bluuebunny/crossref_metadata_2025_split huggingface dataset:
The ecology of achievement among students diverse in ethnicity and ability
Authors: McMahon Susan D. , Keys Christopher B. , Berardi Luciano , Crouch Ronald 
Published: July 2011

AbstractThis longitudinal study uses an ecological framework to examine school and individual influences on academic achievement among African American and Latino students with and without disabilities who had recently transferred to more inclusive schools. The authors' ecological framework includes four domains: organizational policies and practices, school environment, student–school connections, and psychological symptoms. The authors tested a comprehensive model with 111 students from 16 schools over 3 years, as well as an organizational model with a smaller sample. Organizational policies and practices of inclusion and student–school connections of belonging each predicted higher academic achievement, and psychological symptoms of aggressive behavior predicted lower academic achievement across time. Their findings are consistent with and extend existing research through support of a comprehensive ecological model across time. Findings also yield significant implications for ecological theory and research in community psychology, school planning, intervention, and implementation of inclusive best practices for students with and without disabilities. © 2011 Wiley Periodicals, Inc.
Perceived neighborhood violence and use of verbal aggression, corporal punishment, and physical abuse by a national sample of parents in Israel
Authors: Winstok Zeev , Straus Murray A. 
Published: July 2011

AbstractThis study, based on an ecological perspective, examined the relation of perceived neighborhood violence, child misbehavior, parental attitudes to aggressive discipline tactics, and the actual use of aggressive discipline tactics. Research questions were: To what extent is perceived neighborhood violence associated with aggressive discipline by parents? What is the mechanism through which perceived neighborhood violence is linked to aggressive discipline? Data were obtained from a stratified probability sample of 1,649 women. Findings indicated that the more the study participants perceived their neighborhood as violent, the more frequent is the parental use of aggressive discipline. It seems that child misbehavior and parental approval of corporal punishment are affected by perceived neighborhood violence and, in turn, affect parental use of aggressive disciplines. Furthermore, the relationships of child misbehavior, parental approval of aggressive discipline, and the use of aggressive discipline are different in low and high levels of perceived neighborhood violence. © 2011 Wiley Periodicals, Inc.
Impacts of the duration of Head Start enrollment on children's academic outcomes: moderation effects of family risk factors and earlier outcomes
Authors: Lee Kyunghee 
Published: July 2011

AbstractThis study examined effects of the duration of Head Start enrollment on children's academic outcomes. Study questions are as follows: (a) Do Head Start children's baseline characteristics differ among those who entered at age 3 and enrolled in Head Start for 1 year, those who entered at age 4 and stayed for 1 year, and those who entered at age 3 and stayed for 2 years? (b) Do children's academic scores differ among the three groups? (c) Do these effects differ depending on the number of family risk factors and on children's scores at the beginning of the year? Findings indicate that children who entered Head Start at age 3 and stayed for 2 years showed higher academic outcomes than those enrolled later or for less time. Benefits were greater among children with more family risk factors and among those whose academic scores at the beginning of the study year were lower. © 2011 Wiley Periodicals, Inc.
The critical role of JNK in the ER‐mitochondrial crosstalk during apoptotic cell death
Authors: Verma Gaurav , Datta Malabika 
Published: July 2011

