bluuebunny/crossref_metadata_2025_split huggingface dataset:
Women's experience of ageing with a chronic condition
Authors: Giddings Lynne S. , Roy Dianne E. , Predeger Elizabeth 
Published: May 2007

Abstract Title. Women's experience of ageing with a chronic condition Aim.  This paper is a report of a study to explore the experiences of ‘almost old’ women as they grow older while living with a chronic condition.Background.  Little is known about the contextual effects of ageing and how it shapes and is shaped by a woman's chronic illness experience. Nurses’ understanding of this phenomenon can have positive effects on how their client accesses and responds to healthcare.Method.  Seven women aged between 50 and 58 years participated in this interpretive descriptive study that explored the issues of ageing with a chronic condition. Three focus groups were held between March 2003 and March 2004. Transcriptions were analyzed after each focus group. Participants were given the opportunity to respond to the findings as the analysis progressed.Findings.  The experience of living with a chronic illness foreshadowed what was to come with ageing and embodied the ageing process: it was just part of their lives. Alongside this, the women now felt less out of place. Their peers were catching up and beginning to experience aspects of participants’ everyday reality. The women, however, experienced double jeopardy because ageing amplified the ongoing vulnerabilities of living with a chronic condition.Conclusion.  Nurses who recognize the resourcefulness and expertise of women who live with a chronic condition can effectively be co‐strategists in their helping them to age well.
Impact of intravenous drug use on quality of life for patients with venous ulcers
Authors: Palfreyman Simon J. , Tod Angela M. , King Brenda , Tomlinson Darlene , Brazier John E. , Michaels Jonathan A. 
Published: May 2007

AbstractTitle.  Impact of intravenous drug use on quality of life for patients with venous ulcers Aim.  This paper is a report of a study to examine, from the perspective of patients, the impact of venous leg ulcers on health‐related quality of life in current and former intravenous drug users and the general population.Background.  Venous ulceration can be caused by intravenous drug use. There has been little examination on how this affects the quality of life of this group of patients and how they compare with other patients who have venous ulcers.Method.  A qualitative approach was adopted, using framework analysis. Semi‐structured interviews with 19 participants who had a venous leg ulcer were conducted between August 2005 and February 2006. Interview audiotapes were analysed to identify recurring themes relating to the impact of venous leg ulcers on overall quality of life.Findings.  A complex interaction between symptoms, social restriction and attribution of illness influenced the impact of venous leg ulcers. Smell and pain were the symptoms that had the most profound impacts. In addition to the physical and psychological consequences, participants’ activities and social interactions were restricted. Intravenous drug users experienced more social isolation and difficulties in accessing treatment for their venous ulcers.Conclusion.  While leg ulcer services remain focused on the needs of older people, services for young intravenous drug users are unlikely to improve. A more coherent and earlier intervention, when the ulcers are not as difficult to treat, would decrease time and costs to the health service. The challenge is to find new ways of providing effective and accessible care to this growing population.
Genetic monogamy despite social promiscuity in the pot‐bellied seahorse (Hippocampus abdominalis)
Authors: WILSON A. B. , MARTIN‐SMITH K. M. 
Published: May 2007

AbstractSexual selection theory predicts a positive correlation between relative parental investment and mate choice. In syngnathid fishes (seahorses and pipefish), males brood offspring in specialized brooding structures. While female‐female mating competition has been demonstrated in some pipefishes, all seahorses (genus Hippocampus) studied to date have been found to have conventional sex roles with greater male–male competition for access to mates despite possessing the most complex brood structures in the family. Although multiple mating is common in pipefish, seahorses are again exceptional, exhibiting strict genetic monogamy. Both demographic and behavioural explanations have been offered to explain the lack of multiple mating in seahorse species, but these hypotheses have not yet been explicitly addressed. We investigated mating systems and brood parentage of the pot‐bellied seahorse, Hippocampus abdominalis, a temperate‐water species that is socially promiscuous with conventional sex roles in laboratory populations. We observed promiscuous courtship behaviour and sex‐role reversal in high density, female‐biased field populations of H. abdominalis. We hypothesize that sex roles are plastic in H. abdominalis, depending on local population density and sex ratio. Despite promiscuous courtship behaviour, all assayed male seahorses were genetically monogamous in both laboratory and wild populations. Physiological limitations associated with embryo incubation may explain the absence of multiple mating in seahorses and may have played an important role in the development of the unique reproductive behaviour typical in these species.
Genetic consequences of Pleistocene range shifts: contrast between the Arctic, the Alps and the East African mountains
Authors: EHRICH DOROTHEE , GAUDEUL MYRIAM , ASSEFA ADANE , KOCH MARCUS A. , MUMMENHOFF KLAUS , NEMOMISSA SILESHI , CONSORTIUM INTRABIODIV , BROCHMANN CHRISTIAN 
Published: May 2007

