bluuebunny/crossref_metadata_2025_split huggingface dataset:
‘Weak‐Center’ Gentrification and the Contradictions of Containment: Deconcentrating Poverty in Downtown Los Angeles
Authors: REESE ELLEN , DEVERTEUIL GEOFFREY , THACH LEANNE 
Published: April 2010

AbstractThis case study of recent efforts to deconcentrate poverty within the Skid Row area of Los Angeles examines processes of ‘weak‐center’ gentrification as it applies to a ‘service dependent ghetto,’ thus filling two key gaps in prior scholarship. We document the collaboration between the government, business and development interests, and certain non‐profit agencies in this process and identify two key mechanisms of poverty deconcentration: housing/service displacement and the criminalization of low income residents. Following Harvey, we argue that these efforts are driven by pressures to find a ‘spatial fix’ for capital accumulation through Downtown redevelopment. This process has been hotly contested, however, illustrating the strength of counter‐pressures to gentrification/poverty deconcentration within ‘weak‐center’ urban areas.Résumé Cette étude de cas porte sur les efforts entrepris récemment pour déconcentrer la pauvreté dans le quartier de Skid Row à Los Angeles. Elle examine les processus de gentrification d'un ‘centre faible’ lorsqu'ils s'appliquent à un ‘ghetto de populations dépendantes de services’, et comble ainsi deux grandes lacunes des recherches antérieures. Elle montre comment les intérêts du gouvernement, des entreprises et de l'urbanisme se joignent à certains organismes non lucratifs impliqués dans le processus. De plus, elle identifie deux mécanismes clés de la déconcentration de la pauvreté: le déplacement des logements et/ou services, et la criminalisation des habitants à faible revenu. Dans le sillage de Harvey, l'étude préconise que les efforts entrepris sont suscités par des pressions visant à trouver une ‘solution spatiale’à l'accumulation de capital en réaménageant le centre‐ville. Toutefois, cette démarche a été vivement contestée, illustrant ainsi la vigueur de la résistance à l'encontre de la gentrification et de la déconcentration de la pauvreté dans le cadre d'un modèle urbain à‘centre faible’.
High frequency, diversity and severity of skin diseases in a paediatric emergency department
Authors: Kramkimel N , Soussan V , Beauchet A , Duhamel A , Saiag P , Chevallier B , Mahé E 
Published: April 2010

AbstractBackground  Skin disorders are a major concern in the Paediatric Emergency Department (PED). We provide an accurate evaluation of the incidence, characteristics and severity of skin disorders seen in our PED over a 1‐year period.Methods  A total of 20 652 children’s medical notes were reviewed in a single centre, retrospective study in the PED of a University Hospital over a 1‐year period. The dermatological disorders were analysed on the basis of different criteria including their incidence, patient age, sex ratio, diagnosis, seasonal variations and hospitalization rates.Results  A total of 1897 (9.2%, F/M: 1.2; mean age: 4.1 ± 3.6 years) children presented with 1999 skin diseases and 69 different diagnoses. This frequency increased in the summer months (more than 14% of all patients). A total of 46.5% of diseases were infectious in nature (27.6% viral and 14.4% bacterial), inflammatory diseases accounted for 26.2% (urticaria and angio‐oedema 15.9%, atopic dermatitis 3.5%, Henoch‐Schönlein purpura: 2.1%), non‐specific focal disease (balanitis, vulvitis, etc.) and insect bites, burns, transient diseases of the newborn and drug reactions for 9.2%, 7.8%, 6.4%, 3.7% and 1.2% respectively. More than 90% of children presented at the hospital for an acute condition and 155 (8.2% of children with skin disorders; F/M: 0.9; age: 4.0 ± 4.0 years) were hospitalized. More than 90% of hospitalizations were for infectious and inflammatory diseases.Conclusion  Our data reveal the extremely high frequency, diversity and potential severity of paediatric emergency skin disorders. Specific educational measures and closer co‐operation between Dermatologists and Paediatricians are essential if the skin care dispensed to children and teenagers is to be improved.
Calcium channels in photosynthetic eukaryotes: implications for evolution of calcium‐based signalling
Authors: Verret Frédéric , Wheeler Glen , Taylor Alison R. , Farnham Garry , Brownlee Colin 
Published: May 2010

