bluuebunny/crossref_metadata_2025_split huggingface dataset:
Structural characterization of the regioisomers of di(hydroxybutyl) ether by GC‐EI MS and theoretical calculations
Authors: Staccioli Serena , Altamura Maria , Giorgi Gianluca , Triolo Antonio 
Published: April 2009

AbstractDi(hydroxybutyl) ether (DHBE), a liver protecting drug, is composed of a mixture of three regioisomers: 4‐(3‐hydroxybutoxy)‐2‐butanol (1), 3‐(4‐hydroxy‐2‐butoxy)‐1‐butanol (2), and 3‐(3‐hydroxybutoxy)‐1‐butanol (3). Unequivocal differentiation of each regioisomer of DHBE was rapidly obtained without isolation of the single components, using GC‐MS with electron ionization (EI).The mass spectrum of 1 showed a rearrangement ion at m/z 118, characteristic of the 3‐hydroxybutyl chain, deriving from loss of acetaldehyde from the molecular ion, whereas 2 and 3 were characterized by the ion at m/z 117, expected from α‐cleavage of the 4‐hydroxy‐2‐butyl chain. The species at m/z 118, in turn, loses a water molecule via a mechanism involving both alcohol hydrogens, as shown by deuterium exchange experiments. Both this finding and theoretical calculations support a mechanism in which the loss of acetaldehyde in 1 occurs via a cyclic intermediate, stabilized by a strong hydrogen bond between the alcohol oxygen bearing the charge and the other alcohol oxygen, and involves initial hydrogen transfer from the former to the latter.The EI spectrum of 2, having two 4‐hydroxy‐2‐butyl chains, showed the fragmentations expected from classical fragmentation rules of aliphatic ethers and alcohols, whereas the EI spectrum of 3, bearing one 4‐hydroxy‐2‐butyl and one 3‐hydroxybutyl chain, showed essentially the characteristic fragments of both chains. Copyright © 2009 John Wiley & Sons, Ltd.
An efficient neural network approach for nanoscale FinFET modelling and circuit simulation
Authors: Alam M. S. , Kranti A. , Armstrong G. A. 
Published: April 2009

AbstractThe present paper demonstrates the suitability of artificial neural network (ANN) for modelling of a FinFET in nano‐circuit simulation. The FinFET used in this work is designed using careful engineering of source–drain extension, which simultaneously improves maximum frequency of oscillation ƒmaxbecause of lower gate to drain capacitance, and intrinsic gainAV0 = gm/gds, due to lower output conductancegds. The framework for the ANN‐based FinFET model is a common source equivalent circuit, where the dependence of intrinsic capacitances, resistances and dc drain currentIdon drain–sourceVdsand gate–sourceVgsis derived by a simple two‐layered neural network architecture. All extrinsic components of the FinFET model are treated as bias independent. The model was implemented in a circuit simulator and verified by its ability to generate accurate response to excitations not used during training. The model was used to design a low‐noise amplifier. At low power (Jds∼10 µA/µm) improvement was observed in both third‐order‐interceptIIP3(∼10 dBm) and intrinsic gainAV0(∼20 dB), compared to a comparable bulk MOSFET with similar effective channel length. This is attributed to higher ratio of first‐order to third‐order derivative ofIdwith respect to gate voltage and lowergdsin FinFET compared to bulk MOSFET. Copyright © 2009 John Wiley & Sons, Ltd.
Development of microglia in the chick embryo spinal cord: Implications in the regulation of motoneuronal survival and death
Authors: Calderó Jordi , Brunet Núria , Ciutat Dolors , Hereu Marta , Esquerda Josep E. 
Published: April 2009

AbstractThe role of microglia during normal development of the nervous system is still not well understood. In the present study, a chick embryo model was used to examine the development of microglia in the spinal cord and characterize their changes in response to naturally occurring and pathological death of motoneurons (MNs). The microglial response to MN axotomy and the effects of microglial activation on MN survival were also studied. We found that: 1) macrophages/microglial cells were present in the spinal cord at early developmental stages (E3) and that they were recruited after normal and induced MN apoptosis; 2) although many microglial cells were seen phagocytosing apoptotic bodies, a proportion of dying cells were devoid of engulfing microglia; 3) axotomy of mature MNs was accompanied by microglial activation in the absence of MN death; 4) excitotoxic (necrotic) MN death provoked a rapid and massive microglial recruitment with phagocytic activity; 5) lipopolysaccharide‐induced microglial activation in vivo resulted in the death of immature, but not mature, microglia; and 6) overactivation of microglia modulated the survival of mature MNs, either by killing them or by enhancing their vulnerability to die in response to a mild injury. Taken together, these observations indicate that normal microglia do not play an active role in triggering apoptosis of developing MNs. Rather, they act as phagocytes for the removal of dying cells during the process of programmed cell death. © 2009 Wiley‐Liss, Inc.
In vitro analysis of glial cell function in ganglioside‐deficient mice
Authors: Silajdžić Edina , Willison Hugh J. , Furukawa Koichi , Barnett Susan C. 
Published: April 2009

