bluuebunny/crossref_metadata_2025_split huggingface dataset:
How hippocampus and cortex contribute to recognition memory: Revisiting the complementary learning systems model
Authors: Norman Kenneth A. 
Published: September 2010

AbstractWe describe how the Complementary Learning Systems neural network model of recognition memory (Norman and O'Reilly (2003) Psychol Rev 104:611–646) can shed light on current debates regarding hippocampal and cortical contributions to recognition memory. We review simulation results illustrating three critical differences in how (according to the model) hippocampus and cortex contribute to recognition memory, all of which derive from the hippocampus' use of pattern separated representations. Pattern separation makes the hippocampus especially well‐suited for discriminating between studied items and related lures; it makes the hippocampus especially poorly suited for computing global match; and it imbues the hippocampal ROC curve with a Y‐intercept > 0. We also describe a key boundary condition on these differences: When the average level of similarity between items in an experiment is very high, hippocampal pattern separation can fail, at which point the hippocampal model will start to behave like the cortical model. We describe the implications of these simulation results for extant debates over how to describe hippocampal versus cortical contributions and how to measure these contributions. © 2010 Wiley‐Liss, Inc.
Spatial learning deficits in mice lacking A‐type K+ channel subunits
Authors: Lockridge Amber , Yuan Li‐Lian 
Published: September 2010

AbstractKv4.2‐mediated A‐type K+ channels in dendrites act to dampen back‐propagating action potentials, constrain coincidence detection, and modify synaptic properties. Because of naturally high concentrations in the hippocampus, genetic deletion of this protein results in enhanced CA1 dendritic excitability and a broader signal integration time window with potential implications for spatial learning. In this investigation, we tested Kv4.2 knockout mice in the Morris water maze to assess their spatial reference acquisition and recall abilities. These mice demonstrated prolonged latencies and pathlength to reach a hidden platform during learning trials that was correlated to a decreased use of spatial search strategies in favor of repetitive looping. Knockout mice also showed no preference for target areas in recall‐based probe trials but were less impaired by a switch in the platform location at the start of reversal learning. We discuss the possibility that these behavior discrepancies may be attributable to an enhancement in synaptic plasticity and loss of selectivity among synaptic pathways bearing different information into the CA1 region. © 2010 Wiley Periodicals, Inc.
Heat transfer augmentation in a plate‐fin heat exchanger using a rectangular winglet
Authors: Gupta Munish , Kasana K.S. , Vasudevan R. 
Published: September 2010

AbstractThis study presents numerical computation results on laminar convection heat transfer in a plate‐fin heat exchanger, with triangular fins between the plates of a plate‐fin heat exchanger. The rectangular winglet type vortex generator is mounted on these triangular fins. The performance of the vortex generator is evaluated for varying angles of attack of the winglet i.e., 20, 26, and 37° and Reynolds number 100, 150, and 200. The computations are also performed by varying the geometrical size and location of the winglet. The complete Navier–Stokes equation and the energy equation are solved by the (Marker and Cell) MAC algorithm using the staggered grid arrangement. The constant wall temperature thermal boundary conditions are considered. Air is taken as the working fluid. The heat transfer enhancement is seen by introducing the vortex generator. Numerical results show that the average Nusselt number increases with an increase in the angle of attack and Reynolds number. For the same area of the LVG, the increase in length of the LVG brings more heat transfer enhancement than increasing the height. The increase in heat transfer comes with a moderate pressure drop penalty. © 2010 Wiley Periodicals, Inc. Heat Trans Asian Res; Published online in Wiley Online Library (wileyonlinelibrary.com). DOI 10.1002/htj.20318
Characteristics of heat transfer inside a tube during sodium‐water reaction in a FBR steam generator
Authors: Kurihara Akikazu , Ohshima Hiroyuki , Monde Masanori 
Published: September 2010