SummaryMuch of our current knowledge on the mechanisms by which Ca2+ signals are generated in photosynthetic eukaryotes comes from studies of a relatively small number of model species, particularly green plants and algae, revealing some common features and notable differences between ‘plant’ and ‘animal’ systems. Physiological studies from a broad range of algal cell types have revealed the occurrence of animal‐like signalling properties, including fast action potentials and fast propagating cytosolic Ca2+ waves. Genomic studies are beginning to reveal the widespread occurrence of conserved channel types likely to be involved in Ca2+ signalling. However, certain widespread ‘ancient’ channel types appear to have been lost by certain groups, such as the embryophytes. More recent channel gene loss is also evident from comparisons of more closely related algal species. The underlying processes that have given rise to the current distributions of Ca2+ channel types include widespread retention of ancient Ca2+ channel genes, horizontal gene transfer (including symbiotic gene transfer and acquisition of bacterial genes), gene loss and gene expansion within taxa. The assessment of the roles of Ca2+ channel genes in diverse physiological, developmental and life history processes represents a major challenge for future studies.

Contents

Summary
23

I.
Introduction
24

II.
Physiological features of Ca2+ channel activity ineukaryotic photoautotrophs
25

III.
Expansion, loss and horizontal gene transfer of Ca2+‐permeable channels in photoautotrophs
28

IV.
Conclusions
36

Acknowledgements
37

References
37
Visual field function in school‐aged children with spastic unilateral cerebral palsy related to different patterns of brain damage
Authors: JACOBSON LENA , RYDBERG AGNETA , ELIASSON ANN‐CHRISTIN , KITS ANNIKA , FLODMARK OLOF 
Published: May 2010

Aim  To relate visual field function to brain morphology in children with unilateral cerebral palsy (CP).Method  Visual field function was assessed using the confrontation technique and Goldmann perimetry in 29 children (15 males, 14 females; age range 7–17y, median age 11y) with unilateral CP classified at Gross Motor Function Classification System (GMFCS) level I and Manual Ability Classification System levels I to III. The type and extent of brain lesions were determined using cerebral imaging.Results  Eighteen children had subnormal visual field function. The visual fields were severely restricted in six. The underlying brain lesions were malformation (n=7), white matter damage of immaturity (WMDI; n=13), and cortical–subcortical lesions (n=9). Visual field function could be correlated with the pattern of brain damage in children with cortical–subcortical lesions or extensive lesions caused by malformation or WMDI. Total homonymous hemianopia was common in the cortical–subcortical group but rare in children with malformation or WMDI. Five children had normal visual field function despite having malformation or WMDI involving parts of the brain usually encompassing the visual system.Interpretation  Visual field function may be preserved by plasticity of the immature brain in children with malformation and WMDI. Severely restricted visual fields were more often associated with lesions occurring later in the developing brain. All children with severely restricted visual fields were identified by the confrontation technique. Goldmann perimetry was a suitable method to identify relative visual field defects.
Functioning and health‐related quality of life of adolescents with cerebral palsy: self versus parent perspectives
Authors: GATES PHILIP , OTSUKA NORMAN , SANDERS JAMES , MCGEE‐BROWN JEANIE 
Published: May 2010

Aim  To determine whether there is a difference between perspectives of functioning and health‐related quality of life (HRQL) of parents and ambulatory adolescents with spastic cerebral palsy (CP).Method A total of 139 parent patient pairs (73 females, 66 males; median age 14y 6mo, age range 11–18y, Gross Motor Function Classification System [GMFCS] levels I–III, with hemiplegia [n=23], diplegia [n=103], triplegia [n=9], and quadriplegia [n=4]) were recruited from outpatient CP clinics at three pediatric orthopaedic hospitals, between 2000 and 2006, from whom Pediatric Outcomes Data Collection Instrument (PODCI) responses were collected.Results Cross‐sectional data, calculated with intraclass correlation coefficients [ICC], showed parents and adolescents agreed more on functioning (ICC=0.488–0.748) than HRQL (ICC=0.242–0.568; PODCI). Parents and adolescents both recognized significant comorbidities (ICC=0.502–0.713), but adolescents saw themselves as less limited (ICC=0.330) than parents. The greatest differences between parents and adolescents were in HRQL scales for male adolescents, with only a small part explained by GMFCS level difference between sexes (effect size 0.002–0.143). Age, parent well‐being, and parent sex had little effect and comorbidities had no effect. GMFCS level was the most common predictor.Interpretation Most scales on health conditions, function, and HRQL agreed between parents and adolescents aged11 to 18 years. Parent proxy is reasonable when necessary, but assessing both parents and adolescents gives additional insight. Adolescents do not consider themselves as limited by health conditions as parents do; parents have greater satisfaction with current level of symptoms than adolescents, and findings vary on expectations for treatment.
Construct validity of the Infant Motor Profile: relation with prenatal, perinatal, and neonatal risk factors
Authors: HEINEMAN KIRSTEN R , LA BASTIDE‐VAN GEMERT SACHA , FIDLER VACLAV , MIDDELBURG KARIN J , BOS AREND F , HADDERS‐ALGRA MIJNA 
Published: May 2010

