Sea otter, Enhydra lutris, containment management: field studies and feasibility assessment

Limiting sea otter geographic distribution in California (containment management) has long been recognized as being necessary to preserve human recreational and commercial uses of shellfish resources. However, passage of federal legislation that focused preferentially on marine mammal protection and the 1977 listing of the California sea otter population as "threatened" effectively precluded any range-limiting management program. Research, however, that evaluated various non-lethal means of influencing sea otter movements and distribution was encouraged. Our research suggests that herding and acoustical devices may not have any real potential use in this context. Based on research-related capture success rates, capture and relocation techniques may be useful in influencing sea otter geographical distribution. The translocation of sea otters to San Nicolas Island provided the first opportunity to test the technical feasibility of maintaining a large area free of sea otters. Capture success rates were appreciably poorer than those achieved during research-related efforts. We identify several logistical and behavioral influences that contributed to the relatively poor success rate. Based on this evaluation, we discuss the factors likely to limit application of these techniques in the future. We feel that capture techniques can be useful in a long-term management program, if used in conjunction with efforts to limit the sea otter population growth rate. Consequently, we feel future research should focus on assessing individual health effects from using chemical contraceptives and assessing the feasibility of their use to safely control population growth. (12pp.

Sea Otter, Enhydra lutris, mortalities in California, 1968 through 1993

Sea otter, Enhydra lutris, mortality in California and the relative contribution from specific causes was assessed for the 26 years from 1968 through 1993. There were 2,082 dead sea otters recorded from Tomales Bay (Marin County) south to Bluff Cove (Los Angeles County) during that period. The average number of carcasses recorded was 80 per year and seven per month. Sex was identified in 87% (n=1,819) of the cases and was composed of 47% female and 53% male. A relative age was assigned to 97% (n=2,017) of the cases and was composed of 28% pup, 18% subadult and 54% adult. Specific causes of death were determined for 26% (n=55 1) of the cases. The majority of these (n=381) were considered to be due to natural causes and included the following specific causes: shark bitten (n=78), probably shark bitten (n=106), other natural causes (n=140), and mating wounds (n=57). The remaining (n=170) were considered to be due to human-related causes and included the following specific causes: shot (n=72), probably shot (n=8), net drowned (n=76), and other human causes (n=14). The large proportion of carcasses without an identified specific cause of death prompted a more detailed necropsy effort in 1992 and 1993. During that period, 78 of the 232 recovered carcasses were examined by veterinary pathologists and a specific cause of death was determined in 76% (n=59) of the cases. This effort identified a wide range of specific causes of death that otherwise may have been categorized as "unknown without trauma". Considering the variety of diseases diagnosed in this expanded necropsy program, it would be prudent to continue this level of examination to refine our knowledge of sea otter pathology. (48pp.

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 hospitalization2–4 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

Towards a cross-cultural assessment of binge-watching: Psychometric evaluation of the “watching TV series motives” and “binge-watching engagement and symptoms” questionnaires across nine languages

In view of the growing interest regarding binge-watching (i.e., watching multiple episodes of television (TV) series in a single sitting) research, two measures were developed and validated to assess binge-watching involvement (“Binge-Watching Engagement and Symptoms Questionnaire”, BWESQ) and related motivations (“Watching TV Series Motives Questionnaire”, WTSMQ). To promote international and cross-cultural binge-watching research, the present article reports on the validation of these questionnaires in nine languages (English, French, Spanish, Italian, German, Hungarian, Persian, Arabic, Chinese). Both questionnaires were disseminated, together with additional self-report measures of happiness, psychopathological symptoms, impulsivity and problematic internet use among TV series viewers from a college/university student population (N = 12,616) in 17 countries. Confirmatory factor, measurement invariance and correlational analyses were conducted to establish structural and construct validity. The two questionnaires had good psychometric properties and fit in each language. Equivalence across languages and gender was supported, while construct validity was evidenced by similar patterns of associations with complementary measures of happiness, psychopathological symptoms, impulsivity and problematic internet use. The results support the psychometric validity and utility of the BWESQ and WTSMQ for conducting cross-cultural research on binge-watching

A new polymorph of dicesium tetracyanoplatinate monohydrate with unusual platinum stacking

We wish to report the discovery of a new and unexpected polymorph of dicesium tetracyanoplatinate. Short, linear chains of five platinum atoms (platinum “needles”) appear in a zigzag arrangement, interspersed by isolated tetracyanoplatinate ions

Preclinical deposition of pathological prion protein PrP(Sc) in muscles of hamsters orally exposed to scrapie

Recently, pathological prion protein PrP(Sc), the putative key constituent of infectious agents causing transmissible spongiform encephalopathies (TSEs), was found in muscles of rodents experimentally infected with scrapie and in patients with Creutzfeldt-Jakob disease (CJD). For the assessment of risk scenarios originating from these findings (e.g., alimentary transmission of pathogens associated with bovine spongiform encephalopathy [BSE] and chronic wasting disease [CWD] via tainted beef and game or iatrogenic dissemination of CJD agent through contaminated surgical instruments) more detailed information about the time course of PrP(Sc) accumulation in muscles at preclinical and clinical stages of incubation is needed. Here we show that PrP(Sc) in muscles of hamsters fed with scrapie can be detected prior to the onset of clinical symptoms, but that the bulk of PrP(Sc) was deposited late in clinical disease. Additionally, regarding the question of how muscles become invaded, we report on the intramuscular location of PrP(Sc) and substantial indications for centrifugal spread of infection from spinal motor neurons to myofibers. Our findings in a well-established animal model for TSEs contribute to a better assessment of the risks for public health emanating from “Prions in skeletal muscle” and provide new insights into the pathophysiological spread of TSE agents through the body

Differential inhibition of macrophage foam-cell formation and atherosclerosis in mice by PPARα, β/δ, and γ

PPARα, β/δ, and γ regulate genes involved in the control of lipid metabolism and inflammation and are expressed in all major cell types of atherosclerotic lesions. In vitro studies have suggested that PPARs exert antiatherogenic effects by inhibiting the expression of proinflammatory genes and enhancing cholesterol efflux via activation of the liver X receptor–ABCA1 (LXR-ABCA1) pathway. To investigate the potential importance of these activities in vivo, we performed a systematic analysis of the effects of PPARα, β, and γ agonists on foam-cell formation and atherosclerosis in male LDL receptor–deficient (LDLR(–/–)) mice. Like the PPARγ agonist, a PPARα-specific agonist strongly inhibited atherosclerosis, whereas a PPARβ-specific agonist failed to inhibit lesion formation. In concert with their effects on atherosclerosis, PPARα and PPARγ agonists, but not the PPARβ agonist, inhibited the formation of macrophage foam cells in the peritoneal cavity. Unexpectedly, PPARα and PPARγ agonists inhibited foam-cell formation in vivo through distinct ABCA1-independent pathways. While inhibition of foam-cell formation by PPARα required LXRs, activation of PPARγ reduced cholesterol esterification, induced expression of ABCG1, and stimulated HDL-dependent cholesterol efflux in an LXR-independent manner. In concert, these findings reveal receptor-specific mechanisms by which PPARs influence macrophage cholesterol homeostasis. In the future, these mechanisms may be exploited pharmacologically to inhibit the development of atherosclerosis