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This paper presents a theoretical line loss calculation of distribution network containing an uncertainty power of wind turbine. First, this paper establishes the theoretical line loss mathematical model considering wind turbine power constraint within the sampling period. Then this paper gets multi group wind turbine output data satisfied the power constraints through Monte Carlo simulation. By combining with the first power coefficient method and Monte Carlo simulation technique, this paper also generates multi groups load pseudo measurement test of non real time. By combining the real-time measurement of power flow calculation, a group of simulated data with minimum error between the power flow results and the real time measurement are selected. Finally based on the selected pseudo measurement, the theoretical line loss within the given time period based on periodic accumulative calculation of real-time measurement are calculated. 14 nodes example is given to verify the accuracy and practicality of the algorithm.

Accurate Partial discharge (PD) detection and location is of great significance for the power cable insulation condition monitoring. To achieve this, an adequate cable model to analyze pulse propagation is needed. Considering the complex structure of the cable, the equivalent circuit model is no longer applicable. In this paper a numerical electromagnetic method, FDTD, is applied. To analysis wave propagation characteristics in time domain, a well-established cable model is constructed. By simulating the electromagnetic (EM) field propagation inside the cable and the cable joint, the components of the electric fields excited by the PD source in different directions are calculated in order to evaluate the influence of the cable joint in practice, the calculated PD waveforms in the cable are compared with those of the cable joint model in FDTD.

In Beijing, capital of China, decreasing visibility has become a serious problem on people's life, thus a hot environmental concern. An urban roadside site in Beijing was chosen to collect 24-h TSP, PM10 and PM2.5 samples for one month each season from June 2009 to March 2010. The PM mass concentrations, and the concentrations of ions, EC, OC and metals in PM10 and PM2.5 were measured, and their correlation with visibility, as well as the influence of weather factors on visibility were studied. The results showed that daily mean concentrations of TSP, PM10 and PM2.5 were 75-1350 μg/m^3 (mean 275.8), 29-448 μg/m^3 (mean 187) and up to 300 μg/m^3 (mean 92.6), with the number of days exceeding the secondary standard (GB3095-2012) representing 33.3%, 59.8% and 51.0%, respectively. All PM concentrations were higher in spring than in other seasons. Obvious seasonal variations were observed for certain ions, OC, EC and metal concentrations in PM10 and PM2.5. Average mean visibility was low (5.64 km), showing better visibility in summer than in other seasons. PM10 and PM2.5 showed stronger negative correlation with visibility giving coefficients of -0.52 and -0.50. Almost all significant correlations were negative and occurred in autumn for visibility with TSP, PM10 and PM2.5, and with ions, EC and OC in both PM10 and PM2.5. The only positive and significant correlation was found between fine OC and visibility. Negative and significant correlations were also observed for visibility with humidity in autumn and winter, and with minimum temperature in all seasons but summer.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is effective in reducing axonal damage associated with traumatic brain injury (TBI), and has immunomodulatory properties. Toll-like receptor 4 (TLR4) is an important mediator of the innate immune response. It significantly contributes to neuroinflammation induced by brain injury. However, it remains unknown whether exogenous PACAP can modulate TBI through the TLR4/adapter protein myeloid differentiation factor 88 (MyD88)/nuclear factor-κB (NF-κB) signaling pathway. In this study, we investigated the potential neuroprotective mechanisms of PACAP pretreatment in a weight-drop model of TBI. PACAP38 was microinjected intracerebroventricularly before TBI. Brain samples were extracted from the pericontusional area in the cortex and hippocampus. We found that TBI induced significant upregulation of TLR4, with peak expression occurring 24 h post-trauma, and that pretreatment with PACAP significantly improved motor and cognitive dysfunction, attenuated neuronal apoptosis, and decreased brain edema. Pretreatment with PACAP inhibited upregulation of TLR4 and its downstream signaling molecules MyD88, p-IκB, and NF-κB, and suppressed increases in the levels of the downstream inflammatory agents interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), in the brain tissue around the injured cortex and in the hippocampus. Administration of PACAP both in vitro and in vivo attenuated the ability of the TLR4 agonist lipopolysaccharide (LPS) to increase TLR4 protein levels. Therefore, PACAP exerts a neuroprotective effect in this rat model of TBI, by inhibiting a secondary inflammatory response mediated by the TLR4/MyD88/NF-κB signaling pathway in microglia and neurons, thereby reducing neuronal death and improving the outcome following TBI.

