bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cross‐cultural comparison of the neurobehavioral characteristics of Chinese and Japanese neonates
Authors: Loo Kek Khee , Ohgi Shohei , Zhu Honglin , Howard Judy , Chen Lian 
Published: July 2005

Abstract
Background
: Similarities and differences in the neurobehavioral repertoire of neonates from different cultures have been noted using the Brazelton Neonatal Behavioral Assessment Scale (NBAS). By identifying the behavioral attributes of newborns that are seen more universally versus those that are culture‐specific, comparative studies increase understanding of the roles of cultural factors in shaping the behavioral trajectory of infants. This study compared the neurobehavioral characteristics of neonates in Chengdu, China and Nagasaki, Japan.
Methods
: The Brazelton NBAS was administered within the first week of life to 40 Chinese and 62 Japanese healthy, full‐term neonates in Chengdu and Nagasaki.
Results
: The two groups differed significantly in birthweight, gender, age at time of exam, mode of delivery, and gestational age. When these variables, in addition to group status (Chinese or Japanese), were entered into multiple linear analyses with NBAS cluster scores as dependent variables, group status independently predicted Range of State and Habituation scores. The group status did not predict Orientation, Motor, Regulation of States, Autonomic Stability, and Abnormal Reflexes cluster scores.
Conclusion
: These results suggest that Japanese newborns habituated more readily to stimuli, and were less irritable than newborns in the Chinese sample. The infants in the two groups shared many similar neurobehavioral characteristics as well. The implications of these similarities and differences were discussed.
Proteasome inhibition by lactacystin in primary neuronal cells induces both potentially neuroprotective and pro‐apoptotic transcriptional responses: a microarray analysis
Authors: Yew Elaine Hau Jin , Cheung Nam Sang , Choy Meng Shyan , Qi Robert Z. , Lee Alan Yiu‐Wah , Peng Zhao Feng , Melendez Alirio J. , Manikandan Jayapal , Koay Evelyn Siew‐Chuan , Chiu Lily‐Lily , Ng Wooi Loon , Whiteman Matthew , Kandiah Jeyaseelan , Halliwell Barry 
Published: July 2005

AbstractAlthough inhibition of the ubiquitin proteasome system has been postulated to play a key role in the pathogenesis of neurodegenerative diseases, studies have also shown that proteasome inhibition can induce increased expression of neuroprotective heat‐shock proteins (HSPs). The global gene expression of primary neurons in response to treatment with the proteasome inhibitor lactacystin was studied to identify the widest range of possible pathways affected. Our results showed changes in mRNA abundance, both at different time points after lactacystin treatment and at different lactacystin concentrations. Genes that were differentially up‐regulated at the early time point but not when most cells were undergoing apoptosis might be involved in an attempt to reverse proteasome inhibitor‐mediated apoptosis and include HSP70, HSP22 and cell cycle inhibitors. The up‐regulation of HSP70 and HSP22 appeared specific towards proteasome inhibitor‐mediated cell death. Overexpression of HSP22 was found to protect against proteasome inhibitor‐mediated loss of viability by up to 25%. Genes involved in oxidative stress and the inflammatory response were also up‐regulated. These data suggest an initial neuroprotective pathway involving HSPs, antioxidants and cell cycle inhibitors, followed by a pro‐apoptotic response possibly mediated by inflammation, oxidative stress and aberrant activation of cell cycle proteins.
Differential effects ofl‐DOPA on monoamine metabolism, cell survival and glutathione production in midbrain neuronal‐enriched cultures from parkin knockout and wild‐type mice
Authors: Casarejos M. J. , Solano R. M. , Menéndez J. , Rodríguez‐Navarro J. A. , Correa C. , García de Yébenes J. , Mena M. A. 
Published: July 2005

