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<P><B>Abstract</B></P><P>Ataxia is often associated with altered cerebellar motor control, a process in which Purkinje cells (PCs) play a principal role. Pogo mice display severe motor deficits characterized by an ataxic gait accompanying hindlimb hyperextension. Here, using whole‐cell patch‐clamp recordings, we show that parallel fiber (PF)‐excitatory post‐synaptic currents (PF‐EPSCs) are reduced, paired‐pulse facilitation (PPF) is increased and PF‐PC long‐term depression (LTD) is impaired in Pogo mice; in contrast, climbing‐fiber EPSCs are preserved. In control mice, treatment with the calmodulin antagonist calmidazolium (5 μ<SMALL>m</SMALL>) impaired PPF and LTD. Notably, cerebellar calmodulin expression was significantly reduced in Pogo mice compared with control mice. Control PCs predominantly exhibited a tonic firing pattern, whereas the firing pattern in Pogo PCs was mainly a complex burst type. These results implicate alterations in PC responses and calmodulin content in the abnormal cerebellar function of Pogo mice.</P>
Xin, Li‐,Ping,Liang, En‐,Wei,Wei, Jian‐,Yan,Zhang, Bing,Lv, Hou‐,Jun,Zheng, Wei‐,Kang,Urata, Yuji,Im, Myungshin,Wang, Jing,Qiu, Yu‐,Lei,Deng, Jin‐,Song,Huang, Blackwell Publishing Ltd 2011 MONTHLY NOTICES- ROYAL ASTRONOMICAL SOCIETY Vol.410 No.1
<P><B>ABSTRACT</B></P><P>GRB 090426 is a short‐duration burst detected by <I>Swift</I> (<IMG src='/wiley-blackwell_img/equation/MNR_17419_mu1.gif' alt ='inline image'/> s in the observer frame and <IMG src='/wiley-blackwell_img/equation/MNR_17419_mu2.gif' alt ='inline image'/> s in the burst frame at <I>z</I>= 2.609). Its host galaxy properties and some gamma‐ray‐related correlations are analogous to those seen in long‐duration gamma‐ray bursts (GRBs), which are believed to be of a massive star origin (so‐called Type II GRBs). We present the results of its early optical observations with the 0.8‐m Tsinghua University–National Astronomical Observatory of China Telescope (TNT) at Xinglong Observatory and the 1‐m LOAO telescope at Mt Lemmon Optical Astronomy Observatory in Arizona. Our well‐sampled optical afterglow light curve covers from <IMG src='/wiley-blackwell_img/equation/MNR_17419_mu3.gif' alt ='inline image'/> to 10<SUP>4</SUP> s after the GRB trigger. It shows two shallow decay episodes that are likely due to energy injection, which end at <IMG src='/wiley-blackwell_img/equation/MNR_17419_mu4.gif' alt ='inline image'/> and 7100 s, respectively. The decay slopes after the injection phases are consistent with each other (<IMG src='/wiley-blackwell_img/equation/MNR_17419_mu5.gif' alt ='inline image'/>). The X‐ray afterglow light curve appears to trace the optical, although the second energy‐injection phase was missed due to visibility constraints introduced by the <I>Swift</I> orbit. The X‐ray spectral index is <IMG src='/wiley-blackwell_img/equation/MNR_17419_mu6.gif' alt ='inline image'/> without temporal evolution. Its decay slope is consistent with the prediction of the forward shock model. Both X‐ray and optical emission are consistent with being in the same spectral regime above the cooling frequency (<IMG src='/wiley-blackwell_img/equation/MNR_17419_mu7.gif' alt ='inline image'/>). The fact that <IMG src='/wiley-blackwell_img/equation/MNR_17419_mu8.gif' alt ='inline image'/> is below the optical band from the very early epoch of the observation provides a constraint on the burst environment, which is similar to that seen in classical long‐duration GRBs. We therefore suggest that death of a massive star is the possible progenitor of this short burst.</P>
Xiao, Fang,Li, Junhua,Singh, Anurag Kumar,Riederer, Brigitte,Wang, Jiang,Sultan, Ayesha,Park, Henry,Lee, Min Goo,Lamprecht, Georg,Scholte, Bob J.,De Jonge, Hugo R.,Seidler, Ursula Blackwell Publishing Ltd 2012 The Journal of physiology Vol.590 No.21
