fed either standard chow or a lithogenic diet were intraperitoneally injected with phosphate-buffered saline (PBS) or MIC-1 (200 μg/kg/week). Among lithogenic diet–fed mice, MIC-1 treatment resulted in increased gallstone formation compared with PBS treatment. Compared with PBS treatment, MIC-1 treatment decreased hepatic cholesterol and bile acid levels and reduced expression of HMG-CoA reductase (HMGCR), the master cholesterol metabolism regulator sterol regulatory element-binding protein 2, cholesterol 7α-hydroxylase (CYP7A1), mitochondrial sterol 27-hydroxylase, and oxysterol 7α-hydroxylase. Compared with PBS treatment, MIC-1 treatment had no effect on small heterodimer partner, farnesoid X receptor, or pregnane X receptor expression, and extracellular signal–related kinase and c-Jun N-terminal kinase phosphorylation decreased, suggesting that these factors do not contribute to the MIC-1–induced reduction in CYP7A1 expression. Compared with PBS treatment, MIC-1 treatment increased AMP-activated protein kinase (AMPK) phosphorylation. Treatment with the AMPK activator 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) reduced CYP7A1 and HMGCR expression, whereas the AMPK inhibitor Compound C reversed MIC-1-induced reductions in CYP7A1 and HMGCR expression. Furthermore, in MIC-1-treated mice, total biliary cholesterol levels increased together with increased ATP-binding cassette subfamily G (ABCG)5 and ABCG8 expression. Compared with PBS treatment, MIC-1 treatment did not affect expression of liver X receptors α and β, liver receptor homolog 1, hepatocyte nuclear factor 4α, or NR1I3 (also known as constitutive androstane receptor), which are upstream of ABCG5/8; however, MIC-1 treatment increased ABCG5/8 expression and promoter activities. Our study indicates that MIC-1 influences gallstone formation by increasing AMPK phosphorylation, reducing CYP7A1 and HMGCR expression, and increasing ABCG5 and ABCG8 expression.

The characteristics of the cell type(s) responsible for initiating protective gut immune responses are not fully defined. Akira and colleagues show that TLR5 + lamina propria dendritic cells trigger, in a retinoic-dependent way, the production of interleukin 17 and immunoglobulin A. The intestinal cell types responsible for defense against pathogenic organisms remain incompletely characterized. Here we identify a subset of CD11c hi CD11b hi lamina propria dendritic cells (LPDCs) that expressed Toll-like receptor 5 (TLR5) in the small intestine. When stimulated by the TLR5 ligand flagellin, TLR5 + LPDCs induced the differentiation of naive B cells into immunoglobulin A–producing plasma cells by a mechanism independent of gut-associated lymphoid tissue. In addition, by a mechanism dependent on TLR5 stimulation, these LPDCs promoted the differentiation of antigen-specific interleukin 17–producing T helper cells and type 1 T helper cells. Unlike spleen DCs, the LPDCs specifically produced retinoic acid, which, in a dose-dependent way, supported the generation and retention of immunoglobulin A–producing cells in the lamina propria and positively regulated the differentiation interleukin 17–producing T helper cells. Our findings demonstrate unique properties of LPDCs and the importance of TLR5 for adaptive immunity in the intestine.

Noise exposure can destroy the synaptic connections between hair cells and auditory nerve fibers without damaging the hair cells, and this synaptic loss could contribute to difficult hearing in noisy environments. In this study, we investigated whether delivering lithium chloride to the round-window can regenerate synaptic loss of cochlea after acoustic overexposure. Our rat animal model of noise-induced cochlear synaptopathy caused about 50% loss of synapses in the cochlear basal region without damaging hair cells. We locally delivered a single treatment of poloxamer 407 (vehicle) containing lithium chloride (either 1 mM or 2 mM) to the round-window niche 24 hours after noise exposure. Controls included animals exposed to noise who received only the vehicle. Auditory brainstem responses were measured 3 days, 1 week, and 2 weeks post-exposure treatment, and cochleas were harvested 1 week and 2 weeks post-exposure treatment for histological analysis. As documented by confocal microscopy of immunostained ribbon synapses, local delivery of 2 mM lithium chloride produced synaptic regeneration coupled with corresponding functional recovery, as seen in the suprathreshold amplitude of auditory brainstem response wave 1. Western blot analyses revealed that 2 mM lithium chloride suppressed N -methyl-D-aspartate (NMDA) receptor expression 7 days after noise-exposure. Thus, round-window delivery of lithium chloride using poloxamer 407 reduces cochlear synaptic loss after acoustic overexposure by inhibiting NMDA receptor activity in rat model.

