bluuebunny/crossref_metadata_2025_split huggingface dataset:
Institutional and industrial changes in the Italian South: the case of Brindisi
Authors: Greco Lidia 
Published: May 2004

SummaryThis article proposes an institutionalist reading of the processes of industrial and employment change taking place in the clothing industry in Brindisi, Italy, during the 1990s. In contrast to more orthodox economic interpretations that focus on the separation between the economy and institutions, this article assumes the centrality of institutions for an understanding of industrial and employment performances and their change over time. Institutions profoundly affect the pursuit of the objectives of profit and efficiency in that they influence the definition of what can be considered as rational in a given institutional configuration and compatible with the values that a given society holds as socially and economically legitimate.
Integration or marginalization? The failures of social policy for the Roma in Rome
Authors: Marinaro Isabella Clough 
Published: May 2004

SummaryThis article examines Rome City Council's policies concerning the Roma during Francesco Rutelli's two terms as mayor (1993-2001). It demonstrates that the Rutelli administration's policies for these minority communities shifted from a superficial but genuine attempt to overcome aspects of marginalization to a criminalizing strategy of exclusion. It is argued here that the failure significantly to improve the social conditions of the Roma was due to (a) a refusal to tackle the inter-related causes of their social exclusion and (b) submission to the anti-Roma hostility of parts of the voting public. Following the demolition of Rome's largest shanty town in October 2000, the Council was unable to house many of the Roma it had made homeless. It would seem that a ‘cleaning-up’ campaign was intro duced to distance undocumented individuals and those with criminal records from the city through a notable rise in police raids. This change in approach was accompanied and justified by an intensification of ethnicized public order discourse.
Moving in and out of poverty
Authors: Layte Richard , Whelan Christopher T. 
Published: May 2004

Although many of the debates around social exclusion and cumulative disadvantage relate to processes that occur across time, there has been relatively little research into poverty dynamics except in a few notable countries such as Britain, the USA and Germany. This neglect is almost entirely because of the absence of comparative longitudinal data on income for other countries, but it is regrettable given the central importance of this area. By studying poverty dynamics we not only get a better insight into the processes leading to patterns of disadvantage and inequality, but we can also understand better the influence of different welfare state regimes on the social risks experienced by different types of individuals and households. The extent to which different national contexts protect their citizens from poverty persistence, or vary in the factors leading to poverty persistence, tells us a great deal about the workings of their socioeconomic systems and welfare regimes.
In this article we use the recent availability of five waves of the European Community Household Panel Survey to outline the nature of poverty persistence and poverty dynamics across a large number of countries. In doing so we ask three important questions. First, is poverty a more common experience when viewed longitudinally rather than cross-sectionally, and how is this affected by the income poverty line used? Second, can we identify a tendency toward poverty persistence, and does this vary in its extent across countries? Third and lastly, what types of events are more likely to lead to entry into and exit from poverty, and does the importance of these events differ between countries? The article shows that the experience of poverty is far wider than is appreciated from cross-sectional data, and also tends to be more concentrated on a particular population than would be expected from cross-sectional rates. Moreover, the pattern of poverty persistence is congruent with welfare regime theory. The importance of country institutions and welfare regimes is also underlined by the finding that social welfare and market incomes play different roles in poverty transitions across countries, and that Southern European, or residualist, welfare regimes focus poverty risks on the experience of the household's primary earner to a far greater extent than Northern European welfare states do.
Educational systems and perceived social inequality
Authors: Groß Martin 
Published: May 2004

This paper investigates the effect of intra-generational mobility patterns on collective social action. We start with the assumption that employees tend to collective action in pursuing their economic interests only if their social position is homogeneous, stable in time and characterized by privileges (or structural disadvantages). We believe that patterns of intra-generational mobility (and not only those of inter-generational mobility) are crucial for these preconditions of collective action. These conditions can come into effect only in systems of ‘closed positions’, where intra-generational mobility is restricted. In systems of open positions, a high degree of intra-generational mobility prevents the existence of homogeneous, stable and privileged social positions.
In addition, the institutional arrangements of a given society, especially the educational system, determine to a great extent whether occupational positions are closed or not. In societies with standardized, stratified and differentiated educational systems, intra-generational mobility is restricted by credentialist allocation regimes so that the three conditions are fulfilled and patterns of collective action have a high probability of arising.
This hypothesis is tested by an international comparison of effects on perceived social inequality using data from the International Social Justice Project (1991, 1996). It turns out that, as expected, in credentialist countries, educational titles and class position have stronger effects on perceived social inequality than in non-credentialist societies. But it was found that the economic system also plays an important role in the structuring of perceived inequality.
Separation Performance of PVC and PP Plastic Mixture Using Air Table
Authors: Dodbiba G. , Shibayama A. , Miyazaki T. , Fujita T. 
Published: May 2004

