bluuebunny/crossref_metadata_2025_split huggingface dataset:
Genetic Evaluation of Elbow Angles as Predictors of Elbow Dysplasia in German Shepherd Dogs
Authors: Janutta V. , Hamann H. , Klein S. , Tellhelm B. , Distl O. 
Published: June 2005

SummaryElbow angles were measured in X‐rays of both elbows to elucidate the usefulness of such data for selecting against elbow dysplasia (ED) in German shepherd dogs. These measurements record the size, proportions and alignments of the anconeal process (PA), the radius (RA), the olecranon (OL), and the ulnar trochlear notch (UL). The reference system for evaluating the information content of the measurements was the score for ED (ED‐SV) as recommended by the International Elbow Working Group. Data from 2645 X‐rayed dogs born from 1998 to 2001 in 1331 kennels were analysed by using residual maximum likelihood procedures to estimate heritabilities, additive genetic correlations and residual correlations. The pedigree file included 11 426 dogs and contained ancestors for up to six generations. ED‐SV was significantly influenced by sex, by age within sex and by month of birth. The elbow angles were significantly influenced by the month and year of birth, X‐ray positioning of the dog's forelimbs, angle of elbow flection, litter size and number of dogs X‐rayed by the veterinary practitioners. The following heritability estimates were found:h2 = 0.18 ± 0.04 for ED;h2 = 0.76 ± 0.04 for OL;h2 = 0.52 ± 0.05 for PA;h2 = 0.50 ± 0.04 for UL; andh2 = 0.39 ± 0.04 for RA. The additive genetic correlations of ED‐SV with three elbow angles (OL, UL and RA) were close to zero. A higher additive genetic correlation to ED‐SV was found only for PA, for whichrg = 0.31. The distributions of predicted breeding values for susceptibility to ED were not affected by regarding the elbow angles as additional traits in the multivariate prediction procedure. Measurements of elbow angles were thus shown to be unsuitable for use in selection programmes against ED in German shepherd dogs.
Mitochondrial Damage as an Early Event of Monensin‐induced Cell Injury in Cultured Fibroblasts L929
Authors: Souza A. C. , Machado F. S. , Celes M. R. N. , Faria G. , Rocha L. B. , Silva J. S. , Rossi M. A. 
Published: June 2005

SummaryThe present study was designed to identify, submicroscopically, the primary organelle or target structure for monensin in cultured murine fibroblasts L929. In addition, the effect of the drug on cell size and surface membranes of the cells were analysed; cellular proliferation, collagen secretion, and necrosis and apoptosis were re‐evaluated. At the lowest concentration of monensin the foremost ultrastructural alteration occurred in the mitochondria, characterized by increased matrix density with disorganized and less distinct crystae. Incubation with monensin at higher concentrations resulted in severe mitochondrial damage and marked dilatation of the Golgi apparatus and rough endoplasmic reticulum cisternae. Fibroblasts exposed to higher concentrations of monensin were enlarged with decreased number of filopodia and hollows in the surface membrane. Moreover, monensin inhibited the cell proliferation, increased immunohistochemical positiveness for collagen type I in a dose‐dependent manner, and, at high concentrations, caused cell necrosis whereas apoptosis was not induced. Taken together, these results show that monensin induces early mitochondrial damage, possibly causing an energy deficit that led to inhibition of fibroblasts proliferation and accumulation of collagen causing dilatation of Golgi apparatus and rough endoplasmic reticulum. Moreover, the mitochondrial damage would also explain the monensin‐induced necrosis.
Smith'sSentiments(1759) and Wright'sPassions(1601): the beginnings of sociology
Authors: Barbalet Jack 
Published: June 2005

