bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of temperature and ration size on carbon and nitrogen stable isotope trophic fractionation
Authors: BARNES CAROLYN , SWEETING CHRISTOPHER J. , JENNINGS SIMON , BARRY JON T. , POLUNIN NICHOLAS V. C. 
Published: January 2007

Summary

Stable isotope data are widely used to track the origins and transformations of materials in food webs. Reliable interpretation of these data requires knowledge of the factors influencing isotopic fractionation between diet and consumer. For practical reasons, isotopic fractionation is often assumed to be constant but, in reality, a range of factors may affect fractionation.
To investigate effects of temperature and feeding rate on fractionation of carbon and nitrogen stable isotopes in a marine predator, we reared European sea bass Dicentrarchus labrax on identical diets at 11 and 16 °C on three ration levels for 600 days.
Nitrogen trophic fractionation (Δδ15N) was affected by temperature. Bass Δδ15N was 4·41‰ at 11 °C and 3·78‰ at 16 °C.
Carbon fractionation (Δδ13C) was also affected by temperature. Bass Δδ13C was 1·18‰ at 11 °C and 1·64‰ at 16 °C. The higher lipid content in the tissues of bass reared at cooler temperatures accounted for the temperature effect on Δδ13C. When Δδ13C was determined using mathematically defatted values, there was a direct effect of ration size and Δδ13C was 2·51, 2·39 and 2·31‰ for high, medium and low rations, respectively.
Reported Δδ15N for all treatments exceeded the mean of 3·4‰ widely used in ecological studies of fish populations and communities. This would confound the interpretation of δ15N as an indicator of trophic level when comparing populations that are exposed to different temperatures.
The Δδ13C of 0–1‰ commonly applied in food web studies did not hold under any of the temperature or feeding regimes considered and a value of 2‰ would be more appropriate.
Improving paediatric nurses' knowledge and attitudes in childhood fever management
Authors: Edwards Helen , Walsh Anne , Courtney Mary , Monaghan Sarah , Wilson Jenny , Young Jeanine 
Published: January 2007

Abstract Title. Improving paediatric nurses' knowledge and attitudes in childhood fever management Aim.  This paper reports an evaluation of the effectiveness of a peer education programme in developing paediatric nurses’ evidence‐based knowledge and attitudes towards fever management and the sustainability of these changes.Background.  In general, paediatric nurses’ fever management knowledge seems to be mediocre. They believe fever to be harmful, causing febrile convulsions and brain damage. Antipyretics are administered to prevent febrile convulsions and alternate antipyretics are given when temperatures are not reduced.Method.  A quasi‐experiment was conducted from August 2002 to March 2003. An experimental group of Registered Nurses received the peer education programme and peer support and education were promoted for those unable to attend the sessions. A control group continued its normal practices. Seventy‐seven nurses were eligible to attend the programme; 74·0% attended at least one session, 52% two or more. Questionnaire data were collected 1 month before and 1 and 4 months after the peer education programme from 56·3% to 77·8% of eligible experimental and 40·9% to 51·6% of eligible control group nurses.Findings.  Interaction effects between group and time were found in overall knowledge (P = 0·01), specifically knowledge of the physiology of fever (P = 0·001), and attitudes towards evidence‐based fever management (P = 0·05). In addition, experimental group nurses demonstrated statistically significantly more knowledge of general fever management principles at 4 months after the intervention than control group nurses (P = 0·01), and compared with their own knowledge at baseline (P < 0·001).Conclusions.  Educational programmes targeting practice change must be theoretically based and target knowledge, attitudes and barriers to change. The programme tested here, which incorporated peer education and support and facilitated group change, is adaptable to other practices, groups and settings.
What degree of work overload is likely to cause increased sickness absenteeism among nurses? Evidence from the RAFAELA patient classification system
Authors: Rauhala Auvo , Kivimäki Mika , Fagerström Lisbeth , Elovainio Marko , Virtanen Marianna , Vahtera Jussi , Rainio Anna‐Kaisa , Ojaniemi Kati , Kinnunen Juha 
Published: January 2007

