The Marin County Livestock Protection Program: 15 Years in Review

Predation by wild carnivores challenges livestock producers worldwide. To reduce or offset losses due to predation, a variety of predator control methods and compensation schemes have been developed. In 2001, Marin County, California, USA replaced its U.S. Department of Agriculture Wildlife Services (WS) cooperative predator damage management program with a county-run program that emphasized nonlethal methods for preventing and controlling coyote (Canis latrans) predation on domestic sheep (Ovis aries). This new Livestock Protection Program (LPP) cost-shared with livestock producers’ efforts to improve fencing, obtain and maintain guard animals, and other such nonlethal methods, and initially it compensated producers for documented losses to predators. In 2006, 5 years into the program, 17 sheep producers were surveyed to compare the former WS program to the LPP with regard to rancher satisfaction and preferences, lethality to predators, livestock losses, uses of nonlethal predator deterrent techniques, and costs. In 2016, 15 years after the program was replaced by a county-administered nonlethal program, we surveyed sheep producers to determine if their perceptions of the program had changed. Although the lack of standardized data collection complicated our evaluation, the number of sheep and lambs produced in Marin County has continued to decline; 5 producers left the sheep business and others who remain graze less acreage with smaller flocks, predation by coyotes remains a high concern to producers, and producers are generally dissatisfied with the Livestock Protection Program. Recommendations include increased programmatic funding for management practices, payments for losses, and seasonal hiring of wildlife specialists during critical times, especially during lambing seasons

Perturbed cholesterol and vesicular trafficking associated with dengue blocking in Wolbachia-infected Aedes aegypti cells

Wolbachia are intracellular maternally inherited bacteria that can spread through insect populations and block virus transmission by mosquitoes, providing an important approach to dengue control. To better understand the mechanisms of virus inhibition, we here perform proteomic quantification of the effects of Wolbachia in Aedes aegypti mosquito cells and midgut. Perturbations are observed in vesicular trafficking, lipid metabolism and in the endoplasmic reticulum that could impact viral entry and replication. Wolbachia-infected cells display a differential cholesterol profile, including elevated levels of esterified cholesterol, that is consistent with perturbed intracellular cholesterol trafficking. Cyclodextrins have been shown to reverse lipid accumulation defects in cells with disrupted cholesterol homeostasis. Treatment of Wolbachia-infected Ae. aegypti cells with 2-hydroxypropyl-β-cyclodextrin restores dengue replication in Wolbachia-carrying cells, suggesting dengue is inhibited in Wolbachia-infected cells by localised cholesterol accumulation. These results demonstrate parallels between the cellular Wolbachia viral inhibition phenotype and lipid storage genetic disorders

High-Density Lipoprotein Metabolism in Human Apolipoprotein B\u3csub\u3e100\u3c/sub\u3e Transgenic/Brown Adipose Tissue Deficient Mice: A Model of Obesity-Induced Hyperinsulinemia

Obese and diabetic humans display decreased plasma high-density lipoprotein cholesterol (HDL-C) concentrations and an increased risk for coronary heart disease. However, investigation on HDL metabolism in obesity with a particular emphasis on hepatic ATP-binding cassette transporter A1 (ABCA1), the primary factor for HDL formation, has not been well studied. Human apolipoprotein B100 transgenic (hApoBtg) and brown adipose tissue deficient (BATless) mice were crossed to generate hApoBtg/BATless mice. Male and female hApoBtg and hApoBtg/BATless mice were maintained on either a regular rodent chow diet or a diet high in fat and cholesterol until 24 weeks of age. The hApoBtg/BATless mice that were fed a HF/HC diet became obese, developed hepatic steatosis, and had significantly elevated plasma insulin levels compared with their hApoBtg counterparts, but plasma concentrations of total cholesterol, HDL-C, triglycerides, and free fatty acids and lipoprotein distribution between genotypes were not significantly different. Hepatic expression of genes encoding HDL-modifying factors (e.g., scavenger receptor, class B, type I, hepatic lipase, lecithin:cholesterol acyltransferase, and phospholipid transfer protein) was either altered significantly or showed a trend of difference between 2 genotypes of mice. Importantly, hepatic protein levels of ABCA1 were significantly lowered by ∼35% in male obese hApoBtg/BATless mice with no difference in mRNA levels compared with hApoBtg counterparts. Despite reduced hepatic ABCA1 protein levels, plasma HDL-C concentrations were not altered in male obese hApoBtg/BATless mice. The result suggests that hepatic ABCA1 may not be a primary contributing factor for perturbations in HDL metabolism in obesity-induced hyperinsulinemia

Promoting Bicycle Commuter Safety, Research Report 11-08

We present an overview of the risks associated with cycling to emphasize the need for safety. We focus on the application of frameworks from social psychology to education, one of the 5 Es—engineering, education, enforcement, encouragement, and evaluation. We use the structure of the 5 Es to organize information with particular attention to engineering and education in the literature review. Engineering is essential because the infrastructure is vital to protecting cyclists. Education is emphasized since the central focus of the report is safety

