bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fungal foot infection, cellulitis and diabetes: a review
Authors: Bristow I. R. , Spruce M. C. 
Published: April 2009

AbstractAims  To review the current evidence for the presence of fungal foot infection (tinea pedis and toenail onychomycosis) as a risk factor for the development of cellulitis within the lower limb, particularly for those individuals with diabetes.Methods  A structured review of medline, embase and cinahl databases was undertaken to identify publications investigating fungal foot infection as a risk factor for the development of cellulitis.Results  Sixteen studies were identified. Eight studies adopted a case–control methodology, with the remainder being cross‐sectional surveys. The majority of studies established the presence of tinea infection by clinical rather than established microbiological methods. Although the majority of papers suggested a link, only two case–control studies employed microbiological diagnosis to demonstrate that fungal foot infection was a risk for the development of lower limb cellulitis, particularly when infection was located between the toes. There were insufficient data to suggest that fungal foot infection posed an increased risk to patients with diabetes.Conclusion  There is some evidence to suggest that fungal infection of the foot is a factor in the development of lower limb cellulitis, but further robust research is needed to confirm these findings and quantify the risk that fungi pose, particularly to the diabetic foot. Meanwhile, improved surveillance and treatment of tinea infections on the foot by healthcare professionals should be encouraged to reduce potential complications.
Randomized controlled trial to assess the impact of continuous glucose monitoring on HbA1c in insulin‐treated diabetes (MITRE Study)
Authors: Cooke D. , Hurel S. J. , Casbard A. , Steed L. , Walker S. , Meredith S. , Nunn A. J. , Manca A. , Sculpher M. , Barnard M. , Kerr D. , Weaver J. U. , Ahlquist J. , Newman S. P. 
Published: April 2009

AbstractAims  To determine whether continuous glucose information provided through use of either the GlucoWatch G2 Biographer or the MiniMed continuous glucose monitoring system (CGMS) results in improved glycated haemoglobin (HbA1c) for insulin‐treated adults with diabetes mellitus, relative to an attention control and standard care group.Methods  Four hundred and four adults taking at least two daily insulin injections and with two consecutive HbA1c values ≥ 7.5% were recruited to this randomized controlled trial (RCT). All were trained at baseline to use the same monitor for traditional capillary glucose testing throughout the 18‐month study. The CGMS group were asked to wear the device three times during the first 3 months of the trial and on another three occasions thereafter. The GlucoWatch group wore the device a minimum of four times per month and a maximum of four times per week during the first 3 months and as desired for the remainder of the trial. Trained diabetes research nurses used downloaded data to guide therapy adjustments. Proportional reduction in HbA1c from baseline to 18 months was the primary outcome measure.Results  Neither an intention‐to‐treat nor per‐protocol analysis showed improvement in HbA1c in the device groups compared with standard care. For the intention‐to‐treat analysis, when the standard care group was compared with each of the other groups, this equated to differences in mean relative HbA1c reduction (95% confidence interval) from baseline to 18 months of 3.5% (−1.3 to 8.3; GlucoWatch), 0.7% (−4.1 to 5.5; CGMS), and −0.1% (−4.6 to 4.3; attention control).Conclusions  The additional information provided by these devices did not result in improvements in HbA1c in this population.
Effects of rosiglitazone and pioglitazone on lipoprotein metabolism in patients with Type 2 diabetes and normal lipids
Authors: Brackenridge A. L. , Jackson N. , Jefferson W. , Stolinski M. , Shojaee‐Moradie F. , Hovorka R , Umpleby A. M. , Russell‐Jones D. 
Published: April 2009

