Polarity engineering in polycrystalline ZnO by inversion boundaries

Two distinctive polarity-engineered microstructures were obtained in polycrystalline ZnO ceramics by inducing two different types of inversion boundaries (IBs) inside individual grains to examine the effect of the different polarities on the varistor performances. The presence of head-to-head IBs induced by the addition of Sb and tail-to-tail IBs by doping Ti was directly confirmed by the characteristic geometry of the chemical etch pits. It was proposed that a consequent polarity on the grain boundary planes, which are affected by the presence of head-to-head IBs is crucial in exhibiting the superior performance of ZnO varistors.open2

Observation of transverse spin Nernst magnetoresistance induced by thermal spin current in ferromagnet/non-magnet bilayers

Electric generation of spin current via spin Hall effect is of great interest as it allows an efficient manipulation of magnetization in spintronic devices. Theoretically, spin current can be also created by a temperature gradient, which is known as spin Nernst effect. Here, we report spin Nernst effect-induced transverse magnetoresistance in ferromagnet (FM)/non-magnetic heavy metal (HM) bilayers. We observe that the magnitude of transverse magnetoresistance (i.e., planar Nernst signal) in FM/HM bilayers is significantly modified by HM and its thickness. This strong dependence of transverse magnetoresistance on HM evidences the spin Nernst effect in HM; the generation of thermally-induced spin current in HM and its subsequent reflection at the FM/HM interface. Our analysis of transverse magnetoresistance shows that the spin Nernst angles of W and Pt have the opposite sign to their spin Hall angles. Moreover, our estimate implies that the magnitude of the spin Nernst angle would be comparable to that of the spin Hall angle, suggesting an efficient generation of spin current by the spin Nernst effect

Epidemiology of Complex Regional Pain Syndrome: A Retrospective Chart Review of 150 Korean Patients

Complex regional pain syndrome (CRPS) is a chronically painful and disabling disorder. However, no data are available even on the epidemiology of CRPS in Korea. This study was undertaken to retrospectively assess the epidemiologic characteristics of CRPS in 150 consecutive patients at a tertiary chronic pain center from March 2002 to February 2006. Information was obtained regarding patients' demographics, nature of injury, and treatment modalities. Seventy-one percent of patients had CRPS type I. The mean 11-point verbal numerical rating scale score at initial examinations and at the time of study were 8.0 and 5.7, respectively. Thirty-two percent of patients showed no change or increase in pain intensity during follow-up at our pain center. The mean duration of CRPS symptoms prior to our pain center evaluation and prior to the time of study were 27 months and 50 months, respectively. These patients had seen on average 5 different physicians before being referred to our center. This study shows that the majority of CRPS patients were referred to our center after more than 2 yr of symptoms. The clinical implication of such delayed transfer and strategies to avoid this problem are discussed

Homeobox gene Dlx-2 is implicated in metabolic stress-induced necrosis

<p>Abstract</p> <p>Background</p> <p>In contrast to tumor-suppressive apoptosis and autophagic cell death, necrosis promotes tumor progression by releasing the pro-inflammatory and tumor-promoting cytokine high mobility group box 1 (HMGB1), and its presence in tumor patients is associated with poor prognosis. Thus, necrosis has important clinical implications in tumor development; however, its molecular mechanism remains poorly understood.</p> <p>Results</p> <p>In the present study, we show that Distal-less 2 (Dlx-2), a homeobox gene of the Dlx family that is involved in embryonic development, is induced in cancer cell lines dependently of reactive oxygen species (ROS) in response to glucose deprivation (GD), one of the metabolic stresses occurring in solid tumors. Increased Dlx-2 expression was also detected in the inner regions, which experience metabolic stress, of human tumors and of a multicellular tumor spheroid, an <it>in vitro </it>model of solid tumors. Dlx-2 short hairpin RNA (shRNA) inhibited metabolic stress-induced increase in propidium iodide-positive cell population and HMGB1 and lactate dehydrogenase (LDH) release, indicating the important role(s) of Dlx-2 in metabolic stress-induced necrosis. Dlx-2 shRNA appeared to exert its anti-necrotic effects by preventing metabolic stress-induced increases in mitochondrial ROS, which are responsible for triggering necrosis.</p> <p>Conclusions</p> <p>These results suggest that Dlx-2 may be involved in tumor progression via the regulation of metabolic stress-induced necrosis.</p

