bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cryo‐X‐ray analysis—A novel tool to better understand the physicochemical reactions at the bioglass/biological fluid interface
Authors: Balamurugan Anbalagan , Benhayoune Hicham , Kannan Sanjeevi , Laquerriere Patrice , Michel Jean , Balossier Gerard , Ferreira José M.F. 
Published: July 2008

AbstractThe present study deals with the short‐term physicochemical reactions at the interface between bioactive glass particles [55SiO2‐20CaO‐9P2O5‐12Na2O‐4MgO. mol%] and biological fluid (Dulbecco Modified Eagle's Medium (DMEM)). The physicochemical reactions within the interface are characterized by scanning transmission electron microscopy (TEM) (STEM) associated with Energy‐dispersive X‐ray spectroscopy (EDXS). Microanalysis of diffusible ions such as sodium, potassium, or oxygen requires a special care. In the present investigation the cryo‐technique was adopted as a suitable tool for the specimen preparation and characterization. Cryosectioning is essential for preserving the native distribution of ions so that meaningful information about the local concentrations can be obtained by elemental microanalysis. The bioglass particles immersed in biological fluid for 24 h revealed five reaction stages: (i) dealkalization of the surface by cationic exchange (Na+, Ca2+ with H+ or H3O+); (ii) loss of soluble silica in the form of Si(OH)4 to the solution resulting from the breakdown of SiOSi bonds (iii); repolymerization of Si(OH)4 leading to condensation of SiO2); (iv) migration of Ca2+ and PO43− to the surface through the SiO2‐rich layer to form CaO‐P2O5 film; (v) crystallization of the amorphous CaO‐P2O5 by incorporating OH or CO32− anions with the formation of three different surface layers on the bioactive glass periphery. The thickness of each layer is ≈300 nm and from the inner part to the periphery they consist of SiOH, which permits the diffusion of Ca2+ and PO43− ions and the formation of the middle CaP layer, and finally the outer layer composed of NaO, which acts as an ion exchange layer between Na+ ions and H+ or H3O+ from the solution. Microsc. Res. Tech., 2008. © 2008 Wiley‐Liss, Inc.
Restricted transgene persistence after lentiviral vector‐mediated fetal gene transfer in the pregnant rabbit model
Authors: Moreno Rafael , Rosal Marta , Martinez Itziar , Vilardell Felip , Gonzalez Juan Ramón , Petriz Jordi , Hernandez‐Andrade Edgard , Gratacós Eduard , Aran Josep M. 
Published: July 2008

AbstractBackgroundPrenatal gene transfer may enable early causal intervention for the treatment or prevention of many devastating diseases. Nevertheless, permanent correction of most inherited disorders requires a sustained level of expression from the therapeutic transgene, which could theoretically be achieved with integrating vectors.MethodsRabbit fetuses received 8.5 × 106 HIV‐based recombinant lentivirus particles containing the enhanced green fluorescent protein (EGFP) transgene by intrahepatic, intra‐amniotic or intraperitoneal injection at 22 days of gestation. Provirus presence and transgene expression in rabbit tissues were evaluated at both 1.5 and 16 weeks post‐in utero intervention by polymerase chain reaction (PCR) and reverse transcriptase‐PCR, respectively. Moreover, we assessed persistence of EGFP by immunohistochemistry. Enzyme‐linked immunosorbent assays confirmed the development of antibodies specific against both the viral vector and the reporter protein.ResultsRegardless of the route of administration employed, lentiviral vector‐based in utero gene transfer was safe and reached 85% of the intervened fetuses at birth. However, the integrated provirus frequency was significantly reduced to 50% of that in young rabbits at 16 weeks post‐treatment. In these animals, EGFP expression was evident in many tissues, including cytokeratin 5‐rich basal cells from stratified and pseudostratified epithelia, suggesting that the lentiviral vector might have reached progenitor cells. Conversely, we identified the presence of immune‐inflammatory infiltrates in several EGFP‐expressing tissues. Moreover, almost 70% of the lentiviral vector‐treated rabbits elicited a humoral immune response against the viral envelope and/or the EGFP.ConclusionsAt two‐thirds gestational age, the adaptive immune system of the rabbit appears a relevant factor limiting transgene persistence and expression following lentiviral vector‐mediated in utero gene transfer. Copyright © 2008 John Wiley & Sons, Ltd.
Improved retroviral vector design results in sustained expression after adult gene therapy in mucopolysaccharidosis I mice
Authors: Sedaghat Herati Ramin , Ma Xiucui , Tittiger Mindy , Ohlemiller Kevin K. , Kovacs Attila , Ponder Katherine P. 
Published: July 2008

