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A statistical approach has been applied in order to evaluate chemical interaction between groundwater and river water by using electrical conductivity (EC) in the Changnyeong-Haman river barrage (CHRB), Korea. The EC values in groundwater have been decreased an average of 50 μS/cm and 160 μS/cm. According to factor analysis using the EC data, the EC in groundwater has been disturbed by the CHRB construction as well as dredging of the Nakdong River during the construction work and with time ealpse the groundwater quality became stabilized. It is also demonstrated that hydrologic environment has been changed due to the CHRB construction, comparing the 1st period and 4th period. Hence, a long-term monitoring is required in order to reveal the change of hydrologic environment that can adversely affect plant growth.

Estimating the groundwater recharge rate is essential in all groundwater-related fields, including groundwater development, use, management, modeling, and contamination analysis. In this study, we proposed a combined method of water budget and climate change scenario for estimating the net groundwater recharge rate in the Nakdong River watershed (NRW), South Korea. For the climate change scenario method, the representative concentration pathway (RCP) 4.5 and 8.5 climate scenarios were adopted. First, using the water budget method from 2009 to 2018, the net groundwater recharge rate (NGRR) of 12.15–18.10% relative to annual precipitation (AP) was obtained, subtracting direct runoff (DR) of 21.18–25.32% relative to AP, evapotranspiration (EP) of 40.53–52.29% relative to AP, and baseflow of 12.42–17.84% relative to AP, from the AP (865–1494 mm). The average annual NGRR of the NRW was 200 mm (15.59%). Second, the mean NGRRs from 2009 to 2100 under the RCP 4.5 and RCP 8.5 scenarios were anticipated as 8.73% and 7.63%, respectively. The similarity between the water budget and climate change scenarios was confirmed using data from 2009 and 2018. According to the simple climate change scenario, it is predicted that annual precipitation will increase over the years while the groundwater level and net groundwater recharge rate will decrease. Nonetheless, the estimated NGRR by the water budget method in this study possesses uncertainty due to using potential ET instead of actual ET which should be estimated by considering soil water content.

Investigating the physical and chemical properties of riverine wetlands is necessary to understand their distribution characteristics and depositional environment. This study investigated the physical (particle size, color, and type) and chemical properties (organic, inorganic, and moisture contents) of sediments in Samrak wetland, located in the Nakdong River estuary area in Busan, South Korea. The particle size analysis indicated that the hydraulic conductivity values for the coarse grain and the mixture of coarse and fine grains ranged from 2.03 to 3.49×10−1 cm s−1 and 7.18×10−3 to 1.24×10−7 cm s−1 , respectively. In-situ water quality and laboratory-based chemical analyses and radon-222 measurement were performed on groundwater and surface water in the wetland and water from the nearby Nakdong River. The physical and chemical properties of Samrak wetland was characterized by the sediments in the vertical and lateral direction. The concentrations of chemical components in the wetland groundwater were distinctly higher than those in the Nakdong River water though the wetland groundwater and Nakdong River water equally belonged to the Ca-HCO3 type.

The demand for water resources is consistently increasing due to industrialization and urbanization. Water resource management can become difficult because of climate change and social issues. Due to the difficulty in securing stable water resources, reasonable utilization and management of water is crucial for the sustainable development of groundwater resources that are an efficient alternative to surface water. For groundwater management, the National Groundwater Information Management Service (GIMS) Center for K-Water measures groundwater data hourly (groundwater level, water temperature, and electrical conductivity) at national groundwater monitoring stations and analyzes the long-term variation of groundwater with regard to climate change. According to the Groundwater Act (1993), auxiliary groundwater monitoring stations for groundwater use and water quality are activated by local governments. The observed data after the calibration process are provided for utilization by citizens, industries, schools, institutes, and government policies through annual reports on groundwater monitoring by the GIMS Center. In 2018, the Korean government merged water resources affairs that were once divided between the Ministry of Environment and the Ministry of Land, Infrastructure, and Transport. The change will be favorable for effective management of the surface water and groundwater resources as well as ensuring both quality and quantity.

Rehabilitation work is required to increase well productivity, which decreases with the elapsed time of pumping owing to the clogging of the water well. Clogging causes not only a reduction in the well productivity but also a deterioration of the water quality. For unclogging and rehabilitating wells, several techniques are used such as brushing, air surging, surge blocks, and gas impulse. In this study, the high-pressure air impulse technique, which effectively and economically rehabilitates wells, was applied to a riverbank filtration site in Korea for the same objective. At most of the wells, the hydraulic parameters (transmissivity, storage coefficient, and specific capacity) were increased by the application of the high-pressure air impulse technique. The well loss change values also indicate an increase in the hydraulic parameters by the air impulse implementation. Thus, the high-pressure air impulse technique can be efficiently and economically applied to water and riverbank filtration wells for rehabilitating the decreased productivity.

