bluuebunny/crossref_metadata_2025_split huggingface dataset:
Long‐term effects of infant learning on adult conditioned odor aversion are determined by the last preweaning experience
Authors: Sevelinges Yannick , Mouly Anne‐Marie , Lévy Frédéric , Ferreira Guillaume 
Published: May 2009

AbstractWe recently showed that odorizing mother's nipples from birth to weaning attenuated adult conditioned odor aversion (COA). The present study evaluated whether shorter durations of preweaning olfactory experiences could induce similar long‐term effects. We first showed that late preweaning odorization (PN13–PN25) impaired adult COA similarly to odorization from birth to weaning (PN0–PN25) whereas early odorization (PN0–PN12) had no effect on adult COA. As early odorization was followed by an odorless suckling period, we evaluated whether this odorless suckling could have interfered with early associative learning. We therefore weaned the animals either immediately after early odorization or 7 days later. Early odorization (PN0–PN18) followed by late odorless suckling (PN19–PN25) had no effect on adult COA. However, pups with early odorization (PN0–PN18) but without late odorless suckling (weaned at PN18) showed attenuated COA. These results support the hypothesis that interference between early and late preweaning experiences with the mother determines the long‐term impact on adult COA. © 2009 Wiley Periodicals, Inc. Dev Psychobiol 51: 389–398, 2009.
Generation of mice with a conditional allele for transforming growth factor beta 1 gene
Authors: Azhar Mohamad , Yin Moying , Bommireddy Ramireddy , Duffy John J. , Yang Junqi , Pawlowski Sharon A. , Boivin Gregory P , Engle Sandra J. , Sanford L.P. , Grisham Christina , Singh Ram R. , Babcock George F. , Doetschman Thomas 
Published: May 2009

AbstractTransforming growth factor β1 (TGFβ1) is a multifunctional growth factor involved in wound healing, tissue fibrosis, and in the pathogenesis of many syndromic diseases (e.g., Marfan syndrome, Camurati‐Engelmann disease) and muscular, neurological, ophthalmic, cardiovascular and immunological disorders, and cancer. Since the generation of Tgfb1 knockout mice, there has been extraordinary progress in understanding its physiological and pathophysiological function. Here, we report the generation of a conditional knockout allele for Tgfb1 in which its exon 6 is flanked with LoxP sites. As proof of principle, we crossed these mice to LckCre transgenic mice and specifically disrupted Tgfb1 in T cells. The results indicate that T‐cell‐produced TGFβ1 is required for normal in vivo regulation of peripheral T‐cell activation, maintenance of T‐cell homeostasis, and suppression of autoimmunity. genesis 47:423–431, 2009. © 2009 Wiley‐Liss, Inc.
Generation of a mouse line expressing Sox17‐driven Cre recombinase with specific activity in arteries
Authors: Liao W. Perry , Uetzmann Lena , Burtscher Ingo , Lickert Heiko 
Published: May 2009

AbstractThe HMG‐box transcription factor Sox17 has been shown to play important roles in both endoderm formation and cardiovascular development. To conditionally inactivate genes in these domains, we have targeted a codon improved Cre Recombinase (iCre) into exon 1 of the Sox17 gene. Surprisingly, Cre‐mediated recombination in the Rosa26 reporter mouse line revealed largely specific activity within the vasculature rather than in endoderm‐derived tissues. Here we report a new Cre knock‐in mouse line, Sox17iCre with activity in the vascular endothelial cells of arteries in the cardiovascular system but not in veins. Cre‐mediated recombination was also strongly detected in the liver and spleen, the two organs associated with hematopoiesis. Thus, these results indicate that the Sox17iCre would be an appropriate tool for conditional mutagenesis of genes in the vasculature and could be used in studies of blood vessel development and angiogenesis. Additionally, we provide evidence that two different promoters drive Sox17 expression in the endodermal and vascular system. genesis 47:476–483, 2009. © 2009 Wiley‐Liss, Inc.
On the mechanism underlying the divergent retinal and bristle defects of M8* (E(spl)D) in Drosophila
Authors: Kahali Bhaskar , Bose Anasua , Karandikar Umesh , Bishop Clifton P. , Bidwai Ashok P. 
Published: May 2009