<P><B>Key points</B></P><P><P>Cystic fibrosis (CF) is a lethal disease characterized by low rates of epithelial Cl<SUP>−</SUP> and HCO<SUB>3</SUB><SUP>−</SUP> secretion and obstruction of the airways and gastrointestinal and reproductive organs by sticky mucus. HCO<SUB>3</SUB><SUP>−</SUP> secretion has recently been demonstrated to be necessary for mucus hydration.</P><P>The most frequent CF mutation is F508del. This mutant protein is usually degraded in the proteasome. New therapeutic strategies have been developed which deliver F508del to the plasma membrane.</P><P>Utilizing transgenic F508del mutant and cystic fibrosis transmembrane conductance regulator (CFTR) knockout mice, apical membrane expression of F508del protein was found to be associated with enhanced stimulation of intestinal HCO<SUB>3</SUB><SUP>−</SUP> secretion.</P><P>The predominant molecular mechanism for enhanced F508del HCO<SUB>3</SUB><SUP>−</SUP> stimulation appeared to be the activation of a Cl<SUP>−</SUP> recycling pathway, with Cl<SUP>−</SUP> exit via membrane‐resident F508del protein and Cl<SUP>−</SUP> entry in exchange for HCO<SUB>3</SUB><SUP>−</SUP> by apical Cl<SUP>−</SUP>/HCO<SUB>3</SUB><SUP>−</SUP> exchange. In contrast, the predominant molecular mechanism for cAMP‐activated HCO<SUB>3</SUB><SUP>−</SUP> secretion in WT intestine appears to be HCO<SUB>3</SUB><SUP>−</SUP> exit via CFTR itself.</P></P><P><B>Abstract </B> This study investigated whether expression of the common cystic fibrosis transmembrane conductance regulator (CFTR) mutant F508del in the apical membrane of enterocytes confers increased bicarbonate secretory capacity on the intestinal epithelium of F508del mutant mice compared to that of CFTR knockout (KO) mice. CFTR KO mice, F508del mutant mice (F508del) and wild‐type (WT) littermates were bred on the FVB/N background. F508del isolated brush border membrane (BBM) contained approximately 5–10% fully glycosylated band C protein compared to WT BBM. Similarly, the forskolin (FSK)‐induced, CFTR‐dependent short‐circuit current (Δ<I>I</I><SUB>sc</SUB>) of F508del mucosa was approximately 5–10% of WT, whereas the HCO<SUB>3</SUB><SUP>−</SUP> secretory response (<IMG src='/wiley-blackwell_img/equation/TJP_5291_mu1.gif' alt ='inline image'/>) was almost half that of WT in both duodenum and mid‐colon studied <I>in vitro</I> and <I>in vivo.</I> While WT intestine retained full FSK‐induced <IMG src='/wiley-blackwell_img/equation/TJP_5291_mu2.gif' alt ='inline image'/> in the absence of luminal Cl<SUP>−</SUP>, the markedly higher <IMG src='/wiley-blackwell_img/equation/TJP_5291_mu3.gif' alt ='inline image'/> than Δ<I>I</I><SUB>sc</SUB> in F508del intestine was dependent on the presence of luminal Cl<SUP>−</SUP>, and was blocked by CFTR inhibitors. The Ste20‐related proline–alanine‐rich kinases (SPAK/OSR1), which are downstream of the with‐no‐lysine (K) protein kinases (WNK), were rapidly phosphorylated by FSK in WT and F508del, but significantly more slowly in CFTR KO intestine. In conclusion, the data demonstrate that low levels of F508del membrane expression in the intestine of F508del mice significantly increased FSK‐induced HCO<SUB>3</SUB><SUP>−</SUP> secretion mediated by Cl<SUP>−</SUP>/HCO<SUB>3</SUB><SUP>−</SUP> exchange. However, in WT mucosa FSK elicited strong SPAK/OSR1 phosphorylation and Cl<SUP>−</SUP>‐independent HCO<SUB>3</SUB><SUP>−</SUP> efflux. This suggests that therapeutic strategies which deliver F508del to the apical membrane have the potential to significantly enhance epithelial HCO<SUB>3</SUB><SUP>−</SUP> secretion.</P>