Abstract Title. What degree of work overload is likely to cause increased sickness absenteeism among nurses? Evidence from the RAFAELA patient classification system Aim.  This paper reports a study examining whether nurses’ work overload is associated with increased sick leave and quantifying the loss of working days from work overload.Background.  The RAFAELA patient classification system indicates nursing care intensity in relation to an optimum and is one of the few validated monitoring instruments of patient‐associated workload among nurses. However, it is not clear whether work overload is a risk factor for increased sickness absenteeism, an important occupational problem in health care.Method.  An observational cohort study was carried out with 877 nurses, 31 wards and five Finnish hospitals. Patient‐associated workload scores from the RAFAELA system were based on a 6‐month monitoring period in 2004. Records of 12‐month self certified (1–3 days) and medically certified (>3 days) periods of sick leave in the same year were obtained from employers’ registers.Findings.  The mean workload was 9% (sd = 8%) above the optimum. There was a linear trend between increasing workload and increasing sick leave (P ≤ 0·006). Among nurses with workload ≥30% above the optimum the rate of self certified periods of sick leave was 1·44 (95% CI 1·13–1·83) times higher than among those with an optimum workload. The corresponding rate ratio for medically certified sick leave was 1·49 (1·10–2·03). These excess rates of sickness absence resulted in 12 extra sick leave days per person‐year.Conclusion.  Measuring nurses’ workload may be an important part of strategic human resource management of nurses to reduce sick leave among nurses.
Insulin‐like growth factor I (IGF‐I) and its receptor (IGF‐1R) in the rat anterior pituitary
Authors: Eppler Elisabeth , Jevdjovic Tanja , Maake Caroline , Reinecke Manfred 
Published: January 2007

AbstractFew and controversial results exist on the cellular sites of insulin‐like growth factor (IGF)‐I synthesis and the type 1 IGF receptor (IGF‐1R) in mammalian anterior pituitary. Thus, the present study analysed IGF‐I and the IGF‐1R in rat pituitary. Reverse transcription‐polymerase chain reaction revealed IGF‐I and IGF‐1R mRNA expression in pituitary. The sequences of both were identical to the corresponding sequences in other rat organs. In situ hybridization localized IGF‐I mRNA in endocrine cells. The majority of the growth hormone (GH) cells and numerous adrenocorticotropic hormone (ACTH) cells exhibited IGF‐1R‐immunoreactivity at the cell membrane. At lower densities, IGF‐1 receptors were also present at the other hormone‐producing cell types, indicating a physiological impact of IGF‐I for all endocrine cells. IGF‐I‐immunoreactivity was located constantly in almost all ACTH‐immunoreactive cells. At the ultrastructural level, IGF‐I‐immunoreactivity was confined to secretory granules in co‐existence with ACTH‐immunoreactivity, indicating a concomitant release of both hormones. Occasionally, IGF‐I‐immunoreactivity was detected in an interindividually varying number of GH cells. In some individuals, weak IGF‐I‐immunoreactions were also detected also in follicle‐stimulating hormone and luteinizing hormone cells. Thus, IGF‐I seems to be produced as a constituent in ACTH cells, possibly indicating its particular importance in stress response. Generally, IGF‐I from the endocrine cells may regulate synthesis and/or release of hormones in an autocrine/paracrine manner as well as prevent apoptosis and stimulate proliferation. Production of IGF‐I in GH cells may depend on the physiological status, most likely the serum IGF‐I level. IGF‐I released from GH cells may suppress GH synthesis and/or release by an autocrine feedback mechanism in addition to the endocrine route.
Deep brain stimulation in a rat model modulates TH, CaMKIIa and Homer1 gene expression
Authors: Henning Jeannette , Koczan Dirk , Glass Änne , Karopka Thomas , Pahnke Jens , Rolfs Arndt , Benecke Reiner , Gimsa Ulrike 
Published: January 2007

AbstractHigh‐frequency stimulation (HFS) of subthalamic nucleus (STN) is a therapy for late‐stage Parkinson's disease. Its mechanisms of action are not yet fully understood. In the present study, gene expression analyses were performed in a rat model of Parkinson's disease, i.e. striatal 6‐hydroxydopamine (6‐OHDA) lesion. Using microarrays, gene expression was analysed in 1‐mm‐thick sagittal brain slices, including basal ganglia of five groups of male Wistar rats. These were unmanipulated rats (group A), unlesioned rats with implanted electrode but without stimulation (group B), unlesioned, stimulated rats (group C), 6‐OHDA‐lesioned rats with implanted electrode but without stimulation (group D), and finally 6‐OHDA‐lesioned and stimulated rats (group E). A statistically significant downregulation of tyrosine hydroxylase (TH) mRNA expression induced by 6‐OHDA lesion and an HFS‐induced TH upregulation in 6‐OHDA‐lesioned rats could be detected. It could be hypothesized that the HFS‐induced upregulation of TH is the result of neuronal STN modulation and mediated via projections from STN to substantia nigra pars compacta. Furthermore, a downregulation of calcium/calmodulin‐dependent protein kinase type IIA and Homer1 was observed. This downregulation could result in a reduced sensitivity towards glutamate in basal ganglia downstream of STN.
Concomitant short‐ and long‐duration response to levodopa in the 6‐OHDA‐lesioned rat: a behavioural and molecular study
Authors: Marin C. , Aguilar E. , Mengod G. , Cortés R. , Obeso J. A. 
Published: January 2007

