Objective. Glaucoma is a leading cause of severe visual impairment and blindness. Although high intraocular pressure (IOP) is an established risk factor for the disease, the role of abnormal ocular vessel function in the pathophysiology of glaucoma gains more and more attention. We tested the hypothesis that elevated intraocular pressure (IOP) causes vascular dysfunction in the retina. Methods. High IOP was induced in one group of mice by unilateral cauterization of three episcleral veins. The other group received sham surgery only. Two weeks later, retinal vascular preparations were studied by video microscopy in vitro. Reactive oxygen species (ROS) levels and expression of hypoxia markers and of prooxidant and antioxidant redox genes as well as of inflammatory cytokines were determined. Results. Strikingly, responses of retinal arterioles to stepwise elevation of perfusion pressure were impaired in the high-IOP group. Moreover, vasodilation responses to the endothelium-dependent vasodilator, acetylcholine, were markedly reduced in mice with elevated IOP, while no differences were seen in response to the endothelium-independent nitric oxide donor, sodium nitroprusside. Remarkably, ROS levels were increased in the retinal ganglion cell layer including blood vessels. Expression of the NADPH oxidase isoform, NOX2, and of the inflammatory cytokine, TNF-α, was increased at the mRNA level in retinal explants. Expression of NOX2, but not of the hypoxic markers, HIF-1α and VEGF-A, was increased in the retinal ganglion cell layer and in retinal blood vessels at the protein level. Conclusion. Our data provide first-time evidence that IOP elevation impairs autoregulation and induces endothelial dysfunction in mouse retinal arterioles. Oxidative stress and inflammation, but not hypoxia, appear to be involved in this process.

Objective: Coronavirus disease 2019 (COVID-19) has high morbidity and mortality, and spreads rapidly in the community to result in a large number of infection cases. This study aimed to compare clinical features in adult patients with coronavirus disease 2019 (COVID-19) pneumonia to those in adult patients with community-acquired pneumonia (CAP). Methods: Clinical presentations, laboratory findings, imaging features, complications, treatment and outcomes were compared between patients with COVID-19 pneumonia and patients with CAP. The study group of patients with COVID-19 pneumonia consisted of 120 patients. One hundred and thirtyfour patients with CAP were enrolled for comparison. Results: Patients with COVID-19 pneumonia had lower levels of abnormal laboratory parameters (white blood cell count, lymphocyte count, procalcitonin level, erythrocyte sedimentation rate and Creactive protein level) and more extensive radiographic involvement. More severe respiratory compromise resulted in a higher rate of intensive care unit admission, acute respiratory distress syndrome (ARDS) and mechanical ventilation (36% vs 15%, 34% vs 15% and 32% vs 12%, respectively; all p < .05). The 30 day mortality was more than twice as high in patients with COVID-19 pneumonia (12% versus 5%; p ¼ .063), despite not reaching a statistically significant difference. Conclusions: Lower levels of abnormal laboratory parameters, more extensive radiographic involvement, more severe respiratory compromise, and higher rates of ICU admission, ARDS and mechanical ventilation are key characteristics that distinguish patients with COVID-19-associated pneumonia from patients with CAP.

The paradigmatic example of a topological phase of matter, the two-dimensional (2D) Chern insulator 1-5 , is characterized by a topological invariant consisting of a single integer, the scalar Chern number. Extending the Chern insulator phase from 2D to three dimensions (3D) requires the generalization of the Chern number to a 3-vector 6-7 , similar to the 3D quantum Hall effect 8-13 . Such Chern vectors for 3D Chern insulators have never been explored experimentally. Here, we use magnetically tunable 3D photonic crystals to achieve the experimental demonstration of Chern vectors and their topological surface states. We demonstrate Chern vector magnitudes of up to six, higher than all previously realized scalar 2 / 31

Background Detailed descriptions of the patterns of disease progression of deceased coronavirus disease 2019 (COVID‐19) patients have not been well explored. Objectives This study sought to explore disease progression patterns and risk factors associated with mortality of deceased patients with COVID‐19. Materials and Methods Epidemiological, clinical, laboratory, and imaging data (from 15 January to 26 March 2020) of laboratory‐confirmed COVID‐19 patients were collected retrospectively from two hospitals, Hubei province, China. Disease progression patterns of patients were analyzed based on laboratory data, radiological findings, and Sequential Organ Failure Assessment (SOFA) score. Risk factors associated with death were analyzed. Results A total of 792 patients were enrolled in this study, of whom 68 died and 724 survived. Complications during hospitalization, such as sepsis, severe acute respiratory distress syndrome, acute cardiac injury, and acute kidney injury, were markedly more frequent in deceased patients than in surviving patients. Deceased patients presented progressive deterioration pattern in laboratory variables, chest computed tomography evaluation, and SOFA score, while surviving patients presented initial deterioration to peak level involvement followed by improvement pattern over time. Days 10 to 14 after illness onset was a critical stage of disease course. Older age, number of preexisting comorbidities ≥2, and SOFA score were independently associated with death for COVID‐19. Conclusions Multiorgan dysfunction was common in deceased COVID‐19 patients. Deceased patients presented progressive deterioration pattern, while surviving patients presented a relatively stable pattern during disease progression. Older age, number of preexisting comorbidities ≥2, and SOFA score were independent risk factors for death for COVID‐19.