bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased hippocampal neurogenesis in the progressive stage of Alzheimer's disease phenotype in an APP/PS1 double transgenic mouse model
Authors: Yu Yingxin , He Jue , Zhang Yanbo , Luo Huanmin , Zhu Shenghua , Yang Yi , Zhao Tou , Wu Jiang , Huang Yuangui , Kong Jiming , Tan Qingrong , Li Xin‐Min 
Published: March 2009

AbstractAlzheimer's disease (AD) is a progressive neurodegenerative disease associated with senile β‐amyloid (Aβ) plaques and cognitive decline. Neurogenesis in the adult hippocampus is implicated in regulating learning and memory, and is increased in human postmortem brain of AD patients. However, little is currently known about the changes of hippocampal neurogenesis in the progression of AD. As brain tissues from patients during the progression of AD are generally not available, an amyloid precursor protein (APP)/presenilin1 (PS1) double transgenic mouse model of AD was studied. Bromodeoxyuridine (BrdU) labeling supported by doublecortin staining was used to detect proliferating hippocampal cells in the mice. Compared with age‐matched wild‐type controls, 9‐month‐old transgenic mice with memory impairment and numerous brain Aβ deposits showed increased numbers of proliferating hippocampal cells. However, 3‐month‐old transgenic mice with normal memory and subtle brain Aβ deposits showed normal hippocampal proliferation. Double immunofluorescent labeling with BrdU and either NeuN or glial fibrillary acidic protein was conducted in mice at 10 months (28 days after the last BrdU injection) to determine the differentiation of proliferating cells. The number of hippocampal BrdU‐positive cells and BrdU‐positive cells differentiating into neurons (neurogenesis) in 10‐month‐old mice was greater in transgenic mice compared with age‐matched controls, but the ratio of hippocampal BrdU‐positive cells differentiating into neurons and astroglia was comparable. These results suggest hippocampal neurogenesis may increase during the progression of AD. Targeting this change in neurogenesis and understanding the underlying mechanism could lead to the development of a new treatment to control the progression of AD. © 2009 Wiley‐Liss, Inc.
Long‐term treadmill exposure protects against age‐related neurodegenerative change in the rat hippocampus
Authors: O'Callaghan Rachel M. , Griffin Éadaoin W. , Kelly Áine M. 
Published: March 2009

AbstractThe potential of exercise or environmental enrichment to prevent or reverse age‐related cognitive decline in rats has been widely investigated. The data suggest that the efficacy of these interventions as neuroprotectants may depend upon the duration and nature of the protocols and age of onset. Investigations of the mechanisms underlying these neuroprotective strategies indicate a potential role for the neurotrophin family of proteins, including nerve growth factor (NGF) and brain‐derived neurotrophic factor (BDNF). In this study, we have assessed the effects of 8 months of forced exercise, begun in middle‐age, on the expression of long‐term potentiation (LTP) and on spatial learning in the Morris water maze in aged Wistar rats. We also assessed these measures in a cage control group and in a group of rats exposed to the stationary treadmill for the same duration as the exercised rats. Our data confirm an age‐related decline in expression of LTP and in spatial learning concomitant with decreased expression of NGF and BDNF mRNA in dentate gyrus (DG). The age‐related impairments in both plasticity and growth factor expression were prevented in the long‐term exercised group and, surprisingly, the treadmill control group. Given the extensive handling that the treadmill control group received and their regular exposure to an environment outside the home cage, this group can be considered to have experienced environmentally enriched conditions when compared with the cage control group. Significant correlations were observed between both learning and LTP and the expression of NGF and BDNF mRNA in the dentate gyrus. We conclude that decreased expression of NGF and BDNF in the dentate gyrus of aged rats is associated with impaired LTP and spatial learning. We suggest that the reversal of these age‐related impairments by enrichment and exercise may be linked with prevention of the age‐related decline in expression of these growth factors and, furthermore, that enrichment is as efficacious as exercise in preventing this age‐related decline. © 2009 Wiley‐Liss, Inc.
Decreased neuronal differentiation of newly generated cells underlies reduced hippocampal neurogenesis in chronic temporal lobe epilepsy
Authors: Hattiangady Bharathi , Shetty Ashok K. 
Published: March 2009

