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Manganese does not alter the severe neurotoxicity of MPTP
Baek, S Y,Kim, Y H,Oh, S O,Lee, C-R,Yoo, C I,Lee, J H,Lee, H,Sim, C S,Park, J,Kim, J-W,Yoon, C S,Kim, Y Scientific & Medical Division,Macmillan Press 2007 Human & experimental toxicology Vol.26 No.3
<P>We utilized a mice model of Parkinsonism: (1) to evaluate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity; and (2) to evaluate whether manganese (Mn) exposure can affect MPTP-induced neurotoxicity. A 2 × 3 experimental design (MPTP ×± Mn) was as follows: SS, MPTP(-) × Mn(-); SLMn, MPTP(-) × low Mn(+); SHMn, MPTP(-) × high Mn(+); MpS, MPTP(+) × Mn(-); MpLMn, MPTP(+) × low Mn(+); MpHMn, MPTP(+) × high Mn(+). We administered MPTP (30 mg/kg per day) to male C57BL/6 mice intraperitoneally, once a day for 5 days. Subsequently, mice were treated with either 2 or 8 mg/kg of MnCl<SUB>2</SUB>.4H<SUB>2</SUB>O intraperitoneally, once a day for 3 weeks.</P><P>Blood and striatal Mn levels were elevated in the Mnexposed groups. The number of tyrosine hydroxylase (TH)-immunoreactive (ir) neurons in the substantia nigra pars compacta were decreased significantly in the MPTP-exposed groups. The densities of TH-ir axon terminals in caudate-putamen (CPU) were significantly decreased in the MPTP-treated groups. However, Mn treatment did not affect MPTP neurotoxicity. The densities of glial fibrillary acidic protein (GFAP)-ir astrocytes in the CPU or globus pallidus were significantly increased in the MPTP-treated groups. Concentrations of dopamine in the striatum were decreased significantly in the MPTP-exposed groups only, but Mn had no effect.</P>
Vu, Phuong-Lan,Shin, Jung-Ah,Lee, Yun-Jeung,Nam, Ha-Young,Lee, Jeung-Hee,Akoh, Casimir C,Lee, Ki-Teak Scientific and Medical Division, Macmillan Press 2008 International journal of food sciences and nutriti Vol.59 No.2
<P>Recently, dietary oil with high diacylglycerol (DAG) contents, so called DAG-oil, was introduced in Japan and the USA. It was claimed that the oil mostly composed of DAG is metabolized differently from conventional triacylglycerol oil, reducing body weight and fat mass because DAG tends to be oxidized to provide energy rather than stored as fat in the body. Monoacylglcyerol and DAG could be prepared by lipase-catalyzed reactions including hydrolysis, esterification, and glycerolysis. In this study, modified lipid containing some DAG esterified with the health-beneficial medium-chain fatty acids and conjugated linoleic acid was produced by lipase-catalyzed reactions. Many health benefits of medium-chain fatty acids (C6:0-C12:0) and conjugated linoleic acid isomers have been reported, including anticarcinogenic and antiatherogenic activities, and being rapid energy sources for humans with little or no deposition as body fat. The produced lipid molecules in this study have potential applications as functional healthy dietary fats and oils.</P>
A case of methanol intoxication caused by methomyl pesticide ingestion.
Gil, H W,Hong, J R,Song, H Y,Hong, S Y Scientific Medical Division, Macmillan Press 2012 Human & experimental toxicology Vol.31 No.12
<P>When clinicians treat patients with pesticide poisoning, they often pay attention only to the chief toxic agent and ignore the toxicity of the pesticide's additives or solvents. Occasionally, however, a solvent (e.g. methanol) may itself be the cause of poisoning. We report a case of acute methanol intoxication that occurred after ingestion of a methomyl pesticide that contained methanol as an additive. A 49-year-old man was brought to the emergency department in an unconscious state after ingestion of 20 ml of a carbamate pesticide (chief ingredient: methomyl; active ingredient: methanol). Upon arrival, he was semicomatose and did not breathe spontaneously; however, his cholinesterase level was within normal limits and cholinergic symptoms were not observed. High anion gap metabolic acidosis was present. His blood ethanol level was 74.8 mg/dL. The urine methanol level was 55.60 mg/dL, and urine ethanol level was 22.0 mg/dL. He was treated with hemodialysis; subsequently, his metabolic acidosis resolved and he returned to normal mental status. We guessed that methanol, as the solvent of the methomyl, had produced the symptoms. When treating pesticide-poisoned patients, clinicians should identify the solvent used in the pesticide, because solvents such as methanol may exacerbate the symptoms of poisoned patients.</P>
Lee, J,Jung, H-S,Nam, H-C,Kwok, S-K,Ju, J H,Park, K-S,Kim, H-Y,Park, S-H Scientific Medical Division, Macmillan Press Ltd 2012 Lupus Vol.21 No.12
