bluuebunny/crossref_metadata_2025_split huggingface dataset:
Adipose tissue at entheses: the innervation and cell composition of the retromalleolar fat pad associated with the rat Achilles tendon
Authors: Shaw H. M. , Santer R. M. , Watson A. H. D. , Benjamin M. 
Published: August 2007

AbstractThis study set out to determine whether the fat pad at the attachment of the Achilles tendon has features enabling it to function as an immune organ and a mechanosensory device, and to be a source of pain in insertional tendon injuries. Sections for histology and immunohistochemistry were cut from the Achilles tendon enthesis organ of 1 day old, 1 month, 4 month and 24 month old rats. For fluorescence and peroxidase immunohistochemistry, cryosections were labelled with primary antibodies directed against PGP9.5, substance P, neurofilament 200, calcitonin gene related peptide, CD68, CD36, myeloid related protein 14, actin and vinculin. The fat pad contained not only adipocytes, but also fibrous tissue, mast cells, macrophages, fibroblasts and occasional fibrocartilage cells. It was richly innervated with nerve fibres, some of which were likely to be nociceptive, and others mechanoreceptive (myelinated fibres, immunoreactive for neurofilament 200). The fibres lay between individual fat cells and in association with blood vessels. In marked contrast, the enthesis itself and all other components of the enthesis organ were aneural at all ages. The presence of putative mechanoreceptive and nociceptive nerve endings between individual fat cells supports the hypothesis that the fat pad has a proprioceptive role monitoring changes in the insertional angle of the Achilles tendon and that it may be a source of pain in tendon injuries. The abundance of macrophages suggests that the adipose tissue could have a role in combating infection and/or removing debris from the retrocalcaneal bursa.
Depressive symptoms among rural Bangladeshi mothers: implications for infant development
Authors: Black Maureen M. , Baqui Abdullah H. , Zaman K. , McNary Scot W. , Le Katherine , Arifeen Shams El , Hamadani Jena D. , Parveen Monowara , Yunus Md. , Black Robert E. 
Published: August 2007

Objective:  To examine how maternal depressive symptoms are related to infant development among low‐income infants in rural Bangladesh and to examine how the relationship is affected by maternal perceptions of infant irritability and observations of caregiving practices.Methods:  Development was measured among 221 infants at 6 and 12 months with the Bayley Scales II. Mothers reported on their depressive symptoms and on perceptions of their infant's temperament, and a home visit was made to complete the HOME Inventory.Results:  Half (52%) the mothers reported depressive symptoms. In bivariate analyses, maternal depressive symptoms were related to low scores on the Bayley Scales. Infants whose mothers reported depressive symptoms and perceived their infants to be irritable acquired fewer cognitive, motor, and Orientation/Engagement skills between 6–12 months than infants whose mothers reported neither or only one condition. The relationship linking maternal depressive symptoms and perceived infant irritability with infant cognitive skills was partially mediated by parental responsiveness and opportunities for play in the home.Conclusions:  The intergenerational risks of maternal depressive symptoms on infant development extend to rural Bangladesh and are accentuated when mothers perceive their infants as irritable. Mothers who report depressive symptoms and infant irritability may lack the capacity to provide responsive, developmentally‐oriented caregiving environments.
Predicting the impact of changing CO2 on crop yields: some thoughts on food
Authors: Ziska Lewis H. , Bunce James A. 
Published: August 2007

SummaryRecent breakthroughs in CO2 fumigation methods using free‐air CO2 enrichment (FACE) technology have prompted comparisons between FACE experiments and ‘enclosure studies’ with respect to quantification of the effects of projected atmospheric CO2 concentrations on crop yields. On the basis of one such comparison, it was argued that model projections of future food supply (some of which are based on older enclosure data) may have significantly overestimated the positive effect of elevated CO2 concentration on crop yields and, by extension, food security. However, in the comparison, no effort was made to differentiate ‘enclosure study’ methodologies with respect to maintaining projected CO2 concentration or to consider other climatic changes (e.g. warming) that could impact crop yields. In this review, we demonstrate that relative yield stimulations in response to future CO2 concentrations obtained using a number of enclosure methodologies are quantitatively consistent with FACE results for three crops of global importance: rice (Oryza sativa), soybean (Glycine max) and wheat (Triticum aestivum). We suggest, that instead of focusing on methodological disparities per se, improved projections of future food supply could be achieved by better characterization of the biotic/abiotic uncertainties associated with projected changes in CO2 and climate and incorporation of these uncertainties into current crop models.

