bluuebunny/crossref_metadata_2025_split huggingface dataset:
Combined Experimental and Density Functional Theory Studies on the Crystal Structures and Magnetic Properties of Mg(Mg1–xMnx)2Sb2 (x ≈ 0.25) and BaMn2Sb2
Authors: Xia Sheng‐Qing , Myers Chad , Bobev Svilen 
Published: August 2008

AbstractReported are the synthesis and structural characterization of two ternary transition metal intermetallic compounds, Mg(Mg1–xMnx)2Sb2 (where x is approximately 0.25) and BaMn2Sb2·Mg(Mg2.50(3)Mn0.5)2Sb2 crystallizes in the trigonal space group P$\bar {3}$m1 (no. 164) and belongs to the CaAl2Si2‐type, while BaMn2Sb2 is isostructural with the body‐centred tetragonal ThCr2Si2‐type (I4/mmm, no. 139). Both structures have been refined from single‐crystal X‐ray diffraction data and their magnetic properties determined with the aid of a SQUID‐magnetometry. The experimental results have been corroborated by electronic‐structure calculations using the linear muffin‐tin orbital (LMTO) method. Spin‐polarized density‐functional theory calculations confirm the antiferromagntically ordered magnetic structures. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2008)
A Simple Two‐Step Sequence for the Synthesis of Novel 4‐Aryl‐4,5‐dihydro‐6H‐[1,3]dioxolo[4,5‐h]pyrrolo[1,2‐a][1]benzazepin‐6‐ones from 6‐Amino‐3,4‐methylenedioxyacetophenone
Authors: Abonia Rodrigo , Cuervo Paola , Insuasty Braulio , Quiroga Jairo , Nogueras Manuel , Cobo Justo 
Published: August 2008

AbstractHerein is provided an efficient and two‐step short procedure for the synthesis of novel 6H‐[1,3]dioxolobenzo[4,5‐h]pyrrolo[1,2‐a][1]benzazepin‐6‐one derivatives promoted by commercial phosphoric acid. In a parallel approach some pyrrolyl chalcones were isolated that proved to behave as intermediates for the title compounds. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2008)
Protonation of Diarylacetylenes in Superacid HSO3F and Their Oxidation in the HSO3F/PbO2 System: One‐Pot Synthesis of Polysubstituted Naphthalenes
Authors: Vasilyev Aleksander V. , Shchukin Andrey O. , Walspurger Stéphane , Sommer Jean 
Published: August 2008

AbstractIn the superacid HSO3F, diarylacetylenes bearing one electron‐withdrawing group (NO2, CN, COMe, CO2Me) in each arene ring form stable ions, protonated at these groups. Oxidation of such diarylacetylenes in the HSO3F/PbO2 system at –75 to –50 °C over 2–2.5 h, followed by quenching of the reaction mixture with hydrochloric (or hydrobromic) acid at –60 to 25 °C, resulted in the formation of (E,E)‐1,4‐dichloro (or dibromo)‐1,2,3,4‐tetraarylbuta‐1,3‐dienes. These butadienes spontaneously undergo electrocyclic transformation into polysubstituted naphthalenes at room temperature. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2008)
Altruism or psychological escape: Why does empathy promote prosocial behavior?
Authors: Stocks Eric L. , Lishner David A. , Decker Stephanie K. 
Published: August 2008

