bluuebunny/crossref_metadata_2025_split huggingface dataset:
Association of the Ser704Cys DISC1 polymorphism with human hippocampal formation gray matter and function during memory encoding
Authors: Di Giorgio Annabella , Blasi Giuseppe , Sambataro Fabio , Rampino Antonio , Papazacharias Apostolos , Gambi Francesco , Romano Raffaella , Caforio Grazia , Rizzo Miriam , Latorre Valeria , Popolizio Teresa , Kolachana Bhaskar , Callicott Joseph H , Nardini Marcello , Weinberger Daniel R , Bertolino Alessandro 
Published: November 2008

AbstractA common nonsynonymous single nucleotide polymorphism leading to a serine‐to‐cysteine substitution at amino acid 704 (Ser704Cys) in the DISC1 protein sequence has been recently associated with schizophrenia and with specific hippocampal abnormalities. Here, we used multimodal neuroimaging to investigate in a large sample of healthy subjects the putative association of the Ser704Cys DISC1 polymorphism with in vivo brain phenotypes including hippocampal formation (HF) gray matter volume and function (as assessed with functional MRI) as well as HF functional coupling with the neural network engaged during encoding of recognition memory. Individuals homozygous for DISC1 Ser allele relative to carriers of the Cys allele showed greater gray matter volume in the HF. Further, Ser/Ser subjects exhibited greater engagement of the HF together with greater HF–dorsolateral prefrontal cortex functional coupling during memory encoding, in spite of similar behavioral performance. These findings consistently support the notion that Ser704Cys DISC1 polymorphism is physiologically relevant. Moreover, they support the hypothesis that genetic variation in DISC1 may affect the risk for schizophrenia by modifying hippocampal gray matter and function.
Adenosine preconditions against ouabain but not against glutamate on CA1‐evoked potentials in rat hippocampal slices
Authors: Ferguson Alexandra L. , Stone Trevor W. 
Published: November 2008

AbstractHypoxic and ischaemic brain damage are believed to involve excessive release of glutamate, and recent work shows that glutamate‐induced damage in brain slices can be reduced by preconditioning with hypoxia or glutamate itself. Because adenosine is a powerful preconditioning agent, we have investigated whether adenosine could precondition against glutamatein vitro. In rat hippocampal slices, glutamate depolarization reduced the amplitudes of antidromic‐ and orthodromic‐evoked potentials, with only partial recovery. Applying adenosine before these insults failed to increase that recovery. Ouabain also produced depolarization with partial reversibility, but adenosine pretreatment increased the extent of recovery. The preconditioning effect of adenosine on ouabain responses was prevented by blocking receptors forN‐methyl‐d‐aspartate (NMDA), but not receptors for kainate or α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA), and was blocked by inhibiting nitric oxide synthase. Preconditioning was also abolished by the ATP‐dependent potassium channel blockers, glibenclamide (cytoplasmic) or 5‐hydroxydecanoate (mitochondrial). We conclude that adenosine does not precondition against glutamate in hippocampal slices, but that it does precondition against ouabain with a pharmacology similar to studiesin vivo. Ischaemic neuronal damage is a complex of many factors, and because adenosine can precondition against ischaemic neuronal damage, its failure to protect against glutamate highlights limitations of using glutamate alone as a model for ischaemia. Because damage following ischaemia, trauma or excitotoxicity also involves reduced Na+,K+‐ATPase activity, and adenosine can precondition against ouabain, we propose that ouabain‐induced damage represents an additional or alternative model for the contribution to cell damage of Na+,K+‐ATPase loss, this being more relevant to the mechanisms of preconditioning.
A chemical compound commonly used to inhibit PKR, {8‐(imidazol‐4‐ylmethylene)‐6H‐azolidino[5,4‐g] benzothiazol‐7‐one}, protects neurons by inhibiting cyclin‐dependent kinase
Authors: Chen Hsin‐Mei , Wang Lulu , D’Mello Santosh R. 
Published: November 2008