<P>Summary. </P><P><I>Background:</I> Doxorubicin (DOX) is a widely used anticancer drug for solid tumors and hematologic malignancy, but its active use is hampered by serious adverse effects, including thrombocytopenia. Although bone marrow toxicity of DOX has been suggested to be the sole mechanism underlying the reduced platelet counts, the direct effects of DOX on platelets have never been examined. <I>Objective:</I> Here, we investigated the DOX-induced platelet cytotoxicity and its underlying mechanism in an effort to elucidate the contribution of platelet cytotoxicity to DOX-induced thrombocytopenia. <I>Results:</I> In freshly isolated human platelets, DOX induced platelet cytotoxicity in a time-dependent and concentration-dependent manner. Reactive oxygen species (ROS) generation, decreased glutathione levels and subsequent protein thiol depletion were shown to underlie the DOX-induced platelet cytotoxicity. Conspicuously, DOX-treated platelets displayed apoptotic features such as caspase-3 activation, reduced mitochondrial transmembrane potential, and phosphatidylserine exposure. Decreased glutathiolation of procaspase-3 was shown to be a link between protein thiol depletion and caspase-3 activation. It is of note that DOX-mediated platelet cytotoxicity was significantly enhanced by shear stress, a common complicating factor in cancer patients. These <I>in vitro</I> results were further confirmed by an <I>in vivo</I> animal model, where administration of DOX induced a platelet count decrease, ROS generation, caspase-3 activation, protein thiol depletion, and damaged platelet integrity. <I>Conclusion:</I> We demonstrated that DOX can directly induce platelet cytotoxicity through ROS generation, decreased glutathione levels, and protein thiol depletion. We believe that this study provides important evidence for the role of DOX-induced platelet cytotoxicity in the development of thrombocytopenia in DOX-treated patients.</P>
<P>Adenoids are known as immunosecretory organs and those in atopic children present cellular and cytokine profiles different from those of non-atopic children. We hypothesized that locally produced total IgE and allergen-specific antibodies could be involved in the inflammatory responses in adenoid tissue. Local productions of total IgE and <I>Dermatophagoides pteronyssinus</I> (DP)-specific IgE, IgA, IgG1, and IgG4 antibodies were evaluated, as well as their relationships with the markers of allergic inflammation within adenoid tissue. Eighteen atopic subjects, who were sensitized to more than one common aeroallergen, and 22 non-atopic subjects undergoing adenotonsillectomy, were recruited. Immunoassays using adenoid tissue homogenate were performed to quantify the levels of total IgE, eosinophil cationic protein (ECP), and mast cell tryptase. DP-specific IgE, IgA, IgG1, and IgG4 antibodies, soluble IL-2 receptors (sIL-2R), soluble CD23 (sCD23), and IL-6 were measured by ELISA. All parameters measured in adenoid tissue homogenate were presented as a ratio to the albumin level found in the adenoid. Median level of total IgE in adenoid tissue homogenate was significantly higher in atopic individuals than in non-atopic individuals. Median values of DP-specific IgE and IgA antibodies were significantly higher in atopics than in non-atopics (p<I> </I>= 0.001, p<I> </I>= 0.006, respectively), while no differences were seen in DP-specific IgG1 and IgG4 antibodies. ECP and sCD23 levels in adenoid homogenate were significantly higher in atopics than in non-atopics (p<I> </I>= 0.026, p<I> </I>= 0.048, respectively), while no significant differences were noted in tryptase, sIL-2R, and IL-6 levels. The levels of DP-specific IgE, IgA, IgG1, and IgG4 antibodies in adenoid homogenate correlated significantly with ECP levels, but not with those of sIL-2R, sCD23, and IL-6. The presence of total IgE and DP-specific antibodies in adenoid tissue was confirmed to be more prominent in atopics. In conclusion, locally-produced total IgE and DP-specific antibodies may contribute to eosinophilic inflammation in adenoid tissue in atopic children.</P>