AbstractWhy does empathy promote prosocial behavior? Previous research suggests that empathically aroused individuals help those in need, even when physical escape from the need situation is easy, and this evidence has been used to support the claim that empathy evokes an altruistic motive. However, existing research has not addressed the possibility that empathically aroused participants help because ease of physical escape fails to provide adequate psychological escape from awareness of the victim's suffering and the aversive empathic arousal such awareness produces. The two experiments reported here examined this issue by directly manipulating empathic arousal and the perceived ease of psychological escape among potential helpers. In both experiments, higher rates of helping were observed among empathically aroused participants, even under conditions of easy psychological escape. The findings of both experiments suggest that empathy evokes an altruistic motive to reduce the victim's suffering rather than an egoistic aversive‐arousal reduction motive. In addition, the results of Experiment 1 suggest that concern for psychological escape from the suffering of others may constitute an important independent prosocial motive in need of future study. Copyright © 2008 John Wiley & Sons, Ltd.
Expression and mutational analysis of MET in human solid cancers
Authors: Ma Patrick C. , Tretiakova Maria S. , MacKinnon Alexander C. , Ramnath Nithya , Johnson Candace , Dietrich Sascha , Seiwert Tanguy , Christensen James G. , Jagadeeswaran Ramasamy , Krausz Thomas , Vokes Everett E. , Husain Aliya N. , Salgia Ravi 
Published: August 2008

AbstractMET receptor tyrosine kinase and its ligand hepatocyte growth factor (HGF) regulate a variety of cellular functions, many of which can be dysregulated in human cancers. Activated MET signaling can lead to cell motility and scattering, angiogenesis, proliferation, branching morphogenesis, invasion, and eventual metastasis. We performed systematic analysis of the expression of the MET receptor and its ligand HGF in tumor tissue microarrays (TMA) from human solid cancers. Standard immunohistochemistry (IHC) and a computerized automated scoring system were used. DNA sequencing for MET mutations in both nonkinase and kinase domains was also performed. MET was differentially overexpressed in human solid cancers. The ligand HGF was widely expressed in both tumors, primarily intratumoral, and nonmalignant tissues. The MET/HGF likely is functional and may be activated in autocrine fashion in vivo. MET and stem cell factor (SCF) were found to be positively stained in the bronchioalevolar junctions of lung tumors. A number of novel mutations of MET were identified, particularly in the extracellular semaphorin domain and the juxtamembrane domain. MET‐HGF pathway can be assayed in TMAs and is often overexpressed in a wide variety of human solid cancers. MET can be activated through overexpression, mutation, or autocrine signaling in malignant cells. Mutations in the nonkinase regions of MET might play an important role in tumorigenesis and tumor progression. MET would be an important therapeutic antitumor target to be inhibited, and in lung cancer, MET may represent a cancer early progenitor cell marker. © 2008 Wiley‐Liss, Inc.
Multiple recurrent chromosomal breakpoints in mantle cell lymphoma revealed by a combination of molecular cytogenetic techniques
Authors: Salaverria Itziar , Espinet Blanca , Carrió Ana , Costa Dolors , Astier Laura , Slotta‐Huspenina Julia , Quintanilla‐Martinez Leticia , Fend Falko , Solé Francesc , Colomer Dolors , Serrano Sergio , Miró Rosa , Beà Sílvia , Campo Elías 
Published: August 2008

AbstractMantle cell lymphoma (MCL) is genetically characterized by 11q13 translocations leading to the overexpression of CCND1, and additional secondary genomic alterations that may be important in the progression of this disease. We have analyzed 22 MCL cases and 10 MCL cell lines using multicolor fluorescence in situ hybridization (M‐FISH), FISH, and comparative genomic hybridization (CGH). The 19 cases with abnormal karyotype showed the t(11;14)(q13;q32) translocation and, additionally, 89% of cases showed both numerical (n = 58) and structural (n = 77) aberrations. All but one MCL cell line showed t(11;14) and structural and numerical alterations in highly complex karyotypes. Besides 11 and 14, the most commonly rearranged chromosomes were 1, 8, and 10 in the tumors and 1, 8, and 9 in the cell lines. No recurrent translocations other than the t(11;14) were identified. However, we identified 17 recurrent breakpoints, the most frequent being 1p22 and 8p11, each observed in four cases and two cell lines. Interestingly, five tumors and four cell lines displayed a complex t(11;14), cryptic in one case and two cell lines, preferentially involving chromosome 8. In typical MCL, ATM gene deletions were significantly associated with a high number of structural and numerical alterations. In conclusion, MCL does not have recurrent translocations other than t(11;14), but shows recurrent chromosomal breakpoints. Furthermore, most MCL harbor complex karyotypes with a high number of both structural and numerical alterations affecting several common breakpoints, leading to various balanced and unbalanced translocations. © 2008 Wiley‐Liss, Inc.
Astrocytes are very sensitive to develop innate immune responses to lipid‐carried short interfering RNA
Authors: Gorina Roser , Santalucia Tomàs , Petegnief Valérie , Ejarque‐Ortiz Aroa , Saura Josep , Planas Anna M. 
Published: August 2008