AbstractAims  Previous studies have suggested that plasma lipids are affected differently by the peroxisome proliferators‐activated receptor (PPAR)‐γ agonists pioglitazone and rosiglitazone. The aim of this study was to perform a quantitative lipoprotein turnover study to determine the effects of PPAR‐γ agonists on lipoprotein metabolism.Methods  Twenty‐four subjects with Type 2 diabetes treated with diet and/or metformin were randomized in a double‐blind study to receive 30 mg pioglitazone, 8 mg rosiglitazone or placebo once daily for 3 months. Before and after treatment, absolute secretion rate (ASR) and fractional catabolic rate (FCR) of very low‐density lipoprotein (VLDL), intermediate‐density lipoprotein (IDL) and low‐density lipoprotein (LDL) apolipoprotein B100 were measured with a 10‐h infusion of 1‐13C leucine.Results  There was a significant decrease in glycated haemoglobin (HbA1c) and non‐esterified fatty acids with pioglitazone (P = 0.01; P = 0.02) and rosiglitazone (P = 0.04; P = 0.003), respectively, but no change in plasma triglyceride or high‐density lipoprotein (HDL) cholesterol. Following rosiglitazone, there was a significant reduction in VLDL apolipoprotein B100 (apoB) ASR (P = 0.01) compared with baseline, a decrease in VLDL triglyceride/apoB (P = 0.01), an increase in LDL2 cholesterol (P = 0.02) and a decrease in LDL3 cholesterol (P = 0.02). There was a decrease in VLDL triglyceride/apoB (P = 0.04) in the pioglitazone group. There was no significant difference in change in VLDL ASR or FCR among the three groups.Conclusions  In patients with Type 2 diabetes and normal lipids, treatment with rosiglitazone or pioglitazone had no significant effect on lipoprotein metabolism compared with placebo.
Reforming pensions: Principles, analytical errors and policy directions
Authors: Barr Nicholas , Diamond Peter 
Published: April 2009

AbstractThis article, sets out a series of principles for pension design rooted in economic theory: pension systems have multiple objectives, analysis should consider the pension system as a whole, analysis should be framed in a second‐best context, different systems share risks differently, and systems have different effects by generation and by gender. That discussion is reinforced by identification of a series of widespread analytical errors — errors that appear in World Bank work, but by no means only in World Bank work: tunnel vision, improper use of first‐best analysis, improper use of steady‐state analysis, incomplete analysis of implicit pension debt, incomplete analysis of the impact of funding (including excessive focus on financial flows, failure to consider how funding is generated, and improper focus on the type of asset in trust funds), and ignoring distributional effects. The second part of the article considers implications for policy: there is no single best pension design, earlier retirement does little or nothing to reduce unemployment, unsustainable pension promises need to be addressed directly, a move from pay‐as‐you‐go towards funding in a mandatory system may or may not be welfare improving, and implementation matters — policy design that exceeds a country's capacity to implement it is bad policy design. We illustrate the ranges of designs of pension systems that fit the fiscal and institutional capacity constraints typical at different levels of economic development. The potential gains from simplicity imply that a country capable of implementing an administratively demanding plan does not necessarily gain from doing so. New Zealand has a simple pension system through choice, not constraint.
Pension system generosity and reform in Algeria, Morocco and Tunisia
Authors: Ben Braham Mehdi 
Published: April 2009

AbstractPension systems in the North African countries of Algeria, Morocco and Tunisia are facing a certain number of difficulties. Presenting the characteristics and organizational structure of each, this article identifies the specificities of, as well as the common problems confronting, these countries' pension systems. With reference to authorizing legislation and case simulations, the high level of generosity of the different pension systems is discussed and an analysis presented. In a context of population ageing, it is argued that current levels of generosity cannot be maintained; reform is needed. The article discusses different reform options, the challenges of implementation and the possible macroeconomic impacts of reform.
Does a top‐predator provide an endangered rodent with refuge from an invasive mesopredator?
Authors: Letnic M. , Crowther M. S. , Koch F. 
Published: April 2009

AbstractIn arid environments, ecological refuges are often conceptualised as places where animal species can persist through drought owing to the localised persistence of moisture and nutrients. The mesopredator release hypothesis (MRH) predicts that reduced abundance of top‐order predators results in an increase in the abundance of smaller predators (mesopredators) and consequently has detrimental impacts on the prey of the smaller predators. Thus according to the MRH, the existence of larger predators may provide prey with refuge from predation. In this study, we investigated how the abundance of an endangered rodent Notomys fuscus is affected by Australia's largest predator, the dingo Canis lupus dingo, introduced mesopredators, introduced herbivores, kangaroos and rainfall. Our surveys showed that N. fuscus was more abundant where dingoes occurred. Generalised linear modelling showed that N. fuscus abundance was associated positively with dingo activity and long‐term annual rainfall and negatively with red fox Vulpes vulpes activity. Our results were consistent with the hypothesis that areas with higher rainfall and dingoes provide N. fuscus with refuge from drought and predation by invasive red foxes, respectively. Top‐order predators, such as dingoes, could have an important functional role in broad‐scale biodiversity conservation programmes by reducing the impacts of mesopredators.
Screen‐detected invasive cervical carcinoma and its clinical significance during the introduction of organized screening
Authors: Herbert A , Anshu  , Gregory M , Gupta SS , Singh N 
Published: April 2009

