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The western pond turtle (WPT) was formerly considered a single species (Actinemys or Emys marmorata) that ranged from southern British Columbia, Canada to Baja California, México. More recently it was divided into a northern and a southern species. WPTs are found primarily in streams that drain into the Pacific Ocean, although scattered populations exist in endorheic drainages of the Great Basin and Mojave deserts. Populations in the Mojave Desert were long thought to be restricted to the Mojave River, but recently another population was documented in Piute Ponds, a terminal wetland complex associated with Amargosa Creek on Edwards Air Force Base. WPT fossils in the Mojave Desert are known from the Miocene to the Pleistocene. Recently, Pleistocene fossils have been found as far into the desert as Salt Springs, just south of Death Valley. The oldest fossil records suggest that WPTs were present in wetlands and drainages of the geological feature known as the Mojave block prior to the uplift of the Sierra Nevada Range about 8 Ma and prior to the ~ 3 Ma uplift of the Transverse Ranges. Archaeological records document use of turtles by Native Americans for food and cultural purposes 1,000 or more years ago at the Cronese Lakes on the lower Mojave River and Oro Grande on the upper river. The first modern publication documenting their presence in the Mojave River was 1861. Museum specimens were collected as early as 1937. These fossil and early literature records support the indigenous status of WPTs to the Mojave River. However, mtDNA-based genetic evidence shows that Mojave River turtles share an identical haplotype with turtles on the California coast. Limited nuclear data show some minor differences. Overdraft of water from the Mojave River for municipal and agricultural uses, urban development, and saltcedar expansion are threats to the continued survival of WPTs in the Mojave River.

The western pond turtle (WPT), recently separated into two paripatrically distributed species (Emys pallida and Emys marmorata), is experiencing significant reductions in its range and population size. In addition to habitat loss, two potential causes of decline are female-biased road mortality and high juvenile mortality from non-native predatory bullfrogs (Rana catesbeiana). However, quantitative analyses of these threats have never been conducted for either species of WPT. We used a combination of historical museum samples and published and unpublished field studies shared with us through personal communications with WPT field researchers (B. Shaffer, P. Scott, R. Fisher, C. Brown, R. Dagit, L. Patterson, T. Engstrom, 2019, personal communications) to quantify the effect of roads and bullfrogs on WPT populations along the west coast of the United States. Both species of WPT shift toward increasingly male biased museum collections over the last century, a trend consistent with increasing, female-biased road mortality. Recent WPT population studies revealed that road density and proximity were significantly associated with increasingly male-biased sex ratios, further suggesting female-biased road mortality. The mean body size of museum collections of E. marmorata, but not E. pallida, has increased over the last 100 years, consistent with reduced recruitment and aging populations that could be driven by invasive predators. Contemporary WPT population sites that co-occur with bullfrogs had significantly greater average body sizes than population sites without bullfrogs, suggesting strong bullfrog predation on small WPT hatchlings and juveniles. Overall, our findings indicate that both species of WPT face demographic challenges which would have been difficult to document without the use of both historical data from natural history collections and contemporary demographic field data. Although correlational, our analyses suggest that female-biased road mortality and predation on small turtles by non-native bullfrogs are occurring, and that conservation strategies reducing both may be important for WPT recovery.

Understanding the ecological pressures that generate variation in body shape is important because body shape profoundly affects physiology and overall fitness. Using Fundulus, a genus of fish that exhibits considerable morphological and physiological variation with evidence of repeated transitions between freshwater and saltwater habitats, we tested whether habitat salinity has influenced the macroevolution of body shape at different stages in development. After accounting for phylogenetic inertia, we find that body shape deviates from the optimal streamlined shape in a manner consistent with different osmoregulatory pressures exerted by different salinity niches at every stage of ontogeny that we examined. We attribute variation in body shape to differential selection for osmoregulatory efficiency because: (1) saline intolerant species developed body shapes with relatively low surface areas more conducive to managing osmoregulatory demands and (2) inland species that exhibit high salinity tolerances have body shapes similar to saline tolerant species in marine environments.