Contents

Summary
607

I.
Rising CO2 and agricultural crop yields
608

II.
Expanding methodologies
608

III.
Which methodology gives the ‘truest’ prediction   of future yields?
608

IV.
Comparing responses among methodologies
610

V.
Methodology vs future uncertainty
611

VI.
Abiotic uncertainties
612

VII.
Biotic uncertainties
613

VIII.
Uncertainty vs methodology
614

IX.
Modelers and experimentalists
614

X.
Final thoughts
615

Acknowledgements
615

References
615
Understanding the relationship between holiday taking and self‐assessed health: an exploratory study of senior tourism
Authors: Hunter‐Jones Philippa , Blackburn Adele 
Published: August 2007

AbstractThe senior market is particularly attractive to the tourism industry. Alongside evidence of a growing propensity to travel and spend, consumption is often deliberately linked to low seasons, balancing out the peaks and valleys for tourism suppliers. Health is one variable which is particularly significant to this consumer. Personal health influences all patterns of consumer behaviour regardless of age, although the full extent to which this models senior tourism activity is unclear. An exploratory qualitative study was undertaken in the spring of 2005, with 22 senior consumers (aged 55 years plus) interviewed. Utilizing the earlier work by Zimmer et al.into self‐assessed health as a framework, travel propensity, the perceived effects of travel and factors inhibiting full participation were questioned. Conclusions drawn outline both a senior tourism typology and areas for future research. Notably the relationship between caregiving and tourism consumption is singled out for further investigation.
Exploring word‐of‐mouth influences on travel decisions: friends and relatives vs. other travellers
Authors: Murphy Laurie , Mascardo Gianna , Benckendorff Pierre 
Published: August 2007

AbstractTravel research consistently shows the importance of word‐of‐mouth (WOM) information sources in the travel decision‐making process. Friends and relatives have been identified as organic image‐formation agents, and it has been emphasized that this WOM information is one of the most relied‐upon sources of information for destination selection. While there has been recognition of the importance of WOM information sources on consumer behaviour in tourism, little has been performed to understand more specifically how and what behaviour is influenced. This study examined the differing influences of friends and relatives vs. other travellers on the travel choices and behaviours of 412 visitors to the North Queensland Region in Australia. More specifically, the present study compared the following four groups of respondents: those who indicated that they obtained travel information from friends/relatives and other travellers (n = 70); those who obtained information from friends/relatives only (n = 121); those who obtained information from other travellers only (n = 105); and those who obtained information from neither (i.e. no WOM) (n = 116). The results indicated that there were significant differences across the four groups with respect to demographic characteristics, other information sources used, accommodation and transportation used, and travel activities in the destination. However, the groups did not differ in their image of the destination.
Information sources used by older adults for decision making about tourist and travel destinations
Authors: Patterson Ian 
Published: August 2007

AbstractOver the past decade, the older market has emerged as an extremely important one because of its increased purchasing power for most consumer goods and services. The tourism and leisure industry is also targeting people aged 65 years and older, because many possess a relatively large share of discretionary money that they want to spend on travel. This has resulted in increasing attention by the mass media and the advertising industry in particular. This paper discusses the main types of information sources that are used by older adults when they make decisions about tourist and travel destinations, and particularly focuses on the importance of word‐of‐mouth sources and personal experiences. It also explores the influence of the mass media on trip decision making for older adults, and discusses the importance of brochures, magazines and television as information sources for older adults. Finally, it critiques the lack of senior models in advertising campaigns for travel products that are aimed at the older market.
β2‐ and β3‐Adrenoceptors activate glucose uptake in chick astrocytes by distinct mechanisms: a mechanism for memory enhancement?
Authors: Hutchinson Dana S. , Summers Roger J. , Gibbs Marie E. 
Published: August 2007

