bluuebunny/crossref_metadata_2025_split huggingface dataset:
Worker Absenteeism in Search Equilibrium*
Authors: Engström Per , Holmlund Bertil 
Published: October 2007

AbstractIn this paper we introduce a general equilibrium model of search unemployment that incorporates absence from work as a distinct labor force state. Absenteeism is driven by random shocks to the value of leisure that are private information to the workers. Firms maximize profits while recognizing that the compensation package may affect the queue of job applicants and the absence rate. The analysis provides results concerning the effects of social insurance benefits and other determinants of workers' and firms' behavior. The normative analysis identifies externalities associated with firm‐provided sick pay and examines the welfare implications of alternative policies.
Inflation Adjustment and Labour Market Structures: Evidence from a Multi‐country Study*
Authors: Bowdler Christopher , Nunziata Luca 
Published: October 2007

AbstractThe impact of labour market structures on the response of inflation to macroeconomic shocks is analysed empirically. Results based on a 20‐country panel show that if labour market coordination is high, the effect on inflation of movements in unemployment, import prices, tax rates and productivity is dampened, both on impact and dynamically. In contrast, monopoly power in labour supply, measured by the percentage unionisation of the workforce, appears to amplify the response of inflation to its reduced‐form determinants. These findings are attributed to the behaviour of wages following movements in demand‐ and supply‐side conditions.
Taste response and poliomyelitis
Authors: BRAND N. 
Published: October 2007

SUMMARYTaste threshold for phenylthiourea was measured in 115 paralytic poliomyelitis subjects and 120 healthy people of both sexes from 6 to 40 years of age originating from various countries (Israel, Europe, Asia and North Africa Jews).A significant difference of non‐tasters frequency was found between paralytic poliomyelitis and healthy subjects, i.e. 31.3 and 16.7%, respectively.It may be suggested that the non‐tasters of paralytic poliomyelitis patients are more susceptible to polio virus.I wish to thank Prof. M. Makin, Director of the orthopedic hospital ‘Alyn’for crippled children in Jerusalem, Drs Mandel, Head of the Pediatric Department of the Government Hospital Sarafand, Goldman, Head of the Orthopedic Department of the Government Hospital Poriah for allowing me full access to their patients, and Dr A. Salamonovitsh, Head of the Health Centre Kiryath Shmonah for permission to examine school children.
An investigation into the fertility rates of mentally ill patients
Authors: MACSORLEY KATE 
Published: October 2007

SUMMARYAn investigation into celibacy and reproduction rates of 187 male and 203 female mentally ill patients has been described. Comparisons were made between patients and their sibs. Two control populations were used1. Figures taken from the Registrar General's Reports.2. An independent population drawn from the medical and surgical wards of Paddington General Hospital.The mean ages of onset were calculated. The marital states and reproduction rates of all patients and controls were considered. It was found that the celibacy rate of patients was more than 50 % above that in the general population and almost as much above that of the independent control population, at least for the schizophrenic diseases. It was found that a fairly large group of patients (forty‐eight males and twenty females) designated as ‘Atypical’resembled the schizophrenic groups very closely in mean age of onset and low marriage and reproductive rates.The number of children per marriage of patients was a good deal below, and the percentage of childless marriages a good deal above, that of the control population.There was evidence of assortative mating.I am grateful to the Medical Research Council for their financial support. I also wish to express my thanks to the Medical Superintendents of Horton, Paddington and St Bernard's Hospitals who permitted me to interview their patients. My special thanks are due to Drs B. A. J. C. Gregory, H. R. Rollin, L. W. Russell and P. J. F. Walsh who generously gave their time and opinions.
Distances which involve satellited chromosomes in metaphase preparations
Authors: MERRINGTON MAXINE , PENROSE L. S. 
Published: October 2007

SUMMARYInvestigations of distance measurements between centromeres of human chromosomes in metaphase photographs show that there is a general tendency for homologous pairs to lie closer to one another than would be expected on the hypothesis of random arrangement. In the present analysis no significant divergence from random arrangement of their distances was found for the specific pairs nos. 1, 2 and 3. However, there is strong evidence that the groups of large and small acrocentrics tend to lie closer to one another than would be expected on the random hypothesis. The distances between no. 1 and nos. 21 or 22 chromosomes were not found to be significantly less than expected.The writers wish to thank Mr N. P. Bishun, Dr Joy D. A. Delhanty, Dr J. R. Ellis and Miss Ruth Marshall for supplying photographs of cells and Miss Patricia Jackson and Miss Katharine Solomon for assistance in measurement and standardization calculations.
Birth weight and some other factors in relation to infant survival. A study on an Indian sample
Authors: JAYANT K. 
Published: October 2007