AbstractOur results, using endogenous mutants and Gal4‐UAS driven transgenes, implicate multisite phosphorylation in repression by E(spl)M8. We propose that these phosphorylations occur in the morphogenetic furrow (MF) to reverse an auto‐inhibited state of M8, enabling repression of Atonal during R8 specification. Our studies address the paradoxical behavior of M8*, the truncated protein encoded by E(spl)D. We suggest that differences in N signaling in the bristle versus the eye underlie the antimorphic activity of M8* in N+ (ectopic bristles) and hypermorphic activity in Nspl (reduced eye). Ectopic M8* impairs eye development (in Nspl) only during establishment of the atonal feedback loop (anterior to the MF), but is ineffective after this time point. In contrast, a CK2 phosphomimetic M8 lacking Groucho (Gro) binding, M8SDΔGro, acts antimorphic in N+ and suppresses the eye/R8 and bristle defects of Nspl, as does reduced dosage of E(spl) or CK2. Multisite phosphorylation could serve as a checkpoint to enable a precise onset of repression, and this is bypassed in M8*. Additional implications are discussed. genesis 47:456–468, 2009. © 2009 Wiley‐Liss, Inc.
Transthyretin mouse transgenes direct RFP expression or Cre‐mediated recombination throughout the visceral endoderm
Authors: Kwon Gloria S. , Hadjantonakis Anna‐Katerina 
Published: May 2009

AbstractTransthyretin (Ttr) is a thyroid hormone transport protein secreted by cells of the visceral yolk sac and fetal liver in developing embryos, and by hepatocytes and the choroid plexus epithelium of the brain in adult mice. Spatiotemporal localization of Ttr mRNA during embryogenesis suggested that Ttr regulatory elements might drive transgene expression throughout the visceral endoderm of early mouse embryos. We use Ttr cis‐regulatory elements to generate Ttr::RFP and Ttr::Cre strains of mice, driving red fluorescent protein (RFP) and a nuclear‐localized Cre recombinase, respectively. Visualization of RFP fluorescence in Ttr::RFP transgenics confirms reporter localization throughout the visceral endoderm in early embryos and in the visceral yolk sac and fetal liver of later stage embryos. Using both GFP‐based and LacZ‐based Cre reporter strains, we demonstrate that in Ttr::Cre transgenics, Cre‐mediated recombination occurs throughout the visceral endoderm. The Ttr::Cre strain can therefore be used as a tool for genetic modifications within the visceral endoderm lineage. genesis 47:447–455, 2009. © 2009 Wiley‐Liss, Inc.
Generation of Smad7‐Cre recombinase mice: A useful tool for the study of epithelial‐mesenchymal transformation within the embryonic heart
Authors: Snider Paige , Tang Sunyong , Lin Goldie , Wang Jian , Conway Simon J. 
Published: May 2009

AbstractSmad7 can be induced by various transforming growth factor‐β superfamily ligands and negatively modulates their signaling, thus acting in a negative, autocrine feedback manner. Previous analyses have demonstrated that although Smad7 is widely expressed, it is predominantly found in the vascular endothelium. Because of the restricted spatiotemporal reporter expression driven via a novel 4.3 kb Smad7 promoter in endocardial cells overlying the hearts atrioventricular (AV) cushions; we hypothesized that a transgenic Cre line would prove useful for the analysis of endocardial cushion and valve formation. Here we describe a mouse line, Smad7Cre, where Cre is robustly expressed within both cardiac outflow and AV endocardial cushions. Additionally, as endocardial cells are thought to contribute at least in part to the formation of the endocardial cushion mesenchyme, we crossed the Smad7Cre mice to the ROSA26eGFP‐DTA diphtheria toxin A‐expressing mice in order to genetically ablate Smad7Cre expressing cells. Ablation of Smad7Cre cells resulted in embryonic lethality by E11.5 and largely acellular endocardial cushions. genesis 47:469–475, 2009. © 2009 Wiley‐Liss, Inc.
FlEx‐based transgenic reporter lines for visualization of Cre and Flp activity in live zebrafish
Authors: Boniface Emily J. , Lu Jianjun , Victoroff Tristan , Zhu Meiying , Chen Wenbiao 
Published: May 2009

