bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monetary and Financial Integration in the EMU: Push or Pull?
Authors: Spiegel Mark M. 
Published: August 2009

AbstractThis paper examines the channels through which monetary union increased financial integration, using panel data on bilateral international commercial bank claims from 1998–2006. I decompose the increase in claims into three channels: a “borrower effect,” as a country's EMU membership may leave its borrowers more creditworthy in the eyes of foreign lenders; a “creditor effect,” as membership in a monetary union may increase the attractiveness of a nation's commercial banks as intermediaries, perhaps through increased scale economies or through an improved regulatory environment after the advent of monetary union; and a “pairwise effect,” as joint membership in a monetary union increases the quality of intermediation between borrowers and creditors when both are in the union. Isolating these three channels through a series of difference‐in‐differences specifications, I find that the pairwise effect is the primary source of increased financial integration. This result is robust to a number of sensitivity exercises.
Sterilization, Monetary Policy, and Global Financial Integration
Authors: Aizenman Joshua , Glick Reuven 
Published: August 2009

AbstractThis paper investigates the changing pattern and efficacy of sterilization within emerging market countries as they liberalize markets and integrate with the world economy. We estimate the marginal propensity to sterilize foreign asset accumulation associated with net balance of payments inflows, across countries, and over time. We find that the extent of sterilization of foreign reserve inflows has risen in recent years to varying degrees in Asia as well as in Latin America, consistent with greater concerns about the potential inflationary impact of reserve inflows. We also find that sterilization depends on the composition of balance of payments inflows.
Abacavir and risk of myocardial infarction in HIV‐infected patients on highly active antiretroviral therapy: a population‐based nationwide cohort study
Authors: Obel N , Farkas DK , Kronborg G , Larsen CS , Pedersen G , Riis A , Pedersen C , Gerstoft J , Sørensen HT 
Published: August 2009

ObjectiveThe aim of the study was to examine whether exposure to abacavir increases the risk for myocardial infarction (MI).Design, setting and subjectsThis was a prospective nationwide cohort study which included all Danish HIV‐infected patients on highly active antiretroviral therapy (HAART) from 1995 to 2005 (N=2952). Data on hospitalization for MI and comorbidity were obtained from Danish medical databases. Hospitalization rates for MI after HAART initiation were calculated for patients who used abacavir and those who did not. We used Cox's regression to compute incidence rate ratios (IRR) as a measure of relative risk for MI, while controlling for potential confounders (as separate variables and via propensity score) including comorbidity.Main outcomeRelative risk of hospitalization with MI in abacavir users compared with abacavir nonusers.ResultsHospitalization rates for MI were 2.4/1000 person‐years (PYR) [95% confidence interval (CI) 1.7–3.4] for abacavir nonusers and 5.7/1000 PYR (95% CI 4.1–7.9) for abacavir users. The risk of MI increased after initiation of abacavir [unadjusted IRR=2.22 (95% CI 1.31–3.76); IRR adjusted for confounders=2.00 (95% CI 1.10–3.64); IRR adjusted for propensity score=2.00 (95% CI 1.07–3.76)]. This effect was also observed among patients initiating abacavir within 2 years after the start of HAART and among patients who started abacavir as part of a triple nucleoside reverse transcriptase inhibitor (NRTI) regimen.ConclusionsWe confirmed the association between abacavir use and increased risk of MI. Further studies are needed to control for potential confounding not measured in research to date.
A 12‐month longitudinal study of calcium metabolism and bone turnover during valproate monotherapy
Authors: Verrotti A. , Agostinelli S. , Coppola G. , Parisi P. , Chiarelli F. 
Published: August 2009

