bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chronic illness self‐management: locating the ‘self’
Authors: Koch Tina , Jenkin Peter , Kralik Debbie 
Published: November 2004

Aim.  In this paper, we present the findings of a recent research project in which we explored self‐ management with older people who were diagnosed with asthma.Background.  Asthma self‐management literature has focused on the need for the patient to ‘adhere’ to prescribed therapies, in particular the taking of medications, monitoring of respiratory function or recognizing and avoiding triggers.Method.  Data were generated during a period of 9 months from three sources; in‐depth interviews with 24 older participants, an open‐ended questionnaire and two mixed‐gender participatory action research groups.Findings.  Based on current literature, our previous research findings which have ‘unpacked’ what is ‘self’‐management, and data generated in this project, we propose that three asthma management models are in operation: Medical Model of Self‐management, Collaborative Model of Self‐management and Self‐Agency Model of Self‐management. Locating the ‘self’ in self‐management means acknowledging that many people living with a chronic condition are already self‐determining and their expertise should be acknowledged as such.Conclusion.  Health care professionals can best facilitate people toward self‐agency by embracing new understandings of self‐management in long‐term illness. This process is enhanced when the expertise a person brings to the management of their condition is given the respect it deserves. There needs to be a focus on providing people with the means to grow and learn in a participative relationship that cannot be fully realized with ‘off the shelf’ self‐management solutions.
Case of recalcitrant necrobiotic xanthogranuloma
Authors: Wells Jillian , Gillespie Rod , Zardawi Ibrahim 
Published: November 2004

SUMMARY A 53‐year‐old woman with necrobiotic xanthogranuloma presented as infiltrated eyelid plaques, with later development of arm and thigh lesions. Clinical features, including association with immunoglobulin G‐κ paraprotein, and pathological findings were typical of this disorder. Treatment for 15 months with varying combinations of prednisone and multiple chemotherapeutic agents (melphalan, cyclophosphamide and chlorambucil) has led to minimal or no improvement in the clinical lesions or paraprotein. The case demonstrates some of the difficulties in managing this unusual disorder.
Monitoring and assessment of restoration of a rainforest remnant at Wingham Brush, NSW
Authors: Harden Gwen J. , Fox Marilyn D. , Fox Barry J. 
Published: November 2004

Abstract  Wingham Brush is a 9‐ha remnant of lowland subtropical rainforest, on mid‐north coast New South Wales, Australia, with high floristic diversity (about 200 species, more than 70 endemic trees and 27 endemic vines). A history of disturbance, environmental mismanagement and flooding from the Manning River resulted in many exotic species vigorously invading the rainforest. By the late 1970s weeds blanketed large sections of the forest, preventing regeneration of native species and destroying the canopy. By 1978 rainforest ecologists thought it ‘doubtful whether the rainforest could be saved from extinction.’ In 1980 a restoration program funded by the National Trust of Australia (NSW), used the Bradley Method of bush regeneration. However, this method did not consider the unique character of the rainforest community, which required the highest priority to be restoring the canopy. The National Herbarium of New South Wales became involved in 1984 as an independent agency to monitor the progress of the regeneration and assess the techniques being used, in particular the use of glyphosate. Monitoring provided evidence of beneficial change, showed how it occurred and has since been used as a basis for planning, documenting and assessing progress in rainforest regeneration. Reformation of the canopy allowed the forest floor to stabilize under a more constant microclimate, encouraging germination of shade‐loving rainforest species. Maximum and minimum temperature values demonstrated the buffering effect of the closed rainforest canopy. After 20 years, Wingham Brush has changed from a degraded forest, dominated by exotic vines, with many large gaps in the canopy, to a rainforest with an intact canopy, enlarged core forest area and reduced edge effect, that supports the diversity and structure of a healthy subtropical rainforest. Techniques developed in the ‘Wingham Brush Method’, have become the basis for restoration programs in other rainforest areas. The principles are: be canopy‐focused, be flexible, assess each site individually, and use techniques appropriate to problems encountered and goals of the long‐term program.
Exotic plant invasions in an endemic‐rich habitat: The spread of an introduced Australian grass, Agrostis avenacea J. F. Gmel., in California vernal pools
Authors: Zedler Paul H. , Black Charles 
Published: November 2004