AbstractGangliosides are a family of sialic acid–containing glycosphingolipids highly enriched in neuronal and glial membranes, where they play pleiotropic roles in nervous system function. In this glial cell biological study, we used mice deficient in glycosyltransferases involved in ganglioside biosynthesis to gain insights into the possible role of ganglioside overexpression or deficiency on glial cell proliferation, migration, and differentiation in vitro. Primary cultures of olfactory ensheathing cells, oligodendrocyte lineage cells, and Schwann cells isolated from β1,4‐N‐acetylgalactosaminyl (β1,4‐GalNAc) transferase– and α‐2,8‐sialyltransferase‐deficient mice demonstrated subtle differences in their behavior when compared with wild‐type glia. Oligodendrocyte–axonal interactions were investigated in dissociated embryonic mixed spinal cord cultures in which axonal ensheathment with myelin internodes and organized nodes of Ranvier form. In these myelinating cultures, deficiency of complex gangliosides, as found in β1,4‐GalNAc T−/− mice, resulted in the temporal disorganization of Kv and Na+ channels at the nodes of Ranvier, similar to that seen in β1,4‐GalNAc T−/− mice in vivo. These data show that glycosyltransferase deficiency and the consequent ganglioside imbalance has subtle effects on a range of glial cell functions and that in vitro systems can be used to explore these in ways that complement whole animal physiology. Our results are also consistent with the absence of gross neurodevelopmental dysfunction in mice lacking a variety of different gangliosides, suggesting that ganglioside redundancy and substitution are mechanisms that compensate for the lack of a full complement of complex gangliosides. © 2009 Wiley‐Liss, Inc.
Functional and immunocytochemical characterization of D‐serine transporters in cortical neuron and astrocyte cultures
Authors: Shao Zongjun , Kamboj Amit , Anderson Christopher M. 
Published: April 2009

AbstractD‐serine is an endogenous coagonist of N‐methyl‐D‐aspartate (NMDA) receptors that plays an important role in synaptic function, neuronal development, and excitotoxicity. Mechanisms of D‐serine transport are important in regulation of extracellular D‐serine concentration and therefore of these critical processes. D‐serine can be transported with low affinity through the Na+‐dependent amino acid transporter termedASCT2, whereas high‐affinity D‐serine uptake has been reported through the Na+‐independent transporter termedasc‐1. We investigated immunoreactivity for ASCT2 and asc‐1 and D‐serine transport kinetics in cultured cortical neurons and astrocytes to gain insight into how D‐serine transporters regulate CNS D‐serine levels. Both neurons and astrocytes exhibited low‐affinity Na+‐dependent D‐serine uptake (KT> 1 mM) with broad substrate selectivity that was consistent with uptake through ASCT2. Both neurons and astrocytes also stained positively for ASCT2 in immunocytochemistry studies. Neurons but not astrocytes stained positively for the high‐affinity D‐serine transporter asc‐1, but no evidence of functional asc‐1 could be detected in neurons with conditions that produced such activity in cortical synaptosomes. These data support ASCT2 function in both neuron and astrocyte cultures and identify a discrepancy between observed asc‐1 immunoreactivity and lack of functional asc‐1 activity in neuron cultures. Together these findings further our knowledge of the processes that govern D‐serine regulation. © 2009 Wiley‐Liss, Inc.
Possible promotion of neuronal differentiation in fetal rat brain neural progenitor cells after sustained exposure to static magnetism
Authors: Nakamichi Noritaka , Ishioka Yukichi , Hirai Takao , Ozawa Shusuke , Tachibana Masaki , Nakamura Nobuhiro , Takarada Takeshi , Yoneda Yukio 
Published: April 2009

