Miracle-dz/UniFAR-FTUs huggingface dataset:
Metabolic indicators of fibre recruitment in mammalian muscles during locomotion.

Fast-twitch-oxidative-glycolytic (FOG), fast-twitch-glycolytic (FG) and slow-twitch-oxidative (SO) fibres are distributed within and among physiological extensor muscles in mammals in predictable patterns. Deep muscles and the deep portions of extensor muscles are primarily composed of SO and FOG fibres, and the more peripheral portions of the muscles have higher concentrations of FG fibres. During terrestrial locomotion, the fibres are recruited in this same general order from postural standing through high speed running to jumping (i.e. during standing deep SO fibres are active and during locomotion there is a progressive peripheral recruitment of fibres from SO to FOG to FG). Several metabolic indicators may be used to map these fibre recruitment patterns, including glycogen loss in fibres, metabolic enzyme changes during training at different speeds, and distribution of blood flow within and among the muscles. Concerning the latter, during standing in rats blood flows in the hindlimb muscles are directly proportional to the SO fibre populations in the muscles. However, during locomotion the elevations in blood flow over pre-exercise are a function of the populations of FOG fibres in the muscles. Blood flows in the peripheral white portions (FG fibres) of extensor muscles are not significantly elevated until the rats run at high speeds, when the FG fibres presumably are recruited. During swimming, when flexor muscles are relatively more active than extensor muscles (as compared with terrestrial locomotion), blood flows in the flexors are correspondingly higher. Thus, there exists a clear 'biological economy' in the matching of blood flow to the specific fibres that are active within and among muscles during exercise.
Choroidal Thickness after Treatment for Myopic Choroidal Neovascularization

Purpose To evaluate choroidal thickness in highly myopic eyes with choroidal neovascularization (CNV), 3 or more years after treatment with photodynamic therapy (PDT), intravitreal ranibizumab (IVR), or both (PDT + IVR). Methods The medical records of patients with high myopia and CNV treated with PDT or IVR in our department were reviewed. Eyes meeting the inclusion criteria were assigned to 3 groups: PDT, IVR, and PDT + IVR. A fourth group, “dry myopic maculopathy,” included the contralateral highly myopic eyes that never developed CNV. All patients performed a cross-sectional evaluation with best-corrected visual acuity (BCVA), measurement of axial length, color fundus photography, and enhanced depth imaging with spectral domain optical coherence tomography. Results Forty-two eyes (21 patients) were included: 11 eyes (26.2%) in the PDT group, 8 (19.0%) in the IVR group, 9 (21.4%) in the PDT + IVR group, and 14 (33.3%) in the dry maculopathy group. Subfoveal choroidal thickness showed no significant differences between groups (p>0.05). Positive correlation was found between BCVA and macular choroidal thickness (r = +0.293, p<0.001). Regression analysis showed that age (p<0.001), axial length (p<0.001), sex (p = 0.001), and myopic lesions such as tessellated fundus (p = 0.046) and patchy atrophy (p = 0.008) were predictive of choroidal thickness. Type of treatment was not predictive of choroidal thickness. Conclusions Older age and greater axial length are the major factors associated with macular choroidal thinning in highly myopic eyes submitted to CNV treatment. The type of treatment performed for myopic CNV had no predictive contribution for choroidal thickness.
Dynamic microgrid-based operations: A new operational paradigm for distribution networks

This paper expands the conventional concept of microgrids - predetermined groups of loads and generators electrically connected to each other and possibly to the main power grid - into a new concept of dynamic microgrids (DMs) which allows different groupings of these resources based on actual real time supply and demand conditions in the network. Under the DM paradigm, the distribution network is continuously partitioned into dynamically changing microgrid cells which can be leveraged to improve the operational performance of distribution networks. The paper describes algorithms to define DMs based on real time conditions and also proposes a DM-based operational strategy wherein DMs operate in tandem during normal operations and can function as islands during faults to minimize customer interruptions. Simulations on standard test systems are used to demonstrate how such a strategy can be leveraged to minimize the impact of disturbances on customers, maximize the deployment of renewable generation and improve asset utilization.
Antagonism of Antinociception Produced by Intrathecal Clonidine by Ketorolac in the Rat: The Role of the Opioid System