Aim  The Infant Motor Profile (IMP) is a qualitative assessment of motor behaviour of infants aged 3 to 18 months. The aim of this study was to investigate construct validity of the IMP through the relation of IMP scores with prenatal, perinatal, and neonatal variables, including the presence of brain pathology indicated by neonatal ultrasound imaging of the brain.Method  A longitudinal prospective study was performed in a group of 30 term infants (12 females, 18 males; median gestational age 40.1wks, range 37.6–42wks) and 59 preterm infants (25 females, 34 males; median gestational age 29.7wks, range 25–34.7wks). IMP assessments were performed at (corrected) ages of 4, 6, 10, 12, and 18 months. Socio‐economic and perinatal data were collected, which, in the case of preterm infants, included information on periventricular leukomalacia and intraventricular haemorrhage based on neonatal cranial ultrasound. Data were analysed by fitting mixed‐effects models.Results  Gestational age, socio‐economic status, and 5‐minute Apgar scores were significant determinants of IMP scores in the total group of infants (p<0.001, <0.002, and <0.042 respectively). In the subgroup of preterm infants, IMP scores were significantly affected by brain lesions on neonatal ultrasound (p<0.001) and by socio‐economic status (p=0.001).Interpretation  The findings support the construct validity of the IMP: IMP scores are clearly associated with relevant determinants of neuromotor function.
Neuroimaging in childhood arterial ischaemic stroke: evaluation of imaging modalities and aetiologies
Authors: BUERKI SARAH , ROELLIN KATJA , REMONDA LUCA , MERCATI DANIELLE GUBSER , JEANNET PIERRE‐YVES , KELLER ELMAR , LUETSCHG JUERG , MENACHE CAROLINE , RAMELLI GIAN PAOLO , SCHMITT‐MECHELKE THOMAS , WEISSERT MARKUS , BOLTSHAUSER EUGEN , STEINLIN MAJA 
Published: May 2010

Aim  The aim of this study was to describe neuroimaging patterns associated with arterial ischaemic stroke (AIS) in childhood and to differentiate them according to stroke aetiology.Method  Clinical and neuroimaging (acute and follow‐up) findings were analysed prospectively in 79 children (48 males, 31 females) aged 2 months to 15 years 8 months (median 5y 3mo) at the time of stroke by the Swiss Neuropaediatric Stroke Registry from 2000 to 2006.Results  Stroke was confirmed in the acute period in 36 out of 41 children who underwent computed tomography, in 53 of 57 who underwent T2‐weighted magnetic resonance imaging (MRI) and in all 48 children who underwent diffusion‐weighted MRI. AIS occurred in the anterior cerebral artery (ACA) in 63 participants and in all cases was associated with lesions of the middle cerebral artery (MCA). The lesion was cortical–subcortical in 30 out of 63 children, cortical in 25 out of 63, and subcortical in 8 of 63 children. Among participants with AIS in the posterior circulation territory, the stroke was cortical–subcortical in 8 out of 16, cortical in 5 of 16, and thalamic in 3 out of 16 children.Interpretation  AIS mainly involves the anterior circulation territory, with both the ACA and the MCA being affected. The classification of Ganesan is an appropriate population‐based classification for our Swiss cohort, but the neuroimaging pattern alone is insufficient to determine the aetiology of stroke in a paediatric population. The results show a poor correlation between lesion pattern and aetiology.
Effects of social responsibility labelling and brand on willingness to pay for apparel
Authors: Hustvedt Gwendolyn , Bernard John C. 
Published: April 2010

