11 research outputs found
Mountain lions prey selectively on prion-infected mule deer
The possibility that predators choose prey selectively based on age or condition has been suggested but rarely tested. We examined whether mountain lions (Puma concolor) selectively prey upon mule deer (Odocoileus hemionus) infected with chronic wasting disease, a prion disease. We located kill sites of mountain lions in the northern Front Range of Colorado, USA, and compared disease prevalence among lion-killed adult (â„2 years old) deer with prevalence among sympatric deer taken by hunters in the vicinity of kill sites. Hunter-killed female deer were less likely to be infected than males (odds ratios (OR) = 0.2, 95% confidence intervals (CI) = 0.1â0.6; p = 0.015). However, both female (OR = 8.5, 95% CI = 2.3â30.9) and male deer (OR = 3.2, 95% CI = 1â10) killed by a mountain lion were more likely to be infected than same-sex deer killed in the vicinity by a hunter (p < 0.001), suggesting that mountain lions in this area actively selected prion-infected individuals when targeting adult mule deer as prey items
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WildSense: Monitoring Interactions among Wild Deer in Harsh Outdoor Environments Using a Delay-Tolerant WSN
Biologists and ecologists often monitor the spread of disease among deer in the wild by using tracking systems that record their movement patterns, locations, and interaction behavior. The existing commercial systems for monitoring wild deer utilize collars with GPS sensors, deployed on captured and rereleased deer. The GPS sensors record location data every few hours, enabling researchers to approximate the interaction behavior of tracked deer with their GPS locations. However, the coarse granularity of periodically recorded GPS location data provides only limited precision for determining deer interaction behavior. We have designed a novel system to monitor wild deer interaction behavior more precisely in harsh wilderness environments. Our system combines the functionalities of both GPS and RF-radio sensors with low-cost and minimal-resource motes. We designed and built our system to be able to operate robustly for a period of up to several months for continual tracking and monitoring of the locations and interaction behaviors of wild deer in harsh environments. We successfully deployed six deer collars on six wild deer that were captured and rereleased in the Soapstone Prairie Natural Area of northern Colorado over a one-month period. In this paper, we describe how we designed and built this system and evaluate its successful operation in a wilderness area
Wild Felids as Hosts for Human Plague, Western United States
Plague seroprevalence was estimated in populations of pumas and bobcats in the western United States. High levels of exposure in plague-endemic regions indicate the need to consider the ecology and pathobiology of plague in nondomestic felid hosts to better understand the role of these species in disease persistence and transmission
Meta-analysis of SHANK Mutations in Autism Spectrum Disorders: A Gradient of Severity in Cognitive Impairments.
International audienceSHANK genes code for scaffold proteins located at the post-synaptic density of glutamatergic synapses. In neurons, SHANK2 and SHANK3 have a positive effect on the induction and maturation of dendritic spines, whereas SHANK1 induces the enlargement of spine heads. Mutations in SHANK genes have been associated with autism spectrum disorders (ASD), but their prevalence and clinical relevance remain to be determined. Here, we performed a new screen and a meta-analysis of SHANK copy-number and coding-sequence variants in ASD. Copy-number variants were analyzed in 5,657 patients and 19,163 controls, coding-sequence variants were ascertained in 760 to 2,147 patients and 492 to 1,090 controls (depending on the gene), and, individuals carrying de novo or truncating SHANK mutations underwent an extensive clinical investigation. Copy-number variants and truncating mutations in SHANK genes were present in âŒ1% of patients with ASD: mutations in SHANK1 were rare (0.04%) and present in males with normal IQ and autism; mutations in SHANK2 were present in 0.17% of patients with ASD and mild intellectual disability; mutations in SHANK3 were present in 0.69% of patients with ASD and up to 2.12% of the cases with moderate to profound intellectual disability. In summary, mutations of the SHANK genes were detected in the whole spectrum of autism with a gradient of severity in cognitive impairment. Given the rare frequency of SHANK1 and SHANK2 deleterious mutations, the clinical relevance of these genes remains to be ascertained. In contrast, the frequency and the penetrance of SHANK3 mutations in individuals with ASD and intellectual disability-more than 1 in 50-warrant its consideration for mutation screening in clinical practice
Mountain lions prey selectively on mule deer infected with chronic wasting disease
The possibility that predators choose prey selectively based on age or condition has been suggested but rarely tested. We examined whether mountain lions (Puma concolor) selectively prey upon mule deer (Odocoileus hemionus) infected with chronic wasting disease, a prion disease. We located kill sites of mountain lions in the northern Front Range of Colorado, USA, and compared disease prevalence among lion-killed adult (2 years old) deer with prevalence among sympatric deer taken by hunters in the vicinity of kill sites. Hunter-killed female deer were less likely to be infected than males (odds ratios (OR) 5 0.2, 95% confidence intervals (CI) 5 0.1 â0.6; p 5 0.015). However, both female (OR 5 8.5, 95% CI 5 2.3 â30.9) and male deer (OR 5 3.2, 95% CI 5 1 â10) killed by a mountain lion were more likely to be infected than samesex deer killed in the vicinity by a hunter (p \u3c 0.001), suggesting that mountain lions in this area actively selected prion-infected individuals when targeting adult mule deer as prey items
EXT418, a novel longâacting ghrelin, mitigates Lewis lung carcinoma induced cachexia in mice
