bluuebunny/crossref_metadata_2025_split huggingface dataset:
DEGREE, ITERATION AND PERMUTATION IN IMPROVING BONFERRONI‐TYPE BOUNDS
Authors: Seneta E. 
Published: February 2008

summaryThis note has as its starting points: 1) the upper bound of Worsley (1982) for the probability of union of n events: 2) the iterative procedure of Hoppe (1985) for deriving successive upper and lower Bonferroni‐type bounds, in alternation, for the probability of such a union. We first show that Worsley's bound (and hence successive bounds based on it) can be sharpened by an initial application of 2) to an appropriate lower bound due to Boole (1854). Subsequently, we show that if the n events are exchangeable, the sequence of bounds obtained from this starting point is that due to Sobel and Uppuluri (1972). The role of degree of a bound is explored, as well as sharpening of bounds by permutation when events are not necessarily exchangeable.
BAYESIAN ANALYSIS OF THE LINEAR REGRESSION MODEL WITH NON‐NORMAL DISTURBANCES
Authors: Chaturvedi Anoop , Hasegawa Hikaru , Asthana Sheel 
Published: February 2008

SummaryThis paper considers the Bayesian analysis of a linear regression model with identically independently distributed non‐normal disturbances. The distribution of disturbances is approximated by an Edgeworth series distribution with cumulants, of order higher than fourth, negligible. The posterior distribution of the regression coefficients vector is obtained under the assumption of a g‐prior distribution for the parameters of the model. The Bayes estimator and its Bayes risk of the estimator are derived under a quadratic loss structure.
RIGHTS, INDIRECT HARMS AND THE NON‐IDENTITY PROBLEM
Authors: MCBRAYER JUSTIN PATRICK 
Published: February 2008

ABSTRACTThe non‐identity problem is the problem of grounding moral wrongdoing in cases in which an action affects who will exist in the future. Consider a woman who intentionally conceives while on medication that is harmful for a fetus. If the resulting child is disabled as a result of the medication, what makes the woman's action morally wrong? I argue that an explanation in terms of harmful rights violations fails, and I focus on Peter Markie's recent rights‐based defense. Markie's analysis rests on the notion of an indirect harm, and I show that the calculation of an indirect harm relies on an improper baseline for the determination of whether or not an action adversely affects a patient's interests. I also defend an impersonal duty‐based analysis of the wrongdoing in non‐identity cases against an objection by Markie. I close by arguing that the rights‐based analysis is insensitive to context and that context is morally relevant in the determination of the moral valence of actions in cases of non‐identity. This failure provides a pro tanto reason to favor an impersonal duty‐based analysis of the wrongdoing in non‐identity cases.
MORAL QUALMS, FUTURE PERSONS, AND EMBRYO RESEARCH
Authors: SHAW DAVID MARTIN 
Published: February 2008

ABSTRACTMany people have moral qualms about embryo research, feeling that embryos must deserve some kind of protection, if not so much as is afforded to persons. This paper will show that these qualms serve to camouflage motives that are really prudential, at the cost of also obscuring the real ethical issues at play in the debate concerning embryo research and therapeutic cloning. This in turn leads to fallacious use of the Actions/Omissions Distinction and ultimately neglects the duties that we have towards future persons.
Inflation and Unemployment in General Equilibrium*
Authors: Rocheteau Guillaume , Rupert Peter , Wright Randall 
Published: February 2008

AbstractWhen labor is indivisible, there exist efficient outcomes with some agents randomly unemployed, as in Rogerson (1988). We integrate this idea into the modern theory of monetary exchange, where some trade occurs in centralized markets and some in decentralized markets, as in Lagos and Wright (2005). This delivers a general equilibrium model of unemployment and money, with explicit microeconomic foundations. We show that the implied relation between inflation and unemployment can be positive or negative, depending on simple preference conditions. Our Phillips curve provides a long‐run, exploitable, trade‐off for monetary policy; it turns out, however, that the optimal policy is the Friedman rule.
Heterogeneity, Job Creation and Unemployment Volatility
Authors: Guerrieri Veronica 
Published: February 2008

AbstractIn this paper, I explore the impact of match‐specific heterogeneity at the job creation margin on business cycle fluctuations. I show that this form of heterogeneity alone does not help to amplify labor market volatility, either under full or under asymmetric information. First, I show analytically that, under full information, heterogeneity has no first‐order effect on the response of unemployment and job creation to productivity, and actually tends to dampen the response of market tightness. Then, in a series of calibrations, I show that with both full and asymmetric information, the model delivers labor market volatilities close to the representative‐agent, full‐information benchmark.
Testing and the Composition of the Labor Pool
Authors: Boone Johnathan , Watson Joel 
Published: February 2008