The management of severe pain may require “balanced analgesia,” involving the use of analgesics with different modes of action. Clonidine, an &agr;2-adrenoreceptor agonist produces analgesia by itself as well as when given with morphine and local anesthetics. Ketorolac is indicated for the management of moderately severe acute pain and causes analgesia equivalent to morphine. This study was designed to investigate whether the addition of ketorolac promotes antinociception produced by intrathecal administration of clonidine in male Sprague-Dawley rats. Intrathecal injection of clonidine (1–30 &mgr;g) induced a dose-dependent increase in antinociception as measured by the tail flick (TF) and hot plate tests. Ketorolac alone (150–600 &mgr;g) increased the antinociception by 50%–60% only in the TF test. Ketorolac (10 &mgr;g) decreased clonidine (10 &mgr;g)-induced antinociception from 69.1% ± 7.8% to 23.5% ± 1.6% (P < 0.05) in the TF test and 35.7% ± 4.7% to 4.5% ± 0.1% (P < 0.05) maximum possible effect in the hot plate test. Ketorolac also antagonized the effect of 30 &mgr;g of clonidine. The opioid receptor antagonist naloxone antagonized the antinociceptive effect of clonidine and ketorolac, indicating the involvement of the opioid system in the antinociception produced by clonidine or ketorolac. However, neither clonidine nor ketorolac (10−8 to 10−3 M) inhibited the binding of specific ligands to &mgr;-, &dgr;-, and &kgr;-opioid receptors, indicating a lack of direct interaction of clonidine and ketorolac with opioid receptors. These results suggest that intrathecal injection of ketorolac antagonizes the antinociception produced by clonidine. Implications Clonidine and ketorolac are two important drugs used to give pain relief to patients. We observed that ketorolac inhibits clonidine-induced analgesia in the rat. We recommend that this drug interaction should be taken into account when both clonidine and ketorolac are used together to alleviate pain in patients.
Oxidative-Stress Resistance Mutants of Helicobacter pylori

ABSTRACT Within a large family of peroxidases, one member that catalyzes the reduction of organic peroxides to alcohols is known as alkyl hydroperoxide reductase, or AhpC. Gene disruption mutations in the gene encoding AhpC of Helicobacter pylori (ahpC) were generated by screening transformants under low-oxygen conditions. Two classes of mutants were obtained. Both types lack AhpC protein, but the major class (type I) isolated was found to synthesize increased levels (five times more than the wild type) of another proposed antioxidant protein, an iron-binding, neutrophil-activating protein (NapA). The other class of mutants, the minor class (type II), produced wild-type levels of NapA. The two types of AhpC mutants differed in their frequencies of spontaneous mutation to rifampin resistance and in their sensitivities to oxidative-stress chemicals, with the type I mutants exhibiting less sensitivity to organic hydroperoxides as well as having a lower mutation frequency. The napA promoter regions of the two types of AhpC mutants were identical, and primer extension analysis revealed their transcription start site to be the same as for the wild type. Gene disruption mutations were obtained in napA alone, and a double mutant strain (ahpC napA) was also created. All four of the oxidative-stress resistance mutants could be distinguished from the wild type in oxygen sensitivity or in some other oxidative-stress resistance phenotype (i.e., in sensitivity to stress-related chemicals and spontaneous mutation frequency). For example, growth of the NapA mutant was more sensitive to oxygen than that of the wild-type strain and both of the AhpC-type mutants were highly sensitive to paraquat and to cumene hydroperoxide. Of the four types of mutants, the double mutant was the most sensitive to growth inhibition by oxygen and by organic peroxides and it had the highest spontaneous mutation frequency. Notably, two-dimensional gel electrophoresis combined with protein sequence analysis identified another possible oxidative-stress resistance protein (HP0630) that was up-regulated in the double mutant. However, the transcription start site of the HP0630 gene was the same for the double mutant as for the wild type. It appears that H. pylori can readily modulate the expression of other resistance factors as a compensatory response to loss of a major oxidative-stress resistance component.
Osteochondral defects: present situation and tissue engineering approaches