Genetic evidence indicates that haploinsufficiency of ARID1B causes intellectual disability (ID) and autism spectrum disorder (ASD), but the neural function of ARID1B is largely unknown. Using both conditional and global Arid1b knockout mouse strains, we examined the role of ARID1B in neural progenitors. We detected an overall decrease in the proliferation of cortical and ventral neural progenitors following homozygous deletion of Arid1b, as well as altered cell cycle regulation and increased cell death. Each of these phenotypes was more pronounced in ventral neural progenitors. Furthermore, we observed decreased nuclear localization of β-catenin in Arid1b-deficient neurons. Conditional homozygous deletion of Arid1b in ventral neural progenitors led to pronounced ID- and ASD-like behaviors in mice, whereas the deletion in cortical neural progenitors resulted in minor cognitive deficits. This study suggests an essential role for ARID1B in forebrain neurogenesis and clarifies its more pronounced role in inhibitory neural progenitors. Our findings also provide insights into the pathogenesis of ID and ASD.

The rheological properties of polycarbonate/acrylonitrile-butadiene-styrene (PC/ABS) blends with various blend ratios are investigated at different temperatures to determine the shear dependent chain motions in a heterogeneous blend system. At low frequency levels under 0.1 rad/s, the viscosity of the material with a blend ratio of 3:7 (PC:ABS) is higher than that of pure ABS polymer. As the temperature increases, the viscosities of ABS-rich blends increase rather than decrease, whereas PC-rich blends exhibit decrease in viscosity. Results from the time sweep measurements indicate that ordered structures of PC and the formation and breakdown of internal network structures of ABS polymer occur simultaneously in the blend systems. Newly designed sequence test results show that the internal structures formed between PC and ABS polymers are dominant at low shear conditions for the blend ratio of 3:7 and effects of structural change and the presence of polybutadiene (PBD) become dominant at high shear conditions for pure ABS. The results of yield stress and relaxation time for PC/ABS blends support this phenomenon. The specimen with a blend ratio of 3:7 exhibited the highest value of yield stress at high temperature among others, which implies that the internal structure become stronger at higher temperature. The heterogeneity of ABS-rich blends increases whereas that of PC-rich blends decreases as temperature increases.

Selective autolysosomal degradation of damaged mitochondria, also called mitophagy, is an indispensable process for maintaining integrity and homeostasis of mitochondria. One well-established mechanism mediating selective removal of mitochondria under relatively mild mitochondria-depolarizing stress is PINK1-Parkin-mediated or ubiquitin-dependent mitophagy. However, additional mechanisms such as LC3-mediated or ubiquitin-independent mitophagy induction by heavy environmental stress exist and remain poorly understood. The present study unravels a novel role of stress-inducible protein Sestrin2 in degradation of mitochondria damaged by transition metal stress. By utilizing proteomic methods and studies in cell culture and rodent models, we identify autophagy kinase ULK1-mediated phosphorylation sites of Sestrin2 and demonstrate Sestrin2 association with mitochondria adaptor proteins in HEK293 cells. We show that Ser-73 and Ser-254 residues of Sestrin2 are phosphorylated by ULK1, and a pool of Sestrin2 is strongly associated with mitochondrial ATP5A in response to Cu-induced oxidative stress. Subsequently, this interaction promotes association with LC3-coated autolysosomes to induce degradation of mitochondria damaged by Cu-induced ROS. Treatment of cells with antioxidants or a Cu chelator significantly reduces Sestrin2 association with mitochondria. These results highlight the ULK1-Sestrin2 pathway as a novel stress-sensing mechanism that can rapidly induce autophagic degradation of mitochondria under severe heavy metal stress.

Electroplating of metals on polymer materials is one of the best decorative processes for achieving low cost and light weight. However, low interfacial adhesion often limits practical utilization due to the potential peel-off behavior of metal layers. The interface between the metal layers and acrylonitrile-butadiene-styrene (ABS) substrate and its peeling mechanism are investigated as a function of etching time. Sa, the arithmetic average roughness of the unit area, and Sdr, the interfacial area ratio, are adopted instead of linear roughness, Ra, to quantify the surface profile. As the etching time increases, both Sa and Sdr for the etched ABS and corresponding metal side increase. The failure mode changes from adhesive to cohesive as the etching time increases, and the peel-off strength of the electroplated ABS exhibits a dependence on the tensile strength of the substrate. The peel-off strength of the electroplated ABS specimens increases to 8.46 N/cm after 30 min of etching time, but the interface degrades, forming inner voids. The Sdr ratio (Sdr, polymer / Sdr, plating) is proposed as a surface parameter to predict the peel-off strength of electroplated ABS and represents a new attempt to quantitatively correlate the interfacial morphology with the adhesion strength.

Haploinsufficiency of the chromatin remodeling factor ARID1B leads to autism spectrum disorder and intellectual disability. Several independent research groups, including our own, recently examined the effects of heterozygous deletion of Arid1b in mice and reported severe behavioral abnormalities reminiscent of autism spectrum disorders and intellectual disability as well as marked changes in gene expression and decreased body size. Arid1b heterozygous mice also display significant cortical excitatory/inhibitory imbalance due to altered GABAergic neuron numbers and impaired inhibitory synaptic transmission. Abnormal epigenetic modifications, including histone acetylation and methylation, are additionally associated with Arid1b haploinsufficiency in the brain. Treating adult Arid1b mutant mice with a positive GABA allosteric modulator, however, rescues multiple behavioral abnormalities, such as cognitive and social impairments, as well as elevated anxiety. While treating Arid1b haploinsufficient mice with recombinant mouse growth hormone successfully increases body size, it has no effect on aberrant behavior. Here we summarize the recent findings regarding the role of ARID1B in brain development and behavior and discuss the utility of the Arid1b heterozygous mouse model in neurodevelopmental and psychiatric research. We also discuss some of the opportunities and potential challenges in developing translational applications for humans and possible avenues for further research into the mechanisms of ARID1B pathology in the brain.

