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Pollution flashover occurs when soluble and nonsoluble materials cover the surface of an insulator, and this may ultimately cause a reduction in its performance. In this paper, the common type of sodium chloride (NaCl) was used as a soluble pollutant (ESDD) and kaolin as a nonsoluble pollutant (NSDD). Samples of silicone rubber (SiR) insulators were selected for this study and fabricated at the Advanced High Voltage Engineering Research Centre (AHIVEC) at Cardiff University. The samples were preconditioned and polluted according to standard specifications. Additionally, the AC voltage ramp technique was used to achieve flashover (FOV) voltage with different pollution levels. The aim of this work was to investigate the effect of nonsoluble materials on flashover characteristics to understand their interaction with dry-band arcs by using FOV electrical equations and experimental data. The test results show that the FOV voltage of the silicone rubber insulator substantially decreased with the increase in both ESDD and NSDD values. It was also identified from these results that the dry-band arcs were considerably influenced by both ESDD and NSDD levels. This impact can be quantified by determining the variation of discharge parameters (N, n). Based on the FOV equations and experimental data, a mathematical model was suggested, taking into account the effect of both ESDD and NSDD.

This paper assesses the dry-band formation and location during artificial pollution tests performed on a 4-shed 11kV insulator with conventional and textured surface designs in a clean-fog chamber and with the application of a voltage ramp-shape source. The different designs present the same overall geometrical dimensions, but the textured ones are characterized by the application of a patented insulator surface design. Three pollution levels, extremely high, high and moderate, were considered. A newly developed MATLAB procedure is able to automatically recognize the perimeter of the insulator, the trunk and shed areas on infra-red recordings. In addition, using the vertical axis identification, all trunks are subdivided into zones and into left and right areas, significantly increasing the capability of abnormalities detection. Any temperature increase within these areas enables to detect the appearance and the extension of dry bands. The results of the analysis of the statistical location and extension development over time of the dry bands during these set of comparative tests show a clear distinction between designs and pollution levels. These results may offer interesting design guidelines for dry-band control.

The aim of this study is the presentation of the results of an in-lab comparative study of electrical and thermal monitoring of artificially polluted, HTV-textured silicone rubber insulators, with different pollution levels. This work is a preliminary study of an in-situ monitoring of 400 kV SiR textured in a polluted environment. The results showed that the rms leakage current magnitude and pulses, and the average dissipated power depended on the pollution levels and the dry-bands formation. The discharge activity and their nature are governed by the pollution level and the voltage. A differentiation and a quantification between dry-band discharge onset and dry-band arc inception is highlighted.

This paper investigates the possible options for achieving a substantial reduction in a substation footprint using air-insulated switchgear as a more environmentally-friendly alternative to gas-insulated substations that use SF6 gas. Adopting a new approach to surge arrester location and numbers, International Electrotechnical Commission (IEC) minimum clearances can be successfully selected instead of the maximum clearances as currently adopted by many utilities, as is the case in the UK. In addition, innovative alternative compact busbar arrangements using vertical and delta configurations have been proposed by the authors. A further opportunity for compaction is offered by the application of compact and integrated technology offered from several manufacturers. The full overvoltage control within the entire substation under any surge condition is a key aspect of the feasibility of this type of substation. This work demonstrates that the new design option can be an attractive alternative for future substation configuration with minimum footprint.

Modelling for very fast transients (VFTs) requires good knowledge of the behaviour of gas insulated substation (GIS) components when subjected to high frequencies. Modelling usually takes the form of circuit-based insulation coordination type studies, in an effort to determine the maximum overvoltages and waveshapes present around the system. At very high frequencies, standard transmission line modelling assumptions may not be valid. Therefore, the approach to modelling of these transients must be re-evaluated. In this work, the high frequency finite element analysis (FEA) was used to enhance circuit-based models, allowing direct computation of parameters from geometric and material characteristics. Equivalent models that replicate a finite element model’s frequency response for bus-spacer and 90° elbow components were incorporated in alternative transients program-electromagnetic transients program (ATP-EMTP) using a pole-residue equivalent circuit derived following rational fitting using the well-established and robust method of vector fitting (VF). A large model order is often required to represent this frequency dependent behaviour through admittance matrices, leading to increased computational burden. Moreover, while highly accurate models can be derived, the data extracted from finite element solutions can be non-passive, leading to instability when included in time domain simulations. A simple method of improved stability for FEA derived responses along with a method for identification of a minimum required model order for stability of transient simulations is proposed.

The incidence of postoperative delirium in patients undergoing cardiac surgery is very high and increases morbidity and mortality. The possibility of pharmacological means to reduce its incidence is very attractive. At present, there is still no clear demonstration that any drug can prevent postoperative delirium in these patients. The aim of this Bayesian network meta-analysis (NMA) was to evaluate whether there is evidence that a drug is effective in reducing the incidence of POD in cardiac surgical patients. Our NMA showed that preoperative ketamine at subanesthetic doses can significantly reduce the incidence of POD. Risperidone also decreases the incidence of POD, but not significantly.

Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related death worldwide. In the recent years nonalcoholic fatty liver disease (NAFLD) is becoming a growing cause of HCCs and the incidence of NAFLD-related HCCs is expected to further dramatically increase by the next decade. Chronic inflammation is regarded as the driving force of NAFLD progression and a key factor in hepatic carcinogenesis. Hepatic inflammation in NAFLD results from the persistent stimulation of innate immunity in response to hepatocellular injury and gut dysbiosis as well as by the activation of adaptive immunity. However, the relative roles of innate and adaptive immunity in the processes leading to HCC are still incompletely characterized. This is due to the complex interplay between different liver cell populations, which is also strongly influenced by gut-derived bacterial products, metabolic/nutritional signals. Furthermore, carcinogenic mechanisms in NAFLD/NASH appear to involve the activation of signals mediated by hypoxia inducible factors. This review discusses recent data regarding the contribution of different inflammatory cells to NAFLD-related HCC and their possible impact on patient response to current treatments.

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously non-alcoholic fatty liver disease (NAFLD), is a leading cause of chronic liver disease worldwide. In 20%-30% of MASLD patients, the disease progresses to metabolic dysfunction-associated steatohepatitis (MASH, previously NASH) which can lead to fibrosis/cirrhosis, liver failure as well as hepatocellular carcinoma (HCC). Here we investigated the role of histidine-rich glycoprotein (HRG), a plasma protein produced by hepatocytes, in MASLD/MASH progression and HCC development. The role of HRG was investigated by morphological, cellular, and molecular biology approaches in (a) HRG mice (HRG mice) fed on a CDAA dietary protocol or a MASH related diethyl-nitrosamine/CDAA protocol of hepatocarcinogenesis, (b) THP1 monocytic cells treated with purified HRG, and (c) well-characterized cohorts of MASLD patients with or without HCC. In non-neoplastic settings, murine and clinical data indicate that HRG increases significantly in parallel with disease progression. In particular, in MASLD/MASH patients, higher levels of HRG plasma levels were detected in subjects with extensive fibrosis/cirrhosis. When submitted to the pro-carcinogenic protocol, HRG mice showed a significant decrease in the volume and number of HCC nodules in relation to decreased infiltration of macrophages producing pro-inflammatory mediators, including IL-1β, IL-6, IL-12, IL-10, and VEGF as well as impaired angiogenesis. The histopathological analysis (H-score) of MASH-related HCC indicate that the higher HRG positivity in peritumoral tissue significantly correlates with a lower overall patient survival and an increased recurrence. Moreover, a significant increase in HRG plasma levels was detected in cirrhotic (F4) patients and in patients carrying HCC vs. F0/F1 patients. Murine and clinical data indicate that HRG plays a significant role in MASLD/MASH progression to HCC by supporting a specific population of tumor-associated macrophages with pro-inflammatory response and pro-angiogenetic capabilities which critically support cancer cell survival. Furthermore, our data suggest HRG as a possible prognostic predictor in HCC patients with MASLD/MASH-related HCCs.

Non-Alcoholic Fatty Liver Disease (NAFLD) is a major form of chronic liver disease in the general population in relation to its high prevalence among overweight/obese individuals and patients with diabetes type II or metabolic syndrome. NAFLD can progress to steatohepatitis (NASH), fibrosis and cirrhosis and end-stage of liver disease but mechanisms involved are still incompletely characterized. Within the mechanisms proposed to mediate the progression of NAFLD, lipotoxicity is believed to play a major role. In the present study we provide data suggesting that microvesicles (MVs) released by fat-laden cells undergoing lipotoxicity can activate NLRP3 inflammasome following internalization by either cells of hepatocellular origin or macrophages. Inflammasome activation involves NF-kB-mediated up-regulation of NLRP3, pro-caspase-1 and pro-Interleukin-1, then inflammasome complex formation and Caspase-1 activation leading finally to an increased release of IL-1β. Since the release of MVs from lipotoxic cells and the activation of NLRP3 inflammasome have been reported to occur in vivo in either clinical or experimental NASH, these data suggest a novel rational link between lipotoxicity and increased inflammatory response.

Non-alcoholic fatty liver disease (NAFLD) is becoming the most common chronic liver disease worldwide. In 20-30% of patients, NAFLD can progress into non-alcoholic steatohepatitis (NASH), eventually leading to fibrosis, cirrhosis and hepatocellular carcinoma development. SerpinB3 (SB3), a hypoxia-inducible factor-2α dependent cysteine protease inhibitor, is up-regulated in hepatocytes during progressive NAFLD and proposed to contribute to disease progression. In this study we investigated the pro-inflammatory role of SB3 by employing phorbol-myristate acetate-differentiated human THP-1 macrophages exposed in vitro to human recombinant SB3 (hrSB3) along with mice overexpressing SB3 in hepatocytes (TG/SB3) or knockout for SB3 (KO/SB3) in which NASH was induced by feeding methionine/choline deficient (MCD) or a choline-deficient, L-amino acid defined (CDAA) diets. In vivo experiments showed that the induction of NASH in TG/SB3 mice was characterized by an impressive increase of liver infiltrating macrophages that formed crown-like aggregates and by an up-regulation of hepatic transcript levels of pro-inflammatory cytokines. All these parameters and the extent of liver damage were significantly blunted in KO/SB3 mice. In vitro experiments confirmed that hrSB3 stimulated macrophage production of M1-cytokines such as TNFα and IL-1β and reactive oxygen species along with that of TGFβ and VEGF through the activation of the NF-kB transcription factor. The opposite changes in liver macrophage activation observed in TG/SB3 or KO/SB3 mice with NASH were associated with a parallel modulation in the expression of triggering receptor expressed on myeloid cells-2 (TREM2), CD9 and galectin-3 markers, recently detected in NASH-associated macrophages. From these results we propose that SB3, produced by activated/injured hepatocytes, may operate as a pro-inflammatory mediator in NASH contributing to the disease progression.