AbstractWe consider a continuous‐time labor matching model with endogenous separation. Firms initially lack information about the quality of workers with whom they are matched. They acquire information both from pre‐employment testing and, in the case in which a labor relationship is established, on‐the‐job performance. Testing provides a signal of a worker's quality. A firm can pick the accuracy level of its test, but it pays a cost that increases in the accuracy. Workers who perform poorly on the test are not offered employment; those who perform poorly on the job are eventually fired (after some delay). Worker quality is not match‐specific; low‐quality workers are less productive with all firms. We show that, in equilibrium, there is an inverse and complementary relation between the level of testing that firms optimally perform and the overall quality of the workers in the matching pool. We consider the properties of a steady‐state, stable equilibrium in such an environment. The complementarity between testing and the composition of the unemployed pool introduces the possibility of multiple equilibria.
PROFIT, SURPLUS PRODUCT, EXPLOITATION AND LESS THAN MAXIMIZED UTILITY: A NEW EQUIVALENCE PROPOSITION ON THE FUNDAMENTAL MARXIAN THEOREM
Authors: Matsuo Tadasu 
Published: February 2008

ABSTRACTMorishima's Generalized Fundamental Marxian Theorem (GFMT) is an extended form of Okishio's Fundamental Marxian Theorem, which showed the equivalence between positive profit and the exploitation of labor. GFMT is not developed as a system of equivalence proposition between five conditions, which I call ‘The Strong System of Exploitation Theory’. But by the definition of this system, there remains the possibility of positive profit without exploitation. In this paper, I demonstrated an alternative system of equivalence proposition, naming it ‘The Weak System of Exploitation Theory’, in which positive profits always mean exploitation. Here I introduced workers' utility function to define the exploitation concept. Then I could also show that the exploitation is equivalent with the situation where workers' utilities are under‐maximized.
THEORETICAL FOUNDATIONS OF PAY‐AS‐YOU‐GO DEFINED‐CONTRIBUTION PENSION SCHEMES
Authors: Gronchi Sandro , Nisticò Sergio 
Published: February 2008

ABSTRACTThe paper inquires into notional defined contribution pension schemes, which retain the pay‐as‐you‐go financing method while adopting the award and indexation formulas typical of funded, defined‐contribution systems. It examines the properties of the new arrangement and compares them with those of the traditional defined‐benefit pay‐as‐you‐go schemes.
MICRO EMPIRICAL RESULTS OF A KALECKIAN‐TYPE CAPITAL ACCUMULATION MODEL COMPARED WITH MACRO RESULTS FOR SOME EUROPEAN ECONOMIES
Authors: Gander James P. 
Published: February 2008

ABSTRACTA micro economic model of the rate of capital accumulation that corresponds to a macro Kaleckian‐type post‐Keynesian investment function is hypothesized. Firm‐level accounting data on industrial and commercial firms over the time period 1994–2000 for three European economies and the USA are used to test the consistency of the micro model with the macro model of Hein and Ochsen (2003, Metroeconomica, 54, pp. 404–33). The micro empirical results were very consistent with the macro results, suggesting a strong micro foundation to the macro investment function. In addition country differences and industry differences were included in the analysis.
A Bootstrap Method for Identifying and Evaluating a Structural Vector Autoregression*
Authors: Demiralp Selva , Hoover Kevin D. , Perez Stephen J. 
Published: February 2008

AbstractGraph‐theoretic methods of causal search based on the ideas of Pearl (2000), Spirtes et al. (2000), and others have been applied by a number of researchers to economic data, particularly by Swanson and Granger (1997) to the problem of finding a data‐based contemporaneous causal order for the structural vector autoregression, rather than, as is typically done, assuming a weakly justified Choleski order. Demiralp and Hoover (2003) provided Monte Carlo evidence that such methods were effective, provided that signal strengths were sufficiently high. Unfortunately, in applications to actual data, such Monte Carlo simulations are of limited value, as the causal structure of the true data‐generating process is necessarily unknown. In this paper, we present a bootstrap procedure that can be applied to actual data (i.e. without knowledge of the true causal structure). We show with an applied example and a simulation study that the procedure is an effective tool for assessing our confidence in causal orders identified by graph‐theoretic search algorithms.
Informationist programme in support of biomedical research: a programme description and preliminary findings of an evaluation
Authors: Whitmore Susan C. , Grefsheim Suzanne F. , Rankin Jocelyn A. 
Published: February 2008