AbstractSite‐specific recombinases such as Cre and Flp are invaluable tools for genetic manipulations, but their usage in zebrafish has been limited. Incorporating recently developed flip‐excision (FlEx) design that allows stable inversions, we have established zebrafish reporter lines that express bright and ubiquitous EGFP, but switch to express mCherry in the presence of Cre or Flp. Here, we demonstrate the stable inversion in the reporter lines, both in somatic cells and in the germ line by Cre or Flp, and the subsequent reinversion using the other recombinase. Using the reporter lines, we characterized cardiomyocyte‐specific Cre lines and neuronal progenitor‐specific and tamoxifen‐dependent Cre lines. We also used the reporter lines for screening Cre‐ and Flp‐based enhancer trap lines. Similar to the widely used Cre reporter lines in mice, these FlEx‐based reporter lines will facilitate the use of recombinases for genetic manipulations in zebrafish. genesis 47:484–491, 2009. © 2009 Wiley‐Liss, Inc.
Precise temporal regulation of roughest is required for correct salivary gland autophagic cell death in Drosophila
Authors: Simon Claudio R. , Moda Livia M.R. , Octacilio‐Silva Shirlei , Anhezini Lucas , Machado‐Gitai Luciana C.H. , Ramos Ricardo Guelerman P. 
Published: May 2009

AbstractThe Drosophila roughest (rst) locus encodes an immunoglobulin superfamily transmembrane glycoprotein implicated in a variety of embryonic and postembryonic developmental processes. Here we demonstrate a previously unnoticed role for this gene in the autophagic elimination of larval salivary glands during early pupal stages by showing that overexpression of the Rst protein ectodomain in early pupa leads to persistence of salivary glands up to at least 12 hours after head eversion, although with variable penetrance. The same phenotype is observed in individuals carrying the dominant regulatory allele rstD, but not in loss of function alleles. Analysis of persistent glands at the ultrastructural level showed that programmed cell death starts at the right time but is arrested at an early stage of the process. Finally we describe the expression pattern and intracellular distribution of Rst in wild type and rstD mutants, showing that its downregulation in salivary glands at the beginning of pupal stage is an important factor in the correct implementation of the autophagic program of this tissue in space and time. genesis 47:492–504, 2009. © 2009 Wiley‐Liss, Inc.
Synthesis of the Clathrate‐II K8.6(4)Ge136 by Oxidation of K4Ge9 in an Ionic Liquid
Authors: Guloy Arnold M. , Tang Zhongjia , Ramlau Reiner , Böhme Bodo , Baitinger Michael , Grin Yuri 
Published: May 2009

AbstractThe new clathrate‐II K8.6(4)Ge136 has been synthesized by mild oxidation of K4Ge9 in the ionic liquid n‐dodecyltrimethylammonium chloride (DTAC)/AlCl3 at 300 °C and subsequent annealing at 370 °C. Refinement of the crystal structure from X‐ray powder diffraction data revealed the composition K8.6(4)Ge136 [space group Fd$\bar {3}$m, a = 15.302(1) Å], which was also confirmed by energy‐dispersive X‐ray spectrometry (EDXS), transmission electron microscopy, and scanning electron microscopy on the bulk material. K atoms preferably occupy the larger Ge28 cages rather than the Ge20 cages in the clathrate‐II structure. K8.6(4)Ge136 is metastable and was found to decompose exothermically at 471 °C. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2009)
Direct Electron Transfer of Horseradish Peroxidase in Gellan Gum–Hydrophilic Ionic Liquid Gel Film
Authors: Shangguan Xiaodong , Zheng Jianbin , Sheng Qinglin 
Published: May 2009