AbstractShort interfering RNA (siRNA) inhibits the synthesis of specific proteins through RNA interference (RNAi). However, siRNA can induce innate immune responses that are mediated by toll‐like receptors (TLRs) in cells of the immune system. Here, we sought to evaluate whether siRNA can induce such responses in glial cells. We examined the effects of various siRNA sequences prepared with lipids (oligofectamine). Lipid‐siRNA induced variable degrees of silencing‐independent nonspecific effects, e.g. increased Stat1 and Cox‐2 expression and release of IL‐6 and IP‐10 in primary astroglia. This was prevented through chemical modification of siRNA by nucleoside 2′‐O‐methylation, without impairing specific gene silencing. Lipid‐siRNA also induced nonspecific responses in purified astroglia, but not in microglia, or 3T3 cells. The highest TLR7 and TLR3 mRNA expression was found in microglia and purified astroglia, respectively. Accordingly, the TLR3 agonist poly(I:C) (PIC) induced higher release of IFN‐β in primary and purified astroglia than in microglia. As siRNA, PIC induced IP‐10, Stat1, VCAM‐1, and Cox‐2 and increased TLR3 mRNA expression. The effects of lipid‐siRNA in purified astrocytes were attenuated after silencing TLR3 or TLR7 expression, and by the PKR inhibitor 2‐aminopurine. Furthermore, lipid‐siRNA induced the expression of RIG‐I. In contrast, siRNA devoid of lipids did not enter the astrocytes, did not silence gene expression, and did not induce Stat1 or Cox‐2. The results show that, in astroglia, lipid‐siRNA induces innate immune responses that are mediated, at least in part, by intracellular mechanism dependent on TLR7, TLR3, and helicases. © 2008 Wiley‐Liss, Inc.
Ultrastructural and antigenic properties of neural stem cells and their progeny in adult rat subventricular zone
Authors: Danilov Alexandre I. , Gomes‐Leal Walace , Ahlenius Henrik , Kokaia Zaal , Carlemalm Eric , Lindvall Olle 
Published: August 2008

AbstractNeural stem cells (NSCs) in the subventricular zone (SVZ) continuously generate olfactory bulb interneurons in the adult rodent brain. Based on their ultrastructural and antigenic properties, NSCs, transient amplifying precursor cells, and neuroblasts (B, C, and A cells, respectively) have been distinguished in mouse SVZ. Here, we aimed to identify these cell types in rat SVZ ultrastructurally and at the light microscopy level, and to determine the antigenic properties of each cell type using gold and fluorescence immunolabeling. We found astrocytes with single cilia (NSCs, correspond to B cells) and neuroblasts (A cells). We also observed mitotic cells, ependymal cells, displaced ependymal cells, and mature astrocytes. In contrast, transient amplifying precursor cells (C cells) were not detected. The NSCs and neuroblasts had epidermal growth factor receptor (EGFR) and platelet‐derived growth factor receptor alpha (PDGFRα) expressed on the ciliary apparatus and were the only cell types incorporating the proliferation marker BrdU. Throughout mitosis, EGFR and PDGFRα were associated with the microtubule of the mitotic spindle. Ependymal and displaced ependymal cells also expressed EGFR and PDGFRα on their cilia but did not incorporate BrdU. Our findings indicate that the NSCs in adult rat SVZ give rise directly to neuroblasts. During mitosis, the NSCs disassemble the primary cilium and symmetrically distribute EGFR and PDGFRα among their progeny. © 2008 Wiley‐Liss, Inc.
The localization and non‐genomic function of the membrane‐associated estrogen receptor in oligodendrocytes
Authors: Hirahara Yukie , Matsuda Ken‐Ichi , Gao Wen , Arvanitis Dina N. , Kawata Mitsuhiro , Boggs Joan M. 
Published: August 2008

