Background: Cancer patients are regarded as a highly vulnerable group in the current Coronavirus Disease 2019 (COVID-19) pandemic. To date, the clinical characteristics of COVID-19-infected cancer patients remain largely unknown. Patients and methods: In this retrospective cohort study, we included cancer patients with laboratory-confirmed COVID-19 from three designated hospitals in Wuhan, China. Clinical data were collected from medical records from 13 January 2020 to 26 February 2020. Univariate and multivariate analyses were carried out to assess the risk factors associated with severe events defined as a condition requiring admission to an intensive care unit, the use of mechanical ventilation, or death. Results: A total of 28 COVID-19-infected cancer patients were included; 17 (60.7%) patients were male. Median (interquartile range) age was 65.0 (56.0e70.0) years. Lung cancer was the most frequent cancer type (n ¼ 7; 25.0%). Eight (28.6%) patients were suspected to have hospital-associated transmission. The following clinical features were shown in our cohort: fever (n ¼ 23, 82.1%), dry cough (n ¼ 22, 81%), and dyspnoea (n ¼ 14, 50.0%), along with lymphopaenia (n ¼ 23, 82.1%), high level of high-sensitivity C-reactive protein (n ¼ 23, 82.1%), anaemia (n ¼ 21, 75.0%), and hypoproteinaemia (n ¼ 25, 89.3%). The common chest computed tomography (CT) findings were ground-glass opacity (n ¼ 21, 75.0%) and patchy consolidation (n ¼ 13, 46.3%). A total of 15 (53.6%) patients had severe events and the mortality rate was 28.6%. If the last antitumour treatment was within 14 days, it significantly increased the risk of developing severe events [hazard ratio (HR) ¼ 4.079, 95% confidence interval (CI) 1.086e15.322, P ¼ 0.037]. Furthermore, patchy consolidation on CT on admission was associated with a higher risk of developing severe events (HR ¼ 5.438, 95% CI 1.498e19.748, P ¼ 0.010). Conclusions: Cancer patients show deteriorating conditions and poor outcomes from the COVID-19 infection. It is recommended that cancer patients receiving antitumour treatments should have vigorous screening for COVID-19 infection and should avoid treatments causing immunosuppression or have their dosages decreased in case of COVID-19 coinfection.

Enhanced degradation of damaged components of NP cells by autophagy may be a crucial survival response against mechanical overload, and extensive autophagy may trigger autophagic cell death. Regulating autophagy and reducing the generation of intracellular ROS may retard IVD degeneration.

Using a 3D multispecies magnetohydrodynamic model, we investigated the effect of the solar wind dynamic pressure (Pd) with different densities and velocities on the subsolar standoff distance (r0) of the Martian magnetic pileup boundary (MPB). We fixed the solar maximum condition, the strongest crustal field located in the dayside region, and the Parker spiral interplanetary magnetic field at Mars. We simulated 35 cases with a Pd range of 0.1494 to 7.323 nPa (solar wind number density n ∈ [1, 9] cm−3, and solar wind velocity V ∈ [−258, −1344] km s−1). The main results are as follows. (1) r0 decreases with increasing Pd according to the power-law relations. For the same Pd, a higher solar wind velocity (lower density) results in a larger r0 of the Martian MPB. (2) A higher solar wind density leads to a lower ratio of the compressed magnetic field strength to the crustal field strength and a larger plasma β under the same Pd. This indicates that the thermal pressure at the Martian MPB plays a significant role for the compressed magnetic field. Because the magnetic pileup process is stronger for a higher solar wind velocity, the magnetic pressure at the Martian MPB is increased. As a result, the thermal pressure decreases and r0 of the Martian MPB increases. (3) We present a new formula of r0 with the parameters of the solar wind dynamic pressure, number density, and velocity.