Articular cartilage is often damaged due to trauma or degenerative diseases, resulting in severe pain and disability. Most clinical approaches have been shown to have limited capacity to treat cartilage lesions. Tissue engineering (TE) has been proposed as an alternative strategy to repair cartilage. Cartilage defects often penetrate to the subchondral bone, or full‐thickness defects are also produced in some therapeutic procedures. Therefore, in TE strategies one should also consider the need for a simultaneous regeneration of both cartilage and subchondral bone in situations where osteochondral defects are present, or to provide an enhanced support for the cartilage hybrid construct. In this review, different concepts related to TE in osteochondral regeneration will be discussed. The focus is on the need to produce new biphasic scaffolds that will provide differentiated and adequate conditions for guiding the growth of the two tissues, satisfying their different biological and functional requirements. Copyright © 2007 John Wiley & Sons, Ltd.
A Bcl‐2 antisense oligonucleotide increases α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid (AMPA) toxicity in cortical cultures

Both α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid (AMPA) receptor–mediated neurotoxicity and the induction of death‐regulatory genes have been implicated in the pathophysiology of delayed ischemic neuronal injury. To assess the role of the antiapoptotic gene Bcl‐2 in the modulation of AMPA toxicity, we exposed neuron‐enriched cultures from rat cerebral cortex to AMPA, in the absence or presence of an antisense oligodeoxynucleotide (ODN) directed against Bcl‐2. AMPA produced concentration‐dependent toxicity detected by a decrease in fluorescence of the redox indicator Alamar blue and by an increase in lactic acid dehydrogenase release. This effect was accompained by the induction of Bcl‐2 protein expression, with maximal induction at 100 μM AMPA. A phosphorothioate antisense ODN against Bcl‐2 reduced the AMPA‐stimulated induction of Bcl‐2 protein levels, detected by western blotting, by about 70%. In the presence of the antisense ODN, but not sense or scrambled ODNs, the toxicity of 100 μM AMPA was increased by about 60%. These findings suggest that induction of Bcl‐2 expression by AMPA may have a protective role to limit AMPA receptor–mediated neuronal damage and that modifying Bcl‐2 expression could have therapeutic potential in ischemia.
Using rubrics in IT: Experiences of assessment and feedback at Deakin University

This paper explores the use of analytical rubrics as a form of assessment and feedback in Information Technology (IT) Higher Education. Rubrics are a tool for assessment, however, they can also be used to provide a mapping of learning outcomes and graduate attributes within minimum standards to allow students to evidence their skills beyond the assignment criteria. This paper will discuss how rubrics are used in IT at Deakin and present, via a small case study, outcomes from the evaluation of two rubrics used. While the results are not broad, this study demonstrates that rubrics can be useful for students studying IT as they assist with students understanding the alignment of learning outcomes with assessment.
Estimating stature in fossil hominids: which regression model and reference sample to use?

coResearchers have long appreciated the significant relationship between body size and an animal's overall adaptive strategy and life history. However, much more emphasis has been placed on interpreting body size than on the actual calculation of it. One measure of size that is especially important for human evolutionary studies is stature. Despite a long history of investigation, stature estimation remains plagued by two methodological problems: (1) the choice of the statistical estimator, and (2) the choice of the reference population from which to derive the parameters. This work addresses both of these problems in estimating stature for fossil hominids, with special reference to A.L. 288-1 (Australopithecus afarensis) and WT 15000 (Homo erectus). Three reference samples of known stature with maximum humerus and femur lengths are used in this study: a large (n=2209) human sample from North America, a smaller sample of modern human pygmies (n=19) from Africa, and a sample of wild-collected African great apes (n=85). Five regression techniques are used to estimate stature in the fossil hominids using both univariate and multivariate parameters derived from the reference samples: classical calibration, inverse calibration, major axis, reduced major axis and the zero-intercept ratio model. We also explore a new diagnostic to test extrapolation and allometric differences with multivariate data, and we calculate 95% confidence intervals to examine the range of variation in estimates for A.L. 288-1, WT 15000 and the new Bouri hominid (contemporary with [corrected] Australopithecus garhi). Results frequently vary depending on whether the data are univariate or multivariate. Unique limb proportions and fragmented remains complicate the choice of estimator. We are usually left in the end with the classical calibrator as the best choice. It is the maximum likelihood estimator that performs best overall, especially in scenarios where extrapolation occurs away from the mean of the reference sample. The new diagnostic appears to be a quick and efficient way to determine at the outset whether extrapolation exists in size and/or shape of the long bones between the reference sample and the target specimen.
Role of the type I interferons in allograft rejection