AbstractApoptosis or programmed cell death is an extremely coordinated phenomenon that involves the participation of a complex interacting crosstalk between the endoplasmic reticulum and mitochondria. This involves a series of signaling molecules like stress kinases, caspases, Bcl‐2 family of proteins, etc. that coordinately induce apoptosis by releasing apoptotic proteins from the mitochondria and mediate DNA damage of the cell. Among the stress kinases, JNK, a member of the MAPK family has been believed to be critically mediating these apoptotic phenomena. The involvement of JNK has been clouded by controversies because of its role both as a pro‐apoptotic and an anti‐apoptotic mediator. A very significant initiator of JNK activation is the pro‐inflammatory cytokine, IL‐1β, levels of which are significantly elevated in varied diseases especially diabetes where it is believed to significantly contribute to pancreatic β‐cell death. During apoptotic cell death, the endoplasmic reticulum and the mitochondrion participate in a relay of cellular events that determine the onset of the classical apoptotic pathways. Here we discuss the details of this ER‐mitochondrial crosstalk and the role of JNK herein that ultimately culminates into apoptotic cell death that is evident in various pathophysiological conditions. J. Cell. Physiol. 227: 1791–1795, 2012. © 2011 Wiley Periodicals, Inc.
mda‐7/IL‐24 differentially regulates soluble and nuclear clusterin in prostate cancer
Authors: Bhutia Sujit K. , Das Swadesh K. , Kegelman Timothy P. , Azab Belal , Dash Rupesh , Su Zhao‐zhong , Wang Xiang‐Yang , Rizzi Federica , Bettuzzi Saverio , Lee Seok‐Geun , Dent Paul , Grant Steven , Curiel David T. , Sarkar Devanand , Fisher Paul B. 
Published: July 2011

AbstractMelanoma differentiation‐associated gene‐7/interleukin‐24 (mda‐7/IL‐24), a unique member of the IL‐10 gene family, displays a broad range of antitumor properties including cancer‐specific induction of apoptosis, inhibition of tumor angiogenesis, and modulation of anti‐tumor immune responses. Here, we identify clusterin (CLU) as a MDA‐7/IL‐24 interacting protein in DU‐145 cells and investigate the role of MDA‐7/IL‐24 in regulating CLU expression and mediating the antitumor properties of mda‐7/IL‐24 in prostate cancer. Ad.mda‐7 decreased expression of soluble CLU (sCLU) and increased expression of nuclear CLU (nCLU). In the initial phase of Ad.mda‐7 infection sCLU expression increased and CLU interacted with MDA‐7/IL‐24 producing a cytoprotective effect. Infection of stable clones of DU‐145 prostate cancer cells expressing sCLU with Ad.mda‐7 resulted in generation of nCLU that correlated with decreased cell viability and increased apoptosis. In the presence of mda‐7/IL‐24, sCLU‐DU‐145 cells displayed G2/M phase arrest followed by apoptosis. Similarly, Ad.mda‐7 infection decreased cell migration by altering cytoskeleton in sCLU‐DU‐145 cells. Ad.mda‐7‐treated sCLU‐DU‐145 cells displayed a significant reduction in tumor growth in mouse xenograft models and reduced angiogenesis when compared to the vector control group. Tumor tissue lysates demonstrated enhanced nCLU generated from sCLU with increased apoptosis in the presence of MDA‐7/IL‐24. Our findings reveal novel aspects relative to the role of sCLU/nCLU in regulating the anticancer properties of MDA‐7/IL‐24 that may be exploited for developing enhanced therapies for prostate cancer. J. Cell. Physiol. 227: 1805–1813, 2012. © 2011 Wiley Periodicals, Inc.
Possible role of RKIP in cytotrophoblast migration: immunohistochemical and in vitro studies
Authors: Ciarmela Pasquapina , Marzioni Daniela , Islam Md. Soriful , Gray Peter Clarke , Terracciano Luigi , Lorenzi Teresa , Todros Tullia , Petraglia Felice , Castellucci Mario 
Published: July 2011