Abstract  The present abundance and historical spread of an exotic grass, Agrostis avenacea, is documented for California, USA, and for the vernal pools of San Diego County in particular. Agrostis avenacea is native to Australia where it is a common grass of ephemeral and fluctuating wetlands. California vernal pools, by reason of their extreme variability and high endemism, have been thought to be relatively resistant to invasion. The recent expansion of A. avenacea in San Diego County demonstrates, however, that the alleged resistance is probably a function of a relatively small pool of invaders and a low probability of targeted dispersal. Although A. avenacea is now abundant in pools with little current disturbance, human disturbance appears to have been a major factor that facilitated its initial establishment. This specific instance adds to the mounting evidence that there are probably few, if any, habitats immune to invasion.
Estrogen receptor beta is expressed in human embryonic brain cells and is regulated by 17β‐estradiol
Authors: Fried G. , Andersson E. , Csöregh L. , Enmark E. , Gustafsson J.‐Å. , Aanesen A. , Österlund C. 
Published: November 2004

AbstractIn order to study estrogen effects on developing human neurons, we have established primary cultures of neurons and glia from 8–13‐week human embryo cortex and spinal cord. The neuronal identity of the cultures was verified using the neuronal synaptic vesicle and neuronal endosomal membrane markers synaptotagmin, synapsin and synaptophysin, and the glial contribution to the mixed glial–neuronal cultures was verified using the glial marker glial fibrillary acidic protein (GFAP). We here report expression of estrogen receptor beta (ERβ) in these cells using RT‐PCR and sequencing, RNAse protection assay, immunohistochemistry and immunoblotting. We found that both neuronal and mixed glial–neuronal cultures expressed ERβ. Treatment with 17β‐estradiol gave an increased expression of ERβ in both types of cultures. These results suggest that ERβ is expressed in fetal brain and thus may mediate effects of estrogen in the developing nervous system. Furthermore, the results suggest that expression of ERβ in fetal brain may be regulated by estrogen.
NGF and GDNF differentially regulate TRPV1 expression that contributes to development of inflammatory thermal hyperalgesia
Authors: Amaya Fumimasa , Shimosato Goshun , Nagano Masatoshi , Ueda Masashi , Hashimoto Satoru , Tanaka Yoshifumi , Suzuki Hidenori , Tanaka Masaki 
Published: November 2004

AbstractThe transient receptor potential ion channel, TRPV1 plays an essential role in the development of inflammatory thermal hyperalgesia. We investigated the dependence of inflammatory TRPV1 induction on neurotrophic factor. Rat dorsal root ganglia (DRG) neurons were classified according to immunostaining for trk‐A and IB4 and the effects of antibodies against NGF or GDNF on TRPV1 expression within the groups were then analysed by immunohistochemical means. The data were compared with the time course of trophic factor expression and the effects of their antibodies on thermal hyperalgesia against radiant heat after inflammation. Although the levels of both NGF and GDNF were increased by inflammation, NGF rapidly and transiently increased whereas GDNF increased gradually over a period of approximately one week. TRPV1 expression was increased within both trk‐A positive and IB4 positive neurons after inflammation. Increased TRPV1 expression within trk‐A positive neurons was prevented by anti‐NGF but not by anti‐GDNF, whereas TRPV1 induction within the IB4 positive group was blocked by anti‐GDNF but not by anti‐NGF. Both antibodies prevented the short latency of withdrawing an inflamed paw from radiant heat. These results suggest that inflammation differentially increases both NGF and GDNF, which facilitate TRPV1 expression within distinctive neurons to induce thermal hyperalgesia.
Isolation of an mRNA binding protein homologue that is expressed in nociceptors
Authors: Eilers Helge , Trilk Sharon L. , Lee Sook Young , Xue Qing , Jong Beverly E. , Moff Irene , Levine Jon D. , Schumacher Mark A. 
Published: November 2004