AbstractActivation of the double‐stranded RNA‐dependent protein kinase (PKR) has been implicated in the pathogenesis of several neurodegenerative diseases. We find that a compound widely used as a pharmacological inhibitor of this enzyme, referred to as PKR inhibitor (PKRi), {8‐(imidazol‐4‐ylmethylene)‐6H‐azolidino[5,4‐g]benzothiazol‐7‐one}, protects against the death of cultured cerebellar granule and cortical neurons. PKRi also prevents striatal neurodegeneration and improves behavioral outcomes in a chemically induced mouse model of Huntington’s disease. Surprisingly, PKRi fails to block the phosphorylation of eIF2α, a downstream target of PKR, and does not reduce the autophosphorylation of PKR enzyme immunoprecipitated from neurons. Furthermore, neurons lacking PKR are fully protected from apoptosis by PKRi, demonstrating that neuroprotection by this compound is not mediated by PKR inhibition. Using in vitro kinase assays we investigated whether PKRi affects any other protein kinase. These analyses demonstrated that PKRi has no major inhibitory effect on pro‐apoptotic kinases such as the c‐Jun N‐terminal kinases, the p38 MAP kinases and the death‐associated protein kinases, or on other kinases including c‐Raf, MEK1, MKK6 and MKK7. PKRi does, however, inhibit the activity of certain cyclin‐dependent kinases (CDKs), including CDK1, CDK2 and CDK5 both in vitro and in low potassium‐treated neurons. Consistent with its inhibitory action on mitotic CDKs, the treatment of HT‐22 and HEK293T cell lines with PKRi sharply reduces the rate of cell cycle progression. Taken together with the established role of CDK activation in the promotion of neurodegeneration, our results suggest that PKRi exerts its neuroprotective action by inhibiting CDK.
Use of stable isotope‐labelled cells to identify active grazers of picocyanobacteria in ocean surface waters
Authors: Frias‐Lopez Jorge , Thompson Anne , Waldbauer Jacob , Chisholm Sallie W. 
Published: November 2008

Summary Prochlorococcus and Synechococcus are the two most abundant marine cyanobacteria. They represent a significant fraction of the total primary production of the world oceans and comprise a major fraction of the prey biomass available to phagotrophic protists. Despite relatively rapid growth rates, picocyanobacterial cell densities in open‐ocean surface waters remain fairly constant, implying steady mortality due to viral infection and consumption by predators. There have been several studies on grazing by specific protists on Prochlorococcus and Synechococcus in culture, and of cell loss rates due to overall grazing in the field. However, the specific sources of mortality of these primary producers in the wild remain unknown. Here, we use a modification of the RNA stable isotope probing technique (RNA‐SIP), which involves adding labelled cells to natural seawater, to identify active predators that are specifically consuming Prochlorococcus and Synechococcus in the surface waters of the Pacific Ocean. Four major groups were identified as having their 18S rRNA highly labelled: Prymnesiophyceae (Haptophyta), Dictyochophyceae (Stramenopiles), Bolidomonas (Stramenopiles) and Dinoflagellata (Alveolata). For the first three of these, the closest relative of the sequences identified was a photosynthetic organism, indicating the presence of mixotrophs among picocyanobacterial predators. We conclude that the use of RNA‐SIP is a useful method to identity specific predators for picocyanobacteria in situ, and that the method could possibly be used to identify other bacterial predators important in the microbial food‐web.
Volatile organic compounds: a potential direct long‐distance mechanism for antagonistic action of Fusarium oxysporum strain MSA 35
Authors: Minerdi Daniela , Bossi Simone , Gullino Maria Lodovica , Garibaldi Angelo 
Published: November 2008

Summary Fusarium oxysporum MSA 35 [wild‐type (WT) strain] is an antagonistic Fusarium that lives in association with a consortium of bacteria belonging to the genera Serratia, Achromobacter, Bacillus and Stenotrophomonas in an Italian soil suppressive to Fusarium wilt. Typing experiments and virulence tests provided evidence that the F. oxysporum isolate when cured of the bacterial symbionts [the cured (CU) form], is pathogenic, causing wilt symptoms identical to those caused by F. oxysporum f. sp. lactucae. Here, we demonstrate that small volatile organic compounds (VOCs) emitted from the WT strain negatively influence the mycelial growth of different formae speciales of F. oxysporum. Furthermore, these VOCs repress gene expression of two putative virulence genes in F. oxysporum lactucae strain Fuslat10, a fungus against which the WT strain MSA 35 has antagonistic activity. The VOC profile of the WT and CU fungus shows different compositions. Sesquiterpenes, mainly caryophyllene, were present in the headspace only of WT MSA 35. No sesquiterpenes were found in the volatiles of ectosymbiotic Serratia sp. strain DM1 and Achromobacter sp. strain MM1. Bacterial volatiles had no effects on the growth of the different ff. spp. of F. oxysporum examined. Hyphae grown with VOC from WT F. oxysporum f. sp. lactucae strain MSA 35 were hydrophobic whereas those grown without VOCs were not, suggesting a correlation between the presence of volatiles in the atmosphere and the phenotype of the mycelium. This is the first report of VOC production by antagonistic F. oxysporum MSA 35 and their effects on pathogenic F. oxysporum. The results obtained in this work led us to propose a new potential direct long‐distance mechanism for antagonism by F. oxysporum MSA 35 mediated by VOCs. Antagonism could be the consequence of both reduction of pathogen mycelial growth and inhibition of pathogen virulence gene expression.
Thrombolysis in recurrent lacunar stroke: a case example
Authors: Nguyen T. H. , Vo D. , Ngo M. B. , Truong A. L. T. , Bui C. Q. , Nguyen L. K. , Le T. V. 
Published: November 2008