AbstractTreatments of sources of Adam Smith's sociological theory of the self and associated ideas inThe Theory of Moral Sentimentstypically refer to classical antecedents or the work of his teacher Francis Hutcheson or his contemporary David Hume. During the seventeenth century, however, many books on the passions were published in London that arguably constitute an important but neglected source of Smith's treatment of moral sentiments. These works are largely forgotten today but at the time were widely read. They are not philosophical, partly devotional and predominantly psychological. Although Smith does not refer to these works his argument resembles theirs in many places. The importance of the seventeenth‐century books on the passions, apart from their role in the history of psychology, is their bearing on contemporary economic practices. In this paper the connections between Smith and one of these books, Thomas Wright'sThe Passions of the Minde in Generall, are indicated.
Symbolic interactionism and the concept of power
Authors: Dennis Alex , Martin Peter J. 
Published: June 2005

AbstractSymbolic interactionism is often represented as a perspective which is limited by its restriction to ‘micro’ aspects of social organization. As such, it is allegedly unable to adequately conceptualize ‘macro’ phenomena such as social structure, patterns of inequality, and power. Such a view is routinely presented in undergraduate textbooks. This paper contests such a view through a consideration of the concept of power. We argue that the interactionist research tradition does show a fundamental concern with power phenomena, and that a reconsideration of the concept is timely in light of theoretical developments in sociology more generally. An increasing concern with the analysis of culture, the continuing influence of Foucault, the development of feminist perspectives, and the emerging consensus around neo‐Weberian thought have all contributed to a renewal of interest in themes long ago explored by interactionists. As examples we suggest that interactionist studies in the fields of deviance and education have been concerned above all with the authoritative imposition of consequential identities, i.e., with the social processes through which power is enacted and institutionalized in real situations. Such developments have led some to argue that interactionism has now been incorporated into the mainstream of sociology. We conclude, however, by arguing that such a view runs the risk of granting to orthodox sociological thought a legitimacy which is analytically unwarranted, and which fails to recognize the alternative theoretical and philosophical foundations of symbolic interactionist thought.
Choosing Buddhism in Australia: towards a traditional style of reflexive spiritual engagement1
Authors: Phillips Tim , Aarons Haydn 
Published: June 2005

AbstractThere has been little dedicated sociological research on the appeal Buddhism holds for many individuals in the West. It is suggested that this absence reflects a current tendency within the discipline to highlight a new age approach to spiritual involvement and to overlook other optional styles of engagement. Such a pattern of study is concerning because the propensity to privilege the new age style would seem to be less an outcome of a coherent research agenda than a result of the currency that the idea of postmodern religion has come to assume in theoretical accounts of spiritual transformation in contemporary societies. Using data from a modest quantitative survey, the study investigates spiritual style among a sample of Australians who have developed an interest in Buddhist practice and belief. The results point to the prevalence of a traditional approach to involvement, whereby the individual decides to engage solely with Buddhism for the long duration. Given its possession of these qualities, the research goes on to examine the social patterning of spiritual commitment. The findings suggest that comprehending the social restrictions to any kind of involvement is a more pressing sociological question than explaining social divergences among the engaged.
Reciprocity in relationships: socio‐economic and health influences on intergenerational exchanges between Third Age parents and their adult children in Great Britain
Authors: Grundy Emily 
Published: June 2005

AbstractIn this paper data from a nationally representative British longitudinal study are used to analyse exchanges of support between Third Age parents (aged 55–75) and their adult children. Results show that between two thirds and three quarters of parents in this age group were involved in some sort of exchange relationship with at least one of their children. Generally, more Third Age parents were providers than recipients of help, but there was a strong reciprocal element to intergenerational exchange with, for example, married parents who provided support to at least one child being twice as likely as those who did not to receive support from a child, after allowance for a range of relevant parental and child characteristics. Parental characteristics associated with higher probability of providing help included higher income, home ownership and being married or widowed rather than divorced. Higher income and home ownership were, however, negatively associated with odds of receiving help from a child, again after adjustment for other co‐variates, suggesting socio‐economic differences in the balance of support exchanges. Children seem responsive to parental needs in that receipt of help from a child was positively associated with older parental age and with parental disability. The paper shows that in Britain, as in the USA, the balance of intergenerational exchanges involving Third Age adults is downward rather than upward, in contravention of depictions of older adults as ‘burdens’ on younger generations. Current demographic and social changes are, it is argued, likely to increase support demands from adult children to Third Age parents in coming decades.
2004 American Sociological Association Presidential address: For public sociology*
Authors: Burawoy Michael 
Published: June 2005