<P>Abstract</P><P>The sea squirt <I>Halocynthia roretzi</I> is an important marine food resource species that is found in the waters around Korea. We describe the isolation and characterization of 13 new polymorphic microsatellite loci in 96 sea squirt samples that were collected from the marine environment of Samcheok on the east coast of Korea. The number of alleles that were observed for each locus ranged from six to 32, and the value of expected and observed heterozygosities was 0.504–0.922 and 0.396–0.813, respectively. These markers will be useful tools for future population studies.</P>
<P>Abstract</P><P>To understand the deformation mechanism and seismic anisotropy in the uppermost mantle beneath Spitsbergen, Svalbard, in the Arctic, the deformation microstructures of olivine in the peridotite of Spitsbergen were studied. Seismic anisotropy in the upper mantle can be explained mainly by the lattice-preferred orientation (LPO) of olivine. The LPOs of the olivine in the peridotites were determined using electron backscattered diffraction patterns. Eight specimens out of 10 showed that the  axis of the olivine was aligned subparallel to the lineation and that the (010) plane was subparallel to the foliation, showing a type A LPO. In the other two specimens the  axis of olivine was aligned subparallel to the lineation and both the  and  axes were distributed in a girdle nearly perpendicular to the lineation, showing a type D LPO. The dislocation density of the olivine in the samples showing a type D LPO was higher than that in the samples showing a type A LPO. The result of an Fourier transformation infrared study showed that both the types A and D samples were dry. These observations were in good agreement with a previous experimental study (<I>Tectonophysics</I>, <B>421</B>, 2006, 1): samples showing a type D LPO for olivine were observed at a high stress condition and samples showing both types A and D LPO were deformed under dry condition. Observations of both strong LPOs and dislocations of olivine indicate that the peridotites studied were deformed by dislocation creep. The seismic anisotropy calculated from the LPOs of the olivine could be used to explain the seismic anisotropy of <I>P</I>- and <I>S</I>-waves in the lithospheric mantle beneath Spitsbergen, Svalbard.</P>
<P>Summary</P><P>Objective: </P><P>Although the pathogenesis of aspirin-induced urticaria (AIU) is not fully understood, mast cell activation has been noted in patients with AIU. Tumour necrosis factor (TNF)-&agr;, a potent pro-inflammatory cytokine, is released by human skin mast cells and other inflammatory cells in patients with urticaria. To investigate the role of TNF-&agr; promoter polymorphisms in the development of AIU, we performed an association study of TNF-&agr; promoter polymorphisms with AIU phenotype.</P><P>Methods: </P><P>Two hundred thirty-nine patients with AIU consisting of 120 patients with aspirin intolerant chronic urticaria (AICU) and 119 with aspirin-intolerant acute urticaria (AIAU), and 524 normal controls were enrolled. AIU was confirmed by oral aspirin challenge test. Five SNPs in the TNF-&agr; gene (-1031T>C, -863C>A, -857C>T, -308G>A, -238G>A) were genotyped by a single-base extension method. Haplotype analyses were done.</P><P>Results: </P><P>The genotype frequencies of TNF-1031T>C and TNF-863C>A were significantly higher in the AIU patients than in the normal controls in both co-dominant (<I>P </I>= 0·014, <I>P </I>= 0·007) and dominant (<I>P </I>= 0·007, <I>P </I>= 0·004) models. The frequency of <I>TNF-ht2[CACGG]</I> containing a genotype in the AIU group was significantly higher in the normal controls with both co-dominant (<I>P </I>= 0·004, <I>Pc </I>= 0·02) and dominant models (<I>P </I>= 0·002, <I>Pc </I>= 0·01).</P><P>Conclusions: </P><P>These findings suggest that the two promoter polymorphisms of TNF-&agr; at -1031T>C and -863C>A may contribute to the development of AIU.</P>