AbstractIsoprenaline, acting at β‐adrenoceptors (ARs), enhances memory formation in single trial discriminated avoidance learning in day‐old chicks by mechanisms involving alterations in glucose and glycogen metabolism. Earlier studies of memory consolidation in chicks indicated that β3‐ARs enhanced memory by increasing glucose uptake, whereas β2‐ARs enhance memory by increasing glycogenolysis. This study examines the ability of β‐ARs to increase glucose uptake in chick forebrain astrocytes. The β‐AR agonist isoprenaline increased glucose uptake in a concentration‐dependent manner, as did insulin. Glucose uptake was increased by the β2‐AR agonist zinterol and the β3‐AR agonist CL316243, but not by the β1‐AR agonist RO363. In chick astrocytes, reverse transcription‐polymerase chain reaction studies showed that β1‐, β2‐, and β3‐AR mRNA were present, whereas radioligand‐binding studies showed the presence of only β2‐ and β3‐ARs. β‐AR or insulin‐mediated glucose uptake was inhibited by phosphatidylinositol‐3 kinase and protein kinase C inhibitors, suggesting a possible interaction between the β‐AR and insulin pathways. However β2‐ and β3‐ARs increase glucose uptake by two different mechanisms: β2‐ARs via a Gs‐cAMP‐protein kinase A‐dependent pathway, while β3‐ARs via interactions with Gi. These results indicate that activation of β2‐ and β3‐ARs causes glucose uptake in chick astrocytes by distinct mechanisms, which may be relevant for memory enhancement.
Canine distemper virus infection of primary hippocampal cells induces increase in extracellular glutamate and neurodegeneration
Authors: Brunner Jean‐Marc , Plattet Philippe , Majcherczyk Paul , Zurbriggen Andreas , Wittek Riccardo , Hirling Harald 
Published: August 2007

AbstractThe canine distemper virus (CDV) belongs to the Morbillivirus genus which includes important human pathogens like the closely related measles virus. CDV infection can reach the nervous system where it causes serious malfunctions. Although this pathology is well described, the molecular events in brain infection are still poorly understood. Here we studied infection in vitro by CDV using a model of dissociated cell cultures from newborn rat hippocampus. We used a recombinant CDV closely related to the neurovirulent A75/17 which also expresses the enhanced green fluorescent protein. We found that infected neurons and astrocytes could be clearly detected, and that infection spreads only slowly to neighboring cells. Interestingly, this infection causes a massive cell death of neurons, which includes also non‐infected neurons. Antagonists of NMDA‐type or alpha‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propinate (AMPA)‐type glutamate receptors could slow down this neuron loss, indicating an involvement of the glutamatergic system in the induction of cell death in infected and non‐infected cells. Finally, we show that, following CDV infection, there is a steady increase in extracellular glutamate in infected cultures. These results indicate that CDV infection induces excitotoxic insults on neurons via glutamatergic signaling.
Inhibition of heat shock proteins (HSP) expression by quercetin and differential doxorubicin sensitization in neuroblastoma and Ewing’s sarcoma cell lines
Authors: Zanini Cristina , Giribaldi Giuliana , Mandili Giorgia , Carta Franco , Crescenzio Nicoletta , Bisaro Brigitte , Doria Alessandra , Foglia Luiselda , Di Montezemolo Luca Cordero , Timeus Fabio , Turrini Franco 
Published: August 2007

AbstractNeuroblastoma (NB) and Ewing’s sarcoma (ES) represent the most common extracranial solid tumors of childhood. Heat shock proteins (HSP) are elevated in cancer cells and their over‐expression was correlated to drug‐resistance. In this work we identified the HSP by a sensitive proteomic analysis of NB and ES cell lines, then, we studied the HSP response to doxorubicin. Some identified HSP were constitutively more expressed in NB than in ES cells. Doxorubicin‐stimulated HSP response only in NB cells. Quercetin was found to inhibit HSP expression depleting heat shock factor 1 (HSF1) cellular stores. Quercetin caused a higher anti‐proliferative effect in NB (IC50: 6.9 ± 5.8 μmol/L) than in ES cells (IC50: 85.5 ± 53.1 μmol/L). Moreover, quercetin caused a very pronounced doxorubicin sensitizing effect in NB cells (241 fold IC50 decrease) and a moderate effect in ES cells. HSP involvement in NB cells sensitization was confirmed by the silencing of HSF1. Quercetin treatment and HSF1 silencing increased the pro‐apoptotic effect of doxorubicin. In conclusion, the higher HSP levels, observed in NB cells, did not confer increased resistance to doxorubicin; on the contrary, HSP inhibition by quercetin or gene silencing caused higher sensitization to doxorubicin. These results may have a potential application in the treatment of NB.
Ethanol alters lipid profiles and phosphorylation status of AMP‐activated protein kinase in the neonatal mouse brain
Authors: Saito Mariko , Chakraborty Goutam , Mao Rui‐Fen , Wang Ray , Cooper Thomas B. , Vadasz Csaba , Saito Mitsuo 
Published: August 2007