AbstractThe peripheral detection of painful stimuli requires the activation of small‐diameter primary afferent neurons known as nociceptors. We have exploited two features of nociceptor biology, expression of the high affinity receptor for nerve growth factor (TrkA) and sensitivity to capsaicin, to isolate novel proteins using a differential display cloning scheme. A resulting ∼4.3‐kb cDNA was isolated and sequence analysis inferred a ∼157‐kDa protein containing a signal/mitochondrial targeting peptide sequence. Due to its molecular weight and significant amino acid identity with ‘human leucine‐rich protein 130’[leucine‐rich pentatricopeptide motif containing (LRPPRC)], we termed the cDNA candidate leucine‐rich protein 157 (rLRP157). Western blot analysis of HEK293 cells over‐expressing the candidate cDNA showed a single protein product of similar size to that found in rat dorsal root ganglion as well as in other neuronal tissues and cell lines. Although expressed in a wide variety of tissues, in situ hybridization and immunohistochemistry in dorsal root ganglion revealed that rLRP157 expression was restricted to the small‐diameter neurons. Sequence identity with previously characterized mRNA binding proteins and its subcellular localization in sensory neurons suggest that rLRP157 is associated with mitochondrial function. Moreover, the genetic basis of French‐Canadian Leigh syndrome, which confers a loss of mitochondrial cytochrome c oxidase and is characterized by neurodegeneration, was recently mapped to a mutation in the LRPPRC gene. Taken together with its expression in small‐diameter sensory neurons, we hypothesize that rLRP157, the rat orthologue of the human LRPPRC, may play a role in the modulation of peripheral pain transduction and serve as a novel marker for nociceptor subtypes.
The human perirhinal cortex and semantic memory
Authors: Davies R. R. , Graham Kim S. , Xuereb John H. , Williams Guy B. , Hodges John R. 
Published: November 2004

AbstractStudies in macaque monkeys indicate that the perirhinal cortex in the temporal lobe participates in object memory. This function may be analogous to aspects of human semantic memory (knowledge of objects, concepts, faces and words). To date, the status of perirhinal cortex has not specifically been investigated in patients with semantic deficits as seen in semantic dementia, the temporal lobe variant of frontotemporal dementia. High‐resolution three‐dimensional magnetic resonance imaging was performed in subjects with semantic dementia and Alzheimer's disease (characterized in its early stages by selective episodic memory impairment) and in healthy age‐matched controls. Hippocampal, perirhinal, temporopolar and entorhinal cortex volumes were measured by outlining areas on successive scan slices according to recognized landmarks. The entorhinal and hippocampal regions were further subdivided into anterior and posterior parts. In keeping with the hypothesized contribution of the perirhinal cortex to semantic memory function, we found greater involvement of this region, together with the temporopolar and anterior entorhinal cortices, in semantic dementia than in either Alzheimer's disease patients or control subjects. Performance on a range of semantic tests also correlated with perirhinal volume. Bilateral reduction in hippocampal volume compared with controls was seen in Alzheimer's disease. In conclusion, atrophy of the human perirhinal cortex, and of directly connected areas, was associated with semantic memory impairment but not episodic memory impairment, as predicted from the primate work.
Dynamic or inert metabolism? Turnover of N‐acetyl aspartate and glutathione from d‐[1‐13C]glucose in the rat brain in vivo
Authors: Choi In‐Young , Gruetter Rolf 
Published: November 2004

AbstractThe rate of 13C‐label incorporation into both aspartyl (NAA C3) and acetyl (NAA C6) groups of N‐acetyl aspartate (NAA) was simultaneously measured in the rat brain in vivo for up to 19 h of [1‐13C]glucose infusion (n = 8). Label incorporation was detected in NAA C6 approximately 1.5 h earlier than in NAA C3 because of the delayed labeling of the precursor of NAA C3, aspartate, compared to that of NAA C6, glucose. The time courses of NAA were fitted using a mathematical model assuming synthesis of NAA in one kinetic compartment with the respective precursor pools of aspartate and acetyl coenzyme A (acetyl‐CoA). The turnover rates of NAA C6 and C3 were 0.7 ± 0.1 and 0.6 ± 0.1 µmol/(g h) with the time constants 14 ± 2 and 13 ± 2 h, respectively, with an estimated pool size of 8 µmol/g. The results suggest that complete label turnover of NAA from glucose occurs in approximately 70 h. Several hours after starting the glucose infusion, label incorporation into glutathione (GSH) was also detected. The turnover rate of GSH was 0.06 ± 0.02 µmol/(g h) with a time constant of 13 ± 2 h. The estimated pool size of GSH was 0.8 µmol/g, comparable to the cortical glutathione concentration. We conclude that NAA and GSH are completely turned over and that the metabolism is extremely slow (< 0.05% of the glucose metabolic rate).
Molecular modeling of human MT2 melatonin receptor: the role of Val204, Leu272 and Tyr298 in ligand binding
Authors: Mazna Petr , Obsilova Veronika , Jelinkova Irena , Balik Ales , Berka Karel , Sovova Zofie , Ettrich Rüdiger , Svoboda Petr , Obsil Tomas , Teisinger Jan 
Published: November 2004