Abstractl‐DOPA is the most effective treatment for Parkinson's disease but in isolated neuronal cultures it is neurotoxic for dopamine (DA) neurones. Experimentsin vivoand clinical studies have failed to show toxicity ofl‐DOPA in animals or patients but that does not exclude the possibility of a toxic effect ofl‐DOPA on patients with certain genetic risk factors. Mutations of the parkin gene are the most frequent cause of hereditary parkinsonism. Parkin null mice have a mild phenotype that could be modified by different neurotoxins. The aim of this study was to investigate whether the toxic effects ofl‐DOPA on DA neurones are amplified in parkin null mice. We have measured the effects ofl‐DOPA on cell viability, tyrosine hydroxylase (TH) expression, DA metabolism and glutathione levels of parkin knockout (PK‐KO) midbrain cultures. Neuronal‐enriched cultures from PK‐KO mice have similar proportions of the different cell types with the exception of a significant increment of microglial cells.l‐DOPA (400 µmfor 24 h) reduced the number of TH‐immunoreactive cells to 50% of baseline and increased twofold the percentage of apoptotic cells in cultures of wild‐type (WT) animals. The PK‐KO mice, however, are not only resistant to thel‐DOPA‐induced pro‐apoptotic effects but they have an increased number of TH‐immunoreactive neurones after treatment withl‐DOPA, suggesting thatl‐DOPA is toxic for neurones of WT mice but not those of parkin null mice. MAPK and phosphatidylinositol‐3 kinase signalling pathways are not involved in the differentiall‐DOPA effects in WT and PK‐KO cultures. Intracellular levels ofl‐DOPA were not different in WT and parkin null mice but the intracellular and extracellular levels of DA and 3‐4‐dihydroxyphenylacetic acid, however, were significantly increased in parkin null animals. Furthermore, monoamine oxidase activity was significantly increased in parkin null mice, suggesting that these animals have an increased metabolism of DA. The levels of glutathione were further increased in parkin null mice than in controls both with and without treatment withl‐DOPA, suggesting that a compensatory mechanism may protect DA neurones from neuronal death. This study opens new avenues for understanding the mechanisms of action ofl‐DOPA on DA neurones in patients with Park‐2 mutations.
Inhibition of Rac GTPase triggers a c‐Jun‐ and Bim‐dependent mitochondrial apoptotic cascade in cerebellar granule neurons
Authors: Le Shoshona S. , Loucks F. Alexandra , Udo Hiroshi , Richardson‐Burns Sarah , Phelps Reid A. , Bouchard Ron J. , Barth Holger , Aktories Klaus , Tyler Kenneth L. , Kandel Eric R. , Heidenreich Kim A. , Linseman Daniel A. 
Published: July 2005

AbstractRho GTPases are key transducers of integrin/extracellular matrix and growth factor signaling. Although integrin‐mediated adhesion and trophic support suppress neuronal apoptosis, the role of Rho GTPases in neuronal survival is unclear. Here, we have identified Rac as a critical pro‐survival GTPase in cerebellar granule neurons (CGNs) and elucidated a death pathway triggered by its inactivation. GTP‐loading of Rac1 was maintained in CGNs by integrin‐mediated (RGD‐dependent) cell attachment and trophic support. Clostridium difficile toxin B (ToxB), a specific Rho family inhibitor, induced a selective caspase‐mediated degradation of Rac1 without affecting RhoA or Cdc42 protein levels. Both ToxB and dominant–negative N17Rac1 elicited CGN apoptosis, characterized by cytochrome c release and activation of caspase‐9 and ‐3, whereas dominant–negative N19RhoA or N17Cdc42 did not cause significant cell death. ToxB stimulated mitochondrial translocation and conformational activation of Bax, c‐Jun activation, and induction of the BH3‐only protein Bim. Similarly, c‐Jun activation and Bim induction were observed with N17Rac1. A c‐jun N‐terminal protein kinase (JNK)/p38 inhibitor, SB203580, and a JNK‐specific inhibitor, SP600125, significantly decreased ToxB‐induced Bim expression and blunted each subsequent step of the apoptotic cascade. These results indicate that Rac acts downstream of integrins and growth factors to promote neuronal survival by repressing c‐Jun/Bim‐mediated mitochondrial apoptosis.
Celastrol protects against MPTP‐ and 3‐nitropropionic acid‐induced neurotoxicity
Authors: Cleren Carine , Calingasan Noel Y. , Chen Junya , Beal M. Flint 
Published: July 2005

AbstractOxidative stress and inflammation are implicated in neurodegenerative diseases including Parkinson's disease (PD) and Huntington's disease (HD). Celastrol is a potent anti‐inflammatory and antioxidant compound extracted from a perennial creeping plant belonging to theCelastraceaefamily.Celastrol is known to prevent the production of proinflammatory cytokines, inducible nitric oxide synthase and lipid peroxidation. Mice were treated with celastrol before and after injections of MPTP, a dopaminergic neurotoxin, which produces a model of PD. A 48% loss of dopaminergic neurons induced by MPTP in the substantia nigra pars compacta was significantly attenuated by celastrol treatment. Moreover, celastrol treatment significantly reduced the depletion in dopamine concentration induced by MPTP. Similarly, celastrol significantly decreased the striatal lesion volume induced by 3‐nitropropionic acid, a neurotoxin used to model HD in rats. Celastrol induced heat shock protein 70 within dopaminergic neurons and decreased tumor necrosis factor‐α and nuclear factor κ B immunostainings as well as astrogliosis. Celastrol is therefore a promising neuroprotective agent for the treatment of PD and HD.
RanBPM is an L1‐interacting protein that regulates L1‐mediated mitogen‐activated protein kinase activation
Authors: Cheng Ling , Lemmon Sandra , Lemmon Vance 
Published: July 2005