AbstractThe long‐duration response (LDR) is a sustained improvement in parkinsonism due to chronic levodopa therapy and lasts after discontinuation of treatment. We have investigated the molecular changes that underlie the LDR in rats with a unilateral 6‐hydroxydopamine (6‐OHDA) lesion. Animals were treated for 22 days with levodopa or saline. Forelimb akinesia was evaluated prior and following a test dose of levodopa. Rotational behaviour was weekly evaluated. Levodopa induced an improvement in the parkinsonian limb akinesia that lasted for 48 h after withdrawal. A shortening in the duration of rotational behaviour was observed. After 3 days of washout, levodopa treatment maintained elevated striatal preproenkephalin mRNA expression, also inducing an increase in preprodynorphin (PDyn) and dopamine D‐3 receptor mRNAs, but without any modification of the adenosine A2A mRNA expression induced by 6‐OHDA. Levodopa reversed the lesion‐induced increase in the expression of cytochrome oxidase mRNA in the subthalamic nucleus and glutamate decarboxylase mRNA in the pars reticulata of the substantia nigra. After 7 days of levodopa washout, the molecular markers show a decline in the basal ganglia evolving towards the parkinsonian state, being statistically significant for the striatal PDyn mRNA. This study characterizes the concomitant presence of the short‐duration response and LDR to levodopa in the 6‐OHDA model of parkinsonism and shows that the molecular changes induced by levodopa in the basal ganglia are not permanent and that this reversal after levodopa washout may be responsible for the gradual motor deterioration that characterize the LDR.
Environmental enrichment enhances neurogenesis and improves functional outcome after cranial irradiation
Authors: Fan Yang , Liu Zhengyan , Weinstein Philip R. , Fike John R. , Liu Jialing 
Published: January 2007

AbstractRadiation therapy is a widely used treatment for brain tumors but it can cause delayed progressive cognitive decline and memory deficits. Previous studies suggested that this neurocognitive dysfunction might be linked to the impairment of hippocampal neurogenesis. However, little is known regarding how to reduce the cognitive impairment caused by radiation therapy. To investigate whether environmental enrichment (EE) promotes neurogenesis and cognitive function after irradiation, irradiated gerbils were housed in EE for 2 months and evaluated by neurobehavioral testing for learning and memory function, and immunohistochemical analysis for neurogenesis. Our results demonstrated that even relatively low doses (5–10 Gy) of irradiation could acutely abolish precursor cell proliferation in the dentate gyrus by more than 90%. This reduction in precursor proliferation was persistent and led to a significant decline in the granule cell population 9 months later. EE housing enhanced the number of newborn neurons and increased residual neurogenesis. EE also significantly increased the total number of immature neurons in the dentate gyrus. Furthermore, irradiated animals after EE housing showed a significant improvement in spatial learning and memory during the water‐maze test and in rotorod motor learning over a 5‐day training paradigm. In conclusion, EE has a positive impact on hippocampal neurogenesis and functional recovery in irradiated adult gerbils. Our data suggest that there is still a considerable amount of plasticity remaining in the hippocampal progenitor cells in adult animals after radiation injury, which can become a target of therapeutic intervention for radiation‐induced cognitive dysfunction.
Local administration of N‐acetylaspartylglutamate (NAAG) peptidase inhibitors is analgesic in peripheral pain in rats
Authors: Yamamoto Tatsuo , Saito Osamu , Aoe Tomohiko , Bartolozzi Alessandra , Sarva Jayaprakash , Zhou Jia , Kozikowski Alan , Wroblewska Barbara , Bzdega Tomasz , Neale Joseph H. 
Published: January 2007