AbstractSodium reacts chemically with water in the case of an unexpected tube failure of a steam generator (SG) in a fast breeder reactor (FBR). In order to predict the event with high accuracy, it is very important to understand the characteristics of heat transfer inside the tube in detail during the tube failure due to the sodium–water reaction. Experiments were performed by using purified water under the following conditions: initial pressure of 11.2–13.4 MPa, initial water temperature of 200 °C, and water mass flux of 45.7 to 3630 kg/(m2s). The test tube was heated rapidly by high‐frequency induction current. The time averaged heat flux was estimated by using an inverse solution from the measured temperatures at two points on three different locations along the tube. It was confirmed that the derived values agreed with the measured heat fluxes on the outer surface within 20% accuracy. It was found that the characteristics of the heat transfer strongly depend on the flow rate. The heat transfer on the wall changed from nucleate boiling to transient‐film boiling during increasing the heat flux and returned to the nucleate boiling during decreasing the heat flux. A counterclockwise cycle always appeared in the transition boiling region, where the nucleate and film boiling coexisted and the area ratio of these varied with time. The adequacy of heat transfer correlations to evaluate tube overheating was confirmed. © 2010 Wiley Periodicals, Inc. Heat Trans Asian Res; Published online in Wiley Online Library (wileyonlinelibrary.com). DOI 10.1002/htj.20320
LAPTM4B overexpression is a novel predictor of epithelial ovarian carcinoma metastasis
Authors: Yin Mingzhu , Xu Ye , Lou Ge , Hou Yan , Meng Fanling , Zhang Haiyu , Li Cong , Zhou Rouli 
Published: September 2010

AbstractLAPTM4B is a novel tumor‐associated gene. To date, there have been no published data regarding the role of LAPTM4B expression in epithelial ovarian carcinoma metastasis. Therefore, this study was performed to determine whether LAPTM4B overexpression is a new predictor of epithelial ovarian carcinoma metastasis. LAPTM4B expression was evaluated in 22 normal ovarian specimens and 139 ovarian carcinomas by western blotting analyses and immunohistochemistry. Univariate and multivariate analyses were used to determine the association between LAPTM4B expression and epithelial ovarian carcinoma metastasis. Western blotting analysis demonstrated that LAPTM4B was overexpressed in metastatic tissues from patients with ovarian cancers, and immunohistochemistry results revealed that among 59 patients with LAPTM4B overexpression, 57 (96.6%) presented intraperitoneal metastasis and 31 (52.5%) had lymph node metastasis. The results of the univariate and multivariate analyses demonstrated that LAPTM4B overexpression correlated with metastasis. The odds ratio of high‐to‐low expression for intraperitoneal metastasis was 11.410 (95% CI: 2.357, 55.239) and that for lymph node metastasis was 6.332 (95% CI: 2.533, 15.831). For intraperitoneal metastasis, the sensitivity and specificity of LAPTM4B overexpression were 48.7% and 90.9%; for lymph node metastasis, they were 73.8%% and 71.1%, respectively. LAPTM4B overexpression is a new predictor of epithelial ovarian carcinoma metastasis and an important potential biomarker for the early diagnosis of ovarian carcinoma.
TNF‐α increases αvβ3 integrin expression and migration in human chondrosarcoma cells
Authors: Hou Chun‐Han , Yang Rong‐Sen , Hou Sheng‐Mou , Tang Chih‐Hsin 
Published: September 2010