Contains fulltext : 171765.pdf (Publisher’s version ) (Closed access) Myelination, the process by which oligodendrocytes form the myelin sheath around axons, is key to axonal signal transduction and related motor function in the central nervous system (CNS). Aging is characterized by degenerative changes in the myelin sheath, although the molecular underpinnings of normal and aberrant myelination remain incompletely understood. Here we report that axon myelination and related motor function are dependent on BubR1, a mitotic checkpoint protein that has been linked to progeroid phenotypes when expressed at low levels and healthy lifespan when overabundant. We found that oligodendrocyte progenitor cell proliferation and oligodendrocyte density is markedly reduced in mutant mice with low amounts of BubR1 (BubR1H/H mice), causing axonal hypomyelination in both brain and spinal cord. Expression of essential myelin-related genes such as MBP and PLP1 was significantly reduced in these tissues. Consistent with defective myelination, BubR1H/H mice exhibited various motor deficits, including impaired motor strength, coordination, and balance, irregular gait patterns and reduced locomotor activity. Collectively, these data suggest that BubR1 is a key determinant of oligodendrocyte production and function and provide a molecular entry point to understand age-related degenerative changes in axon myelination.

Since 2018, groundwater resource is expected to be more efficiently managed by the unified management of the surface water and groundwater resources as well as both quality and quantity at the same time.

Exendin-4 (Ex-4), a glucagon-like peptide-1 receptor (GLP-1R) agonist, has been known to reverse hepatic steatosis in ob/ob mice. Although many studies have evaluated molecular targets of Ex-4, its mechanism of action on hepatic steatosis and fibrosis has not fully been determined. In the liver, glucose transporter 4 (GLUT4) is mainly expressed in hepatocytes, endothelial cells and hepatic stellate cells (HSCs). In the present study, the effects of Ex-4 on GLUT4 expression were determined in the liver of ob/ob mice. Ob/ob mice were treated with Ex-4 for 10 weeks. Serum metabolic parameters, hepatic triglyceride levels, and liver tissues were evaluated for hepatic steatosis. The weights of the whole body and liver in ob/ob mice were reduced by long-term Ex-4 treatment. Serum metabolic parameters, hepatic steatosis, and hepatic fibrosis in ob/ob mice were reduced by Ex-4. Particularly, Ex-4 improved hepatic steatosis by enhancing GLUT4 via GLP-1R activation in ob/ob mice. Ex-4 treatment also inhibited hepatic fibrosis by decreasing expression of connective tissue growth factor in HSCs of ob/ob mice. Our data suggest that GLP-1 agonists exert a protective effect on hepatic steatosis and fibrosis in obesity and type 2 diabetes.

Obesity-induced fatty liver disease is associated with increased hypothalamic inflammation. Previous reports have demonstrated that the deletion of SIRT1 in hepatocytes increases hepatic steatosis and inflammation. Using myeloid cell-specific SIRT1 knockout (KO) mice, we investigated whether ablation of SIRT1 in macrophages plays a role in regulating hepatic steatosis and hypothalamic inflammation. When challenged with a high-fat diet (HFD) for 24 weeks, hyperleptinemia, hyperinsulinemia, hepatic steatosis and macrophage infiltrations in HFD-fed KO mice were increased compared with HFD-fed WT mice. Hypothalamic expression levels of iba1 were increased in HFD-fed KO mice compared with HFD-fed WT mice. In particular, the expression levels of choline acetyltransferase were decreased in the hypothalamus of HFD-fed KO mice compared with HFD-fed WT mice. Thus, our findings suggest that SIRT1 plays a key role for hepatic steatosis and hypothalamic inflammation and that anti-inflammatory effect of SIRT1 may be important for the prevention of obesity-induced metabolic syndromes.

Several association studies have implicated the PARK2 gene that encodes parkin – the key molecule orchestrating the mitochondrial quality control system – as a candidate susceptibility gene for diabetes. A total of 7551 unrelated Korean KARE cohort subjects were analyzed to investigate the association between the PARK2 single nucleotide polymorphism (SNP) and quantitative glycemic traits. Two SNPs, rs10455889 and rs9365294, were significantly associated with fasting plasma glucose level ( p = ∼1.2 × 10 −4 ) and insulin secretion indices ( p = ∼7.4 × 10 −5 ) in male KARE subjects. Parkin was expressed predominantly in the rat pancreatic islets. Downregulation of the Park2 gene in rat INS-1 β-cells resulted in a significant decrease in the glucose-stimulated insulin secretion, intracellular insulin gene expression, and intracellular ATP level. The Park2 -depleted β-cells also exhibited increased mitochondrial fragmentation and ROS production and decreased mitochondrial membrane potential. Both population-based statistical evaluation and experimental evidence demonstrated a fundamental role of the PARK2 gene in the maintenance of β-cell function.