Background and purpose: Treatment with valproate (VPA) can cause changes in bone mineral metabolism, but the real influences and the underlying pathologic mechanisms are still unclear and under discussion. The aim of this study was to examine the changes on calcium metabolism and bone turnover in post‐pubertal male patients with newly diagnosed idiopathic generalized epilepsy (IGE) before (baseline evaluation) and 12 months after VPA monotherapy (second evaluation).Methods: Participants included 20 post‐pubertal males with IGE, aged 16.5–22.1 years. Also 20 post‐pubertal sex‐ and age‐matched healthy controls were evaluated. Physical activity, calcium and vitamin D intake were determined. Laboratory samples were obtained to measure biochemical parameters of bone metabolism and bone turnover: serum calcium, phosphate, magnesium, 25‐hydroxyvitamin D, 1,25‐dihydroxyvitamin D, intact parathyroid hormone, total alkaline phosphatase, bone alkaline phosphatase (bone‐ALP), osteocalcin (OC), carboxy‐terminal propeptide of type I procollagen (PICP) and carboxy‐terminal telopeptide of type I collagen (ICTP).Results: At baseline evaluation, there were no significant differences between controls and patients parameters. At second evaluation, patients showed both markers of bone formation and resorption significantly higher than baseline values (bone‐ALP: 51.2 ± 9.9 vs. 57.3 ± 9.3 U/l,P < 0.01; OC: 8.1 ± 1.1 vs. 10.4 ± 1.5 μg/l,P < 0.01; PICP: 138.7 ± 16.4 vs. 152.6 ± 17.1 μg/l,P < 0.01; ICTP: 3.8 ± 0.8 vs. 5.9 ± 0.6 μg/l,P < 0.01).Conclusions: Valproate monotherapy in epileptic post‐pubertal males causes a significant increase of bone turnover.
Cytoprotective effect of polypeptide from Chlamys farreri on neuroblastoma (SH‐SY5Y) cells following H2O2 exposure involves scavenging ROS and inhibition JNK phosphorylation
Authors: Ye Junli , Han Yantao , Wang Chunbo , Yu Wengong 
Published: August 2009

AbstractOxidative stress has long been linked to cell death in many neurodegenerative conditions. Treatment with antioxidants is a promising approach for slowing disease progression. In this study, we used the neuroblastoma SH‐SY5Y cells as an in vitro model to first assess the effect of polypeptide from Chlamys farreri (PCF), a natural marine antioxidant, on H2O2‐induced neuronal cell death. Pre‐treatment of SH‐SY5Y cells with PCF inhibited H2O2‐induced cell death in a concentration‐dependent manner. In parallel, intracellular reactive oxygen species generation and lipid peroxidation were inhibited by PCF. Under severe H2O2 insult, PCF promoted endogenous antioxidant defense components including glutathione peroxidase, catalase, superoxide dismutase, and glutathione. PCF also protected DNA from oxidative damage and enhanced the removal of 8‐oxo‐7,8‐dihydro‐2′‐deoxyguanosine from DNA. Further, we found that PCF potentially prevented H2O2–induced cell apoptosis. When investigated mitogen‐activated protein kinase signaling pathway, we found that pre‐treatment of cells with PCF significantly blocked H2O2–induced phosphorylation of c‐Jun N‐terminal kinase of the mitogen‐activated protein kinase family. However, PCF had little inhibitory effect on the H2O2–induced activation of extracellular signal‐regulated kinase. Taken together, these data demonstrate that PCF prevents oxidative stress‐induced reactive oxygen species production and c‐Jun N‐terminal kinase activation and may be useful in the treatment of neurodegenerative diseases.
Penelope’s web: using α‐latrotoxin to untangle the mysteries of exocytosis
Authors: Silva John‐Paul , Suckling Jason , Ushkaryov Yuri 
Published: August 2009

AbstractFor more than three decades, the venom of the black widow spider and its principal active components, latrotoxins, have been used to induce release of neurotransmitters and hormones and to study the mechanisms of exocytosis. Given the complex nature of α‐latrotoxin (α‐LTX) actions, this research has been continuously overshadowed by many enigmas, misconceptions and perpetual changes of the underlying hypotheses. Some of the toxin’s mechanisms of action are still not completely understood. Despite all these difficulties, the extensive work of several generations of neurobiologists has brought about a great deal of fascinating insights into pre‐synaptic processes and has led to the discovery of several novel proteins and synaptic systems. For example, α‐LTX studies have contributed to the widespread acceptance of the vesicular theory of transmitter release. Pre‐synaptic receptors for α‐LTX – neurexins, latrophilins and protein tyrosine phosphatase σ– and their endogenous ligands have now become centrepieces of their own areas of research, with a potential of uncovering new mechanisms of synapse formation and regulation that may have medical implications. However, any future success of α‐LTX research will require a better understanding of this unusual natural tool and a more precise dissection of its multiple mechanisms.
The neurokinin‐1 receptor modulates the methamphetamine‐induced striatal apoptosis and nitric oxide formation in mice
Authors: Zhu Judy , Xu Wenjing , Wang Jing , Ali Syed F. , Angulo Jesus A. 
Published: August 2009

