bluuebunny/crossref_metadata_2025_split huggingface dataset:
Peripheral facial nerve axotomy in mice causes sprouting of motor axons into perineuronal central white matter: Time course and molecular characterization
Authors: Makwana Milan , Werner Alexander , Acosta‐Saltos Alejandro , Gonitel Roman , Pararajasingham Abirami , Ruff Crystal , Rumajogee Prakasham , Cuthill Dan , Galiano Mathias , Bohatschek Marion , Wallace Adam S. , Anderson Patrick N. , Mayer Ulrike , Behrens Axel , Raivich Gennadij 
Published: October 2009

AbstractGeneration of new axonal sprouts plays an important role in neural repair. In the current study, we examined the appearance, composition and effects of gene deletions on intrabrainstem sprouts following peripheral facial nerve axotomy. Axotomy was followed by the appearance of galanin+ and calcitonin gene‐related peptide (CGRP)+ sprouts peaking at day 14, matching both large, neuropeptide+ subpopulations of axotomized facial motoneurons, but with CGRP+ sprouts considerably rarer. Strong immunoreactivity for vesicular acetylcholine transporter (VAChT) and retrogradely transported MiniRuby following its application on freshly cut proximal facial nerve stump confirmed their axotomized motoneuron origin; the sprouts expressed CD44 and alpha7beta1 integrin adhesion molecules and grew apparently unhindered along neighboring central white matter tracts. Quantification of the galanin+ sprouts revealed a stronger response following cut compared with crush (day 7–14) as well as enhanced sprouting after recut (day 8 + 6 vs. 14; 14 + 8 vs. 22), arguing against delayed appearance of sprouting being the result of the initial phase of reinnervation. Sprouting was strongly diminished in brain Jun‐deficient mice but enhanced in alpha7 null animals that showed apparently compensatory up‐regulation in beta1, suggesting important regulatory roles for transcription factors and the sprout‐associated adhesion molecules. Analysis of inflammatory stimuli revealed a 50% reduction 12–48 hours following systemic endotoxin associated with neural inflammation and a tendency toward more sprouts in TNFR1/2 null mutants (P = 10%) with a reduced inflammatory response, indicating detrimental effects of excessive inflammation. Moreover, the study points to the usefulness of the facial axotomy model in exploring physiological and molecular stimuli regulating central sprouting. J. Comp. Neurol. 518:699–721, 2010. © 2009 Wiley‐Liss, Inc.
Chronic expression of PPAR‐δ by oligodendrocyte lineage cells in the injured rat spinal cord
Authors: Almad Akshata , McTigue Dana M. 
Published: October 2009

AbstractThe transcription factor peroxisome proliferator‐activated receptor (PPAR)‐δ promotes oligodendrocyte differentiation and myelin formation in vitro and is prevalent throughout the brain and spinal cord. Its expression after injury, however, has not been examined. Thus, we used a spinal contusion model to examine the spatiotemporal expression of PPAR‐δ in naïve and injured spinal cords from adult rats. As previously reported, PPAR‐δ was expressed by neurons and oligodendrocytes in uninjured spinal cords; PPAR‐δ was also detected in NG2 cells (potential oligodendrocyte progenitors) within the white matter and gray matter. After spinal cord injury (SCI), PPAR‐δ mRNA and protein were present early and increased over time. Overall PPAR‐δ+ cell numbers declined at 1 day post injury (dpi), likely reflecting neuron loss, and then rose through 14 dpi. A large proportion of NG2 cells expressed PPAR‐δ after SCI, especially along lesion borders. PPAR‐δ+ NG2 cell numbers were significantly higher than naive by 7 dpi and remained elevated through at least 28 dpi. PPAR‐δ+ oligodendrocyte numbers declined at 1 dpi and then increased over time such that >20% of oligodendrocytes expressed PPAR‐δ after SCI compared with ∼10% in uninjured tissue. The most prominent increase in PPAR‐δ+ oligodendrocytes was along lesion borders where at least a portion of newly generated oligodendrocytes (bromodeoxyuridine+) were PPAR‐δ+. Consistent with its role in cellular differentiation, the early rise in PPAR‐δ+ NG2 cells followed by an increase in new PPAR‐δ+ oligodendrocytes suggests that this transcription factor may be involved in the robust oligodendrogenesis detected previously along SCI lesion borders. J. Comp. Neurol. 518:785–799, 2010. © 2009 Wiley‐Liss, Inc.
Localization of a GABA transporter to glial cells in the developing and adult olfactory pathway of the moth Manduca sexta
Authors: Oland Lynne A. , Gibson Nicholas J. , Tolbert Leslie P. 
Published: October 2009

