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To optimize the performance and operation of shared-bicycle systems, this study aims to evaluate the efficiency of shared-bicycle stations and to find factors affecting their efficiency scores. We analyzed the efficiency of 1,260 shared-bicycle stations in the City of Seoul using shared-bicycle rental and trajectory data as of June 2018. In this study, the two-stage bootstrap data envelopment analysis, which is a non-parametric frontier technique, was applied to estimate each shared-bicycle station’s efficiency. In the first stage, we evaluated efficiency scores by employing the number of bicycle racks and bicycle path ratio as input variables, and bicycle turnover rate and balancing rate as output variables. The efficiency scores were regressed on potential covariates using a bootstrapped truncated regression in the second stage. From our results, the efficiencies of shared-bicycle stations were found to be diverse depending on the nature of land use around the station location. The results present evidence to show that shared-bicycle stations located in residential and school-dominated areas are likely to be efficient, whereas those in semi-industrial areas, commercial, and business districts are generally inefficient. Furthermore, the effect of variables like the commuting population, the number of registered vehicles, and the number of bicycle-related accidents per year were statistically significant, thus affecting shared-bicycle station performance. This study offers essential insights into the efficiency of shared-bicycle stations, which could be incorporated into shared-transportation strategies to improve mobility in urban cities.

This research explores the efficiency of Transit-Oriented Development (TOD) at transit stations in Seoul using a two-stage bootstrap Data Envelopment Analysis with truncated regression. The ridership, in terms of the bus, subway, and shared bicycle usage within the transit stations' impact area, is judged as an immediate output of TOD performance, and indicators relating to the core concepts of TOD are selected as inputs. In the first-phase, TOD efficiency estimates are computed and regressed on environmental variables in the subsequent phase to identify contributory factors of TOD efficiency. Assessing the performance of TOD at the transit station revealed that the stations located around the CBD where commercial activities highly concentrated and transit stations are connected were more efficient compared to those located at the periphery of the city. The second-stage results indicate that a rise in pedestrian volume, the number of shared-bicycle stations and bus stops, commercial floor area, and traffic congestion around a transit station improves the efficiency of TOD. Our study makes a significant contribution to the literature by employing a more robust approach to explore TOD efficiency at transit stations. The findings of this study provide useful implications and insights for urban planners and policymakers across cities.

During pregnancy, the progesterone metabolite, allopregnanolone (ALLO), becomes elevated and has been associated with altered levels within the CNS and resulting changes in GABAA receptor function. Pregnant animals poorly compensate reflexes for a decrease in blood pressure during hemorrhage. Previous works suggested that ALLO decreases baroreflex responses by central actions, however, the underlying mechanisms are poorly understood. In this study, we tested ALLO actions on visceral afferent synaptic transmission at second-order neurons within medial portions of the nucleus tractus solitarius (NTS) using hindbrain slices from non-pregnant female rats. Solitary tract (ST) stimulation-evoked excitatory postsynaptic currents (ST-eEPSCs) in NTS neurons directly connected to vagal afferents within the ST. ST-eEPSCs were functionally identified as monosynaptic by the latency characteristics (low jitter = standard deviation of latency, ≤200 μs) to ST stimulation. Such second-order neurons all displayed spontaneous inhibitory postsynaptic currents (sIPSCs), and low micromolar concentrations of ALLO increased frequency and decay time. At submicromolar concentrations, ALLO induced a tonic, GABAergic inhibitory current and suppressed ST-eEPSCs' amplitude. While GABAA receptor antagonist, bicuculline, blocked all ALLO effects, gabazine only blocked sIPSC actions. In current-clamp mode, ALLO perfusion increased failure of ST stimulation to trigger action potentials in most neurons. Thus, our results indicate that ALLO acts to suppress visceral afferent ST synaptic transmission at first synapses by activating pharmacologically distinct GABAA subtypes at different concentration ranges. This ALLO-mediated attenuated visceral afferent signal integration in NTS may underlie reflex changes in blood pressure during gestation.

PR interval is the period from the onset of P wave to the start of the QRS complex on electrocardiograms. A recent genomewide association study (GWAS) suggested that GAREM1 was linked to the PR interval on electrocardiograms. This study was designed to validate this correlation using additional subjects and examined the function of Garem1 in a mouse model. We analyzed the association of rs17744182, a variant in the GAREM1 locus, with the PR interval in 5646 subjects who were recruited from 2 Korean replication sets, Yangpyeong (n = 2471) and Yonsei (n = 3175), and noted a significant genomewide association by meta-analysis (P = 2.39 × 10−8). To confirm the function of Garem1 in mice, Garem1 siRNA was injected into mouse tail veins to reduce the expression of Garem1. Garem1 transcript levels declined by 53% in the atrium of the heart (P = 0.029), and Garem1-siRNA injected mice experienced a significant decrease in PR interval (43.27 ms vs. 44.89 ms in control, P = 0.007). We analyzed the expression pattern of Garem1 in the heart by immunohistology and observed specific expression of Garem1 in intracardiac ganglia. Garem1 was expressed in most neurons of the ganglion, including cholinergic and adrenergic cells. We have provided evidence that GAREM1 is involved in the PR interval of ECGs. These findings increase our understanding of the regulatory signals of heart rhythm through intracardiac ganglia of the autonomic nervous system and can be used to guide the development of a therapeutic target for heart conditions, such as atrial fibrillation.

Hepatocellular carcinoma (HCC) belongs to the most deadly types of cancer since it has a poor prognosis due to its aggressive metastatic phenotype. Endoplasmic reticulum (ER) stress is closely associated with the incidences of a variety of liver diseases including liver injury, regeneration, fibrosis, cirrhosis and often HCC. G protein-coupled receptor (GPCR) signals lead to activation of their downstream pathways through G proteins. Previously, we reported that Gα12 overexpression enhances HCC malignancy, promoting cancer migration and microvascular invasion. However, the role of Gα12 in ER stress-associated pathophysiology in the liver was unclear. Given the link between ER stress and HCC malignancy, this study investigated the effect of ER stress on Gα12, the role of Gα12 in ER stress-mediated hepatocyte death, and the underlying pathway. In the analyses of RNA-sequencing data from mouse liver or primary mouse embryonic fibroblasts challenged with ER stress, Gα12 and C/EBP homologous protein (CHOP) levels correlated with each other. Increases in Gα12 level by unfolded protein response (UPR) under ER stress condition was verified using primary hepatocytes or hepatocyte-derived cell line, confirmative of the close association between Gα12 and UPR. Of note, enforced Gα12 expression under ER stress condition augmented IRE1α level in a RhoA/Rock-dependent pathway. Among the canonical pathways, IRE1α gene silencing distinctly inhibited Gα12 induction elicited by ER stress in hepatocytes. Consistently, overexpression of IRE1α enhanced Gα12 level upon tunicamycin treatment. Similar outcomes were obtained in cells or mice treated with acetaminophen, a representative liver toxicant inducing ER stress response. Overall, our results provide evidence that IRE1α-dependent increase of Gα12 potentiates ER stress response in the liver as mediated by the RhoA-ROCK pathway, enhancing catastrophic death of hepatocytes. Citation Format: Jihoon Tak, Tae Hyun Kim, Sang Geon Kim. IRE1á-dependent increase of Gá12, a gep oncogene, augments ER stress-induced catastrophic cell death [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2659.