bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sonographic appearances of the normal ulnar nerve in the cubital tunnel
Authors: Ozturk Ersin , Sonmez Guner , Çolak Ahmet , Sildiroglu H. Onur , Mutlu Hakan , Senol Mehmet Guney , Basekim C. Cinar , Kizilkaya Esref 
Published: April 2008

AbstractPurpose.To investigate the sonographic characteristics of the normal ulnar nerve in the cubital tunnel, as well as any differences related to age, sex, and dominant arm.Method.Two hundred twelve elbows in healthy volunteers were evaluated sonographically. The cross‐sectional area (CSA) of the ulnar nerve within the cubital tunnel was measured with the elbow in extension and in flexion. The presence and number of fascicles was determined. The displacement of the ulnar nerve out of the cubital tunnel in full elbow flexion was also investigated.Results.The mean ± SD CSA of the ulnar nerve was 6.6 ± 1.7 mm2 (6.7 ± 1.8 mm2 in men and 6.5 ± 1.7 mm2 in women). The mean CSA of the ulnar nerve was highest for subjects aged 50–59 years, and lowest for subjects aged 30–39 years. Forty‐two of 212 (19.8%) ulnar nerves had 2 fascicles, and 5 (2.4%) had 3 fascicles. The remaining 165 (77.8%) nerves had 1 fascicle. During elbow flexion, 49 of 212 (23.1%) ulnar nerves showed subluxation, and 18 (8.5%) were dislocated.Conclusion:There were differences in the CSA of the ulnar nerve between some age groups, but there was no variation with sex or handedness. Sonography can evaluate the morphologic changes of the nerve during flexion of the elbow. © 2008 Wiley Periodicals, Inc. J Clin Ultrasound, 2008
Surfing in the air: a grounded theory of the dynamics of street life and its policy implications
Authors: Conticini Alessandro 
Published: April 2008

AbstractNearly 20 years after the emergence of a specialised literature dealing with homeless children and youth, best practices are still rare and a divide remains between our understanding of street life, and the policy and programmes that are promoted to reach out to street‐living children: a persisting dichotomy between theory and practice.While much of the literature available is still entrapped in a sort of ‘pathology of case studies’ unable to provide systematic information to policy makers and practitioners, this paper claims originality in presenting an inter‐disciplinary understanding of the processes of street adaptation followed by children. In doing so, the paper presents a grounded theory to predict the consequences of street life and to plan interventions accordingly. Copyright © 2008 John Wiley & Sons, Ltd.
Pacific islands' bilateral trade: the role of remoteness and of transport costs
Authors: Borgatti Lisa 
Published: April 2008

AbstractBilateral trade of geographically distant countries is likely to be negatively affected by the distance separating them from their trading partners and positively affected by their remoteness, defined as the average weighted distance between two countries with weights reflecting the absorptive capacity of the partner country. In presence of competitive transport costs, the effect of remoteness and distance is diluted. An augmented gravity model applied to the Pacific islands' bilateral trade from 1980 to 2004 shows that a doubling of the elasticity of distance would decrease their average bilateral trade by 80 per cent. Remoteness positively affects the Pacific islands' bilateral trade, but does not compensate for the negative effect of distance. The opposite is found for the Caribbean islands, where the elasticity of trade with respect to remoteness is six times bigger than that for the Pacific islands. By lowering transport costs, improved infrastructure fosters trade. A cluster analysis for 30 small island developing states shows that the Pacific islands belong to the clusters with the weaker infrastructure stocks, leaving them with a large scope for improvement. Copyright © 2008 John Wiley & Sons, Ltd.
Public sector efficiency, foreign aid and small island developing states
Authors: Feeny Simon , Rogers Mark 
Published: April 2008

AbstractThis paper examines the efficiency of public sector expenditures and foreign aid at achieving social sector outcomes in Small Island Developing States (SIDS). Efficiency is estimated using a Stochastic Production Function (SPF) approach and panel data since 1990. A second stage of the analysis examines the determinants of efficiency. Results indicate that the efficiency of aid and public sectors at improving life expectancy has deteriorated during the 1990s but efficiency at improving school enrolments has increased. Higher levels of governance are associated with higher efficiency. There is also evidence to suggest that efficiency is lower in SIDS, as well as in Sub‐Saharan Africa. Copyright © 2008 John Wiley & Sons, Ltd.
Brain‐derived neurotrophic factor stimulates the neural differentiation of human umbilical cord blood‐derived mesenchymal stem cells and survival of differentiated cells through MAPK/ERK and PI3K/Akt‐dependent signaling pathways
Authors: Lim Jung Yeon , Park Sang In , Oh Ji Hyeon , Kim Seong Muk , Jeong Chang Hyun , Jun Jin Ae , Lee Kwan‐Sung , Oh Wonil , Lee Jae‐Kwon , Jeun Sin‐Soo 
Published: April 2008

