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The current platoon control strategies of connected autonomous vehicles (CAVs) focus on controlling the fixed intervehicle distance, i.e., the string stability of the platoon system. Here, we aimed to design a CAV platoon control strategy based on a constraint-following approach to solve the problem of platoon starting. As the resistance of the vehicle during driving varies with time, this study regarded the CAV platoon system as a changing dynamic system and introduced the Udwadia-Kalaba (U-K) approach to simplify the solution. Apart from adding an equality constraint, unlike most other studies, this study imposed a bilateral inequality constraint on the intervehicle distance between successive CAVs to prevent collisions. Meanwhile, a diffeomorphism method was introduced to transform the bounded state into an unbounded state. The proposed control strategy could render each CAV compliant with both the original imposed bilateral inequality constraint and the equality constraint. The former avoids collisions, and the latter indicates the string stability of the designed CAV platoon system. The effectiveness of the proposed controller was verified by numerical experiments. The gap errors tend to converge to zero, which is not amplified by the propagation of traffic flow., Author(s): Mengyan Hu [1]; Ying Gao (corresponding author) [1]; Xiangmo Zhao [1]; Bin Tian [1]; Zhigang Xu [1] 1. Introduction With the increasing growth of the automobile industry, urban transportation [...]

Introduction: Intracranial branch atheromatous disease (BAD) has been applied to occlusions that occur at the origin of large caliber penetrating arteries due to the microatheromas or large parent artery plaques. This study aimed to explore the association between culprit plaques of large parent arteries, neuroimaging markers of cerebral small vessel disease (CSVD), and the risk of early neurological deterioration (END) in stroke patients with BAD. Methods: A total of 97 stroke patients with BAD in the vascular territories of the lenticulostriate arteries or paramedian pontine arteries, diagnosed using high-resolution magnetic resonance imaging, were prospectively recruited in this observational study. A culprit plaque in the middle cerebral artery was defined as the only arterial plaque on the ipsilateral side of an infarction visible on diffusion-weighted imaging. A culprit plaque in the basilar artery (BA) was identified when it was observed within the same axial slices of an infarction or on the adjacent upper or lower slice, whereas a plaque within the BA located in the ventral region was considered non-culprit. If more than one plaque was present in the same vascular territory, the most stenotic plaque was chosen for the analysis. Four CSVD neuroimaging markers, including white matter hyperintensity, lacunes, microbleeds, and enlarged perivascular spaces, were evaluated in accordance with the total CSVD score. The associations between neuroimaging features of lesions within large parent arteries, neuroimaging markers of CSVD, and the risk of END in stroke patients with BAD were investigated using logistic regression analysis. Results: END occurred in 41 stroke patients (42.27%) with BAD. The degree of large parent artery stenosis (p < 0.001), culprit plaques of large parent arteries (p < 0.001), and plaque burden (p < 0.001) were significantly different between the END and non-END groups in stroke patients with BAD. In logistic regression analysis, culprit plaques of large parent arteries (odds ratio, 32.258; 95% confidence interval, 4.140–251.346) were independently associated with the risk of END in stroke patients with BAD. Conclusions: Culprit plaques of large parent arteries could predict the risk of END in stroke patients with BAD. These results suggest that lesions in the large parent arteries, rather than damage to the cerebral small vessels, contribute to END in stroke patients with BAD. [ABSTRACT FROM AUTHOR]

Objective: To examine the association of a combined healthy lifestyle in early pregnancy with gestational diabetes mellitus (GDM) risk. Design, setting and population: A Chinese prospective cohort study with 6980 pregnant women. Methods: Individual modifiable lifestyle factors were assessed in early pregnancy and a combined lifestyle score was derived from the sum of the lifestyle factors, with a higher score indicating a healthier lifestyle. The association of a combined healthy lifestyle with GDM risk was examined. Main outcome measures: Gestational diabetes mellitus was diagnosed in middle pregnancy according to the International Association of Diabetes and Pregnancy Study Group criteria or diagnoses in medical records. Results: Overall, 501 (7.2%) pregnant women were diagnosed with GDM. Being physically active (total energy expenditure in upper three quintiles, i.e. ≥100.1 metabolic equivalent of task [MET]‐hours/week; odds ratio [OR] 0.76, 95% confidence interval [CI] 0.63–0.92), healthy diet (total intake of vegetables and fruits ≥5 times/day; OR 0.74, 95% CI 0.59–0.94), sufficient sleep (night‐time sleep duration ≥7 hours/night; OR 0.66, 95% CI 0.48–0.90) and healthy weight (early‐pregnancy BMI <24.0 kg/m2; OR 0.57, 95% CI 0.46–0.71) were associated with lower GDM risk. The GDM risk decreased linearly across the combined lifestyle score (Ptrend <0.001): women with 2, 3 and 4 lifestyle factors compared with those with 0–1 factor had 38% (OR 0.62, 95% CI 0.46–0.84), 57% (OR 0.43, 95% CI 0.31–0.58) and 66% (OR 0.34, 95% CI 0.22–0.52) lower risks of GDM, respectively. Conclusion: A healthy lifestyle in early pregnancy was associated with a substantially lower GDM risk. [ABSTRACT FROM AUTHOR]