AbstractResponding to the growing gap between the sociological ethos and the world we study, the challenge of public sociology is to engage multiple publics in multiple ways. These public sociologies should not be left out in the cold, but brought into the framework of our discipline. In this way we make public sociology a visible and legitimate enterprise, and, thereby, invigorate the discipline as a whole. Accordingly, if we map out the division of sociological labor, we discover antagonistic interdependence among four types of knowledge: professional, critical, policy, and public. In the best of all worlds the flourishing of each type of sociology is a condition for the flourishing of all, but they can just as easily assume pathological forms or become victims of exclusion and subordination. This field of power beckons us to explore the relations among the four types of sociology as they vary historically and nationally, and as they provide the template for divergent individual careers. Finally, comparing disciplines points to the umbilical chord that connects sociology to the world of publics, underlining sociology's particular investment in the defense of civil society, itself beleaguered by the encroachment of markets and states.
Brain‐derived neurotrophic factor modulates dopaminergic deficits in a transgenic mouse model of Huntington's disease
Authors: Pineda José R. , Canals Josep M , Bosch Miquel , Adell Albert , Mengod Guadalupe , Artigas Francesc , Ernfors Patrik , Alberch Jordi 
Published: June 2005

AbstractDysfunction of dopaminergic neurons may contribute to motor impairment in Huntington's disease. Here, we study the role of brain‐derived neurotrophic factor (BDNF) in alterations of the nigrostriatal system associated with transgenics carrying mutant huntingtin. Using huntingtin‐BDNF+/– double‐mutant mice, we analyzed the effects of reducing the levels of BDNF expression in a model of Huntington's disease (R6/1). When compared with R6/1 mice, these mice exhibit an increased number of aggregates in the substantia nigra pars compacta. In addition, reduction of BDNF expression exacerbates the dopaminergic neuronal dysfunction seen in mutant huntingtin mice, such as the decrease in retrograde labelling of dopaminergic neurons and striatal dopamine content. However, mutant huntingtin mice with normal or lowered BDNF expression show the same decrease in the anterograde transport, number of dopaminergic neurons and nigral volume. In addition, reduced BDNF expression causes decreased dopamine receptor expression in mutant huntingtin mice. Examination of changes in locomotor activity induced by dopamine receptor agonists revealed that, in comparison with R6/1 mice, the double mutant mice exhibit lower activity in response to amphetamine, but not to apomorphine. In conclusion, these findings demonstrate that the decreased BDNF expression observed in Huntington's disease exacerbates dopaminergic neuronal dysfunction, which may participate in the motor disturbances associated with this neurodegenerative disorder.
The antimicrobial peptide rCRAMP is present in the central nervous system of the rat
Authors: Bergman Peter , Termén Stefan , Johansson Linda , Nyström Lisbeth , Arenas Ernest , Jonsson Ann‐Beth , Hökfelt Tomas , Gudmundsson Gudmundur H. , Agerberth Birgitta 
Published: June 2005

AbstractThe brain is protected against invading pathogens by the blood–brain barrier, and also by its own innate defence system consisting of microglia and neurons in a coordinated network. Antimicrobial peptides are a part of the innate immune system at epithelial surfaces, and may also have important functions in the brain. Recently, we characterized the rat homologue of the human cathelicidin LL‐37, designated rCRAMP. Here we present several lines of evidence for this peptide being expressed in rat CNS. (1) A peptide/protein extract of rat brain is active against bacteria in a salt‐dependent manner. (2) Western blot analysis demonstrates the presence of rCRAMP in rat brain extract. (3) rCRAMP peptide and mRNA are present mainly in specific CNS regions (olfactory bulb, cerebellum, medulla oblongata and spinal cord). (4) rCRAMP‐like immunoreactivity is detected in olfactory bulb, cerebellum and spinal cord by immunohistochemistry. (5) Moreover, the transcript of rCRAMP is detected in primary cultures from hippocampus, striatum, cerebellum and spinal cord, as shown with RT–PCR and Southern blot analyses. In addition, the rCRAMP peptide exhibits in vitro activity against the neuropathogenic bacterium Neisseria meningitidis. Taken together, these data suggest that the cathelicidin rCRAMP may play a role in the innate immunity of the CNS.
Green tea polyphenol (–)‐epigallocatechin‐3‐gallate induces neurorescue of long‐term serum‐deprived PC12 cells and promotes neurite outgrowth
Authors: Reznichenko L. , Amit T. , Youdim M. B. H. , Mandel S. 
Published: June 2005