Type I interferons are potent immuno‐modulatory cytokines that enhance expression of the major histocompatibility complex (MHC) class I antigens, T‐cell cytotoxicity, and natural killer (NK) cell activity, all of which are implicated in graft rejection. A monoclonal antibody (mAb) directed against the extracellular domain of the human interferon α (IFN‐α) receptor (IFN‐αR), which inhibits both the binding and biological activity of all the type I IFNs tested, exerted a dose‐dependent inhibition of the mixed lymphocyte reaction and induced permanent survival of skin allografts in MHC‐divergent Cynomologus monkeys treated with a subeffective dose of cyclosporin A. Marked differences were observed in the composition of T lymphocyte sub‐populations in anti‐IFN‐αR mAb‐treated animals relative to the various control groups. Skin biopsies from animals treated with anti‐IFN‐R Mab + cyclosporin A revealed very low levels of MHC class I and class II antigen expression and the absence of histological signs of rejection, whereas skin biopsies from control animals exhibited high levels of MHC antigen expression and the histological signs of acute rejection, including a pronounced lymphocytic infiltrate, edema, and necrosis. No monkey antibodies (IgG) to the mouse anti‐human IFN‐αR mAb were detected in the serum of any of the animals treated with the anti‐IFN‐αR mAb either alone or together with cyclosporin A. Treatment of lethally irradiated Cynomologus monkeys with the anti‐IFN‐αR mAb together with a subeffective dose of cyclosporin A was also found to markedly enhance the survival of animals grafted with allogeneic bone marrow cells from donors differing in both MHC class I and class II antigens. These results show that selective and lasting immunosuppression can be obtained by the short‐term administration of an IFN‐α antagonist together with a subeffective dose of cyclosporin A, and may have important implications for the therapy of human allograft rejection.
Human platelet‐rich plasma stimulates migration and chondrogenic differentiation of human subchondral progenitor cells

In cartilage repair, platelet‐rich plasma (PRP) is used in one‐step approaches utilizing microfracture and matrix‐induced chondrogenesis procedures, bone marrow‐derived cell transplantation, or intra‐articular injection. The aim of our study was to evaluate the effect of human PRP on the migration and chondrogenic differentiation of human subchondral progenitors. Human progenitors were derived from subchondral cortico‐spongious bone (CSP), were analyzed for their migration capacity upon PRP treatment in 96‐well chemotaxis assays and cultured in high‐density pellet cultures under serum‐free conditions in the presence of 5% PRP. Chemotaxis assays showed that 0.1–100% PRP significantly (p < 0.05) stimulate the migration of CSP compared to untreated controls. Histological staining of proteoglycan and immuno‐staining of type II collagen indicated that progenitors stimulated with PRP show significantly increased cartilage matrix formation compared to untreated progenitors. Real‐time gene expression analysis of typical chondrocyte marker genes as well as osteogenic and adipogenic markers like osteocalcin and fatty acid binding protein showed that PRP induces the chondrogenic differentiation sequence of human progenitors in high‐density pellet cultures, while osteogenic or adipogenic differentiation was not evident. These results suggest that human PRP may enhance the migration and stimulate the chondrogenic differentiation of human subchondral progenitor cells known from microfracture. © 2011 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:845–852, 2012
Two factors that bind to highly conserved sequences in mammalian type C retroviral enhancers