AbstractA yeast two‐hybrid screen using the last 28 amino acids of the cytoplasmic domain of the neural cell adhesion molecule L1 identified RanBPM as an L1‐interacting protein. RanBPM associates with L1 in vivo and the N‐terminal region of RanBPM (N‐RanBPM), containing the SPRY domain, is sufficient for the interaction with L1 in a glutathione S‐transferase pull‐down assay. L1 antibody patching dramatically changes the subcellular localization of N‐RanBPM in transfected COS cells. Overexpression of N‐RanBPM in COS cells reduces L1‐triggered extracellular signal‐regulated kinase 1/2 activation by 50% and overexpression of N‐RanBPM in primary neurons inhibits L1‐mediated neurite outgrowth and branching. These data suggest that RanBPM is an adaptor protein that links L1 to the extracellular signal‐regulated kinase/MAPK pathway.
Treatment of YAC128 mice and their wild‐type littermates with cystamine does not lead to its accumulation in plasma or brain: implications for the treatment of Huntington disease
Authors: Pinto John T. , Van Raamsdonk Jeremy M. , Leavitt Blair R. , Hayden Michael R. , Jeitner Thomas M. , Thaler Howard T. , Krasnikov Boris F. , Cooper Arthur J. L. 
Published: July 2005

AbstractCystamine is beneficial to Huntington disease (HD) transgenic mice. To elucidate the mechanism, cystamine metabolites were determined in brain and plasma of cystamine‐treated mice. A major route for cystamine metabolism is thought to be: cystamine → cysteamine → hypotaurine → taurine. Here we describe an HPLC system with coulometric detection that can rapidly measure underivatized cystamine, cysteamine and hypotaurine, as well as cysteine and glutathione in the same deproteinized tissue sample. A method is also described for the coulometric estimation of taurine as its isoindole‐sulfonate derivative. Using this new methodology we showed that cystamine and cysteamine are undetectable (≤ 0.2 nmol/100 mg protein) in the brains of 3‐month‐old HD transgenic (YAC128) mice (or their wild‐type littermates) treated daily for 2 weeks with cystamine (225 mg/kg) in their drinking water. No significant changes were observed in brain glutathione and taurine but significant increases were observed in brain cysteine. Cystamine and cysteamine were not detected in the plasma of YAC128 mice treated daily with cystamine between the ages of 4 and 12 or 7 and 12 months. These findings suggest that cystamine is not directly involved in mitigating HD but that increased brain cysteine or uncharacterized sulfur metabolites may be responsible.
Neurotoxicity and behavioral deficits associated with Septin 5 accumulation in dopaminergic neurons
Authors: Son Jin H. , Kawamata Hibiki , Yoo Myung S. , Kim Dae J. , Lee Young K. , Kim SooYoul , Dawson Ted M. , Zhang Hui , Sulzer David , Yang Lichuan , Beal M. Flint , DeGiorgio Lorraine A. , Chun Hong S. , Baker Harriet , Peng Chu 
Published: July 2005

AbstractSeptin 5, a parkin substrate, is a vesicle‐ and membrane‐associated protein that plays a significant role in inhibiting exocytosis. The regulatory function of Septin 5 in dopaminergic (DAergic) neurons of substantia nigra (SN), maintained at relatively low levels, has not yet been delineated. As loss of function mutations of parkin are the principal cause of a familial Parkinson's disease, a prevailing hypothesis is that the loss of parkin activity results in accumulation of Septin 5 which confers neuron‐specific toxicity in SN‐DAergic neurons. In vitro and in vivo models were used to support this hypothesis. In our well‐characterized DAergic SN4741 cell model, acute accumulation of elevated levels of Septin 5, but not synphilin‐1 (another parkin substrate), resulted in cytotoxic cell death that was markedly reduced by parkin co‐transfection. A transgenic mouse model expressing a dominant negative parkin mutant accumulated moderate levels of Septin 5 in SN‐DAergic neurons. These mice acquired a progressive l‐DOPA responsive motor dysfunction that developed despite a 25% higher than normal level of striatal dopamine (DA) and no apparent loss of DAergic neurons. The phenotype of this animal, increased striatal dopamine and reduced motor function, was similar to that observed in parkin knockout animals, suggesting a common DAergic alteration. These data suggest that a threshold level of Septin 5 accumulation is required for DAergic cell loss and that l‐DOPA‐responsive motor deficits can occur even in the presence of elevated DA.
Evidence that gabapentin reduces neuropathic pain by inhibiting the spinal release of glutamate
Authors: Coderre Terence J. , Kumar Naresh , Lefebvre Celeste D. , Yu Jonathan S. C. 
Published: July 2005

