Novasignal’s Lucid robotic system reveals insights into COVID-19
Novasignal Corp. (formerly Neural Analytics), of Los Angeles, reported that data published Aug. 6, 2020, in the American Journal of Respiratory and Critical Care Medicine used the company’s noninvasive Lucid robotic system to remotely assess and monitor patients with COVID-19. Critical care teams at Mount Sinai Health System used the company’s autonomous robotic ultrasound to monitor cerebral blood flow of 18 mechanically ventilated patients with COVID-19 and revealed insights into the pathophysiology of the virus. The study included 18 mechanically ventilated patients with severe COVID-19 pneumonia, low lung compliance and clinical markers of hypoxemia. While monitoring these critically ill patients with the Lucid robotic system, physicians discovered an overabundance of pulmonary shunting, a physical dysfunction whereby deoxygenated blood bypasses the normal circulatory system resulting in lower levels of oxygen in the blood and contributing to respiratory distress in patients with COVID-19. The researchers found that 83% of patients had detectable microbubbles signaling vascular shunting. The study reports that the quantity of bubbles corresponds to the level of hypoxemia and lung function in patients with COVID-19. The shunting is likely due to pulmonary dilatation leading to hypoxemia. follow-up study is currently being conducted to generate additional findings on the pathophysiology of COVID-19.
Sensing eye mask developed to improve data capture in neuro studies
University of Massachusetts Amherst scientists are working on a lightweight eye mask that can unobtrusively capture pulse, eye movement and sleep signals, for example, when worn in an everyday environment. Named Chesma, the smart eye mask is fitted with two kinds of fabric electrodes that can simply be sewn onto a variety of pre-made garments and further miniaturized, if desired. This capability allows them to integrate electrodes into a lightweight foam mask for recording electro-oculography and cardiac signals. Their design automatically positions the electrodes on the face with no need for custom fitting. The mask also contains one fabric pressure sensor positioned over an artery to monitor pulse as a proxy for cardiac function, with the whole linked to two microcontrollers with water-repellant silver threads as connectors. The combination of electrode network with the pressure sensor will enable studies for investigating sleep quality, sleep disorders, mental health, neurodegenerative diseases and more. The researchers published their work Aug. 20, 2020, in Matter.
Multiple sclerosis’ early days
By looking at the immune signatures of monozygotic twins where one twin had multiple sclerosis (MS) and the other did not, researchers at the University Clinic Muenster have been able to gain new insights into how the disease starts. As with many neurological diseases, cell damage in MS starts long before clinical symptoms are apparent. As a result, how MS begins is still unclear. In their work, the authors compared the immune systems of individuals with MS to their apparently healthy siblings. Immune system signatures overall were “remarkably” similar, but by focusing on a group of healthy siblings with subtle signs of neuroinflammation but no overt MS, the authors were able to identify differences in memory T cells between sibling pairs. The authors argued that “insight into the immunological mechanisms associated with the initiation of the disease is relevant not only to the therapy but also for prevention of the disease.” They published their paper in the Aug. 17, 2020, online issue of the Proceedings of the National Academy of Sciences.
How antidepressants inhibit fibrosis
Researchers at the University of California at San Francisco have identified the mechanism by which tricyclic antidepressants (TCAs) can inhibit fibrosis. Fibrosis, the formation of excessive scar tissue after injury, ultimately leads to organ failure. Its origins are poorly understood, but the UCSF team had previously demonstrated that liver fibrosis was driven by hepatic stellate cells, and that TCAs inhibited fibrosis by inhibiting the enzyme acid ceramidase (aCDase), which catalyzes the formation of ceramide. In followup work now published in the Aug. 19, 2020, issue of Science Translational Medicine, the team linked this effect to inhibition of the transcriptional co-activators YAP/TAZ, which had also been shown to reduce fibrosis previously. YAP/TAZ proteasomal degradation could be achieved by inhibiting aCDase. The team also showed that “a signature of the genes most down-regulated by ceramide identifies patients with advanced fibrosis who could benefit from aCDase targeting. The findings implicate ceramide as a critical regulator of YAP/TAZ signaling and HSC activation and highlight aCDase as a therapeutic target for the treatment of fibrosis,” they wrote.