A kinematic wave theory of capacity drop

Capacity drop at active bottlenecks is one of the most puzzling traffic phenomena, but a thorough understanding is practically important for designing variable speed limit and ramp metering strategies. In this study, we attempt to develop a simple model of capacity drop within the framework of kinematic wave theory based on the observation that capacity drop occurs when an upstream queue forms at an active bottleneck. In addition, we assume that the fundamental diagrams are continuous in steady states. This assumption is consistent with observations and can avoid unrealistic infinite characteristic wave speeds in discontinuous fundamental diagrams. A core component of the new model is an entropy condition defined by a discontinuous boundary flux function. For a lane-drop area, we demonstrate that the model is well-defined, and its Riemann problem can be uniquely solved. We theoretically discuss traffic stability with this model subject to perturbations in density, upstream demand, and downstream supply. We clarify that discontinuous flow-density relations, or so-called "discontinuous" fundamental diagrams, are caused by incomplete observations of traffic states. Theoretical results are consistent with observations in the literature and are verified by numerical simulations and empirical observations. We finally discuss potential applications and future studies.Comment: 29 pages, 10 figure

(2,2′-Bipyridine-κ2 N,N′){N-[2-oxido-5-(phenyl­diazen­yl)benzyl­idene-κO]glycinato-κ2 N,O}copper(II)

In the title compound, [Cu(C15H11N3O3)(C10H8N2)], the CuII atom is five-coordinated in a distorted square-pyramidal CuN3O2 geometry. The basal positions are occupied by three donor atoms from the tridentate Schiff base ligand and by one N atom from the 2,2′-bipyridine ligand. The axial position is occupied by the other N atom of the 2,2′-bipyridine ligand. The crystal structure is consolidated by weak C—H⋯O hydrogen bonds. In addition, π–π inter­actions between adjacent pyridine rings (centroid–centroid distances = 3.238 and 3.313 Å) may also stabilize the crystal packing

The unidirectional valve patch provides no benefits to early and long-term survival in patients with ventricular septal defect and severe pulmonary artery hypertension

ObjectiveOur aim was to test whether a unidirectional valve patch would provide benefit to early and long-term survival for patients with ventricular septal defect and severe pulmonary artery hypertension.MethodsEight hundred seventy-six cases of ventricular septal defect with severe pulmonary artery hypertension were closed with or without a unidirectional valve patch and were classified as the unidirectional valve patch (UVP) group (n = 195) and nonvalve patch (NVP) group (n = 681), respectively. Propensity scores of inclusion into the UVP group were used to match 138 pairs between the 2 groups. Kaplan–Meier survival curves were constructed to compare early and long-term survival.ResultsFor the 138 propensity-matched pairs, there were 7 and 9 early deaths (in-hospital deaths) in the UVP and NVP groups, respectively. The difference in early mortality between the 2 groups did not reach statistical significance (χ2 = 0.265, P = .6064). With a mean of 9.2 ± 4.92 years' and 2511 patient-years' follow-up, there were 6 late deaths in the UVP group and 7 late deaths in the NVP group. The difference in actuarial survival at 5, 10, 15, and 18 years between the 2 groups was not significant (log-rank test, χ2 = 0.565, P = .331). The difference in the late mortality between the groups with or without a patent patch at the time of discharge did not reach statistical significance (χ2 = 1.140, P = .2856). There was no difference between the 2 groups in the 6-minute walk distance assessed at the last follow-up (525.9 ± 88.0 meters for the UVP group and 536.5 ± 95.8 meters for the NVP group, F = 1.550, P = .214).ConclusionA unidirectional valve patch provides no benefits to early and long-term survival when it is used to deal with ventricular septal defect and severe pulmonary artery hypertension

A study of factors influencing long-term glycemic variability in patients with type 2 diabetes: a structural equation modeling approach