AbstractBackgroundMucopolysaccharidosis I (MPS I) is a lysosomal storage disease due to α‐L‐iduronidase (IDUA) deficiency that results in the accumulation of glycosaminoglycans (GAG). Gene therapy can reduce most clinical manifestations, but mice that receive transfer as adults lose expression unless they receive immunosuppression. Increasing liver specificity of transgene expression has reduced immune responses to other genes.MethodsA gamma retroviral vector was generated with a liver‐specific human α1‐antitrypsin promoter and the canine IDUA cDNA inverted relative to the retroviral long‐terminal repeat. Adult MPS I mice received the vector intravenously at 6 weeks of age and were assessed for expression via serial serum IDUA assays. Functional testing and organ analysis were performed at 8 months.ResultsThis vector resulted in high specificity of expression in liver, and serum IDUA activity was stable in 90% of animals. Although the average serum IDUA activity was relatively low at 12.6 ± 8.1 units/ml in mice with stable expression, a relatively high percentage of enzyme contained the mannose 6‐phosphorylation necessary for uptake by other cells. At 6.5 months after transduction, most organs had high IDUA activity and normalized GAG levels. There was complete correction of hearing and vision abnormalities and significant improvements in bone, although the aorta was refractory to treatment.ConclusionsStable expression of IDUA in adult MPS I mice can be achieved without immunosuppression by modifying the vector to reduce expression in the spleen. This approach may be effective in patients with MPS I or other lysosomal storage diseases. Copyright © 2008 John Wiley & Sons, Ltd.
A new red fluorescent protein that allows efficient marking of murine hematopoietic stem cells
Authors: Sanuki Seiko , Hamanaka Sanae , Kaneko Shin , Otsu Makoto , Karasawa Satoshi , Miyawaki Atsushi , Nakauchi Hiromitsu , Nagasawa Toshiro , Onodera Masafumi 
Published: July 2008

AbstractBackgroundGenetic marking of hematopoietic stem cells (HSCs) with multiple fluorescent proteins (FPs) would allow analysis of their features, including interaction with adjacent cells. However, there are few red FPs that are comparable to green FPs in terms of low toxicity and high fluorescent intensity. This study has evaluated the usefulness of Kusabira Orange (KO) originated from the coral stone Fungia concinna as a red FP for marking of HSCsMethodsA vector used was the MSCV‐type retroviral vector, DΔNsap that has the PCC4 cell‐passaged myeloproliferative sarcoma virus derived long terminal repeat devoid of a binding site for YY1 and the primer‐binding site derived from the dl587rev, respectively. The vector was cloned with the codon‐optimized KO cDNA for higher expression in mammalian cells (huKO) and converted to the corresponding retroviruses pseudotyped with the vesicular stomatitis virus G envelope protein, then transduced into c‐KIT+Sca‐1+Lineage− cells obtained from C57BL/6 (Ly5.1) mice followed by transplantation into lethally irradiated Ly5.2 mice.ResultsApproximately 70% of donor‐derived cells highly expressed huKO at 16 weeks post‐transplantation. Furthermore, the high expression of huKO was also detected in serially transplanted mice, suggesting that expression of huKO per se had little deleterious effect on murine hematopoiesis. In double marking experiments, huKO‐expressing hematopoietic cells were easily distinguished from those expressing EGFP by flow cytometery and fluorescent microscope analysis.ConclusionsOverall, the results obtained from the present study suggest that huKO can be used as a valuable and versatile red fluorescent marker for HSCs. Copyright © 2008 John Wiley & Sons, Ltd.
Internationalisation and firm performance: Evidence from estimates of efficiency in banking in Namibia and Tanzania
Authors: Okeahalam Charles C. 
Published: July 2008

AbstractThis paper assesses and compares the impact of internationalisation on the economic performance of firms in the banking sector in Namibia and Tanzania. With the aid of financial ratios and econometric analysis, measures of efficiency are used as proxies for overall economic performance and comparisons are made. In Namibia, the market is more concentrated than in Tanzania, all the foreign banks are from one country, and they have had a presence in the country for a long time. In Tanzania, the market is less concentrated than in Namibia, foreign entry is from a number of countries and has been more recent. The study finds that in Namibia, all the foreign banks are larger but more inefficient than domestically owned banks. In Tanzania, foreign banks are more efficient than domestic banks. These results suggest that the generation of foreign entry and industry structure are significant determinants of positive spillovers of internationalisation. They also indicate that the type of foreign entrant, not, just foreign entry determines the impact on efficiency and the competitive landscape. Copyright © 2008 John Wiley & Sons, Ltd.
Has private participation in water and sewerage improved coverage? Empirical evidence from Latin America
Authors: Clarke George R.G. , Kosec Katrina , Wallsten Scott 
Published: July 2008