AbstractThere is general acceptance that the estrogen receptor can act as a transcription factor. However, estrogens can also bind to receptors that are located at the plasma membrane and stimulate rapid intracellular signaling processes. We recently showed that a membrane‐associated estrogen receptor (mER) is present within myelin and at the oligodendrocyte (OL) plasma membrane. To understand the physiological function of mER in OLs, we investigated its cellular localization and involvement in rapid signaling in CG4 cells and OL primary cultures. An ERα was expressed along the lacy network of veins in the membrane sheets and in the perikaryon and nucleus in OLs. ERβ was located in the nucleus, and to a lesser extent along the veins. The expression of ERα and ERβ in OL membranes was confirmed by Western analysis of isolated membranes. OL membranes mainly had truncated forms of ERα, 53 and 50 kDa, in addition to some 65 kDa form, whereas ERβ was a 54 kDa form. CG4 cells and OLs were pulsed with 17α‐ and 17β‐estradiol for various times and the total lysates were analyzed for phosphorylated kinases. Both 17α‐ and 17β‐estradiol elicited rapid phosphorylation of p42/44MAPK, Akt, and GSK‐3β within 8 min. This rapid signaling is consistent with estradiol ligation of a membrane form of ER. Since 17α‐estradiol is produced at higher concentrations than 17β‐estradiol in the brain of both sexes, signaling via 17α‐estradiol‐liganded mER may have an important function in OLs. © 2008 Wiley‐Liss, Inc.
Mitogen‐activated protein kinase‐signaling stimulates Müller glia to proliferate in acutely damaged chicken retina
Authors: Fischer Andy J. , Scott Melissa A. , Tuten William 
Published: August 2008

AbstractMüller glia in the mature retina have the capacity to become progenitor‐like cells in a many different vertebrate classes. The cell‐signaling pathways that control the ability of mature Müller glia to become progenitor‐like cells remain uncertain. The purpose of this study was to investigate the roles of the Mitogen‐Activated Protein Kinase (MAPK) pathway in regulating the activity of Müller glia in the chicken retina. In response to acute retinal damage, we found that Müller glia accumulated phosphorylated ERK1/2 and phospho‐CyclicAMP Response Element Binding‐protein (pCREB), and transiently expressed immediate early genes, cFos and Egr1, that are known to be downstream of MAPK‐signaling. Egr1 and pCREB were normally expressed by retinal progenitors in the circumferential marginal zone (CMZ), whereas cFos and pERK1/2 were not. In addition, small molecule inhibitors of MEK (UO126) and the FGF‐receptor (SU5402) suppressed the proliferation of Müller glia‐derived progenitor‐like cells. These inhibitors suppressed the accumulation of Egr1 and pCREB, whereas levels of cFos were unaffected in the glial cells. These findings suggest that Egr1 and pCREB are downstream of the signaling cascade activated by FGF‐receptors and ERK1/2. Further, our findings suggest that Egr1 and pCREB may promote glial proliferation. We propose that activation of both the FGF‐receptor and ERK1/2‐pathway is required for the proliferation and transdifferentiation of Müller glia into progenitor‐like cells. © 2008 Wiley‐Liss, Inc.
Night‐time work predisposes to non‐Hodgkin lymphoma
Authors: Lahti Tuuli A. , Partonen Timo , Kyyrönen Pentti , Kauppinen Timo , Pukkala Eero 
Published: August 2008