Objective  To assess the clinical significance of screen‐detected cancer compared with symptomatic cervical cancer during the introduction of organized screening.Study design  Screen‐detected and symptomatic cancers were analysed according to International Federation of Obstetrics and Gynecology stage and histological type of cancer and age of women during four 3‐year periods.Setting  Southampton and South West Hampshire (SSWH).Population  Women resident in SSWH registered with invasive cervical carcinoma between 1985 and 1996.Methods  Screen‐detected and symptomatic cancers were defined on the basis of clinical information obtained at the time of diagnosis and recorded together with date of diagnosis, age group, histology and cytology results. Data were held for analysis on an anonymous spreadsheet.Main outcome measures  Incidence of screen‐detected and symptomatic cancers per 100 000 women; association between route to diagnosis, age group, stage of cancer and screening history during four 3‐year periods.Results  Of 382 cancers, 256 were symptomatic, 78 screen‐detected fully invasive and 48 screen‐detected microinvasive. Incidence of symptomatic cancers fell from 13.0 to 6.4 per 100 000 total female population (P = 0.0005), and there was a trend towards screen‐detected cancers as a proportion of all cancers (P = 0.002). By the latest period of the study (1994–96), the likelihood of cancers being screen‐detected was strongly associated with younger age groups (P = 0.001). Screen‐detected fully invasive cancers were significantly less likely (P = 0.001) to be diagnosed at stage II or above (16.6%) compared with symptomatic cancers (63.3%). Women with screen‐detected microinvasive cancers were significantly more likely (P < 0.001) to have been screened within 5 years (83.3%) than screen‐detected fully invasive cancers (60.2%) or symptomatic cancers (33.6%).Conclusion  Screen‐detected cancers were more likely to be diagnosed at an earlier stage, in younger women and in women who had previously been screened and became relatively more frequent as symptomatic cancers declined.
Treating miscarriages: a randomised study of cost‐effectiveness in medical or surgical choice
Authors: Niinimäki M , Karinen P , Hartikainen A‐L , Pouta A 
Published: April 2009

Objective  The aim was to carry out a cost effectiveness analysis (CEA) of medical and surgical treatment of miscarriage using quantitative and qualitative indicators.Design  A prospective study where the data of the clinical course of the treatment and the patients` experiences (pain and satisfaction) were collected from a previous randomised study.Setting  Department of Obstetrics and Gynecology, Oulu University Hospital, Oulu, Finland.Population  Ninety‐eight eligible women with a diagnosed miscarriage.Methods  The incremental cost‐effectiveness ratio (ICER) was calculated by using institutional prices (provider’s aspect) of the medical care and the number of patients who experienced pain, dissatisfaction or unsuccessful treatment while treated for the miscarriage.Main outcome measures  Primary (uncomplicated treatment) and secondary (complications and other unplanned events) costs of the treatments.Results  Primary costs of the surgical treatment were higher, but the more frequent unplanned events and complications in the medical group brought the costs to the same level. In the medical group, based on the ICER, 12 patients more experienced pain, 7 patients more were dissatisfied with the treatment and 5 patients more had unsuccessful treatment compared with surgically treated patients. In theory, these negative outcomes could have been avoided by investing €1688 more in the surgical treatment.Conclusions  Medical treatment of miscarriage was not more cost‐effective, when the adverse events were considered. As neither of these two methods was economically superior, the treatment choice should be made on an individual basis by respecting the patient’s choice.
Rescue of Aβ1–42‐induced memory impairment in day‐old chick by facilitation of astrocytic oxidative metabolism: implications for Alzheimer’s disease
Authors: Gibbs Marie E. , Gibbs Zoe , Hertz Leif 
Published: April 2009