A beneficial radioprotective agent has been used to treat the radiation-induced lung injury. This study was performed to investigate whether curcumin, which is known to have anti-inflammatory and antioxidant properties, could ameliorate radiation-induced pulmonary inflammation and fibrosis in irradiated lungs. Rats were given daily doses of intragastric curcumin (200 mg/kg) prior to a single irradiation and for 8 weeks after radiation. Histopathologic findings demonstrated that macrophage accumulation, interstitial edema, alveolar septal thickness, perivascular fibrosis, and collapse in radiation-treated lungs were inhibited by curcumin administration. Radiation-induced transforming growth factor-β1 (TGF-β1), connective tissue growth factor (CTGF) expression, and collagen accumulation were also inhibited by curcumin. Moreover, western blot analysis revealed that curcumin lowered radiation-induced increases of tumor necrosis factor-α (TNF-α), TNF receptor 1 (TNFR1), and cyclooxygenase-2 (COX-2). Curcumin also inhibited the nuclear translocation of nuclear factor-κ B (NF-κB) p65 in radiation-treated lungs. These results indicate that long-term curcumin administration may reduce lung inflammation and fibrosis caused by radiation treatment.

Non-alcoholic fatty liver disease (NAFLD) is one of the most frequent causes of liver disease and its prevalence is a serious and growing clinical problem. Caloric restriction (CR) is commonly recommended for improvement of obesity-related diseases such as NAFLD. However, the effects of CR on hepatic metabolism remain unknown. We investigated the effects of CR on metabolic dysfunction in the liver of obese diabetic db/db mice. We found that CR of db/db mice reverted insulin resistance, hepatic steatosis, body weight and adiposity to those of db/m mice. 1H-NMR- and UPLC-QTOF-MS-based metabolite profiling data showed significant metabolic alterations related to lipogenesis, ketogenesis, and inflammation in db/db mice. Moreover, western blot analysis showed that lipogenesis pathway enzymes in the liver of db/db mice were reduced by CR. In addition, CR reversed ketogenesis pathway enzymes and the enhanced autophagy, mitochondrial biogenesis, collagen deposition and endoplasmic reticulum stress in db/db mice. In particular, hepatic inflammation-related proteins including lipocalin-2 in db/db mice were attenuated by CR. Hepatic metabolomic studies yielded multiple pathological mechanisms of NAFLD. Also, these findings showed that CR has a therapeutic effect by attenuating the deleterious effects of obesity and diabetes-induced multiple complications.

Rho-associated coil kinase (ROCK) inhibitors reportedly prevent neurodegeneration, and abnormal ROCK activation in the central nervous system induces neurite collapse and retraction. However, it is unclear whether the ROCK inhibitor Y-27632 directly protects hippocampal neurons from excitotoxicity. Here, we determined the effects of Y-27632 on neuroprotection following kainic acid (KA)-induced seizures in mice and during glutamate-induced excitotoxicity in HT22 cells. One day after Y-27632 injection, mice were treated with KA and killed 1-2 days later. Fluoro-Jade B and rapid Golgi staining showed that Y-27632 protected against KA-induced neurodegeneration and neurite dystrophy. Y-27632 inhibited increases in hippocampal RhoA and ROCK2 in KA-treated mice as determined by western blot analysis. Immunohistochemical analysis revealed ROCK2-positive neurons and astrocytes in the KA-treated hippocampus. In HT22 cells, Y-27632 also protected neurons and neurite formation during glutamate-induced excitotoxicity in vitro. These results indicate that ROCK inhibition modulates neurite growth and protects neurons from excitotoxicity-induced cell death.

Obesity-induced diabetes is associated with chronic inflammation and is considered a risk factor for neurodegeneration. We tested the hypothesis that an AMP-activated protein kinase activator, resveratrol (RES), which is known to exert potent anti-inflammatory effects, would attenuate peripheral and central inflammation and improve memory deficit in mice fed a high-fat diet (HFD). C57BL/6J mice were fed an HFD or an HFD supplemented with RES for 20 weeks. Metabolic parameters in serum were evaluated, and Western blot analysis and immunohistochemistry in peripheral organs and brain were completed. We used the Morris water maze test to study the role of RES on memory function in HFD-treated mice. RES treatment reduced hepatic steatosis, macrophage infiltration, and insulin resistance in HFD-fed mice. In the hippocampus of HFD-fed mice, the protein levels of tumor necrosis factor-α and Iba-1 expression were reduced by RES treatment. Choline acetyltransferase was increased, and the phosphorylation of tau was decreased in the hippocampus of HFD-fed mice upon RES treatment. In particular, we found that RES significantly improved memory deficit in HFD-fed mice. These findings indicate that RES reverses obesity-related peripheral and central inflammation and metabolic derangements and improves memory deficit in HFD-fed diabetic mice.

