Negative input-resistance compensator for a constant power load

A negative input-resistance compensator is designed to stabilize a power electronic brushless dc motor drive with constant power-load characteristics. The strategy is to feed a portion of the changes in the dc-link voltage into the current control loop to modify the system input impedance in the midfrequency range and thereby to damp the input filter. The design process of the compensator and the selection of parameters are described. The impact of the compensator is examined on the motor-controller performance, and finally, the effectiveness of the controller is verified by simulation and experimental testing.

The interaction of sodium chlorite with phospholipids and glutathione:a comparison of effects in vitro, in mammalian and in microbial cells

In this study the interaction of the preservative sodium chlorite with unsaturated lipids and glutathione was investigated, in comparison with peroxides, sodium hypochlorite, and benzalkonium chloride. The aim was to determine whether the action of sodium chlorite could involve membrane lipid damage or antioxidant depletion, and how this related to toxicity in both mammalian and microbial cells. The treatment of phospholipids with chlorite yielded low levels of hydroperoxides, but sodium chlorite oxidized the thiol-containing antioxidant glutathione to its disulfide form very readily in vitro, with a 1:4 oxidant:GSH stoichiometry. In cultured cells, sodium chlorite also caused a substantial depletion of intracellular glutathione, whereas lipid oxidation was not very prominent. Sodium chlorite had a lower toxicity to ocular mammalian cells than benzalkonium chloride, which could be responsible for the different effects of long-term application in the eye. The fungal cells, which were most resistant to sodium chlorite, maintained higher percentage levels of intracellular glutathione during treatment than the mammalian cells. The results show that sodium chlorite can cause oxidative stress in cells, and suggest that cell damage is more likely to be due to interaction with thiol compounds than with cell membrane lipids. The study also provides important information about the differential resistance of ocular cells and microbes to various preservatives and oxidants.

Differential moderating effect of locus of control on effect of driving experience in young male and female drivers

Investigations of relationships between the specific personality variable, locus of control (LOC, Rotter, 1966) and driver behaviour or accidents have returned contrasting results. Review suggests dependence on gender or experience characteristics of participants, suggesting these factors interact with LOC to influence driving. Relationships were investigated in terms of influence on the eight driving styles of the Multidimensional Driving Style Inventory (MDSI, Taubman-Ben-Ari, Mikulincer & Gillarth, 2004) in young drivers (18-29 years). Gender and LOC differences in driving styles previously related to accidents were proposed. It was also proposed that driving experience influences driving style, and LOC influences effect of driving experience. Gender differences were found for dissociative, anxious, patient, risky, angry and high velocity styles. Women had more external LOC than men, and driver stress styles increased with more external LOC, but reduced with increased driving experience, but so did patient style. High velocity style increased with experience. Controlling for LOC revealed important gender differences in effect of experience: positive effects for men (reducing angry and high velocity, increasing carefulness) and negative effects for women (increasing angry and higher velocity, reducing carefulness). Findings suggest negative influence of high internal LOC on young men in terms of its interaction with experience.

A study of potential serum markers for a diagnosis of gram-positive and gram-negative bacterial sepsis

Sepsis continues to be a major cause of morbidity and mortality as it can readily lead tosevere sepsis, septic shock, multiple organ failure and death. The onset can be rapid and difficult to define clinically. Despite the numerous candidate markers proposed in the literature, to date a serum marker for sepsis has not been found. The aim of this study was to assay the serum of clinically diagnosed patients with eithera Gram-negative or Gram- positive bacterial sepsis for elevated levels of nine potentialmarkers of sepsis, using commercially produced enzyme linked immunosorbent assays(ELISA). The purpose was to find a test marker for sepsis that would be helpful toclinicians in cases of uncertain sepsis and consequently expose false positive BC'scaused by skin or environmental contaminants. Nine test markers were assayed including IL-6, IL-I 0, ILI2, TNF-α, lipopolysaccharide binding protein, procalcitonin, sE-selectin, sICAM -1 and a potential differential marker for Gram-positive sepsis- anti-lipid S antibody. A total of 445 patients were enrolled into this study from the Queen Elizabeth Hospital and Selly Oak Hospital (Birmingham). The results showed that all the markers were elevated in patients with sepsis and that patients with a Gram-negative sepsis consistently produced higher median/range serum levels than those with a Gram-positive sepsis. No single marker was able to identify all the septic patients. Combining two markers caused the sensitivities and specificities for a diagnosis of sepsis to increase to within a 90% to 100% range. By a process of elimination the markers that survived into the last phase were IL-6 with sICAM -1, and anti-lipid S IgG assays Defining cut-off levels for a diagnosis of sepsis became problematic and a semi-blind trial was devised to test the markers in the absence of both clinical details and positive blood cultures. Patients with pyrexia of unknown origin and negative BC were included in this phase (4). The results showed that IL-6 with sICAM-l are authentic markers of sepsis. There was 82% agreement between the test marker diagnosis and the clinical diagnosis for sepsis in patients with a Gram-positive BC and 78% agreement in cases of Gram-negative Be. In the PUO group the test markers identified 12 cases of sepsis and the clinical diagnosis 15. The markers were shown to differentiate between early sepsis and sepsis, inflammatory responses and infection. Anti-lipid S with IL-6 proved be a sensitive marker for Gram-positive infections/sepsis.