The transcriptional enhancers of the Moloney and Friend murine leukemia viruses (MLV) are important determinants of viral pathogenicity. We used electrophoretic mobility shift and methylation interference assays to study nuclear factors which bind to a region of these enhancers whose sequence is identical between Moloney and Friend viruses and particularly highly conserved among 35 mammalian type C retroviruses whose enhancer sequences have been aligned (E. Golemis, N. A. Speck, and N. Hopkins, J. Virol. 64:534-542, 1990). Previous studies identified sites for the leukemia virus factor b (LVb) and core proteins in this region (N. A. Speck and D. Baltimore, Mol. Cell. Biol. 7:1101-1110, 1987) as well as a site, overlapping those for LVb and core, for a third factor (N. R. Manley, M. A. O'Connell, P. A. Sharp, and N. Hopkins, J. Virol. 63:4210-4223, 1989). Surprisingly, the latter factor appeared to also bind two sites identified in the Friend MLV enhancer, Friend virus factor a and b1 (FVa and FVb1) sites, although the sequence basis for the ability of the protein to bind these diverse sites was not apparent. Here we describe the further characterization of this binding activity, termed MCREF-1 (for mammalian type C retrovirus enhancer factor 1), and the identification of a consensus sequence for its binding, GGN8GG. We also identify a factor, abundant in mouse T-cell lines and designated LVt, which binds to two sites in the Moloney MLV enhancer, overlapping the previously identified LVb and LVc binding sites. These sites contain the consensus binding site for the Ets family of proteins. We speculate on how distinct arrays of these factors may influence the disease-inducing phenotype.
Mission creep in the application of wildlife law: The progressive dilution of legal requirements regarding a wild-born orca kept for ‘research’ purposes

Environmental law contributes to biodiversity conservation insofar as it is properly drafted and implemented. This article explores one way in which its effectiveness can be impaired: progressive dilution. This occurs when consecutive steps are taken in the law's application which in isolation may not appear much out of line and are presented as legal, but eventually render a result contrary to the law's intentions – like a military mission creeping beyond its mandate. This phenomenon is explored using the case of an orca found emaciated in the Netherlands’ waters in 2010. Captured for rehabilitation purposes and subsequently retained for strictly circumscribed scientific research, the animal somehow ended up in a commercial Spanish entertainment park, used for public performances and breeding purposes – all with express approval of various governmental authorities, including courts. The entire chain of events is analysed in light of requirements imposed by diverse (inter)national legal instruments, including the Agreement on the Conservation of Small Cetaceans of the Baltic, North East Atlantic, Irish and North Seas (ASCOBANS), the Convention on International Trade in Endangered Species (CITES) and European Union regulations.
Effects of infection on growth in Sudanese children.

A cohort of 439 infants from poor districts of Greater Khartoum were examined at intervals of 2 weeks from birth to 1 year. At each visit symptoms suggesting infection were recorded--diarrhoea, fever, vomiting and cough or cold. On average 30 per cent of children had episodes of diarrhoea and 40 per cent had episodes of cold or cough in each 4-week period, the incidence being somewhat lower in the first 2 months of life. The average duration of an episode was 5 d. The effect of illness on weight gain was calculated by regressing weight gain against number of days ill. Diarrhoea produced a deficit in weight gain of 32 g per day ill, and cough/cold a deficit of 16.4g per day ill. From these data the overall impact of illness on weight gain was calculated. In the average child between 12 and 24 weeks diarrhoea produced a reduction in growth of 160g, and cough/cold a reduction of 95g. In most periods the frequency of episodes of diarrhoea was not significantly greater in supplemented than in exclusively breast-fed children. In the first 3 months of life episodes of diarrhoea had little effect on weight gain, but thereafter an episode of diarrhoea in any 2-week period reduced the gain in that period to less than 50 per cent of that found in uninfected children. 'Faltering' was defined as a weight increment below -2 s.d. of the reference mean. Diarrhoea did not always lead to faltering, but it seems to have been an initiating factor in some 50 per cent of those children who did falter. (ABSTRACT TRUNCATED AT 250 WORDS)