AbstractBrain‐derived neurotrophic factor (BDNF) plays an important role in the differentiation, development, and survival of neural stem cells. In this study, we analyzed its effects on the stimulation of human umbilical cord blood‐derived mesenchymal stem cells in terms of their potential to differentiate into neuron‐like cells, their survival characteristics, and the molecular mechanisms involved. The treatment of cells with neural induction medium (NIM) and BDNF generated more cells that were neuron‐like and produced stronger expression of neural‐lineage markers than cells treated with NIM and without BDNF. Raf‐1 and ERK phosphorylation and p35 expression levels increased significantly in cells treated with both NIM and BDNF. This treatment also effectively blocked cell death following neural induction and increased Akt phosphorylation and Bcl2 expression compared with cells treated with NIM without BDNF. Inhibition of ERKs inhibited the BDNF‐stimulated up‐regulation of p35 and Bcl2. In addition, the inhibition of PI3K abrogated Akt phosphorylation and Bcl2 expression, but not p35 expression. Thus, MAPK/ERK‐dependent p35 up‐regulation and MAPK/ERK‐dependent and PI3K/Akt‐dependent Bcl2 up‐regulation contribute to BDNF‐stimulated neural differentiation and to the survival of differentiated cells. © 2008 Wiley‐Liss, Inc.
Role of Rho kinase pathway in chondroitin sulfate proteoglycan‐mediated inhibition of neurite outgrowth in PC12 cells
Authors: Gopalakrishnan Sujatha M. , Teusch Nicole , Imhof Christiane , Bakker Margot H. M. , Schurdak Mark , Burns David J. , Warrior Usha 
Published: April 2008

AbstractActivation of the Rho kinase (ROCK) pathway has been associated with inhibition of neurite regeneration and outgrowth in spinal cord injury. Growth‐inhibitory substances present in the glial scar such as chondroitin sulfate proteoglycans (CSPGs) have been shown to create a nonpermissive environment for axon regeneration that results in growth cone collapse. In this study, an in vitro model was developed in nerve growth factor‐differentiated PC12 cells where the Rho/ROCK pathway was modulated by CSPG. CSPG elicited concentration‐dependent inhibition of neurite outgrowth in PC12 cells, which was reversed by ROCK inhibitors such as fasudil, dimethylfasudil, and Y27632. Further studies on the interactions of CSPG with ROCK inhibitors revealed that the modulation of ROCK by CSPG is noncompetitive in nature. It was also observed that ROCK inhibitors increased neurite outgrowth in undifferentiated PC12 cells, indicating constitutive ROCK activity in the cells. Analysis of signaling pathways demonstrated that the effect of CSPG increases the phosphorylation of myosin phosphatase, a substrate immediately downstream of ROCK activation. Fasudil, dimethylfasudil, and Y27632 inhibited the phosphorylation of myosin phosphatase induced by CSPG with rank order potencies comparable to those observed in the neurite outgrowth assay. In addition, ROCK inhibitors reversed cofilin phosphorylation induced by CSPG with similar rank order potencies. Taken together, our data demonstrate that the interaction of CSPG with the ROCK pathway involves downstream effectors of ROCK such as myosin phosphatase and cofilin. © 2008 Wiley‐Liss, Inc.
Maternal immune activation in mice delays myelination and axonal development in the hippocampus of the offspring
Authors: Makinodan Manabu , Tatsumi Kouko , Manabe Takayuki , Yamauchi Takahira , Makinodan Eri , Matsuyoshi Hiroko , Shimoda Shigero , Noriyama Yoshinobu , Kishimoto Toshifumi , Wanaka Akio 
Published: April 2008