AbstractBackground:  The informationist programme at the Library of the National Institutes of Health (NIH) in Bethesda, MD, USA has grown to 14 informationists working with 40 clinical and basic science research teams.Purpose:  This case report, intended to contribute to the literature on informationist programmes, describes the NIH informationist programme, including implementation experiences, the informationists’ training programme, their job responsibilities and programme outcomes.Brief description:  The NIH informationist programme was designed to enhance the library's service capacity. Over time, the steps for introducing the service to new groups were formalized to ensure support by leadership, the team being served and the library. Job responsibilities also evolved from traditional library roles to a wide range of knowledge management activities. The commitment by the informationist, the team and the library to continuous learning is critical to the programme's success.Results / outcomes:  NIH scientists reported that informationists saved them time and contributed to teamwork with expert searching and point‐of‐need instruction. Process evaluation helped refine the programme.Evaluation method:  High‐level, preliminary outcomes were identified from a survey of scientists receiving informationist services, along with key informant interviews. Process evaluation examined service implementation, informationists’ training and service components. Anecdotal evidence has also indicated a favourable response to the programme.
Characterization of folate uptake by choroid plexus epithelial cells in a rat primary culture model
Authors: Wollack Jan B. , Makori Benedette , Ahlawat Stuti , Koneru Rajeth , Picinich Sonia C. , Smith Angela , Goldman I. David , Qiu Andong , Cole Peter D. , Glod John , Kamen Barton 
Published: February 2008

J. Neurochem. (2008) 104, 1494–1503.AbstractReduced derivatives of folic acid (folates) play a critical role in the development, function and repair of the CNS. However, the molecular systems regulating folate uptake and homeostasis in the central nervous system remain incompletely defined. Choroid plexus epithelial cells express high levels of folate receptor α (FRα) suggesting that the choroid plays an important role in CNS folate trafficking and maintenance of CSF folate levels. We have characterized 5‐methyltetrahydrofolate (5‐MTHF) uptake and metabolism by primary rat choroid plexus epithelial cells in vitro. Two distinct processes are apparent; one that is FRα dependent and one that is independent of the receptor. FRα binds 5‐MTHF with high affinity and facilitates efficient uptake of 5‐MTHF at low extracellular folate concentrations; a lower affinity FRα independent system accounts for increased folate uptake at higher concentrations. Cellular metabolism of 5‐MTHF depends on the route of folate entry into the cell. 5‐MTHF taken up via a non‐FRα ‐mediated process is rapidly metabolized to folylpolyglutamates, whereas 5‐MTHF that accumulates via FRα remains non‐metabolized, supporting the hypothesis that FRα may be part of a pathway for transcellular movement of the vitamin. The proton‐coupled folate transporter, proton‐coupled folate transporter (PCFT), mRNA was also shown to be expressed in choroid plexus epithelial cells. This is consistent with the role we have proposed for proton‐coupled folate transporter in FRα‐mediated transport as the mechanism of export of folates from the endocytic compartment containing FRα.
Altered expression and subcellular distribution of GRK subtypes in the dopamine‐depleted rat basal ganglia is not normalized byl‐DOPA treatment
Authors: Ahmed M. Rafiuddin , Bychkov Evgeny , Gurevich Vsevolod V. , Benovic Jeffrey L. , Gurevich Eugenia V. 
Published: February 2008