AbstractA new composite film of microbial exocellular polysaccharide‐gellan gum (GG) and hydrophilic room temperature ionic liquid 1‐butyl‐3‐methyl‐imidazolium tetrafluoroborate (BMIMBF4) was firstly used as an immobilization matrix to entrap horseradish peroxidase (HRP), and its properties were studied by UV/vis spectroscopy, cyclic voltammetry and electrochemical impedance spectroscopy. The results showed that BMIMBF4 could promote the electron transfer between HRP and electrode surface, and the existence of GG could successfully immobilize BMIMBF4 on the electrode surface with improved stability. HRP–BMIMBF4–GG/GCE exhibited a pair of well‐defined and quasireversible cyclic voltammetric peaks in 0.1 M pH 7.0 phosphate buffer solutions at 1.8 V/s, which was the characteristic of HRP Fe(III)/Fe(II) redox couples. The formal potentials (E°′) was −0.368 V (vs. SCE) and the peak‐to‐peak potential separation (ΔEP) was 0.058 V. The peak currents were five times as large as those of HRP–GG/GCE. The average surface coverage (Γ*) and the apparent Michaelis‐Menten constant (Km) were 4.5×10−9 mol/cm2 and 0.67 μM, respectively. The electron transfer rate constant was estimated to be 15.8 s−1. The proposed electrode showed excellent electrocatalytic activity towards hydrogen peroxide (H2O2). The linear dynamic range for the detection of H2O2 was 0.05–0.5 μM with a correlation coefficient of 0.9945 and the detection limit was estimated at about 0.02 μM (S/N=3). BMIMBF4–GG composite film was promising to immobilize other redox enzymes or proteins and attain their direct electrochemistry.
High hyperdiploid childhood acute lymphoblastic leukemia
Authors: Paulsson Kajsa , Johansson Bertil 
Published: May 2009

AbstractHigh hyperdiploidy (51–67 chromosomes) is the most common cytogenetic abnormality pattern in childhood B‐cell precursor acute lymphoblastic leukemia (ALL), occurring in 25–30% of such cases. High hyperdiploid ALL is characterized cytogenetically by a nonrandom gain of chromosomes X, 4, 6, 10, 14, 17, 18, and 21 and clinically by a favorable prognosis. Despite the high frequency of this karyotypic subgroup, many questions remain regarding the epidemiology, etiology, presence of other genetic changes, the time and cell of origin, and the formation and pathogenetic consequences of high hyperdiploidy. However, during the last few years, several studies have addressed some of these important issues, and these, as well as previous reports on high hyperdiploid childhood ALL, are reviewed herein. © 2009 Wiley‐Liss, Inc.
Blockade of TRPC6 channels induced G2/M phase arrest and suppressed growth in human gastric cancer cells
Authors: Cai Rong , Ding Xia , Zhou Kechun , Shi Yu , Ge Ruiliang , Ren Gang , Jin Yening , Wang Yizheng 
Published: May 2009

AbstractChannels formed by the canonical transient receptor potential (TRPC) subfamily of proteins are Ca2+‐permeable, nonselective cation channels with various functions. Through a phospholipase C (PLC)‐dependent mechanism TRPC6, a member of TRPC subfamily, can be activated by receptor tyrosine kinases (RTK) or G protein‐coupled receptors (GPCR), which are implicated in cell proliferation and human malignancies. Here, we report that TRPC6 has a critical role in human gastric cancer development. Expression of TRPC6 was greatly upregulated in human gastric cancer epithelial cells compared with that in normal gastric epithelial cells. Treatment of AGS or MKN45 cells, human gastric cancer cell lines, with SKF96365, an agent known to inhibit TRPC channels, arrested cell cycle in G2/M phase and suppressed cell growth. Importantly, expressing a dominant negative mutant of TRPC6 (DNC6) in these cells also arrested cell cycle in G2/M phase and inhibited cell growth. The Ca2+ elevation in the MKN45 cells evoked by histamine was inhibited by SKF96365 and DNC6. Moreover, inhibition of TRPC6 suppressed the formation of gastric tumors in nude mice. These results suggest that Ca2+ elevation regulated by TRPC6 channels is essential for G2/M phase transition and for the development of gastric cancers. © 2009 UICC
Serum hepatocyte growth factor as a prognostic marker for stage II or III colorectal cancer patients
Authors: Toiyama Yuji , Miki Chikao , Inoue Yasuhiro , Okugawa Yoshinaga , Tanaka Kouji , Kusunoki Masato 
Published: May 2009