AbstractOur aim was to find out whether non‐Hodgkin lymphoma (NHL) was more common than expected among night‐time shift workers. The Finnish job‐exposure matrix (FINJEM) provided estimates of the proportion of exposed persons and the mean level of exposure among the exposed in each occupation. The probability of night‐time work in each occupation was assessed, the observed and expected numbers of cancer cases in a cohort of persons born in 1906–1945 during the years of 1971–1995 were calculated, and the cumulative index of night‐time work was scored. The cohort compromised of 1,669,272 persons of whom 6,307 (3,813 men and 2,494 women) had NHL during the follow‐up. Night‐time work increased significantly (p = 0.01) the risk of NHL in men, the overall relative risk being 1.10 (95% confidence interval of 1.03–1.19). Using the lag period of 10 years, the risk ratio was 1.28 (1.03–1.59) for men who worked in night‐time shifts to a high degree as compared with those who had not been exposed to night‐time work. Night‐time workers are cancer prone and have a greater risk of NHL than population on average. © 2008 Wiley‐Liss, Inc.
Frequent promoter hypermethylation and transcriptional downregulation of the NDRG2 gene at 14q11.2 in primary glioblastoma
Authors: Tepel Martin , Roerig Peter , Wolter Marietta , Gutmann David H. , Perry Arie , Reifenberger Guido , Riemenschneider Markus J. 
Published: August 2008

AbstractThe N‐myc downstream‐regulated gene 2 (NDRG2) at 14q11.2 has been reported to be downregulated in glioblastoma, and NDRG2 overexpression represses glioblastoma cell proliferation in vitro (Deng et al., Int J Cancer 2003;106;342–7). To further address the role of NDRG2 as a candidate tumor suppressor in human gliomas, we analyzed 67 astrocytic tumors (10 diffuse astrocytomas, 11 anaplastic astrocytomas, 34 primary glioblastomas and 12 secondary glioblastomas) for NDRG2 gene mutation, promoter methylation and expression at the mRNA and protein levels. Using real‐time reverse transcription PCR analysis, we found decreased NDRG2 mRNA levels in primary glioblastomas as compared to diffuse and anaplastic astrocytomas. Similarly, immunohistochemistry revealed low or absent NDRG2 protein expression in primary glioblastomas. Mutational analysis of the entire NDRG2 coding sequence did not reveal any tumor‐associated DNA sequence alterations. However, sequencing of sodium bisulfite‐modified DNA identified hypermethylation of the NDRG2 promoter region in 21 of 34 primary glioblastomas (62%). Moreover, NDRG2 promoter hypermethylation was associated with decreased NDRG2 mRNA expression. In contrast to primary glioblastomas, NDRG2 promoter hypermethylation was detected in only 1 of 11 anaplastic astrocytomas (9%) and was absent in 10 diffuse astrocytomas and 12 secondary glioblastomas. Taken together, our data support NDRG2 as a candidate tumor suppressor gene that is epigenetically silenced in the majority of primary glioblastomas, but not in lower grade astrocytomas and secondary glioblastomas. © 2008 Wiley‐Liss, Inc.
Ebselen sensitizes glioblastoma cells to Tumor Necrosis Factor (TNFα)‐induced apoptosis through two distinct pathways involving NF‐κB downregulation and Fas‐mediated formation of death inducing signaling complex
Authors: Sharma Vivek , Tewari Richa , Sk Ugir Hossain , Joseph Christy , Sen Ellora 
Published: August 2008