AbstractEpidemiological data suggest a relationship between maternal infection and a high incidence of schizophrenia in offspring. An animal model based on this hypothesis was made by injecting double‐stranded RNA, polyinosinic‐polycytidylic acid (poly‐I:C), into early pregnant mice, and their offspring were examined for biochemical and histological abnormalities. Mouse brains were examined with special reference to oligodendrocytes, which have been implicated in several neurodevelopmental disorders. We detected a significant decrease of myelin basic protein (MBP) mRNA and protein at early postnatal periods in poly‐I:C mice. MBP immunocytochemistry and electron microscopy revealed that the hippocampus of juvenile poly‐I:C mice was less myelinated than in PBS mice, with no significant loss of oligodendrocytes. In addition, axonal diameters were significantly smaller in juvenile poly‐I:C mice than in control mice. These abnormalities reverted to normal levels when the animals reached the adult stage. These findings suggest that retarded myelination and axonal abnormalities in early postnatal stages caused by maternal immune activation could be related to schizophrenia‐related behaviors in adulthood. © 2008 Wiley‐Liss, Inc.
Histone deacetylase‐related protein inhibits AES‐mediated neuronal cell death by direct interaction
Authors: Zhang Xiaoguang , Chen Hsin‐Mei , Jaramillo Eduardo , Wang Lulu , D'Mello Santosh R. 
Published: April 2008

AbstractHistone deacetylase‐related protein (HDRP), an alternatively spliced and truncated form of histone deacetylase‐9 that lacks a C‐terminal catalytic domain, protects neurons from death. In an effort to understand the mechanism by which HDRP mediates its neuroprotective effect, we screened for proteins in the brain that interact with HDRP by using a yeast two‐hybrid assay. One of the HDRP‐interacting proteins identified in this screen was amino enhancer of split (AES), a 197–amino acid protein belonging to the Groucho family. Interaction between HDRP and AES was verified by in vitro binding assays, coimmunoprecipitation, and colocalization studies. To investigate the significance of the HDRP‐AES association to the regulation of neuronal survival, we used cultured cerebellar granule neurons, which undergo apoptosis when treated with low potassium (LK) medium. We found that in contrast to HDRP, whose expression is markedly reduced by LK treatment, AES expression was not appreciably altered. Forced expression of AES in healthy neurons results in cell death, an action that is blocked by the coexpression of HDRP. AES is a truncated version of larger Groucho‐related proteins, one of which is transducin‐like enhancer of split (TLE)‐1. We found that the expression of TLE1 is reduced in LK‐treated neurons and the forced expression of TLE1 blocks LK‐induced neuronal death as well as death induced by AES. Our results show that AES has apoptotic activity in neurons and suggest that neuroprotection by HDRP is mediated by the inhibition of this activity through direct interaction. © 2008 Wiley‐Liss, Inc.
Triptolide modulates T‐cell inflammatory responses and ameliorates experimental autoimmune encephalomyelitis
Authors: Wang Ying , Mei Yunhua , Feng Dechun , Xu Lingyun 
Published: April 2008

AbstractTriptolide (TPT), a diterpenoid triepoxide, is the major component isolated from the Chinese herb Tripterygium wilfordii Hook. f. Previous studies have shown that TPT has immunosuppressive properties and is effective in prolonging graft survival and suppressing autoimmune responses. The aim of this study was to investigate theprotective effect of TPT in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. Treatment of C57BL/6 mice with TPT from the date of EAE induction significantly delayed EAE onset and suppressed disease severity, accompanied with reduced inflammation and demyelination in the central nervous system. TPT treatment lead to a significant inhibition of the mRNA expression of both Th1/ThIL‐17 and Th2 cytokines in spleen mononuclear cells (MNC) as well as in spinal cord tissues. In addition, the expression of Forkhead box p3 (Foxp3) was up‐regulated in spleen MNC after TPT treatment. Furthermore, we detected apparent inhibition of nuclear factor–kappa B (NF‐κB)‐DNA binding activity, increased expression of the inhibitor of nuclear factor–kappa Bα (IκBα) and decreased expression of pIκBα in spleen MNC in TPT‐treated EAE mice. Taken together, these findings indicate that TPT has profound immunoregulatory functions and potential protective values for the treatment of autoimmune inflammatory disorders. © 2008 Wiley‐Liss, Inc.
Increase in dopaminergic neurons from mouse embryonic stem cell‐derived neural progenitor/stem cells is mediated by hypoxia inducible factor‐1α
Authors: Kim Tae‐Sun , Misumi Sachiyo , Jung Cha‐Gyun , Masuda Tadashi , Isobe Yoshiaki , Furuyama Fujiya , Nishino Hitoo , Hida Hideki 
Published: April 2008