AbstractWe have previously shown significant potentiation of Ca2+ influx mediated by N‐methyl‐D‐aspartate receptors, along with decreased microtubules‐associated protein‐2 (MAP2) expression, in hippocampal neurons cultured under static magnetism without cell death. In this study, we investigated the effects of static magnetism on the functionality of neural progenitor cells endowed to proliferate for self‐replication and differentiate into neuronal, astroglial, and oligodendroglial lineages. Neural progenitor cells were isolated from embryonic rat neocortex and hippocampus, followed by culture under static magnetism at 100 mT and subsequent determination of the number of cells immunoreactive for a marker protein of particular progeny lineages. Static magnetism not only significantly decreased proliferation of neural progenitor cells without affecting cell viability, but also promoted differentiation into cells immunoreactive for MAP2 with a concomitant decrease in that for an astroglial marker, irrespective of the presence of differentiation inducers. In neural progenitors cultured under static magnetism, a significant increase was seen in mRNA expression of several activator‐type proneural genes, such as Mash1, Math1, and Math3, together with decreased mRNA expression of the repressor type Hes5. These results suggest that sustained static magnetism could suppress proliferation for self‐renewal and facilitate differentiation into neurons through promoted expression of activator‐type proneural genes by progenitor cells in fetal rat brain. © 2009 Wiley‐Liss, Inc.
Desacyl‐ghrelin and synthetic GH‐secretagogues modulate the production of inflammatory cytokines in mouse microglia cells stimulated by β‐amyloid fibrils
Authors: Bulgarelli Ilaria , Tamiazzo Laura , Bresciani Elena , Rapetti Daniela , Caporali Simona , Lattuada Donatella , Locatelli Vittorio , Torsello Antonio 
Published: April 2009

AbstractData from Alzheimer's disease (AD) patients and AD animal models demonstrate the accumulation of inflammatory microglia at sites of insoluble fibrillar β‐amyloid protein (fAβ) deposition. It is known that fAβ binds to CD36, a type B scavenger receptor also involved in internalization of oxidized low‐density lipoprotein (LDL), and initiate a signaling cascade that regulates microglial recruitment, activation, and secretion of inflammatory mediators leading to neuronal dysfunction and death. The recent demonstration of a binding site for the growth hormone secretagogues (GHS) on CD36 prompted us to ascertain whether ghrelin and synthetic GHS could modulate the synthesis of inflammatory cytokines in fAβ‐activated microglia cells. We demonstrate that N9 microglia cells express the CD36 and are a suitable model to study the activation of inflammatory cytokines synthesis. In fact, in N9 cells exposed to fAβ25–35 for 24 hr, the expression of interleukin (IL)‐1β and IL‐6 mRNA significantly increased. Interestingly, 10−7 M desacyl‐ghrelin, hexarelin, and EP80317 in the nanomolar range effectively counteracted fAβ25–35 stimulation of IL‐6 mRNA levels, whereas ghrelin was ineffective. Similarly, the effects of fAβ25–35 on IL‐1β mRNA levels were attenuated by desacyl‐ghrelin, hexarelin, and EP80317, but not ghrelin. Because we have observed that the specific GHS receptor GHS‐R1a is not expressed in N9 cells, the actions of GHS should be mediated by different receptors. Reportedly, hexarelin and EP80317 are capable of binding the CD36 in mouse macrophages and reducing atherosclerotic plaque deposition in mice. We conclude that desacyl‐ghrelin, hexarelin, and EP80317 might interfere with fAβ activation of CD36 in microglia cells. © 2009 Wiley‐Liss, Inc.
Sustained hydrogen peroxide stress decreases lactate production by cultured astrocytes
Authors: Liddell Jeff R. , Zwingmann Claudia , Schmidt Maike M. , Thiessen Anette , Leibfritz Dieter , Robinson Stephen R. , Dringen Ralf 
Published: April 2009

