690 research outputs found

    The Cambridge Crime Harm Index: Measuring Total Harm from Crime Based on Sentencing Guidelines

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    The logic of simply summing crimes of all kind into a single total has long been challenged as misleading. All crimes are not created equal. Counting them as if they are fosters distortion of risk assessments, resource allocation, and accountability. To solve this problem, Sherman (2007, 2010, 2011 and 2013) has offered a general proposal to create a weighted 'Crime Harm Index (CHI).' This article provides and explicates a detailed procedure for operationalizing this idea in UK: what we call the 'Cambridge CHI.' The new elements of the Cambridge CHI presented here are (1) the use of the 'starting point' in the national Sentencing Guidelines to define the number of days in prison for each offence type; (2) the exclusion of proactively detected, previously unreported offences, and (3) a comparative analysis of the Cambridge and other approaches to weighting crime harm, judged by a three-pronged test of democracy, reliability, and cost

    Intramuscular Contributions to Low-Frequency Force Potentiation Induced by a High-Frequency Conditioning Stimulation.

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    Electrically-evoked low-frequency (submaximal) force is increased immediately following high-frequency stimulation in human skeletal muscle. Although central mechanisms have been suggested to be the major cause of this low-frequency force potentiation, intramuscular factors might contribute. Thus, we hypothesized that two intramuscular Ca(2+)-dependent mechanisms can contribute to the low-frequency force potentiation: increased sarcoplasmic reticulum Ca(2+) release and increased myofibrillar Ca(2+) sensitivity. Experiments in humans were performed on the plantar flexor muscles at a shortened, intermediate, and long muscle length and electrically evoked contractile force and membrane excitability (i.e., M-wave amplitude) were recorded during a stimulation protocol. Low-frequency force potentiation was assessed by stimulating with a low-frequency tetanus (25 Hz, 2 s duration), followed by a high-frequency tetanus (100 Hz, 2 s duration), and finally followed by another low-frequency (25 Hz, 2 s duration) tetanus. Similar stimulation protocols were performed on intact mouse single fibers from flexor digitorum brevis muscle, whereby force and myoplasmic free [Ca(2+)] ([Ca(2+)]i) were assessed. Our data show a low-frequency force potentiation that was not muscle length-dependent in human muscle and it was not accompanied by any increase in M-wave amplitude. A length-independent low-frequency force potentiation could be replicated in mouse single fibers, supporting an intramuscular mechanism. We show that at physiological temperature (31°C) this low-frequency force potentiation in mouse fibers corresponded with an increase in sarcoplasmic reticulum (SR) Ca(2+) release. When mimicking the slower contractile properties of human muscle by cooling mouse single fibers to 18°C, the low-frequency force potentiation was accompanied by minimally increased SR Ca(2+) release and hence it could be explained by increased myofibrillar Ca(2+) sensitivity. Finally, introducing a brief 200 ms pause between the high- and low-frequency tetanus in human and mouse muscle revealed that the low-frequency force potentiation is abolished, arguing that increased myofibrillar Ca(2+) sensitivity is the main intramuscular mechanism underlying the low-frequency force potentiation in humans

    Are There Critical Fatigue Thresholds? Aggregated vs. Individual Data

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    The mechanisms underlying task failure from fatiguing physical efforts have been the focus of many studies without reaching consensus. An attractive but debated model explains effort termination with a critical peripheral fatigue threshold. Upon reaching this threshold, feedback from sensory afferents would trigger task disengagement from open-ended tasks or a reduction of exercise intensity of closed-ended tasks. Alternatively, the extant literature also appears compatible with a more global critical threshold of loss of maximal voluntary contraction force. Indeed, maximal voluntary contraction force loss from fatiguing exercise realized at a given intensity appears rather consistent between different studies. However, when looking at individual data, the similar maximal force losses observed between different tasks performed at similar intensities might just be an "artifact" of data aggregation. It would then seem possible that such a difference observed between individual and aggregated data also applies to other models previously proposed to explain task failure from fatiguing physical efforts. We therefore suggest that one should be cautious when trying to infer models that try to explain individual behavior from aggregated data

    Muscle Fatigue Affects the Interpolated Twitch Technique When Assessed Using Electrically-Induced Contractions in Human and Rat Muscles

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    The interpolated twitch technique (ITT) is the gold standard to assess voluntary activation and central fatigue. Yet, its validity has been questioned. Here we studied how peripheral fatigue can affect the ITT. Repeated contractions at submaximal frequencies were produced by supramaximal electrical stimulations of the human adductor pollicis muscle in vivo and of isolated rat soleus fiber bundles; an extra stimulation pulse was given during contractions to induce a superimposed twitch. Human muscles fatigued by repeated 30-Hz stimulation trains (3 s on-1 s off) showed an ~80% reduction in the superimposed twitch force accompanied by a severely reduced EMG response (M-wave amplitude), which implies action potential failure. Subsequent experiments combined a less intense stimulation protocol (1.5 s on-3 s off) with ischemia to cause muscle fatigue, but which preserved M-wave amplitude. However, the superimposed twitch force still decreased markedly more than the potentiated twitch force; with ITT this would reflect increased "voluntary activation." In contrast, the superimposed twitch force was relatively spared when a similar protocol was performed in rat soleus bundles. Force relaxation was slowed by >150% in fatigued human muscles, whereas it was unchanged in rat soleus bundles. Accordingly, results similar to those in the human muscle were obtained when relaxation was slowed by cooling the rat soleus muscles. In conclusion, our data demonstrate that muscle fatigue can confound the quantification of central fatigue using the ITT
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