SUMMARYEffect of parity, maternal age, birth weight and sex of the child on infant survival have been studied in 3822 eases belonging to the upper socio‐economic group and the relationship of birth weight to survival in 2279 cases of a lower socio‐economic group have also been studied. It has been suggested that for the upper socio‐economic group a child with a birth weight of less than 5| lb., if it is a male, and 5 J lb., if it is a female, may be considered as premature whereas for the lower socio‐economic group the corresponding birth weight is 4J lb. for both males and females. In the latter group, the critical weight of 4½ lb. would have to be revised, if perinatal mortality rate improves.I am indebted to the management of the Chamanlal Mehta Hospital for women for allowing me to collect the data from their hospital. I am grateful to Prof. M. C. Chakrabarti, University Department of Statistics for giving me all the facilities for the statistical analysis. I would like to record my gratitude to Miss Mary N. Karn, Galton Laboratory, London and to Dr A. M. Kshirsagar, University of Bombay for taking interest in this paper.Grateful acknowledgement is due to Dr T. H. Rindani, the Dean, T.N. Medical College for permission to make use of outside resources for collection and analysis of the data and to Dr V. N. Panse, Professor, Department of Preventive and Social Medicine for his encouragement and advice.
Finger‐print patterns in mongolism
Authors: HOLT SARAH B. 
Published: October 2007

SUMMARYThe frequencies of arches, ulnar and radial loops and whorls on the fingers of 310 mongolian imbeciles and 1000 controls are given. In both sexes the mongols show a reduction in the frequencies of whorls, arches and radial loops, with a corresponding increase in the frequency of ulnar loops. In contrast with the controls, all the major pattern types occur with similar frequencies in both sexes.Individuals with arches on all ten fingers are nearly seven times as common in mongols as in the control population.
Promyelocytic leukemia‐nuclear body formation is an early event leading to retinoic acid‐induced differentiation of neuroblastoma cells
Authors: Delaune A. , Corbière C. , Benjelloun F. D , Legrand E. , Vannier J. P. , Ripoll C. , Vasse M. 
Published: October 2007

AbstractNeuroblastoma is one of the most common cancers in children. Neuroblastoma differentiation is linked to the presence of the promyelocytic leukemia (PML) protein. Retinoic acid, a powerful differentiation‐inducer in vitro, is a potent agent for the treatment of neuroblastoma. Using two different human neuroblastoma cell lines, SH‐SY5Y and LA‐N‐5, we show here that PML protein leads to the formation of nuclear bodies (PML‐NB) after only 1 h of retinoic acid treatment and that this formation is mediated by the extracellular signal‐regulated kinase (ERK) pathway. Inhibition of protein kinase C also leads to formation of PML‐NB via the ERK pathway. Both sumoylation and phosphorylation of PML in an ERK‐dependent pathway are also required for formation of PML‐NB. Finally, we show that PML‐NB formation in neuroblastoma cells is associated with neurite outgrowth. These results support the proposal that the formation of PML‐NB is correlated with the differentiation of neuroblastoma cells.
Gi‐coupled P2Y‐ADP receptor mediates GSK‐3 phosphorylation and β‐catenin nuclear translocation in granule neurons
Authors: Ortega Felipe , Pérez‐Sen Raquel , Miras‐Portugal MªTeresa 
Published: October 2007

AbstractGlycogen synthase kinase‐3 (GSK‐3) is a multifaceted enzyme involved in development, neurogenesis, and survival at the CNS. We investigated nucleotides signaling to GSK‐3 in cerebellar granule neurons and found that the metabotropic agonist 2‐methyl‐thio‐ADP (2MeSADP) was able to induce GSK‐3 phosphorylation and inhibition of its catalytic activity. 2MeSADP could be acting through several P2Y‐ADP receptors expressed in granule neurons, as RT‐PCR expression was found for P2Y1, P2Y12, and P2Y13receptors, but the pharmacological data fitted well with a Gi‐coupled P2Y13receptor: the effect was sensitive to pertussis toxin, was unaffected by specific antagonists of P2Y1and P2Y12receptors, such as 2′‐deoxy‐N6‐methyl‐adenosine 3′,5′‐diphosphate and 2‐methyl‐thio‐AMP, respectively, and the EC50values for 2MeSADP and ADP were in the same low nanomolar range. 2MeSADP was able to phosphorylate and activate extracellular signal‐regulated kinase (ERK)‐1,2 and Akt proteins, but its effect on GSK‐3 phosphorylation was primarily dependent on the phosphatidyl inositol‐3 kinase (PI3‐K)/Akt pathway, as it was abolished by the PI3‐K inhibitor wortmannin. GSK‐3 inactivation by 2MeSADP in granule neurons resulted in nuclear translocation of its substrate β‐catenin, which functions as a transcriptional regulator, this effect being lost with wortmaninn. The present study first describes the coupling of a Gi‐coupled P2Y13‐like receptor to GSK‐3 and β‐catenin through PI3‐K/Akt signaling.
Arachidonic acid induces both Na+ and Ca2+ entry resulting in apoptosis
Authors: Fang Kwang‐Ming , Chang Wei‐Luen , Wang Su‐Mei , Su Ming‐Jai , Wu Mei‐Lin 
Published: October 2007

