A report on the sea otter, Enhydra lutris L., in California

This report discusses in detail findings and observations of 5 years of research on the sea otter population and its relationship to the nearshore marine environment in California. Initial efforts were directed at providing some relief to the commercial abalone fishery in the Cambria - Point Estero area north of Morro Bay. This fishery has subsequently collapsed along with other commercial and sport abalone and sport crab fisheries throughout the sea otter's range due to continued sea otter foraging. Capturing, tagging and translocation studies, censusing studies, examination of sea otter remains, habitat surveys, food habits observations and studies on otters in captivity provide a broad base of information on the expanding sea otter population in California and its effects on resources utilized by man. Recommendations for sea otter management consistent with esthetic, recreational, and commercial uses of marine resources are included in this report. (95pp.

A review of California sea otter, Enhydra lutris, surveys

Recent surveys (1977 to 1983) of the sea otter, Enhydra lutris, in California were summarized and compared to past surveys, to evaluate the adequacy of current survey design and to-make inferences about current population status. Ground counts within selected index areas provided the best indicator of population trends. These data suggest a rather remarkable stability in the long-term occupied range. Rangewide aerial surveys with ground truth stations provided the best available data for estimating total population size. The most recent (1979) survey yielded a population estimate of approximately 1500 sea otters. Comparisons with past surveys suggest there have been no demonstrable changes in population size since at least 1976. (34pp.

A simulated translocation of sea otters, Enhydra lutris, with a review of capture, transport and holding techniques

A number of techniques and pieces of equipment judged necessary for the translocation of sea otters were field tested. Captures were accomplished with either a scuba diver operated capture device (Wilson trap), a surface set tangle net or a dip net. A portable floating pen proved very satisfactory for simultaneously holding at least ten otters for several days. Commercially available pet transport kennels, with the capability of holding water, were adequate for maintaining the otter's pelage in good condition during a transport of approximately five hours duration. Subsequent observations indicated no apparent stress related dispersal. (17pp.

An assessment of the accidental take of sea otters, Enhydra lutris, in gill and trammel nets

The sea otter, Enhydra 1utris, is fully protected in California by both state and federal law. Despite this protection the population has not grown appreciably since at least 1976. Research efforts directed at identifying the reasons for the lack of population growth have concentrated on sources of mortality and their contribution to total mortality. The accidental drowning of sea otters in gill and trammel nets used to take California halibut, Para1ichthys ca1ifornicus, was identified as a source of mortality which has probably increased as the sea otter population expanded into areas of intense fishing. As a result, an existing gill and trammel net fishery observation program in Monterey Bay was expanded to assess the extent and significance of the accidental drownings of sea otters in the areas near Morro Bay and Port San Luis. Three different estimates of the number of sea otters drowned annually in gill and trammel nets were generated using comparable data bases. The average of these estimates was approximately 80 sea otters per year for the level of fishing effort expended during the June 1982 through June 1984 study period. Back calculations of the annual take of sea otters by the gill and trammel net fishery for California halibut were made for each year from 1973 through 1983. These calculations suggest that the level of accidental take of sea otters during the last decade may have been high enough to be a significant factor in the lack of sea otter population growth. (31pp.

Post mortem studies of sea otters, Enhydra lutris L., in California

Dead sea otters found on or near beaches in central California from January 1968 through June 1974 were collected for study. Necropsies were conducted on many of these carcasses. Sea otter mortalities are related to: (1) area of recovery; (2) sex; (3) relative age; (4) general cause of death; and (5) sea surface roughness. Selected specific aspects of necropsies are summarized. Tables for estimating weight from total length and estimating total length from tail length and foot length are given. Organ weights are discussed. Criteria for establishing relative age based on degree of fusion of cranial sutures, eruption and wear of dentition, and development of the glenoid fossa are given. A method of estimating relative age of male otters is given based on baculum length or volume. Methods useful for sexing dissociated skeletal remains based on osteological differences in pelves are presented. (87pp.

Enteric bacterial pathogen detection in southern sea otters (Enhydra lutris nereis) is associated with coastal urbanization and freshwater runoff

Although protected for nearly a century, California’s sea otters have been slow to recover, in part due to exposure to fecally-associated protozoal pathogens like Toxoplasma gondii and Sarcocystis neurona. However, potential impacts from exposure to fecal bacteria have not been systematically explored. Using selective media, we examined feces from live and dead sea otters from California for specific enteric bacterial pathogens (Campylobacter, Salmonella, Clostridium perfringens, C. difficile and Escherichia coli O157:H7), and pathogens endemic to the marine environment (Vibrio cholerae, V. parahaemolyticus and Plesiomonas shigelloides). We evaluated statistical associations between detection of these pathogens in otter feces and demographic or environmental risk factors for otter exposure, and found that dead otters were more likely to test positive for C. perfringens, Campylobacter and V. parahaemolyticus than were live otters. Otters from more urbanized coastlines and areas with high freshwater runoff (near outflows of rivers or streams) were more likely to test positive for one or more of these bacterial pathogens. Other risk factors for bacterial detection in otters included male gender and fecal samples collected during the rainy season when surface runoff is maximal. Similar risk factors were reported in prior studies of pathogen exposure for California otters and their invertebrate prey, suggesting that land-sea transfer and/or facilitation of pathogen survival in degraded coastal marine habitat may be impacting sea otter recovery. Because otters and humans share many of the same foods, our findings may also have implications for human health

