Bearing damage analysis by calculation of capacitive coupling between inner and outer races of a ball bearing

Bearing damage in modern inverter-fed AC drive systems is more common than in motors working with 50 or 60 Hz power supply. Fast switching transients and common mode voltage generated by a PWM inverter cause unwanted shaft voltage and resultant bearing currents. Parasitic capacitive coupling creates a path to discharge current in rotors and bearings. In order to analyze bearing current discharges and their effect on bearing damage under different conditions, calculation of the capacitive coupling between the outer and inner races is needed. During motor operation, the distances between the balls and races may change the capacitance values. Due to changing of the thickness and spatial distribution of the lubricating grease, this capacitance does not have a constant value and is known to change with speed and load. Thus, the resultant electric field between the races and balls varies with motor speed. The lubricating grease in the ball bearing cannot withstand high voltages and a short circuit through the lubricated grease can occur. At low speeds, because of gravity, balls and shaft voltage may shift down and the system (ball positions and shaft) will be asymmetric. In this study, two different asymmetric cases (asymmetric ball position, asymmetric shaft position) are analyzed and the results are compared with the symmetric case. The objective of this paper is to calculate the capacitive coupling and electric fields between the outer and inner races and the balls at different motor speeds in symmetrical and asymmetrical shaft and balls positions. The analysis is carried out using finite element simulations to determine the conditions which will increase the probability of high rates of bearing failure due to current discharges through the balls and races.

Corneal confocal microscopy : a novel means to detect nerve fibre damage in idiopathic small fibre neuropathy

Patients with idiopathic small fibre neuropathy (ISFN) have been shown to have significant intraepidermal nerve fibre loss and an increased prevalence of impaired glucose tolerance (IGT). It has been suggested that the dysglycemia of IGT and additional metabolic risk factors may contribute to small nerve fibre damage in these patients. Twenty-five patients with ISFN and 12 aged-matched control subjects underwent a detailed evaluation of neuropathic symptoms, neurological deficits (Neuropathy deficit score (NDS); Nerve Conduction Studies (NCS); Quantitative Sensory Testing (QST) and Corneal Confocal Microscopy (CCM)) to quantify small nerve fibre pathology. Eight (32%) patients had IGT. Whilst all patients with ISFN had significant neuropathic symptoms, NDS, NCS and QST except for warm thresholds were normal. Corneal sensitivity was reduced and CCM demonstrated a significant reduction in corneal nerve fibre density (NFD) (Pb0.0001), nerve branch density (NBD) (Pb0.0001), nerve fibre length (NFL) (Pb0.0001) and an increase in nerve fibre tortuosity (NFT) (Pb0.0001). However these parameters did not differ between ISFN patients with and without IGT, nor did they correlate with BMI, lipids and blood pressure. Corneal confocal microscopy provides a sensitive non-invasive means to detect small nerve fibre damage in patients with ISFN and metabolic abnormalities do not relate to nerve damage.

An improved modal strain energy method for damage assessment

The modal strain energy method, which depends on the vibration characteristics of the structure, has been reasonably successful in identifying and localising damage in the structure. However, existing strain energy methods require the first few modes to be measured to provide meaningful damage detection. Use of individual modes with existing strain energy methods may indicate false alarms or may not detect the damage at or near the nodal points. This paper proposes a new modal strain energy based damage index which can detect and localize the damage using any one of the modes measured and illustrates its application for beam structures. It becomes evident that the proposed strain energy based damage index also has potential for damage quantification.

Property damage crash equivalency factors to solve crash frequency-severity dilemma: Case study on South Korean rural roads

Safety interventions (e.g., median barriers, photo enforcement) and road features (e.g., median type and width) can influence crash severity, crash frequency, or both. Both dimensions—crash frequency and crash severity—are needed to obtain a full accounting of road safety. Extensive literature and common sense both dictate that crashes are not created equal, with fatalities costing society more than 1,000 times the cost of property damage crashes on average. Despite this glaring disparity, the profession has not unanimously embraced or successfully defended a nonarbitrary severity weighting approach for analyzing safety data and conducting safety analyses. It is argued here that the two dimensions (frequency and severity) are made available by intelligently and reliably weighting crash frequencies and converting all crashes to property-damage-only crash equivalents (PDOEs) by using comprehensive societal unit crash costs. This approach is analogous to calculating axle load equivalents in the prediction of pavement damage: for instance, a 40,000-lb truck causes 4,025 times more stress than does a 4,000-lb car and so simply counting axles is not sufficient. Calculating PDOEs using unit crash costs is the most defensible and nonarbitrary weighting scheme, allows for the simple incorporation of severity and frequency, and leads to crash models that are sensitive to factors that affect crash severity. Moreover, using PDOEs diminishes the errors introduced by underreporting of less severe crashes—an added benefit of the PDOE analysis approach. The method is illustrated with rural road segment data from South Korea (which in practice would develop PDOEs with Korean crash cost data).