AbstractHippocampal neurogenesis declines substantially in chronic temporal lobe epilepsy (TLE). However, it is unclear whether this decline is linked to altered production of new cells and/or diminished survival and neuronal fate‐choice decision of newly born cells. We quantified different components of hippocampal neurogenesis in rats exhibiting chronic TLE. Through intraperitoneal administration of 5′‐bromodeoxyuridine (BrdU) for 12 days, we measured numbers of newly born cells in the subgranular zone‐granule cell layer (SGZ‐GCL) at 24 h and 2.5 months post‐BrdU administration. Furthermore, the differentiation of newly added cells into neurons and glia was quantified via dual immunofluorescence for BrdU and various markers of neurons and glia. Addition of new cells to the SGZ‐GCL over 12 days was comparable between the chronically epileptic hippocampus and the age‐matched intact hippocampus. Furthermore, comparison of BrdU+ cells measured at 24 h and 2.5 months post‐BrdU administration revealed similar survival of newly born cells between the two groups. However, only 4–5% of newly born cells (i.e., BrdU+ cells) differentiated into neurons in the chronically epileptic hippocampus, in comparison to 73–80% of such cells exhibiting neuronal differentiation in the intact hippocampus. Moreover, differentiation of newly born cells into S‐100β+ astrocytes or NG2+ oligodendrocyte progenitors increased to ∼79% in the chronically epileptic hippocampus from ∼25% observed in the intact hippocampus. Interestingly, the extent of proliferation of astrocytes and microglia (identified through Ki‐67 and S‐100β and Ki‐67 and OX‐42 dual immunofluorescence) in the SGZ‐GCL was similar between the chronically epileptic hippocampus and the age‐matched intact hippocampus, implying that the proliferation of neural stem/progenitor cells in the SGZ‐GCL of the chronically epileptic hippocampus was not obscured by an increased division of glia. Thus, severely diminished DG neurogenesis in chronic TLE is not associated with either decreased production of new cells or reduced survival of newly born cells in the SGZ‐GCL. Rather, it is linked to a dramatic decline in the neuronal fate‐choice decision of newly generated cells. Overall, the differentiation of newly born cells turns mainly into glia with chronic TLE from predominantly neuronal differentiation seen in control conditions. © 2009 Wiley‐Liss, Inc.
5‐HT1Aand NMDA receptors interact in the rat medial septum and modulate hippocampal‐dependent spatial learning
Authors: Elvander‐Tottie Elin , Eriksson Therese M. , Sandin Johan , Ögren Sven Ove 
Published: March 2009

AbstractCholinergic and GABAergic neurons in the medial septum/vertical limb of the diagonal band of Broca (MS/vDB) projecting to the hippocampus, constitute the septohippocampal projection, which is important for hippocampal‐dependent learning and memory. There is also evidence for an extrinsic as well as an intrinsic glutamatergic network within the MS/vDB. GABAergic and cholinergic septohippocampal neurons express the serotonergic 5‐HT1Areceptor and most likely also glutamatergic NMDA receptors. The aim of the present study was to examine whether septal 5‐HT1Areceptors are important for hippocampal‐dependent long‐term memory and whether these receptors interact with glutamatergic NMDA receptor transmission in a manner important for hippocampal‐dependent spatial memory. Intraseptal infusion of the 5‐HT1Areceptor agonist (R)‐8‐OH‐DPAT (1 or 4 μg/rat) did not affect spatial learning in the water maze task but impaired emotional memory in the passive avoidance task at the higher dose tested (4 μg/rat). While intraseptal administration of (R)‐8‐OH‐DPAT (4 μg) combined with a subthreshold dose of the NMDA receptor antagonist D‐AP5 (1 μg) only marginally affected spatial acquisition, it produced a profound impairment in spatial memory. In conclusion, septal 5‐HT1Areceptors appears to play a more prominent role in emotional than in spatial memory. Importantly, septal 5‐HT1Aand NMDA receptors appear to interact in a manner, which is particularly critical for the expression or retrieval of hippocampal‐dependent long‐term spatial memory. It is proposed that NMDA receptor hypofunction in the septal area may unmask a negative effect of 5‐HT1Areceptor activation on memory, which may be clinically relevant. © 2009 Wiley‐Liss, Inc.
Histone marks and chromatin remodelers on the regulation of neurogenin1 gene in RA induced neuronal differentiation of P19 cells
Authors: Wu Meng , Zhang Ye , Wu Ning‐hua , Shen Yu‐fei 
Published: March 2009