Vehicle platooning is a perspective technique for intelligent transportation systems (ITS). Connected and automated vehicles (CAVs) use dedicated short-range communication (DSRC) to form a convoy, in which the following vehicles can receive the information from their preceding vehicles to achieve safe automated driving and maintain a short headway. Consequently, a vehicle platoon can improve traffic safety and efficiency, further reducing fuel consumption. However, emergency braking inevitably occurs when the platoon meets an accident or a sudden mechanical failure. It is more critical when the wireless communication got delays. Therefore, “how to predefine a minimum safe distance (MSD) considering communication delay” is a challenging issue. To this end, a series of field tests were carried out to measure the communication delay of IEEE 802.11p that is the underlying protocol of DSRC. Subsequently, MSD is modeled and analyzed when the platoon travels at accelerating, cruising, and decelerating states. More importantly, the results of field tests are applied in the models to investigate the impact of communication delay on MSD in practice. The simulation results verify that the proposed model can effectively maintain the platooning vehicles' safety even if emergency braking happens with certain communication delays., Author(s): Mengyan Hu [1]; Xiangmo Zhao [1]; Fei Hui [1]; Bin Tian (corresponding author) [1]; Zhigang Xu [1]; Xinrui Zhang [1] 1. Introduction Nowadays, roadway traffic continues to cause congestion, [...]

Natural killer (NK) cells are enriched in the central nervous system in aging-related atheriosclerotic cerebral small vessel disease (aCSVD), but their roles and underlying mechanism remain to be elucidated. To identify potential cytotoxic molecules released by NK cells in aCSVD lesions, proteomic analysis of cerebrospinal fluid (CSF), plasma, and peripheral NK cells from patients with aCSVD were performed. We found that integrin β2 (ITGB2), cathepsin D (CTSD), and granzyme H (GZMH) were highly expressed in NK cells. ITGB2 interacted with intercellular adhesion molecule 1 in vascular endothelial cells. As assessed by immunofluorescence and scanning electron microscopy of the blood–brain barrier model, transwell membranes covered with primary human brain microvascular endothelial cells and astrocytes, we demonstrated that the CTSD-mediated degradation of collagen in the blood–brain barrier depended on the cytotoxicity of NK cells in aCSVD. With the immunostaining in vitro and in vivo, GZMH disruption of demyelinated nerve fibers was reversed by cotreatment with the inhibitor 3,4-DCIC during white matter hyperintensity (WMH) in aCSVD. Our results indicate that NK cells contribute to CTSD-induced damage to the blood–brain barrier and GZMH-induced disruption of nerve fibers during WMH in aCSVD. [ABSTRACT FROM AUTHOR]

Acute ischemic stroke (AIS) induces cerebral endothelial cell death resulting in the breakdown of the blood–brain barrier (BBB). Endothelial cell autophagy acts as a protective mechanism against cell death. Autophagy is activated in the very early stages of ischemic stroke and declines after prolonged ischemia. Previous studies have shown that Rubicon can inhibit autophagy. The current study aimed to investigate whether continuous long‐term ischemia can inhibit autophagy in endothelial cells after ischemic stroke by regulating the function of Rubicon and its underlying mechanism. Wild‐type male C57BL/6J mice were subjected to transient middle cerebral artery occlusion (tMCAO). ROCK1, ROCK2, and NOX2 inhibitors were injected into male mice 1 h before the onset of tMCAO. Disease severity and BBB permeability were evaluated. bEnd.3 cells were cultured in vitro and subjected to oxygen–glucose deprivation (OGD). bEnd.3 cells were pretreated with or without ROCK1, ROCK2, or NOX2 inhibitors overnight and then subjected to OGD. Cell viability and permeability were also evaluated. The expression of Rubicon, ROCK1, and autophagy‐related proteins were analyzed. Increased BBB permeability was correlated with Rubicon expression in tMCAO mice and Rubicon was upregulated in endothelial cells subjected to OGD. Autophagy was inhibited in endothelial cells after long‐term OGD treatment and knockdown of Rubicon expression restored autophagy and viability in endothelial cells subjected to 6‐h OGD. ROCK1 inhibition decreased the interaction between Beclin1 and Rubicon and restored cell viability and autophagy suppressed by 6‐h OGD treatment in endothelial cells. Additionally, ROCK1 inhibition suppressed Rubicon, attenuated BBB disruption, and brain injury induced by prolonged ischemia in 6‐h tMCAO mice. Prolonged ischemia induced the death of brain endothelial cells and the breakdown of the BBB, thus aggravating brain injury by increasing the interaction of ROCK1 and Rubicon with Beclin1 while inhibiting canonical autophagy. Inhibition of ROCK1 signaling in endothelial cells could be a promising therapeutic strategy to prolong the therapeutic time window in AIS. [ABSTRACT FROM AUTHOR]