AbstractA model of the helical part of the human MT2 melatonin (hMT2) receptor, a member of the G protein‐coupled receptors superfamily has been generated, based on the structure of bovine rhodopsin. Modeling has been combined with site‐directed mutagenesis to investigate the role of the specific amino acid residues within the transmembrane domains (TM) numbers V, VI and VII of hMT2 receptor in the interaction with 2‐iodomelatonin. Saturation binding assays with 2‐iodomelatonin demonstrated that the substitution V204A (TMV) resulted in total loss of binding while the mutation V205A had no effect. The replacement of F209 with alanine led to a significant decrease in the Bmax value of receptor binding while mutations V205A and F209A also within TM V did not significantly change binding properties of the hMT2 receptor. In the case of TM VI, the substitution G271T caused substantial decrease in 2‐iodomelatonin binding to the hMT2 receptor. The change L272A (TM VI) as well as mutation Y298A within TM VII completely abolished ligand binding to the receptor. These data suggest that several new amino acid residues within TM V, VI and VII are involved in ligand–MT2 receptor interaction.
Adenosine receptor‐mediated modulation of dopamine release in the nucleus accumbens depends on glutamate neurotransmission and N‐methyl‐d‐aspartate receptor stimulation
Authors: Quarta Davide , Borycz Janusz , Solinas Marcello , Patkar Kshitij , Hockemeyer Jörg , Ciruela Francisco , Lluis Carme , Franco Rafael , Woods Amina S. , Goldberg Steven R. , Ferré Sergi 
Published: November 2004

AbstractAdenosine, by acting on adenosine A1 and A2A receptors, exerts opposite modulatory roles on striatal extracellular levels of glutamate and dopamine, with activation of A1 inhibiting and activation of A2A receptors stimulating glutamate and dopamine release. Adenosine‐mediated modulation of striatal dopaminergic neurotransmission could be secondary to changes in glutamate neurotransmission, in view of evidence for a preferential colocalization of A1 and A2A receptors in glutamatergic nerve terminals. By using in vivo microdialysis techniques, local perfusion of NMDA (3, 10 µm), the selective A2A receptor agonist 2‐p‐(2‐carboxyethyl)phenethylamino‐5′‐N‐ethylcarboxamidoadenosine (CGS 21680; 3, 10 µm), the selective A1 receptor antagonist 8‐cyclopentyl‐1,3‐dimethylxanthine (CPT; 300, 1000 µm), or the non‐selective A1‐A2A receptor antagonist in vitro caffeine (300, 1000 µm) elicited significant increases in extracellular levels of dopamine in the shell of the nucleus accumbens (NAc). Significant glutamate release was also observed with local perfusion of CGS 21680, CPT and caffeine, but not NMDA. Co‐perfusion with the competitive NMDA receptor antagonist dl‐2‐amino‐5‐phosphonovaleric acid (APV; 100 µm) counteracted dopamine release induced by NMDA, CGS 21680, CPT and caffeine. Co‐perfusion with the selective A2A receptor antagonist MSX‐3 (1 µm) counteracted dopamine and glutamate release induced by CGS 21680, CPT and caffeine and did not modify dopamine release induced by NMDA. These results indicate that modulation of dopamine release in the shell of the NAc by A1 and A2A receptors is mostly secondary to their opposite modulatory role on glutamatergic neurotransmission and depends on stimulation of NMDA receptors. Furthermore, these results underscore the role of A1 vs. A2A receptor antagonism in the central effects of caffeine.
NGFI‐B (Nurr77/Nr4a1) orphan nuclear receptor in rat pinealocytes: circadian expression involves an adrenergic‐cyclic AMP mechanism
Authors: Humphries Ann , Weller Joan , Klein David , Baler Ruben , Carter David A. 
Published: November 2004