No Effect of Exercise Intensity on Appetite in Highly-Trained Endurance Women

In endurance-trained men, an acute bout of exercise is shown to suppress post-exercise appetite, yet limited research has examined this response in women. The purpose of this study was to investigate the effect of exercise intensity on appetite and gut hormone responses in endurance-trained women. Highly-trained women (n = 15, 18–40 years, 58.4 ± 6.4 kg, VO₂ₘₐₓ = 55.2 ± 4.3 mL/kg/min) completed isocaloric bouts (500 kcals or 2093 kJ) of moderate-intensity (MIE, 60% VO2MAX) and high-intensity (HIE, 85% VO2MAX) treadmill running at the same time of day, following a similar 48-h diet/exercise period, and at least 1-week apart. Blood was drawn pre-exercise (baseline), immediately post-exercise and every 20-min for the next 60-min. Plasma concentrations of acylated ghrelin, PYY₃₋₃₆, GLP-1 and subjective appetite ratings via visual analog scale (VAS) were assessed at each time point. Acylated ghrelin decreased (p = 0.014) and PYY3–36 and GLP-1 increased (p = 0.036, p < 0.0001) immediately post-exercise, indicating appetite suppression. VAS ratings of hunger and desire to eat decreased immediately post-exercise (p = 0.0012, p = 0.0031, respectively), also indicating appetite suppression. There were no differences between exercise intensities for appetite hormones or VAS. Similar to males, post-exercise appetite regulatory hormones were altered toward suppression in highly-trained women and independent of energy cost of exercise. Results are important for female athletes striving to optimize nutrition for endurance performance

WISE/NEOWISE observations of Active Bodies in the Main Belt

We report results based on mid-infrared photometry of 5 active main belt objects (AMBOs) detected by the Wide-field Infrared Survey Explorer (WISE) spacecraft. Four of these bodies, P/2010 R2 (La Sagra), 133P/Elst-Pizarro, (596) Scheila, and 176P/LINEAR, showed no signs of activity at the time of the observations, allowing the WISE detections to place firm constraints on their diameters and albedos. Geometric albedos were in the range of a few percent, and on the order of other measured comet nuclei. P/2010 A2 was observed on April 2-3, 2010, three months after its peak activity. Photometry of the coma at 12 and 22 {\mu}m combined with ground-based visible-wavelength measurements provides constraints on the dust particle mass distribution (PMD), dlogn/dlogm, yielding power-law slope values of {\alpha} = -0.5 +/- 0.1. This PMD is considerably more shallow than that found for other comets, in particular inbound particle fluence during the Stardust encounter of comet 81P/Wild 2. It is similar to the PMD seen for 9P/Tempel 1 in the immediate aftermath of the Deep Impact experiment. Upper limits for CO2 & CO production are also provided for each AMBO and compared with revised production numbers for WISE observations of 103P/Hartley 2.Comment: 32 Pages, including 5 Figure

The Web Epoch of Reionization Lyman-α\alpha Survey (WERLS) I. MOSFIRE Spectroscopy of z∼7−8\mathbf{z \sim 7-8} Lyman-α\alpha Emitters

We present the first results from the Web Epoch of Reionization Lyman-$\alpha$ Survey (WERLS), a spectroscopic survey of Lyman-$\alpha$ emission using Keck I/MOSFIRE and LRIS. WERLS targets bright ($J<26$) galaxy candidates with photometric redshifts of $5.5\lesssim z \lesssim 8$ selected from pre-JWST imaging embedded in the Epoch of Reionization (EoR) within three JWST deep fields: CEERS, PRIMER, and COSMOS-Web. Here, we report 11 $z\sim7-8$ Lyman-$\alpha$ emitters (LAEs; 3 secure and 8 tentative candidates) detected in the first five nights of WERLS MOSFIRE data. We estimate our observed LAE yield is $\sim13$%, broadly consistent with expectations assuming some loss from redshift uncertainty, contamination from sky OH lines, and that the Universe is approximately half-ionized at this epoch, whereby observable Lyman-$\alpha$ emission is unlikely for galaxies embedded in a neutral intergalactic medium. Our targets are selected to be UV-bright, and span a range of absolute UV magnitudes with $-23.1 < M_{\text{UV}} < -19.8$. With two LAEs detected at $z=7.68$, we also consider the possibility of an ionized bubble at this redshift. Future synergistic Keck+JWST efforts will provide a powerful tool for pinpointing beacons of reionization and mapping the large scale distribution of mass relative to the ionization state of the Universe.Comment: 27 pages, 8 figures; ApJ submitte

Predominant and novel de novo variants in 29 individuals with ALG13 deficiency: Clinical description, biomarker status, biochemical analysis, and treatment suggestions