<P>Colitis in patients with systemic lupus erythematosus (SLE) is quite rare. It can be caused by intestinal vasculitis, mesenteric vascular thrombosis, concomitant inflammatory bowel disease or infectious colitis. It is important to make an accurate and early diagnosis as the treatments for each condition differ and a delayed diagnosis can result in life-threatening complications. However, non-specific gastrointestinal symptoms make a timely diagnosis challenging. Amoebic colitis is a rare condition in patients with SLE. Here we present a case of fulminant amoebic colitis in a patient with SLE which was initially misdiagnosed as ischemic colitis due to intestinal vasculitis. Her colitis was complicated with multiple intestinal perforations, disseminated intravascular coagulation and acute respiratory distress syndrome; but in the end, the patient was successfully treated with metronidazole and paromomycin.</P>
Halder, D,Mandal, C,Lee, BH,Lee, JS,Choi, MR,Chai, JC,Lee, YS,Jung, KH,Chai, YG Scientific & Medical Division,Macmillan Press 2015 Human & experimental toxicology Vol.34 No.10
<P>Ethanol (EtOH) exposure during embryonic development causes dysfunction of the central nervous system (CNS). Here, we examined the effects of chronic EtOH on gene expression during early stages of neuronal differentiation. Human embryonic carcinoma (NCCIT) cells were differentiated into neuronal precursors/lineages in the presence or absence of EtOH and folic acid. Gene expression profiling and pathway analysis demonstrated that EtOH deregulates many genes and pathways that are involved in early brain development. EtOH exposure downregulated several important genes, such as <I>PCDHB14, GABRB1, CTNND2, NAV3, RALDH1,</I> and <I>OPN5,</I> which are involved in CNS development, synapse assembly, synaptic transmission, and neurotransmitter receptor activity. GeneGo pathway analysis revealed that the deregulated genes mapped to disease pathways that were relevant to fetal alcohol spectrum disorders (FASD, such as neurotic disorders, epilepsy, and alcohol-related disorders). In conclusion, these findings suggest that the impairment of the neurological system or suboptimal synapse formation resulting from EtOH exposure could underlie the neurodevelopmental disorders in individuals with FASD.</P>
Ok, S-H,Yu, J,Lee, Y,Cho, H,Shin, I-W,Sohn, J-T Scientific & Medical Division,Macmillan Press 2016 Human & experimental toxicology Vol.35 No.9
<P>The goal of this in vitro study was to investigate the effect of lipid emulsion on apoptosis induced by a toxic dose of bupivacaine (BPV) in H9c2 rat cardiomyoblast cell lines. The effect of lipid emulsion on the decreased cell viability and count induced by BPV or mepivacaine (MPV) in the H9c2 cells was assessed using an 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide assay or a cell count assay. The effect of BPV or lipid emulsion combined with BPV on cleaved caspase 3, caspase 8, and Bax in H9c2 cells was investigated using Western blotting. A terminal deoxynucleotidyl transferase dUTP2'-deoxyuridine 5'-triphosphate nick end labeling (TUNEL) assay was performed to detect apoptosis of H9c2 cells treated with BPV alone or lipid emulsion combined with BPV. The magnitude of lipid emulsion-mediated attenuation of decreased cell viability induced by BPV was higher than that of lipid emulsion-mediated attenuation of decreased cell viability induced by MPV. Lipid emulsion attenuated the increases in cleaved caspase 3, caspase 8 and Bax induced by BPV. Lipid emulsion attenuated the increases in TUNEL-positive cells induced by BPV. These results suggest that lipid emulsion attenuates a toxic dose of BPV-induced apoptosis via inhibition of the extrinsic and intrinsic apoptotic pathways. The protective effect of lipid emulsion may be partially associated with the relatively high lipid solubility of BPV.</P>
Kwak, Kyeong-Gue,Wang, Jing-Hua,Shin, Jang-Woo,Lee, Dong-Soo,Son, Chang-Gue Scientific Medical Division, Macmillan Press 2011 Human & experimental toxicology Vol.30 No.9
<P>Chunggan extract (CGX) is a hepatotherapeutic herbal formula which has been traditionally used for patients suffering from various hepatic disorders. This study aimed to elucidate antifibrotic effect and mechanisms of CGX in thioacetamide (TAA) model. Hepatic fibrosis was induced in 45 Sprague-Dawley rats by TAA (200 mg kg(-1), intraperitoneally [ip]) on twice per week for 12 weeks. CGX (100 or 200 mg kg(-1), per oral [po]) was administrated once a day throughout the experiment. CGX treatment ameliorated serum biomarkers. CGX administration significantly attenuated distortion of histopathologic finding, and accumulation of hydroxyproline and malondialdehyde (MDA). CGX treatment significantly decreased transforming growth factor-beta (TGF-관) concentrations and inactivated hepatic stellate cells (HSCs). CGX treatment drastically restored glutathione (GSH) system, while inducible nitric oxide synthase (iNOS) and tumor necrosis factor-alpha (TNF-관) significantly down-regulated in liver tissue. CGX showed antifibrotic effect in thioacetamide-induced chronic liver injury model. Its corresponding mechanisms may be mediated via anti-oxidative stress property sustaining GSH system and inhibition of ROS production.</P>