AbstractRaf kinase inhibitor protein (RKIP) regulates growth and differentiation signaling of mitogen‐activated protein kinases (MAPK), GRK2 and NF‐kappaB pathways each of which regulates cytotrophoblast differentiation and normal placental development. We show here that RKIP is expressed in human normal and preeclampic placentas as detected by immunostaining. RKIP was detected in villous cytotrophoblast in normal placenta and switched to syncytiotrophoblast in pre‐eclampsia (PE)‐complicated pregnancies. RKIP was also localized in extravillous cytotrophoblast of cell islands and cell columns both in normal and in PE placentas, although staining was less uniform in the latter specimens. In order to test RKIP involvement in cytotrophoblast function, we performed in vitro studies on HTR‐8/SVneo cells, a first trimester cytotrophoblast cell line. We show that the RKIP inhibitor locostatin reduces ERK phosphorylation and impairs HTR‐8/SV neo cells motility in wound closure experiments. We also document the presence of GRK2 mRNA, the reduction of phosphorylated RKIP expression by locostatin and the induction of PAI mRNA expression in HTR‐8/SV neo cells, suggesting the involvement of GRK2 and NF‐kappaB pathways in these cells. In conclusion, our work provides evidence that RKIP is a novel factor expressed in cytotrophoblast cells where it likely regulates cell migration. J. Cell. Physiol. 227: 1821–1828, 2012. © 2011 Wiley Periodicals, Inc.
Activation of the p53 pathway induces α‐smooth muscle actin expression in both myeloid leukemic cells and normal macrophages
Authors: Secchiero Paola , Rimondi Erika , di Iasio Maria Grazia , Voltan Rebecca , Gonelli Arianna , Zauli Giorgio 
Published: July 2011

AbstractA range of cell types of mesenchymal origin express α‐smooth muscle actin (α‐SMA), a protein that plays a key role in controlling cell motility and differentiation along the fibrocyte and myofibroblast lineages. Although α‐SMA is often expressed in stromal cells associated to a variety of cancers including hematological malignancies, up to now the role of anti‐cancer drugs on α‐SMA has not been deeply investigated. In this study, we demonstrated that Nutlin‐3, the small molecule inhibitor of the MDM2/p53 interactions, significantly up‐regulated the mRNA and protein levels of α‐SMA in normal macrophages as well as in p53wild‐type but not in p53mutated/null myeloid leukemic cells. The p53‐dependence of α‐SMA up‐regulation induced by Nutlin‐3 was demonstrated in experiments performed with siRNA for p53. Of note, Nutlin‐3 mediated up‐regulation of α‐SMA in OCI leukemic cells was accompanied by cell adhesion to plastic substrate and by reduced cell migratory response in transwell assays. Notably, the role of α‐SMA induction in the modulation of myeloid cell migration was clearly documented in α‐SMA gene knockdown experiments. In addition, Nutlin‐3 significantly up‐regulated α‐SMA expression in primary endothelial cells, but not in fibroblasts and mesenchymal stem cells (MSC). Conversely, transforming growth factor‐β1 up‐regulated α‐SMA in fibroblasts and MSC, but not in macrophages and endothelial cells. Taken together, these data indicate that Nutlin‐3 is a potent inducer of α‐SMA in both normal and leukemic myeloid cells as well as in endothelial cells. J. Cell. Physiol. 227: 1829–1837, 2012. © 2011 Wiley Periodicals, Inc.
Inhibitory regulation of osteoclast differentiation by interleukin‐3 via regulation of c‐Fos and Id protein expression
Authors: Oh Jaemin , Lee Myeung Su , Yeon Jeong‐Tae , Choi Sik‐Won , Kim Hun Soo , Shim Hyeok , Lee Sam Youn , Youn Byung Soo , Yokota Yoshifumi , Kim Jung Ha , Kwak Han Bok 
Published: July 2011

