Multi-Agent System for Electric Vehicle Charging Scheduling in Parking Lots

As the number of electric vehicles (EVs) increases, massive numbers of EVs have started to gather in commercial parking lots to charge and discharge, which may significantly impact the operation of the grid. There may also be a deviation in the departure time of charged and discharged EVs in commercial parking lots. This deviation can lead to insufficient battery energy when the EVs leave the parking lot. This study uses the simulation software AnyLogic to build a commercial parking lot multi-agent simulation model, and the agent-based model can fully reflect the autonomy of individual EVs. Based on this simulation model, we propose an EV scheduling algorithm. The algorithm contains two main agents. The first is the power distribution center agent (PDCA), which is used to coordinate the energy output of photovoltaic (PV), energy storage system (ESS), and distribution station (DS) to solve the problem of grid overload. The second is the scheduling center agent (SCA), which is used to solve the insufficient battery energy problem due to EVs’ random departures. The SCA includes two stages. In the first stage, a priority scheduling algorithm is proposed to emphasize the fairness of EV charging. In the second stage, a genetic algorithm is used to accurately determine the time interval between charging and discharging to ensure the maximum benefit of EV owner. Finally, simulation experiments are conducted in AnyLogic, and the results demonstrate the superiority of the algorithm over the classical algorithm

TLR3 Ligand PolyI:C Prevents Acute Pancreatitis Through the Interferon-β/Interferon-α/β Receptor Signaling Pathway in a Caerulein-Induced Pancreatitis Mouse Model

Acute pancreatitis (AP) is a common and devastating inflammatory disorder of the pancreas. However, there are still no effective treatments available for the disease. Therefore, it is important to discover new therapeutic targets and strategies for better treatment and prognosis of AP patients. Toll-like receptor 3 (TLR3) ligand polyI:C is a double-stranded RNA mimic that can be used as an immune stimulant. Our current study indicates that polyI:C exerted excellent anti-inflammatory effects in a caerulein-induced AP mouse model and taurocholate-induced pancreatic acinar cell line injury model. We found that polyI:C triggers type I interferon (IFN) production and downstream IFN-α/β receptor (IFNAR)-dependent signaling, which play key roles in protecting the pancreas from inflammatory injury. Knockout of IFN-β and IFNAR in mice abolished the preventive effects of polyI:C on caerulein-induced AP symptoms, which include pancreatic edema, neutrophil infiltration, the accumulation of reactive oxygen species (ROS), and inflammatory gene expression. Treating pancreatic acinar 266-6 cells with an IFNAR inhibitor, which blocks the interaction between type I IFN and IFNAR, diminishes the downregulation of oxidative stress by polyI:C. Additionally, a subsequent transcriptome analysis on the role of polyI:C in treating pancreatitis suggested that chemotaxis of neutrophils and the production of ROS were inhibited by polyI:C in the pancreases damaged by caerulein injection. Thus, polyI:C may act as a type I IFN inducer to alleviate AP, and it has the potential to be a promising therapeutic agent used at the early stages of AP

DHEA and DHEA-S levels in posttraumatic stress disorder: A meta-analytic review

Differences in hypothalamic-pituitary-adrenocortical (HPA) functioning between patients with posttraumatic stress disorder (PTSD) and controls are among the most consistent neurobiological findings in PTSD. HPA-axis activation results in the output of various steroid hormones including dehydroepiandrosterone (DHEA), which is then converted into dehydroepiandrosterone sulfate (DHEA-S), with anti-glucocorticoid actions among its pleiotropic effects. To investigate whether there is evidence for consistent differences in basal DHEA and DHEA-s levels between individuals with and without PTSD, we performed random-effect meta-analyses aggregating findings of previously published studies. Nine studies reporting on DHEA levels (486 participants) and 8 studies reporting on DHEA-S levels (501 participants) were included. No significant differences in DHEA or DHEA-S levels between PTSD and control groups were found. Exploratory subgroup analyses were performed to"distinguish between effects of PTSD and trauma exposure. A trend for higher DHEA levels was found in PTSD-patients compared to non-trauma-exposed controls-(NTC) (k = 3, SMD = 1.12 95% CI -0.03-2.52, Z = 1.91, p = 0.06). Significantly higher DHEA-S levels were observed in PTSD patients compared to NTC (k = 2, SMD = 0.76, 95% CI 0.38-1.13, Z = 3.94, p <0.001). Additionally, significantly higher DHEA levels were observed in trauma-exposed controls (TC) compared to NTC (k = 3, SMD = 0.66, 95% CI 0.33-0.99, Z = 3.88, p <0.001, I-2 = 86%) this suggests that trauma exposure, irrespective of further PTSD development, might increase basal DHEA and DHEA-S level