The aim of the research presented in this article was to investigate separation performance of the air table when separating a binary mixture of plastics. Separation using the air table, i.e. a dry mechanical process that grades constituents of the mixture with differences in specific gravity, is employed for separation of the PVC/PP mixture. Moreover, the performance of the laboratory‐scale air table is improved by increasing the height of riffles laid on the porous deck.The separation tests in a laboratory‐scale air table showed that the total efficiency of the separation is mainly dependent on superficial velocity of the air, longitudinal vibrating frequency of the deck, end slope, side slope, and height of riffles. The respective influence of these variables upon the total efficiency of separation is demonstrated experimentally.The evaluations of the separation performance for the two‐component mixture are made in terms of grade [%], recovery [%] and total efficiency [%].
Macrophage Migration Inhibitory Factor is a Constitutively Expressed Cytokine in the Human Adrenal Gland
Authors: Jian Ming , Parker Richard 
Published: May 2004

AbstractMacrophage migration inhibitory factor (MIF) has been found to be widely expressed in many cell types throughout the body and appears to play several physiologic roles. We sought to determine the expression and cellular distribution of MIF in human fetal (HFA) and adult (HAA) adrenals. A single band of approximately 0.8 kb was revealed by northern blot hybridization using cDNA probes for MIF in total RNA extracts of both HFA and HAA tissues. Immunohistochemical analysis showed strong immunostaining for MIF in the broad fetal zone of the HFA and in both the zona glomerulosa and zona reticularis of HAA. The cells of the zona fasciculata of the HAA and of the neocortex of the HFA were only minimally, if at all, immunopositive for MIF and medullary elements were consistently negative for MIF. These results are indicative of local production of MIF in adrenocortical cells during intrauterine development and also in adulthood. The role of MIF in cortical cells of the human adrenal gland remains to be determined. IUBMB Life, 55: 155‐158, 2003
Dual Regulation of Proton‐ and Sodium‐Coupled Phosphate Transport Systems in the Yarrowia lipolytica Yeast by Extracellular Phosphate and pH
Authors: Zvyagilskaya R. , Persson BL 
Published: May 2004

AbstractIn this study we used a newly isolated osmo‐, salt‐, and alkali‐tolerant Yarrowia lipolytica yeast strain, with a unique capacity to grow over a wide pH range (3.5‐10.5). A procedure was elaborated to follow phosphate accumulation by Y. lipolytica cells grown at different pH values. In this paper we demonstrate that Pi‐starved Y. lipolytica cells are endowed by derepressible high‐affinity, high‐capacity H+‐ and Na+‐driven Pi uptake systems and that activities of these transport systems are under the dual control by the prevailing extracellular Pi concentrations and pH values. IUBMB Life, 55: 151‐154, 2003
Synergism between Genomic and Non Genomic Estrogen Action Mechanisms
Authors: Acconcia Filippo , Marino Maria 
Published: May 2004

