The Role of Gender Dynamics in the Relationship between Parental Maltreatment and Juvenile Theft in South Korea

Juvenile theft is the leading crime among adolescents in Korea and is a serious social concern. The present study is an examination of youth theft in the framework of general strain theory, which asserts that criminal behavior occurs as a response to various strains, such as parental abuse and neglect. To test the role of parent-youth gender dynamics in the relationship between parental strain and youth theft, the current study analyzed a community-based sample of youth offenders and non-offenders in Korea (N = 374) using multivariate logistic regression models with interaction terms. Paternal physical abuse and maternal neglect predicted greater youth involvement in theft behavior. Regarding parent-youth gender dynamics, there was no difference in the role of maternal or paternal maltreatment in predicting theft behavior in sons or daughters. The exception was fathers' neglect, in which daughters showed higher odds of theft engagement than did sons who experienced even greater paternal neglect. The findings underscored the distinct and detrimental role of parental maltreatment in adolescent theft. The results supported the need to reach out to parents in consideration of the youth's gender and provided important implications for guiding current social services in preventing juvenile theft in Korea

Round-Trip System Available to Measure Path Length Variation in Korea VLBI System for Geodesy

The construction project of Korea Geodetic VLBI officially started in October 2008. The construction of all systems will be completed by the end of 2011. The project was named Korea VLBI system for Geodesy (KVG), and its main purpose is to maintain the Korea Geodetic Datum. In case of the KVG system, an observation room with an H-maser frequency standard is located in a building separated from the antenna by several tens of meters. Therefore KVG system will adopt a so-called round-trip system to transmit reference signals to the antenna with reduction of the effect of path length variations. KVG s round-trip system is designed not only to use either metal or optical fiber cables, but also to measure path length variations directly. We present this unique round trip system for KVG

Myopericarditis in a Korean Young Male With Systemic Lupus Erythematosus

Myocardial involvement with clinical symptoms is a rare manifestation of systemic lupus erythematosus (SLE), despite the relatively high prevalence of myocarditis at autopsies of SLE patients. In this review, we report the case of a 19-year-old male SLE patient who initially presented with myopericarditis and was successfully treated with high dose of glucocorticoids

Regorafenib Regulates AD Pathology, Neuroinflammation, and Dendritic Spinogenesis in Cells and a Mouse Model of AD

The oral multi-target kinase inhibitor regorafenib, which targets the oncogenic receptor tyrosine kinase (RTK), is an effective therapeutic for patients with advanced gastrointestinal stromal tumors or metastatic colorectal cancer. However, whether regorafenib treatment has beneficial effects on neuroinflammation and Alzheimer's disease (AD) pathology has not been carefully addressed. Here, we report the regulatory function of regorafenib in neuroinflammatory responses and AD-related pathology in vitro and in vivo. Regorafenib affected AKT signaling to attenuate lipopolysaccharide (LPS)-mediated expression of proinflammatory cytokines in BV2 microglial cells and primary cultured microglia and astrocytes. In addition, regorafenib suppressed LPS-induced neuroinflammatory responses in LPS-injected wild-type mice. In 5x FAD mice (a mouse model of AD), regorafenib ameliorated AD pathology, as evidenced by increased dendritic spine density and decreased Aβ plaque levels, by modulating APP processing and APP processing-associated proteins. Furthermore, regorafenib-injected 5x FAD mice displayed significantly reduced tau phosphorylation at T212 and S214 (AT100) due to the downregulation of glycogen synthase kinase-3 beta (GSK3β) activity. Taken together, our results indicate that regorafenib has beneficial effects on neuroinflammation, AD pathology, and dendritic spine formation in vitro and in vivo.1

The MAO Inhibitor Tranylcypromine Alters LPS- and A beta-Mediated Neuroinflammatory Responses in Wild-type Mice and a Mouse Model of AD

Monoamine oxidase (MAO) has been implicated in neuroinflammation, and therapies targeting MAO are of interest for neurodegenerative diseases. The small-molecule drug tranylcypromine, an inhibitor of MAO, is currently used as an antidepressant and in the treatment of cancer. However, whether tranylcypromine can regulate LPS- and/or Aβ-induced neuroinflammation in the brain has not been well-studied. In the present study, we found that tranylcypromine selectively altered LPS-induced proinflammatory cytokine levels in BV2 microglial cells but not primary astrocytes. In addition, tranylcypromine modulated LPS-mediated TLR4/ERK/STAT3 signaling to alter neuroinflammatory responses in BV2 microglial cells. Importantly, tranylcypromine significantly reduced microglial activation as well as proinflammatory cytokine levels in LPS-injected wild-type mice. Moreover, injection of tranylcypromine in 5xFAD mice (a mouse model of AD) significantly decreased microglial activation but had smaller effects on astrocyte activation. Taken together, our results suggest that tranylcypromine can suppress LPS- and Aβ-induced neuroinflammatory responses in vitro and in vivo.1

Dasatinib regulates LPS-induced microglial and astrocytic neuroinflammatory responses by inhibiting AKT/STAT3 signaling