Background and purpose:  We report a case of intravenous thrombolysis in a patient with early recurrent stroke. A 62‐year‐old man recovered nearly completely after a lacunar infarct of the left putamen. He suffered stroke recurrence 7 days later due to a new infarct in the left internal capsule. Intravenous alteplase 0.9 mg/kg was administered 40 min after the symptom onset resulting in significant neurologic improvement.Conclusion:  Intravenous thrombolysis may be safe for early recurrent lacunar stroke in patients with relatively small risk of hemorrhage.
Pregabalin as add‐on therapy induces REM sleep enhancement in partial epilepsy: a polysomnographic study
Authors: Romigi A. , Izzi F. , Marciani M. G. , Torelli F. , Zannino S. , Pisani L. R. , Uasone E. , Corte F. , Placidi F. 
Published: November 2008

Background and purpose: To evaluate the effects of pregabalin (PGB) adjunctive therapy on sleepwake cycle and daytime somnolence in adult patients affected by partial epilepsy.Methods: Twelve patients affected by partial epilepsy underwent a 24‐h ambulatory polysomnography and a subjective evaluation of daytime somnolence by means of the Epworth Sleepiness Scale (ESS), before and after 3 months treatment with PGB.Results: Pregabalin therapy reduced seizures by >50% in 8 out of 12 patients. It induced a significant increase of REM sleep and a decrease of stage 2 NREM sleep (S2). A significant increase of the ESS score was observed without reaching the pathological cut‐off value (mean ESS score <10). No statistical correlation between REM sleep and seizure frequency was observed.Discussion: Pregabalin seems to be effective and safe in partial epilepsy. The increase of REM sleep may be indicative of an improvement of nocturnal sleep quality considering the involvement of REM sleep in learning and memory processes. REM sleep enhancement may be the result of both a direct effect of PGB on sleep generators and an indirect effect due to its clinical efficacy. The increase of ESS score within normal range suggests that daytime somnolence is a minor adverse effect of PGB.
Locating Backup Facilities to Enhance Supply Chain Disaster Resilience
Authors: RATICK SAMUEL , MEACHAM BRIAN , AOYAMA YUKO 
Published: November 2008

ABSTRACTThe use of emergency backup and storage facilities to supplement existing facilities in response to the potential effects of various natural and anthropogenic hazards (e.g., floods, fires, outages, and acts of malice) can be an effective way of reducing vulnerability and enhancing the resilience of supply chain and other logistics functions. Although there can be additional costs associated with utilizing emergency backup and storage facilities, they can be a particularly attractive and cost‐effective alternative in those cases where long‐term disruptions can, or should, be expected. In this paper we use set cover location modeling as a decision to determine the number of backup facilities to locate under varying cover, anticover, and complementary anticover distances. We then add the flexibility of allowing existing facilities to serve as backup facilities and explore the interrelationships among hazards, vulnerability, and location. Finally, these model formulations are applied to an example data set over 900 cities and towns in New England and New York.
Demography of a socially natural herd of Przewalski's horses: an example of a small, closed population
Authors: Tatin L. , King S. R. B. , Munkhtuya B. , Hewison A. J. M. , Feh C. 
Published: November 2008