AbstractThe 17β‐estradiol (E2) action mechanism for inducing target gene expression can be attributed to both the direct binding of its receptor (ER) to specific sequences, the estrogen response element (ERE), and to the interaction between ER and other DNA‐binding transcription factors. At the present meagre information is available for the role played by the rapid hormone action mechanism(s) (i.e., activation of ERK, PI(3)K, PKC‐α) in modulating E2‐induced gene promoter activity. Here the involvement of the rapid non genomic mechanism in triggering the transcriptional activity of two E2‐regulated target genes in human hepatoma HepG2 cells has been studied, taking into consideration the cyclin D1 (ERE‐devoid) and the complement protein 3 (ERE‐containing) promoter‐luciferase report constructs. The results indicate that the activation of the ERK pathway is essential for the E2‐induced activity of both promoters, whereas the other rapid E2‐induced membrane‐starting signal transduction pathways (i.e., PI(3)K and PKC‐α) were differently required. These results permit the amplification of the E2 action mechanism by the addition of synergy between the non genomic and genomic molecular actions of the E2‐induced gene transcription. IUBMB Life, 55: 145‐150, 2003
Detection of Mitochondrial DNA Deletion by a Modified PCR Method in a 60Co Radiation‐exposed Patient
Authors: Zhen‐Cheng Wang , Xue‐Min Wang , Bing‐Hua Jiao , You‐Xin Jin , Ming‐Yong Miao , Ke‐Jun Zhu , Qing‐Gui Ni 
Published: May 2004

AbstractA new PCR based method was developed to detect deleted mitochondrial DNA (mtDNA). Peripheral blood cell DNA was obtained from a victim who was accidently exposed to a 60Co radiation source in 1990. Using the DNA as template, first PCR was performed to generate multiple products including true deletions and artifacts. The full length product was recovered and used as template of secondary PCR. The suspicious deletion product of mtDNA could be confirmed only if it was yielded by first PCR. Using either original primers or their nested primers, the suspicious deletion product was amplified and authenticated as a true deletion product. The template was recovered and determined to be a deletion by sequencing directly. The results show that a new mtDNA deletion, which spans 889 bp from nt 11688 to nt 12576, was detected in the peripheral blood cells of the victim. It indicates that this new PCR‐based method was more efficient at detecting small populations of mtDNA deletion than other routine methods. MtDNA deletion was found in the victim, suggesting the relationship between the deletion and phenotypes of the disease. IUBMB Life, 55: 133‐137, 2003
Search for Difference in Aminoacylation of Mitochondrial DNA‐encoded Wild‐type and Mutant Human tRNALeu?(UUR)
Authors: Zhen‐Cheng Wang , Xue‐Min Wang , You‐Xin Jin , Bing‐Hua Jiao , Feng Xu , Ming‐Yong Miao , Ke‐Jun Zhu 
Published: May 2004

AbstractThe pathogenetic mechanism of the most extensively investigated A3243G mutated tRNALeu (UUR) gene, which causes the MELAS encephalomyopathy, maternally inherited diabetes, or chronic progressive external ophlthalmoplegia, is still unresolved, despite the numerous investigations on the topic. Previous evidences presented in published work suggested that the mitochondrial DNA harboring A3243G mutation result decreases in the rates of mitochondrial protein synthesis. To search for differences in aminoacylation of mitochondrial DNA‐encoded wild‐type and mutant human tRNALeu (UUR), we have expressed and purified the two kinds of tRNAsLeu (UUR), and have expressed human mitochondrial leucyl‐tRNA synthetase for in vitro assays of aminoacylation of wild‐type and mutant human tRNALeu (UUR). The results indicate human mitochondrial tRNALeu (UUR) gene A3243G point mutant can remarkably reduce its aminoacylation, suggesting it could be one of the mechanisms that the mutation can produce in such clinical phenotypes. IUBMB Life, 55: 139‐144, 2003
The KRAB Domain of Zinc Finger Gene ZNF268: a Potential Transcriptional Repressor
Authors: Sun Yan , Gou De‐ming , Liu Hui , Peng Xiao , Li Wen‐xin 
Published: May 2004

AbstractNearly one‐third of Krupple‐type C2H2 zinc finger proteins have a krupple‐associated box (KRAB) domain, which may act as a transcriptional repressor. ZNF268, which was novelty isolated from early human embryo, is a typical krupple‐type C2H2 zinc finger protein with a conserved KRAB domain. In this report, the KRAB domain of ZNF268 is identified to localize in the nucleus and has transcriptional repressor activity. IUBMB Life, 55: 127‐131, 2003
PDK1 and PKB/Akt: Ideal Targets for Development of New Strategies to Structure‐Based Drug Design
Authors: Harris Thomas 
Published: May 2004