Abrasion resistance of concrete

This thesis describes an experimental study of the abrasion resistance of concrete at both the macro and micro levels. This is preceded by a review related to friction and wear, methods of test for assessing abrasion resistance, and factors influencing the abrasion resistance of concrete. A versatile test apparatus was developed to assess the abrasion resistance of concrete. This could be operated in three modes and a standardised procedure was established for all tests. A laboratory programme was undertaken to investigate the influence, on abrasion resistance, of three major factors - finishing techniques, curing regimes and surface treatments. The results clearly show that abrasion resistance was significantly affected by these factors, and tentative mechanisms were postulated to explain these observations. To substantiate these mechanisms, the concrete specimens from the macro-study were subjected to micro-structural investigation, using such techniques as 'Mercury Intrusion Forosimetry, Microhardness, Scanning Electron Microscopy, Petrography and Differential Thermal Analysis. The results of this programme clearly demonstrated that the abrasion resistance of concrete is primarily dependent on the microstructure of the concrete nearest to the surface. The viability of indirectly assessing the abrasion resistance was investigated using three non-destructive techniques - Ultrasonic Pulse Velocity, Schmidt Rebound Hardness, and the Initial Surface Absorption Test. The Initial Surface Absorption was found to be most sensitive to factors which were shown to have influenced the abrasion resistance of concrete. An extensive field investigation was also undertaken. The results were used to compare site and laboratorypractices, and the performance in the accelerated abrasion test with the service wear. From this study, criteria were developed for assessing the quality of concrete floor slabs in terms of abrasion resistance.

Defective peroxisomal proliferators activated receptor gamma activity due to dominant-negative mutation synergizes with hypertension to accelerate cardiac fibrosis in mice

Aims: Humans with inactivating mutations in peroxisomal proliferators activated receptor gamma (PPAR?) typically develop a complex metabolic syndrome characterized by insulin resistance, diabetes, lipodystrophy, hypertension, and dyslipidaemia which is likely to increase their cardiovascular risk. Despite evidence that the activation of PPAR? may prevent cardiac fibrosis and hypertrophy, recent evidence has suggested that pharmacological activation of PPAR? causes increased cardiovascular mortality. In this study, we investigated the effects of defective PPAR? function on the development of cardiac fibrosis and hypertrophy in a murine model carrying a human dominant-negative mutation in PPAR?. Methods and results: Mice with a dominant-negative point mutation in PPAR? (P465L) and their wild-type (WT) littermates were treated with either subcutaneous angiotensin II (AngII) infusion or saline for 2 weeks. Heterozygous P465L and WT mice developed a similar increase in systolic blood pressure, but the mutant mice developed significantly more severe cardiac fibrosis to AngII that correlated with increased expression of profibrotic genes. Both groups similarly increased the heart weight to body weight ratio compared with saline-treated controls. There were no differences in fibrosis between saline-treated WT and P465L mice. Conclusion: These results show synergistic pathogenic effects between the presence of defective PPAR? and AngII-induced hypertension and suggest that patients with PPAR? mutation and hypertension may need more aggressive therapeutic measures to reduce the risk of accelerated cardiac fibrosis. © The Author 2009.

Gender differences in the sensitivity to negative stimuli:cross-modal affective priming study

Background: There is evidence showing that men and women differ with regard to the processing of emotional information. However, the mechanisms behind these differences are not fully understood. Method: The sample comprised of 275 (167 female) right-handed, healthy participants, recruited from the community. We employed a customized affective priming task, which consisted of three subtests, differing in the modality of the prime (face, written word, and sound). The targets were always written words of either positive or negative valence. The priming effect was measured as reaction time facilitation in conditions where both prime and target were emotional (of the same positive or negative valence) compared with conditions where the emotional targets were preceded by neutral primes. Results: The priming effect was observed across all three modalities, with an interaction of gender by valence: the priming effect in the emotionally negative condition in male participants was stronger compared with females. This was accounted for by the differential priming effect within the female group where priming was significantly smaller in the emotionally negative conditions compared with the positive conditions. The male participants revealed a comparable priming effect across both the emotionally negative and positive conditions. Conclusion: Reduced priming in negative conditions in women may reflect interference processes due to greater sensitivity to negative valence of stimuli. This in turn could underlie the gender-related differences in susceptibility to emotional disorders.

Negative feedback regulation of the ERK1/2 MAPK pathway

The extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) signalling pathway regulates many cellular functions, including proliferation, differentiation, and transformation. To reliably convert external stimuli into specific cellular responses and to adapt to environmental circumstances, the pathway must be integrated into the overall signalling activity of the cell. Multiple mechanisms have evolved to perform this role. In this review, we will focus on negative feedback mechanisms and examine how they shape ERK1/2 MAPK signalling. We will first discuss the extensive number of negative feedback loops targeting the different components of the ERK1/2 MAPK cascade, specifically the direct posttranslational modification of pathway components by downstream protein kinases and the induction of de novo gene synthesis of specific pathway inhibitors. We will then evaluate how negative feedback modulates the spatiotemporal signalling dynamics of the ERK1/2 pathway regarding signalling amplitude and duration as well as subcellular localisation. Aberrant ERK1/2 activation results in deregulated proliferation and malignant transformation in model systems and is commonly observed in human tumours. Inhibition of the ERK1/2 pathway thus represents an attractive target for the treatment of malignant tumours with increased ERK1/2 activity. We will, therefore, discuss the effect of ERK1/2 MAPK feedback regulation on cancer treatment and how it contributes to reduced clinical efficacy of therapeutic agents and the development of drug resistance.