AbstractPreviously, we have shown that ethanol‐induced apoptosis in cultured neurons is accompanied by changes in cellular lipid profiles. In the present study, the effects of ethanol on brain lipid metabolism were studied using 7‐day‐old C57BL/6ByJ mice, which display apoptotic neurodegeneration upon exposure to ethanol. The brain lipids were extracted 4–24 h after the ethanol or saline treatment, and analyzed by TLC. We found that the levels of triglyceride, cholesterol ester, ceramide, and N‐acylphosphatidylethanolamine increased significantly in the brains of ethanol‐treated mice compared to those of saline‐treated mice. Concomitantly, ethanol reduced Thr172 phosphorylation of AMP‐activated protein kinase (AMPK) α subunits. Ethanol also reduced phosphorylation of acetyl‐CoA carboxylase, a substrate of AMPK and a lipogenic enzyme known to be activated by dephosphorylation. In contrast, lipid profiles of 19‐day‐old mouse brains, which scarcely manifested neurodegeneration upon ethanol exposure, were not significantly affected by ethanol. Also, the basal levels of Thr172‐phosphorylated AMPK α were lower in these brains than in 7‐day‐old mouse brains, and no detectable changes in the phosphorylation status were observed by ethanol treatment. Our findings indicate that the ethanol‐induced apoptotic neurodegeneration observed in mice during restricted developmental periods is accompanied by alterations in both the lipid content and the activity of AMPK in the brain.
Cone arrestin binding to JNK3 and Mdm2: conformational preference and localization of interaction sites
Authors: Song Xiufeng , Gurevich Eugenia V. , Gurevich Vsevolod V. 
Published: August 2007

AbstractArrestins are multi‐functional regulators of G protein‐coupled receptors. Receptor‐bound arrestins interact with >30 remarkably diverse proteins and redirect the signaling to G protein‐independent pathways. The functions of free arrestins are poorly understood, and the interaction sites of the non‐receptor arrestin partners are largely unknown. In this study, we show that cone arrestin, the least studied member of the family, binds c‐Jun N‐terminal kinase (JNK3) and Mdm2 and regulates their subcellular distribution. Using arrestin mutants with increased or reduced structural flexibility, we demonstrate that arrestin in all conformations binds JNK3 comparably, whereas Mdm2 preferentially binds cone arrestin ‘frozen’ in the basal state. To localize the interaction sites, we expressed separate N‐ and C‐domains of cone and rod arrestins and found that individual domains bind JNK3 and remove it from the nucleus as efficiently as full‐length proteins. Thus, the arrestin binding site for JNK3 includes elements in both domains with the affinity of partial sites on individual domains sufficient for JNK3 relocalization. N‐domain of rod arrestin binds Mdm2, which localizes its main interaction site to this region. Comparable binding of JNK3 and Mdm2 to four arrestin subtypes allowed us to identify conserved residues likely involved in these interactions.
α2‐Adrenergic receptors activate cyclic AMP‐response element‐binding protein through arachidonic acid metabolism and protein kinase A in a subtype‐specific manner
Authors: Karkoulias Georgios , Mastrogianni Orthodoxia , Papathanasopoulos Panagiotis , Paris Hervé , Flordellis Christodoulos 
Published: August 2007

AbstractOn incubation with epinephrine, PC12 cells stably expressing α2‐adrenergic receptor (α2‐AR) undergo morphological and biochemical changes characteristic of neuron‐like differentiation. The present study shows that α2‐AR stimulation increases the phosphorylation of the transcription factor cAMP‐response element‐binding protein (CREB), the activity of a CRE‐reporter plasmid and the expression of cyclin D1 with subtype‐dependent efficiency (α2A ≈ α2C>> α2B). The effects of epinephrine were mimicked by cell exposure to forskolin or to exogenous arachidonic acid (AA) and they were abrogated by prior treatment with the inhibitor of phospholipase C (PLC) (U73122) or the inhibitor of cytochrome P450‐dependent epoxygenase, ketoconazole. On the other hand, treatment of the cells with epinephrine caused activation of protein kinase A (PKA), which was fully abolished by ketoconazole. Inhibition of PKA activity with H89 or ketoconazole abolished the effects of epinephrine on CREB, suggesting that activation of the cAMP/PKA pathway by AA epoxy‐derivatives is responsible for CREB activation by α2‐ARs. The effects of epinephrine were unaffected by LY294002. Furthermore, treatment with staurosporine, tyrphostin AG1478, PP1 or PD98059 did not change the extent of CREB phosphorylation but enhanced its transcriptional activity. Altogether, our results demonstrate that, in PC12 cells, the α2‐AR subtypes cause phosphorylation and activation of CREB through a pathway involving stimulation of PLC, AA release, generation of epoxygenase derivative and increase of PKA activity. They also suggest attenuation of CREB transcriptional activity by mitogen‐activated protein kinase, protein kinase C and Src kinases.
Isolation and characterization of microsatellite markers from the white‐ruffed manakin Corapipo altera (Aves, Pipridae)
Authors: BARNETT JACOB R. , STENZLER LAURA M. , RUIZ‐GUTIERREZ VIVIANA , BOGDANOWICZ STEVEN M. , LOVETTE IRBY J. 
Published: August 2007

