Low-Power Complementary Inverter Based on Graphene/Carbon-Nanotube and Graphene/MoS₂ Barristors

The recent report of a p-type graphene(Gr)/carbon-nanotube(CNT) barristor facilitates the application of graphene barristors in the fabrication of complementary logic devices. Here, a complementary inverter is presented that combines a p-type Gr/CNT barristor with a n-type Gr/MoS2 barristor, and its characteristics are reported. A sub-nW (~0.2 nW) low-power inverter is demonstrated with a moderate gain of 2.5 at an equivalent oxide thickness (EOT) of ~15 nm. Compared to inverters based on field-effect transistors, the sub-nW power consumption was achieved at a much larger EOT, which was attributed to the excellent switching characteristics of Gr barristors

Cytoprotective effects of fermented oyster extracts against oxidative stress-induced DNA damage and apoptosis through activation of the Nrf2/HO-1 signaling pathway in MC3T3-E1 osteoblasts

Osteoblast damage by oxidative stress has been recognized as a cause of bone-related disease, including osteoporosis. Recently, we reported that fermented Pacific oyster (Crassostrea gigas) extracts (FO) inhibited osteoclastogenesis and osteoporosis, while promoting osteogenesis. However, since the beneficial potential of FO on osteoblasts is not well known, in the present study, we investigated the cytoprotective effect of FO against oxidative stress in MC3T3-E1 osteoblasts. Our results demonstrated that FO inhibited hydrogen peroxide (H2O2)-induced DNA damage and cytotoxicity through the rescue of mitochondrial function by blocking abnormal ROS accumulation. FO also prevented apoptosis by suppressing loss of mitochondrial membrane potential and cytosolic release of cytochrome c, decreasing the rate of Bax/Bcl-2 expression and reducing the activity of caspase-9 and caspase-3 in H2O2-stimulated MC3T3-E1 osteoblasts, suggesting that FO protected MC3T3-E1 osteoblasts from the induction of caspase dependent- and mitochondria-mediated apoptosis by oxidative stress. In addition, FO markedly promoted the activation of nuclear factor-erythroid-2-related factor 2 (Nrf2), which was associated with the enhanced expression of heme oxygenase-1 (HO-1). However, inhibiting the expression of HO-1 by artificially blocking the expression of Nrf2 using siRNA significantly eliminated the protective effect of FO, indicating that FO activates the Nrf2/HO-1 signaling pathway in MC3T3-E1 osteoblasts to protect against oxidative stress. Based on the present data, FO is thought to be useful as a potential therapeutic agent for the inhibition of oxidative stress in osteoblasts

Critical thickness for the two-dimensional electron gas in LaTiO3/SrTiO3 superlattices

Transport dimensionality of Ti d electrons in (LaTiO3)(1)/(SrTiO3)(N) superlattices has been investigated using density functional theory with local spin-density approximation + U method. Different spatial distribution patterns have been found between Ti t(2g) orbital electrons. The d(xy) orbital electrons are highly localized near interfaces due to the potentials by positively charged LaO layers, while the degenerate d(yz) and d(xz) orbital electrons are more distributed inside SrTiO3 insulators. For N >= 3 unit cells (u.c.), the Ti d(xy) densities of state exhibit the staircaselike increments, which appear at the same energy levels as the d(xy) flat bands along the Gamma-Z direction in band structures. The k(z)-independent discrete energy levels indicate that the electrons in d(xy) flat bands are two-dimensional electron gases (2DEGs) which can transport along interfaces, but they cannot transport perpendicularly to interfaces due to the confinements in the potential wells by LaO layers. Unlike the d(xy) orbital electrons, the d(yz) and d(xz) orbital electrons have three-dimensional (3D) transport characteristics, regardless of SrTiO3 thicknesses. The 2DEG formation by d(xy) orbital electrons, when N >= 3 u.c., indicates the existence of critical SrTiO3 thickness where the electron transport dimensionality starts to change from 3D to 2D in (LaTiO3)(1)/(SrTiO3)(N) superlatticesclose

Autoimmune Hypoglycemia in a Patient with Characterization of Insulin Receptor Autoantibodies