AbstractOxidative stress and disrupted energy metabolism are common to many pathological conditions of the brain. Because astrocytes play an important role in the glucose metabolism of the brain, we have investigated whether sustained oxidative stress affects astroglial glucose metabolism with cultured primary rat astrocytes as a model system. Cultured astrocytes were exposed to a sustained concentration of approximately 50 μM H2O2 in the presence of [U‐13C]glucose, and cellular and extracellular contents of lactate and glucose were analysed by enzymatic assays and NMR spectroscopy. Exposure of the cells to sustained H2O2 stress for up to 120 min significantly lowered the rate of lactate accumulation in the media to 61% ± 14% of that in cultures incubated without peroxide. In addition, the ratio of lactate release to glucose consumption was lowered in peroxide‐treated astrocytes to 77% ± 13% of that in control cells, and the specific activity of glyceraldehyde‐3‐phosphate dehydrogenase had declined to about 10% of control cells within 90 min. In addition, the 13C enrichment of intracellular and extracellular [13C]lactate was about 30% and 95%, respectively, and was not affected by the presence of peroxide, demonstrating that two metabolic pools of lactate are present in cultured astrocytes. The decreased rate of lactate production by astrocytes that have been exposed to peroxide stress is a new example of an alteration by oxidative stress of an important metabolic pathway in astrocytes. Such alterations could contribute to the pathological conditions that have been connected with oxidative stress and disrupted energy metabolism in the brain. © 2009 Wiley‐Liss, Inc.
Activated retinal glia promote neurite outgrowth of retinal ganglion cells via apolipoprotein E
Authors: Lorber Barbara , Berry Martin , Douglas Michael R. , Nakazawa Toru , Logan Ann 
Published: April 2009

AbstractIn the present study, we investigated the role and mechanism through which activated retinal glia stimulate retinal ganglion cell (RGC) neurite outgrowth. We have found that the level of retinal glial activation correlates directly with enhanced RGC neurite outgrowth after a preconditioning intravitreal Zymosan injection. Reduction in the number of activated glia in primary rat retinal cultures led to significantly reduced RGC neurite outgrowth. Glial‐related neurite outgrowth appears to be, at least in part, mediated via apolipoprotein E (ApoE), which is expressed by activated retinal astrocytes and Müller glia. ApoE‐deficient mice showed significantly reduced RGC neurite outgrowth potential after intravitreal Zymosan injection compared with age‐matched wild‐type animals. These observations suggest that ApoE, expressed by activated retinal glia, stimulates RGC neurite outgrowth after intravitreal Zymosan injection. © 2009 Wiley‐Liss, Inc.
Insulin‐like growth factor‐I‐stimulated Akt phosphorylation and oligodendrocyte progenitor cell survival require cholesterol‐enriched membranes
Authors: Romanelli Robert J. , Mahajan Kedar R. , Fulmer Clifton G. , Wood Teresa L. 
Published: April 2009

AbstractPreviously we showed that insulin‐like growth factor‐I (IGF‐I) promotes sustained phosphorylation of Akt in oligodendrocyte progenitor cells (OPCs) and that Akt phosphorylation is required for survival of these cells. The direct mechanisms, however, by which IGF‐I promotes Akt phosphorylation are currently undefined. Recently, cholesterol‐enriched membranes (CEMs) have been implicated in regulation of growth factor‐mediated activation of the PI3K/Akt pathway and survival of mature oligodendrocytes; however, less is know about their role in OPC survival. In the present study, we investigate the role of CEMs in IGF‐I‐mediated Akt phosphorylation and OPC survival. We report that acute disruption of membrane cholesterol with methyl‐β‐cyclodextrin results in altered OPC morphology and inhibition of IGF‐I‐mediated Akt phosphorylation. We also report that long‐term inhibition of cholesterol biosynthesis with 25‐hydroxycholesterol blocks IGF‐I stimulated Akt phosphorylation and cell survival. Moreover, we show that the PI3K regulatory subunit, p85, Akt, and the IGF‐IR are sequestered within cholesterol‐enriched fractions in steady‐state stimulation of the IGF‐IR and that phosphorylated Akt and IGF‐IR are present in cholesterol‐enriched fractions with IGF‐I stimulation. Together, the results of these studies support a role for CEMs or “lipid rafts” in IGF‐I‐mediated Akt phosphorylation and provide a better understanding of the mechanisms by which IGF‐I promotes OPC survival. © 2009 Wiley‐Liss, Inc.
Effects of the Tibetan Plateau on the Asian summer monsoon: a numerical case study using a regional climate model
Authors: Song Jee‐Hey , Kang Hyun‐Suk , Byun Young‐Hwa , Hong Song‐You 
Published: April 2009

