bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fasting – the ultimate diet?
Authors: Johnstone A. M. 
Published: August 2006

SummaryAdult humans often undertake acute fasts for cosmetic, religious or medical reasons. For example, an estimated 14% of US adults have reported using fasting as a means to control body weight and this approach has long been advocated as an intermittent treatment for gross refractory obesity. There are unique historical data sets on extreme forms of food restriction that give insight into the consequences of starvation or semi‐starvation in previously healthy, but usually non‐obese subjects. These include documented medical reports on victims of hunger strike, famine and prisoners of war. Such data provide a detailed account on how the body adapts to prolonged starvation. It has previously been shown that fasting for the biblical period of 40 days and 40 nights is well within the overall physiological capabilities of a healthy adult. However, the specific effects on the human body and mind are less clearly documented, either in the short term (hours) or in the longer term (days). This review asks the following three questions, pertinent to any weight‐loss therapy, (i) how effective is the regime in achieving weight loss, (ii) what impact does it have on psychology? and finally, (iii) does it work long‐term?
International school‐based interventions for preventing obesity in children
Authors: Sharma M. 
Published: August 2006

SummaryThe purpose of this article was to review international (excluding the United States) school‐based interventions for preventing obesity in children published between 1999 and 2005. A total of 21 such interventions were found from Australia (1), Austria (1), Canada (1), Chile (1), France (1), Germany (3), Greece (1), New Zealand (1), Norway (1), Singapore (1) and the United Kingdom (9). The grade range of these interventions was from pre‐school to high school with the majority (17) from elementary schools. Nine of these interventions targeted nutrition behaviours followed by seven aiming to modify both physical activity and nutrition behaviours. Only five interventions in international settings were based on any explicit behavioural theory which is different than the interventions developed in the United States. Majority of the interventions (9) were one academic year long. It can be speculated that if the interventions are behavioural theory‐based, then the intervention length can be shortened. All interventions that documented parental involvement successfully influenced obesity indices. Most interventions (16) focused on individual‐level behaviour change approaches. Most published interventions (16) used experimental designs with at least 1‐year follow‐up. Recommendations from international settings for enhancing the effectiveness of school‐based childhood obesity interventions are presented.
Obesity, metabolic syndrome and sleep apnoea: all pro‐inflammatory states
Authors: Alam I. , Lewis K. , Stephens J. W. , Baxter J. N. 
Published: August 2006

SummaryObesity is associated with significant morbidity and mortality and is increasing in prevalence worldwide. Associated conditions include insulin resistance (IR), diabetes, hypertension and dyslipidaemia; a clustering of these has recently been termed as metabolic syndrome. Weight gain is a major predictor of the metabolic syndrome with waist circumference being a more sensitive indicator than body mass index as it reflects both abdominal subcutaneous adipose tissue and visceral adipose tissue (VAT). VAT has more metabolic activity and secretes a number of hormones and pro‐inflammatory cytokines which are linked with the metabolic abnormalities listed above. Central obesity also increases the risk of obstructive sleep apnoea syndrome (OSAS), where the sleep disordered breathing may also independently lead to/or exacerbate IR, diabetes and cardiovascular risk. The contribution of OSAS to the metabolic syndrome has been under‐recognized. The putative mechanisms by which OSAS causes or exacerbates these other abnormalities are discussed. We propose that activation of nuclear factor kappa B by stress hypoxia and/or by increased adipokines and free fatty acids released by excess adipose tissue is the final common inflammatory pathway linking obesity, OSAS and the metabolic syndrome both individually and, in many cases, synergistically.
BHAGAVAD GĪTĀ AS DUTY AND VIRTUE ETHICS
Authors: Gupta Bina 
Published: August 2006

ABSTRACTThe paper examines the ethical conception of the most well‐known and much discussed Hindu text, the Bhagavad Gītā, in the context of the Western distinction between duty ethics and virtue ethics. Most of the materials published on the Gītā make much of its conception of duty; however, there is no systematic investigation of the notion of virtue in the Gītā. The paper begins with a discussion of the fundamental characteristics of virtue ethics, before undertaking a discussion of the conceptions of duty and virtue in the Gītā. The paper clearly demonstrates that (1) both duty and virtue coexist in the Gītā, and (2) the Gītā accords virtue an important place.
FRANK CONVERSATIONS
Authors: Dickens W. T. 
Published: August 2006