AbstractMarked accumulation of arachidonic acid (AA) and intracellular Ca2+ and Na+ overloads are seen during brain ischemia. In this study, we show that, in neurons, AA induces cytosolic Na+ ([Na+]cyt) and Ca2+ ([Ca2+]cyt) overload via a non‐selective cation conductance (NSCC), resulting in mitochondrial [Na+]m and [Ca2+]m overload. Another two types of free fatty acids, including oleic acid and eicosapentaenoic acid, induced a smaller increase in the [Ca2+]i and [Na+]i. RU360, a selective inhibitor of the mitochondrial Ca2+ uniporter, inhibited the AA‐induced [Ca2+]m and [Na+]m overload, but not the [Ca2+]cyt and [Na+]cyt overload. The [Na+]m overload was also markedly inhibited by either Ca2+‐free medium or CGP3715, a selective inhibitor of the mitochondrial Na+cyt‐Ca2+m exchanger. Moreover, RU360, Ca2+‐free medium, Na+‐free medium, or cyclosporin A (CsA) largely prevented AA‐induced opening of the mitochondrial permeability transition pore, cytochrome c release, and caspase 3‐dependent neuronal apoptosis. Importantly, Na+‐ionophore/Ca2+‐free medium, which induced [Na+]m overload, but not [Ca2+]m overload, also caused cyclosporin A‐sensitive mitochondrial permeability transition pore opening, resulting in caspase 3‐dependent apoptosis, indicating that [Na+]m overload per se induced apoptosis. Our results therefore suggest that AA‐induced [Na+]m overload, acting via activation of the NSCC, is an important upstream signal in the mitochondrial‐mediated apoptotic pathway. The NSCC may therefore act as a potential neuronal death pore which is activated by AA accumulation under pathological conditions.
Physiological changes in GRK2 regulate CCL2‐induced signaling to ERK1/2 and Akt but not to MEK1/2 and calcium
Authors: Kleibeuker Wendy , Jurado‐Pueyo Maria , Murga Cristina , Eijkelkamp Niels , Mayor Jr Federico , Heijnen Cobi J. , Kavelaars Annemieke 
Published: October 2007

AbstractG protein‐coupled receptor (GPCR) kinase 2 (GRK2) regulates G protein‐coupled receptor signaling via agonist‐induced receptor phosphorylation and desensitization. GRK2 can also modulate cellular activation by interacting with downstream signaling molecules. The intracellular GRK2 level changes during inflammatory conditions. We investigated how IL‐1β‐induced changes in endogenous GRK2 expression influence chemokine receptor signaling in primary astrocytes. Culturing astrocytes with IL‐1β for 24 h induced a 2–3‐fold increase in GRK2 and decreased C–C chemokine ligand 2 (CCL2)‐induced ERK1/2 activation. Conversely, the 45% decrease in GRK2 expression in astrocytes from GRK2+/− animals resulted in a more pronounced CCL2‐induced ERK1/2 phosphorylation. Increased GRK2 inhibited CCL2‐induced Akt phosphorylation at Thr308 and Ser473 as well as pPDK‐1 translocation. In contrast, altered GRK2 levels did not change the CCL2‐induced increase in intracellular calcium or MEK1/2 phosphorylation. These data suggest that altered GRK2 expression modulates chemokine signaling downstream of the receptor. We found that GRK2 kinase activity was not required to decrease chemokine‐induced ERK1/2 phosphorylation, whereas regulation of CCL2‐induced Akt phosphorylation did require an active GRK2 kinase domain. Collectively, these data suggest that changes in endogenous GRK2 expression in primary astrocytes regulate chemokine receptor signaling to ERK1/2 and to PDK‐1‐Akt downstream of receptor coupling via kinase‐dependent and kinase‐independent mechanisms, respectively.
Neural cell adhesion molecule‐180‐mediated homophilic binding induces epidermal growth factor receptor (EGFR) down‐regulation and uncouples the inhibitory function of EGFR in neurite outgrowth
Authors: Povlsen Gro Klitgaard , Berezin Vladimir , Bock Elisabeth 
Published: October 2007

