This study shows that visceral obesity increases the likelihood of a poor prognosis in CRC patients receiving adjuvant chemotherapy thus underlying the value of lifestyle interventions to minimize visceral obesity in this patient cohort.

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Background Analyses of blood biomarkers involved in the host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral infection can reveal distinct biological pathways and inform development and testing of therapeutics for COVID-19. Our objective was to evaluate host endothelial, epithelial and inflammatory biomarkers in COVID-19. Methods We prospectively enrolled 171 ICU patients, including 78 (46%) patients positive and 93 (54%) negative for SARS-CoV-2 infection from April to September, 2020. We compared 22 plasma biomarkers in blood collected within 24 h and 3 days after ICU admission. Results In critically ill COVID-19 and non-COVID-19 patients, the most common ICU admission diagnoses were respiratory failure or pneumonia, followed by sepsis and other diagnoses. Similar proportions of patients in both groups received invasive mechanical ventilation at the time of study enrollment. COVID-19 and non-COVID-19 patients had similar rates of acute respiratory distress syndrome, severe acute kidney injury, and in-hospital mortality. While concentrations of interleukin 6 and 8 were not different between groups, markers of epithelial cell injury (soluble receptor for advanced glycation end products, sRAGE) and acute phase proteins (serum amyloid A, SAA) were significantly higher in COVID-19 compared to non-COVID-19, adjusting for demographics and APACHE III scores. In contrast, angiopoietin 2:1 (Ang-2:1 ratio) and soluble tumor necrosis factor receptor 1 (sTNFR-1), markers of endothelial dysfunction and inflammation, were significantly lower in COVID-19 (p < 0.002). Ang-2:1 ratio and SAA were associated with mortality only in non-COVID-19 patients. Conclusions These studies demonstrate that, unlike other well-studied causes of critical illness, endothelial dysfunction may not be characteristic of severe COVID-19 early after ICU admission. Pathways resulting in elaboration of acute phase proteins and inducing epithelial cell injury may be promising targets for therapeutics in COVID-19.

Lung disaturated phosphatidylcholine (DSPC) turnover was investigated in normal C57 black and mutant beige mice; the latter have been postulated to have microtubular defects. Turnover experiments were performed on 117 black and 74 beige mice that were assayed for lamellar body-rich fraction (LB) and alveolar lavage fluid (AF) DSPC from 0.5 to 100 h after injection of [3H]glycerol. The data were analyzed by a program that derived the best-fit rate constants for an operator-chosen compartmental model. For black mice, a simple model with bidirectional exchange of DSPC between LB and AF compartments fitted the data almost as well as more complex models. This model yielded a turnover time of 5.9 h, a biological half-life of 16 h, and recycling of AF DSPC into LB of 47%. There was some evidence to suggest that DSPC might be degraded rather than recycled as a unit. For beige mice, the DSPC turnover time was 4.8 h, and its biological half-life was 40 h. The AF DSPC pool was smaller than in black mice, but the LB pool was larger. The bidirectional flux of DSPC between AF and LB was much greater than in black mice, the percent of recycling being 85. These data do not support a microtubular defect in beige mice, but the calculations for beige mice are based on a model of questionable validity.