ABSTRACTI contend that Jews, Christians, and Muslims who seek peace should not be reluctant to acknowledge the existence of their sometimes profound disagreements, or to affirm the truth of their own beliefs and practices. Since this places me at odds with John Hick, I analyze his views, granting the strengths of his critical realism and arguing that his revisionist–pluralist theory of religion has significant limitations for interreligious dialogue. Since the veridical–pluralist alternative I propose facilitates rather than stifles disagreement, I examine three different conceptions of dialogue that acknowledge the importance of disputes among those searching for truth. I also discuss three virtues—honesty, empathy, and humility—whose cultivation would make us less likely to fail in our search for truth and the peace that is its sign and fruit.
THE MISFORTUNE OF THE HAPPY
Authors: Ferreira M. Jamie 
Published: August 2006

ABSTRACTLevinas himself raises the question: “why would I feel responsible in the presence of the Face” since “we are separate ontological beings?” This questions the character of our response to the other—both in terms of agency and motivation. While the general reception of Levinas's thought has focused on his description of us as “hostage”—that is, on the moment of assignation (or assignment) by the other—I suggest that Levinas himself also, though not as directly, addresses (as he needs to) the correlative moment, the moment of response. My essay reconstructs Levinas's implicit understanding of the character of our initiative in the light of his concept of Desire. I explore the different dimensions of Desire as appetite and generosity, and I argue that the “transition to moral consciousness” that Levinas wants to “justify” is one from complacent happiness to “non‐complacent happiness” and can be illuminated by the notion of “passion seeking its downfall.”
From Beveridge to Turner: Demography, Distribution and the Future of Pensions in the UK
Authors: Hills John 
Published: August 2006

SummaryThe paper outlines the recommendations of the UK Pensions Commission, and the data and analysis on which they were based, including projections of demographic change, trends in private pension saving and evolution of the State pension system. The Commission concluded that, without reform, structural problems with UK pensions would lead to increasingly inadequate and inequitable provision by 2020–2025. It recommended reforms which would lead to a more generous, more universal and less means-tested State system than would otherwise evolve, and the establishment of a low cost national pension savings scheme, into which employees without good employer provision would automatically be enrolled. The proposals, which have now largely been adopted by the UK Government, imply eventual increases both in state spending on pensions as a share of national income and in State pension age, but accompanied by measures to facilitate later and more flexible retirement.
Cartilage, SOX9 and Notch signals in chondrogenesis
Authors: Hardingham Timothy E. , Oldershaw Rachel A. , Tew Simon R. 
Published: August 2006

AbstractCartilage repair is an ongoing medical challenge. Tissue engineered solutions to this problem rely on the availability of appropriately differentiated cells in sufficient numbers. This review discusses the potential of primary human articular chondrocytes and mesenchymal stem cells to fulfil this role. Chondrocytes have been transduced with a retrovirus containing the transcription factor SOX9, which permits a greatly improved response of the cells to three‐dimensional culture systems, growth factor stimulation and hypoxic culture conditions. Human mesenchymal stem cells have been differentiated into chondrocytes using well‐established methods, and the Notch signalling pathway has been studied in detail to establish its role during this process. Both approaches offer insights into these in vitro systems that are invaluable to understanding and designing future cartilage regeneration strategies.
How to build and rebuild a lens
Authors: Tsonis Panagiotis A. 
Published: August 2006

AbstractEvolution has used many different strategies to build eyes and lenses. However, the genetic regulation involved seems to be quite conserved. Likewise, the regeneration of eye structures is remarkable, especially in salamanders. This review outlines the basic mechanisms of lens regeneration and its induction and the possibility of creating lenses by transdifferentiation of the pigment epithelial cells, by stem cells or by bioengineering.
Neuronal sensitivity to kainic acid is dependent on the Nrf2‐mediated actions of the antioxidant response element
Authors: Kraft Andrew D. , Lee Jong‐Min , Johnson Delinda A. , Kan Yuet Wai , Johnson Jeffrey A. 
Published: August 2006