AbstractGlial cells have several critical roles in the developing and adult olfactory (antennal) lobe of the moth Manduca sexta. Early in development, glial cells occupy discrete regions of the developing olfactory pathway and processes of γ‐aminobutyric acid (GABA)ergic neurons extend into some of these regions. Because GABA is known to have developmental effects in a variety of systems, we explored the possibility that the glial cells express a GABA transporter that could regulate GABA levels to which olfactory neurons and glial cells are exposed. By using an antibody raised against a characterized high‐affinity M. sexta GABA transporter with high sequence homology to known mammalian GABA transporters (Mbungu et al. [1995] Arch. Biochem. Biophys. 318:489–497; Umesh and Gill [2002] J. Comp. Neurol. 448:388–398), we found that the GABA transporter is localized to subsets of centrally derived glial cells during metamorphic adult development. The transporter persists into adulthood in a subset of the neuropil‐associated glial cells, but its distribution pattern as determined by light‐and electron‐microscopic‐level immunocytochemistry indicates that it could not serve to regulate GABA concentration in the synaptic cleft. Instead, its role is more likely to regulate extracellular GABA levels within the glomerular neuropil. Expression in the sorting zone glial cells disappears after the period of olfactory receptor axon ingrowth, but may be important during ingrowth if GABA regulates axon growth. Glial cells take up GABA, and that uptake can be blocked by L‐2,4‐diaminobutyric acid (DABA). This is the first molecular evidence that the central glial cell population in this pathway is heterogeneous. J. Comp. Neurol. 518:815–838, 2010. © 2009 Wiley‐Liss, Inc.
Different Catalytic Effects of a Single Water Molecule: The Gas‐Phase Reaction of Formic Acid with Hydroxyl Radical in Water Vapor
Authors: Anglada Josep M. , Gonzalez Javier 
Published: October 2009

AbstractThe effect of a single water molecule on the reaction mechanism of the gas‐phase reaction between formic acid and the hydroxyl radical was investigated with high‐level quantum mechanical calculations using DFT–B3LYP, MP2 and CCSD(T) theoretical approaches in concert with the 6‐311+G(2df,2p) and aug‐cc‐pVTZ basis sets. The reaction between HCOOH and HO has a very complex mechanism involving a proton‐coupled electron transfer process (pcet), two hydrogen‐atom transfer reactions (hat) and a double proton transfer process (dpt). The hydroxyl radical predominantly abstracts the acidic hydrogen of formic acid through a pcet mechanism. A single water molecule affects each one of these reaction mechanisms in different ways, depending on the way the water interacts. Very interesting is also the fact that our calculations predict that the participation of a single water molecule results in the abstraction of the formyl hydrogen of formic acid through a hydrogen atom transfer process (hat).
Structural Features of Interacting Complementary Liposomes Promoting Formation of Multicompartment Structures
Authors: Sideratou Zili , Sterioti Nikoletta , Tsiourvas Dimitris , Paleos Constantinos M. 
Published: October 2009

AbstractThe structural features of complementary liposomes and factors favoring formation of multicompartment systems are investigated. Specifically, liposomal formulations consisting of PEGylated unilamellar liposomes with guanidinium moieties located at the distal end of polyethylene glycol (PEG) chains interact with complementary multilamellar liposomes bearing phosphate moieties. Furthermore, the number of PEG chains attached to the unilamellar interface of the liposomes is enhanced by incorporating PEGylated cholesterol in their bilayer. While molecular recognition of the liposomes is the driving force for initiating multicompartmentalization, it is the enhanced PEGylation at the liposomal interface that synergistically promotes fusion resulting in large and well‐formed multicompartment systems. A mechanism is proposed according to which initial adhesion of the liposomes, followed by reorganization of their membrane lipids, leads to giant bilayer aggregates incorporating large liposomes.
QoS‐aware fair packet scheduling in IEEE 802.16 wireless mesh networks
Authors: Li Yajun , Yang Yuhang , Zhou Liang , Wei Anne , Cao Chengyu 
Published: October 2009