AbstractInterleukin‐3 (IL‐3) is produced under various pathological conditions and is thought to be involved in the pathogenesis of inflammatory diseases; however, its function in bone homeostasis under normal conditions or nature of the downstream molecular targets remains unknown. Here we examined the effect of IL‐3 on osteoclast differentiation from mouse and human bone marrow‐derived macrophages (BMMs). Although IL‐3 can induce osteoclast differentiation of multiple myeloma bone marrow cells, IL‐3 greatly inhibited osteoclast differentiation of human BMMs isolated from healthy donors. These inhibitory effects of IL‐3 were only observed at early time points (days 0 and 1). IL‐3 inhibited the expression of c‐Fos and NFATc1 in BMMs treated with RANKL. However, IL‐3‐mediated inhibition of osteoclast differentiation was not completely reversed by ectopic expression of c‐Fos or NFATc1. Importantly, IL‐3 induced inhibitor of DNA binding/differentiation (Id)1 in hBMMs, while Id2 were sustained during osteoclast differentiation of mBMMs treated with IL‐3. Ectopic expression of NFATc1 in Id2‐deficient BMMs completely reversed the inhibitory effect of IL‐3 on osteoclast differentiation. Furthermore, inflammation‐induced bone erosion was markedly inhibited by IL‐3 administration. Taken together, our results suggest that IL‐3 plays an inhibitory role in osteoclast differentiation by regulating c‐Fos and Ids, and also exerts anti‐bone erosion effects. J. Cell. Physiol. 227: 1851–1860, 2012. © 2011 Wiley Periodicals, Inc.
The pro‐apoptotic effect of quercetin in cancer cell lines requires ERβ‐dependent signals
Authors: Bulzomi Pamela , Galluzzo Paola , Bolli Alessandro , Leone Stefano , Acconcia Filippo , Marino Maria 
Published: July 2011

AbstractQuercetin has potentially beneficial effects on disease prevention, including cancer. An intriguing issue regarding the mechanisms of action of quercetin is the ability of this drug to modulate estrogen receptor (ER) activities. In a previous study, we demonstrated that quercetin elicited apoptosis through an ERα‐dependent mechanism. However, the contribution of ERβ in quercetin‐induced apoptosis remains elusive. Here, we report that quercetin, at nutritionally relevant concentrations, mimicked the 17β‐estradiol (E2)‐induced apoptotic effect in both ERβ1‐transfected HeLa and in ERβ1‐containing DLD‐1 colon cancer cell lines by inducing the activation of p38. p38 activation is responsible for pro‐apoptotic activation of caspase‐3 and the cleavage of poly(ADP‐ribose) polymerase. Notably, no inactivation or downregulation of the survival kinases (i.e., AKT and ERK1/2) or the antiapoptotic protein Bcl‐2 was observed after quercetin stimulation. On the contrary, quercetin acted similarly to E2 by increasing the levels of the oncosuppressor protein PTEN and by impeding ERβ‐dependent cyclin D1 promoter activity, which subsequently resulted in the transcription of the estrogen‐responsive element remaining unchanged. As a whole, these data indicate that quercetin mimics the E2 effects in the presence of ERβ1, thus maintaining its anti‐carcinogenic potential. In addition, the quercetin pro‐apoptotic action in the presence of ERα may render it as a dual‐sided protective agent against E2‐related cancer in the reduction of tumour growth in organs that express ERα and/or ERβ. J. Cell. Physiol. 227: 1891–1898, 2012. © 2011 Wiley Periodicals, Inc.
Heterogeneity in apoptotic responses of microvascular endothelial cells to oxidative stress
Authors: Grinnell Katie , Duong Huetran , Newton Julie , Rounds Sharon , Choudhary Gaurav , Harrington Elizabeth O. 
Published: July 2011