Primary systemic anaplastic large cell lymphoma in a single Korean institution: Clinical characteristics and treatment outcome

Despite advances in the characterization of anaplastic large cell lymphoma (ALCL), little data is available on Asian patients. We report here upon single Korean institution's experience regarding the clinical characteristics and outcomes of ALCL. We performed a retrospective study of 32 adults with ALCL. Most of the patients received anthracycline-based chemotherapy. Ann Arbor stage III-IV, B symptoms, high-intermediate/high International Prognostic Index (IPI), and extranodal disease at diagnosis were present in 56%, 44%, 41%, and 63%, respectively. Compared with Western studies, the male/female ratio (4.3) was markedly higher and skin (9%) and bone involvement (9%) were less frequent. The staining results for anaplastic lymphoma kinase were positive in 6 (33%) of 18 cases available. The complete response (CR) rate was 62% (95% CI, 44-80%). With a median follow-up of 51.0 months, 5 yr overall survival was 40 +/- 11%. The 3 yr relapse-free survival for the 18 patients who achieved CR was 74 +/- 12%. Age, performance status, lactate dehydrogenase, extranodal disease sites number, and IPI were correlated with treatment response and survival. Our data suggest that Korean ALCL patients appear to have a higher male/female ratio, less frequent skin/bone involvement, and lower CR rate compared with those of Western studies.

Anti-stress effects of ginseng via down-regulation of tyrosine hydroxylase (TH) and dopamine β-hydroxylase (DBH) gene expression in immobilization-stressed rats and PC12 cells

Catecholamines are among the first molecules that displayed a kind of response to prolonged or repeated stress. It is well established that long-term stress leads to the induction of catecholamine biosynthetic enzymes such as tyrosine hydroxylase (TH) and dopamine β-hydroxylase (DBH) in adrenal medulla. The aim of the present study was to evaluate the effects of ginseng on TH and DBH mRNA expression. Repeated (2 h daily, 14 days) immobilization stress resulted in a significant increase of TH and DBH mRNA levels in rat adrenal medulla. However, ginseng treatment reversed the stress-induced increase of TH and DBH mRNA expression in the immobilization-stressed rats. Nicotine as a ligand of the nicotinic acetylcholine receptor (nAChR) in adrenal medulla stimulates catecholamine secretion and activates TH and DBH gene expression. Nicotine treatment increased mRNA levels of TH and DBH by 3.3- and 3.1-fold in PC12 cells. The ginseng total saponin exhibited a significant reversal in the nicotine-induced increase of TH and DBH mRNA expression, decreasing the mRNA levels of TH and DBH by 57.2% and 48.9%, respectively in PC12 cells. In conclusion, immobilization stress induced catecholamine biosynthetic enzymes gene expression, while ginseng appeared to restore homeostasis via suppression of TH and DBH gene expression. In part, the regulatory activity in the TH and DBH gene expression of ginseng may account for the anti-stress action produced by ginseng

Sleep experiences during different lifetime periods and in vivo Alzheimer pathologies