Amyloid-β (Aβ) accumulation in the hippocampus is an essential event in the pathogenesis of Alzheimer’s disease. Insoluble Aβ is formed through the sequential proteolytic hydrolysis of the Aβ precursor protein, which is cleaved by proteolytic secretases. However, the pathophysiological mechanisms of Aβ accumulation remain elusive. Here, we report that rats fed high-phytate diets showed Aβ accumulation and increased apoptotic neuronal cell death in the hippocampus through the activation of the amyloidogenic pathway in the hippocampus. Immunoblotting and immunohistochemical analyses confirmed that the overexpression of BACE1 β-secretase, a critical enzyme for Aβ generation, exacerbated the hippocampal Aβ accumulation in rats fed high-phytate diets. Moreover, we identified that parathyroid hormone, a physiological hormone responding to the phytate-mediated dysregulation of calcium and phosphate homeostasis, plays an essential role in the transcriptional activation of the Aβ precursor protein and BACE1 through the vitamin D receptor and retinoid X receptor axis. Thus, our findings suggest that phytate-mediated dysregulation of calcium and phosphate is a substantial risk factor for elevated Aβ accumulation and apoptotic neuronal cell death in rats.

This paper presents a highly efficient three-port converter to integrate energy storage (ES) and wireless power transfer (WPT) systems. The proposed converter consists of a bidirectional DC-DC converter and an AC-DC converter with a resonant capacitor. By sharing an inductor and four switches in the bidirectional DC-DC converter, the bidirectional DC-DC converter operates as a DC-DC converter for ES systems and simultaneously as a DC-AC converter for WPT systems. Here, four switches are turned on under the zero voltage switching conditions. The AC-DC converter for WPT system achieves high voltage gain by using a resonance between the resonant capacitor and the leakage inductance of a receiving coil. A 100-W prototype was built and tested to verify the effectiveness of the converter; it had a maximum power-conversion efficiency of 95.9% for the battery load and of 93.8% for the wireless charging load.

Hearing and balance depend upon the precise morphogenesis and mechanosensory function of stereocilia, the specialized structures on the apical surface of sensory hair cells in the inner ear. Previous studies of Grxcr1 mutant mice indicated a critical role for this gene in control of stereocilia dimensions during development. In this study, we analyzed expression of the paralog Grxcr2 in the mouse and evaluated auditory and vestibular function of strains carrying targeted mutations of the gene. Peak expression of Grxcr2 occurs during early postnatal development of the inner ear and GRXCR2 is localized to stereocilia in both the cochlea and in vestibular organs. Homozygous Grxcr2 deletion mutants exhibit significant hearing loss by 3 weeks of age that is associated with developmental defects in stereocilia bundle orientation and organization. Despite these bundle defects, the mechanotransduction apparatus assembles in relatively normal fashion as determined by whole cell electrophysiological evaluation and FM1-43 uptake. Although Grxcr2 mutants do not exhibit overt vestibular dysfunction, evaluation of vestibular evoked potentials revealed subtle defects of the mutants in response to linear accelerations. In addition, reduced Grxcr2 expression in a hypomorphic mutant strain is associated with progressive hearing loss and bundle defects. The stereocilia localization of GRXCR2, together with the bundle pathologies observed in the mutants, indicate that GRXCR2 plays an intrinsic role in bundle orientation, organization, and sensory function in the inner ear during development and at maturity.

In this study, we propose a light-emitting diode (LED) driver for automotive headlamps operating at a 2 MHz switching frequency using gallium nitride (GaN) high-electron-mobility transistors (HEMTs). The LED driver satisfies automotive electromagnetic compatibility (EMC) requirements by operating outside the amplitude-modulated frequency range. The power loss of a GaN-based synchronous direct current (DC)–DC buck (GSB) converter was compared with that of a synchronous buck converter using metal-oxide-semiconductor field-effect transistors (MOSFETs) and an asynchronous buck converter using a MOSFET and an external diode using SPICE simulation tools. The GSB converter operating at the 2 MHz switching frequency was built using the optimal printed circuit board (PCB) layout design, ensuring stable operation, and tested. The maximum power conversion efficiency of the GSB converter was measured to be 91.9% and 88.5% at two separate experimental conditions. The maximum operating temperature of the GaN intelligent power module was 68.2 °C. These results show that the GSB converter, which was built using the optimized PCB layout, demonstrated the superior performance of GaN HEMTs.

Heart failure (HF) is a global health burden, and its management in the emergency department (ED) is important. This study aimed to evaluate the association between focused cardiac ultrasound (FoCUS) and early administration of diuretics in patients with acute HF admitted to the ED. This retrospective observational study was conducted at a tertiary academic hospital. Patients with acute HF patients who were admitted to the ED and receiving intravenous medication between January 2018 and December 2019 were enrolled. The main exposure was a FoCUS examination performed within 2 h of ED triage. The primary outcome was the time to furosemide administration. Of 1154 patients with acute HF, 787 were included in the study, with 116 of them having undergone FoCUS. The time to furosemide was significantly shorter in the FoCUS group (median time (q1–q3), 112 min; range, 65–163 min) compared to the non-FoCUS group (median time, 131 min; range, 71–229 min). In the multivariable logistic regression analysis adjusting for age, sex, chief complaint, mode of arrival, triage level, shock status, and desaturation at triage, early administration of furosemide within 2 h from triage was significantly higher in the FoCUS group (adjusted odds ratio, 1.63; 95% confidence intervals, 1.04–2.55) than in the non-FoCUS group. Early administration of intravenous furosemide was associated with FoCUS examination in patients with acute HF admitted to the ED. An early screening protocol could be useful for improving levels in clinical practice at EDs.