AbstractGabapentin is an anticonvulsant that successfully treats many neuropathic pain syndromes, although the mechanism of its antihyperalgesic action remains elusive. This study aims to help delineate gabapentin's antihyperalgesic mechanisms. We assessed the effectiveness of gabapentin at decreasing mechanical and cold hypersensitivity induced in a rat model of neuropathic pain. Thus, we compared the effectiveness of pre‐ or post‐treatment with systemic or intrathecal (i.t.) gabapentin at reducing the development and maintenance of the neuropathic pain symptoms. Gabapentin successfully decreased mechanical and cold hypersensitivity, both as a pretreatment and post‐treatment. Furthermore, both i.t. and systemic administration of gabapentin were effective in reducing the behavioral hypersensitivity; however, the i.t. administration was superior to the systemic. We also examined gabapentin's effects at inhibiting hindpaw formalin‐induced release of excitatory amino acids (EAAs) in the spinal cord dorsal horn (SCDH) both in naïve rats and in rats with neuropathic pain. We present the first evidence that gabapentin reduces the formalin‐induced release of both glutamate and aspartate in SCDH. Furthermore, i.t. gabapentin reduces the enhanced noxious stimulus‐induced spinal release of glutamate seen in neuropathic rats. These data suggest that gabapentin reduces neuropathic pain symptoms by inhibiting the release of glutamate in the SCDH.
Prostaglandin H2‐derived adducts of proteins correlate with Alzheimer's disease severity
Authors: Zagol‐Ikapitte Irene , Masterson Tina S. , Amarnath V. , Montine Thomas J. , Andreasson Katrin I. , Boutaud Olivier , Oates John A. 
Published: July 2005

AbstractThe formation of cyclooxygenase‐derived lipid adducts of protein in brains of patients who had Alzheimer's disease has been investigated. The enzymatic product of the cyclooxygenases, prostaglandin H2, rearranges in part to highly reactive γ‐ketoaldehydes, levuglandin (LG) E2 and LGD2. These γ‐ketoaldehydes react with free amines on proteins to yield a covalent adduct. Utilizing analysis of the levuglandinyl‐lysine adducts by liquid chromatography‐tandem mass spectrometry, we now find that this post‐translational modification is increased significantly in the hippocampus in Alzheimer's disease. The magnitude of the increase correlates with the pathological evidence of severity.
Characterization of a novel D2‐like dopamine receptor with a truncated splice variant and a D1‐like dopamine receptor unique to invertebrates from Caenorhabditis elegans
Authors: Sugiura Mai , Fuke Satoshi , Suo Satoshi , Sasagawa Noboru , Van Tol Hubert H. M. , Ishiura Shoichi 
Published: July 2005

AbstractWe have cloned two novel Caenorhabditis elegans dopamine receptors, DOP‐3 and DOP‐4. DOP‐3 shows high sequence homology with other D2‐like dopamine receptors. As a result of alternative splicing, a truncated splice variant of DOP‐3, DOP‐3nf, was produced. Because of the in‐frame insertion of a stop codon in the third intracellular loop, DOP‐3nf lacks the sixth and seventh transmembrane domains that are found in the full‐length DOP‐3 receptor. Reporter gene assay showed that DOP‐3 attenuates forskolin‐stimulated cAMP formation in response to dopamine stimulation, whereas DOP‐3nf does not. When DOP‐3 was coexpressed with DOP‐3nf, the ability to inhibit forskolin‐stimulated cAMP formation was reduced. DOP‐4 shows high sequence homology with D1‐like dopamine receptors unique to invertebrates, which are distinct from mammalian D1‐like dopamine receptors. Reporter gene assay showed that DOP‐4 stimulates cAMP accumulation in response to dopamine stimulation. These two receptors provide new opportunities to understand dopaminergic signaling at the molecular level.
Ratzinger Is Right
Authors: GIRARD RENÉ 
Published: July 2005