AbstractIn this paper, we address the problem of heterogeneous quality‐of‐service (QoS) provisioning in IEEE 802.16‐based wireless mesh networks. Our objective is to provide a novel service differentiation scheme based on distributed scheduling in the IEEE 802.16‐based mesh mode, thereby offering QoS guarantees. We first devise a novel scheme for the traffic class differentiation, which can be implemented at the medium access control layer. We then present a QoS‐aware fair packet scheduling (QFPS) algorithm to fulfill the QoS provisioning. With QFPS, a traffic flow with urgent QoS demand is guaranteed to be given priority in wireless resource allocation over those ones with mild QoS requirements. A shorter end‐to‐end delay is therefore expected to be offered for the traffic flows with time‐urgent requirements. Moreover, we propose a new fairness model among different traffic flows traversing the same node. All traffic flows passing through a node are served by the Deficit Round‐Robin scheduling algorithm to achieve fairness within the same priority group. The experimental results of the QFPS demonstrate that various traffic flows are provided with a differentiated service that offers QoS guarantees. Copyright © 2009 John Wiley & Sons, Ltd.
A Probasin‐MerCreMer BAC allows inducible recombination in the mouse prostate
Authors: Birbach Andreas , Casanova Emilio , Schmid Johannes A. 
Published: October 2009

AbstractTissue‐specific transgene expression in the prostate epithelium has previously been achieved using short prostate‐specific promoters, rendering transgenic mouse lines susceptible to integration site‐dependent effects. Here we demonstrate the applicability of bacterial artificial chromosome (BAC) technology to transgene expression in the prostate epithelium. We present mouse lines expressing an inducible Cre protein (MerCreMer) under the control of regulatory elements of the probasin gene on a BAC. These mouse lines show high organ specificity, high transgene expression in anterior, dorsal and lateral prostate lobes, no background Cre recombination using a reporter strain and adjustable amounts of Cre‐induced recombination upon tamoxifen induction. Together with two recently reported transgenic lines expressing the Cre‐ERT2 protein from small prostate‐specific promoters, these mouse lines will be useful in research focused on prostate‐specific disorders such as benign hyperplasia or cancer. genesis 47:757–764, 2009. © 2009 Wiley‐Liss, Inc.
Oligodendroglial and pan‐neural crest expression of Cre recombinase directed by Sox10 enhancer
Authors: Stine Zachary E. , Huynh Jimmy L. , Loftus Stacie K. , Gorkin David U. , Salmasi Amirali H. , Novak Thomas , Purves Todd , Miller Ronald A. , Antonellis Anthony , Gearhart John P. , Pavan William J. , McCallion Andrew S. 
Published: October 2009

AbstractUtilizing a recently identified Sox10 distal enhancer directing Cre expression, we report S4F:Cre, a transgenic mouse line capable of inducing recombination in oligodendroglia and all examined neural crest derived tissues. Assayed using R26R:LacZ reporter mice expression was detected in neural crest derived tissues including the forming facial skeleton, dorsal root ganglia, sympathetic ganglia, enteric nervous system, aortae, and melanoblasts, consistent with Sox10 expression. LacZ reporter expression was also detected in non‐neural crest derived tissues including the oligodendrocytes and the ventral neural tube. This line provides appreciable differences in Cre expression pattern from other transgenic mouse lines that mark neural crest populations, including additional populations defined by the expression of other SoxE proteins. The S4F:Cre transgenic line will thus serve as a powerful tool for lineage tracing, gene function characterization, and genome manipulation in these populations. genesis 47:765–770, 2009. © 2009 Wiley‐Liss, Inc.
Generation and analysis of a mouse line harboring GFP in the Eomes/Tbr2 locus
Authors: Arnold Sebastian J. , Sugnaseelan Jacintha , Groszer Matthias , Srinivas Shankar , Robertson Elizabeth J. 
Published: October 2009

AbstractDuring mouse embryonic development, the T‐box transcription factor Eomes/Tbr2 is expressed in highly dynamic patterns in various progenitor cell types. Those include the undifferentiated cells of the trophectoderm, ingressing nascent mesoderm at the primitive streak, and intermediate progenitor cells of the developing cerebral cortex. We generated an EomesGFP‐ targeted allele to follow the highly dynamic patterns of Eomes expression and to allow for the identification of novel expression domains. We show that our novel allele recapitulates endogenous gene expression at known sites of expression and confirm our results by anti‐Eomes immunofluorescent staining. Using this novel allele we were able to identify previously undocumented domains of Eomes expression within the visceral endoderm and at various locations in the developing and adult mouse brain. genesis 47:775–781, 2009. © 2009 Wiley‐Liss, Inc.
Placenta‐specific gene activation and inactivation using integrase‐defective lentiviral vectors with the Cre/LoxP system
Authors: Morioka Yuka , Isotani Ayako , Oshima Robert G. , Okabe Masaru , Ikawa Masahito 
Published: October 2009