AbstractThe transcription factor, nuclear factor E2 (erythroid‐derived 2)‐related factor 2 (Nrf2), is essential for the induction of a battery of phase II detoxification genes through the antioxidant response element (ARE) that lies in their promoter region. Genes driven by the ARE are up‐regulated in response to various stressors of the cellular environment. These genetic changes to the cellular reducing potential may reflect an intrinsic damage response to harmful toxicants. Analysis of transgenic reporter mice following kainate injection revealed selective ARE activation within the damaged hippocampus. Further, 2 × 2 microarray analyses comparing Nrf2 knockout versus wild‐type hippocampi unmasked gene changes associated with ion movement and myelination, in addition to alterations to detoxification‐related genes. Nrf2 knockout mice were more sensitive to kainate toxicity, as evidenced by elevated seizure severity, seizure duration, hippocampal neuron damage and mortality. Knockout mice injected with kainate displayed altered glial fibrillary acidic protein immunoreactivity and increased microglial infiltration. The wild‐type to knockout damage differential was not dependent on the peripheral metabolism of the excitotoxin, was well correlated with increased seizure susceptibility, and was therefore not necessarily the neuroprotective effects of Nrf2. These results combine to support a role for Nrf2 in the neural cell defense response of the adult brain.
Post‐ versus presynaptic plasticity in L‐DOPA‐induced dyskinesia
Authors: Cenci M. Angela , Lundblad Martin 
Published: August 2006

AbstractL‐3,4‐dihydroxyphenylalanine (L‐DOPA) remains the most efficacious drug for the treatment of Parkinson's disease (PD), but causes adverse effects that limit its utility. L‐DOPA‐induced dyskinesia (abnormal involuntary movements) is a significant clinical problem that attracts growing scientific interest. Current notions attribute the development of dyskinesia to two main factors, viz. the loss of nigrostriatal dopamine (DA) projections and the maladaptive changes produced by L‐DOPA at sites postsynaptic to the nigrostriatal neuron. Basic research in the past 15 years has placed a lot of emphasis on the postsynaptic plasticity associated with dyskinesia, but recent experimental work shows that also some presynaptic factors, involving the regulation of L‐DOPA/DA release and metabolism in the brain, may show plasticity during treatment. This review summarizes significant studies of L‐DOPA‐induced dyskinesia in patients and animal models, and outlines directions for future experiments addressing mechanisms of presynaptic plasticity. These investigations may uncover clues to the varying susceptibility to L‐DOPA‐induced dyskinesia among PD patients, paving the way for tailor‐made treatments.
Rapid co‐release of interleukin 1β and caspase 1 in spinal cord inflammation
Authors: Clark Anna K. , D'Aquisto Fulvio , Gentry Clive , Marchand Fabien , McMahon Stephen B. , Malcangio Marzia 
Published: August 2006

AbstractMounting evidence supports the hypothesis that pro‐inflammatory cytokines secreted by astrocytes and microglia modulate nociceptive function in the injured CNS and following peripheral nerve damage. Here we examine the involvement of interleukin‐1β (IL‐1β) and microglia activation in nociceptive processing in rat models of spinal cord inflammation. Following application of lipopolysaccharide (LPS) to anex vivodorsal horn slice preparation, we observed rapid secretion of IL‐1β which was prevented by inhibition of glial cell metabolism and by inhibitors of either p38 mitogen‐activated protein kinase (MAPK) or caspase 1. LPS superfusion also induced rapid secretion of active caspase 1 and apoptosis‐associated speck‐like protein containing a caspase recruitment domain from the isolated dorsal horn. Extensive microglial cell activation in the dorsal horn, as determined by immunoreactivity for phosphorylated p38 MAPK, was found to correlate with the occurrence of IL‐1β secretion. In behavioural studies, intrathecal injection of LPS in the lumbar spinal cord produced mechanical hyperalgesia in the rat hind‐paws which was attenuated by concomitant injections of a p38 MAPK inhibitor, a caspase 1 inhibitor or the rat recombinant interleukin 1 receptor antagonist. These data suggest a critical role for the cytokine IL‐1β and caspase 1 rapidly released by activated microglia in enhancing nociceptive transmission in spinal cord inflammation.
Neuroprotectant FK506 inhibits glutamate‐induced apoptosis of astrocytes in vitro and in vivo
Authors: Szydlowska Kinga , Zawadzka Malgorzata , Kaminska Bozena 
Published: August 2006

