As practical interest in flexible/or wearable power-conversion devices increases, the demand for high-performance alternatives to thermoelectric (TE) generators based on brittle inorganic materials is growing. Herein, we propose a flexible and ultralight TE generator (TEG) based on carbon nanotube yarn (CNTY) with excellent TE performance. The as-prepared CNTY shows a superior electrical conductivity of 3147 S/cm due to increased longitudinal carrier mobility derived from a highly aligned structure. Our TEG is innovative in that the CNTY acts as multifunctions in the same device. The CNTY is alternatively doped into n- and p-types using polyethylenimine and FeCl, respectively. The highly conductive CNTY between the doped regions is used as electrodes to minimize the circuit resistance, thereby forming an all-carbon TEG without additional metal deposition. A flexible TEG based on 60 pairs of n- and p-doped CNTY shows the maximum power density of 10.85 and 697 μW/g at temperature differences of 5 and 40 K, respectively, which are the highest values among reported TEGs based on flexible materials. We believe that the strategy proposed here to improve the power density of flexible TEG by introducing highly aligned CNTY and designing a device without metal electrodes shows great potential for the flexible/or wearable power-conversion devices.

In Noonan Syndrome (NS) 30% to 50% of subjects show cognitive deficits of unknown etiology and with no known treatment. Here, we report that knock-in mice expressing either of two NS-associated Ptpn11 mutations show hippocampal-dependent spatial learning impairments and deficits in hippocampal long-term potentiation (LTP). In addition, viral overexpression of the PTPN11D61G in adult hippocampus results in increased baseline excitatory synaptic function, deficits in LTP and spatial learning, which can all be reversed by a MEK inhibitor. Furthermore, brief treatment with lovastatin reduces Ras-Erk activation in the brain, and normalizes the LTP and learning deficits in adult Ptpn11D61G/+ mice. Our results demonstrate that increased basal Erk activity and corresponding baseline increases in excitatory synaptic function are responsible for the LTP impairments and, consequently, the learning deficits in mouse models of NS. These data also suggest that lovastatin or MEK inhibitors may be useful for treating the cognitive deficits in NS.

The metabolic syndrome is common in an urban Korean population when using Asian-Pacific waist criteria. The prevalence of the metabolic syndrome increased with increasing tertiles of insulin resistance.

OBJECTIVE -To investigate whether the peripheral blood mtDNA (pb-mtDNA) content is decreased and linked to insulin resistance in the offspring of type 2 diabetic patients.RESEARCH DESIGN AND METHODS -A total of 82 offspring of type 2 diabetic patients and 52 age-, sex-, and BMI-matched normal subjects from the Mokdong, Korea, population were selected for this study by stratified, randomized sampling. Of the offspring of diabetic patients, 52 had normal glucose tolerance (NGT), 21 had impaired glucose tolerance (IGT), and 9 had newly diagnosed type 2 diabetes. The pb-mtDNA content was measured by real-time polymerase chain reaction with a mitochondria-specific fluorescent probe, normalized by a nuclear DNA, 28S rRNA gene. The associations between pb-mtDNA content and several parameters of insulin resistance were studied.RESULTS -The pb-mtDNA contents tended to be lower in the 82 offspring of type 2 diabetic patients (1,084.7 Ϯ 62.6 vs. 1,304.0 Ϯ 99.2 in the offspring and control subjects, respectively, P ϭ 0.051) and was significantly lower in the combined NGT and IGT offspring group (NGTϩIGT, 1,068.0 Ϯ 67.8, P Ͻ 0.05) than in the control subjects. In NGTϩIGT offspring, the pb-mtDNA content was significantly correlated with logarithmically transformed insulin sensitivity (r ϭ 0.253, P Ͻ 0.05) and was the main predictor of insulin sensitivity.CONCLUSIONS -Quantitative mtDNA status might be a hereditary factor associated with type 2 diabetes and could serve as an indicator for insulin sensitivity. Diabetes Care 24:865-869, 2001T he mitochondria are the major site of intracellular respiration and energy metabolism, and their function is intimately related to insulin secretion and possibly insulin action (1,2). Moreover, the mitochondria contain their own genome, with mtDNA coding for some proteins of the respiratory chain. The mutation of mtDNA was believed to cause ϳ0.5-1% of diabetes (3,4). The content of mtDNA is vital for maintaining the mitochondrial function and the energy demands of the body, but little attention has been paid to the quantitative aspects of mtDNA in diabetes. Several animal and human studies have described variations in mtDNA content. Decreased mtDNA content was found in the pancreatic islets of diabetes-prone Goto-Kakizaki rats (5) and in mitochondrial transcriptional factor A (Tfam)-defective mice (4). Decreased mtDNA content was also found in the skeletal muscle of type 1 and type 2 diabetic patients (6). Although the changes resulting from diabetes might influence the mtDNA content, decreases in peripheral blood mtDNA (pb-mtDNA) were observed before the onset of diabetes (7). Peripheral blood could provide an alternative sample type to skeletal muscle in the diagnosis of mitochondrial pathology because the data on the mitochondrial state in skeletal muscles and peripheral blood lymphocytes were comparable (8). Decreased pb-mtDNA was found to be related to insulin resistance or the development of type 2 diabetes (7).Although maximum oxygen consumption (VO 2max ) was positively related to m...