AbstractChondrosarcoma is a type of highly malignant tumour with a potent capacity to invade locally and cause distant metastasis. Chondrosarcoma shows a predilection for metastasis to the lungs. Tumour necrosis factor (TNF)‐α is a key cytokine involved in inflammation, immunity, cellular homeostasis and tumour progression. Integrins are the major adhesive molecules in mammalian cells and have been associated with metastasis of cancer cells. However, the effects of TNF‐α in migration and integrin expression in chondrosarcoma cells are largely unknown. In this study, we found that TNF‐α increased the migration and the expression of αvβ3 integrin in human chondrosarcoma cells. Activations of MAPK kinase (MEK), extracellular signal‐regulating kinase (ERK) and nuclear factor‐κB (NF‐κB) pathways after TNF‐α treatment were demonstrated, and TNF‐α‐induced expression of integrin and migration activity was inhibited by the specific inhibitor and mutant of MEK, ERK and NF‐κB cascades. Taken together, our results indicated that TNF‐α enhances the migration of chondrosarcoma cells by increasing αvβ3 integrin expression through the MEK/ERK/NF‐κB signal transduction pathway. J. Cell. Physiol. 226: 792–799, 2011. © 2010 Wiley‐Liss, Inc.
Expression pattern of receptor activator of NFκB (RANK) in a series of primary solid tumors and related bone metastases
Authors: Santini Daniele , Perrone Giuseppe , Roato Ilaria , Godio Laura , Pantano Francesco , Grasso Donatella , Russo Antonio , Vincenzi Bruno , Fratto Maria Elisabetta , Sabbatini Roberto , Della Pepa Chiara , Porta Camillo , Del Conte Alessandro , Schiavon Gaia , Berruti Alfredo , Tomasino Rosa Maria , Papotti Mauro , Papapietro Nicola , Onetti Muda Andrea , Denaro Vincenzo , Tonini Giuseppe 
Published: September 2010

AbstractReceptor activator of NFκB ligand (RANKL), RANK, and osteoprotegerin (OPG) represent the key regulators of bone metabolism both in normal and pathological conditions, including bone metastases. To our knowledge, no previous studies investigated and compared RANK expression in primary tumors and in bone metastases from the same patient. We retrospectively examined RANK expression by immunohistochemistry in 74 bone metastases tissues from solid tumors, mostly breast, colorectal, renal, lung, and prostate cancer. For 40 cases, tissue from the corresponding primary tumor was also analyzed. Sixty‐six (89%) of the 74 bone metastases were RANK‐positive and, among these, 40 (59.5%) showed more than 50% of positive tumor cells. The median percentage of RANK‐positive cells was 60% in primary tumors and metastases, without any statistically significant difference between the two groups (P = 0.194). The same percentage was obtained by considering only cases with availability of samples both from primary and metastasis. Our study shows that RANK is expressed by solid tumors, with high concordance between bone metastasis and corresponding primary tumor. These data highlight the central role of RANK/RANKL/OPG pathway as potential therapeutic target not only in bone metastasis management, but also in the adjuvant setting. J. Cell. Physiol. 226: 780–784, 2011. © 2010 Wiley‐Liss, Inc.
Fibroblast growth factor‐2 stimulates directed migration of periodontal ligament cells via PI3K/AKT signaling and CD44/hyaluronan interaction
Authors: Shimabukuro Yoshio , Terashima Hiroaki , Takedachi Masahide , Maeda Kenichiro , Nakamura Tomomi , Sawada Keigo , Kobashi Mariko , Awata Toshihito , Oohara Hiroyuki , Kawahara Takanobu , Iwayama Tomoaki , Hashikawa Tomoko , Yanagita Manabu , Yamada Satoru , Murakami Shinya 
Published: September 2010