AbstractOxidative stress contributes to disease and can alter endothelial cell (EC) function. EC from different vascular beds are heterogeneous in structure and function, thus we assessed the apoptotic responses of EC from lung and heart to oxidative stress. Since protein kinase Cδ (PKCδ) is activated by oxidative stress and is an important modulator of apoptosis, experiments assessed the level of apoptosis in fixed lung and heart sections of PKCδ wild‐type (PKCδ+/+) and null (PKCδ−/−) mice housed under normoxia (21% O2) or hyperoxia (∼95% O2). We noted a significantly greater number of TUNEL‐positive cells in lungs of hyperoxic PKCδ+/+ mice, compared to matched hearts or normoxic organs. We found that 33% of apoptotic cells identified in hyperoxic lungs of PKCδ+/+ mice were EC, compared to 7% EC in hyperoxic hearts. We further noted that EC apoptosis was significantly reduced in lungs of PKCδ−/− hyperoxic mice, compared to lungs of PKCδ+/+ hyperoxic mice. In vitro, both hyperoxia and H2O2 promoted apoptosis in EC isolated from microvasculature of lung (LMVEC), but not from the heart (HMVEC). H2O2 treatment significantly increased p38 activity in LMVEC, but not in HMVEC. Inhibition of p38 attenuated H2O2‐induced LMVEC apoptosis. Baseline expression of total PKCδ protein, as well as the caspase‐mediated, catalytically active PKCδ cleavage fragment, was higher in LMVEC, compared to HMVEC. PKCδ inhibition significantly attenuated H2O2‐induced LMVEC p38 activation. Conversely, overexpression of wild‐type PKCδ or the catalytically active PKCδ cleavage product greatly increased H2O2‐induced HMVEC caspase and p38 activation. We propose that enhanced susceptibility of lung EC to oxidant‐induced apoptosis is due to increased PKCδ → p38 signaling, and we describe a PKCδ‐centric pathway which dictates the differential response of EC from distinct vascular beds to oxidative stress. J. Cell. Physiol. 227: 1899–1910, 2012. © 2011 Wiley Periodicals, Inc.
Duplicated chromosomal fragments stabilize shortened telomeres in normal human IMR‐90 cells before transition to senescence
Authors: Zahnreich Sebastian , Krunic Damir , Melnikova Larissa , Szejka Agnes , Drossel Barbara , Sabatier Laure , Durante Marco , Ritter Sylvia , Fournier Claudia 
Published: July 2011

AbstractTo assess why during in vitro aging of fibroblasts the maintenance of chromosomal stability is effective or occasionally fails, a detailed cytogenetic analysis was performed in normal human IMR‐90 fetal lung fibroblasts. The onset of senescence was inferred from proliferation activity, expression pattern of cell cycle regulating proteins, activity of β‐galactosidase, and morphological features. Over the period of proliferation, a moderate increase of non‐transmissible structural chromosomal aberrations was observed. In addition, using fluorescence in situ hybridization (mFISH and mBAND) techniques, we detected clonally expanding translocations in up to 70% of the analyzed metaphases, all involving one homolog of chromosome 9 as an acceptor. Notably, chromosomes are randomly involved as donor‐chromosomes of the translocated terminal acentric fragments. These fragments result from duplication because the donor chromosomes are apparently unchanged. Interstitial telomeric signals were detectable at fusion sites, most likely belonging to chromosome 9. Quantitative fluorescence in situ hybridization (QFISH) detecting telomere sequences, followed by mFISH technique revealed that already in young cells the respective telomeres of one chromosome 9 were particularly short. For the first time, we have observed dysfunctional telomeres of one specific chromosome in normal human cells that have been stabilized by duplicated terminal sequences. J. Cell. Physiol. 227: 1932–1940, 2012. © 2011 Wiley Periodicals, Inc.
Functional ion channels and cell proliferation in 3T3‐L1 preadipocytes
Authors: Zhang Xiao‐Hua , Zhang Ying‐Ying , Sun Hai‐Ying , Jin Man‐Wen , Li Gui‐Rong 
Published: July 2011