AbstractIn wide‐ranging species, the genetic consequences of range shifts in response to climate change during the Pleistocene can be predicted to differ among different parts of the distribution area. We used amplified fragment length polymorphism data to compare the genetic structure of Arabis alpina, a widespread arctic‐alpine and afro‐alpine plant, in three distinct parts of its range: the North Atlantic region, which was recolonized after the last ice age, the European Alps, where range shifts were probably primarily altitudinal, and the high mountains of East Africa, where the contemporary mountain top populations result from range contraction. Genetic structure was inferred using clustering analyses and estimates of genetic diversity within and between populations. There was virtually no diversity in the vast North Atlantic region, which was probably recolonized from a single refugial population, possibly located between the Alps and the northern ice sheets. In the European mountains, genetic diversity was high and distinct genetic groups had a patchy and sometimes disjunct distribution. In the African mountains, genetic diversity was high, clearly structured and partially in accordance with a previous chloroplast phylogeography. The fragmented structure in the European and African mountains indicated that A. alpina disperses little among established populations. Occasional long‐distance dispersal events were, however, suggested in all regions. The lack of genetic diversity in the north may be explained by leading‐edge colonization by this pioneer plant in glacier forelands, closely following the retracting glaciers. Overall, the genetic structure observed corresponded to the expectations based on the environmental history of the different regions.
Amyloid fibrils of mammalian prion protein induce axonal degeneration in NTERA2‐derived terminally differentiated neurons
Authors: Novitskaya Vera , Makarava Natallia , Sylvester Ian , Bronstein Igor B. , Baskakov Ilia V. 
Published: May 2007

AbstractDefects in axonal transport and synaptic dysfunctions are associated with early stages of several neurodegenerative diseases including Alzheimer’s, Huntington’s, Parkinson’s, and prion diseases. Here, we tested the effect of full‐length mammalian prion protein (rPrP) converted into three conformationally different isoforms to induce pathological changes regarded as early subcellular hallmarks of prion disease. We employed human embryonal teratocarcinoma NTERA2 cells (NT2) that were terminally differentiated into neuronal and glial cells and co‐cultured together. We found that rPrP fibrils but not α‐rPrP or soluble β‐sheet rich oligomers caused degeneration of neuronal processes. Degeneration of processes was accompanied by a collapse of microtubules and aggregation of cytoskeletal proteins, formation of neuritic beads, and a dramatic change in localization of synaptophysin. Our studies demonstrated the utility of NT2 cells as valuable human model system for elucidating subcellular events of prion pathogenesis, and supported the emerging hypothesis that defects in neuronal transport and synaptic abnormalities are early pathological hallmarks associated with prion diseases.
GluR2‐free α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionate receptors intensify demyelination in experimental autoimmune encephalomyelitis
Authors: Bannerman Peter , Horiuchi Makoto , Feldman Daniel , Hahn Ashleigh , Itoh Aki , See Jill , Jia Zheng Ping , Itoh Takayuki , Pleasure David 
Published: May 2007

AbstractWe adopted a genetic approach to test the importance of edited GluR2‐free, Ca2+‐permeable, α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionate (AMPA) receptors in the pathophysiology of experimental autoimmune encephalomyelitis, an inflammatory demyelinative disorder resembling multiple sclerosis. Initial studies showed that oligodendroglial lineage cells from mice lacking functional copies of the gene encoding the GluR3 AMPA receptor subunit (Gria3) had a diminished capacity to assemble edited GluR2‐free AMPA receptors, and were resistant to excitotoxicity in vitro. Neurological deficits and spinal cord demyelination elicited by immunization with myelin oligodendrocyte glycoprotein peptide were substantially milder in these Gria3 mutant mice than in their wild‐type littermates. These results support the hypothesis that oligodendroglial excitotoxicity mediated by AMPA receptors that do not contain edited GluR2 subunits contributes to demyelination in experimental autoimmune encephalomyelitis, and suggest that inhibiting these Ca2+‐permeable AMPA receptors would be therapeutic in multiple sclerosis.
Differential effects of Parkin and its mutants on protein aggregation, the ubiquitin‐proteasome system, and neuronal cell death in human neuroblastoma cells
Authors: Kyratzi Elli , Pavlaki Maria , Kontostavlaki Dimitra , Rideout Hardy J. , Stefanis Leonidas 
Published: May 2007