AbstractIntroducing private sector participation (PSP) into the water and sewerage sectors is difficult and controversial. Empirical studies on its effects are scant and generally inconclusive. Case studies tend to find improvements following privatisation, but they suffer from selection bias and it is difficult to generalise their results. To explore empirically the effects of private sector participation on coverage, we assemble a new dataset of connections to water and sewerage services at the city and province level based on household surveys in Argentina, Bolivia and Brazil. The household surveys, conducted over a number of years, allow us to compile data before and after the introduction of private sector participation as well as from similar (control) regions did not privatise. Our analysis reveals that, in general, the share of households connected to piped water and sewerage improved following the introduction of private sector participation, consistent with the case study literature. We also find, however, that the share of households connected similarly improved in the control regions, suggesting that private sector participation,per se, may not have been responsible for those improvements. Results are similar when looking only at the poorest households. The share of poor households connected to piped water and sewerage increased similarly in areas both with and without private sector participation, suggesting that—in terms of connections at least—private sector participation did not harm the poor. Copyright © 2008 John Wiley & Sons, Ltd.
Memantine leads to behavioral improvement and amyloid reduction in Alzheimer's‐disease‐model transgenic mice shown as by micromagnetic resonance imaging
Authors: Scholtzova Henrieta , Wadghiri Youssef Z. , Douadi Moustafa , Sigurdsson Einar M. , Li Yong‐Sheng , Quartermain David , Banerjee Pradeep , Wisniewski Thomas 
Published: July 2008

AbstractMemantine, an N‐methyl‐D‐aspartate (NMDA) receptor antagonist, has been shown to improve learning and memory in several preclinical models of Alzheimer's disease (AD). Memantine has also been shown to reduce the levels of amyloid β (Aβ) peptides in human neuroblastoma cells as well as to inhibit Aβ oligomer‐induced synaptic loss. In this study, we assessed whether NMDA receptor inhibition by memantine in transgenic mice expressing human amyloid‐beta precursor protein (APP) and presenilin 1 (PS1) is associated with cognitive benefit and amyloid burden reduction by using object recognition, micromagnetic resonance imaging (μMRI), and histology. APP/PS1 Tg mice were treated either with memantine or with vehicle for a period of 4 months starting at 3 months of age. After treatment, the mice were subjected to an object recognition test and analyzed by ex vivo μMRI, and histological examination of amyloid burden. μMRI was performed following injection with gadolinium‐DTPA‐Aβ1–40. We found that memantine‐treated Tg mice performed the same as wild‐type control mice, whereas the performance of vehicle‐treated Tg mice was significantly impaired (P = 0.0081, one‐way ANOVA). Compared with vehicle‐treated animals, memantine‐treated Tg mice had a reduced plaque burden, as determined both histologically and by μMRI. This reduction in amyloid burden correlates with an improvement in cognitive performance. Thus, our findings provide further evidence of the potential role of NMDA receptor antagonists in ameliorating AD‐related pathology. In addition, our study shows, for the first time, the utility of μMRI in conjunction with gadolinium‐labeled Aβ labeling agents to monitor the therapeutic response to amyloid‐reducing agents. © 2008 Wiley‐Liss, Inc.
Functional contribution of α3L8′ to the neuronal nicotinic α3 receptor
Authors: Nieves‐Cintrón Madeline , Caballero‐Rivera Daniel , Silva Walter I. , Navedo Manuel F. , Lasalde‐Dominicci José A. 
Published: July 2008