Objective: Visceral fat accumulation is more strongly related to insulin resistance than to excess total adiposity. The visceral adiposity index (VAI) has recently been suggested as an indicator of the visceral adiposity measured by magnetic resonance imaging. To evaluate whether the VAI could replace visceral computed tomography (CT) scanning and predict insulin resistance in young women with polycystic ovary syndrome (PCOS) was presented. Design and Methods: One hundred and eighty Korean women aged 16-41 years who were diagnosed with PCOS using the Rotterdam criteria were included. The VAI was derived from a formula using body mass index, waist circumference, triglycerides, and high-density lipoprotein cholesterol. Visceral adiposity was defined as a visceral fat area (VFA) measuring > 100 cm 2 by CT scanning. Insulin sensitivity was evaluated by insulinmediated glucose utilization (M value), which was obtained using a euglycemic hyperinsulinemic clamp. Results:The VAI positively correlated with VFA, the visceral-to-subcutaneous fat ratio, and systolic and diastolic blood pressure, and negatively correlated with the M value. In a linear regression analysis, the VAI was an independent determinant of the insulin sensitivity after controlling for age, systolic blood pressure, fasting glucose, fasting insulin, and testosterone levels. In a logistic regression analysis, the VAI odds ratio was 3.5 (95% CI 1.2-9.8) for predicting visceral adiposity after controlling for the various metabolic parameters and testosterone. Conclusion: The VAI can replace visceral CT scanning as a marker for visceral adiposity, and it predicts insulin resistance in young women with PCOS.

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This work was supported in part by the grant from the Korea Centers for Disease Control and Prevention (2009-E00591-00). The work was also supported by the Ewha Global Top5 Grant 2013 of Ewha Womans University. None of the authors has any conflict of interest to declare.

Granular corneal dystrophy type 2 (GCD2) is an autosomal dominant disease characterized by a progressive age-dependent extracellular accumulation of transforming growth factor β-induced protein (TGFBI). Corneal fibroblasts from GCD2 patients also have progressive degenerative features, but the mechanism underlying this degeneration remains unknown. Here we observed that TGFBI was degraded by autophagy, but not by the ubiquitin/proteasome-dependent pathway. We also found that GCD2 homozygous corneal fibroblasts displayed a greater number of fragmented mitochondria. Most notably, mutant TGFBI (mut-TGFBI) extensively colocalized with microtubule-associated protein 1 light chain 3β (MAP1LC3B, hereafter referred to as LC3)-enriched cytosolic vesicles and CTSD in primary cultured GCD2 corneal fibroblasts. Levels of LC3-II, a marker of autophagy activation, were significantly increased in GCD2 corneal fibroblasts. Nevertheless, levels of SQSTM1/p62 and of polyubiquitinated protein were also significantly increased in GCD2 corneal fibroblasts compared with wild-type (WT) cells. However, LC3-II levels did not differ significantly between WT and GCD2 cells, as assessed by the presence of bafilomycin A 1, the fusion blocker of autophagosomes and lysosomes. Likewise, bafilomycin A 1 caused a similar change in levels of SQSTM1. Thus, the increase in autophagosomes containing mut-TGFBI may be due to inefficient fusion between autophagosomes and lysosomes. Rapamycin, an autophagy activator, decreased mut-TGFBI, whereas inhibition of autophagy increased active caspase-3, poly (ADP-ribose) polymerase 1 (PARP1) and reduced the viability of GCD2 corneal fibroblasts compared with WT controls. These data suggest that defective autophagy may play a critical role in the pathogenesis of GCD2.