The jack mackerel (Trachurus symmetricus) resource of the eastern North Pacific

The jack mackerel before 1947, was of minor commercial importance having to take a back seat to the better known, more profitable, and more abundant Pacific sardine (Sardinops caeruleus) and the more desirable Pacific mackerel (Scomber japonicus). During these years it was referred to as "horse mackerel" and had relatively little market appeal. Much of the catch between 1926 and 1946 was absorbed by the fresh fish markets and consisted primarily of jack mackerel taken from mixed sardine and Pacific mackerel schools. Landings were low, varying between 183 and 15,573 short tons. During the 1947-48 season, the industry, after being hit hard by poor sardine landings, turned to the jack mackerel as a substitute sardine and landed approximately 71,000 short tons. Jack mackerel have been a major contributor to California's commercial landings ever since (Figure 1). In 1948, the U.S. Pure Food and Drug Administration authorized the use of the common name jack mackerel on all labeling. This name was expected to have more consumer appeal than the original official name "horse mackerel". The California Department of Fish and Game commenced routine length and age sampling of the commercial landings in 1947, the year the fishery first blossomed into being. Due to the apparent healthy condition of the resource and the need for emphasis on other fisheries these sample data have not been subjected to a complete analysis. We have recently completed the assignment of ages to the otoliths sampled and anticipate dedicating most of our effort in 1968 to writing a manuscript describing the fishery, its year-class composition and other factors affecting the yield. The literature on the jack mackerel is somewhat scanty with the greatest part of it pertaining to: (i) taxonomy; (ii) egg and larva distribution, and survival; (iii) yield per area from California waters; and (iv) reviews of the jack mackerel fishery in California and preliminary discussions of biological knowledge. Accordingly, for this paper, I have called upon past work and much unpublished data from our files, including station data from pre-season albacore cruises and the previously mentioned length and age data. (Document has 13 pages

Tocilizumab in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial

Background: In this study, we aimed to evaluate the effects of tocilizumab in adult patients admitted to hospital with COVID-19 with both hypoxia and systemic inflammation. Methods: This randomised, controlled, open-label, platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]), is assessing several possible treatments in patients hospitalised with COVID-19 in the UK. Those trial participants with hypoxia (oxygen saturation <92% on air or requiring oxygen therapy) and evidence of systemic inflammation (C-reactive protein ≥75 mg/L) were eligible for random assignment in a 1:1 ratio to usual standard of care alone versus usual standard of care plus tocilizumab at a dose of 400 mg–800 mg (depending on weight) given intravenously. A second dose could be given 12–24 h later if the patient's condition had not improved. The primary outcome was 28-day mortality, assessed in the intention-to-treat population. The trial is registered with ISRCTN (50189673) and ClinicalTrials.gov (NCT04381936). Findings: Between April 23, 2020, and Jan 24, 2021, 4116 adults of 21 550 patients enrolled into the RECOVERY trial were included in the assessment of tocilizumab, including 3385 (82%) patients receiving systemic corticosteroids. Overall, 621 (31%) of the 2022 patients allocated tocilizumab and 729 (35%) of the 2094 patients allocated to usual care died within 28 days (rate ratio 0·85; 95% CI 0·76–0·94; p=0·0028). Consistent results were seen in all prespecified subgroups of patients, including those receiving systemic corticosteroids. Patients allocated to tocilizumab were more likely to be discharged from hospital within 28 days (57% vs 50%; rate ratio 1·22; 1·12–1·33; p<0·0001). Among those not receiving invasive mechanical ventilation at baseline, patients allocated tocilizumab were less likely to reach the composite endpoint of invasive mechanical ventilation or death (35% vs 42%; risk ratio 0·84; 95% CI 0·77–0·92; p<0·0001). Interpretation: In hospitalised COVID-19 patients with hypoxia and systemic inflammation, tocilizumab improved survival and other clinical outcomes. These benefits were seen regardless of the amount of respiratory support and were additional to the benefits of systemic corticosteroids. Funding: UK Research and Innovation (Medical Research Council) and National Institute of Health Research

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease