Nonalcoholic fatty liver disease (NAFLD) is related to risk factors of coronary artery disease, such as dyslipidemia, diabetes, and metabolic syndrome, which are closely linked with visceral adiposity. The aim of this study was to investigate whether NAFLD was associated with coronary artery calcification (CAC), which is used as a surrogate marker for coronary atherosclerosis independent of computed tomography (CT)-measured visceral adiposity. Out of 5,648 subjects who visited one of health screening centers between 2003 and 2008, we enrolled 4,023 (mean age 56.9 ± 9.4 years, 60.7% males) subjects without known liver disease or a history of ischemic heart disease. CAC score was evaluated by the Agatston method. In univariate analyses, the presence of CAC (score >0) was significantly associated with age, sex, body mass index, aspartate aminotransferase, alanine aminotransferase, high-density lipoprotein cholesterol, triglycerides and increased odds of diabetes, hypertension, smoking, and NAFLD. Increasing CAC scores (0, <10, 10-100, ≥100) were associated with higher prevalence of NAFLD (OR 1.84, 95% CI 1.61-2.10, P<0.001). Multivariate ordinal regression analysis adjusted for traditional risk factors, and CT-measured visceral adipose tissue area in a subgroup of subjects showed that the increased CAC scores were significantly associated with the presence of NAFLD (OR 1.28, 95% CI 1.04-1.59, P=0.023) independent of visceral adiposity. CONCLUSIONS Patients with NAFLD are at increased risk for coronary atherosclerosis independent of classical coronary risk factors, including visceral adiposity. These data suggest that NAFLD per se might be an independent risk factor for coronary artery disease.

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Wireless-power-transfer-system (WPTS) based wireless electric vehicles (WEVs), classified into roadway powered electric vehicles (RPEVs) and stationary charging electric vehicles (SCEVs), are in the spotlight as future mainstream transportations. RPEVs are free from serious battery problems such as large, heavy, and expensive battery packs and long charging time because they get power directly from the road while moving. The power transfer capacity, efficiency, lateral tolerance, EMF, air-gap, size, weight, and cost of the WPTSs have been improved by virtues of innovative semiconductor switches, better coil designs, roadway construction techniques, and higher operating frequency. Recent advances in WPTSs for RPEVs are summarized in this review paper. The fifth-(5G) and sixth-generation (6G) on-line electric vehicles (OLEVs), which reduce infrastructure cost for commercialization, and the interoperability between RPEVs and SCEVs are addressed in detail in this paper. Major milestones of the developments of other RPEVs are also summarized. The rest of this paper deals with a few important technical issues such as coil structures, power supply schemes, and segmentation switching techniques of a lumped inductive power transfer system (IPTS) for RPEVs. Index Terms-Wireless electric vehicle (WEV), roadway powered electric vehicle (RPEV)Manuscript

Social deficits are observed in diverse psychiatric disorders, including autism spectrum disorders and schizophrenia. We found that mice lacking the excitatory synaptic signaling scaffold IRSp53 (also known as BAIAP2) showed impaired social interaction and communication. Treatment of IRSp53(-/-) mice, which display enhanced NMDA receptor (NMDAR) function in the hippocampus, with memantine, an NMDAR antagonist, or MPEP, a metabotropic glutamate receptor 5 antagonist that indirectly inhibits NMDAR function, normalized social interaction. This social rescue was accompanied by normalization of NMDAR function and plasticity in the hippocampus and neuronal firing in the medial prefrontal cortex. These results, together with the reduced NMDAR function implicated in social impairments, suggest that deviation of NMDAR function in either direction leads to social deficits and that correcting the deviation has beneficial effects.

Autism spectrum disorders (ASDs) are four times more common in males than in females, but the underlying mechanisms are poorly understood. We characterized sexually dimorphic changes in mice carrying a heterozygous mutation in Chd8 (Chd8) that was first identified in human CHD8 (Asn2373LysfsX2), a strong ASD-risk gene that encodes a chromatin remodeler. Notably, although male mutant mice displayed a range of abnormal behaviors during pup, juvenile, and adult stages, including enhanced mother-seeking ultrasonic vocalization, enhanced attachment to reunited mothers, and isolation-induced self-grooming, their female counterparts do not. This behavioral divergence was associated with sexually dimorphic changes in neuronal activity, synaptic transmission, and transcriptomic profiles. Specifically, female mice displayed suppressed baseline neuronal excitation, enhanced inhibitory synaptic transmission and neuronal firing, and increased expression of genes associated with extracellular vesicles and the extracellular matrix. Our results suggest that a human CHD8 mutation leads to sexually dimorphic changes ranging from transcription to behavior in mice.