AbstractNeuron–astrocyte interactions are critical for signalling, energy metabolism, extracellular ion and glutamate homeostasis, volume regulation and neuroprotection in the CNS. Glutamate uptake by astrocytes may prevent excitotoxic glutamate elevation and determine neuronal survival. However, an excess of glutamate can cause the death of astrocytes. FK506, an inhibitor of calcineurin, and an immunosuppressive drug, is neuroprotective in animal models of neurologic diseases, including focal and global ischaemia. In the present work, we demonstrate that a single injection of FK506 60 min after a transient middle cerebral artery occlusion (MCAo) significantly decreases the number of terminal deoxynucleotidyl transferase nick‐end labelling (TUNEL)‐positive cells in the ischaemic cortex and striatum. Using 3‐D confocal microscopy we found that, 24 h after MCAo, many TUNEL‐positive cells in the ischaemic striatum and cortex are astrocytes. Furthermore, we demonstrate that exposure of cultured cortical astrocytes to 50–100 mM Glu for 24 h induces apoptotic alterations in nuclear morphology, DNA fragmentation, dissipation of mitochondrial transmembrane potential (ΔΨ) and caspase activation. FK506 (1 μM) efficiently inhibits Glu‐induced apoptosis of cultured astrocytes, DNA fragmentation and changes in mitochondrial ΔΨ. Our findings suggest that modulation of glutamate‐induced astrocyte death early after reperfusion may be a novel mechanism of FK506‐mediated neuroprotection in ischaemia.
Noncoding mitochondrial loci for corals
Authors: CONCEPCION GREGORY T. , MEDINA MONICA , TOONEN ROBERT J. 
Published: August 2006

AbstractWe developed five degenerate primer pairs for the amplification and sequencing of two noncoding regions found in the mitochondrial genome of corals. These primers amplify products ranging from 380 to 950 bp, and work in a wide variety of scleractinian taxa from both the Pacific and Caribbean. Based on our initial analysis of ∼300 sequences from 13 scleractinian taxa, both these noncoding regions appear to have equivalent levels of variability to the most variable of previously published coral mitochondrial loci, but work in a wider variety of taxa. We believe these primers will be of use to coral biologists studying questions above the level of species; as with other mithochondrial DNA markers in corals, these loci will likely provide little resolution for within‐species studies.
Identification of microsatellite loci in Collinsia verna (Veronicaceae)
Authors: DUNN JESSICA L. , DIERKES LINDSAY , PICÓ F. XAVIER , KALISZ SUSAN 
Published: August 2006

AbstractWe developed eight polymorphic microsatellite loci for Collinsia verna (Veronicaceae). In a sample of 18–35 individuals from a single population, we found two to 15 alleles per locus (mean 8.3). We also tested these loci for cross‐amplification in all 22 species in the tribe Collinseae. Overall, more than half the species in the tribe amplified one microsatellite while three species most closely related to C. verna (Collinsia violacea, Collinsia parviflora and Collinsia grandiflora) amplified multiple microsatellite loci. These microsatellite loci will be used in future studies of mating system in this tribe and other quantitative genetic and population genetic studies.
Polymorphic microsatellite markers isolated from partially enriched genomic library of Chitala chitala
Authors: PUNIA PEYUSH , GUPTA HARI SHANKAR , SINGH RAJEEV K , MOHINDRA VINDHYA , LAL KULDEEP K , RANJANA  , CHAUHAN V S , LAKRA W S 
Published: August 2006

AbstractA total eight polymorphic microsatellite loci were obtained from genomic library of Indian feather back, Chitala chitala (order Osteoglossiformes, family Notopteridae) and the 46 samples were analysed to determine genetic variation. The mean number of alleles per locus ranged from 4.50 to 5.25, and expected heterozygosity ranged from 0.124 to 0.852. Deviation from Hardy–Weinberg equilibrium expectations (P < 0.002) was observed at loci Cch2, Cch9 (Bhaghirathi) and Cch9 (Brahmaputra). The identified microsatellite loci were found promising for population genetics studies of C. chitala and related species Notopterus notopterus (family Notopteridae).
Oxygen supplementation increases glucose tolerance during euglycaemic hyperinsulinaemic glucose clamp procedure in patients with severe COPD and chronic hypoxaemia
Authors: Jakobsson P. , Jorfeldt L. 
Published: August 2006