AbstractThe role of position L8′, located in transmembrane domain 1 of the neuronal nicotinic α3 subunit, was characterized by using two‐electrode voltage clamp inXenopusoocytes. Four amino acids (Ala, Ser, Phe, and Tyr) were inserted at this conserved position, and the mutant subunit was coexpressed with either wild‐type β2 or β4 subunits. These substitutions led to significant alterations in the pharmacodynamic parameters of cholinergic agents, resulting in loss of function. Ala and Ser substitutions resulted in losses in agonist (ACh, nicotine, and DMPP) potency and intrinsic activity at both α3β2 and α3β4 receptors. Similarly, significant changes in antagonist potency were produced by the Ala and Ser substitutions. Phe and Tyr mutations did not alter the receptor's EC50for ACh or nicotine but reduced the EC50for DMPP at both receptors. The Phe mutation also reduced the intrinsic activity of all agonists tested at both receptors. The Tyr mutation, though, led to a decrease in intrinsic activity for all agonists at the α3β2 receptor, yet resulted in no changes for DMPP, a decrease for nicotine, and an increase for ACh at the α3β4 receptor. The most dramatic changes in the receptor's functional properties were produced by substitutions that introduced the largest changes in amino acid volume. Additional replacements (Gly, Thr, and Val) suggested an inverse correlation between amino acid volume at position α3L8′ and EC50for α3β4 nAChRs; however, α3β2 nAChRs displayed a nonlinear correlation. These data demonstrate that structural alterations at position α3L8′ could propagate to the agonist‐binding site. © 2008 Wiley‐Liss, Inc.
Pyramidal cell responses to γ‐aminobutyric acid differ in type I and type II cortical dysplasia
Authors: André Véronique M. , Cepeda Carlos , Vinters Harry V. , Huynh My , Mathern Gary W. , Levine Michael S. 
Published: July 2008

AbstractAbnormalities in the γ‐aminobutyric acid (GABA)‐ergic system could be responsible for seizures in cortical dysplasia (CD). We examined responses of pyramidal neurons to exogenous application of GABA, as well as alterations of GABAergic interneuron number and size in pediatric epilepsy surgery patients with non‐CD, type I CD, and type II CD pathologies. We used the dissociated cell preparation for electrophysiology along with immunohistochemistry to identify number and size of GABAergic cells. Pyramidal neurons from type I CD tissue showed increased EC50and faster kinetics compared with cells from non‐CD and type II CD tissue. Cytomegalic pyramidal neurons showed increased GABA peak currents and decreased peak current densities, longer kinetics, and decreased sensitivity to zolpidem and zinc compared with normal pyramidal cells from non‐CD and type I CD. There were fewer but larger glutamic acid decarboxylase (GAD)‐containing cells in type II CD tissue with cytomegalic neurons compared with non‐CD, type I CD, and type II CD without cytomegalic neurons. In addition, GABA transporters (VGAT and GAT‐1) showed increased staining surrounding cytomegalic neurons in type II CD tissue. These results indicate that there are differences in GABAAreceptor‐mediated pyramidal cell responses in type I and type II CD. Alterations in zolpidem and zinc sensitivities also suggest that cytomegalic neurons have altered GABAAreceptor subunit composition. These findings support the hypothesis that patients with type I and type II CD will respond differently to GABA‐mediated antiepileptic drugs and that cytomegalic neurons have features similar to immature neurons with prolonged GABAAreceptor open channel times. © 2008 Wiley‐Liss, Inc.
Comparative study of the influence of Thy1 deficiency and dietary iron deficiency on dopaminergic profiles in the mouse striatum
Authors: Connor James R. , Wang Xin‐Sheng , Neely Elizabeth B. , Ponnuru Padmavathi , Morita Hokuto , Beard John 
Published: July 2008

AbstractThy‐1, a glycosyl‐phosphatidylinositol (GPI)‐linked integral membrane protein, may play a role in stabilizing synapses. Thy1 was identified in a gene expression analysis as iron responsive, and subsequent cell culture and animal models of iron deficiency expanded this finding to the protein. The importance of Thy1 in influencing neurotransmitter feedback mechanisms led to this study to determine the relative effects of Thy1 deficiency and dietary iron deficiency on the dopaminergic system in the mouse striatum. The model for this analysis was the Thy1 null mutant mouse in the presence or absence of dietary iron deficiency. The results revealed significant differences in dopaminergic profiles associated with Thy1 and iron deficiency and also a sex effect. For example, both iron deficiency and the absence of Thy1 are associated with increased dopamine in both sexes, but the dopamine transporter is increased in these experimental groups only in female mice. In male mice, the increase in dopamine transporter is found only in the Thy1 null mutants. Increases in vesicular monoamine transporter and phosphorylated tyrosine hydroxlyase are found only in iron‐deficient mice. In contrast decreased release of dopamine from synaptosomes is found only in the Thy1 null mutant animals. In general, these results indicate that a loss of Thy1 can influence the dopaminergic profile in the striatum. Furthermore, the results reveal consistent differences in the dopaminergic profile in Thy1 knockout mice compared with iron‐deficient mice, indicating that the effects of iron deficiency are not due only to a change in Thy1 expression. © 2008 Wiley‐Liss, Inc.
Reduced brain injury in CD18‐deficient mice after experimental intracerebral hemorrhage
Authors: Titova Elena , Ostrowski Robert P. , Kevil Christopher G. , Tong Wenni , Rojas Hugo , Sowers Lawrence C. , Zhang John H. , Tang Jiping 
Published: July 2008