Asparagine-linked glycosylation 13 homolog (ALG13) encodes a nonredundant, highly conserved, X-linked uridine diphosphate (UDP)-N-acetylglucosaminyltransferase required for the synthesis of lipid linked oligosaccharide precursor and proper N-linked glycosylation. De novo variants in ALG13 underlie a form of early infantile epileptic encephalopathy known as EIEE36, but given its essential role in glycosylation, it is also considered a congenital disorder of glycosylation (CDG), ALG13-CDG. Twenty-four previously reported ALG13-CDG cases had de novo variants, but surprisingly, unlike most forms of CDG, ALG13-CDG did not show the anticipated glycosylation defects, typically detected by altered transferrin glycosylation. Structural homology modeling of two recurrent de novo variants, p.A81T and p.N107S, suggests both are likely to impact the function of ALG13. Using a corresponding ALG13-deficient yeast strain, we show that expressing yeast ALG13 with either of the highly conserved hotspot variants rescues the observed growth defect, but not its glycosylation abnormality. We present molecular and clinical data on 29 previously unreported individuals with de novo variants in ALG13. This more than doubles the number of known cases. A key finding is that a vast majority of the individuals presents with West syndrome, a feature shared with other CDG types. Among these, the initial epileptic spasms best responded to adrenocorticotropic hormone or prednisolone, while clobazam and felbamate showed promise for continued epilepsy treatment. A ketogenic diet seems to play an important role in the treatment of these individuals.Fil: Ng, Bobby G.. Sanford Burnham Prebys Medical Discovery Institute; Estados UnidosFil: Eklund, Erik A.. Sanford Burnham Prebys Medical Discovery Institute; Estados Unidos. Lund University; SueciaFil: Shiryaev, Sergey A.. Sanford Burnham Prebys Medical Discovery Institute; Estados UnidosFil: Dong, Yin Y.. University of Oxford; Reino UnidoFil: Abbott, Mary Alice. University of Massachusetts Medical School; Estados UnidosFil: Asteggiano, Carla Gabriela. Universidad Católica de Córdoba; Argentina. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Estudios de las Metabolopatías Congénitas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; ArgentinaFil: Bamshad, Michael J.. University of Washington; Estados UnidosFil: Barr, Eileen. University of Emory; Estados UnidosFil: Bernstein, Jonathan A.. University of Stanford; Estados UnidosFil: Chelakkadan, Shabeed. Monash Children's Hospital; AustraliaFil: Christodoulou, John. Sydney Medical School; Australia. University of Melbourne; AustraliaFil: Chung, Wendy K.. Columbia University; Estados UnidosFil: Ciliberto, Michael A.. University of Iowa; Estados UnidosFil: Cousin, Janice. National Human Genome Research Institute ; Estados UnidosFil: Gardiner, Fiona. University of Melbourne; AustraliaFil: Ghosh, Suman. University of Florida; Estados UnidosFil: Graf, William D.. University of Connecticut; Estados UnidosFil: Grunewald, Stephanie. University College London; Estados UnidosFil: Hammond, Katherine. University of Alabama at Birmingahm; Estados UnidosFil: Hauser, Natalie S.. Inova, Fairfax Hospital Falls Church; Estados UnidosFil: Hoganson, George E.. University Of Illinois At Chicago; Estados UnidosFil: Houck, Kimberly M.. Baylor College of Medicine; Estados UnidosFil: Kohler, Jennefer N.. University of Stanford; Estados UnidosFil: Morava, Eva. Mayo Clinic; Estados UnidosFil: Larson, Austin A.. University Of Colorado Anschutz Medical Campus.; Estados UnidosFil: Liu, Pengfei. Baylor Genetics; Estados Unidos. Baylor College Of Medicine; Estados UnidosFil: Madathil, Sujana. University of Iowa; Estados UnidosFil: McCormack, Colleen. University of Stanford; Estados UnidosFil: Meeks, Naomi J.L.. University Of Colorado Anschutz Medical Campus.; Estados UnidosFil: Papazoglu, Gabriela Magali. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Estudios de las Metabolopatías Congénitas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentin

The home environment and childhood obesity in low-income households: indirect effects via sleep duration and screen time

Background Childhood obesity disproportionally affects children from low-income households. With the aim of informing interventions, this study examined pathways through which the physical and social home environment may promote childhood overweight/obesity in low-income households. Methods Data on health behaviors and the home environment were collected at home visits in low-income, urban households with either only normal weight (n = 48) or predominantly overweight/obese (n = 55) children aged 6–13 years. Research staff conducted comprehensive, in-person audits of the foods, media, and sports equipment in each household. Anthropometric measurements were collected, and children’s physical activity was assessed through accelerometry. Caregivers and children jointly reported on child sleep duration, screen time, and dietary intake of foods previously implicated in childhood obesity risk. Path analysis was used to test direct and indirect associations between the home environment and child weight status via the health behaviors assessed. Results Sleep duration was the only health behavior associated with child weight status (OR = 0.45, 95% CI: 0.27, 0.77), with normal weight children sleeping 33.3 minutes/day longer on average than overweight/obese children. The best-fitting path model explained 26% of variance in child weight status, and included paths linking chaos in the home environment, lower caregiver screen time monitoring, inconsistent implementation of bedtime routines, and the presence of a television in children’s bedrooms to childhood overweight/obesity through effects on screen time and sleep duration. Conclusions This study adds to the existing literature by identifying aspects of the home environment that influence childhood weight status via indirect effects on screen time and sleep duration in children from low-income households. Pediatric weight management interventions for low-income households may be improved by targeting aspects of the physical and social home environment associated with sleep