AbstractAdministration of small oligomeric β‐amyloid (Aβ)1–42 45 min before one‐trial bead discrimination learning in day‐old chicks abolishes consolidation of learning 30 min post‐training (Gibbs et al. Neurobiol. Aging, in press). Administration of the β3‐adrenergic agonist CL316243, which specifically stimulates astrocytic but not neuronal glucose uptake, rescues Aβ impaired memory. Weakly reinforced training can be consolidated by various metabolic substrates and we have demonstrated neuronal dependence on oxidative metabolism of glucose soon after training versus astrocytic glucose dependence 20 min later. Based on these findings we examined whether different metabolic substrates were able to counteract memory inhibition by Aβ1–42. Although lactate, the medium‐chain fatty acid octanoate, and the ketone body β‐hydroxybutyrate consolidated weakly reinforced training when injected close to learning, none of them were able to salvage Aβ‐impaired memory; at this early time. All three metabolites and the astrocytic‐specific acetate consolidated weak learning and rescued Aβ‐impaired memory when injected 10–20 min post‐training. However, neither glucose nor insulin rescued memory when injected at 20 min. Rescue of memory by providing astrocytes with alternative substrates for oxidative metabolism suggests that Aβ1–42 exerts its amnestic effects specifically by impairing astrocytic glycolysis.
Cerebral oxygen demand for short‐lived and steady‐state events
Authors: Herman Peter , Sanganahalli Basavaraju G. , Blumenfeld Hal , Hyder Fahmeed 
Published: April 2009

AbstractBecause of the importance of oxidative energetics for cerebral function, extraction of oxygen consumption (CMRO2) from blood oxygenation level‐dependent (BOLD) signal using multi‐modal measurements of blood flow (CBF) and volume (CBV) has become an accepted functional magnetic resonance imaging (fMRI) technique. This approach, termed calibrated fMRI, is based on a biophysical model which describes tissue oxygen extraction at steady‐state. A problem encountered for calculating dynamic CMRO2 relates to concerns whether the conventional BOLD model can be applied transiently. In particular, it is unclear whether calculation of CMRO2 differs between short and long stimuli. Linearity was experimentally demonstrated between BOLD‐related components and neural activity, thereby making it possible to use calibrated fMRI in a dynamic manner. We used multi‐modal fMRI and electrophysiology, in α‐chloralose anesthetized rats during forepaw stimulation to show that respective transfer functions (of BOLD, CBV, CBF) generated by deconvolution with neural activity are time invariant, for events in the millisecond to minute range. These results allowed extraction of a significant component of the BOLD signal that can be ascribed to CMRO2 transients. We discuss the importance of minimizing residual signal, represented by the difference between modeled and raw signals, in convolution analysis of multi‐modal signals.
The role of abnormal mitochondrial dynamics in the pathogenesis of Alzheimer’s disease
Authors: Wang Xinglong , Su Bo , Zheng Ling , Perry George , Smith Mark A. , Zhu Xiongwei 
Published: April 2009

AbstractMitochondria play critical roles in neuronal function and almost all aspects of mitochondrial function are altered in Alzheimer neurons. Emerging evidence shows that mitochondria are dynamic organelles that undergo continuous fission and fusion, the balance of which not only controls mitochondrial morphology and number, but also regulates mitochondrial function and distribution. In this review, after a brief overview of the basic mechanisms involved in the regulation of mitochondrial fission and fusion and how mitochondrial dynamics affects mitochondrial function, we will discuss in detail our and others’ recent work demonstrating abnormal mitochondrial morphology and distribution in Alzheimer’s disease (AD) models and how these abnormalities may contribute to mitochondrial and synaptic dysfunction in AD. We propose that abnormal mitochondrial dynamics plays a key role in causing the dysfunction of mitochondria that ultimately damage AD neurons.
Acetate transport and utilization in the rat brain
Authors: Deelchand Dinesh K. , Shestov Alexander A. , Koski Dee M. , Uğurbil Kâmil , Henry Pierre‐Gilles 
Published: April 2009