AimThe present study aims to utilize structural equation modeling (SEM) to investigate the factors impacting long-term glycemic variability among patients afflicted with type 2 diabetes.MethodThe present investigation is a retrospective cohort study that involved the collection of data on patients with type 2 diabetes mellitus who received care at a hospital located in Chengdu, Sichuan Province, over a period spanning from January 1, 2013, to October 30, 2022. Inclusion criteria required patients to have had at least three laboratory test results available. Pertinent patient-related information encompassing general demographic characteristics and biochemical indicators was gathered. Variability in the dataset was defined by standard deviation (SD) and coefficient of variation (CV), with glycosylated hemoglobin variation also considering variability score (HVS). Linear regression analysis was employed to establish the structural equation models for statistically significant influences on long-term glycemic variability. Structural equation modeling was employed to analyze effects and pathways.ResultsDiabetes outpatient special disease management, uric acid variability, mean triglyceride levels, mean total cholesterol levels, total cholesterol variability, LDL variability, baseline glycated hemoglobin, and recent glycated hemoglobin were identified as significant factors influencing long-term glycemic variability. The overall fit of the structural equation model was found to be satisfactory and it was able to capture the relationship between outpatient special disease management, biochemical indicators, and glycated hemoglobin variability. According to the total effect statistics, baseline glycated hemoglobin and total cholesterol levels exhibited the strongest impact on glycated hemoglobin variability.ConclusionThe factors that have a significant impact on the variation of glycosylated hemoglobin include glycosylated hemoglobin itself, lipids, uric acid, and outpatient special disease management for diabetes. The identification and management of these associated factors can potentially mitigate long-term glycemic variability, thereby delaying the onset of complications and enhancing patients’ quality of life

Contribution of basal ganglia activity to REM sleep disorder in Parkinson’s disease

Background: Rapid eye movement (REM) sleep behaviour disorder (RBD) is one of the most common sleep problems and represents a key prodromal marker in Parkinson’s disease (PD). It remains unclear whether and how basal ganglia nuclei, structures that are directly involved in the pathology of PD, are implicated in the occurrence of RBD. Method: Here, in parallel with whole-night video polysomnography, we recorded local field potentials from two major basal ganglia structures, the globus pallidus internus and subthalamic nucleus, in two cohorts of patients with PD who had varied severity of RBD. Basal ganglia oscillatory patterns during RBD and REM sleep without atonia were analysed and compared with another age-matched cohort of patients with dystonia that served as controls. Results: We found that beta power in both basal ganglia nuclei was specifically elevated during REM sleep without atonia in patients with PD, but not in dystonia. Basal ganglia beta power during REM sleep positively correlated with the extent of atonia loss, with beta elevation preceding the activation of chin electromyogram activities by ~200 ms. The connectivity between basal ganglia beta power and chin muscular activities during REM sleep was significantly correlated with the clinical severity of RBD in PD. Conclusions: These findings support that basal ganglia activities are associated with if not directly contribute to the occurrence of RBD in PD. Our study expands the understanding of the role basal ganglia played in RBD and may foster improved therapies for RBD by interrupting the basal ganglia-muscular communication during REM sleep in PD

Metabolically Specific In Situ Fluorescent Visualization of Bacterial Infection on Wound Tissues

The ability to effectively detect bacterial infection in human tissues is important for the timely treatment of the infection. However, traditional techniques fail to visualize bacterial species adhered to host cells in situ in a target-specific manner. Dihydropteroate synthase (DHPS) exclusively exists in bacterial species and metabolically converts p-aminobenzoic acid (PABA) to folic acid (FA). By targeting this bacterium-specific metabolism, we have developed a fluorescent imaging probe, PABA-DCM, based on the conjugation of PABA with a long-wavelength fluorophore, dicyanomethylene 4H-pyran (DCM). We confirmed that the probe can be used in the synthetic pathway of a broad spectrum of Gram-positive and negative bacteria, resulting in a significantly extended retention time in bacterial over mammalian cells. We validated that DHPS catalytically introduces a dihydropteridine group to the amino end of the PABA motif of PABA-DCM, and the resulting adduct leads to an increase in the FA levels of bacteria. We also constructed a hydrogel dressing containing PABA-DCM and graphene oxide (GO), termed PABA-DCM@GO, that achieves target-specific fluorescence visualization of bacterial infection on the wounded tissues of mice. Our research paves the way for the development of fluorescent imaging agents that target species-conserved metabolic pathways of microorganisms for the in situ monitoring of infections in human tissues. </p