AbstractFibroblast growth factor‐2 (FGF‐2) regulates a variety of functions of the periodontal ligament (PDL) cell, which is a key player during tissue regeneration following periodontal tissue breakdown by periodontal disease. In this study, we investigated the effects of FGF‐2 on the cell migration and related signaling pathways of MPDL22, a mouse PDL cell clone. FGF‐2 activated the migration of MPDL22 cells and phosphorylation of phosphatidylinositol 3‐kinase (PI3K) and akt. The P13K inhibitors, Wortmannin and LY294002, suppressed both cell migration and akt activation in MPDL22, suggesting that the PI3K/akt pathway is involved in FGF‐2‐stimulated migration of MPDL22 cells. Moreover, in response to FGF‐2, MPDL22 showed increased CD44 expression, avidity to hyaluronan (HA) partly via CD44, HA production and mRNA expression of HA synthase (Has)‐1, 2, and 3. However, the distribution of HA molecular mass produced by MPDL22 was not altered by FGF‐2 stimulation. Treatment of transwell membrane with HA facilitated the migration of MPDL22 cells and an anti‐CD44 neutralizing antibody inhibited it. Interestingly, the expression of CD44 was colocalized with HA on the migrating cells when stimulated with FGF‐2. Furthermore, an anti‐CD44 antibody and small interfering RNA for CD44 significantly decreased the FGF‐2‐induced migration of MPDL22 cells. Taken together, PI3K/akt and CD44/HA signaling pathways are responsible for FGF‐2‐mediated cell motility of PDL cells, suggesting that FGF‐2 accelerates periodontal regeneration by regulating the cellular functions including migration, proliferation and modulation of extracellular matrix production. J. Cell. Physiol. 226: 809–821, 2011. © 2010 Wiley‐Liss, Inc.
Preclinical testing of the Akt inhibitor triciribine in T‐cell acute lymphoblastic leukemia
Authors: Evangelisti Camilla , Ricci Francesca , Tazzari Pierluigi , Chiarini Francesca , Battistelli Michela , Falcieri Elisabetta , Ognibene Andrea , Pagliaro Pasqualepaolo , Cocco Lucio , McCubrey James A. , Martelli Alberto M. 
Published: September 2010

AbstractOver the past 20 years, survival rates of T‐cell acute lymphoblastic leukemia (T‐ALL) patients have improved, mainly because of advances in polychemotherapy protocols. Despite these improvements, we still need novel and less toxic treatment strategies targeting aberrantly activated signaling networks which increase proliferation, survival, and drug resistance of T‐ALL cells. One such network is represented by the phosphatidylinositol 3‐kinase (PI3K)/Akt axis. PI3K inhibitors have displayed some promising effects in preclinical models of T‐ALL. Here, we have analyzed the therapeutic potential of the Akt inhibitor, triciribine, in T‐ALL cell lines. Triciribine caused cell cycle arrest and caspase‐dependent apoptosis. Western blots demonstrated a dose‐dependent dephosphorylation of Akt1/Akt2, and of mammalian target of rapamycin complex 1 downstream targets in response to triciribine. Triciribine induced autophagy, which could be interpreted as a defensive mechanism, because an autophagy inhibitor (chloroquine) increased triciribine‐induced apoptosis. Triciribine synergized with vincristine, a chemotherapeutic drug employed for treating T‐ALL patients, and targeted the side population of T‐ALL cell lines, which might correspond to leukemia initiating cells. Our findings indicate that Akt inhibition, either alone or in combination with chemotherapeutic drugs, may serve as an efficient treatment towards T‐ALL cells requiring upregulation of this signaling pathway for their proliferation and survival. J. Cell. Physiol. 226: 822–831, 2011. © 2010 Wiley‐Liss, Inc.
Developmentally regulated inhibition of cell cycle progression by glucocorticoids through repression of cyclin a transcription in primary osteoblast cultures
Authors: Gabet Yankel , Noh Tommy , Lee Christopher , Frenkel Baruch 
Published: September 2010