AbstractAcetate, a glial‐specific substrate, is an attractive alternative to glucose for the study of neuronal‐glial interactions. The present study investigates the kinetics of acetate uptake and utilization in the rat brainin vivoduring infusion of [2‐13C]acetate using NMR spectroscopy. When plasma acetate concentration was increased, the rate of brain acetate utilization (CMRace) increased progressively and reached close to saturation for plasma acetate concentration > 2–3 mM, whereas brain acetate concentration continued to increase. The Michaelis–Menten constant for brain acetate utilization ( = 0.01 ± 0.14 mM) was much smaller than for acetate transport through the blood–brain barrier (BBB) ( = 4.18 ± 0.83 mM). The maximum transport capacity of acetate through the BBB ( = 0.96 ± 0.18 μmol/g/min) was nearly twofold higher than the maximum rate of brain acetate utilization ( = 0.50 ± 0.08 μmol/g/min). We conclude that, under our experimental conditions, brain acetate utilization is saturated when plasma acetate concentrations increase above 2–3 mM. At such high plasma acetate concentration, the rate‐limiting step for glial acetate metabolism is not the BBB, but occurs after entry of acetate into the brain.
Delayed cerebral oxidative glucose metabolism after traumatic brain injury in young rats
Authors: Scafidi Susanna , O’Brien Janet , Hopkins Irene , Robertson Courtney , Fiskum Gary , McKenna Mary 
Published: April 2009

AbstractTraumatic brain injury (TBI) results in a cerebral metabolic crisis that contributes to poor neurologic outcome. The aim of this study was to characterize changes in oxidative glucose metabolism in early periods after injury in the brains of immature animals. At 5 h after controlled cortical impact TBI or sham surgery to the left cortex, 21–22 day old rats were injected intraperitoneally with [1,6‐13C]glucose and brains removed 15, 30 and 60 min later and studied by ex vivo 13C‐NMR spectroscopy. Oxidative metabolism, determined by incorporation of 13C into glutamate, glutamine and GABA over 15–60 min, was significantly delayed in both hemispheres of brain from TBI rats. The most striking delay was in labeling of the C4 position of glutamate from neuronal metabolism of glucose in the injured, ipsilateral hemisphere which peaked at 60 min, compared with the contralateral and sham‐operated brains, where metabolism peaked at 30 and 15 min, respectively. Our findings indicate that (i) neuronal‐specific oxidative metabolism of glucose at 5–6 h after TBI is delayed in both injured and contralateral sides compared with sham brain; (ii) labeling from metabolism of glucose via the pyruvate carboxylase pathway in astrocytes was also initially delayed in both sides of TBI brain compared with sham brain; (iii) despite this delayed incorporation, at 6 h after TBI, both sides of the brain showed apparent increased neuronal and glial metabolism, reflecting accumulation of labeled metabolites, suggesting impaired malate aspartate shuttle activity. The presence of delayed metabolism, followed by accumulation of labeled compounds is evidence of severe alterations in homeostasis that could impair mitochondrial metabolism in both ipsilateral and contralateral sides of brain after TBI. However, ongoing oxidative metabolism in mitochondria in injured brain suggests that there is a window of opportunity for therapeutic intervention up to at least 6 h after injury.
Transcranial flavoprotein fluorescence imaging of mouse cortical activity and plasticity
Authors: Tohmi Manavu , Takahashi Kuniyuki , Kubota Yamato , Hishida Ryuichi , Shibuki Katsuei 
Published: April 2009

AbstractEndogenous fluorescence signals derived from mitochondria reflect activity‐dependent changes in brain metabolism and may be exploited in functional brain imaging. Endogenous flavoprotein fluorescence imaging in mice is especially important because many genetically manipulated strains of mice are available and the transparent skull of mice allows transcranial fluorescence imaging of cortical activities. In the primary sensory areas of mice, cortical activities and experience‐dependent plasticity have been investigated using transcranial fluorescence imaging. Furthermore, differential imaging, based on stimulus specificity of cortical areas, distinguished activities in higher visual areas around the primary visual cortex from those in primary visual cortex. The combination of transcranial fluorescence imaging with the suppression of cortical activities using photobleaching of flavoproteins is expected to aid in elucidating the roles of sensory cortices including higher areas in mice.