AbstractMutations in Parkin, an E3 ligase, which participates in the ubiquitin‐proteasome system (UPS), cause juvenile onset Parkinson’s disease (PD). Some mutants aggregate upon over‐expression, but the effects of such aggregation on the UPS and neuronal survival have not been characterized. We show in this study that transient over‐expression of wild type (WT) Parkin or various mutants in human neuroblastoma cells leads to localized accumulation of green fluorescent protein (GFPu), an artificial proteasomal substrate, indicative of UPS dysfunction. Parkin mutants, but not WT, aggregated, and GFPu and ubiquitin accumulated within such aggregates. Apoptotic death occurred only with mutant Parkin over‐expression, and correlated with aggregation, but not GFPu accumulation. Enzymatic proteasomal activity was slightly increased with WT Parkin and decreased with mutant Parkin over‐expression. This decrease was, at least in part, due to caspase activation. We conclude that mutant forms of Parkin can exert toxic effects on neuronal cells, possibly through their propensity to aggregate. Both WT and mutant forms can induce localized UPS dysfunction, likely through different mechanisms. This raises a note of caution regarding forced over‐expression of Parkin as a neuroprotective strategy in PD or other neurodegenerative conditions and suggests a possible toxic gain of function for certain mutant forms of Parkin.
Cleavage of neuronal synaptosomal‐associated protein of 25 kDa by exogenous matrix metalloproteinase‐7
Authors: Szklarczyk Arek , Oyler George , McKay Ron , Gerfen Charles , Conant Katherine 
Published: May 2007

AbstractMatrix metalloproteinases (MMPs) belong to a family of zinc dependent enzymes best studied for their role in cancer and inflammation. Though MMPs typically target extracellular proteins, here we show that MMP‐7, an MMP family member which lacks a C‐terminal hemopexin‐like domain, can cleave an intraneuronal protein that is critical to vesicular fusion and neurotransmitter release, synaptosomal‐associated protein of 25 kDa (SNAP‐25). Western blot analysis using an N‐terminal specific antibody on extracts from cultured neurons suggests that cleavage occurs towards the C‐terminal portion of SNAP 25. Additional studies with recombinant SNAP‐25 demonstrate that cleavage occurs at amino acid 129. The ability of MMP‐7 to cleave SNAP‐25 is diminished by chlorpromazine and phenylarsine oxide, inhibitors of clathrin dependent endocytosis. Together, these results imply that exogenous MMP‐7 can access an intraneuronal substrate and suggest that additional studies may be warranted to determine if SNAP function is impaired with brain inflammation.
Curcumin suppresses growth and chemoresistance of human glioblastoma cells via AP‐1 and NFκB transcription factors
Authors: Dhandapani Krishnan M. , Mahesh Virendra B , Brann Darrell W 
Published: May 2007

AbstractMalignant gliomas are a debilitating class of brain tumors that are resistant to radiation and chemotherapeutic drugs, contributing to the poor prognosis associated with these tumors. Over‐expression of transcription factors such as NFκB and AP‐1 contribute to the enhanced glioma survival, radioresistance, and chemoresistance. Curcumin, which may inhibit these pathways, was therefore investigated for a potential therapeutic role in glioma. The effect of curcumin on glioma survival was investigated in human (T98G, U87MG, and T67) and rat (C6) glioma cell lines. The ability of curcumin to overcome glioma cell radioresistance and chemoresistance was also explored. Curcumin reduced cell survival in a p53‐ and caspase‐independent manner, an effect correlated with the inhibition of AP‐1 and NFκB signaling pathways via prevention of constitutive JNK and Akt activation. Curcumin‐sensitized glioma cells to several clinically utilized chemotherapeutic agents (cisplatin, etoposide, camptothecin, and doxorubicin) and radiation, effects correlated with reduced expression of bcl‐2 and IAP family members as well as DNA repair enzymes (MGMT, DNA‐PK, Ku70, Ku80, and ERCC‐1). These findings support a role for curcumin as an adjunct to traditional chemotherapy and radiation in the treatment of brain cancer.
Atmospheric Pressure and Seizure Frequency in the Epilepsy Unit: Preliminary Observations
Authors: Doherty Michael J. , Youn Clover , Gwinn Ryder P. , Haltiner Alan M. 
Published: May 2007