AbstractSynthetic glucocorticoids (GCs) like dexamethasone (DEX) are effective immunosuppressants indicated for autoimmune and inflammatory diseases. However, they often promote osteoporosis and bone fractures. Here, we investigated the anti‐mitogenic effect of GCs in primary osteoblast cultures. DEX did not affect cell cycle progression in confluent (day 2), or early post‐confluent cultures. Starting on day 5, however, DEX strongly inhibited the G1/S cell cycle transition. Day 5 also marked the beginning of a ∼2‐day commitment stage, during which cultures acquired resistance to the inhibitory effect of DEX on mineralization. Considering the importance of Wnt signaling in osteoblast development, we analyzed the effect of DEX on the Wnt pathway. DEX treatment did not inhibit the TOPGAL Wnt reporter before, but only during and after the commitment stage. However, this inhibition was not associated with repression of neither cyclin D1 nor c‐Myc mRNA, well‐established Wnt targets regulating cell cycle progression. On the other hand, acute (24‐h) and chronic (7 days) DEX treatment significantly reduced both the mRNA and protein levels of cyclin A, another cell cycle regulator. Moreover, cyclin A repression by DEX was not observed before, but only during and after the commitment stage. Using gel shift and reporter assays, we identified an ATF/CREB‐binding site critical for the DEX‐mediated repression of cyclin A transcription. Furthermore, and similar to cyclin A, Atf4 expression was repressed by DEX only during and after commitment. Our data suggest that GCs attenuate cell cycle progression in osteoblasts in a developmental stage‐specific manner by repressing Atf4‐dependent cyclin A gene expression. J. Cell. Physiol. 226: 991–998, 2011. © 2010 Wiley‐Liss, Inc.
Homocysteine induces smooth muscle cell proliferation through differential regulation of cyclins A and D1 expression
Authors: Chiang Jui‐Kun , Sung Mao‐Lin , Yu Hong‐Ren , Chang Hsin‐I , Kuo Hsing‐Chun , Tsai Tzung‐Chieh , Yen Chia‐Kuang , Chen Cheng‐Nan 
Published: September 2010

AbstractThe mechanism of homocysteine‐induced cell proliferation in human vascular smooth muscle cells (SMCs) remains unclear. We investigated the molecular mechanisms by which homocysteine affects the expression of cyclins A and D1 in human umbilical artery SMCs (HUASMCs). Homocysteine treatment induced proliferation of HUASMCs and increased the expression levels of cyclins A and D1. Knocking down either cyclin A or cyclin D1 by small interfering RNA (siRNA) inhibited homocysteine‐induced cell proliferation. Furthermore, treatment with extracellular signal‐related kinase (ERK) inhibitor (PD98059) and dominant negative Ras (RasN17) abolished homocysteine‐induced cyclin A expression; and treatment with phosphatidylinositol 3‐kinase (PI3K) inhibitor (LY294002) and mammalian target of rapamycin (mTOR) inhibitor (rapamycin) attenuated the homocysteine‐induced cyclin D1 expression. Homocysteine also induced transient phosphorylation of ERK, Akt, and p70 ribosomal S6 kinase (p70S6K). Neutralizing antibody and siRNA for β1 integrin blocked cell proliferation, expression of cyclins A and D1, and phosphorylation of ERK and Akt. In conclusion, homocysteine‐induced differential activation of Ras/ERK and PI3K/Akt/p70S6K signaling pathways and consequent expression of cyclins A and D1 are dependent on β1 integrin. Homocysteine may accelerate progression of atherosclerotic lesions by promoting SMC proliferation. J. Cell. Physiol. 226: 1017–1026, 2011. © 2010 Wiley‐Liss, Inc.
Artefactual effects of oxygen on cell culture models of cellular senescence and stem cell biology
Authors: Toussaint Olivier , Weemaels Geoffroy , Debacq‐Chainiaux Florence , Scharffetter‐Kochanek Karin , Wlaschek Meinhard 
Published: September 2010

AbstractIn life sciences, modelling of the in vivo conditions using in vitro models is an important tool to generate knowledge. Although aerobic organisms including mammals depend on accurate oxygen tension, mimicking physiological conditions in cell culture experiments is not very common. Due to the need for simple technical and experimental design, the requirement for simulating the in vivo oxygen tension parameters has been neglected over long time. Fortunately, due to increasing knowledge in recent years the attention has shifted towards this scientific demand. In this short review, we summarize data substantiating the necessity to adequately mimic physiological oxygen tension using cell culture models in life science research. J. Cell. Physiol. 226: 315–321, 2011. © 2010 Wiley‐Liss, Inc.
Acetylcholine inhibits hypoxia‐induced tumor necrosis factor‐α production via regulation of MAPKs phosphorylation in cardiomyocytes
Authors: Li Dong‐Ling , Liu Jin‐Jun , Liu Bing‐Hang , Hu Hao , Sun Lei , Miao Yi , Xu Hai‐Fei , Yu Xiao‐Jiang , Ma Xin , Ren Jun , Zang Wei‐Jin 
Published: September 2010