AbstractIn a previous study we showed that pharmacological blockade of the neurokinin‐1 receptors attenuated the methamphetamine (METH)‐induced toxicity of the striatal dopamine terminals. In the present study we examined the role of the neurokinin‐1 receptors on the METH‐induced apoptosis of some striatal neurons. To that end, we administered a single injection of METH (30 mg/kg, i.p.) to male mice. METH induced the apoptosis (terminal deoxyncleotidyl transferase‐mediated dUTP nick end labeling) of approximately 20% of striatal neurons. This percentage of METH‐induced apoptosis was significantly attenuated by either a single injection of the neurokinin‐1 receptor antagonist, 17‐β‐hydroxy‐17‐a‐ethynyl‐5‐a‐androstano[3,2‐β]pyrimido[1,2‐a]benzimidazole (WIN‐51,708) (5 mg/kg, i.p.), or the ablation of the striatal interneurons expressing the neurokinin‐1 receptors (cholinergic and somatostatin) with the selective neurotoxin [Sar9,Met(O2)11] substance P–saporin. Next we assessed the levels of striatal 3‐nitrotyrosine (3‐NT) by HPLC and immunohistochemistry. METH increased the levels of striatal 3‐NT and this increase was attenuated by pre‐treatment with WIN‐51,708. Our data support the hypothesis that METH‐induced striatal apoptosis occurs via a mechanism involving the neurokinin‐1 receptors and the activation of nitric oxide synthesis. Our findings are relevant for the treatment of METH abuse and may be relevant to certain neurological disorders involving the dopaminergic circuitry of the basal ganglia.
The blood–brain barrier transport and cerebral distribution of guanidinoacetate in rats: involvement of creatine and taurine transporters
Authors: Tachikawa Masanori , Kasai Yasuyuki , Yokoyama Reiji , Fujinawa Jun , Ganapathy Vadivel , Terasaki Tetsuya , Hosoya Ken‐ichi 
Published: August 2009

AbstractAlthough the cerebral accumulation of guanidinoacetate (GAA) contributes to neurological complications inS‐adenosylmethionine:guanidinoacetateN‐methyltransferase (GAMT) deficiency, how GAA is abnormally distributed in the brain remains unknown. The purpose of this study was to investigate the transport of GAA across the blood–brain barrier (BBB) and in brain parenchymal cells in rats. [14C]GAA microinjected into the rat cerebrum was not eliminated from the brain, implying the negligible contribution of GAA efflux transport across the BBB. In contrast,in vivoanalysis and an uptake study by TR‐BBB cells, a ratin vitroBBB model, revealed that GAA was transported from the circulating blood across the BBB most likely via a creatine transporter (CRT). Although CRT at the BBB is almost saturated by endogenous creatine under physiological conditions, the creatine level in the blood significantly decreases in GAMT deficiency. This might lead to the increase of CRT‐mediated blood‐to‐brain transport of GAA at the BBB. Furthermore, [14C]GAA was taken up by brain parenchymal cells in a concentrative manner most likely via taurine transporter and CRT. These characteristics of GAA transport across the BBB and in the brain parenchymal cells could be the key factors that facilitate GAA accumulation in the brains of patients with GAMT deficiency.
Astrocytes are poised for lactate trafficking and release from activated brain and for supply of glucose to neurons
Authors: Gandhi Gautam K. , Cruz Nancy F. , Ball Kelly K. , Dienel Gerald A. 
Published: August 2009

AbstractBrain is a highly‐oxidative organ, but during activation, glycolytic flux is preferentially up‐regulated even though oxygen supply is adequate. The biochemical and cellular basis of metabolic changes during brain activation and the fate of lactate produced within brain are important, unresolved issues central to understanding brain function, brain images, and spectroscopic data. Because in vivo brain imaging studies reveal rapid efflux of labeled glucose metabolites during activation, lactate trafficking among astrocytes and between astrocytes and neurons was examined after devising specific, real‐time, sensitive enzymatic fluorescent assays to measure lactate and glucose levels in single cells in adult rat brain slices. Astrocytes have a 2‐ to 4‐fold faster and higher capacity for lactate uptake from extracellular fluid and for lactate dispersal via the astrocytic syncytium compared to neuronal lactate uptake from extracellular fluid or shuttling of lactate to neurons from neighboring astrocytes. Astrocytes can also supply glucose to neurons as well as glucose can be taken up by neurons from extracellular fluid. Astrocytic networks can provide neuronal fuel and quickly remove lactate from activated glycolytic domains, and the lactate can be dispersed widely throughout the syncytium to endfeet along the vasculature for release to blood or other brain regions via perivascular fluid flow.
Effect of soybean administration on the pharmacokinetics of carbamazepine and omeprazole in rats
Authors: Singh Dharmender , Asad Mohammed 
Published: August 2009