AbstractTransgenic and knockout studies have advanced our understanding of the genetic control of embryonic development over the past decades. However, interpretation of the phenotype of mutant mice is potentially complicated, since the commonly used knockout approach modifies both the fetal and placental genome. To circumvent this problem, we previously developed a placenta‐specific gene manipulation system by lentiviral vector transduction of embryos at the blastocyst stage. In the present study, by combination with the Cre/LoxP system, we successfully demonstrate placenta‐specific gene activation and inactivation in EGFP reporter mice and Ets2 floxed mice, respectively. Transient expression using integrase‐defective lentiviral (IDLV) vectors diminished the toxic effect of Cre expression and solved the dilemma of mosaic recombination with lower concentrations and toxic effects with higher concentrations of Cre recombinase. We also show that placenta‐specific Ets2 disruption causes embryonic lethality and reconfirmed the critical role of Ets2 during placentation. This technology facilitates both gain and loss of gene function analyses in placental development during pregnancy. Since IDLV vectors can efficiently transduce a variety of cell types similarly to wild‐type vectors, our IDLV‐Cre strategy is potentially useful for a wide range of applications. genesis 47:793–798, 2009. © 2009 Wiley‐Liss, Inc.
Generation of an allele to inactivate Wnt4 gene function conditionally in the mouse
Authors: Shan Jingdong , Jokela Tiina , Peltoketo Hellevi , Vainio Seppo 
Published: October 2009

AbstractThe Wnt family member Wnt4 is critical for the development of several organs, including the kidney, gonad, and adrenal, mammary, and pituitary glands. To study its potential postnatal functions, we generated a floxed Wnt4 allele. A single loxP site was targeted to the second intron, while a loxP‐Neo‐loxP cassette was placed 3′ from Exon 5. The floxed Neo cassette was subsequently removed by crossing with MeuCre40 transgenic mice. The Wnt4 gene was specifically inactivated with CAGCre and another Wnt4 allele, Wnt4EGFPCre, in which the Cre is driven by the endogenous Wnt4 promoter. Deletion of Wnt4 gene function with CAGCre impaired kidney development, as is the case with the conventional knockout. Similarly, the Wnt4EGFPCre‐mediated inactivation of Wnt4 function considerably reduced the amount of Wnt4 transcripts, led to a severe defect in kidney development, and caused the female embryos to undergo partial sex reversal to males. All in all, the floxed Wnt4 allele serves as a useful tool for studying the roles of Wnt4 signaling during the life cycle. genesis 47:782–788, 2009. © 2009 Wiley‐Liss, Inc.
Regulation of NK cell trafficking by CD81
Authors: Krämer Benjamin , Schulte Daniela , Körner Christian , Zwank Claudia , Hartmann Agathe , Michalk Monika , Söhne Jennifer , Langhans Bettina , Nischalke Hans‐Dieter , Coenen Martin , Möhl Christoph , Vogt Annabelle , Hennenberg Martin , Sauerbruch Tilman , Spengler Ulrich , Nattermann Jacob 
Published: October 2009

AbstractNK cells, a heterogeneous sub‐population of lymphocytes, are critically involved in the regulation of both innate and adaptive immune responses in humans. Besides their participation in the control of tumors and viral infections, they also regulate inflammatory processes, mediating both beneficial and detrimental effects. To effectively fulfil their role in immune surveillance, proper trafficking of NK cells is essential. However, the mechanisms and factors governing NK cell recruitment are only poorly dissected. Here, we describe the functional role of tetraspanins, a family of evolutionary conserved cell‐surface proteins, in modulating migration and transmigration of human NK cells. We demonstrate expression of various tetraspanins on NK cells. Furthermore, we show that stimulation of the NK cell‐expressed tetraspanin CD81 induces phosphorylation of ezrin/radixin/moesin proteins and leads to NK cell polarization thereby facilitating NK cell migration toward various chemokines/cytokines. Finally, we provide evidence for a role of CD81 in promoting adhesion of NK cells to components of the extracellular matrix, a prerequisite for extravasation of lymphocytes in inflamed tissues. Thus, our data suggest that the tetraspanin CD81 is importantly involved in the regulation of NK cell recruitment.
ERK/p38 MAP‐kinases and PI3K are involved in the differential regulation of B7‐H1 expression in DC subsets
Authors: Karakhanova Svetlana , Meisel Stefan , Ring Sabine , Mahnke Karsten , Enk Alexander H. 
Published: October 2009