AbstractTo understand impacts of the Tibetan Plateau (TP) upon the Asian summer monsoon (ASM), including both the Indian summer monsoons (ISM) and East Asian summer monsoons (EASM), a series of numerical experiments using the National Centers for Environmental Prediction (NCEP) regional spectral model (RSM) are conducted with various TP heights ranging from the flat surface (1.2 km) to 140% of the actual height. It was found that an increase in the TP height leads to an increase in the simulated ISM precipitation over northern India and conversely a decrease in the height leads to a decrease in precipitation. This sensitivity is associated with both the thermal and dynamical effects of the TP; however, although the ISM precipitation over India is affected by the changes in atmospheric circulation, it is not directly affected by the thermal effect. The thermal effect of surface heating plays a role in developing positive vorticity with a consequent increase in monsoon precipitation over northern India. The width of the plateau also seems to be associated with the intensity of the sensitivity for the ISM region. For the EASM region, the orographic effect caused by changes in the lower‐atmospheric circulation and its link with upper‐atmospheric circulation are crucial to the monsoon circulation and precipitation. With increased TP height, the monsoon precipitation moves inland in a northwestward direction, which qualitatively follows the previous findings based on general circulation models (GCMs), but with a detailed dynamical mechanism in linkage between the lower‐ and upper‐atmospheric circulation in the regional climate modelling (RCM) framework in this study. Copyright © 2009 Royal Meteorological Society
Rules of engagement in turbulent times: How Verizon Wireless uses a robust HR portal for employee communication
Authors: Poglianich Antonio , Antonek Matt 
Published: April 2009

AbstractTurbulent times such as these will test the resilience of many companies' communication capabilities, particularly for rapid response with consistent messaging to focus and engage a wary and distracted workforce on the many challenges ahead. The answer may be an HR portal like that at Verizon Wireless, where it is a core part of an engagement strategy that is the envy of the industry. The article discusses the importance of engagement for organizational and business performance; the role communication can play in driving engagement; and five principles for accomplishing this. The article goes on to explore how Verizon Wireless has developed and positioned its HR portal for rapid as well as sustained messaging, personalization, and self‐service tools that all help define the employee experience. © 2009 Wiley Periodicals, Inc.
Creating growth with externalization of R&D results—the spin‐along approach
Authors: Rohrbeck René , Döhler Mario , Arnold Heinrich 
Published: April 2009

AbstractAfter a long period of restructuring and outsourcing, companies are increasingly looking for new growth opportunities. Growth with existing products or by expansion in new markets is limited. Therefore, companies are searching for ways to expand their activities in new businesses. A frequently used tool of multinational enterprises is corporate venturing. Within corporate venturing, a further differentiation can be made between internal venturing and external venturing. Internal venturing promotes business ideas generated within the organization, whereas external venturing integrates business ideas developed outside the company.This article presents a special case of corporate venturing: the spin‐along approach of Deutsche Telekom Laboratories. It can be seen as a combination of internal and external venturing. In the spin‐along approach, employees of the corporate research and development (R&D) department are encouraged to take their technology or business idea external by founding a separate company. Successful companies might later be bought and integrated back into Deutsche Telekom. © 2009 Wiley Periodicals, Inc.
Formation of cartilage repair tissue in articular cartilage defects pretreated with microfracture and covered with cell‐free polymer‐based implants
Authors: Erggelet Christoph , Endres Michaela , Neumann Katja , Morawietz Lars , Ringe Jochen , Haberstroh Kathrin , Sittinger Michael , Kaps Christian 
Published: April 2009

AbstractThe aim of our study was to evaluate the mid‐term outcome of a cell‐free polymer‐based cartilage repair approach in a sheep cartilage defect model in comparison to microfracture treatment. Cell‐free, freeze‐dried implants (chondrotissue®) made of a poly‐glycolic acid (PGA) scaffold and hyaluronan were immersed in autologous serum and used for covering microfractured full‐thickness articular cartilage defects of the sheep (n = 4). Defects treated with microfracture only served as controls (n = 4). Six months after implantation, cartilage implants and controls were analyzed by immunohistochemical staining of type II collagen, histological staining of proteoglycans, and histological scoring. Histological analysis showed the formation of a cartilaginous repair tissue rich in proteoglycans. Histological scoring documented significant improvement of repair tissue formation when the defects were covered with the cell‐free implant, compared to controls treated with microfracture. Immunohistochemistry showed that the cell‐free implant induced cartilaginous repair tissue and type II collagen. Controls treated with microfracture showed marginal formation of a mixed‐type repair tissue consisting of cartilaginous tissue and fibro‐cartilage. Covering of microfractured defects with the cell‐free polymer‐based cartilage implant is suggested to be a promising treatment option for cartilage defects and improves the regeneration of articular cartilage. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 27:1353–1360, 2009