The neuroprotective effects of pituitary adenylate cyclise-activating polypeptide (PACAP) have been well documented in vivo and in vitro. However, the mechanisms by which PACAP protected microglia from ischemic/hypoxic injury via inhibition of microglia activation remain unclear. Toll-like receptor 4 (TLR4) plays a considerable role in the induction of innate immune and inflammatory responses. The purpose of this study is to investigate the effect of PACAP on the oxygen and glucose deprivation (OGD)/reoxygenation BV2 microglia and to explore the role of TLR4/myeloid differentiation protein 88 (MyD88)/nuclear factor-kappa B (NF-kappaB) pathway in the neuroprotective effects of PACAP.We conducted OGD/reoxygenation by placing BV2 microglia into an airtight chamber and in glucose-free medium. BV2 microglia cell viability was determined by MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide] assay. Western blot was utilized to detect TLR4, MyD88 expression, inhibitory protein of NF-kappaB (IkappaB) phosphorylation/degradation, NF-kappaB activation. Level of tumor necrosis factor-alpha (TNF-alpha) in culture medium was measured with enzyme-linked immunosorbent assay (ELISA). Apoptosis was determined by flow cytometry.We found that pretreatment with PACAP to BV2 cells immediately before OGD/reoxygenation significantly alleviated microglia hypoxic injury. PACAP inhibited upregulation of TLR4, MyD88 and NF-kappaB in BV2 microglial cells exposed to OGD/reoxygenation. PACAP administration also significantly reduced the production of proinflammatory cytokines and apoptosis in BV2 microglia exposed to OGD/reoxygenation.Pretreatment with PACAP inhibited activation of the TLR4/MyD88/NF-kappaB signaling pathway and decreased inflammatory cytokine levels, as well as apoptosis in microglia, thereby attenuating microglia hypoxic injury. Our results suggested that TLR4-mediated MyD88-dependent signaling pathway contributed to neuroprotection of PACAP to microglia against OGD/reoxygenation.

Propofol exhibits neuroprotective effects against hypoxic-ischemic brain injury, but the underlying mechanisms are still not clear. Toll-like receptor 4 (TLR4) plays a considerable role in the induction of innate immune and inflammatory responses. The purposes of this study are to investigate the effect of propofol on the oxygen and glucose deprivation (OGD)/reoxygenation (OGD/R) BV2 microglia and to explore the role of TLR4/myeloid differentiation protein 88 (MyD88)/nuclear factor-kappa B (NF-κB) pathway in the neuroprotective effects of propofol. BV2 microglia were placed into an airtight chamber and in glucose-free medium for OGD/reoxygenation. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide assay. TLR4 and its downstream signaling molecules, MyD88 and NF-κB expressions were detected by Western blotting. Level of tumor necrosis factor alpha (TNF-α) in culture medium was determined with enzyme-linked immunosorbent assay. BV2 microglia apoptosis was determined by flow cytometry. We found that pretreatment with propofol significantly alleviated the hypoxic injury in BV2 microglia. Propofol inhibited upregulation of TLR4, MyD88, and NF-κB expressions in BV2 microglia exposed to OGD/reoxygenation. Propofol pretreatment also significantly reduced the production of TNF-α and apoptosis in OGD/reoxygenation BV2 microglia. The results indicated that TLR4 and its downstream MyD88-dependent signaling pathway contributed to neuroprotection of propofol to microglia exposed to OGD/reoxygenation.

Assessing the insulation condition of high-voltage transformers is essential for repairing and maintaining based on condition of equipment. For the instant diagnostic examination of PD with oil-paper insulated transformers, basically physical method directly related to PD is currently used electric signals. Based on advanced sensor technology, PD detectors with enhanced options for discriminating disturbances were carried out on-site and on-line. PD values condition changes of the insulation system can early be identified and evaluated with simple trending. Consequently, PD monitoring and diagnosis systems allow conditioned based maintenance strategies, serve asset appraisements and permit continuous risk assessment. The reliability and safety of the HV equipment and the system operation of the power network can be increased. The application of on-line and on site PD diagnosis of power transformers in service is a powerful tool to detect defects in the coil insulation. The approach with long term monitoring with remote access through substation communications or the web is important for the lifetime management of ageing transformers The techniques are described, together with cased studies of their application on the engineering practice field.