Aim It is known that garlic has antioxidative and anti-inflammatory properties. Aged red garlic (ARG), a novel aged garlic formulation, has higher antioxidant effects than fresh raw garlic. This study was performed to examine the anti-inflammatory effects of ARG extract (ARGE). Methods The anti-inflammatory effects of ARGE were evaluated in the lipopolysaccharide (LPS)-treated Raw 264.7 macrophages and acute lung inflammatory mice. NO production was determined by the Griess method, and iNOS, HO-1 and COX-2 expressions were measured using Western blot analysis. Histology and inflammation extent of lung were analysed using haematoxylin–eosin staining and immunohistochemistry. Results ARGE treatment markedly reduced LPS-induced nitrite production in RAW 264.7 macrophages and reduced inducible nitric oxide synthase (iNOS) expression. Treatment of cells with ARGE led to a significant increase in haeme oxygenase-1 (HO-1) protein expression, which was mediated by stimulating the expression of nuclear factor erythroid 2-related factor 2 (Nrf2). Treatment with zinc protoporphyrin, a selective inhibitor of HO-1, significantly reversed the ARGE-mediated inhibition of nitrite production (P

Summary Status epilepticus causes significant damage to the brain, and cellular injury due to prolonged seizures may cause the pathogenesis of epilepsy or cognitive deficits. Clusterin mediates several cell signaling pathways, including cell death or survival pathways in the brain. A nuclear form of clusterin protein has been suggested to have pro-apoptotic properties. Bcl-x L functions as a dominant-negative modulator of the pro-apoptotic protein Bax. However, the relationship between clusterin and Bcl-x L in cell death signaling in the brain remains unknown. Therefore, we examined whether clusterin interacts with Bcl-x L after seizures or whether this interaction is related to neuronal death. We found increased levels of nuclear clusterin and cleaved caspase-3 in CA3 neurons after prolonged seizures induced by systemic kainic acid, along with extensive hippocampal cell death, as evidenced by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) and anti-active caspase-3 staining. Furthermore, co-immunoprecipitation and double immunofluorescence analyses revealed that clusterin interacted with Bcl-x L in dying CA3 neurons while the levels of Bcl-x L , Bad or Bax remained constant. These findings provide evidence that nuclear clusterin signals cell death at least via an interaction with Bcl-x L in the hippocampus after seizures, suggesting that targeting nuclear clusterin may be a promising novel strategy to protect against seizure-induced neuronal injury.

Calcineurin (CaN)-mediated excitotoxicity impairs γ-aminobutyric acid (GABA) transmission and induces neuronal apoptosis. Ca(2+)-dependent K(+)-Cl(-) cotransporter 2 (KCC2) participates in GABAergic inhibitory transmission. However, the mechanism by which CaN mediates GABA receptor-mediated KCC2 in seizures is not fully understood. In the present study, we investigated the altered expression of KCC2 and the effects of the CaN inhibitor FK506 on KCC2 expression in the mouse hippocampus following kainic acid (KA) treatment. FK506 was injected twice 24 h and 30 min before KA treatment and then mice were treated with KA and killed 2 days later. FK506 had anticonvulsant effect on KA-induced seizure activities. CaN cleavage was evident in the hippocampus 24 h after KA treatment. FK506 pretreatment blocked the truncation of CaN in the KA-treated hippocampus. Cresyl violet and TUNEL staining showed that FK506 prevented KA-induced hippocampal cell death. In particular, Western blot analysis showed that KCC2 expression was time dependent, with a peak at 6 h and a return to decreased levels at 48 h, whereas FK506 pretreatment inhibited the KA-induced decrease in KCC2 expression in the hippocampus. Immunofluorescence showed that FK506 pretreatment protected the loss of inhibitory GABAergic KCC2-expressing neurons following KA treatment. Taken together, these results provide evidence that altered KCC2 expression may be associated with Ca(2+)-mediated seizure activity and indicate that neuron-specific KCC2 may be involved in neuroprotection after seizures.

Similar to fasting, the ketogenic diet (KD) has anti-inflammatory effects and protects against excitotoxicity-mediated neuronal cell death. Recent studies have shown that peroxisome proliferator-activated receptor (PPAR)γ has anti-inflammatory effects in seizure animal models. However, the exact mechanisms underlying the anti-inflammatory effects of the KD have not been determined for seizures. Here we investigated the effect of the KD and acetoacetate (AA) on neuroinflammation in a seizure animal model and glutamate-treated HT22 cells, respectively. Mice were fed the KD for 4 weeks and sacrificed 2 or 6h after KA injection. The KD reduced hippocampal tumor necrosis factor alpha (TNF-α) levels and nuclear factor (NF)-κB translocation into the nucleus 2h after KA treatment. KD-induced PPARγ activation was decreased by KA in neurons as assessed by western blotting and immunofluorescence. Finally, the KD inhibited cyclooxygenase (COX)-2 and microsomal prostaglandin E(2) synthase-1 (mPGES-1) expression in the hippocampus 6h after KA treatment. AA treatment also protected against glutamate-induced cell death in HT22 cells by reducing TNF-α and PPARγ-mediated COX-2 expression. Thus, the KD may inhibit neuroinflammation by suppressing a COX-2-dependent pathway via activation of PPARγ by the KD or AA.