AbstractWe previously reported that a combination of serum hepatocyte growth factor (HGF) and carcinoembryonic antigen (CEA) was useful for selecting early‐stage colorectal cancer patients with aggressive disease. The aim of the present study was to determine whether serum HGF could provide CEA‐independent prognostic information on patients undergoing surgery with curative intent. Serum samples were collected from 184 patients with colorectal cancer and 30 controls. Reverse‐transcription polymerase chain reaction was used to detect HGF expression in colorectal cancer cell lines. Serum and tissue levels of HGF were measured by enzyme‐linked immunosorbent assay. The serum HGF levels in colorectal cancer patients were compared with those in healthy controls, and we retrospectively assessed the association between serum HGF levels and clinicopathological findings and survival. Expression of HGF was significantly higher in colorectal cancer tissues compared with non‐tumor tissues. The serum HGF levels were closely correlated with the HGF levels in cancer tissue. The mean serum HGF level in patients was significantly higher than that in controls, and significantly higher in patients with large tumor, lymph‐node involvement and distant metastasis. According to the receiver operating characteristic (ROC) analysis, elevated serum HGF levels can predict patients with larger tumor, lymph‐node and distant metastasis. Elevated serum HGF level demonstrated a significant association with poor survival, and was only an independent risk factor for poor survival in Stage II or/and III. Elevated serum HGF level is significantly associated with colorectal cancer development, lymph or distant invasive phenotypes and survival, especially in Stage II or III patients. © 2009 UICC
Increased intratumoral regulatory T cells are related to intratumoral macrophages and poor prognosis in hepatocellular carcinoma patients
Authors: Zhou Jia , Ding Tong , Pan Weidong , Zhu Ling‐yan , Li Lian , Zheng Limin 
Published: May 2009

AbstractImmunosuppression mediated by regulatory T cells (Tregs) is a key facilitator of tumor immune evasion, but the source of these Tregs and their contribution to human cancer progression remains unclear. This study investigated the properties of FoxP3+ Tregs, their prognostic value in patients with hepatocellular carcinoma (HCC) and the underlying mechanisms of FoxP3+ Treg intratumoral accumulation. In addition to an increased number of circulating FoxP3+ Tregs, the results also showed that FoxP3+ Tregs gathered in the tumor site, where they suppressed tissue‐derived CD4+CD25− T‐cell activation (p < 0.001), promoting disease progression and poor prognosis in HCC patients (< 0.01). The intratumoral prevalence of FoxP3+ Tregs was associated with a high density of macrophages (Mφ) (p < 0.001). Depletion of tissue Mφ thus attenuated the increase of liver FoxP3+ Treg frequency attributed to in vivo inoculation with hepatoma (p = 0.01), whereas Mφ exposed to tumor culture supernatants from hepatoma‐derived cell lines increased FoxP3+ Treg frequency in vitro (p < 0.001). This increase was partially blocked by antiinterleukin‐10 antibody (p < 0.01). In conclusion, tumor‐associated Mφ may trigger a rise of the intratumoral FoxP3+ Treg population, which in turn may promote HCC progression. © 2009 UICC
Embryonic fates for extraembryonic lineages: New perspectives
Authors: Fraser Stuart T. , Baron Margaret H. 
Published: May 2009