AbstractThe peptide neurotransmitter N‐acetylaspartylglutamate (NAAG) selectively activates group II metabotropic glutamate receptors (mGluRs). Systemic administration of inhibitors of the enzymes that inactivate NAAG results in decreased pain responses in rat models of inflammatory and neuropathic pain. These effects are blocked by a group II mGluR antagonist. This research tested the hypothesis that some analgesic effects of NAAG peptidase inhibition are mediated by NAAG acting on sensory neurite mGluRs at the site of inflammation. Group II mGluR agonists, SLx‐3095‐1, NAAG and APDC, or NAAG peptidase inhibitors, ZJ‐43 and 2‐PMPA, injected into the rat footpad reduced pain responses in carrageenan or formalin models. The analgesic effects of SLx‐3095‐1, APDC, ZJ‐43, 2‐PMPA and NAAG were blocked by co‐injection of LY341495, a selective group II mGluR antagonist. Injection of group II mGluR agonists, NAAG or the peptidase inhibitors into the contralateral rat footpad had no effect on pain perception in the injected paw. At 10–100 µm ZJ‐43 and 2‐PMPA demonstrated no consistent agonist activity at mGluR2 or mGluR3. Consistent with the conclusion that peripherally administered NAAG peptidase inhibitors increase the activation of mGluR3 by NAAG that is released from peripheral sensory neurites, we found that the tissue average concentration of NAAG in the unstimulated rat hind paw was about 6 µm. These data extend our understanding of the role of this peptide in sensory neurons and reveal the potential for treatment of inflammatory pain via local application of NAAG peptidase inhibitors at doses that may have little or no central nervous system effects.
Low‐frequency stimulation of the direct cortical input to area CA1 induces homosynaptic LTD and heterosynaptic LTP in the rat hippocampal–entorhinal cortex slice preparation
Authors: Wöhrl Robert , Von Haebler Dorothea , Heinemann Uwe 
Published: January 2007

AbstractThe entorhinal cortex (EC) innervates area CA1 and the subiculum directly via the portion of the perforant path, which originates from EC layer III cells referred to as direct cortical input (dCI), and indirectly via the trisynaptic loop through the dentate gyrus and area CA3. The dCI is of great importance as it mediates positional information for activation of place cells that is not prevented after interrupting information flow from area CA3 to CA1. In this study, we investigated the effects of low‐frequency stimulation of the dCI on homo‐ and heterosynaptic plasticity in area CA1 and tested for the contribution of NMDA, GABAA, GABAB, kainate and group I mGlu receptors. We demonstrate that 1 Hz stimulation of the dCI induces homosynaptic long‐term depression (LTD) and that 1 Hz stimulation of the dCI induces a long‐lasting augmentation of stratum radiatum‐induced population spikes in area CA1 (heterosynaptic long‐term potentiation). Additionally we show that homosynaptic effects depend on activation of GABAB and kainate receptors, whereas the heterosynaptic effects are GABAA and mGlu receptor dependent.
Changes in blood–brain barrier permeability to large and small molecules following traumatic brain injury in mice
Authors: Habgood M. D. , Bye N. , Dziegielewska K. M. , Ek C. J. , Lane M. A. , Potter A. , Morganti‐Kossmann C , Saunders N. R. 
Published: January 2007

AbstractThe entry of therapeutic compounds into the brain and spinal cord is normally restricted by barrier mechanisms in cerebral blood vessels (blood–brain barrier) and choroid plexuses (blood–CSF barrier). In the injured brain, ruptured cerebral blood vessels circumvent these barrier mechanisms by allowing blood contents to escape directly into the brain parenchyma. This process may contribute to the secondary damage that follows the initial primary injury. However, this localized compromise of barrier function in the injured brain may also provide a ‘window of opportunity’ through which drugs that do not normally cross the blood–brain barriers are able to do so. This paper describes a systematic study of barrier permeability in a mouse model of traumatic brain injury using both small and large inert molecules that can be visualized or quantified. The results show that soon after trauma, both large and small molecules are able to enter the brain in and around the injury site. Barrier restriction to large (protein‐sized) molecules is restored by 4–5 h after injury. In contrast, smaller molecules (286–10 000 Da) are still able to enter the brain as long as 4 days postinjury. Thus the period of potential secondary damage from barrier disruption and the period during which therapeutic compounds have direct access to the injured brain may be longer than previously thought.
Neurochemical identification of stereotypic burst‐firing neurons in the rat dorsal raphe nucleus using juxtacellular labelling methods
Authors: Hajós Mihály , Allers Kelly A. , Jennings Katie , Sharp Trevor , Charette Guy , Sík Attila , Kocsis Bernát 
Published: January 2007