AbstractNeurogenin1 is an important bHLH protein that plays crucial role in neurogenesis. We first show that the expression of ngn1 increases drastically in RA induced neuronal differentiation. During which, a three successive stages of the epigenetic changes surrounding the ngn1 gene are found correlated with a repression to activation of the gene in P19 cells. Recruiting of a repressive histone code H3K27me3 on the ngn1 gene is the dominant change in first repression stage, which is followed by the binding of the active codes of H3K9ac, H3K14ac, and the H3K4me3 in the second and third stages of RA treatment. Additionally, BRM but not BRG1 is specifically recruited to ngn1 gene at the third stage and is positively involved in the RA induced ngn1 expression. We propose that histone modifiers and chromatin remodelers are pivotal in the activation of the ngn1 gene in RA induced differentiation of P19 cells. J. Cell. Biochem. 107: 264–271, 2009. © 2009 Wiley‐Liss, Inc.
The SUMO‐E3 ligase PIAS3 targets pyruvate kinase M2
Authors: Spoden Gilles A. , Morandell Dieter , Ehehalt Daniela , Fiedler Marc , Jansen‐Dürr Pidder , Hermann Martin , Zwerschke Werner 
Published: March 2009

AbstractPyruvate kinase M2 (M2‐PK) controls the rate‐limiting step at the end of the glycolytic pathway in normal proliferating and tumor cells. Other functions of M2‐PK in addition to its role in glycolysis are little understood. The aim of this study was to identify new cellular interaction partners of M2‐PK in order to discover novel links between M2‐PK and cellular functions. Here we show that the SUMO‐E3 ligase protein PIAS3 (inhibitor of activated STAT3) physically interacts with M2‐PK and its isoenzyme M1‐PK. Moreover, we demonstrate that endogenous SUMO‐1‐M2‐PK conjugates exist in mammalian cells. Furthermore, we show that transient expression of PIAS3 but not the RING domain mutant PIAS3 (C299S, H301A) is consistent with nuclear localization of M2‐PK and PIAS3 and M2‐PK partially co‐localize in the nucleus of these cells. This study suggests a link between PIAS3 and nuclear pyruvate kinase. J. Cell. Biochem. 107: 293–302, 2009. © 2009 Wiley‐Liss, Inc.
Control mechanisms of differential translation of Hsp90 isoforms in 9L rat gliosarcoma cells
Authors: Lo Chih‐Wei , Chang Yuo‐Sheng , Chao Chih‐Chung , Chang Margaret Dah‐Tsyr , Chang Kun‐Che , Lai Yiu‐Kay 
Published: March 2009

AbstractAlthough the differential expression of heat shcok proteins, Hsp90α and Hsp90β was extensively studied in many kinds of cells, the post‐transcriptional regulation of Hsp90 isoforms remains unclear. In control and GA‐treated rat gliosarcoma cells, it has been reported that the translational efficiency of hsp90α is higher than hsp90β. In this study, we present evidences identifying the roles for leaky scanning and 5′‐UTR sequence in translational regulation of Hsp90β. The result of in vitro transcription and translation (IVTT) experiment showed that hsp90α exhibited higher translation efficiency than hsp90β. Sequence analysis revealed that there is an out‐of‐frame downstream AUG codon in hsp90β gene. However, elimination of the downstream AUG by site‐directly mutagenesis or introducing Kozak context sequence around the initiator AUG of hsp90β open reading frame increased its translational efficiency, which indicated that leaky scanning might be a possible mechanism regulating hsp90β. Furthermore, we also constructed a firefly luciferase reporter system to verify the effect of subsequent translation at the downstream out‐of‐frame AUG codon in 9L and A549 cells. Furthermore, it is believed that 5′‐untranslated region (5′‐UTR) also plays a significant role in translational control. We showed hsp90β 5′‐UTR gives rise to the reduction of the translation efficiency in IVTT experiment. Additionally, the reductive effect of hsp90β 5′‐UTR was further confirmed by luciferase reporter assay using truncated deletion analyses of 5′‐UTR of hsp90β. Our results support the hypothesis that ribosome leaky scanning mechanism and 5′‐UTR sequence acts as negative regulators in hsp90β mRNA. J. Cell. Biochem. 107: 418–427, 2009. © 2009 Wiley‐Liss, Inc.
Daxx inhibits muscle differentiation by repressing E2A‐mediated transcription
Authors: Gupta Amitabh , Hou Rong , Liu Liming , Hiroyasu Shungo , Hadix Jennifer A. , Huggins Gordon S. , Sibinga Nicholas E.S. 
Published: March 2009