No sooner had John Paul II stepped across the threshold of Heaven than Cardinal Ratzinger, now elected Pope Benedict, declared the new mission of the Catholic Church would be to fight “the dictatorship of relativism.”To explore this theme, NPQ spoke with René Girard, the famous anthropologist and author of the seminal study Violence and the Sacred. We then asked Pankaj Mishra, one of the most exciting new non‐fiction writers and author of An End to Suffering: The Buddha in the World, to respond.
Estrogen Treatment Abrogates Neointima Formation in Human C-Reactive Protein Transgenic Mice
Authors: Wang Dajun , Oparil Suzanne , Chen Yiu-Fai , McCrory Mark A. , Skibinski Gregory A. , Feng Wenguang , Szalai Alexander J. 
Published: July 2005

Objective—Previously we established that the vascular injury response was attenuated in ovariectomized wild-type rodents treated with 17β-estradiol (E2). We also showed that the response to acute vascular injury in transgenic mice expressing human C-reactive protein (CRPtg) is exaggerated compared with their nontransgenic (NTG) counterparts. Herein we tested the hypothesis that E2modulates vascular injury in the CRPtg mouse.Methods and Results—Intact (INT) or ovariectomized (OVX) CRPtg and NTG, treated with E2or vehicle, had their right common carotid artery ligated. Resultant neointima formation was exaggerated in CRPtg compared with NTG, whether INT or OVX, but was prevented in both genotypes by E2. Expression of human CRP protein (immunohistochemical analysis) and mRNA (laser microdissection followed by real-time quantitative RT-PCR) was detected in the neointima of OVX CRPtg and was greatly diminished by E2treatment. CRP was not detected in uninjured arteries or in the media of injured arteries, and blood CRP level was consistently low.Conclusions—The exaggerated response to vascular injury in CRPtg is associated with increased neointimal expression of human CRP. E2reduces both neointima formation and neointimal expression of human CRP, suggesting that E2is vasoprotective.
101 and Counting: Dalmatians in Film and Advertising
Authors: Sheen Erica 
Published: July 2005

AbstractIn both academic and animal welfare circles, Disney's live action films 101 and 102 Dalmatians have been criticised as a commercial exploitation of the breed. From this perspective, it was widely held that the Dalmatian has been subject to over-breeding and abandonment as a direct result of these films, and that Disney should be held responsible for this abuse. I question these assumptions. I discuss the Hollywood animal image as a form of intellectual property and provide a detailed account of negotiations between Disney and Dalmatian breed associations in America and the UK. In response to critics who described the films as "an advertisement for the breed", I suggest that Disney's animal imagery should be seen as a more complex cultural and economic negotiation between filmmaker and audience, and conclude that our understanding of the commercial deployment of the Dalmatian image must be situated in a more nuanced account of the relationship between advertising and film.
CD11c- and CD11b-expressing mouse leukocytes transport single Toxoplasma gondii tachyzoites to the brain
Authors: Courret Nathalie , Darche Sylvie , Sonigo Pierre , Milon Geneviève , Buzoni-Gâtel Dominique , Tardieux Isabelle 
Published: July 2005

AbstractThe protozoan parasite Toxoplasma gondii enters hosts through the intestinal mucosa and colonizes distant tissues such as the brain, where its progeny persists for a lifetime. We investigated the role of CD11c- and CD11b-expressing leukocytes in T gondii transport during the early step of parasitism from the mouse small intestine and during subsequent parasite localization in the brain. Following intragastric inoculation of cyst-containing parasites in mice, CD11c+ dendritic cells from the intestinal lamina propria, the Peyer patches, and the mesenteric lymph nodes were parasitized while in the blood, parasites were associated with the CD11c- CD11b+ monocytes. Using adoptive transfer experiments, we demonstrated that these parasitized cells triggered a parasitic process in the brain of naive recipient mice. Ex vivo analysis of parasitized leukocytes showed that single tachyzoites remained at the cell periphery, often surrounded by the host cell plasma membrane, but did not divide. Using either a dye that labels circulating leukocytes or an antibody known to prevent CD11b+ circulating leukocytes from leaving the microvascular bed lumen, and chimeric mice in which the hematopoietic cells expressed the green fluorescent protein, we established that T gondii zoites hijacked CD11b+ leukocytes to reach the brain extravascular space.