SummaryInvestigations in chronic obstructive pulmonary disease (COPD) patients have shown impaired glucose tolerance in hypoxic COPD patients, compared with COPD patients with normal arterial blood gases. In healthy subjects, hypoxaemia or stay at altitude, have been shown to alter glucose metabolism. At altitude the effect seems to be dependent on duration of stay. A short stay is associated with insulin resistance, a longer stay gives rise to increased glucose uptake. The euglycaemic hyperinsulinaemic glucose clamp technique is a method to study glucose tolerance and enables determinations of glucose clearance in peripheral tissues. We investigated six COPD patients [forced expiratory volume in 1 s 0·7 ± 0·2 l (mean ± SD)] with chronic hypoxaemia (PaO2 7·9 ± 0·6 kPa at rest, breathing air), with and without oxygen supplementation, using the glucose clamp technique. Net peripheral glucose uptake was 5·5 ± 1·2 and 7·1 ± 1·6 mg (kg*min)−1 (+29%) breathing air and supplemental oxygen, respectively (P = 0·03). The tissue sensitivity to insulin increased 32% (P = 0·03) with oxygen supplementation. The results indicate that normalization of oxygen saturation in COPD patients with chronic hypoxaemia may have an immediate effect on glucose tolerance and tissue sensitivity to insulin in these patients.
Influence of cardiac output level on oxygen exchange in chronic obstructive pulmonary disease patients
Authors: Manier Gérard , Pillet Odile , Castaing Yves 
Published: August 2006

SummaryStudy objectives:  In the course of chronic obstructive pulmonary disease (COPD), pulmonary gas exchange deteriorates as a result of ventilation/perfusion inequalities and hypoxaemia. The aim of the present study was to evaluate the influence of cardiac output (CO) level observed at rest in COPD patients on interaction between central and peripheral O2 exchange.Methods:  One hundred and nine patients with advanced but stable COPD were analysed in a retrospective study by the multiple inert gas elimination technique. As a function of CO, simulations were conducted to evaluate the respective part of PvO2 and inequalities on the degree of hypoxaemia.Measurements and results:  PaO2 was linked (i) to cardiac index (CI), (ii) to mean ratio of blood flow distribution and (iii) to PvO2, but PvO2 was not correlated with CO. By comparing two groups with CI above and below the mean value of the series respectively, a significant difference was identified in PaO2 (57 ± 9 mmHg in the high CI group versus 63 ± 10 mmHg in the low CI group, P<0·05) because of higher inequalities in the high CI group. Comparing two other groups with values of PvO2 above and below the mean value of the series respectively, a significant difference was identified in PaO2: (mean ± SD was 65 ± 8 in high PvO2 group versus 56 ± 9 mmHg, P<0·001) but with no difference in either CI or perfusion distribution. Analysis of the cumulated effects of PvO2 and CI values, indicated that high CI and low PvO2 gave rise to the lowest PaO2 (53 ± 8 mmHg), with the highest PaO2 (68 ± 8 mmHg) being found in the low CI and normal PvO2 group.Conclusions:  We concluded that in COPD patients, PaO2 appeared to be maintained better when peripheral gas exchange coped with tissue demand without an increase in CO. Conversely, when the physiological increase in CO could not maintain adequate tissue gas exchange, PaO2 continued to fall due to the cumulative effects of increasing CO on inequalities and low PvO2.
Prognostic value of myocardial perfusion imaging in patients with known or suspected stable angina pectoris: Evaluation in a setting in which myocardial perfusion imaging did not influence the choice of treatment
Authors: Johansen Allan , Høilund‐Carlsen Poul F. , Vach Werner , Christensen Henrik W. , Møldrup Mette , Haghfelt Torben 
Published: August 2006

SummaryObjective:  Previous investigations on the prognostic value of myocardial perfusion imaging (MPI) were performed under circumstances in which the test result was known to the patient's physician. We wanted to examine the prognostic value of MPI in patients with known or suspected stable angina in a setting in which MPI could not influence the diagnostic and therapeutic strategy.Design:  A prospective series of 507 patients referred to coronary angiography for this condition were examined by MPI before angiography. Management was based on symptoms and angiographic findings, as the results of MPI were not communicated. Patients were followed for a mean of 45·3 ± 7·7 months.Results:  During follow‐up, 20 patients (3·9%) suffered from myocardial infarction, 19 (3·8%) died and eight (1·6%) were revascularized >1 year after MPI resulting in a combined annual event rate of 2·5%. Patients with normal MPI had a low annual event rate of 1·6% (or 1·1% with regard to myocardial infarction or death only). In contrast, event rates in patients with reversible or mixed ischaemia were 4·0% per year. MPI added independent prognostic value to standard clinical data in a multivariate Cox model.Conclusion:  We could confirm that in patients with known or suspected stable angina, MPI is a valuable risk stratifying tool.