We examined the interactions between surface and groundwater through (1) flowmeter logging, (2) measurements of seasonal and vertical changes in temperature within a well, and (3) geochemical analyses of water samples from nine groundwater-monitoring wells. At two wells adjacent to a stream, subsurface water was found to flow from the stream to a surrounding alluvial fan, and the seasonal change in groundwater temperature is similar to those of surface water and air. Geochemical analyses at two wells indicated hydro-geochemical features affected by streamwater inflow, showing seasonal variations. Accordingly, these two wells are located in an area with active interaction between surface water and groundwater. The Thermochron I-button used in the present study is useful for this type of study of groundwater?surface water interaction because of its low cost and small size.

Novel heteroleptic Pd0 complexes with an N-heterocyclic carbene (NHC) ligand [(Me3P)Pd(NHC)] (NHC = IPr, 1; SIPr, 2) were obtained from [Pd(CH2=CHPh)(PMe3)2] and an equivalent of NHC [NHC = 1,3-bis(2,6-diisopropylphenyl)imidazol-2-ylidene (IPr) or 1,3-bis(2,6-diisopropylphenyl)-4,5-dihydroimidazol-2-ylidene (SIPr)]. Further treatments of complexes 1 and 2 with an additional equimolar NHCafforded the corresponding bis(NHC)–Pd0 complexes [Pd(NHC)2] (NHC = IPr, 3; SIPr, 4). Complexes 1–4 readily reacted with dichloromethane or chloroform to give C–Cl oxidative addition products. In addition, the reactivity of complex 2 toward other organic halides such as bromobenzene, trans-1,2-dichloroethylene, and 5,5′-dibromo-2,2′-bithiophene to produce the corresponding oxidative addition products was investigated. Finally, the ligand replacement of complex 1 with a chelating phosphane was examined.

The bis(silyl) palladium(II) complex [Pd(SiHPh 2 ) 2 (dmpe)] (dmpe = 1,2-bis(dimethylphosphino)ethane) reacted with organic isothiocyanates R–NCS (R = Ph, i Pr, allyl) to give a dithiocarbonimidato [Pd(S 2 C N–Ph)(dmpe)] ( 1 ), a diphenylsilanedithiolato [Pd(S 2 SiPh 2 )(dmpe)] ( 2 ), or a π-allyl [( η 3 -allyl)Pd](NCS) ( 3 ) palladium complex, depending on the isothiocyanate type and reaction conditions. In addition, various dithiocarbonimidato Pd(II) complexes were also obtained from trans -[PdEt 2 L 2 ] (L = PMe 3 , PMe 2 Ph) ( 4 – 6 ) or [Pd(styrene)L 2 ] and organic isothiocyanates.

Chronic airway inflammation is a characteristic feature of destructive cigarette smoking (CS)-induced lung disease, particularly in patients with emphysema. Celecoxib, a specific cyclooxygenase-2 (COX-2) inhibitor, is widely used to treat inflammation. However, the exact mechanisms underlying this drug's anti-inflammatory effects have not yet been determined in pulmonary emphysema. Here, we explore whether celecoxib attenuates CS-induced inflammation in rat lungs. Rats were exposed to smoke and received celecoxib via intragastric feeding daily for 20 wk. We found that celecoxib inhibited interalveolar wall distance and pulmonary inflammation in the lungs of CS-treated rats. Celecoxib inhibited serum NO production, iNOS, COX-2 expression, and PGE2production in CS-treated lung tissues. Our immunohistochemical data showed that CS-induced CD68 and COX-2 expression were inhibited by celecoxib. Furthermore, celecoxib attenuated the activation of phospho-IκBα and NF-κB in CS-treated rat lung. In addition, there was an inhibitory effect of celecoxib on the COX-2 expression and NF-κB activation in LPS-stimulated RAW 264.7 macrophages. Celecoxib also attenuated NF-κB activation in COX-2 siRNA-transfected RAW 264.7 macrophages. Thus, our findings suggest that the anti-inflammatory effects of celecoxib are mediated by its effects on NF-κB-regulated gene expression, which ultimately reduces the progression of CS-induced pulmonary emphysema.

Oxidative stress-induced cell death leads to phosphorylation of 14-3-3ζ at serine 58. 14-3-3ζ is detected at significant levels in cerebrospinal fluid after kainic acid (KA)-induced seizures. Here we examined temporal changes in 14-3-3ζ phosphorylation in the hippocampus and amygdala of mice after KA treatment. Mice were killed at 2, 6, 24, or 48 h after KA (30 mg/kg) injection. We observed an increase in TUNEL and Fluoro-Jade B (FJB)-stained neurons in the hippocampus and amygdala of KA-treated mice. Phospho (p)-14-3-3ζ and p-JNK expression was increased in the hippocampus 2 and 6 h after KA treatment, respectively. In immunohistochemical analysis, p-14-3-3ζ-positive cells were present in the CA3 region of the hippocampus and the central nucleus of amygdala (CeA) of KA-treated mice. Thus, phosphorylation of 14-3-3ζ at serine 58 may play an important role in KA-induced hippocampal and amygdaloid neuronal damage.