BackgroundType B insulin resistance syndrome is a manifestation of autoantibodies to the insulin receptor that results in severe hyperglycemia and acanthosis nigricans. However, the mechanisms by which these autoantibodies induce hypoglycemia are largely unknown. In this paper, we report the case of patient with type B insulin resistance syndrome who presented with frequent severe fasting hypoglycemia and acanthosis nigricans.MethodsTo evaluate the mechanism of hypoglycemia, we measured the inhibition of insulin binding to erythrocytes and IM9 lymphocytes in a sample of the patient's dialyzed serum before and after immunosuppressive therapy.ResultsIn the patient's pre-treatment serum IgG, the binding of 125I-insulin to erythrocytes was markedly inhibited in a dose-dependent manner until the cold insulin level reached 10-9 mol/L. We also observed dose-dependent inhibition of insulin binding to IM9 lymphocytes, which reached approximately 82% inhibition and persisted even when diluted 1:20. After treatment with glucocorticoids, insulin-erythrocyte binding activity returned to between 70% and 80% of normal, while the inhibition of insulin-lymphocyte binding was reduced by 17%.ConclusionWe treated a patient with type B insulin resistance syndrome showing recurrent fasting hypoglycemia with steroids and azathioprine. We characterized the patient's insulin receptor antibodies by measuring the inhibition of insulin binding

Warfarin-Induced Eosinophilic Pleural Effusion

A 29-year-old man suffering from dyspnea and eosinophilic pleural effusion after being on warfarin for pulmonary thromboembolism for a period of one month, was readmitted to our hospital. Etiology of pleural effusion other than warfarin was excluded. To the best of our knowledge, this is the first case of warfarin-induced pleural effusion reported in Korea

Easy Diagnosis of Asthma: Computer-Assisted, Symptom-Based Diagnosis

Diagnosis of asthma is often challenging in primary-care physicians due to lack of tools measuring airway obstruction and variability. Symptom-based diagnosis of asthma utilizing objective diagnostic parameters and appropriate software would be useful in clinical practice. A total of 302 adult patients with respiratory symptoms responded to a questionnaire regarding asthma symptoms and provoking factors. Questions were asked and recorded by physicians into a computer program. A definite diagnosis of asthma was made based on a positive response to methacholine bronchial provocation or bronchodilator response (BDR) testing. Multivariate logistic regression analysis was used to evaluate the significance of questionnaire responses in terms of discriminating asthmatics. Asthmatic patients showed higher total symptom scores than non-asthmatics (mean 5.93 vs. 4.93; p<0.01). Multivariate logistic regression analysis identified that response to questions concerning the following significantly discriminated asthmatics; wheezing with dyspnea, which is aggravated at night, and by exercise, cold air, and upper respiratory infection. Moreover, the presence of these symptoms was found to agree significantly with definite diagnosis of asthma (by kappa statistics). Receiver-operating characteristic curve analysis revealed that the diagnostic accuracy of symptom-based diagnosis was high with an area under the curve of 0.647±0.033. Using a computer-assisted symptom-based diagnosis program, it is possible to increase the accuracy of diagnosing asthma in general practice, when the facilities required to evaluate airway hyperresponsiveness or BDR are unavailable

Vitamin D deficiency is associated with disease activity in patients with Crohn’s disease

Background/Aims Previous data suggest that vitamin D has a significant role in inflammatory bowel disease (IBD). We investigated the incidence of vitamin D deficiency in Korean patients with IBD and the correlation between serum vitamin D level and disease activity. Methods We retrospectively analyzed the medical records of patients with IBD whose serum vitamin D levels were checked. Deficiency of 25-hydroxyvitamin D was defined as <20 ng/mL. Disease activity was evaluated using the partial Mayo score for ulcerative colitis (≥2 defined as active disease) and Harvey-Bradshaw index for Crohn’s disease (≥4 defined as active disease). Results We enrolled 87 patients with IBD (ulcerative colitis [UC], 45; Crohn’s disease [CD], 42). Among them, 65.5% (57/87) were men, with a mean age of 44.9±15.1 years (range, 18–75 years). The mean duration of disease was 4.7±4.8 years (range, 0.1–17.1 years). Vitamin D deficiency was found in 73.6% (64/87) of patients with IBD. Patients with IBD (mean vitamin D level, 16.3±9.0 ng/mL) showed lower vitamin D level than the healthy control group (mean vitamin D level, 20.4±7.0 ng/mL), with no statistically significant difference (P=0.136). Disease activity was inversely correlated with vitamin D deficiency in patients with CD (P=0.007). However, no correlation was observed in patients with UC (P=0.134). Conclusions Approximately 75% of Korean patients with IBD showed vitamin D deficiency state. Vitamin D deficiency is associated with disease activity, particularly in patients with CD