AbstractResistance to tumor necrosis factor (TNFα)‐induced apoptosis in various cancer cells has been attributed to the activation of the transcription factor NF‐κB. Ebselen (2‐phenyl‐1,2‐benzisoselenazol‐3[2H]one)—a selenoorganic compound is known to prevent TNFα‐mediated NF‐κB activity. As glioblastoma are resistant to the cytotoxic effect of TNFα, we investigated the potential of Ebselen in sensitizing glioma cells to TNFα‐induced apoptosis. Although treatment with Ebselen reduced viability of glioma cells, cotreatment with TNFα enhanced apoptosis further through alteration of TNFα‐mediated signaling pathways. Sensitization of TNFα activated glioma cells to apoptosis by Ebselen involved 2 pathways: (i) abrogation of TNFα induced NF‐κB activation and (ii) induction of Fas‐associated death inducing signaling complex (DISC) formation. Ebselen inhibited the prosurvival pathway mediated by NF‐κB by altering the association of TNF receptor associated factor 2 (TRAF2) with TNFα receptor associated death domain (TRADD) in the TNFR1‐TRADD‐TRAF2 complex —an interaction crucial for mediating NF‐κB activity. Ebselen also induced the formation of DISC involving Fas, Fas‐associated death domain (FADD) and active caspase 8 to transduce apoptotic signals in situations where NF‐κB function was inhibited. Cotreatment with Ebselen and TNFα induced G2/M phase arrest in cell cycle and modulated the expression of molecules involved in cell cycle progression. These results raise the possibility of overcoming resistance to TNFα‐induced apoptosis by cotreatment with organoselenium Ebselen as a strategy to kill glioma cells. © 2008 Wiley‐Liss, Inc.
Adiponectin and alcoholic fatty liver disease
Authors: Rogers Christopher Q. , Ajmo Joanne M. , You Min 
Published: August 2008

AbstractWorldwide, one of the most prevalent forms of chronic disease is alcoholic fatty liver, which may progress to more severe forms of liver injury including steatohepatitis, fibrosis, and cirrhosis. The molecular mechanisms by which ethanol consumption causes accumulation of hepatic lipid are multiple and complex. Chronic ethanol exposure is thought to cause enhanced hepatic lipogenesis and impaired fatty acid oxidation by inhibiting key hepatic transcriptional regulators such as AMP‐activated kinase (AMPK), sirtuin 1 (SIRT1), PPAR‐gamma coactivator alpha (PGC‐1α), peroxisome proliferator‐activated receptor alpha (PPARα), and sterol regulatory element‐binding protein 1 (SREBP‐1). Adiponectin is an adipose‐derived hormone with a variety of beneficial biological functions. Increasing evidence suggests that altered adiponectin production in adipose tissue and impaired expression of hepatic adiponectin receptors (AdipoRs) are associated with the development of alcoholic liver steatosis in several rodent models. More importantly, studies have demonstrated a protective role of adiponectin against alcoholic liver steatosis. The hepato‐protective effect of adiponectin is largely mediated by the coordination of multiple signaling pathways in the liver, leading to enhanced fat oxidation, reduced lipid synthesis and prevention of hepatic steatosis. This review begins with an assessment of the current understanding of the role of adiponectin and its receptors in the regulation of lipid homeostasis in liver, with emphasis on their relationship to the development of alcoholic liver steatosis. Following sections will review hepatic signaling molecules involved in the protective actions of adiponectin against alcoholic fatty liver and summarize the current knowledge of regulatory mechanisms of adiponectin expression and secretion in response to chronic ethanol exposure. We will conclude with a discussion of potential strategies for treating human alcoholic fatty liver disease (AFLD), including nutritional and pharmacological modulation of adiponectin and its receptors. © 2008 IUBMB IUBMB Life, 60(12): 790–797, 2008
Comprehensive ab initio calculation and simulation on the low‐lying electronic states of TlX (X = F, Cl, Br, I, and At)
Authors: Zou Wenli , Liu Wenjian 
Published: August 2008

AbstractThe low‐lying electronic states of TlX (X = F, Cl, Br, I, and At) are investigated using the configuration interaction based complete active space third‐order perturbation theory [CASPT3(CI)] with spin‐orbit coupling accounted for. The potential energy curves and the corresponding spectroscopic constants are reported. The results are grossly in good agreement with the available experimental data. The absorption spectra are simulated as well to reassign the experimental bands. The present results are also useful for guiding future experimental measurements. © 2008 Wiley Periodicals, Inc. J Comput Chem, 2009