Pd(II)– and Pt(II)–azido complexes, [M(N3)(PMe3)2(C–L)] {LH = 2-(2′)-thienyl pyridine; M = Pd (1), Pt(2)}, which contain σ-bonded heterocycles (L), were treated with aryl isothiocyanate (Me2C6H3–NCS) to afford the corresponding Pd(II) and Pt(II) tetrazole–thiolato complexes, trans-{M[SCN4(2,6-Me2C6H3)](PMe3)2(C–L)} {M = Pd (3), Pt (4)}. Complexes 3 and 4 have a 1-D helical network formed by the intermolecular M⋯S van der Waals contacts.

The ketogenic diet (KD) prevents kainic acid (KA)-induced hippocampal cell death. There are reports that AMP-activated protein kinase (AMPK) activation regulates the intracellular signaling pathways involved in cellular survival or apoptotic cell death. In this study, we investigated the effect of the KD consumption on the expression of signaling pathway proteins AMPK and ACC, and heat shock protein (HSP) 70 in mouse hippocampus after KA treatment. Mice were fed the KD for 6 weeks and then sacrificed 48 h after KA (30 mg/kg) injection. The marked cell death found commonly in normal diet (ND)-fed mice treated with KA was not observed in the KD-fed KA-treated mice. Western blot analysis revealed that phosphorylation of AMPK and ACC was increased after KA treatment. However, phosphorylation of these proteins was reduced in those animals that received the KD. In addition, increased expression of HSP70 in the hippocampus of KA-treated mice was decreased in animals receiving the KD. These results indicate that the KD promotes neuroprotective effects through suppression of the AMPK cascade and that HSP70 is involved in neuronal cell death or oxidative stress.

Kainic acid (KA)-induced seizure induces the hippocampal cell death. There are reports that AMP-activated protein kinase (AMPK), which is an important regulator of energy homeostasis of cells, has been proposed as apoptotic molecule. In this study, we investigated the altered expression of AMPK cascade in the hippocampus of mice during KA-induced hippocampal cell death. Mice were killed at 2, 6, 24 or 48 h after KA (30 mg/kg) injection. Histological evaluation of KA-treated hippocampus revealed hippocampal cell death first at 6 h and appearing prominently by 48 h after KA injection. Immunoreactivity of Ca(2+)/calmodulin-dependent protein kinase kinasebeta (CaMKKbeta) was increased after KA treatment. In Western blot analysis, AMPK activation was increased 2 h after KA treatment. The proteins of downstream AMPK, including those of glucose transporter1 (GLUT1) and phosphorylation of Acetyl CoA Carboxylase (ACC) were increased in the hippocampus after KA treatment. These results indicate that sustained AMPK activation might be a mechanism by which KA-induced seizure causes hippocampal cell death of mice.

Summary Introduction Ghost cell odontogenic carcinoma is a rare neoplastic variant of calcifying odontogenic cyst, with aggressive growth characteristics. A painful swelling in the jaws with local paraesthesia is the most common symptom. Although it often causes irregular destruction of the adjacent bone, immunohistochemical expression of tartrate-resistant acid phosphatase (TRAP) and vitronectin receptor has not previously been described in this carcinoma. Case report This article describes a ghost cell odontogenic carcinoma affecting the mandible of a 55-year-old man. The patient was treated by segmental mandibulectomy and there was no evidence of recurrence or metastasis for 1.8 years. Cytological features including the immunohistochemical expression of TRAP and vitronectin receptor were studied. Conclusion Specimens revealed varying sized islands of anucleate cell clusters with homogenous, pale eosinophilic cytoplasm, so called ghost cells, admixed with sheets of tumour. TRAP and vitronectin receptor were detected in the ghost cells, but they were not expressed in the tumour cells. Our findings suggest that some of the cytokines produced by ghost cells may play important roles in causing extensive bone resorption in the ghost cell odontogenic carcinoma.

Bis(phosphine) Pd–azido complexes containing heterocycles such as tetrazolyl, pyrazinyl, and thienyl groups reacted with aryl isocyanides to give the corresponding Pd–carbodiimido or –imidoyl carbodiimido complexes. These products were formed by the insertion of the isocyanides into the Pd–N (azido) or the Pd–C (heterocycles) bond.

Aqueous polyurethane dispersions based on isophorone diisocyanate (IPDI), poly (tetramethylene adipate) glycol (PTAd), and dimethylolproprionic acid (DMPA) were synthesized by a prepolymer mixing process. Effects of the molecular weight of PTAd and types of hybridizations, viz. blending, semi-interpenetrating polymer network (IPN), and full IPNs with polybutylacrylate have been determined. It was found that thermal, mechanical, and adhesion properties of the polyurethane dispersions increased with increasing molecular weight of polyols. Regarding the effects of hybridization, full IPNs gave the greatest tensile strength and elongation at break with a fast drying rate, whereas semi-IPNs gave the greatest initial as well as final adhesion, implying that a certain degree of chain mobility would augment the penetrations of adhesive molecules into the soft polyurethane foam substrates.