AbstractMany studies have indicated leukocytes are a major contributor to brain injuries caused by intracerebral hemorrhage (ICH). Leukocyte‐expressed CD18 is important for neutrophil–endothelial interactions in the vasculature, and CD18 deficiency protects against ischemia‐reperfusion injury. We investigated whether CD18 deficiency provides protection against ICH‐induced brain injury. Male wild‐type (WT) CD18+/+ mice and CD18−/−‐knockout mice were used in this study. ICH was induced by a collagenase injection. Mortality, neurological function, brain edema, and myeloperoxidase (MPO) activity as well as tissue expression of nitrotyrosine and MPO were evaluated 24 hr after ICH. We discovered significantly reduced brain edema and diminished mortality with a concomitant decrease in MPO and nitrotyrosine immunoreactivity in brains of CD18‐knockout mice. © 2008 Wiley‐Liss, Inc.
Opposing effects of P2X7and P2Y purine/pyrimidine‐preferring receptors on proliferation of astrocytes induced by fibroblast growth factor‐2: Implications for CNS development, injury, and repair
Authors: Neary Joseph T. , Shi You‐Fang , Kang Yuan , Tran Minh D. 
Published: July 2008

AbstractExtracellular nucleotides play important trophic roles in development and central nervous system (CNS) injury, but the functions of distinct purinergic receptors and related signaling pathways have not been fully elucidated. In the present study we identified opposing effects of P2X and P2Y receptors on the ability of FGF2 to induce proliferation in primary cultures of rat cortical astrocytes. Low concentrations of ATP enhanced DNA synthesis induced by FGF2, whereas high concentrations inhibited FGF2‐induced proliferation. Comparison of concentration–response experiments with ATP and 2′,3′‐O‐(4‐benzoyl)‐benzoyl‐ATP (BzATP) indicated that the inhibitory effect was mediated by P2X7receptors. Interestingly, activation of P2X7receptors led to a state of reversible growth arrest rather than cell death. Selectivity studies showed that proliferation evoked by epidermal growth factor and platelet‐derived growth factor was also inhibited by P2X7receptors, but P2X1or P2X3receptors did not inhibit proliferation induced by FGF2. A marker of mitosis, phosphohistone‐3, was reduced by BzATP and increased by UTP, suggesting that the enhancing effect of ATP on FGF2‐induced proliferation was mediated by P2 purine/pyrimidine receptors. Phosphorylation of the growth arrest–related protein kinases p38/MAPK and SAPK/JNK was strongly increased by BzATP but only weakly affected by UTP. We conclude that P2Y purine/pyrimidine receptors enhance proliferation induced by FGF2 in astrocytes, whereas stimulation of P2X7receptors inhibits proliferation by shifting cells to a state of reversible growth arrest that may be mediated by protein kinase signaling. These trophic actions of P2X7and P2Y purine/pyrimidine receptors may contribute to the regulation of CNS development, adult neurogenesis, and the response of astrocytes to injury. © 2008 Wiley‐Liss, Inc.
Peripheral nerve regeneration is delayed in neuropilin 2–deficient mice
Authors: Bannerman Peter , Ara Jahan , Hahn Ashleigh , Hong Lindy , McCauley Erica , Friesen Katie , Pleasure David 
Published: July 2008

AbstractPeripheral nerve transection or crush induces expression of class 3 semaphorins by epineurial and perineurial cells at the injury site and of the neuropilins neuropilin‐1 and neuropilin‐2 by Schwann and perineurial cells in the nerve segment distal to the injury. Neuropilin‐dependent class 3 semaphorin signaling guides axons during neural development, but the significance of this signaling system for regeneration of adult peripheral nerves is not known. To test the hypothesis that neuropilin‐2 facilitates peripheral‐nerve axonal regeneration, we crushed sciatic nerves of adult neuropilin‐2‐deficient and littermate control mice. Axonal regeneration through the crush site and into the distal nerve segment, repression by the regenerating axons of Schwann cell p75 neurotrophin receptor expression, remyelination of the regenerating axons, and recovery of normal gait were all significantly slower in the neuropilin‐2‐deficient mice than in the control mice. Thus, neuropilin‐2 facilitates peripheral‐nerve axonal regeneration. © 2008 Wiley‐Liss, Inc.