J. Neurochem. (2008)104,1622–1636.AbstractDysregulation of dopamine (DA) receptors is believed to underlie Parkinson’s disease pathology andl‐DOPA‐induced motor complications. DA receptors are subject to regulation by G protein‐coupled receptor kinases (GRKs) and arrestins. DA lesion with 6‐hydroxydopamine caused multiple protein‐ and brain region‐specific changes in the expression of GRKs. In the globus pallidus, all four GRK isoforms (GRK2, 3, 5, 6) were reduced in the lesioned hemisphere. In the caudal caudate‐putamen (cCPu) three GRK isoforms (GRK2, 3, 6) were decreased by DA depletion. The decrease in GRK proteins in globus pallidus, but not cCPu, was mirrored by reduction in mRNA. GRK3 protein was reduced in the rostral caudate‐putamen (rCPu), whereas other isoforms were either unchanged or up‐regulated. GRK6 protein and mRNA were up‐regulated in rCPu and nucleus accumbens.l‐DOPA (25 mg/kg, twice daily for 10 days) failed to reverse changes caused by DA depletion, whereas D2/D3agonist pergolide (0.25 mg/kg daily for 10 days) restored normal levels of expression of GRK5 and 6. In rCPu, GRK2 protein was increased in most subcellular fractions byl‐DOPA but not by DA depletion alone. Similarly,l‐DOPA up‐regulated arrestin3 in membrane fractions in both regions. GRK5 was down‐regulated byl‐DOPA in cCPu in the light membrane fraction, where this isoform is the most abundant. The data suggest that alterations in the expression and subcellular distribution of arrestins and GRKs contribute to pathophysiology of Parkinson’s disease. Thus, these proteins may be targets for antiparkinsonian therapy.
Curcumin binds to the α‐helical intermediate and to the amyloid form of prion protein – a new mechanism for the inhibition of PrPSc accumulation
Authors: Hafner‐Bratkovič Iva , Gašperšič Jernej , Šmid Lojze M. , Bresjanac Mara , Jerala Roman 
Published: February 2008

J. Neurochem. (2008) 104, 1553–1564.AbstractConversion of the native, predominantly α‐helical conformation of prion protein (PrP) into the β‐stranded conformation is characteristic for the transmissible spongiform encephalopathies such as Creutzfeld–Jakob disease. Curcumin, an extended planar molecule and a dietary polyphenol, inhibits in vitro conversion of PrP and formation of protease resistant PrP in neuroblastoma cell lines. Curcumin recognizes the converted β‐form of the PrP both as oligomers and fibrils but not the native form. Curcumin binds to the prion fibrils in the left‐handed chiral arrangement as determined by circular dichroism. We show that curcumin labels the plaques of the brain sections of variant Creutzfeld–Jakob disease cases and stains the same structures as antibodies against the PrP. In contrast to thioflavin T, curcumin also binds to the α‐helical intermediate of PrP present at acidic pH at stoichiometry of 1 : 1. Congo red competes with curcumin for binding to the α‐intermediate as well as to the β‐form of PrP but is toxic and binds also to the native form of PrP. We therefore show that the partially unfolded structural intermediate of the PrP can be targeted by non‐toxic compound of natural origin.
Differential activation of the calcium/protein kinase C and the canonical β‐catenin pathway by Wnt1 and Wnt7a produces opposite effects on cell proliferation in PC12 cells
Authors: Spinsanti Paola , De Vita Teresa , Caruso Alessandra , Melchiorri Daniela , Misasi Roberta , Caricasole Andrea , Nicoletti Ferdinando 
Published: February 2008

J. Neurochem. (2008) 104, 1588–1598.AbstractWe examined the effect of Wnt1 and Wnt7a on cell proliferation using undifferentiated PC12 cells, which originate from the neural crest and are widely employed as a neuronal cell model. Heterologous expression of Wnt1 enhanced [3H]thymidine incorporation and expression of cyclin D1 and cylin E in PC12 cells. Opposite effects were observed in PC12 cells expressing Wnt7a. Searching for the mechanisms underlying the opposite effects of Wnt1 and Wnt7a on PC12 cell proliferation, we examined the activation of the canonical β‐catenin/T‐cell–lymphoid enhancer‐binding protein transcription factor pathway and the ‘calcium pathway’ by co‐transfecting the cells with a reporter gene controlled by either T‐cell–lymphoid enhancer‐binding protein transcription factor or the calcium‐activated transcription factor, NFAT. Wnt1 and Wnt7a activated both pathways, but to a different extent. While Wnt1 preferentially activated the calcium pathway, Wnt7a mainly activated the canonical pathway. Pharmacological inhibition of protein kinase C, which is a component of the calcium pathway, abrogated the increase in cell proliferation induced by Wnt1 without affecting the antiproliferative action of Wnt7a. The action of Wnt7a was instead occluded by lithium ions, which mimic the activation of the canonical pathway, and was largely reduced by Dickkopf‐1, which acts as an inhibitor of the canonical pathway. In addition, expression of a constitutively active mutant of β‐catenin potently activated the canonical Wnt pathway and reduced [3H]thymidine incorporation. These data challenge the view that the canonical Wnt pathway invariably supports cell growth and suggest that, at least in PC12 cells, cell proliferation is regulated by the balance between the calcium/protein kinase C pathway and the canonical pathway.
Identification of poly‐ADP‐ribosylated mitochondrial proteins after traumatic brain injury
Authors: Lai Yichen , Chen Yaming , Watkins Simon C. , Nathaniel Paula D. , Guo Fengli , Kochanek Patrick M. , Jenkins Larry W. , Szabó Csaba , Clark Robert S. B. 
Published: February 2008