AbstractOwing to habitat loss and fragmentation, large mammal populations all over the world are becoming increasingly small and isolated. It is therefore a conservation priority to understand mechanisms influencing the demography of such populations, which can easily be driven to extinction. The Przewalski's horse Equus ferus przewalskii remains one of the world's most endangered species and reintroduced animals are still vulnerable. Over 9 years, we analysed factors affecting mortality and female fecundity at the individual level in a predator‐free, closed population of Przewalski's horses, which grew from 11 to 55 individuals. Similar to other wild equids, the annual growth rate of the population was r=0.169. Typically, adult mortality was much lower than juvenile mortality, the latter being correlated with neither inbreeding coefficient of foals nor population density. We found no link between female fecundity and operational sex ratio of the herd, or inbreeding coefficient, lactation status and body condition of the mares. Although food therefore seemed not to be limiting in this population, density (number of horses ha−1) clearly reduced fecundity, especially in subadult mares. Thus, our results show that space can slow the growth rate of a population before resources become limited, a potential source of concern for increasingly shrinking habitats of endangered large mammals. Possible mechanisms causing this may be found in incest avoidance or other social parameters. Finally, in large herbivores, population density is said to exert influence in a sequential order: juvenile survival first, followed by fecundity of young females, then adult females, and adult survival last. Although we observed no link between density and juvenile survival in the studied population, our results otherwise support this hypothesis.
Shaping the calcium signature
Authors: McAinsh Martin R. , Pittman Jon K. 
Published: November 2008

SummaryIn numerous plant signal transduction pathways, Ca2+is a versatile second messenger which controls the activation of many downstream actions in response to various stimuli. There is strong evidence to indicate that information encoded within these stimulus‐induced Ca2+oscillations can provide signalling specificity. Such Ca2+signals, or ‘Ca2+signatures’, are generated in the cytosol, and in noncytosolic locations including the nucleus and chloroplast, through the coordinated action of Ca2+influx and efflux pathways. An increased understanding of the functions and regulation of these various Ca2+transporters has improved our appreciation of the role these transporters play in specifically shaping the Ca2+signatures. Here we review the evidence which indicates that Ca2+channel, Ca2+‐ATPase and Ca2+exchanger isoforms can indeed modulate specific Ca2+signatures in response to an individual signal.ContentsSummary275I.Introduction276II.Ca2+signalling pathways276III.Shaping Ca2+signatures278IV.Ca2+influx channels278V.Ca2+influx channels as modulators of Ca2+signatures281VI.Ca2+efflux transporters282VII.Ca2+efflux transporters as modulators of Ca2+signatures284VIII.The shaping of noncytosolic Ca2+signatures285IX.Future insights into the role of Ca2+oscillators from modelling studies287X.Conclusions and perspectives288Acknowledgements288References288
Relationship of CSF neurotransmitter metabolite levels to disease severity and disability in multiple sclerosis
Authors: Markianos Manolis , Koutsis Georgios , Evangelopoulos Maria‐Eleftheria , Mandellos Dimitrios , Karahalios Georgios , Sfagos Constantin 
Published: November 2008

AbstractAxonal degeneration and brain tissue loss occur during disease progression in multiple sclerosis (MS) and are expected to influence neurotransmitter activities, with consequences on neurologic and psychiatric symptomatology. We searched for relationships of disease duration, disability, and severity of MS patients to CSF levels of the major metabolites of noradrenaline, dopamine, and serotonin, MHPG, methoxyhydroxyphenylglycol (MHPG), homovanillic acid, and 5‐hydroxyindoleacetic acid (5‐HIAA), respectively, in 39 patients with relapsing–remitting (RR) MS in remission, and 26 patients with progressive (PR) MS. Disability and Disease Severity were assessed by the Expanded Disability Status Scale (EDSS) and the Multiple Sclerosis Severity Score (MSSS). Compared with the levels of 50 control subjects, MHPG levels were not different in either MS group, correlated negatively to duration of illness and number of relapses in the RRMS group, but not to EDSS score or to MSSS. Homovanillic acid levels were significantly lower only in the PRMS group, with a negative correlation to duration of illness, and a strong negative correlation to EDSS score, but not to MSSS. 5‐HIAA was significantly lower in both RRMS and PRMS groups. In the RRMS group, 5‐HIAA levels were negatively related to EDSS and to MSSS. Multiple regression analyses revealed a significant association of MHPG to duration of illness, and a strong negative association of 5‐HIAA to MSSS rather than to EDSS. The strong negative correlation of MSSS to CSF 5‐HIAA levels in RRMS group of patients indicates that deficits in central serotonergic activity are related to the rate of disability accumulation in RRMS, and could be linked to the reported reduction of disease activity by serotonergic drugs.
Role of oxidative stress and caspase 3 in CD47‐mediated neuronal cell death
Authors: Xing Changhong , Lee Sunryung , Kim Woo Jean , Jin Guang , Yang Yong‐Guang , Ji Xunming , Wang Xiaoying , Lo Eng H. 
Published: November 2008