Abstract Background Ghrelin is a potential therapy for cachexia due to its orexigenic properties and anabolic effects on muscle and fat. However, its clinical use is limited by the short halfâlife of active (acylated) ghrelin (~11 min in humans). EXT418 is a novel longâacting, constitutively active ghrelin analog created by covalently linking it to a vitamin D derivative. Here, we evaluated the effects and mechanisms of action of EXT418 on Lewis lung carcinoma (LLC)âinduced cachexia in mice. Methods Male C57BL/6J mice (5â to 7âmonthâold) were implanted with 1 Ă 106 heatâkilled (HK) or live LLC cells. When the tumour was palpable, mice were injected with vehicle (T + V) or EXT418 daily (T + 418 Daily, 0.25 mg/kg/day) or every other day (T + 418 EOD, 0.5 mg/kg/EOD) for up to 14 days, whereas HKâtreated mice were given vehicle (HK + V). Subsets of T + 418 Daily or EODâtreated mice were pairâfed to the T + V group. Body composition and grip strength were evaluated before tumour implantation and at the end of the experiment. Molecular markers were probed in muscles upon termination. Results In tumourâbearing mice, administration of EXT418 daily or EOD partially prevented weight loss (T + V vs. T + 418 Daily, P = 0.030; and vs. T + 418 EOD, P = 0.020). Similar effects were observed in whole body fat and lean body mass. Grip strength in tumourâbearing mice was improved by EXT418 daily (P = 0.010) or EOD (P = 0.008) administration compared with vehicleâtreated mice. These effects of EXT418 on weight and grip strength were partially independent of food intake. EXT418 daily administration also improved type IIA (P = 0.015), IIB (P = 0.037) and IIX (P = 0.050) fibre crossâsectional area (CSA) in tibialis anterior (TA) and EXT418 EOD improved CSA of IIB fibres in red gastrocnemius (GAS; P = 0.005). In skeletal muscles, tumourâinduced increases in atrogenes Fbxo32 and Trim63 were ameliorated by EXT418 treatments (TA and GAS/plantaris, PL), which were independent of food intake. EXT418 administration decreased expression of the mitophagy marker Bnip3 (GAS/PL; P â€Â 0.010). Similar effects of EXT418 EOD were observed in p62 (GAS/PL; P = 0.039). In addition, EXT418 treatments ameliorated the tumourâinduced elevation in muscle Il6 transcript levels (TA and GAS/PL), independently of food intake. Ilâ6 transcript levels in adipose tissue and circulating ILâ10 were elevated in response to the tumour but these increases were not significant with EXT418 administration. Tumour mass was not altered by EXT418. Conclusions EXT418 mitigates LLCâinduced cachexia by attenuating skeletal muscle inflammation, proteolysis, and mitophagy, without affecting tumour mass and partially independent of food intake
Detecting significant genotypeâphenotype association rules in bipolar disorder: market research meets complex genetics
Background
Disentangling the etiology of common, complex diseases is a major challenge in genetic research. For bipolar disorder (BD), several genome-wide association studies (GWAS) have been performed. Similar to other complex disorders, major breakthroughs in explaining the high heritability of BD through GWAS have remained elusive. To overcome this dilemma, genetic research into BD, has embraced a variety of strategies such as the formation of large consortia to increase sample size and sequencing approaches. Here we advocate a complementary approach making use of already existing GWAS data: a novel data mining procedure to identify yet undetected genotypeâphenotype relationships. We adapted association rule mining, a data mining technique traditionally used in retail market research, to identify frequent and characteristic genotype patterns showing strong associations to phenotype clusters. We applied this strategy to three independent GWAS datasets from 2835 phenotypically characterized patients with BD. In a discovery step, 20,882 candidate association rules were extracted.
Results
Two of these rulesâone associated with eating disorder and the other with anxietyâremained significant in an independent dataset after robust correction for multiple testing. Both showed considerable effect sizes (odds ratioâ~â3.4 and 3.0, respectively) and support previously reported molecular biological findings.
Conclusion
Our approach detected novel specific genotypeâphenotype relationships in BD that were missed by standard analyses like GWAS. While we developed and applied our method within the context of BD gene discovery, it may facilitate identifying highly specific genotypeâphenotype relationships in subsets of genome-wide data sets of other complex phenotype with similar epidemiological properties and challenges to gene discovery efforts.Open-Access-Publikationsfonds 201
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Detecting significant genotype-phenotype association rules in bipolar disorder: market research meets complex genetics.
BACKGROUND: Disentangling the etiology of common, complex diseases is a major challenge in genetic research. For bipolar disorder (BD), several genome-wide association studies (GWAS) have been performed. Similar to other complex disorders, major breakthroughs in explaining the high heritability of BD through GWAS have remained elusive. To overcome this dilemma, genetic research into BD, has embraced a variety of strategies such as the formation of large consortia to increase sample size and sequencing approaches. Here we advocate a complementary approach making use of already existing GWAS data: a novel data mining procedure to identify yet undetected genotype-phenotype relationships. We adapted association rule mining, a data mining technique traditionally used in retail market research, to identify frequent and characteristic genotype patterns showing strong associations to phenotype clusters. We applied this strategy to three independent GWAS datasets from 2835 phenotypically characterized patients with BD. In a discovery step, 20,882 candidate association rules were extracted. RESULTS: Two of these rules-one associated with eating disorder and the other with anxiety-remained significant in an independent dataset after robust correction for multiple testing. Both showed considerable effect sizes (odds ratioâ~â3.4 and 3.0, respectively) and support previously reported molecular biological findings. CONCLUSION: Our approach detected novel specific genotype-phenotype relationships in BD that were missed by standard analyses like GWAS. While we developed and applied our method within the context of BD gene discovery, it may facilitate identifying highly specific genotype-phenotype relationships in subsets of genome-wide data sets of other complex phenotype with similar epidemiological properties and challenges to gene discovery efforts