AbstractNGFI‐B (Nur77/Nr4a1) is a member of a nuclear steroid receptor subgroup that includes the related factors Nurr1 (Nr4a2) and NOR‐1 (Nr4a3). These proteins do not have recognized ligands and in fact function independently as orphan receptors with transcriptional regulatory activity. In the present study, expression of the NGFI‐B gene in the rat pineal gland was found to exhibit a robust circadian rhythm, with elevated levels of NGFI‐B mRNA occurring at night. The rhythm of NGFI‐B mRNA is translated into a circadian rhythm of NGFI‐B protein, which accumulates in the nucleus of pinealocytes. In addition, there is a parallel marked nocturnal increase in pineal DNA binding activity to a NGFI‐B response element (NBRE, AAAGGTCA). Pharmacological studies indicate that NGFI‐B mRNA and protein levels are elevated via activation of adrenergic receptors. NGFI‐B protein levels are also elevated by dibutyryl cyclic AMP, as in other systems. In the pineal gland, regulation of NGFI‐B expression also involves the AP‐1 protein Fra‐2, based on studies with a transgenic Fra‐2 knockdown rat, in which pineal NGFI‐B expression increases. This set of observations extends the number of pineal genes that are known to be regulated by Fra‐2, and also provides the first indication that a member of the NGFI‐B group of nuclear receptors is involved in controlling gene expression in the pineal gland.
Amyloid Aβ1−40preconditions non‐apoptotic signalsin vivoand protects fetal rat brain from intrauterine ischemic stress
Authors: Kuperstein Faina , Brand Annette , Yavin Ephraim 
Published: November 2004

AbstractThe dualistic activities of the amyloid beta (Aβ) peptide as a pro‐oxidant and ubiquitous constituent of amyloid deposits in Alzheimer's disease plaques and as an antioxidant of purported physiological function has been suggested but the mechanisms are far from being understood. In this report we measure several oxidative stress parameters and signaling cascades in brains of fetal rats subjected to global ischemia in order to evaluate the putative bifunctional properties of the Aβ1−40peptide. Intraperitoneal injection of 6 µg Aβ1−40into 18‐days‐old rat fetuses (approximately 3 g body weight) resulted after 24 h in the appearance of the peptide in various fetal organs including brain where it enhanced the levels of glutathione (GSH), glutathione reductase, glutathione peroxidase, and stimulated the levels of pro‐survival signaling activities such as Akt serine/threonine kinase, extracellular signal‐regulated kinase (ERK) and protein kinase C enzymes. Moreover, pretreatment with Aβ1−40reversed the consequences of a transient hypovolemic/hypotensive oxidative stress by restoring GSH levels via its recycling enzymes and by lowering the production of lipid peroxides presumably by activating the aforementioned pro‐survival signaling cascades. It also caused a reduction in the number of DAPI‐enhanced reactive cells and a decrease in p38 kinase phosphorylation and caspase‐9 and ‐3 activity. These data suggest that pre‐exposure to Aβ1−40stimulates fetal tolerance to ischemia via regulation of GSH metabolism and as such may be considered as neuroprotective.
Microarray analysis of gene expression in the rat vestibular nucleus complex following unilateral vestibular deafferentation
Authors: Horii Arata , Masumura Chisako , Smith Paul F. , Darlington Cynthia L. , Kitahara Tadashi , Uno Atsuhiko , Mitani Kenji , Kubo Takeshi 
Published: November 2004

AbstractTo investigate the molecular background of vestibular compensation, a model of lesion‐induced plasticity, we used a microarray analysis to examine genes that show asymmetrical expression between the bilateral vestibular nucleus complexes (VNCs) 6 h following unilateral vestibular deafferentation (UVD). Asymmetrical gene expression was then validated by a real‐time quantitative PCR. Among the 88 genes for which the ipsilateral (ipsi) : contralateral (contra) was > 1.35, the number of known genes was 33 (38%), and the number of expressed sequence tag (EST) sequences was 55 (62%). Among the 130 genes for which the contra : ipsi was > 1.35, the number of known genes was 55 (42%), and the number of EST sequences was 75 (58%). Changes in some of the genes were consistent with previous studies; however, we found several new genes which could be functionally related to the molecular basis of the electrophysiological asymmetry between the VNCs following UVD. Ipsi > contra genes included the GABAA receptor rho subunit, regulatory proteins of G protein signaling, calcium signaling related molecules such as the voltage‐dependent calcium channel α2/δ subunit 1, calcineurin subunit Aβ and Ca2+ pump. Contra > ipsi genes included the neuronal high affinity glutamate transporter, 5‐hydroxytryptamine receptor 1D, mitogen‐activated protein kinase 12 and ubiquitin carboxy‐terminal hydrolase L1.