AbstractGrowth factor binding events to receptor tyrosine kinases result in activation of phosphatidylinositol 3‐kinase (PI3K), and activated PI3K generates the membrane‐bound second messengers phosphatidylinositol 3,4‐diphosphate [PI(3,4)P2] and PI(3,4,5)P3, which mediate membrane translocation of the phosphoinositide‐dependent kinase‐1 (PDK1) and protein kinase B (PKB, also known as Akt). In addition to the kinase domain, PDK1 and PKB contain a pleckstrin homology (PH) domain that binds to the second messenger, resulting in the phosphorylation and activation of PKB by PDK1. Recent evidence indicates that constitutive activation of PKB contributes to cancer progression by promoting proliferation and increased cell survival. The indicating of PDK1 and PKB as primary targets for discovery of anticancer drugs, together with the observations that both PDK1 and PKB contain small‐molecule regulatory binding sites that may be in proximity to the kinase active site, make PDK1 and PKB ideal targets for the development of new strategies to structure‐based drug design. While X‐ray structures have been reported for the kinase domains of PDK1 and PKB, no suitable crystals have been obtained for either PDK1 or PKB with their PH domains intact. In this regard, a novel structure‐based strategy is proposed, which utilizes segmental isotopic labeling of the PH domain in combination with site‐directed spin labeling of the kinase active site. Then, long‐range distance restraints between the 15N‐labeled backbone amide groups of the PH domain and the unpaired electron of the active site spin label can be determined from magnetic resonance studies of the enhancement effect that the paramagnetic spin label has on the nuclear relaxation rates of the amide protons. The determination of the structure and position of the PH domain with respect to the known X‐ray structure of the kinase active site could be useful in the rational design of potent and selective inhibitors of PDK1 and PKB by 'linking' the free energies of binding of substrate (ATP) analogs with analogs of the inositol polar head group of the phospholipid second messenger. The combined use of X‐ray crystallography, segmental isotopic and spin labeling, and magnetic resonance studies can be further extended to the study of other dynamic multidomain proteins and targets for structure‐based drug design. IUBMB Life, 55: 117‐126, 2003
Involvement of the Tyrosine Phosphorylation on GSH Transport in NIH3T3 Fibroblasts
Authors: Iantomasi Teresa , Favilli Fabio , Catarzi Serena , Giannoni Elisa , Biagioni Chiara , Vincenzini Maria 
Published: May 2004

AbstractThis study demonstrates the involvement of phosphotyrosine phosphatases on the activity and regulation of GSH ATP‐dependent transport system that we have previously identified in NIH3T3 fibroblasts. This is shown by the fact that increases of the initial rate of GSH uptake were measured in NIH3T3 overexpressing a synthetic gene coding for a low‐Mr‐phosphotyrosine protein phosphatase (LMW‐PTP), while decreases were obtained in NIH3T3 overexpressing the phosphatase inactive mutant (LMW‐C12SPTP), with respect to NIH3T3neo. Moreover, these results have been confirmed by experiments performed in the same cells by vanadate, and H2O2 treatment on both GSH transport and mediated passive transport of glucose. A possible regulation of this transport system by platelet‐derived growth factor receptor (PDGFr) with tyrosine kinase activity is also demonstrated. Moreover, these data show a relationship among GSH, PDGFr and phosphotyrosine phosphatase activity, and suggest a role of GSH transport systems on the cell proliferation process. IUBMB Life, 55: 159‐165, 2003
The Differential Susceptibility of Specific Neuronal Populations: Insights from Huntington's Disease
Authors: Mitchell Ian , Griffiths Mark 
Published: May 2004

AbstractRecent successes in identifying the genes and associated proteins underlying several familial neurodegenerative conditions have not always resulted in accounts as to why the associated patterns of neuronal damage are so specific and limited. Here, with reference to Huntington's disease, we present a general scheme to show how the mutant protein could interact with associated proteins to form an aggregation product. This could lead to neuronal death by direct actions on caspases, or by raising the levels of intracellular calcium ions and reactive oxygen species above a threshold that cannot be resisted by the protection normally conferred by endogenous factors such as calcium binding proteins, free radical scavengers and trophic factors. The local distributions of vulnerability and protective factors could ultimately dictate the pattern of damage induced by the mutant gene. IUBMB Life, 55: 293‐298, 2003
Trophic Factors in Neurodegenerative Disorders
Authors: Weis Joachim , Saxena Smita , Evangelopoulos Maria , Kruttgen Alex 
Published: May 2004