AbstractThe prevailing view of the functions of the extraembryonic lineages of the mammalian embryo has been that they serve solely to support its intrauterine development. In recent years, a number of studies have suggested that the extraembryonic mesoderm and visceral endoderm in fact contribute cells to tissues of the developing animal. In this mini‐review, we discuss evidence that the yolk sac is an early source of hematopoietic stem and progenitor cells and that the cells of the visceral endoderm, once thought to be segregated solely to the yolk sac, constitute a subpopulation of cells within the developing gut tube and perhaps other endodermal structures. Fascinating questions remain to be addressed and are likely to establish a new paradigm for studying early mammalian development. Understanding the processes that give rise to stem cell populations in development may lead to advances in stem cell therapies and regenerative medicine. J. Cell. Biochem. 107: 586–591, 2009. © 2009 Wiley‐Liss, Inc.
Human mesenchymal stem cells express vascular cell phenotypes upon interaction with endothelial cell matrix
Authors: Lozito Thomas P. , Kuo Catherine K. , Taboas Juan M. , Tuan Rocky S. 
Published: May 2009

AbstractMesenchymal stem cells (MSCs) are thought to occupy a perivascular niche where they are exposed to signals originating from vascular cells. This study focused on the effects of endothelial cell (EC)‐derived signals on MSC differentiation toward vascular cell lineages. Upon co‐culture with two types of ECs, macrovascular (macro) ECs and microvascular (micro) ECs, the former caused MSCs to increase expression of both EC and smooth muscle cell (SMC) markers, while the latter induced expression of EC markers only. These marker changes in MSCs were linked to the extracellular matrixes secreted by the ECs (EC‐matrix) rather than soluble EC‐secreted factors. Beyond enhanced marker expression, EC‐matrix also induced functional changes in MSCs indicative of development of a genuine vascular cell phenotype. These included enhanced incorporation into vessels and cytoskeletal localization of vascular SMC‐specific contractile elements. The bioactivity of EC‐matrix was sensitive to EDTA washes and required sulfated glycosaminoglycans. However, neither soluble VEGF nor substrate surfaces coated with fibronectin, collagen type IV, or laminin recreated the effects of EC‐matrix on MSC vascular differentiation. In conclusion, these results identified EC‐matrix as a critical regulator of vascular cell differentiation of MSCs. Elucidating these MSC–EC‐matrix interactions and identifying the specific EC‐matrix components involved will shed light on the perivascular signals seen by MSCs in vivo. J. Cell. Biochem. 107: 714–722, 2009. Published 2009 Wiley‐Liss, Inc.
Effects of resveratrol on H2O2‐induced apoptosis and expression of SIRTs in H9c2 cells
Authors: Yu Wei , Fu Yu‐Cai , Zhou Xiao‐Hui , Chen Chun‐Juan , Wang Xin , Lin Rui‐Bo , Wang Wei 
Published: May 2009

AbstractResveratrol, a polyphenol found in fruits, has been demonstrated to activate Sir2. Though many studies have demonstrated that resveratrol can activate SIRT1, whether it has effect on other sirtuins (SIRT2–7) are unknown. The present study shows that exposure of H9c2 cells to 50 µM H2O2 for 6 h caused a significant increase in apoptosis, as evaluated by TUNEL and flow cytometry (FCM), but pretreatment of resveratrol (20 µM) eliminated H2O2‐induced apoptosis. Resveratrol also prevented H2O2‐induced caspase‐3 activation. Exposure of cells to resveratrol caused rapid activation of SIRT1,3,4,7. Sirtuin inhibitor, nicotinamide (20 mM) attenuated resveratrol's inhibitory effect on cell apoptosis and caspase‐3 activity. These results suggest that resveratrol protects cardiomyocytes from H2O2‐induced apoptosis by activating SIRT1,3,4,7. J. Cell. Biochem. 107: 741–747, 2009. © 2009 Wiley‐Liss, Inc.