AbstractCD47 or integrin‐associated protein promotes cell death in blood and tumor cells. Recently, CD47 signaling has been identified in neurons as well. In this study, we investigated the role of CD47 in neuronal cell death. Exposure of primary mouse cortical neurons to the CD47 ligand thrombospondin‐1 or the specific CD47‐activating peptide 4N1K induced cell death. Activation of CD47 elevated levels of active caspase 3 and increased the generation of reactive oxygen species (ROS) in a time‐dependent manner. Both ROS scavengers and caspase inhibitors attenuated cell death. But ROS scavenging did not reduce the activation of caspase 3, and combination treatments with a caspase inhibitor plus free radical scavenger did not yield additive protection. Taken together, these data suggest that parallel and redundant pathways of oxidative stress and caspase‐mediated cell death are involved. We conclude that CD47 mediates neuronal cell death through caspase‐dependent and caspase‐independent pathways.
Glutamate and nitric oxide modulate ERK and CREB phosphorylation in the avian retina: evidence for direct signaling from neurons to Müller glial cells
Authors: Socodato Renato Esteves da Silva , Magalhães Cristiane Rosa , Paes‐de‐Carvalho Roberto 
Published: November 2008

AbstractGlutamate signaling in the mature retinal tissue is very important for accurate sensory decoding by retinal neurons and orchestrates the fine‐tuned output from the retina to higher‐order centers at the cerebral cortex. In this study, we show that glutamate induces a rapid extracellular‐regulated kinase and cAMP‐responsive element binding protein (CREB) phosphorylation in cultured developing retinal neurons. This process is reliant on α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate receptors and nitric oxide (NO) signaling and independent of NMDA receptors activation, as it is blocked by α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate/kainate antagonists as well as inhibiting NO synthase with NG‐nitro‐l‐arginine methyl ester but not by the NMDA channel blocker dizocilpine maleate. The effect of NO on extracellular‐regulated kinase and CREB is mediated by the classical NO/soluble guanylyl cyclase/protein kinase G pathways as it is inhibited by the soluble guanylyl cyclase blocker 1H‐[1,2,4]oxadiazole[4,3‐a]quinoxalin‐1‐one and the protein kinase G inhibitor KT5823, respectively. Immunocytochemical data suggest that increased CREB phosphorylation in response to glutamate occurs in glial cell nuclei. We also have supporting evidence suggesting that neuronally produced NO directly reaches the glial cells and stimulates CREB phosphorylation. Hence, the results indicate the importance of neuronal–glial communication and glutamate/NO/CREB linkage during retinal development.
International rivers and national security: The Euphrates, Ganges–Brahmaputra, Indus, Tigris, and Yarmouk rivers1
Authors: Zawahri Neda A. 
Published: November 2008

AbstractTo understand a state's incentives to invest in conflict or cooperation over their international rivers, this paper argues that it is necessary to appreciate the relationships a river can create and the national security threat riparians may confront. Rivers impose interdependent and vulnerable relationships, which can compromise a state's ability to respond effectively to floods and droughts, meet its domestic food and energy needs, dredge the river, maintain its drainage systems, and allocate its domestic water budget. The inability to accomplish these tasks can contribute to social, economic, and political losses that may threaten a state's territorial integrity. Regardless of whether a state is upstream or downstream, from these relationships it acquires leverage to manipulate the interdependence and vulnerability to inflict losses on its riparian neighbour. This argument challenges several assumptions within the existing literature, including the belief that a shortage of freshwater is the initial force producing a national security threat and that an upstream–downstream river bequeaths all advantages on the upstream state and leaves the downstream state purely dependent. As the paper shows, riparians confront a more complex relationship than captured by the existing literature.
Urokinase Immobilized on Medical Polymeric Materials: Fundamental and Clinical Studies
Authors: Ohshiro Takeshi , Kosaki Goro 
Published: November 2008

ABSTRACTOne of the methods of preparing an antithrombogenic material is to immobilize a fibrinolytic enzyme on the surface of a carrier. The clinical trial of such a material must be subject to not only a basic study on the quality of a carrier, the technique of immobilization, and the method of disinfection, but also an in vivo study on its antithrombotic effect.Reported herein is the evaluation of the fibrinolytic ability, at fundamental and clinical levels, of the urokinase that was immobilized on the surface of various polymeric materials. The results were favorable.