AbstractNeuronal survival is dependent on continuous trophic stimulation by neurotrophic factors. Anterograde and retrograde transport of neurotrophic factors and their receptors within neurites is essential for the communication of these survival signals. Lack of neurotrophic input has been proposed as a pathomechanism leading to neurodegenerative disease. The present short review provides a summary of some of the recent data on neurotrophic factors in neurodegenerative disorders and describes how disturbances of axonal trafficking might deprive neurons from trophic input. IUBMB Life, 55: 00‐00, 2003
Molecular Mechanisms of Neurodegeneration in Parkinson's Disease: Clues from Mendelian Syndromes
Authors: Lim Kah Leong , Lim Tit Meng 
Published: May 2004

AbstractThe recent identification and characterization of gene products responsible for familial forms of Parkinson disease (PD) have provided significant insights into the pathogenesis of PD. Collectively, these studies point towards ubiquitin‐proteasome system (UPS) dysfunction as an underlying mechanism responsible for dopaminergic cell death in PD. Emerging evidence further indicates a complex interplay between UPS derangements and other PD pathogenetic factors, all interwoven in an integrated network leading to dopaminergic cell death in PD. Taken together, these findings suggest that neuronal degeneration in PD is a result of a cascade of events, rather than a primary pathogenic event. Here, we review the clues uncovered from various Mendelian‐inherited forms of PD that have helped shaped our understanding of the molecular mechanisms underlying PD pathogenesis. IUBMB Life, 55: 315‐322, 2003
A Role for NOX NADPH Oxidases in Alzheimer's Disease and Other Types of Dementia?
Authors: Zekry Dina , Epperson Terry Kay , Krause Karl‐Heinz 
Published: May 2004

AbstractBecause of population ageing, dementias are likely to become a major scourge of the 21st century. Causes of dementia include Alzheimer's disease, cerebrovascular disease, and lesser known entities such as frontotemporal dementia or dementia with Lewy bodies. Neuroinflammation is likely to play an important role in the pathogenesis of dementia by the killing of neurons through inflammatory mechanisms. Such a role of neuroinflammation is well documented for Alzheimer's disease, and it is likely to play a role in other types of dementia as well. Reactive oxygen species (ROS) play a key role in inflammatory tissue destruction. The phagocyte NADPH oxidase NOX2 is the best studied ROS‐generating system. In the central nervous system, it is expressed in microglia and‐‐to a lesser extent‐‐in neurons. Indeed, there is emerging experimental evidence for a role of NOX2 in Alzheimer's and cerebrovascular disease. Recently, six novel ROS‐generating NADPH oxidases with homology to NOX2 have been discovered. Several of them are also expressed in the central nervous system. In this article, we hypothesize a role of NOX‐type NADPH oxidases in inflammatory neuronal loss. We review presently available evidence and suggest that NOX‐type NADPH oxidases may become promising pharmacological targets for the treatment and prevention of dementia. IUBMB Life, 55: 307‐313, 2003
Interactions Between Environmental and Genetic Factors in the Pathophysiology of Parkinson's Disease
Authors: Tsang Fai. , Soong Tuck Wah 
Published: May 2004

AbstractParkinson's disease (PD) is a progressive neurodegenerative disease with no known cure and affects approximately 1% of the elderly population. The major question in PD relates to the selective loss of dopaminergic neurons in patients. The underlying mechanism of genetic dysfunction and environmental toxins in contributing to the pathogenesis of PD may be oxidative stress. The interactions of genetic and environmental factors in PD may provide some answers to the longstanding question. In particular, the possibility that iron may provide selectivity to genetic susceptibility or dopamine reactivity in dopaminergic neuronal death is enhanced by the neuroprotection demonstrated in transgenic mice overexpressing ferritin or the use of iron chelators in MPTP‐induced PD mouse. It will be important to dissect and understand the contributions of genes, environment and intrinsic cellular states in the generation and progression of the pathophysiology of PD. IUBMB Life, 55: 323‐327, 2003