AbstractRecent findings have reported that up‐regulation of tumor necrosis factor‐alpha (TNF‐α) induced by myocardial hypoxia aggravates cardiomyocyte injury. Acetylcholine (ACh), the principle vagal neurotransmitter, protects cardiomyocytes against hypoxia by inhibiting apoptosis. However, it is still unclear whether ACh regulates TNF‐α production in cardiomyocytes after hypoxia. The concentration of extracellular TNF‐α was increased in a time‐dependent manner during hypoxia. Furthermore, ACh treatment also inhibited hypoxia‐induced TNF‐α mRNA and protein expression, caspase‐3 activation, cell death and the production of reactive oxygen species (ROS) in cardiomyocytes. ACh treatment prevented the hypoxia‐induced increase in p38 mitogen‐activated protein kinase (MAPK) and c‐Jun N‐terminal kinase (JNK) phosphorylation, and increased extracellular signal‐regulated kinase (ERK) phosphorylation. Co‐treatment with atropine, a non‐selective muscarinic acetylcholine receptor antagonist, or methoctramine, a selective type‐2 muscarinic acetylcholine (M2) receptor antagonist, abrogated the effects of ACh treatment in hypoxic cardiomyocytes. Co‐treatment with hexamethonium, a non‐selective nicotinic receptor antagonist, and methyllycaconitine, a selective alpha7‐nicotinic acetylcholine receptor antagonist, had no effect on ACh‐treated hypoxic cardiomyocytes. In conclusion, these results demonstrate that ACh activates the M2 receptor, leading to regulation of MAPKs phosphorylation and, subsequently, down‐regulation of TNF‐α production. We have identified a novel pathway by which ACh mediates cardioprotection against hypoxic injury in cardiomyocytes. J. Cell. Physiol. 226: 1052–1059, 2011. © 2010 Wiley‐Liss, Inc.
Tyrosine phosphorylation modulates store‐operated calcium entry in cultured rat epididymal basal cells
Authors: Zuo Wu‐Lin , Du Jian‐Yang , Huang Jie‐Hong , Li Sheng , Zhang Geng , Chen Si‐Liang , Ruan Ye‐Chun , Cheng Christopher H.K. , Zhou Wen‐Liang 
Published: September 2010

AbstractStore‐operated calcium entry (SOCE) is essential for many cellular processes. In this study, we investigated modulation of SOCE by tyrosine phosphorylation in rat epididymal basal cells. The intracellular Ca2+([Ca2+]i) measurement showed that SOCE occurred in rat epididymal basal cells by pretreating the cells with thapsigargin (Tg), the inhibitor of sarco‐endoplasmic reticulum Ca2+‐ATPase. To identify the role of Ca2+ channels in this response, we examined the effects of transient receptor potential canonical channel blockers 2‐aminoethoxydiphenyl borate (2‐APB), 1‐[β‐[3‐(4‐methoxyphenyl)pro‐poxy]‐4‐methoxyphenethyl]‐1H‐imidazole hydrochloride(SKF96365), Gd3+, and non‐selective cation channel blocker Ni2+ respectively on SOCE and found that these blockers could inhibit the Ca2+ influx to different extent. Furthermore, we studied the regulation of SOCE by tyrosine kinase pathway. The inhibitor of tyrosine kinase genistein remarkably suppressed the SOCE response, whereas sodium orthovanadate, the inhibitor of tyrosine phosphatase, greatly enhanced it. The results suggest that tyrosine kinase pathway plays a significant role in the initiation of SOCE and positively modulates SOCE in epididymal basal cells. J. Cell. Physiol. 226: 1069–1073, 2011. © 2010 Wiley‐Liss, Inc.