Summary:  Objective: To demonstrate that seizure frequency in patients undergoing video EEG telemetry does not correlate with atmospheric pressure (AP) changes. Method: Historical automated AP data from weather stations in the Seattle Metropolitan area were correlated to seizure frequency and type in consecutive patients undergoing video EEG telemetry at our institution from April 2005–April 2006. Daily maximum, minimum and range of atmospheric pressures were correlated to daily number of events (seizures, pseudoseizures, unknown) per patient. Alternatively, whether or not events occurred during a change of greater or less than 5.5 mBar per day were used to evaluate odds ratios of events occurring. Results: Of 191 patients, 96 were diagnosed with epilepsy, 60 with pseudoseizures, and 40 had different diagnoses. A total of 159 seizures, 59 pseudoseizures, and 40 unknown events occurred. No correlation between daily mean, maximum or minimum pressure change with seizure or other event frequency was seen. With increased daily AP range an increase in daily seizure per known seizure patient occurred (P = 0.03). Patients with known epilepsy showed an OR of a seizure occurring of 2.80 (95% CI 1.22–6.42 P = 0.02) if pressure changed more than 5.5 mBar that day. Conclusions: Surprisingly, in patients with known epilepsy, increased seizure frequency occurred with changes in barometric pressure, particularly over 5.5 mBar range per day. Speculative mechanisms of AP change on seizure susceptibility are discussed.
A Randomized, Double‐Blind, Placebo‐Controlled Trial of Donepezil to Improve Memory in Epilepsy
Authors: Hamberger Marla J. , Palmese Christina A. , Scarmeas Nikolaos , Weintraub David , Choi Hyunmi , Hirsch Lawrence J. 
Published: May 2007

Summary:  Purpose: To determine whether an acetylcholinesterase inhibitor, such as donepezil, would improve memory or other cognitive/psychological functions in epilepsy patients with subjective memory complaints. Methods: Twenty‐three epilepsy patients with subjective memory difficulty were randomized to either 3 months of donepezil (10 mg/day) or 3 months of placebo treatment, and then crossed over to the other treatment arm. Patients and physicians were blinded to treatment phase throughout data acquisition. Assessment of memory and other cognitive functions, subjective memory, mood, and self‐rated quality of life (QOL) and social functioning was performed at baseline and following completion of both treatment phases. Seizure frequency and severity as well as treatment emergent adverse effects were also monitored. Results: Donepezil treatment was not associated with improvement in memory or other cognitive functions, mood, social functioning or QOL. Comparable increases in self‐rated memory functioning relative to baseline were evident during donepezil and placebo phases. Donepezil treatment was not associated with increased seizure frequency or severity. Similar to group results, analysis of change within individual patients as a function of treatment phase also showed neither significant benefit nor detriment associated with donepezil. Conclusion: This study found no benefit on memory or other cognitive/psychological functions in a heterogeneous group of epilepsy patients with subjective memory difficulty. Further investigation would be required to determine whether individual patients, or those with particular epilepsy syndromes, might benefit from donepezil or other acetylcholinesterase inhibitors, or if a higher dosage might be effective.
Substantial Thalamostriatal Dopaminergic Defect in Unverricht‐Lundborg Disease
Authors: Korja Miikka , Kaasinen Valtteri , Lamusuo Salla , Parkkola Riitta , Någren Kjell , Marttila Reijo J. 
Published: May 2007