AbstractWe describe 15 polymorphic microsatellite loci from the white‐ruffed manakin Corapipo altera, a common understory bird of Neotropical lowland and montane evergreen forests from eastern Honduras to northwestern Colombia. These markers were developed in order to assess population structure and genetic diversity in a fragmented landscape, and to study gene flow between forest fragments. Primers were tested on a population of 159 individuals from the Coto Brus region of southwestern Costa Rica. We found between four and 23 alleles per locus, and observed heterozygosities ranging from 0.23 to 0.93.
Lymphohematopoietic progenitors do not have a synchronized defect with age‐related thymic involution
Authors: Zhu Xike , Gui Jingang , Dohkan Junichi , Cheng Lili , Barnes Peter F. , Su Dong‐Ming 
Published: August 2007

SummaryIt has been speculated that aging lymphohematopoietic progenitor cells (LPC) including hematopoietic stem cells (HSC) and early T‐cell progenitors (ETP) have intrinsic defects that trigger age‐related thymic involution. However, using a different approach, we suggest that that is not the case. We provided a young thymic microenvironment to aged mice by transplanting a fetal thymus into the kidney capsule of aged animals, and demonstrated that old mouse‐derived LPCs could re‐establish normal thymic lymphopoiesis and all thymocyte subpopulations, including ETPs, double negative subsets, double positive, and CD4+ and CD8+ single positive T cells. LPCs derived from aged mice could turn over young RAG−/– thymic architecture by interactions, as well as elevate percentage of peripheral CD4+IL‐2+ T cells in response to costimulator in aged mice. Conversely, intrathymic injection of ETPs sorted from young animals into old mice did not restore normal thymic lymphopoiesis, implying that a shortage and/or defect of ETPs in aged thymus do not account for age‐related thymic involution. Together, our findings suggest that the underlying cause of age‐related thymic involution results primarily from changes in the thymic microenvironment, causing extrinsic, rather than intrinsic, defects in T‐lymphocyte progenitors.
Aging and regulated protein degradation: who has the UPPer hand?
Authors: Vernace Vita A. , Schmidt‐Glenewinkel Thomas , Figueiredo‐Pereira Maria E. 
Published: August 2007

SummaryIn all cells, protein degradation is a constant, ongoing process that is critical for cell survival and repair. The ubiquitin/proteasome pathway (UPP) is the major proteolytic pathway that degrades intracellular proteins in a regulated manner. It plays critical roles in many cellular processes and diseases. Disruption of the UPP is particularly relevant to pathophysiological conditions that provoke the accumulation of aberrant proteins, such as in aging as well as in a variety of neurodegenerative disorders including Alzheimer's and Parkinson's diseases. For unknown reasons, most of these neurodegenerative disorders that include familial and sporadic cases exhibit a late onset. It is possible that these neurodegenerative conditions exhibit a late onset because proteasome activity decreases with aging. Aging‐dependent impairment in proteolysis mediated by the proteasome may have profound ramifications for cell viability. It can lead to the accumulation of modified, potentially toxic proteins in cells and can cause cell injury or premature cell death by apoptosis or necrosis. While it is accepted that aging affects UPP function, the question is why does aging cause a decline in regulated protein degradation by the UPP? Herein, we review some of the properties of the UPP and mechanisms mediating its age‐dependent impairment. We also discuss the relevance of these findings leading to a model that proposes that UPP dysfunction may be one of the milestones of aging.