AbstractMouse 3T3‐L1 preadipocytes are widely used for metabolic study of obesity; however, their cellular physiology is not fully understood. The present study investigates functional ion channels and their role in the regulation of cell proliferation using whole‐cell patch voltage‐clamp, RT‐PCR, Western blot, and cell proliferation assay in undifferentiated 3T3‐L1 preadipocytes. We found three types of ionic currents present in 3T3‐L1 preadipocytes, including an inwardly‐rectifying K+ current (IKir, recorded in 15% of cells) inhibited by Ba2+, a Ca2+‐activated intermediate K+ current (IKCa, recorded in 44% of cells) inhibited by clotrimazole (or TRAM‐34) as well as a chloride current (ICl) inhibited by 4,4′‐diisothiocyanatostilbene‐2,2′‐disulfonic acid (DIDS) in 12% of cells, which can be activated in all cells with hypotonic (0.8 T) insult, implicating a volume‐sensitive ICl (ICl.vol). RT‐PCR and Western blot analysis revealed the expression of KCa3.1 (for IKCa), Kir2.1 (for IKir), and Clcn3 (for ICl.vol). Blockade of IKCa with TRAM‐34 or ICl.vol with DIDS inhibited cell proliferation in a concentration‐dependent manner. Knockdown of KCa3.1 or Clcn3 with specific siRNAs also suppressed cell proliferation. Flow cytometry analysis showed that blockade or silencing of KCa3.1 or Clcn3 channels with corresponding blockers or siRNAs caused an accumulation of cells at the G0/G1 phase. These results demonstrate that three functional ion channel currents, IKCa, ICl.vol, and IKir, are heterogeneously present in 3T3‐L1 preadipocytes. IKCa and ICl.vol participate in the regulation of cell proliferation. J. Cell. Physiol. 227: 1972–1979, 2012. © 2011 Wiley Periodicals, Inc.
X‐rays of inner worlds: The mid‐twentieth‐century American Projective Test Movement
Authors: Lemov Rebecca 
Published: July 2011

AbstractThis essay begins to tell the neglected history of the projective test movement in the U.S. behavioral sciences from approximately 1941 to 1968. This cross‐disciplinary enterprise attempted to use projective techniques as “X‐ray” machines to see into the psyches of subjects tested around the world. The aim was to gather subjective materials en masse, pursuing data on a scope, scale, and manner rarely hazarded before in any science. In particular, the targeted data included the traces of the inner life and elusive aspects of subjective experience including dreams, life stories, and myriad test results from a battery of tests. This essay explores how the movement and the experimental data bank that resulted were unlikely yet telling sites for the practice and pursuit of the Cold War human sciences. To look closely at the encounters that resulted is to show how the most out‐of‐the‐way places and seemingly insignificant moments played a role in heady scientific ambitions and global geopolitical projects. At times, the projective test movement became a mirror of Cold War rationality itself, as tests were employed at the very limits of their possible extension. The essay argues for an off‐kilter centrality in the movement itself, shedding light on the would‐be unified social sciences after World War II and the “subjective turn” they took. © 2011 Wiley Periodicals, Inc.
The lateglacial Quercus expansion in the southern European Alps: rapid vegetation response to a late Allerød climate warming?
Authors: Finsinger W. , Lane C. S. , van Den Brand G. J. , Wagner‐Cremer F. , Blockley S. P. E. , Lotter A. F. 
Published: July 2011

AbstractA pollen‐inferred vegetation shift, from pioneer birch–pine woodland to mixed pine–summergreen oak forests, in the southern Alpine forelands, is commonly attributed to a centennial‐scale warming that occurred between the Gerzensee Oscillation (GO) and the Younger Dryas. Two microtephra layers bracketing the Younger Dryas onset (the Laacher See Tephra and the Vedde Ash) improve the chronology at Lago Piccolo di Avigliana (northern Italy) and allowed accurate correlation with Central European records where the GO is clearly detected. We used pollen percentages, pollen accumulation rates (PARs) and plant macrofossils to assess the population dynamics of Quercus, and leaf‐cuticle analysis for a better taxonomic identification of Quercus. Our results indicate that the species that was locally present was probably Quercus robur. PARs suggest that the population expansion started as early as the Bølling and followed an exponential increase through time. We attribute this gradual shift to increasing summer temperatures and longer growing seasons which contrast with a gradually decreasing temperature trend as recorded in Greenland ice cores and in Central Europe. Breaks or set‐backs in the PAR record may indicate the biotic response to minor Lateglacial cooling events of different life‐history stages in the Quercus population. Copyright © 2011 John Wiley & Sons, Ltd.