AbstractInfluence of soybean administration on the bioavailability of carbamazepine and omeprazole was studied after single dose administration of soybean (10 g/kg p.o.) or after chronic administration of soybean (50% w/w mixed with normal feed) for 15 days in rats. Carbamazepine was administered orally at a dose of 10 mg/kg and omeprazole at a dose of 20 mg/kg. Soybean decreased the bioavailability of carbamazepine after both single dose and chronic administration. It produced a significant decrease in Cmax, Tmax, AUC0–t of carbamazepine after single dose administration and increased the plasma clearance and Vd along with decrease in Cmax, Tmax, AUC0–t and AUC0–∞ after chronic administration. On the contrary, soybean administration increased the bioavailability of omeprazole by producing an increase in Cmax, AUC0–t and AUC0–∞ and a decrease in Vd after single dose administration and a decrease in plasma clearance along with increase in Cmax, AUC0–t and AUC0–∞ after chronic administration. The half‐life of omeprazole was also increased after both acute and chronic administration of soybean. It was concluded that soybean decreases the bioavailability of carbamazepine and increases the bioavailability of omeprazole after both single dose and chronic administration.
Vasorelaxant effects of the monoterpenic phenol isomers, carvacrol and thymol, on rat isolated aorta
Authors: Peixoto‐Neves D. , Silva‐Alves K.S. , Gomes M.D.M. , Lima F.C. , Lahlou S. , Magalhães P.J.C. , Ceccatto V.M. , Coelho‐de‐Souza A.N. , Leal‐Cardoso J.H. 
Published: August 2009

AbstractVarious essential oils are rich in carvacrol, a monoterpenic phenol isomeric with thymol. This study was undertaken to assess the vasorelaxant effects of thymol and carvacrol in rat isolated aorta and the putative mechanisms underlying these effects. Thymol and carvacrol produced a concentration‐dependent relaxation on the aortic ring preparations pre‐contracted using KCl (IC50value of 64.40 ± 4.41 and 78.80 ± 11.91 μm, respectively) or using phenylephrine (PHE, 0.1 μm) (IC50value of 106.40 ± 11.37 and 145.40 ± 6.07 μm, respectively) and inhibited the concentration‐response curves of aortic rings to PHE or KCl. In Ca2+‐free medium with ethylene glycol‐bis(2‐aminoethylether)‐N,N,N′,N′‐tetraacetic acid (2 mm), thymol and carvacrol both at 1000 μmcompletely abolished the phasic component of PHE‐induced endothelium‐containing ring contractions. At 400 μm, thymol and carvacrol significantly reduced the CaCl2‐induced contractions in Ca2+‐free medium. Furthermore, both thymol and carvacrol (300 and 1000 μm) significantly reduced the contraction evoked by phorbol dibutyrate (1 μm), an activator of protein kinase C. Magnitude of this inhibitory effect was enhanced in the presence of the Ca2+pump inhibitor, thapsigargin (1 μm). At 1000 μm, neither thymol nor carvacrol altered the resting potential of vascular smooth muscle cells. In conclusion, thymol and carvacrol induced an endothelium‐independent relaxation in rat isolated aorta, an effect that seems mediated through some mechanisms probably involving a transduction pathway between Ca2+release from sarcoplasmic reticulum and/or regulation of the Ca2+sensitivity of the contractile system. Moreover, it’s conceivable that thymol and carvacrol, at low concentrations, block the Ca2+influx through the membrane.
Inhibition of the JNK signalling pathway enhances proteasome inhibitor‐induced apoptosis of kidney cancer cells by suppression of BAG3 expression
Authors: Wang Hua‐Qin , Liu Bao‐Qin , Gao Yan‐Yan , Meng Xin , Guan Yifu , Zhang Hai‐Yan , Du Zhen‐Xian 
Published: August 2009