AbstractThe neural cell adhesion molecule (NCAM) plays important roles in neuronal development, regeneration, and synaptic plasticity. NCAM homophilic binding mediates cell adhesion and induces intracellular signals, in which the fibroblast growth factor receptor plays a prominent role. Recent studies on axon guidance in Drosophila suggest that NCAM also regulates the epidermal growth factor receptor (EGFR) (Molecular and Cellular Neuroscience, 28, 2005, 141). A possible interaction between NCAM and EGFR in mammalian cells has not been investigated. The present study demonstrates for the first time a functional interaction between NCAM and EGFR in mammalian cells and investigates the molecular mechanisms underlying this interaction. First, NCAM and EGFR are shown to play opposite roles in neurite outgrowth regulation in cerebellar granular neurons. The data presented indicate that negative regulation of EGFR is one of the mechanisms underlying the neuritogenic effect of NCAM. Second, it is demonstrated that expression of the NCAM‐180 isoform induces EGFR down‐regulation in transfected cells and promotes EGFR down‐regulation induced by EGF stimulation. It is demonstrated that the mechanism underlying this NCAM‐180‐induced EGFR down‐regulation involves increased EGFR ubiquitination and lysosomal EGFR degradation. Furthermore, NCAM‐180‐mediated EGFR down‐regulation requires NCAM homophilic binding and interactions of the cytoplasmic domain of NCAM‐180 with intracellular interaction partners, but does not require NCAM‐mediated fibroblast growth factor receptor activation.
Metallothionein and a peptide modeled after metallothionein, EmtinB, induce neuronal differentiation and survival through binding to receptors of the low‐density lipoprotein receptor family
Authors: Ambjørn Malene , Asmussen Johanne W. , Lindstam Mats , Gotfryd Kamil , Jacobsen Christian , Kiselyov Vladislav V. , Moestrup Søren K. , Penkowa Milena , Bock Elisabeth , Berezin Vladimir 
Published: October 2007

AbstractAccumulating evidence suggests that metallothionein (MT)‐I and ‐II promote neuronal survival and regeneration in vivo. The present study investigated the molecular mechanisms underlying the differentiation and survival‐promoting effects of MT and a peptide modeled after MT, EmtinB. Both MT and EmtinB directly stimulated neurite outgrowth and promoted survival in vitro using primary cultures of cerebellar granule neurons. In addition, expression and surface localization of megalin, a known MT receptor, and the related lipoprotein receptor‐related protein‐1 (LRP) are demonstrated in cerebellar granule neurons. By means of surface plasmon resonance MT and EmtinB were found to bind to both megalin and LRP. The bindings were abrogated in the presence of receptor‐associated protein‐1, an antagonist of the low‐density lipoprotein receptor family, which also inhibited MT‐ and EmtinB‐induced neurite outgrowth and survival. MT‐mediated neurite outgrowth was furthermore inhibited by an anti‐megalin serum. EmtinB‐mediated inhibition of apoptosis occurred without a reduction of caspase‐3 activity, but was associated with reduced expression of the pro‐apoptotic B‐cell leukemia/lymphoma‐2 interacting member of cell death (BimS). Finally, evidence is provided that MT and EmtinB activate extracellular signal‐regulated kinase, protein kinase B, and cAMP response element binding protein. Altogether, these results strongly suggest that MT and EmtinB induce their neuronal effects through direct binding to surface receptors belonging to the low‐density lipoprotein receptor family, such as megalin and LRP, thereby activating signal transduction pathways resulting in neurite outgrowth and survival.
Netrin‐1‐independent adenosine A2b receptor activation regulates the response of axons to netrin‐1 by controlling cell surface levels of UNC5A receptors
Authors: McKenna William L. , Wong‐Staal Caroline , Kim Grace C. , Macias Hector , Hinck Lindsay , Bartoe Joseph L. 
Published: October 2007