Neuropsychiatric Disease and Treatment Dovepress Body integrity identity disorder crosses culture: case reports in the Japanese and chinese literature

Abstract: Body integrity identity disorder (BIID) is a condition in which people do not perceive a part of their body as their own, which results in a strong desire for amputation or paralyzation. The disorder is likely to be congenital due to its very early onset. The English literature describes only Western patients with BIID, suggesting that the disorder might be merely prevalent in the West. To scrutinize this assumption, and to extend our knowledge of the etiology of BIID, it is important to trace cases with BIID in non-Western populations. Our objective was to review Chinese and Japanese literature on BIID to learn about its presence in populations with a different genetic background. A systematic literature search was performed in databases containing Japanese and Chinese research, published in the respective languages. Five Japanese articles of BIID were identified which described two cases of BIID, whereas in the Chinese databases only BIID-related conditions were found. This article reports some preliminary evidence that BIID is also present in non-Western countries. However, making general statements about the biological background of the disorder is hampered by the extremely low number of cases found. This low number possibly resulted from the extreme secrecy associated with the disorder, perhaps even more so in Asian countries

The Modified Selenenyl Amide, M-hydroxy Ebselen, Attenuates Diabetic Nephropathy and Diabetes-Associated Atherosclerosis in ApoE/GPx1 Double Knockout Mice

Seleno-organic glutathione peroxidase (GPx) mimetics, including ebselen (Eb), have been tested in in vitro studies for their ability to scavenge reactive oxygen and nitrogen species, including hydrogen peroxide and peroxynitrite. In this study, we investigated the efficacies of two Eb analogues, m-hydroxy ebselen (ME) and ethanol-ebselen (EtE) and compared these with Eb in cell based assays. We found that ME is superior in attenuating the activation of hydrogen peroxide-induced pro-inflammatory mediators, ERK and P38 in human aortic endothelial cells. Consequently, we investigated the effects of ME in an in vivo model of diabetes, the ApoE/GPx1 double knockout (dKO) mouse. We found that ME attenuates plaque formation in the aorta and lesion deposition within the aortic sinus of diabetic dKO mice. Oxidative stress as assessed by 8-OHdG in urine and nitrotyrosine immunostaining in the aortic sinus and kidney tubules, was reduced by ME in diabetic dKO mice. ME also attenuated diabetes-associated renal injury which included tubulointerstitial fibrosis and glomerulosclerosis. Furthermore, the bioactivity of the pro-fibrotic cytokine transforming growth factor-beta (TGF-beta) as assessed by phospho-Smad2/3 immunostaining was attenuated after treatment with ME. TGF-beta-stimulated increases in collagen I and IV gene expression and protein levels were attenuated by ME in rat kidney tubular cells. However, in contrast to the superior activity of ME in in vitro and cell based assays, ME did not further augment the attenuation of diabetes-associated atherosclerosis and renal injury in our in vivo model when compared with Eb. In conclusion, this study strengthens the notion that bolstering GPx-like activity using synthetic mimetics may be a useful therapeutic strategy in lessening the burden of diabetic complications. However, these studies highlight the importance of in vivo analyses to test the efficacies of novel Eb analogues, as in vitro and cell based assays are only partly predictive of the in vivo situation

Altered Global Signal Topography and Its Different Regional Localization in Motor Cortex and Hippocampus in Mania and Depression

Bipolar disorder (BD) is a complex psychiatric disorder characterized by dominant symptom swings across different phases (manic, depressive, and euthymic). Different symptoms in BD such as abnormal episodic memory recall and psychomotor activity have been related to alterations in different regions, ie, hippocampus and motor cortex. How the abnormal regional distribution of neuronal activity relates to specific symptoms remains unclear, however. One possible neuronal mechanism of the relationship is the alteration of the global distribution of neuronal activity manifested in specific local regions; this can be measured as the correlation between the global signal (GS) and local regions. To understand the GS and its relationship to psychopathological symptoms, we here investigated the alteration of both GS variance and its regional topography in healthy controls and 3 phases of BD. We found that the variance of GS showed no significant difference between the 4 groups. In contrast, the GS topography was significantly altered in the different phases of BD, ie, the regions showing abnormally strong topographical GS contribution changed from hippocampus (and parahippocampus/fusiform gyrus) in depression to motor cortex in mania. Importantly, topographical GS changes in these regions correlated with psychopathological measures in both depression and mania. Taken together, our findings demonstrate the central importance of GS topography for psychopathological symptoms. This sheds lights on the neuronal mechanisms of specific psychopathological symptoms in BD, and its relevance in the relationship between global and local neuronal activities for behavior in general