AbstractRecent electrophysiological studies have discovered evidence of heterogeneity of 5‐hydroxytryptamine (5‐HT) neurons in the mesencephalic raphe nuclei. Of particular interest is a subpopulation of putative 5‐HT neurons that display many of the electrophysiological properties of presumed 5‐HT‐containing neurons (regular and slow firing of single spikes with a broad waveform) but fire spikes in short, stereotyped bursts. In the present study we investigated the chemical identity of these neurons in rats utilizing in vivo juxtacellular labelling methods. Of ten dorsal raphe nucleus (DRN) neurons firing short stereotyped bursts within an otherwise regular firing pattern, all exhibited immunoreactivity for either 5‐HT (n = 6) or the 5‐HT synthesizing enzyme, tryptophan hydroxylase (TRH; n = 2) or both (n = 2). Supporting pharmacological experiments demonstrated that the burst firing DRN neurons demonstrated equal sensitivity to 5‐HT1A agonism and α1‐adrenoceptor antagonism to single spiking DRN neurons that we have previously identified as 5‐HT‐containing. Collectively these data provide direct evidence that DRN neurons that exhibit stereotyped burst firing activity are 5‐HT containing. The presence of multiple types of electrophysiologically distinct midbrain 5‐HT neurons is discussed.
Effects of sex and age on regional prefrontal brain volume in two human cohorts
Authors: Cowell Patricia E. , Sluming Vanessa A. , Wilkinson Iain D. , Cezayirli Enis , Romanowski Charles A. J. , Webb Jocasta A. , Keller Simon S. , Mayes Andrew , Roberts Neil 
Published: January 2007

AbstractThis study examined interactive effects of sex and age on prefrontal brain anatomy in humans. It specifically targeted ranges of the adult life span and regions of cortex that previously showed male–female differences. Participants were 68 healthy human males and females aged 20–72 years. Data collection and analysis were conducted in parallel across two cohorts (laboratories) to investigate reproducibility of effects in relation to sex and age. Volumes for four regional prefrontal subfields per hemisphere were obtained from high‐resolution MRI. Regional sex by age interactions were replicated across cohorts. In men, age effects were greatest in medial prefrontal volume, with decreases in dorsal medial and orbital medial regions. In women, age‐related changes in medial prefrontal regions were limited to the dorsal volume, with additional decreases observed in lateral subfields. Cohort and Cohort × Age effects in total brain and total prefrontal volume were linked to a combination of methodological and sampling‐related factors. Findings indicated that neuroanatomical changes throughout adulthood unfold along different time scales in men and women. Results also showed that sex differences in ageing localized to medial prefrontal regions were particularly robust to variation across cohorts.
A multicopper oxidase is essential for manganese oxidation and laccase‐like activity in Pedomicrobium sp. ACM 3067
Authors: Ridge Justin P. , Lin Marianne , Larsen Eloise I. , Fegan Mark , McEwan Alastair G. , Sly Lindsay I. 
Published: January 2007

Summary Pedomicrobium sp. ACM 3067 is a budding‐hyphal bacterium belonging to the α‐Proteobacteria which is able to oxidize soluble Mn2+ to insoluble manganese oxide. A cosmid, from a whole‐genome library, containing the putative genes responsible for manganese oxidation was identified and a primer‐walking approach yielded 4350 bp of novel sequence. Analysis of this sequence showed the presence of a predicted three‐gene operon, moxCBA. The moxA gene product showed homology to multicopper oxidases (MCOs) and contained the characteristic four copper‐binding motifs (A, B, C and D) common to MCOs. An insertion mutation of moxA showed that this gene was essential for both manganese oxidation and laccase‐like activity. The moxB gene product showed homology to a family of outer membrane proteins which are essential for Type I secretion in Gram‐negative bacteria. moxBA has not been observed in other manganese‐oxidizing bacteria but homologues were identified in the genomes of several bacteria including Sinorhizobium meliloti 1021 and Agrobacterium tumefaciens C58. These results suggest that moxBA and its homologues constitute a family of genes encoding an MCO and a predicted component of the Type I secretion system.