J. Neurochem. (2008) 104, 1700–1711.AbstractPoly‐ADP‐ribosylation is a post‐translational modification performed by poly(ADP‐ribose) polymerases (PARP), involved in many diverse cellular functions including DNA repair, transcription, and long‐term potentiation. Paradoxically, PARP over‐activation under pathologic conditions including traumatic brain injury (TBI) results in cell death. We previously demonstrated that intra‐mitochondrial poly‐ADP‐ribosylation occurs following excitotoxic and oxidative injury in vitro. Here we sought to identify mitochondrial proteins modified by poly‐ADP‐ribosylation after TBI in vivo. Poly‐ADP‐ribosylation within mitochondria from injured brain after experimental TBI in rats was first verified using western blot and immuno‐electron microscopy. Poly‐ADP‐ribosylated mitochondrial proteins identified using a targeted proteomic approach included voltage‐dependent anion channel‐1, mitofilin, mitochondrial stress proteins, and the electron transport chain components F1F0 ATPase, cytochrome c oxidase, and cytochrome c reductase. To examine the functional consequences of mitochondrial poly‐ADP‐ribosylation, isolated rat brain mitochondria were exposed to conditions of nitrosative stress known to activate PARP. PARP activation‐induced reductions in State 3 respiration were prevented by the PARP‐1 inhibitor 5‐iodo‐6‐amino‐1,2‐benzopyrone or exogenous poly(ADP‐ribose) glycohydrolase. As the effects of PARP activation on mitochondrial respiration appear regulated by poly(ADP‐ribose) glycohydrolase, a direct effect of poly‐ADP‐ribosylation on electron transport chain function is suggested. These findings may be of relevance to TBI and other diseases where mitochondrial dysfunction occurs.
6‐Hydroxydopamine activates the mitochondrial apoptosis pathway through p38 MAPK‐mediated, p53‐independent activation of Bax and PUMA
Authors: Gomez‐Lazaro Maria , Galindo Maria F. , Concannon Caoimhín G. , Segura Miguel F. , Fernandez‐Gomez Francisco J. , Llecha Nuria , Comella Joan X. , Prehn Jochen H. M. , Jordan Joaquin 
Published: February 2008

J. Neurochem. (2008) 104, 1599–1612.AbstractMitochondrial alterations have been associated with the cytotoxic effect of 6‐hydroxydopamine (6‐OHDA), a widely used toxin to study Parkinson’s disease. In previous work, we have demonstrated that 6‐OHDA increases mitochondrial membrane permeability leading to cytochrome c release, but the precise mechanisms involved in this process remain unknown. Herein we studied the mechanism of increased mitochondrial permeability of SH‐SY5Y neuroblastoma cells in response to 6‐OHDA. Cytochrome c release induced by 6‐OHDA occurred, in both SH‐SY5Y cells and primary cultures, in the absence of mitochondrial swelling or a decrease in mitochondrial calcein fluorescence, suggesting little involvement of the mitochondrial permeability transition pore in this process. In contrast, 6‐OHDA‐induced cell death was associated with a significant translocation of the pro‐apoptotic Bax protein from the cytosol to mitochondria and with a significant induction of the BH3‐only protein PUMA. Experiments in mouse embryonic fibroblasts deficient in Bax or PUMA demonstrated a role for both proteins in 6‐OHDA‐induced apoptosis. Although 6‐OHDA elevated both total and nuclear p53 protein levels, activation of p53 was not essential for subsequent cell death. In contrast, we found that p38 mitogen‐activated protein kinase (MAPK) was activated early during 6‐OHDA‐induced apoptosis, and that treatment with the p38 MAPK inhibitor SKF86002 potently inhibited PUMA induction, green fluorescent protein‐Bax redistribution and apoptosis in response to 6‐OHDA. These data demonstrate a critical involvement of p38 MAPK, PUMA, and Bax in 6‐OHDA‐induced apoptosis.