Damage localisation in beams and plates using vibration characteristics

Dynamic computer simulation techniques are used to develop and apply a multi-criteria procedure, incorporating changes in natural frequencies, modal flexibility and the modal strain energy, for damage localisation in beams and plates. Numerically simulated modal data obtained through finite element analyses are used to develop algorithms based on changes of modal flexibility and modal strain energy before and after damage and used as the indices for assessment of the state of structural health. The proposed procedure is illustrated through its application to flexural members under different damage scenarios and the results confirm its feasibility for damage assessment.

The role of emotional intelligence in moral judgement

In this study we investigated the potential role of emotional intelligence (EI) in moral reasoning (MR). A sample of 131 undergraduate students completed a battery of psychological tests, which included measures of EI, MR and the Big Five dimensions of personality. Results revealed support for a proposed model of the relationship between emotional intelligence, personality and moral reasoning. Specifically, emotional intelligence was found to be a significant predictor of four of the Big Five personality dimensions (extraversion, openness, neuroticism, agreeableness), which in turn were significant predictors of moral reasoning. These results have important implications in regards to our current understanding of the relationships between EI, moral reasoning and personality. We emphasise the need to incorporate the constructs of EI and moral reasoning into a broader, explanatory personality framework.

Leading with moral purpose : insights from community leaders

Leadership has been described as having a moral purpose. This paper argues that theoretical insights from ethical leadership theory and empowerment theory are useful for understanding the work of community leaders. Community leaders tend to be people who are known mainly to their immediate community, work in a voluntary capacity and are committed to a particular goal or cause. The paper begins by referring to Starratt’s (1996) framework that comprises three inter-related ethics: an ethic of care, critique and justice, each of which is said to constitute ethical leadership. It then explores insights from empowerment theory since it is argued that it has some strong connections to ethical leadership. Central to both perspectives is the notion of relationships and ‘power to’ where power is shared and where people work together for change. Based on interviews with nine grassroots voluntary community leaders, this paper contributes to the limited research in the community leadership field by understanding more fully their values, beliefs and leadership practices. It is argued that the insights of ethical leadership and empowerment theory are highly relevant to explain their work and practice. The paper concludes by discussing some implications for leaders in educational settings.

Increased Langerhan cell density and corneal nerve damage in diabetic patients : role of immune mechanisms in human diabetic neuropathy

Aim/hypothesis Immune mechanisms have been proposed to play a role in the development of diabetic neuropathy. We employed in vivo corneal confocal microscopy (CCM) to quantify the presence and density of Langerhans cells (LCs) in relation to the extent of corneal nerve damage in Bowman's layer of the cornea in diabetic patients. Methods 128 diabetic patients aged 58±1 yrs with a differing severity of neuropathy based on Neuropathy Deficit Score (NDS—4.7±0.28) and 26 control subjects aged 53±3 yrs were examined. Subjects underwent a full neurological evaluation, evaluation of corneal sensation with non-contact corneal aesthesiometry (NCCA) and corneal nerve morphology using corneal confocal microscopy (CCM). Results The proportion of individuals with LCs was significantly increased in diabetic patients (73.8%) compared to control subjects (46.1%), P=0.001. Furthermore, LC density (no/mm2) was significantly increased in diabetic patients (17.73±1.45) compared to control subjects (6.94±1.58), P=0.001 and there was a significant correlation with age (r=0.162, P=0.047) and severity of neuropathy (r=−0.202, P=0.02). There was a progressive decrease in corneal sensation with increasing severity of neuropathy assessed using NDS in the diabetic patients (r=0.414, P=0.000). Corneal nerve fibre density (P<0.001), branch density (P<0.001) and length (P<0.001) were significantly decreased whilst tortuosity (P<0.01) was increased in diabetic patients with increasing severity of diabetic neuropathy. Conclusion Utilising in vivo corneal confocal microscopy we have demonstrated increased LCs in diabetic patients particularly in the earlier phases of corneal nerve damage suggestive of an immune mediated contribution to corneal nerve damage in diabetes.