Background and purpose:  Proteasome inhibitors represent a novel class of anti‐tumour agents that have clinical efficacy against haematological and solid cancers. The anti‐apoptotic protein BAG3 is a member of the Bcl‐2‐associated athanogene family. We have previously shown that BAG3 is up‐regulated after exposure to proteasome inhibitors and that inhibition of BAG3 sensitized cells to apoptosis induced by proteasome inhibition. However, the mechanisms by which proteasome inhibition induced BAG3 expression remained unclear and the present experiments were designed to elucidate these mechanisms.Experimental approach:  Effects of the proteasome inhibitor MG132 on activation of mitogenic signalling pathways were evaluated in kidney cancer cells (A498, Caki1, Caki2), with Western blotting. Specific inhibitors against individual mitogenic signalling pathways, real‐time reverse transcription‐polymerase chain reaction and luciferase reporter assays were used to investigate the roles of mitogenic signalling pathways in BAG3 induction after proteasome inhibition. Cell death was evaluated using Annexin V/propidium iodide staining and subsequent FACS.Key results:  MG132 activated several key mitogenic signalling pathways including extracellular signal‐regulated kinase (ERK), c‐Jun N‐terminal kinase (JNK) and p38 mitogen‐activated protein kinase (MAPK) activities. Induction of BAG3 by MG132 was inhibited by blocking JNK, but not ERK1/2 and p38 MAPK signalling pathways. In addition, SP600125 and dominant‐negative JNK1 suppressed BAG3 promoter‐driven reporter gene expression. Furthermore, activation of the JNK pathway induced BAG in kidney cancer cells after treatment with MG132.Conclusions and implications:  Our results suggested that the JNK pathway was associated with the protective response against proteasome inhibition, by mediating induction of BAG3.
The Epidemiology of Dependence in Older People in Nigeria: Prevalence, Determinants, Informal Care, and Health Service Utilization. A 10/66 Dementia Research Group Cross‐Sectional Survey
Authors: Uwakwe Richard , Ibeh Christian C. , Modebe Anne Ifeoma , Bo Emeka , Ezeama Nkiru , Njelita Ifeoma , Ferri Cleusa P. , Prince Martin J. 
Published: August 2009

OBJECTIVES: To describe the prevalence and determinants of dependence in older Nigerians and associations with informal care and health service utilization.DESIGN: A single‐phase cross‐sectional catchment area survey.SETTING: Dunukofia, a rural community in southeastern Nigeria.PARTICIPANTS: One thousand two hundred thirty‐eight adults aged 65 and older, for whom full data were available on 914.MEASUREMENTS: The full 10/66 Dementia Research Group survey protocol was applied, including ascertainment of depression, cognitive impairment, physical impairments, and self‐reported diagnoses. The interviewer rated dependence as not needing care, needing some care, or needing much care. The prevalence of dependence and the independent contribution of underlying health conditions were estimated. Sources of income, care arrangements, caregiver strain, and health service use are described according to level of dependence.RESULTS: The prevalence of dependence was 24.3% (95% confidence interval=22.1–26.5%), with a concentration in participants aged 80 and older. Only 1% of participants received a pension, and fewer than 7% had paid work. Those who were dependent were less likely than others to receive income from their family. Cognitive impairment, physical impairments, stroke, and depression were each independently associated with dependence. Depression made the largest contribution. Dependence was strongly associated with health service use (particularly private doctor and traditional healer services) and with high levels of out‐of‐pocket expenditure.CONCLUSION: In Nigeria, dependence is an important outcome given rapid demographic aging and increases in chronic disease prevalence in all developing regions. Enhancing the social protection of dependent older adults should be a policy priority. Cognitive and mental disorders are important contributors to disability and dependence; more attention should be given to their prevention, detection, and treatment.
Anemia and 9‐Year Domain‐Specific Cognitive Decline in Community‐Dwelling Older Women: The Women's Health and Aging Study II
Authors: Deal Jennifer A. , Carlson Michelle C. , Xue Qian‐Li , Fried Linda P. , Chaves Paulo H. M. 
Published: August 2009

OBJECTIVES: To test the hypothesis that anemia (hemoglobin <12 g/dL) is associated with a faster rate of cognitive decline over 9 years in a community‐dwelling sample of women aged 70 to 80 at baseline.DESIGN: A population‐based, prospective cohort study.SETTING: East Baltimore, Maryland.PARTICIPANTS: Four hundred thirty‐six women sampled to be representative of the two‐thirds least‐disabled women aged 70 to 80 at baseline (1994–1996).MEASUREMENTS: Nine‐year trajectories of cognitive decline, analyzed using linear random effects models, in the domains of immediate verbal recall, delayed verbal recall, psychomotor speed, and executive function.RESULTS: At baseline and after adjustment for demographic and disease covariates, women with anemia were slower to complete a test of executive function; the difference in baseline function between women with anemia and those without was −0.43 standard deviations (SDs) (95% confidence interval (CI)=−0.74 to −0.13) on the Trail Making Test Part B. During follow‐up, anemia was associated with a faster rate of decline in memory. Between baseline and Year 3, the difference in the rates of decline between women with anemia and those without was −0.18 SDs per year (95% CI=−0.29 to −0.06) on the Hopkins Verbal Learning Test (HVLT) and −0.15 SDs per year (95% CI=−0.26 to −0.04) on the HVLT‐Delayed.CONCLUSION: Anemia was associated with poorer baseline performance on a test of executive function and with faster rates of decline on tests of immediate and delayed verbal recall. If this relationship is causal, it is possible that treatment of anemia could prevent or postpone cognitive decline.