Endotoxin-induced lung injury is one of the major causes of death induced by endotoxemia, however, few effective therapeutic options exist. Hydrogen inhalation has recently been shown to be an effective treatment for inflammatory lung injury, but the underlying mechanism is unknown. In the current study we aim to investigate how hydrogen attenuates endotoxin-induced lung injury and provide reference values for the clinical application of hydrogen. LPS was used to establish an endotoxin-induced lung injury mouse model. The survival rate and pulmonary pathologic changes were evaluated. THP-1 and HUVECC cells were cultured in vitro. The thioredoxin 1 (Trx1) inhibitor was used to evaluate the anti-inflammatory effects of hydrogen. Hydrogen significantly improved the survival rate of mice, reduced pulmonary edema and hemorrhage, infiltration of neutrophils, and IL-6 secretion. Inhalation of hydrogen decreased tissue factor (TF) expression and MMP-9 activity, while Trx1 expression was increased in the lungs and serum of endotoxemia mice. LPS-stimulated THP-1 and HUVEC-C cells in vitro and showed that hydrogen decreases TF expression and MMP-9 activity, which were abolished by the Trx1 inhibitor, PX12. Hydrogen attenuates endotoxin-induced lung injury by decreasing TF expression and MMP-9 activity via activating Trx1. Targeting Trx1 by hydrogen may be a potential treatment for endotoxin-induced lung injury.

Fast and efficient semantic segmentation of large-scale Li-DAR point clouds is a fundamental problem in autonomous driving. To achieve this goal, the existing point-based methods mainly choose to adopt Random Sampling strategy to process large-scale point clouds. However, our quantative and qualitative studies have found that Random Sampling may be less suitable for the autonomous driving scenario, since the LiDAR points follow an uneven or even long-tailed distribution across the space, which prevents the model from capturing sufficient information from points in different distance ranges and reduces the model's learning capability. To alleviate this problem, we propose a new Polar Cylinder Balanced Random Sampling method that enables the downsampled point clouds to maintain a more balanced distribution and improve the segmentation performance under different spatial distributions. In addition, a sampling consistency loss is introduced to further improve the segmentation performance and reduce the model's variance under different sampling methods. Extensive experiments confirm that our approach produces excellent performance on both SemanticKITTI and Se-manticPOSS benchmarks, achieving a 2.8% and 4.0% improvement, respectively.

Therapeutic hypothermia (HT) is an important treatment after cardiac arrest to mitigate cerebral ischemia-reperfusion (I/R) injury, but the underlying mechanism is not clear. Studies have shown that cold-inducible RNA binding protein (CIRP), as a stress-response protein, exerts key role on improvement of neurological outcome after therapeutic hypothermia treatment in the global ischemia. Thus, this study focused on investigating the role of CIRP in hippocampal neuronal injury induced by oxygen-glucose deprivation/reoxygenation (OGD/R) and exploring relative mechanisms. In our study, the results of biochemical detection, flow cytometry and western blot showed that HT could significantly inhibit OGD/R-induced neuronal apoptosis and oxidative stress. The results of RT-PCR and western blot indicated that HT could induce CIRP over-expression in neurons and reverse the down-regulation of CIRP induced by OGD/R. In addition, over-expression of CIRP could reduce the release of ROS induced by OGD/R through reducing MDA levels and increasing the level of SOD and GSH, and alleviated OGD/R-induced neuronal apoptosis by down-regulating Caspase-3 expression and up-regulating Bcl-2 expression. Furthermore, CIRP silencing enhanced neuronal OGD/R-induced apoptosis and oxidative stress. Meanwhile, neuron ultrastructure was visualized by transmission electron microscope (TEM). As expected, neurons were seriously damaged and mitochondrial membrane ruptured after OGD/R injury, which were attenuated by CIRP over-expression or HT. Taken together, our results showed that CIRP resisted OGD/R-induced neuronal injury by exhibiting anti-apoptotic and anti-oxidative properties. To sum up, targeting CIRP offers potential therapeutic implications in the treatment of brain I/R injury.

<b><i>Objective:</i></b> The aim of the study was to determine if migraine is associated with fetal-type posterior cerebral artery (PCA) in patients with ischemic stroke. <b><i>Method:</i></b> In this cross-sectional study, patients with acute ischemic stroke were enrolled from two hospitals. The history of migraine headache was evaluated during a face-to-face interview. The variants of fetal-type PCA were assessed with MRA, CTA, or DSA. Patients with and without migraine were compared in terms of fetal-type PCA status and other clinic characteristics. Multivariate logistic regression analyses were performed to adjust for confounders and provide risk estimates for observed associations. <b><i>Result:</i></b> In 750 patients qualified for analysis, 85 (11.3%) were determined with migraine. Patients with migraine had a higher proportion of female gender (51.8% vs. 31.0%, <i>p</i> &#x3c; 0.001), hypertension (72.9% vs. 57.7%, <i>p</i> = 0.007), and fetal-type PCA (36.5% vs. 20.1%, <i>p</i> = 0.001), while lower proportion of current smoking (25.9% vs. 38.3%, <i>p</i> = 0.025) than patients without migraine. National Institutes of Health Stroke Scale (NIHSS) score (3 vs. 2, <i>p</i> = 0.016) was also higher in migraineurs than in non-migraineurs. After adjustment for confounders, fetal-type PCA status was independently associated with migraine (odds ratio [OR] = 2.06; 95% confidence interval [CI], 1.25–3.38; <i>p</i> = 0.005). Other factors associated to migraine included female gender (OR = 2.03; 95% CI, 1.13–3.62; <i>p</i> = 0.017), hypertension (OR = 1.97; 95% CI, 1.17–3.34; <i>p</i> = 0.011), and NIHSS score (OR = 1.08; 95% CI, 1.01–1.16; <i>p</i> = 0.018). <b><i>Conclusion:</i></b> Migraine was associated with fetal-type PCA in patients with ischemic stroke. This finding supported the hypothesis that vascular mechanisms get involved in the migraine-stroke association.