Infrastructure planning for electrified transportation

Due to the climate crisis, the importance of reducing greenhouse gas (GHG) has been recognized by governments, private companies and the general public alike. Yet carbon capturing-based approaches are difficult to integrate with transportation, which is one of the largest GHG producing sectors, Therefore, electrification is the only viable approach to reduce emissions from transportation, by greatly increasing the market share of electric vehicles (EVs). However, the mass adoption of either (or both) of battery EVs (BEVs) and fuel cell EVs (FCEVs) require a large amount of supporting infrastructures, particularly the construction of EV charging stations (EVCSs) for BEVs and hydrogen refuelling stations (HRSs) for FCEVs. The goal of this study is to provide effective approaches for the sizing and sitting of EVCSs and HRSs to facilitate the deployment of BEVs and FCEVs. The background and an overview of the thesis are provided in Chapter 1, where the gaps in the current research are pointed out and the objectives of the thesis are formulated. Chapter 2 reviewed the current state of technologies regarding the hydrogen life cycle as well as the popular planning models for EVCSs and HRSs. In Chapter 3, to achieve a competitive strategy from the perspective of private companies, a market-based framework is proposed for the problem of EVCS planning by leveraging Graph Convolutional Network (GCN) and game theory. In Chapter 4, a multi-objective planning model is developed for EVCSs and the expansion of distribution network with significant renewable components while considering uncertainties in EV charging behaviour. Additionally, in Chapter 5, a planning model of HRS maximises the long-term profit while considering different practical constraints. The HRS planning model also addresses short-term demand uncertainty via redistribution. The models that are developed in this study are validated using either synthetic or real-world case studies, and the simulation results showed the effectiveness of the proposed models. Finally Chapter 6 summarises the major achievements of the thesis and provides directions for further research

Cash dividends, return on equity and earnings persistence

With reference to Ohlson’ model, we optimise earnings persistence model and express earnings persistence measure as a function of return on equity (R.O.E.), dividends payout ratio and other factors. Our theoretical model reveals that dividends payout ratio has little effect on the earnings persistence, while R.O.E. has a decisive effect on earnings persistence. Using quarterly earnings data of 872 listed firms in China over 2011–2020, we calculate the Revised Persistence value of earnings (RPer value) of our earnings persistence model, and find that the Rper value of our model have more explanatory power than that of Kormendi and Lipe’ model. Our study also suggest that quarterly earnings are useful and have information content. Both the theoretical model and empirical results of our research are of great significance to understand and support the implementation of semi-compulsory cash dividends rules in China

Hyperglycemia as a Risk Factor of Ischemic Stroke

Diabetes is considered a major risk factor for stroke and is associated with worsened stroke outcomes. Here, we discuss and summarize the mechanisms that have been associated with the increased risk of stroke due to the hyperglycemia in diabetes mellitus. In diabetic stroke models, hyperglycemia exaggerates the following damaging processes: acidosis, accumulation of reactive oxygen species/reactive nitrogen, inflammation and mitochondrial dysfunction. Understanding the mechanism of diabetes acting as a stroke risk factor will definitely assist to reveal issues related to drug metabolism and toxicity in diabetic stroke. In addition, it is suggested that future studies may focus on the mechanisms mediating blood-brain barrier and astrocytes dysfunction under hyperglycemic stroke.This research was supported in part by a grant from the National Institutes of Health (R01NS058807) and a Kansas University Center for Research startup fund

Hypothalamic Menin Regulates Systemic Aging and Cognitive Decline

Aging is a systemic process, which is a risk factor for impaired physiological functions, and finally death. The molecular mechanisms driving aging process and the associated cognitive decline are not fully understood. The hypothalamus acts as the arbiter that orchestrates systemic aging through neuroinflammatory signaling. Our recent findings revealed that Menin plays important roles in neuroinflammation and brain development. Here, we found that the hypothalamic Menin signaling diminished in aged mice, which correlates with systemic aging and cognitive deficits. Restoring Menin expression in ventromedial nucleus of hypothalamus (VMH) of aged mice extended lifespan, improved learning and memory, and ameliorated aging biomarkers, while inhibiting Menin in VMH of middle-aged mice induced premature aging and accelerated cognitive decline. We further found that Menin epigenetically regulates neuroinflammatory and metabolic pathways, including D-serine metabolism. Aging-associated Menin reduction led to impaired D-serine release by VMH-hippocampus neural circuit, while D-serine supplement rescued cognitive decline in aged mice. Collectively, VMH Menin serves as a key regulator of systemic aging and aging-related cognitive decline

Hypoxia-inducible factor 1 contributes to N-acetylcysteine’s protection in stroke

Stroke is a leading cause of adult morbidity and mortality with very limited treatment options. Evidence from preclinical models of ischemic stroke has demonstrated that the antioxidant N-acetylcysteine (NAC) effectively protects the brain from ischemic injury. Here, we evaluated a new pathway through which NAC exerted its neuroprotection in a transient cerebral ischemia animal model. Our results demonstrated that pretreatment with NAC increased protein levels of hypoxia-inducible factor-1α (HIF-1α), the regulatable subunit of HIF-1, and its target proteins erythropoietin (EPO) and glucose transporter (GLUT)-3, in the ipsilateral hemispheres of rodents subjected to 90 min middle cerebral artery occlusion (MCAO) and 24 h reperfusion. Interestingly, after NAC pretreatment and stroke, the contralateral hemisphere also demonstrated increased levels of HIF-1α, EPO, and GLUT-3, but to a lesser extent. Suppressing HIF-1 activity with two widely used pharmacological inhibitors, YC-1 and 2ME2, and specific knockout of neuronal HIF-1α abolished NAC’s neuroprotective effects. The results also showed that YC-1 and 2ME2 massively enlarged infarcts, indicating that their toxic effect was larger than just abolishing NAC’s neuroprotective effects. Furthermore, we determined the mechanism of NAC-mediated HIF-1α induction. We observed that NAC pretreatment upregulated heat-shock protein 90 (Hsp90) expression and increased the interaction of Hsp90 with HIF-1α in ischemic brains. The enhanced association of Hsp90 with HIF-1α increased HIF-1α stability. Moreover, Hsp90 inhibition attenuated NAC-induced HIF-1α protein accumulation and diminished NAC-induced neuroprotection in the MCAO model. These results strongly indicate that HIF-1 plays an important role in NAC-mediated neuroprotection and provide a new molecular mechanism involved in the antioxidant’s neuroprotection in ischemic stroke

Persistence of an SEIR Model with Immigration Dependent on the Prevalence of Infection

We incorporate the immigration of susceptible individuals into an SEIR epidemic model, assuming that the immigration rate decreases as the spread of infection increases. For this model, the basic reproduction number, R0, is found, which determines that the disease is either extinct or persistent ultimately. The obtained results show that the disease becomes extinct as R01