AbstractThis study examined changes in consumer willingness to pay (WTP) for apparel products as labour‐related information and brand were added. Tobit analysis of auction bids from 121 university students for t‐shirts showed men, Hispanics and consumers who believe in social responsibility and fair trade had significantly higher WTP once labour‐related labelling was added. The amount and complexity of information did not matter, leaving substantial leeway to companies in crafting their message. Adding brand significantly increased WTP for two better‐known brands while not changing WTP for the social responsibility messages. Results suggested brands can benefit from stressing social responsibility‐related attributes of products.
Differential expression patterns of Puma and Hsp70 following proteasomal stress in the hippocampus are key determinants of neuronal vulnerability
Authors: Bonner Helena P. , Concannon Caoimhín G. , Bonner Caroline , Woods Ina , Ward Manus W. , Prehn Jochen H. M. 
Published: May 2010

J. Neurochem. (2010) 114, 606–616.AbstractProteasomal stress is believed to contribute to the pathology of ischemic brain injury and several neurodegenerative disorders, but can activate both cytoprotective and cell death‐inducing pathways. Here we have utilized the complex environment of organotypic hippocampal slice cultures (OHSCs) to investigate the stress responses activated in different neuronal populations following proteasome inhibition. Incubation of OHSCs with the specific proteasome inhibitors, epoxomicin or bortezomib led to a selective injury of the CA1 pyramidal neurons although similarly increased levels of poly‐ubiquitinylated proteins were detected throughout all regions of the hippocampus. Micro‐dissection, quantitative PCR and immunohistochemical analyses of epoxomicin‐treated OHSCs identified a selective activation of cytoprotective genes in non‐vulnerable regions, and a selective activation of p53 target genes within the CA1. Genetic deletion of the pro‐apoptotic p53 target gene, p53‐upregulated modulator of apoptosis (puma), significantly reduced injury within the CA1 following proteasomal inhibition. Activation of cytoprotective genes by treatment with inducers of heat shock protein 70 inhibited the selective activation of p53 signaling within the CA1 and protected CA1 neurons from epoxomicin‐induced cell death. In summary, we demonstrate that the reciprocal activation of p53/p53‐upregulated modulator of apoptosis and heat shock protein 70 signalling determines the selective vulnerability of neurons to proteasome inhibition.
Dopamine D2receptor signaling modulates mutant ataxin‐1 S776 phosphorylation and aggregation
Authors: Hearst Scoty M. , Lopez Mariper E. , Shao Qingmei , Liu Yong , Vig Parminder J. S. 
Published: May 2010

J. Neurochem.(2010)114, 706–716.AbstractSpinocerebellar ataxia 1 (SCA1) is a dominantly inherited neurodegenerative disease associated with progressive ataxia resulting from the loss of cerebellar Purkinje cells (PCs) and neurons in the brainstem. In PCs of SCA1 transgenic mice, the disease causing ataxin‐1 protein mediates the formation of S100B containing cytoplasmic vacuoles and further self‐aggregates to form intranuclear inclusions. The exact function of the ataxin‐1 protein is not fully understood. However, the aggregation and neurotoxicity of the mutant ataxin‐1 protein is dependent on the phosphorylation at serine 776 (S776). Although protein kinase A (PKA) has been implicated as the S776 kinase, the mechanism of PKA/ataxin‐1 regulation in SCA1 is still not clear. We propose that a dopamine D2receptor (D2R)/S100B pathway may be involved in modulating PKA activity in PCs. Using a D2R/S100B HEK stable cell line transiently transfected with GFP‐ataxin‐1[82Q], we demonstrate that stimulation of the D2R/S100B pathway caused a reduction in mutant ataxin‐1 S776 phosphorylation and ataxin‐1 aggregation. Activation of PKA by forskolin resulted in an enhanced S776 phosphorylation and increased ataxin‐1 nuclear aggregation, which was suppressed by treatment with D2R agonist bromocriptine and PKA inhibitor H89. Furthermore, treating SCA1 transgenic PC slice cultures with forskolin induced neurodegenerative morphological abnormalities in PC dendrites consistent with those observedin vivo. Taken together our data support a mechanism where PKA dependent mutant ataxin‐1 phosphorylation and aggregation can be regulated by D2R/S100B signaling.
Storage of GABA in chromaffin granules and not in synaptic‐like microvesicles in rat adrenal medullary cells
Authors: Harada Keita , Matsuoka Hidetada , Nakamura Jun , Fukuda Mitsunori , Inoue Masumi 
Published: May 2010