AbstractGrowth cone response to the bifunctional guidance cue netrin‐1 is regulated by the activity of intracellular signaling intermediates such as protein kinase C‐alpha (PKCα) and adenylyl cyclase. Among the diverse cellular events these enzymes regulate is receptor trafficking. Netrin‐1, itself, may govern the activity of these signaling intermediates, thereby regulating axonal responses to itself. Alternatively, other ligands, such as activators of G protein‐coupled receptors, may regulate responses to netrin‐1 by governing these signaling intermediates. Here, we investigate the mechanisms controlling activation of PKCα and the subsequent downstream regulation of cell surface UNC5A receptors. We report that activation of adenosine receptors by adenosine analogs, or activation of the putative netrin‐1 receptor, the G protein‐coupled receptor adenosine A2b receptor (A2bR) results in PKCα‐dependent removal of UNC5A from the cell surface. This decrease in cell surface UNC5A reduces the number of growth cones that collapse in response to netrin‐1 and converts repulsion to attraction. We show these A2bR‐mediated alterations in axonal response are not because of netrin‐1 because netrin‐1 neither binds A2bR, as assayed by protein overlay, nor stimulates PKCα‐dependent UNC5A surface loss. Our results demonstrate that netrin‐1‐independent A2bR signaling governs the responsiveness of a neuron to netrin‐1 by regulating the levels of cell surface UNC5A receptor.
Widespread immunoreactivity for neuronal nuclei in cultured human and rodent astrocytes
Authors: Darlington Peter J. , Goldman Jen S. , Cui Qiao‐ling , Antel Jack P. , Kennedy Timothy E. 
Published: October 2007

AbstractThe monoclonal antibody (mAb) neuronal nuclei (NeuN) labels the nuclei of mature neurons in vivo in vertebrates. NeuN has also been used to define post‐mitotic neurons or differentiating neuronal precursors in vitro. In this study, we demonstrate that the NeuN mAb labels the nuclei of astrocytes cultured from fetal and adult human, newborn rat, and embryonic mouse brain tissue. A non‐neuronal fibroblast cell line (3T3) also displayed NeuN immunoreactivity. We confirmed that NeuN labels neurons but not astrocytes in sections of P10 rat brain. Western blot analysis of NeuN immunoreactive species revealed a distribution of bands in nucleus‐enriched fractions derived from the different cell lines that was similar, but not identical to adult rat brain homogenates. We then examined the hypothesis that the glial fibrillary acidic protein/NeuN‐double positive population of cells might correspond to neuronal precursors. Although the NeuN‐positive astrocytes were proliferating, no evidence of neurogenesis was detected. Furthermore, expression of additional neuronal precursor markers was not detected. Our results indicate that primary astrocytes derived from mouse, rat, and human brain express NeuN. Our findings are consistent with NeuN being a selective marker of neurons in vivo, but indicate that studies utilizing NeuN‐immunoreactivity as a definitive marker of post‐mitotic neurons in vitro should be interpreted with caution.
Selective enhancement of the activity of C‐terminally truncated, but not intact, acetylcholinesterase
Authors: Zimmermann Martina , Grösgen Sven , Westwell Martin S. , Greenfield Susan A. 
Published: October 2007

AbstractAcetylcholinesterase (AChE) is one of the fastest enzymes approaching the catalytic limit of enzyme activity. The enzyme is involved in the terminal breakdown of the neurotransmitter acetylcholine, but non‐enzymatic roles have also been described for the entire AChE molecule and its isolated C‐terminal sequences. These non‐cholinergic functions have been attributed to both the developmental and degenerative situation: the major form of AChE present in these conditions is monomeric. Moreover, AChE has been shown to lose its typical characteristic of substrate inhibition in both development and degeneration. This study characterizes a form of AChE truncated after amino acid 548 (T548‐AChE), whose truncation site is homologue to that of a physiological form of T‐AChE detected in fetal bovine serum that has lost its C‐terminal moiety supposedly due to proteolytic cleavage. Peptide sequences covered by this C‐terminal sequence have been shown to be crucially involved in both developmental and degenerative mechanisms in vitro. Numerous studies have addressed the structure–function relationship of the AChE C‐terminus with T548‐AChE representing one of the most frequently studied forms of truncated AChE. In this study, we provide new insight into the understanding of the functional characteristics that T548‐AChE acquires in solution: T548‐AChE is incubated with agents of varying net charge and molecular weight. Together with kinetic studies and an analysis of different molecular forms and aggregation states of T548‐AChE, we show that the enzymatic activity of T548‐AChE, an enzyme verging at its catalytic limit is, nonetheless, apparently enhanced by up to 800%. We demonstrate, first, how the activity of T548‐AChE can be enhanced through agents that contain highly positive charged moieties. Moreover, the un‐competitive mechanism of activity enhancement most likely involves the peripheral anionic site of AChE that is reflected in delayed substrate inhibition being observed for activity enhanced T548‐AChE. The data provides evidence towards a mechanistic and functional link between the form of AChE unique to both development and degeneration and a C‐terminal peptide of T‐AChE acting under those conditions.