AbstractA reliable method to induce neural progenitor/stem cells (NPCs) into dopaminergic (DAergic) neurons has not yet been established. As well, the mechanism involved remains to be elucidated. To induce DAergic differentiation from NPCs, a cytokine mixture (C‐Mix) of interleukin (IL)‐1β, IL‐11, leukemia‐inhibitory factor (LIF), and glial‐derived neurotrophic factor or low oxygen (3.5% O2: L‐Oxy) was used to treat embryonic stem (ES) cell‐derived NPCs. Treatment with C‐Mix increased the number of tyrosine hydroxylase (TH)‐positive cells compared with controls (2.20‐fold of control). The C‐Mix effect was induced by mainly LIF or IL‐1β treatment. Although L‐Oxy caused an increase in TH‐positive cells (1.34‐fold), the combination of L‐Oxy with C‐Mix did not show an additive effect. Increases in DA in the medium were shown in the presence of C‐Mix, LIF, and L‐Oxy by high‐performance liquid chromatography. Gene expression patterns of neural markers [tryptophan hydroxylase (TPH), GAD67, GluT1, β‐tubulin III, glial fibrillary acidc protein, and TH] were different in C‐Mix and L‐Oxy treatments. Because increases in hypoxia‐inducible factor (HIF)‐1α protein were found in both treatments, we investigated the effect of HIF‐1α on differentiation of NPCs to DAergic neurons. Inhibition of HIF‐1α by the application of antisense oligodeoxynucleotides (ODNs) to NPCs caused a decrease in TH‐positive cells induced by LIF treatment. Gene expressions of TH, GAD67, and GluT1 were decreased, and those of TPH, β‐tubulin III, and S‐100β were increased by treatment with just ODNs, indicating the importance of the endogenous effect of HIF‐1α on neuronal differentiation. These data suggest that enhanced differentiation into DAergic neurons from ES cell‐derived NPCs was induced by C‐Mix or L‐Oxy mediated by HIF‐1α. © 2008 Wiley‐Liss, Inc.
Effect of cortistatin on tau phosphorylation at Ser262 site
Authors: Rubio Alicia , Pérez Mar , de Lecea Luis , Ávila Jesús 
Published: April 2008

AbstractThe development of intraneuronal lesions as a result of the progressive deposition of hyperphosphorylated tau at specific brain regions (such as hippocampus and cortex) plays a key role in the pathological process of Alzheimer's disease. However, the mechanisms by which tau phosphorylation is regulated, mainly in the pathology found in the cortex, are still poorly understood. Here, we analyzed the effect of cortistatin, a cortical neuropeptide related to somatostatin, on tau phosphorylation at Ser262 in cultures of murine cortical neurons. Both somatostatin and cortistatin induce tau phosphorylation at Ser262, a site modified in Alzheimer's disease, although with different kinetics in cortex. The effect of cortistatin likely is mediated by heterodimeric receptors composed of somatostatin receptor subtypes 2 and 4 and also by protein kinase C signaling. Cortistatin‐deficient mice show decreased tau phosphorylation at Ser262 in the cortex but not in other brain regions tested. Our results suggest an important role for cortistatin in the regulation of tau phosphorylation that may be associated with the pathophysiology of Alzheimer's disease in regions such as the cerebral cortex. © 2008 Wiley‐Liss, Inc.
Localization of N‐methyl‐norsalsolinol within rodent and human brain
Authors: DeCuypere Michael , Kalabokis Vassilios N. , Hao Ruyi , Schroeder Dorothy , Miller Duane D. , LeDoux Mark S. 
Published: April 2008

AbstractThe isoquinoline derivative N‐methyl‐6,7‐dihydroxytetrahydroisoquinoline (N‐methyl‐norsalsolinol) is present in normal human brain and has been identified in the cerebrospinal fluid of patients with Parkinson's disease (PD). Endogenously, N‐methyl‐norsalsolinol may be derived from dopamine by condensation with aldehydes or α‐ketoacids. In vitro experiments suggest that N‐methyl‐norsalsolinol is neurotoxic. In this study, high‐performance liquid chromatography with electrochemical detection (HPLC‐EC) was used to determine N‐methyl‐norsalsolinol concentrations in mouse, rat, normal human, and PD brain. In addition, a monoclonal antibody was generated against N‐methyl‐norsalsolinol and used to determine the cellular localization of N‐methyl‐norsalsolinol in brain. With HPLC‐EC, N‐methyl‐norsalsolinol was detected in all regions of rodent and human brain subjected to analysis. In rodent brains, N‐methyl‐norsalsolinol tissue concentrations were similar among frontal cortex, ventral midbrain, striatum, hippocampus, and cerebellum. Conversely, in normal human control brains, N‐methyl‐norsalsolinol was concentrated in the substantia nigra and striatum. In comparison to normal human controls, N‐methyl‐norsalsolinol levels were significantly lower in the substantia nigra and caudate nuclei from PD patients, a finding possibly related to the death of nigrostriatal dopaminergic neurons. N‐methyl‐norsalsolinol immunoreactivity colocalized with a general neuronal marker (neuron‐specific enolase) and a monoaminergic marker (tyrosine hydroxylase) but not with a glial marker (glial fibrillary acidic protein). The widespread neuronal localization of N‐methyl‐norsalsolinol in several mammalian species suggests that, in isolation, this compound is a “weak” neurotoxin. However, endogeneously derived N‐methyl‐norsalsolinol could contribute to the pathobiology of PD in genetically predisposed individuals after years of accumulation in dopaminergic neurons. © 2008 Wiley‐Liss, Inc.
Expression of the receptor for advanced glycation end products in oligodendrocytes in response to oxidative stress
Authors: Qin Jingdong , Goswami Rajendra , Dawson Sylvia , Dawson Glyn 
Published: April 2008