AbstractRegulatory molecules of the B7‐H‐family expressed by DC are important for immune homeostasis, but their regulation is largely unknown. When investigating the pathways regulating B7‐H1 expression in monocyte‐derived DC (MoDC), freshly isolated myeloid DC (mDC) and plasmacytoid DC, respectively, we showed that in MoDC and mDC B7‐H1 expression was upregulated by a standard cytokine cocktail, poly I:C or LPS. MoDC utilize ERK and PI3K pathways to upregulate B7‐H1 in response to cytokines, whereas p38 kinase was predominantly utilized in response to poly I:C. In mDC, ERK and p38 pathways are involved in B7‐H1 regulation, and similar to MoDC, mainly p38 signaling was required for poly I:C‐induced expression of B7‐H1. Plasmacytoid DC responded only to CpG with upregulation of B7‐H1 and in addition to p38 also utilized the PI3K and ERK pathways to regulate B7‐H1 expression. As a functional consequence of B7‐H1 expression on DC, we demonstrate downmodulation of IFN‐γ production in T cells. Thus, the differential regulation of B7‐H1 on DC subsets may suppress immune responses variably, depending on the target DC population. Further analysis of the regulatory mechanisms may facilitate the development of new immunosuppressive therapies, utilizing the regulation of B7‐H1 expression on DC.
CpG‐enhanced CD8+ T‐cell responses to peptide immunization are severely inhibited by B cells
Authors: Overstreet Michael G. , Freyberger Helen , Cockburn Ian A. , Chen Yun‐Chi , Tse Sze‐Wah , Zavala Fidel 
Published: October 2009

AbstractSynthetic peptides encoding protective pathogen‐derived epitopes represent – in principle – an ideal approach to T‐cell vaccination. Empirically, however, these strategies have not been successful. In the current study, we profiled the early activation of CD8+ T cells by MHC class I‐restricted peptide immunization to better understand the biology of this response. We found that CD8+ T cells proliferated robustly in response to low doses of short synthetic peptides in PBS, but failed to acquire effector function or form memory populations in the absence of the TLR ligand CpG. CpG was unique among TLR ligands in its ability to enhance the response to peptide and its adjuvant effects had strict temporal requirements. Interestingly, CpG treatment modulated T‐cell expression of the surface receptors PD‐1 and CD25, providing insight into its possible adjuvant mechanism. The effects of CpG on peptide immunization were dramatically enhanced in the absence of B cells, demonstrating a unique system of regulation of T‐cell responses by these lymphocytes. The results reported here provide insight into the complex response to a simple vaccination regimen, as well as a framework for a rational peptide‐based vaccine design to both exploit and overcome targeted aspects of the immune response.
Antigen‐specific Treg regulate Th17‐mediated lung neutrophilic inflammation, B‐cell recruitment and polymeric IgA and IgM levels in the airways
Authors: Jaffar Zeina , Ferrini Maria E. , Girtsman Teri A. , Roberts Kevan 
Published: October 2009

AbstractTh17 cells play key roles in mediating autoimmunity, inflammation and mucosal host defense against pathogens. To determine whether naturally occurring Treg (nTreg) limit Th17‐mediated pulmonary inflammation, OVA‐specific CD4+ Th17 cells and expanded CD4+CD25+Foxp3+ nTreg were cotransferred into BALB/c mice that were then exposed to OVA aerosols. Th17 cells, when transferred alone, accumulated in the lungs and posterior mediastinal LN and evoked a pronounced airway hyperreactivity and neutrophilic inflammation, characterized by B‐cell recruitment and elevated IgA and IgM levels. Cotransfer of antigen‐specific nTreg markedly reduced the Th17‐induced pulmonary inflammation and associated neutrophilia, B‐cell influx and polymeric Ig levels in the airways, but did not inhibit airway hyperreactivity. Moreover, the regulation appeared restricted to the site of mucosal inflammation, since transfer of nTreg did not affect the Th17 response developing in the lung draining LN, as evidenced by unaltered levels of IL‐17 production and low numbers of Foxp3+ Treg. Our findings suggest a crucial role for Th17 cells in mediating airway B‐cell influx and IgA response, and demonstrate that antigen‐specific nTreg suppress Th17‐mediated lung inflammation. These results provide new insights into how Th17 responses are limited and may facilitate development of novel approaches for controlling Th17‐induced inflammation.