Diabetes may adversely affect cognitive function and, conversely, caloric restriction (CR) increases longevity and improves memory. To shed light on the unknown underlying mechanisms involved in these observations, we examined the effects of CR on serum metabolic parameters and hippocampal protein expression in the ob/ob mice model of obesity-induced diabetes. We found that CR reduced hepatic steatosis and insulin resistance in ob/ob mice. In addition, CR increased the levels of hippocampal O-linked-N-acetylglucosamine (O-GlcNAc) and GlcNAc transferase and decreased the expression of calcium/calmodulin-dependent protein kinase II, lipocalin-2, and phosphorylated tau. Furthermore, CR lessened the learning deficits that are typically seen in ob/ob mice. These findings indicate that CR may reverse obesity-related brain glucose impairment and intracellular Ca(2+) dysfunction and relieve learning impairment associated with diabetes.

Using a sol–gel process nanometer-scale silicas were incorporated into waterborne polyurethanes (PUs) which were synthesized from isophoronediisocyanate (IPDI), poly(tetramethyleneglycol) (PTMG), dimethylolpropionic acid (DMPA), triethylamine (TEA), diethylenetriamine (DETA) and 3-aminopropyltriethoxysilane as coupling agent. Thermal, mechanical, and dynamic mechanical properties of the hybrid composite have been studied. 29Si-NMR spectra gave evidence of condensation reaction between silica and silanes encaping the PU prepolymers, whereas transmission electron microscopy (TEM) showed the high connectivity of hybrid composites. It was found that greater thermal and mechanical properties of waterborne PU/silica hybrid composite were obtained when chemical networks were formed between PU and silica.

Diabetes-induced cognitive decline has been recognized in human patients of type 2 diabetes mellitus and mouse model of obesity, but the underlying mechanisms or therapeutic targets are not clearly identified. We investigated the effect of caloric restriction on diabetes-induced memory deficits and searched a molecular mechanism of caloric restriction-mediated neuroprotection. C57BL/6 mice were fed a high-fat diet for 40 weeks and RNA-seq analysis was performed in the hippocampus of high-fat diet-fed mice. To investigate caloric restriction effect on differential expression of genes, mice were fed high-fat diet for 20 weeks and continued on high-fat diet or subjected to caloric restriction (2 g/day) for 12 weeks. High-fat diet-fed mice exhibited insulin resistance, glial activation, blood–brain barrier leakage, and memory deficits, in that we identified neurogranin, a down-regulated gene in high-fat diet-fed mice using RNA-seq analysis; neurogranin regulates Ca2+/calmodulin-dependent synaptic function. Caloric restriction increased insulin sensitivity, reduced high-fat diet-induced blood–brain barrier leakage and glial activation, and improved memory deficit. Furthermore, caloric restriction reversed high-fat diet-induced expression of neurogranin and the activation of Ca2+/calmodulin-dependent protein kinase II and calpain as well as the downstream effectors. Our results suggest that neurogranin is an important factor of high-fat diet-induced memory deficits on which caloric restriction has a therapeutic effect by regulating neurogranin-associated calcium signaling.

According to a 2015 study conducted by the Ministry of Environment of Korea, municipal water is supplied to 96.1% of the total Korean population, but 3.9% of the total population (~2.14 million people) in rural myeon or villages, drink groundwater from old and/or unregistered wells that are not a part of the municipal water system. Additionally, accurate statistics are not reported without regular water quality tests, so safety measures alone are insufficient to improve water quality. In this situation, the Korean government is responsible for verifying the quality of groundwater and identifying the cause of groundwater contamination in areas with no municipal water supply. The National Institute of Environmental Research (NIER) under the Ministry of Environment of Korea, conducted the ‘Safe Groundwater Supply Project (SGSP)’ between 2012 and 2016 to secure groundwater quality stability in areas without the benefit of municipal water. This survey identified groundwater quality using a detailed water quality survey and gave recommendations for supplying safe groundwater and providing future improvements and countermeasures in cases of groundwater pollution. This paper presents the SGSP and consists of water quality analysis, the exploration and exploitation of drinking water facilities, the selection of a pilot project area among high-pollution areas, and improvement measures for water quality in the pilot project area.

This study mapped and analyzed groundwater potential using two different models, logistic regression (LR) and multivariate adaptive regression splines (MARS), and compared the results. A spatial database was constructed for groundwater well data and groundwater influence factors. Groundwater well data with a high potential yield of ≥70 m3/d were extracted, and 859 locations (70%) were used for model training, whereas the other 365 locations (30%) were used for model validation. We analyzed 16 groundwater influence factors including altitude, slope degree, slope aspect, plan curvature, profile curvature, topographic wetness index, stream power index, sediment transport index, distance from drainage, drainage density, lithology, distance from fault, fault density, distance from lineament, lineament density, and land cover. Groundwater potential maps (GPMs) were constructed using LR and MARS models and tested using a receiver operating characteristics curve. Based on this analysis, the area under the curve (AUC) for the success rate curve of GPMs created using the MARS and LR models was 0.867 and 0.838, and the AUC for the prediction rate curve was 0.836 and 0.801, respectively. This implies that the MARS model is useful and effective for groundwater potential analysis in the study area.