AbstractOur previous studies have shown that the green tea polyphenol (–)‐epigallocatechin‐3‐gallate (EGCG) prevents neuronal cell death caused by several neurotoxins. The present study sought to determine the neuroprotective effect of EGCG when it is administered after the induction of cell damage (‘neurorescue’). In an attempt to imitate a progressive mode of death, PC12 cells were initially subjected to serum‐starvation conditions for a period of 1 or 3 days before administration of EGCG (0.1–10 µm) for up to 3 days. In spite of the high percentage of cell death, single or repetitive administration of EGCG (1 µm) significantly attenuated cell death. The neurorescue effect of EGCG was abolished by pre‐treatment with the protein kinase C inhibitor GF109203X (2.5 µm), suggesting the involvement of the protein kinase C pathway in neurorescue by the drug. This is consistent with the rapid (15 min) translocation of the protein kinase C alpha isoform to the cell membrane in response to EGCG. The correlative neurite outgrowth activity of EGCG on PC12 cells may also contribute to its neurorescue effect. The present findings suggest that EGCG may have a positive impact on aging and neurodegenerative diseases to retard or perhaps even reverse the accelerated rate of neuronal degeneration.
Loaded dopamine is preferentially stored in the halo portion of PC12 cell dense core vesicles
Authors: Sombers L. A. , Maxson M. M. , Ewing A. G. 
Published: June 2005

AbstractLarge dense core vesicles in rat pheochromocytoma cells are morphologically distinct from dense core vesicles in mast and chromaffin cells in that the dense core occupies a much smaller fraction of the vesicular volume, allowing for a much larger vesicular clear space, or halo. In this work, we present evidence indicating that upon treatment with L‐DOPA the majority of the dopamine loaded into these vesicles is preferentially compartmentalized into the halo portion of the vesicle. Amperometry was used to monitor release of loaded neurotransmitter from cells in both isotonic and hypertonic extracellular conditions, with the latter condition causing inhibition of dense core dissociation. In combination with this we have used transmission electron microscopy to determine the morphological characteristics of dense core vesicles before and after treatment with L‐DOPA in solutions of varied osmolarity. The results provide a more complete understanding of the complex interaction of molecules within dense core vesicles, suggesting that newly loaded dopamine is located in the halo of the vesicle. This finding has fundamental significance for studies of neurotransmitter release from dense core vesicles, as the core appears to have a function involving more than simple storage of neurotransmitter and associated molecules, and the often overlooked vesicular halo appears to be an important storage compartment for neurotransmitter.
Mild prenatal protein malnutrition increases α2C‐adrenoceptor density in the cerebral cortex during postnatal life and impairs neocortical long‐term potentiation and visuo‐spatial performance in rats
Authors: Soto‐Moyano Rubén , Valladares Luis , Sierralta Walter , Pérez Hernán , Mondaca Mauricio , Fernández Victor , Burgos Héctor , Hernández Alejandro 
Published: June 2005

