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A major challenge in studies relating built environment features to health is measurement error in exposure due to geocoding errors. Faulty geocodes in built environment data introduce errors to exposure assessments that may induce bias in the corresponding health effect estimates. In this study, we examine the distribution of the measurement error in measures constructed from point-referenced exposures, quantify the extent of bias in exposure effect estimates due to geocode coarsening, and extend the simulation extrapolation (SIMEX) method to correct the bias. The motivating example focuses on the association between children’s body mass index and exposure to the junk food environment, represented by the number of junk food outlets within a buffer area near their schools. We show, algebraically and through simulation studies, that coarsening of food outlet coordinates results in exposure measurement errors that have heterogeneous variance and non-zero mean, and that the resulting bias in the health effect can be away from the null. The proposed SC-SIMEX procedure accommodates the non-standard measurement error distribution, without requiring external data, and provides the best bias correction compared to other SIMEX approaches.

The boundary, both as social norm and physical form, is an essential element in the development of the structure of urban form. This article explores the role of boundaries: (1) through the transformation of thelilongform in Shanghai by means of a case study of the Guizhoulilongblock and (2) through the extension of the methodology of morphological study. In the urbanization of China, thelilongform tracks successive organizational shifts in society. Over one hundred years, the micro-scale changes of boundaries transformed the morphology of the Guizhoulilongblock from a single-family residence to a mass housing block. Accordingly, the morphological study of the boundaries in Guizhoulilongblock shows how its form was changed by changing regulations applied to it as well as its changing communities. This article uses two-dimensional drawings to investigate the change of boundaries over time extending the Conzen tradition and the understanding of how the social system defines the urban form. Consequently, this article makes an argument for understanding the effect on boundaries of both the conflict and the cooperation between the authorities and the inhabitants in a morphological study following the Conzen School.

Neurite outgrowth is a fundamental process in neurons that produces extensions and, consequently, neural connectivity. Neurite damage and atrophy are observed in various brain injuries and disorders. Understanding the intrinsic pathways of neurite outgrowth is essential for developing strategies to stimulate neurite regeneration. Insulin is a pivotal hormone in the regulation of glucose homeostasis. There is increasing evidence for the neurotrophic functions of insulin, including the induction of neurite outgrowth. However, the associated mechanism remains elusive. Here, we demonstrate that insulin potentiates neurite outgrowth mediated by the small GTPases ADP-ribosylation factor 6 (ARF6) and Ras-related C3 botulinum toxin substrate 1 (Rac1) through the neuronal adaptor FE65. Moreover, insulin enhances atypical protein kinase Cι/λ (PKCι/λ) activation and FE65 phosphorylation at serine 459 (S459) in neurons and mouse brains. In vitro and cellular assays show that PKCι/λ phosphorylated FE65 at S459. Consistently, insulin potentiates FE65 S459 phosphorylation only in the presence of PKCι/λ. Phosphomimetic studies show that an FE65 S459E mutant potently activates ARF6, Rac1, and neurite outgrowth. Notably, this phosphomimetic mutation enhances the FE65-ARF6 interaction, a process that promotes ARF6-Rac1-mediated neurite outgrowth. Likewise, insulin treatment and PKCι/λ overexpression potentiate the FE65-ARF6 interaction. Conversely, PKCι/λ knockdown suppresses the stimulatory effect of FE65 on ARF6-Rac1-mediated neurite outgrowth. The effect of insulin on neurite outgrowth is also markedly attenuated in PKCι/λ knockdown neurons, in the presence and absence of FE65. Our findings reveal a novel mechanism linking insulin with ARF6-Rac1-dependent neurite extension through the PKCι/λ-mediated phosphorylation of FE65.

Objectives To investigate the impact of the SAR-Cov-2 pandemic and lockdown on individuals with bipolar disorder in comparison to healthy controls. Methods A longitudinal study of 560 participants including 147 healthy controls was conducted between April 30 and May 30, 2020 during a state-wide lockdown. Bi-weekly measures included the Coronavirus Impact Scale, the Pittsburg Sleep Quality Index, the Patient Health Questionnaire, 9-item, and the Generalized Anxiety Disorder scale, 7-item. Generalized estimating equations method was used to examine the longitudinal change of the measures within the lockdown and the change from pre-pandemic period to pandemic period. Results All participants reported an impact of lockdown. Individuals with bipolar disorder reported greater impact from the stay-at-home orders with disruptions in routines, income/employment, social support and pandemic related stress. While these measures improved over time, healthy controls recovered quicker and with greater magnitude than persons with bipolar disorder. Comparing mood symptom severity measures in mid-March through May 2020 to the same time window in 2015–2019 (pre- verses post-pandemic), there were no significant differences among individuals with bipolar disorder, whereas healthy controls showed a significant, albeit transient, increase in mood symptoms. Conclusion Everyone was impacted by the SARs-CoV pandemic; however, those with bipolar disorder experienced more life impacting changes from the stay-at-home orders vs healthy controls. These disruptions improved over time but much more slowly than healthy controls. Pre- vs post-pandemic comparisons show a modest but significant increase in mood severity in the healthy controls which was not observed in those with bipolar disorder.

This paper puts forward an emergency dynamic simulation system based on computational experiments method and cellular automata modeling according to the features of mine fire emergency management. The system has characteristics of high performance, open and interact. The system sets initial environmental parameters to simulate fire, and records the fire parameters. Let the staff not only see the whole process of the fire spread and disaster degree of fire in specific environment, but also get fire severity assessment of every experiment. Observation of the whole process can help staff design the actual plan to solve problems, and provide the correct suggestions for promoting emergency capability to reduce casualties and economic loss.

As productive forces developing rapidly, “cluster supply chain” is proposed as a new management pattern to help small and medium-sized enterprises (SMEs) win in the increasingly fierce competition. Facing complex requirements, it is necessary to build an IT system to support them. Modeling is the basic and the most important part in building a system. This paper combines the advantages of agent and Web service based on the common ground between them. According to certain rules, agent models map to Web service models to complete enterprise collaborative modeling in cluster supply chain.