Summary:  Purpose: Unverricht‐Lundborg disease (ULD) is currently classified as progressive myoclonus epilepsy. Myoclonus, the characteristic symptom in ULD, suggests that dopamine neurotransmission may be involved in the pathophysiology of ULD. Our purpose was to examine brain dopaminergic function in ULD patients. Methods: Four genetically and clinically diagnosed ULD patients and eight healthy controls were scanned with [11C]raclopride‐PET. PET images were coregistered to individual 1.5T MR images and region‐of‐interest analysis was performed for the striatum and thalamus. Standardized uptake values and individual voxel‐wise binding potential maps of the patients and controls were also analyzed. Results: ULD patients had markedly higher (31–54%) dopamine D2‐like receptor availabilities than healthy controls in both the striatum and the thalamus. The proportionally highest binding potentials were detected in the thalamus. There were no significant differences in the cerebellar uptake of [11C]raclopride in ULD patients versus healthy controls. Voxel‐based results were in accordance with the region‐of‐interest analysis. Conclusions: These results suggest that dopaminergic modulation at the level of the striatum and thalamus could be a crucial factor contributing to the symptoms of ULD. In the light of our data, we propose that ULD with dopamine dysfunction and dyskinetic symptoms shares certain pathophysiological mechanisms with classical movement disorders. Future studies are therefore warranted to study the effect of dopaminergic pharmacotherapy in ULD.
FTY720 attenuates accumulation of EMAP‐II+ and MHC‐II+ monocytes in early lesions of rat traumatic brain injury
Authors: Zhang Zhiyuan , Zhang Zhiren , Fauser Uwe , Artelt Matthias , Burnet Michael , Schluesener Hermann J. 
Published: May 2007

AbstractFTY720 (Fingolimod) is a novel type of immunosuppressive agent inhibiting lymphocyte egress from secondary lymphoid tissues thereby causing peripheral lymphopenia. FTY720 can inhibit macrophage infiltration into inflammatory lesions under pathological conditions. FTY720 has been clinically evaluated for prophylaxis of allograft rejection and treatment of multiple sclerosis, showing promising immunosuppressive effects. A robust inflammatory response after traumatic brain injury (TBI) plays an important role in the secondary or delayed injuries of TBI. Here we have investigated by immunohistochemistry in a rat TBI model the effects of FTY720 on early cell accumulation into the inflammatory tissue response and on expression of major histo‐compatibility complex class II (MHC‐II) and endothelial‐monocyte activating polypeptide II (EMAP‐II). Accumulation of MHC‐II+ or EMAP‐II+ cells became significant 1 day after injury and continuously increased during the early time periods. Further, double‐staining experiments confirmed that the major cellular sources of MHC‐II were reactive macrophages, however MHC‐II+ cells only constituted a small subpopulation of reactive macrophages. Immediately after TBI, peripheral administration of FTY720 (1 mg/kg in 1 mL saline, every second day) significantly attenuated the accumulation of MHC‐II+ macrophages from Day 1 to 4 and significantly attenuated the accumulation of EMAP‐II+ macrophages/microglia at Day 4. Our findings show that FTY720 attenuates early accumulation of EMAP‐II+ and MHC‐II+ reactive monocytes following TBI, indicating that FTY720 might be a drug candidate to inhibit brain inflammatory reaction following TBI.
5′AMP‐activated protein kinase α deficiency enhances stress‐induced apoptosis in BHK and PC12 cells
Authors: Shaw Margaret M. , Gurr Werner K. , McCrimmon Rory J. , Schorderet Daniel F. , Sherwin Robert S. 
Published: May 2007

Abstract5′AMP‐activated protein kinase (AMPK) activation occurs under a variety of stress conditions but the role of this enzyme in the promotion or inhibition of stress‐induced cell death is unclear. To address this issue, we transformed two different cell lines with shRNA‐expressing plasmids, targeting the alpha subunit of AMPK, and verified AMPKα downregulation. The cell lines were then stressed by exposure to medium without glucose (PC12 cells) or with the viral thymidine kinase‐specific DNA replication inhibitors: acyclovir, penciclovir and ganciclovir (herpes simplex virus thymidine kinase‐expressing Baby Hamster Kidney cells). In non‐AMPK‐downregulated cells, these stress treatments induced AMPK upregulation and phosphorylation, leaving open the question whether the association of AMPK activation with stress‐induced cell death reflects a successful death‐promoting or an ineffective death‐inhibiting activity. In AMPKα‐deficient cells (expressing AMPKα‐specific shRNAs or treated with Compound C) exposure to low glucose medium or DNA replication inhibitors led to an enhancement of cell death, indicating that, under the conditions examined, the role of activated AMPK is not to promote, but to protect from or delay stress‐induced cell death.