AbstractMild reduction in the protein content of the mother's diet from 25 to 8% casein, calorically compensated by carbohydrates, does not alter body and brain weights of rat pups at birth, but leads to significant enhancements in the concentration and release of cortical noradrenaline during early postnatal life. Since central noradrenaline and some of its receptors are critically involved in long‐term potentiation (LTP) and memory formation, this study evaluated the effect of mild prenatal protein malnutrition on the α2C‐adrenoceptor density in the frontal and occipital cortices, induction of LTP in the same cortical regions and the visuo‐spatial memory. Pups born from rats fed a 25% casein diet throughout pregnancy served as controls. At day 8 of postnatal age, prenatally malnourished rats showed a threefold increase in neocortical α2C‐adrenoceptor density. At 60 days‐of‐age, α2C‐adrenoceptor density was still elevated in the neocortex, and the animals were unable to maintain neocortical LTP and presented lower visuo‐spatial memory performance. Results suggest that overexpression of neocortical α2C‐adrenoceptors during postnatal life, subsequent to mild prenatal protein malnutrition, could functionally affect the synaptic networks subserving neocortical LTP and visuo‐spatial memory formation.
Hyposmolarity‐induced ErbB4 phosphorylation and its influence on the non‐receptor tyrosine kinase network response in cultured cerebellar granule neurons
Authors: Lezama Ruth , Ortega Arturo , Ordaz Benito , Pasantes‐Morales Herminia 
Published: June 2005

AbstractExposure of cultured cerebellar granule neurons (24 h serum‐starved) during 3 min to 30% hyposmotic medium activated the tyrosine kinase receptor ErbB4 in the absence of its ligand. Hyposmolarity also activated the non‐receptor tyrosine kinases, Src, focal adhesion kinase (FAK), extracellular signal‐regulated protein kinase (ERK)1/2, and the tyrosine kinase target phosphatidyl‐inositol‐3‐kinase (PI3K). The hyposmotic‐induced activation of these kinases required the prior phosphorylation of ErbB4 as shown by the effect of ErbB4 blockade with AG213 reducing by 85–95% the phosphorylation of FAK and ERK1/2, by 74% and 36% that of PI3K and Src, respectively. These results suggest a key role of ErbB4 as a signal integrator of events associated with hyposmolarity. PI3K seems to be an important connecting element in the signaling network evoked by the hyposmolarity/ErbB4 activation as: (i) the p85 regulatory subunit of PI3K co‐immunoprecipitates with ErbB4 and with FAK; (ii) PI3K blockade with wortmannin reduced the hyposmotic activation of FAK (90%) and ERK1/2 (84–91%). Inhibition of Src with PP2 reduced ErbB4 phosphorylation and inhibited the subsequent cytosolic kinase activation with the same potency as ErbB4 blockade. These results point to Src and ErbB4 and as early targets of the hyposmotic stimulus and osmosignaling. The functional significance for cell volume regulation of the ErbB4‐Src‐PI3K signaling cascade is indicated by the 48–66% decrease of the hyposmotic taurine efflux observed by inhibition of these kinases.
Mitochondrial membrane depolarization and the selective death of dopaminergic neurons by rotenone: protective effect of coenzyme Q10
Authors: Moon Younghye , Lee Kun Ho , Park June‐Hee , Geum Dongho , Kim Kyungjin 
Published: June 2005

AbstractChronic exposure to the pesticide rotenone induces a selective degeneration of nigrostriatal dopaminergic neurons and reproduces the features of Parkinson's disease in experimental animals. This action is thought to be relevant to its inhibition of the mitochondrial complex I, but the precise mechanism of this suppression in selective neuronal death is still elusive. Here we investigate the mechanism of dopaminergic neuronal death mediated by rotenone in primary rat mesencephalic neurons. Low concentrations of rotenone (5–10 nm) induce the selective death of dopaminergic neurons without significant toxic effects on other mesencephalic cells. This cell death was coincident with apoptotic events including capsase‐3 activation, DNA fragmentation, and mitochondrial membrane depolarization. Pretreatment with coenzyme Q10, the electron transporter in the mitochondrial respiratory chain, remarkably reduced apoptosis as well as the mitochondrial depolarization induced by rotenone, but other free radical scavengers such as N‐acetylcysteine, glutathione, and vitamin C did not. Furthermore, the selective neurotoxicity of rotenone was mimicked by the mitochondrial protonophore carbonyl cyanide 4‐(trifluoromethoxy) phenylhydrazone (FCCP), a cyanide analog that effectively collapses a mitochondrial membrane potential. These data suggest that mitochondrial depolarization may play a crucial role in rotenone‐induced selective apoptosis in rat primary dopaminergic neurons.