AbstractDemyelination is a common result of oxidative stress in the nervous system, and we report here that the response of oligodendrocytes to oxidative stress involves the receptor for advanced glycation end products (RAGE). RAGE has not previously been reported in neonatal rat oligodendrocytes (NRO), but, by using primers specific for rat RAGE, we were able to show expression of messenger RNA (mRNA) for RAGE in NRO, and a 55‐kDa protein was detected by Western blotting with antibodies to RAGE. Neonatal rat oligodendrocytes stained strongly for RAGE, suggesting membrane localization of RAGE. Addition of low concentrations of hydrogen peroxide (100 μM) initiated 55‐kDa RAGE shedding from the cell membrane and the appearance of “soluble” 45‐kDa RAGE in the culture medium, followed by restoration of RAGE expression to normal levels. Increasing hydrogen peroxide concentration (>200 μM) resulted in no restoration of RAGE, and the cells underwent apoptosis and necrosis. We further confirmed the observation in a human oligodendroglioma‐derived (HOG) cell line. Both the antioxidant N‐acetyl‐L‐cysteine and the broad‐spectrum metalloproteases inhibitor TAPI0 were able partially to inhibit shedding of RAGE, suggesting involvement of metalloproteases in cleavage to produce soluble RAGE. The level of 55‐kDa RAGE in autopsy brain of patients undergoing neurodegeneration with accompanying inflammation [multiple sclerosis and neuronal ceroid‐lipofuscinosis (Batten's disease)] was much lower than that in age‐matched controls, suggesting that shedding of RAGE might occur as reactive oxygen species accumulate in brain cells and be part of the process of neurodegeneration. © 2008 Wiley‐Liss, Inc.
Blockade of chloride intracellular ion channel 1 stimulates Aβ phagocytosis
Authors: Paradisi Silvia , Matteucci Andrea , Fabrizi Cinzia , Denti Michela A. , Abeti Rosella , Breit Samuel N. , Malchiodi‐Albedi Fiorella , Mazzanti Michele 
Published: April 2008

AbstractIn amyloid‐β (Aβ)‐stimulated microglial cells, blockade of chloride intracellular ion channel 1 (CLIC1) reverts the increase in tumor necrosis factor‐α and nitric oxide (NO) production and results in neuroprotection of cocultured neurons. This effect could be of therapeutic efficacy in Alzheimer's disease (AD), where microglial activation may contribute to neurodegeneration, but it could reduce Aβ phagocytosis, which could facilitate amyloid plaque removal. Here, we analyzed the CLIC1 blockade effect on Aβ‐stimulated mononuclear phagocytosis. In the microglial cell line BV‐2, Aβ25–35 treatment enhanced fluorescent bead phagocytosis, which persisted also in the presence of IAA‐94, a CLIC1 channel blocker. The same result was obtained in rat primary microglia and in BV2 cells, where CLIC1 expression had been knocked down with a plasmid producing small interfering RNAs. To address specifically the issue of Aβ phagocytosis, we treated BV‐2 cells with biotinylated Aβ1–42 and measured intracellular amyloid by morphometric analysis. IAA‐94‐treated cells showed an increased Aβ phagocytosis after 24 hr and efficient degradation of ingested material after 72 hr. In addition, we tested Aβ1–42 phagocytosis in adult rat peritoneal macrophages. Also, these cells actively phagocytosed Aβ1–42 in the presence of IAA‐94. However, the increased expression of inducible NO synthase (iNOS), stimulated by Aβ, was reverted by IAA‐94. In parallel, a decrease in NO release was detected. These results suggest that blockade of CLIC1 stimulates Aβ phagocytosis in mononuclear phagocytes while inhibiting the induction of iNOS and further point to CLIC1 as a possible therapeutic target in AD. © 2008 Wiley‐Liss, Inc.