Background Very little is known for the direction or causality of the relationship between lifetime sleep experiences and in vivo Alzheimers disease (AD) pathologies. This study aimed to examine the relationship between sleep experiences during the young adulthood, midlife, and late-life periods and in vivo cerebral beta-amyloid (Aβ) deposition and AD signature regional neurodegeneration in cognitively normal (CN) old adults. Methods This study included 202 CN old adults who participated in the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimers Disease (KBASE) study. All participants underwent a comprehensive clinical assessment, [11C] Pittsburgh Compound B positron emission tomography (PET), [18F] Fluorodeoxyglucose-PET, and magnetic resonance imaging. The quality and duration of sleep were assessed for the following age periods: 20–30s, 40–50s, and the most recent month. All analyses were adjusted for age, gender, education, apolipoprotein E ε4 status, vascular risk score, Hamilton Depression Rating Scale score, and use of sleep medication. Results Bad sleep quality and short sleep duration during midlife were significantly associated with increased Aβ deposition and AD signature regional hypometabolism, respectively. Although current bad sleep quality appeared to be associated with increased Aβ accumulation, this association disappeared after controlling for the effects of midlife sleep quality. Neither the quality nor duration of sleep during young adulthood was related to Aβ burden or neurodegeneration. Conclusions Bad sleep quality during midlife increases pathological Aβ deposition in the brain, while short sleep duration during the same period accelerates regional hypometabolism.This study was supported by a grant from the Ministry of Science, ICT, and Future Planning, Republic of Korea (Grant No: NRF-2014M3C7A1046042) and a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (Grant No: HI18C0630). The funding source had no role in the design of the study; collection, analysis, and interpretation of the data; and writing of the manuscript

Genetic associations of in vivo pathology influence Alzheimers disease susceptibility

Introduction Although the heritability of sporadic Alzheimers disease (AD) is estimated to be 60–80%, addressing the genetic contribution to AD risk still remains elusive. More specifically, it remains unclear whether genetic variants are able to affect neurodegenerative brain features that can be addressed by in vivo imaging techniques. Methods Targeted sequencing analysis of the coding and UTR regions of 132 AD susceptibility genes was performed. Neuroimaging data using 11C-Pittsburgh Compound B positron emission tomography (PET), 18F-fluorodeoxyglucose PET, and MRI that are available from the KBASE (Korean Brain Aging Study for Early Diagnosis and Prediction of Alzheimers disease) cohort were acquired. A total of 557 participants consisted of 336 cognitively normal (CN) adults, 137 mild cognitive impairment (MCI), and 84 AD dementia (ADD) groups. Results We called 5391 high-quality single nucleotide variants (SNVs) on AD susceptibility genes and selected significant associations between variants and five in vivo AD pathologies: (1) amyloid β (Aβ) deposition, (2) AD-signature region cerebral glucose metabolism (AD-Cm), (3) posterior cingulate cortex (PCC) cerebral glucose metabolism (PCC-Cm), (4) AD-signature region cortical thickness (AD-Ct), and (5) hippocampal volume (Hv). The association analysis for common variants (allele frequency (AF) > 0.05) yielded several novel loci associated with Aβ deposition (PIWIL1-rs10848087), AD-Cm (NME8-rs2722372 and PSEN2-rs75733498), AD-Ct (PSEN1-rs7523) and, Hv (CASS4-rs3746625). Meanwhile, in a gene-based analysis for rare variants (AF < 0.05), cases carrying rare variants in LPL, FERMT2, NFAT5, DSG2, and ITPR1 displayed associations with the neuroimaging features. Exploratory voxel-based brain morphometry between the variant carriers and non-carriers was performed subsequently. Finally, we document a strong association of previously reported APOE variants with the in vivo AD pathologies and demonstrate that the variants exert a causal effect on AD susceptibility via neuroimaging features. Conclusions This study provides novel associations of genetic factors to Aβ accumulation and AD-related neurodegeneration to influence AD susceptibility.The study was supported by grants from the National Research Foundation of Korea (2014M3C7A1046049 and 2018M3C9A5064708 for Choi M and 2014M3C7A1046042 for Lee DY) and grants from the Ministry of Health and Welfare of Korea (HI18C0630 for Mook-Jung IH and Lee DY, and HI19C0149 for Lee DY)