Background: The World Health Organization (WHO) declared coronavirus disease-19 (COVID-19) as a pandemic on March 11, 2020. The impact of COVID-19 on urological services in different geographical areas is unknown. Objective: To investigate the global impact of COVID-19 on urological providers and the provision of urological patient care. Design, setting, and participants: A cross-sectional, web-based survey was conducted from March 30, 2020 to April 7, 2020. A 55-item questionnaire was developed to investigate the impact of COVID-19 on various aspects of urological services. Target respondents were practising urologists, urology trainees, and urology nurses/advanced practice providers. Outcome measurements and statistical analysis: The primary outcome was the degree of reduction in urological services, which was further stratified by the geographical location, degree of outbreak, and nature and urgency of urological conditions. The secondary outcome was the duration of delay in urological services. Results and limitations: A total of 1004 participants responded to our survey, and they were mostly based in Asia,

Reactions of both astrocytes and microglia to central nervous system injury can be beneficial or detrimental to recovery. To gain insights into the functional importance of gliosis, we developed a new model of adolescent closed-head injury (CHI) and interrogated the behavioral, physiological, and cellular outcomes after a concussive CHI in leukemia inhibitory factor (LIF) haplodeficient mice. These mice were chosen because LIF is important for astrocyte and microglial activation. Behaviorally, the LIF haplodeficient animals were equally impaired 4 h after the injury, but in the subsequent 2 weeks, the LIF haplodeficient mice acquired more severe motor and sensory deficits, compared with wild type mice. The prolonged accumulation of neurological impairment was accompanied by desynchronization of the gliotic response, increased cell death, axonal degeneration, diminished callosal compound action potential, and hypomyelination. Our results clearly show that LIF is an essential injury-induced cytokine that is required to prevent the propagation of secondary neurodegeneration.

No abstract

No abstract

No abstract