J. Neurochem. (2010) 114, 617–626.AbstractNeurons and certain kinds of endocrine cells, such as adrenal medullary (AM) cells, have large dense‐core vesicles (LDCVs) and synaptic vesicles or synaptic‐like microvesicles (SLMVs). These secretory vesicles differ in Ca2+ sensitivity and contain different signaling substances. We have recently reported that GABA functions as a paracrine factor in rat AM cells and modulates catecholamine secretion. The present experiment was undertaken to examine the subcellular localization of the GABA system including GABA itself in AM cells. Fractionation analysis with sucrose density gradient and immunocytochemistry indicated that vesicular GABA transporter (VGAT) was localized in LDCVs and not SLMVs in rat and bovine AM cells. In addition, significant amounts of GABA were detected in high density fractions, which contained LDCVs. When green fluorescence protein‐VGAT and green fluorescence protein‐vesicular ACh transporter were exogenously expressed in PC12 cells, the former and the latter were selectively targeted to LDCVs and SLMVs, respectively. We conclude that GABA is stored in chromaffin granules in rat and bovine AM cells through VGAT.
Age‐dependent cardiomyopathy in mitochondrial mutator mice is attenuated by overexpression of catalase targeted to mitochondria
Authors: Dai Dao‐Fu , Chen Tony , Wanagat Jonathan , Laflamme Michael , Marcinek David J. , Emond Mary J , Ngo Calvin P. , Prolla Tomas A. , Rabinovitch Peter S. 
Published: April 2010

SummaryMitochondrial defects have been found in aging and several age‐related diseases. Mice with a homozygous mutation in the exonuclease encoding domain of mitochondrial DNA polymerase gamma (Polgm/m) are prone to age‐dependent accumulation of mitochondrial DNA mutations and have shown a broad spectrum of aging‐like phenotypes. However, the mechanism of cardiac phenotypes in relation to the role of mitochondrial DNA mutations and oxidative stress in this mouse model has not been fully addressed. We demonstrate age‐dependent cardiomyopathy in Polgm/m mice, which by 13–14 months of age displays marked cardiac hypertrophy and dilatation, impairment of systolic and diastolic function, and increased cardiac fibrosis. This age‐dependent cardiomyopathy is associated with increases in mitochondrial DNA (mtDNA) deletions and protein oxidative damage, increased expression of apoptotic and senescence markers, as well as a decline in signaling for mitochondrial biogenesis. The relationship of these changes to mitochondrial reactive oxygen species (ROS) was tested by crossing Polgm/m mice with mice that overexpress mitochondrial targeted catalase (mCAT). All of the above phenotypes were partially rescued in Polgm/m/mCAT mice. These data indicate that accumulation of mitochondrial DNA damage with age can lead to cardiomyopathy and that this phenotype is partly mediated by mitochondrial oxidative stress.
Sustainable Rural Telehealth Innovation: A Public Health Case Study
Authors: Singh Rajendra , Mathiassen Lars , Stachura Max E. , Astapova Elena V. 
Published: May 2010

Objective.To examine adoption of telehealth in a rural public health district and to explain how the innovation became sustainable.Study Setting.Longitudinal, qualitative study (1988–2008) of the largest public health district in Georgia.Study Design.Case study design provided deep insights into the innovation's social dynamics. Punctuated equilibrium theory helped present and make sense of the process. We identified antecedent conditions and outcomes, and we distinguished between episodes and encounters based on the disruptive effects of events.Data Collection.Twenty‐five semistructured interviews with 19 decision makers and professionals, direct observations, published papers, grant proposals, technical specifications, and other written materials.Principal Findings.Strong collaboration within the district, with local community, and with external partners energized the process. Well‐functioning outreach clinics made telehealth desirable. Local champions cultivated participation and generative capability, and overcame barriers through opportunistic exploitation of technological and financial options. Telehealth usage fluctuated between medical and administrative operations in response to internal needs and contextual dynamics. External agencies provided initial funding and supported later expansion.Conclusions.Extensive internal and external collaboration, and a combination of technology push and opportunistic exploitation, can enable sustainable rural telehealth innovation.