Spatiotemporal investigations of DNA damage repair using microbeams

Cellular response to radiation damage is made by a complex network of pathways and feedback loops whose spatiotemporal organisation is still unclear despite its decisive role in determining the fate of the damaged cell. Revealing the dynamic sequence of the repair proteins is therefore critical in understanding how the DNA repair mechanisms work. There are also still open questions regarding the possible movement of damaged chromatin domains and its role as trigger for lesion recognition and signalling in the DNA repair context. The single-cell approach and the high spatial resolution offered by microbeams provide the perfect tool to study and quantify the dynamic processes associated with the induction and repair of DNA damage. We have followed the development of radiation-induced foci for three DNA damage markers (i.e. γ-H2AX, 53BP1 and hSSB1) using normal fibroblasts (AG01522), human breast adenocarcinoma cells (MCF7) and human fibrosarcoma cells (HT1080) stably transfected with yellow fluorescent protein fusion proteins following irradiation with the QUB X-ray microbeam (carbon X-rays <2 µm spot). The size and intensity of the foci has been analysed as a function of dose and time post-irradiation to investigate the dynamics of the above-mentioned DNA repair processes and monitor the remodelling of chromatin structure that the cell undergoes to deal with DNA damage.

INTS3 controls the hSSB1-mediated DNA damage response

Human SSB1 (single-stranded binding protein 1 [hSSB1]) was recently identified as a part of the ataxia telangiectasia mutated (ATM) signaling pathway. To investigate hSSB1 function, we performed tandem affinity purifications of hSSB1 mutants mimicking the unphosphorylated and ATM-phosphorylated states. Both hSSB1 mutants copurified a subset of Integrator complex subunits and the uncharacterized protein LOC58493/c9orf80 (henceforth minute INTS3/hSSB-associated element [MISE]). The INTS3–MISE–hSSB1 complex plays a key role in ATM activation and RAD51 recruitment to DNA damage foci during the response to genotoxic stresses. These effects on the DNA damage response are caused by the control of hSSB1 transcription via INTS3, demonstrating a new network controlling hSSB1 function.

Involvement of Exo1b in DNA damage-induced apoptosis

Apoptosis is essential for the maintenance of inherited genomic integrity. During DNA damage-induced apoptosis, mechanisms of cell survival, such as DNA repair are inactivated to allow cell death to proceed. Here, we describe a role for the mammalian DNA repair enzyme Exonuclease 1 (Exo1) in DNA damage-induced apoptosis. Depletion of Exo1 in human fibroblasts, or mouse embryonic fibroblasts led to a delay in DNA damage-induced apoptosis. Furthermore, we show that Exo1 acts upstream of caspase-3, DNA fragmentation and cytochrome c release. In addition, induction of apoptosis with DNA-damaging agents led to cleavage of both isoforms of Exo1. The cleavage of Exo1 was mapped to Asp514, and shown to be mediated by caspase-3. Expression of a caspase-3 cleavage site mutant form of Exo1, Asp514Ala, prevented formation of the previously observed fragment without any affect on the onset of apoptosis. We conclude that Exo1 has a role in the timely induction of apoptosis and that it is subsequently cleaved and degraded during apoptosis, potentially inhibiting DNA damage repair.

Out of time: The moral temporality of sex, crime and taboo

This paper discusses the relationship between law and morality. Morality does not necessarily coincide with the law, but it contributes to it. An act may be legal but nevertheless considered to be immoral in a particular society. For example, the use of pornography may be considered by many to be immoral. Nevertheless, the sale and distribution of non-violent, non-child related, sexually explicit material is legal (or regulated) in many jurisdictions. Many laws are informed by, and even created by, morality. This paper examines the historical influence of morality on the law and on society in general. It aims to develop a theoretical framework for examining legal moralism and the social construction of morality and crime as well as the relationship between sex, desire and taboo. Here, we refer to the moral temporality of sex and taboo, which examines the way in which moral judgments about sex and what is considered taboo change over time, and the kinds of justifications that are employed in support of changing moralities. It unpacks the way in which abstract and highly tenuous concepts such as ‘‘desire’’, ‘‘art’’ and ‘‘entertainment’’ may be ‘‘out of time’’ with morality, and how morality shapes laws over time, fabricating justifications from within socially constructed communities of practice. This theoretical framework maps the way in which these concepts have become temporally dominated by heteronormative structures such as the family, marriage, reproduction, and longevity. It is argued that the logic of these structures is inexorably tied to the heterosexual life-path, charting individual lives and relationships through explicit phases of childhood, adolescence and adulthood that, in the twenty-first century, delimit the boundaries of taboo surrounding sex more than any other time in history.