Background: The FDA-approved small-molecule drug dasatinib is currently used as a treatment for chronic myeloid leukemia (CML). However, the effects of dasatinib on microglial and/or astrocytic neuroinflammatory responses and its mechanism of action have not been studied in detail. Methods: BV2 microglial cells, primary astrocytes, or primary microglial cells were treated with dasatinib (100 or 250 nM) or vehicle (1% DMSO) for 30 min or 2 h followed by lipopolysaccharide (LPS; 200 ng/ml or 1 μg/ml) or PBS for 5.5 h. RT-PCR, real-time PCR; immunocytochemistry; subcellular fractionation; and immunohistochemistry were subsequently conducted to determine the effects of dasatinib on LPS-induced neuroinflammation. In addition, wild-type mice were injected with dasatinib (20 mg/kg, intraperitoneally (i.p.) daily for 4 days or 20 mg/kg, orally administered (p.o.) daily for 4 days or 2 weeks) or vehicle (4% DMSO + 30% polyethylene glycol (PEG) + 5% Tween 80), followed by injection with LPS (10 mg/kg, i.p.) or PBS. Then, immunohistochemistry was performed, and plasma IL-6, IL-1β, and TNF-α levels were analyzed by ELISA. Results: Dasatinib regulates LPS-induced proinflammatory cytokine and anti-inflammatory cytokine levels in BV2 microglial cells, primary microglial cells, and primary astrocytes. In BV2 microglial cells, dasatinib regulates LPS-induced proinflammatory cytokine levels by regulating TLR4/AKT and/or TLR4/ERK signaling. In addition, intraperitoneal injection and oral administration of dasatinib suppress LPS-induced microglial/astrocyte activation, proinflammatory cytokine levels (including brain and plasma levels), and neutrophil rolling in the brains of wild-type mice. Conclusions: Our results suggest that dasatinib modulates LPS-induced microglial and astrocytic activation, proinflammatory cytokine levels, and neutrophil rolling in the brain. © 2019 The Author(s).1

Contribution of Dietary Intakes of Antioxidants to Homocysteine-Induced Low Density Lipoprotein (LDL) Oxidation in Atherosclerotic Patients

PURPOSE: Elevated circulating oxidized low density lipoprotein (Ox-LDL) levels are associated with increased risk of atherosclerosis, which may be due to high plasma homocysteine (Hcy) and low intakes of antioxidants. We investigated the contribution of dietary intakes of antioxidants to Hcy-induced LDL oxidation in atherosclerotic patients (AP) and controls. MATERIALS AND METHODS: Male AP (n = 101) who were confirmed by coronary angiography and 91 controls were evaluated by blood biochemistry and dietary intakes. To determine whether homocysteine is an independent risk factor for atherosclerosis, subjects were divided into three groups; low- (or= 12.1 uM/L) Hcy. RESULTS: Plasma levels of homocysteine and LDL were higher, but plasma apo A-I in HDL and folate were lower in the AP group. The odds ratio (OR) for the risk of atherosclerosis was 3.002 [95% confidence interval (CI), 1.27-7.09] for patients in the highest tertile with homocysteine >or= 12.1 uM/L. AP having high homocysteine levels had low intakes of vitamin A, beta-carotene and vitamin C. By logistic regression analysis, age, body mass index (BMI), plasma LDL, plasma folate, and low intakes of vitamin A and beta-carotene were found to be risk factors for atherosclerosis in patients with high-Hcy, but dietary B vitamins including folate were not. CONCLUSION: A high-Hcy level was a risk factor for atherosclerosis in patients with high Ox-LDL levels. High intakes of antioxidants appeared to be a protective factor for atherosclerosis, perhaps exerting a pro-oxidative effect on LDL when combined with high levels of Hcy and LDL. However, more evidence for the benefits of B vitamins as a homocysteine-lowering therapy is neededope

Autophagy deficiency leads to protection from obesity and insulin resistance by inducing Fgf21 as a mitokine

Despite growing interest and a recent surge in papers, the role of autophagy in glucose and lipid metabolism is unclear. We produced mice with skeletal muscle–specific deletion of Atg7 (encoding autophagy-related 7). Unexpectedly, these mice showed decreased fat mass and were protected from diet-induced obesity and insulin resistance; this phenotype was accompanied by increased fatty acid oxidation and browning of white adipose tissue (WAT) owing to induction of fibroblast growth factor 21 (Fgf21). Mitochondrial dysfunction induced by autophagy deficiency increased Fgf21 expression through induction of Atf4, a master regulator of the integrated stress response. Mitochondrial respiratory chain inhibitors also induced Fgf21 in an Atf4-dependent manner. We also observed induction of Fgf21, resistance to diet-induced obesity and amelioration of insulin resistance in mice with autophagy deficiency in the liver, another insulin target tissue. These findings suggest that autophagy deficiency and subsequent mitochondrial dysfunction promote Fgf21 expression, a hormone we consequently term a 'mitokine', and together these processes promote protection from diet-induced obesity and insulin resistance

GSK3B induces autophagy by phosphorylating ULK1

Unc-51-like autophagy activating kinase 1 (ULK1), a mammalian homolog of the yeast kinase Atg1, has an essential role in autophagy induction. In nutrient and growth factor signaling, ULK1 activity is regulated by various posttranslational modifications, including phosphorylation, acetylation, and ubiquitination. We previously identified glycogen synthase kinase 3 beta (GSK3B) as an upstream regulator of insulin withdrawal-induced autophagy in adult hippocampal neural stem cells. Here, we report that following insulin withdrawal, GSK3B directly interacted with and activated ULK1 via phosphorylation of S405 and S415 within the GABARAP-interacting region. Phosphorylation of these residues facilitated the interaction of ULK1 with MAP1LC3B and GABARAPL1, while phosphorylation-defective mutants of ULK1 failed to do so and could not induce autophagy flux. Furthermore, high phosphorylation levels of ULK1 at S405 and S415 were observed in human pancreatic cancer cell lines, all of which are known to exhibit high levels of autophagy. Our results reveal the importance of GSK3B-mediated phosphorylation for ULK1 regulation and autophagy induction and potentially for tumorigenesis. © 2021, The Author(s).1