<P>Abstract</P><P>Objective </P><P>Recent reports have demonstrated that mesenchymal stem cells (MSCs) can modulate/suppress immunologic responses through interactions with different immune cells. We performed this study in order to investigate the immunomodulatory effects of MSCs in corneal xenotransplantation.</P><P>Animals studied </P><P>Pig and rat.</P><P>Procedures </P><P>We orthotopically transplanted pig corneas into rats and topically applied allogeneic rat MSCs to the corneas for 2 h immediately after transplantation. Graft survival was clinically assessed using slit-lamp biomicroscopy and the median survival time (MST) was calculated. The rejected grafts were histologically examined using antibodies against CD4, CD8, CD161, and CD68. The expression of IL-2, IL-6, IL-10, and IFN-&ggr; was also evaluated in the rejected grafts using an enzyme-linked immunosorbent assay.</P><P>Results </P><P>The survival of corneal xenografts was not significantly prolonged by MSC application (MST 10.5 days) compared with the controls (MST 9.67 days) (<I>P</I> = 0.4189). Histologically, the rejected grafts in both groups were massively infiltrated with neutrophils and macrophages. Some CD8<SUP>+</SUP> T cells and rare NK cells were found in the rejected grafts. The levels of IL-6 and IL-10 were significantly increased in the rejected grafts from MSC-treated rats compared with the grafts from MSC-untreated rats. However, the levels of IL-2 and IFN-&ggr; were not different between the two groups.</P><P>Conclusions </P><P>Topical application of allogeneic rat MSCs was ineffective in prolonging corneal xenograft survival in a pig-to-rat model.</P>
<P>Abstract – </P><P>Objective </P><P>The aim of this study was to assess the association of chewing ability to oral health-related quality of life (OHRQoL) measured by the Oral Health Impact Profile-14 (OHIP-14) controlling for clinical oral health status, self-reported health status, demographic factors, and socioeconomic conditions among community-dwelling and institutionalized Korean elders.</P><P>Methods </P><P>This cross-sectional study comprised a sample of 307 community-dwelling and 102 institutionalized people over the age of 60, using a cluster sampling procedure. A questionnaire was implemented and a clinical oral examination was completed for each subject. The outcome variable of interest was the OHIP-14 score, and its associations with chewing ability, objective oral health status, self-reported health status, demographic factors, and socioeconomic conditions were assessed. Because of highly-skewed distribution of the OHIP-14 scores, nonparametric analytic methods were used. The final model was developed using a multivariable two-level logistic regression model for a dichotomized OHIP-14 score to account for the cluster sampling method applied to this study.</P><P>Results </P><P>The mean age of the participants was 75.4 years, with 67.7% being women. The median OHIP-14 score was 7. Negative oral health impacts were experienced fairly often or very often by a total of 36.4% of elderly. In the final model, elders who could chew none to three and four to six foods among seven indicator foods were 3.4 (<I>P</I> = 0.010) and 2.0 (<I>P</I> = 0.040) times more likely, respectively, to have worse OHRQoL compared with elders who could chew all seven food types. Also significant associations with worse OHRQoL were shown for being concerned about oral health [Odds Ratio (OR) = 4.9, <I>P</I> = 0.002], fair or better self-reported oral health (OR = 0.12, <I>P</I> = 0.002), very good/good self-reported general health (OR = 0.38, <I>P</I> = 0.008), being married (OR = 2.0, <I>P</I> = 0.054), and having a favourable economic status (OR = 0.43, <I>P</I> = 0.042).</P><P>Conclusions </P><P>This study showed highly significant association between chewing ability and OHRQoL measured by the OHIP-14 score after controlling for related factors. Amelioration of chewing ability might independently contribute to improving the OHRQoL of elders.</P>