The Zinc Dyshomeostasis Hypothesis of Alzheimer's Disease

Alzheimer's disease (AD) is the most common form of dementia in the elderly. Hallmark AD neuropathology includes extracellular amyloid plaques composed largely of the amyloid-β protein (Aβ), intracellular neurofibrillary tangles (NFTs) composed of hyper-phosphorylated microtubule-associated protein tau (MAP-tau), and microtubule destabilization. Early-onset autosomal dominant AD genes are associated with excessive Aβ accumulation, however cognitive impairment best correlates with NFTs and disrupted microtubules. The mechanisms linking Aβ and NFT pathologies in AD are unknown. Here, we propose that sequestration of zinc by Aβ-amyloid deposits (Aβ oligomers and plaques) not only drives Aβ aggregation, but also disrupts zinc homeostasis in zinc-enriched brain regions important for memory and vulnerable to AD pathology, resulting in intra-neuronal zinc levels, which are either too low, or excessively high. To evaluate this hypothesis, we 1) used molecular modeling of zinc binding to the microtubule component protein tubulin, identifying specific, high-affinity zinc binding sites that influence side-to-side tubulin interaction, the sensitive link in microtubule polymerization and stability. We also 2) performed kinetic modeling showing zinc distribution in extra-neuronal Aβ deposits can reduce intra-neuronal zinc binding to microtubules, destabilizing microtubules. Finally, we 3) used metallomic imaging mass spectrometry (MIMS) to show anatomically-localized and age-dependent zinc dyshomeostasis in specific brain regions of Tg2576 transgenic, mice, a model for AD. We found excess zinc in brain regions associated with memory processing and NFT pathology. Overall, we present a theoretical framework and support for a new theory of AD linking extra-neuronal Aβ amyloid to intra-neuronal NFTs and cognitive dysfunction. The connection, we propose, is based on β-amyloid-induced alterations in zinc ion concentration inside neurons affecting stability of polymerized microtubules, their binding to MAP-tau, and molecular dynamics involved in cognition. Further, our theory supports novel AD therapeutic strategies targeting intra-neuronal zinc homeostasis and microtubule dynamics to prevent neurodegeneration and cognitive decline

The case for strategic international alliances to harness nutritional genomics for public and personal health

Nutrigenomics is the study of how constituents of the diet interact with genes, and their products, to alter phenotype and, conversely, how genes and their products metabolise these constituents into nutrients, antinutrients, and bioactive compounds. Results from molecular and genetic epidemiological studies indicate that dietary unbalance can alter gene-nutrient interactions in ways that increase the risk of developing chronic disease. The interplay of human genetic variation and environmental factors will make identifying causative genes and nutrients a formidable, but not intractable, challenge. We provide specific recommendations for how to best meet this challenge and discuss the need for new methodologies and the use of comprehensive analyses of nutrient-genotype interactions involving large and diverse populations. The objective of the present paper is to stimulate discourse and collaboration among nutrigenomic researchers and stakeholders, a process that will lead to an increase in global health and wellness by reducing health disparities in developed and developing countrie

The genetic architecture of the human cerebral cortex

The cerebral cortex underlies our complex cognitive capabilities, yet little is known about the specific genetic loci that influence human cortical structure. To identify genetic variants that affect cortical structure, we conducted a genome-wide association meta-analysis of brain magnetic resonance imaging data from 51,665 individuals. We analyzed the surface area and average thickness of the whole cortex and 34 regions with known functional specializations. We identified 199 significant loci and found significant enrichment for loci influencing total surface area within regulatory elements that are active during prenatal cortical development, supporting the radial unit hypothesis. Loci that affect regional surface area cluster near genes in Wnt signaling pathways, which influence progenitor expansion and areal identity. Variation in cortical structure is genetically correlated with cognitive function, Parkinson’s disease, insomnia, depression, neuroticism, and attention deficit hyperactivity disorder

Exploration of Shared Genetic Architecture Between Subcortical Brain Volumes and Anorexia Nervosa

In MRI scans of patients with anorexia nervosa (AN), reductions in brain volume are often apparent. However, it is unknown whether such brain abnormalities are influenced by genetic determinants that partially overlap with those underlying AN. Here, we used a battery of methods (LD score regression, genetic risk scores, sign test, SNP effect concordance analysis, and Mendelian randomization) to investigate the genetic covariation between subcortical brain volumes and risk for AN based on summary measures retrieved from genome-wide association studies of regional brain volumes (ENIGMA consortium, n = 13,170) and genetic risk for AN (PGC-ED consortium, n = 14,477). Genetic correlations ranged from − 0.10 to 0.23 (all p > 0.05). There were some signs of an inverse concordance between greater thalamus volume and risk for AN (permuted p = 0.009, 95% CI: [0.005, 0.017]). A genetic variant in the vicinity of ZW10, a gene involved in cell division, and neurotransmitter and immune system relevant genes, in particular DRD2, was significantly associated with AN only after conditioning on its association with caudate volume (pFDR = 0.025). Another genetic variant linked to LRRC4C, important in axonal and synaptic development, reached significance after conditioning on hippocampal volume (pFDR = 0.021). In this comprehensive set of analyses and based on the largest available sample sizes to date, there was weak evidence for associations between risk for AN and risk for abnormal subcortical brain volumes at a global level (that is, common variant genetic architecture), but suggestive evidence for effects of single genetic markers. Highly powered multimodal brain- and disorder-related genome-wide studies are needed to further dissect the shared genetic influences on brain structure and risk for AN