AbstractThe basic helix‐loop‐helix (HLH) E2A transcription factors bind to DNA as homodimers or as heterodimers formed with other basic HLH factors, activate gene expression, and promote differentiation of muscle, lymphoid, neuronal, and other cell types. These E2A functions can be inhibited by the Id proteins, HLH factors that sequester E2A in non‐DNA binding dimers. Here we describe the direct interaction of E2A with Daxx, a broadly expressed non‐HLH protein previously associated with apoptosis and transcriptional repression. Daxx inhibits E2A function, but not via an Id‐like mechanism; rather, it recruits histone deacetylase activity to E2A‐dependent promoters. Increased Daxx expression during muscle differentiation inhibits E2A‐dependent expression of key myogenic genes and reduces myotube formation, while decreased Daxx expression promotes myotube formation. These results identify a new mechanism for limiting E2A activity and establish a link between Daxx‐mediated gene regulation and control of cellular differentiation. J. Cell. Biochem. 107: 438–447, 2009. © 2009 Wiley‐Liss, Inc.
OxLDL upregulates caveolin‐1 expression in macrophages: Role for caveolin‐1 in the adhesion of oxLDL‐treated macrophages to endothelium
Authors: Wu Chau‐Chung , Wang Shu‐Huei , Kuan I.‐I. , Tseng Wei‐Kung , Chen Ming‐Fong , Wu Jiahn‐Chun , Chen Yuh‐Lien 
Published: March 2009

AbstractCaveolin‐1, a principle component of caveolae, is present in several cell types known to play an important role in the development of atherosclerosis. In this study, its distribution and expression were studied in the arterial walls of hypercholesterolemic rabbits and apo‐E‐deficient mice and in oxidized low‐density lipoprotein (oxLDL)‐treated RAW264.7 macrophages. Immunohistochemical studies showed that staining for caveolin‐1 expression was stronger in atherosclerotic lesions in hypercholesterolemic rabbits and apo‐E‐deficient mice compared to normal rabbits and mice and was closely associated with macrophages. OxLDL treatment increased caveolin‐1 protein expression in RAW264.7 macrophages in a time‐ and dose‐dependent manner. The increase in caveolin‐1 expression was dependent on phosphorylation of the mitogen‐activated protein kinases (MAPKs) extracellular signal‐regulated kinase1/2 (ERK1/2), p38, and Jun N‐terminal kinase (JNK) and the transcriptional activation and translocation of nuclear factor‐?B (NF‐κB). OxLDL also induced caveolin‐1 mRNA expression and this effect was not seen in the presence of inhibitors for transcription or de novo protein synthesis. OxLDL increased the adhesion of RAW264.7 macrophages to endothelial cells via an increase in caveolin‐1 expression, and the adhesion was reduced by the use of anti‐caveolin‐1 antibody or caveolin‐1‐specific shRNA. These results show that oxLDL increases caveolin‐1 expression in macrophages through the MAPKs/NF‐κB pathway. The caveolin‐1 levels are closely associated with the adherence of monocytes/macrophages to endothelial cells and their accumulation within the arterial intima after hypercholesterolemia insult, resulting in the progression of atherosclerosis. J. Cell. Biochem. 107: 460–472, 2009. © 2009 Wiley‐Liss, Inc.
How long does a mindfulness‐based stress reduction program need to be? A review of class contact hours and effect sizes for psychological distress
Authors: Carmody James , Baer Ruth A. 
Published: March 2009

AbstractThe mindfulness‐based stress reduction (MBSR) program was designed to be long enough for participants to grasp the principles of self‐regulation through mindfulness and develop skill and autonomy in mindfulness practice. It traditionally consists of 26 hours of session time including eight classes of 2‐1/2 hours and an all‐day class. The circumstances of some groups exclude them from participating in this standard form and a number of trials have evaluated programs with abbreviated class time. If lower program time demands can lead to similar outcomes in psychological functioning, it would support their utility in these settings and might lead to greater participation. However, the effect of variation in class hours on outcomes has not been systematically studied. To obtain preliminary information related to this question we examined effect sizes for psychological outcome variables in published studies of MBSR, some of which had adapted the standard number of class hours. The correlation between mean effect size and number of in‐class hours was nonsignificant for both clinical and nonclinical samples and suggests that adaptations that include less class time may be worthwhile for populations for whom reduction of psychological distress is an important goal and for whom longer time commitment may be a barrier to their ability or willingness to participate. However, the standard MBSR format has accrued the most empirical support for its efficacy and session time may be important to the development of other kinds of program outcomes. The result points to the importance of empirical studies systematically examining this question. © 2009 Wiley Periodicals, Inc. J Clin Psychol 65: 1–12, 2009.
Activation of GABA‐A receptor ameliorates homocysteine‐induced MMP‐9 activation by ERK pathway
Authors: Tyagi Neetu , Gillespie William , Vacek Jonathan C. , Sen Utpal , Tyagi Suresh C. , Lominadze David 
Published: March 2009

AbstractHyperhomocysteinemia (HHcy) is a risk factor for neuroinflammatory and neurodegenerative diseases. Homocysteine (Hcy) induces redox stress, in part, by activating matrix metalloproteinase‐9 (MMP‐9), which degrades the matrix and leads to blood–brain barrier dysfunction. Hcy competitively binds to γ‐aminbutyric acid (GABA) receptors, which are excitatory neurotransmitter receptors. However, the role of GABA‐A receptor in Hcy‐induced cerebrovascular remodeling is not clear. We hypothesized that Hcy causes cerebrovascular remodeling by increasing redox stress and MMP‐9 activity via the extracellular signal‐regulated kinase (ERK) signaling pathway and by inhibition of GABA‐A receptors, thus behaving as an inhibitory neurotransmitter. Hcy‐induced reactive oxygen species production was detected using the fluorescent probe, 2′–7′‐dichlorodihydrofluorescein diacetate. Hcy increased nicotinamide adenine dinucleotide phosphate‐oxidase‐4 concomitantly suppressing thioredoxin. Hcy caused activation of MMP‐9, measured by gelatin zymography. The GABA‐A receptor agonist, muscimol ameliorated the Hcy‐mediated MMP‐9 activation. In parallel, Hcy caused phosphorylation of ERK and selectively decreased levels of tissue inhibitors of metalloproteinase‐4 (TIMP‐4). Treatment of the endothelial cell with muscimol restored the levels of TIMP‐4 to the levels in control group. Hcy induced expression of iNOS and decreased eNOS expression, which lead to a decreased NO bioavailability. Furthermore muscimol attenuated Hcy‐induced MMP‐9 via ERK signaling pathway. These results suggest that Hcy competes with GABA‐A receptors, inducing the oxidative stress transduction pathway and leading to ERK activation. J. Cell. Physiol. 220: 257–266, 2009. © 2009 Wiley‐Liss, Inc.
Circle graph obstructions under pivoting
Authors: Geelen Jim , Oum Sang‐il 
Published: March 2009

AbstractA circle graph is the intersection graph of a set of chords of a circle. The class of circle graphs is closed under pivot‐minors. We determine the pivot‐minor‐minimal non‐circle‐graphs; there are 15 obstructions. These obstructions are found, by computer search, as a corollary to Bouchet's characterization of circle graphs under local complementation. Our characterization generalizes Kuratowski's Theorem. © 2009 Wiley Periodicals, Inc. J Graph Theory 61: 1‐11, 2009
Proper path‐factors and interval edge‐coloring of (3,4)‐biregular bigraphs
Authors: Asratian Armen S. , Casselgren Carl Johan , Vandenbussche Jennifer , West Douglas B. 
Published: March 2009

AbstractAn interval coloring of a graph G is a proper coloring of E(G) by positive integers such that the colors on the edges incident to any vertex are consecutive. A (3,4)‐biregular bigraph is a bipartite graph in which each vertex of one part has degree 3 and each vertex of the other has degree 4; it is unknown whether these all have interval colorings. We prove that G has an interval coloring using 6 colors when G is a (3,4)‐biregular bigraph having a spanning subgraph whose components are paths with endpoints at 3‐valent vertices and lengths in {2, 4, 6, 8}. We provide several sufficient conditions for the existence of such a subgraph. © 2009 Wiley Periodicals, Inc. J Graph Theory
On graphs with a given endomorphism monoid
Authors: Koubek Václav , Rödl Vojtěch , Shemmer Benjamin 
Published: March 2009

AbstractHedrlín and Pultr proved that for any monoid M there exists a graph G with endomorphism monoid isomorphic to M. In this paper we give a construction G(M) for a graph with prescribed endomorphism monoid M. Using this construction we derive bounds on the minimum number of vertices and edges required to produce a graph with a given endomorphism monoid for various classes of finite monoids. For example we show that for every monoid M, |M|=m there is a graph G with End(G)≃M and |E(G)|≤(1 + 0(1))m2. This is, up to a factor of 1/2, best possible since there are monoids requiring a graph with \documentclass{article}\footskip=0pc\pagestyle{empty}\begin{document}\begin{eqnarray*} && \frac{m^{2}}{2}(1 -0(1)) \end{eqnarray*}\end{document} edges.We state bounds for the class of all monoids as well as for certain subclasses—groups, k‐cancellative monoids, commutative 3‐nilpotent monoids, rectangular groups and completely simple monoids. © 2009 Wiley Periodicals, Inc. J Graph Theory 62, 241–262, 2009