Molecular ecologists frequently use genome reduction strategies that rely upon restriction enzyme digestion of genomic DNA to sample consistent portions of the genome from many individuals (e.g., RADseq, GBS). However, researchers often find the existing methods expensive to initiate and/or difficult to implement consistently, especially because it is difficult to multiplex sufficient numbers of samples to fill entire sequencing lanes. Here, we introduce a low-cost and highly robust approach for the construction of dual-digest RADseq libraries that build on adapters and primers designed in Adapterama I. Major features of our method include: (1) minimizing the number of processing steps; (2) focusing on a single strand of sample DNA for library construction, allowing the use of a non-phosphorylated adapter on one end; (3) ligating adapters in the presence of active restriction enzymes, thereby reducing chimeras; (4) including an optional third restriction enzyme to cut apart adapter-dimers formed by the phosphorylated adapter, thus increasing the efficiency of adapter ligation to sample DNA, which is particularly effective when only low quantity/quality DNA samples are available; (5) interchangeable adapter designs; (6) incorporating variable-length internal indexes within the adapters to increase the scope of sample indexing, facilitate pooling, and increase sequence diversity; (7) maintaining compatibility with universal dual-indexed primers and thus, Illumina sequencing reagents and libraries; and, (8) easy modification for the identification of PCR duplicates. We present eight adapter designs that work with 72 restriction enzyme combinations. We demonstrate the efficiency of our approach by comparing it with existing methods, and we validate its utility through the discovery of many variable loci in a variety of non-model organisms. Our 2RAD/3RAD method is easy to perform, has low startup costs, has increased utility with low-concentration input DNA, and produces libraries that can be highly-multiplexed and pooled with other Illumina libraries.

Abstract Background The Editorial Board of EJNMMI Radiopharmacy and Chemistry releases a biannual highlight commentary to update the readership on trends in the field of radiopharmaceutical development. Main body This selection of highlights provides commentary on 19 different topics selected by each coauthoring Editorial Board member addressing a variety of aspects ranging from novel radiochemistry to first-in-human application of novel radiopharmaceuticals. Conclusion Trends in radiochemistry and radiopharmacy are highlighted. Hot topics cover the entire scope of EJNMMI Radiopharmacy and Chemistry, demonstrating the progress in the research field in many aspects.

ABSTRACT: Chickens in Australia have recently been identified with symptoms and morphological findings including spondylitis attributed to pathogenic Enterococcus cecorum. Notably, there is limited information on clinical E. cecorum strains in Australia. The cpsO gene, located downstream of the capsular polysaccharide (cps) locus, was recently reported to successfully differentiate between pathogenic and commensal E. cecorum strains, as this gene is highly conserved in the pathogenic strains. In this study, pathogenic E. cecorum, with a conserved cpsO gene, was detected on 1 of the 2 farms studied in Australia. E. cecorum strains isolated from clinical sites of the diseased birds from the second farm did not have the cpsO gene and were distant from the isolates of the first farm. A cpsO PCR of the caecal content of the birds on this farm was positive, while cpsO PCR of washed culture plates where the tissue extracts were spread onto and incubated for bacterial growth was negative. This suggests that pathogenic E. cecorum with the cpsO gene, as detected in Farm 1 and reported in other countries, was present in the second farm but could not grow on the selective agar plates during the initial step of E. cecorum isolation. Nevertheless, E. cecorum isolated from the clinical sites on the second farm might represent the pathogenic strain, but further animal studies are required to validate this possibility. Phylogenetic analysis showed that the pathogenic strains in Australia were most closely related to the clinical strains in North America.

Abstract Using a 50‐compartment Python‐coded mathematical lung model, we compared mixed venous blood flow (Q) distributions and arterial oxygen tension/inspired oxygen fraction (PaO2/FiO2) relationships in lungs modeled with log normal distributions (LND) of inspired (VI) versus expired (VA) alveolar gas volumes. In lungs with normal V/Q heterogeneity, Q versus VA/Q and Q versus VI/Q distributions were similar with either approach, and PaO2/FiO2 sequences remained indistinguishable. In V/Q heterogeneous lungs at high FiO2, VILND generated low Q versus VA/Q shoulders and some negative VA units, while VALND preserved Q versus VA/Q log normality by blood flow diversion from low VI/Q units. We managed VILND‐induced negative VA units either by shunt conversion (VI decreased to 0) or VI redistribution simulating collateral ventilation (VI increased till VA = 0). Comparing oxygen transfer: VALND > VILND (redistribution) > VILND (shunt). In V/Q heterogeneous lungs VALND and VILND (redistribution) regained near optimal oxygen transfer on 100% oxygen, while impairment persisted with VILND (shunt). Unlike VALND, VILND (redistribution) produced Q versus VA/Q distributions in V/Q heterogeneity compatible with multiple inert gas (MIGET) reports. VILND (redistribution) is a physiologically–based MIGET–compatible alternative to West's original VALND lung modeling approach.

Abstract Intestinal infection of many host species with Lawsonia intracellularis are widely reported. Analyses of infections among carnivorous falcons have not previously been reported. Fifty juvenile captive falcons (Falco spp.) with or without Lawsonia infection were investigated in the United Arab Emirates, including clinical laboratory methods. Fresh intestinal biopsy samples were analysed by microbiological techniques for Lawsonia and other bacteria and by standard parasitological and pathological methods. Lawsonia intracellularis infection was diagnosed by microbiological examination and qPCR in 10 of 50 juvenile falcons at case examination. Seven of these 10 falcons were of normal clinical appearance, and the other three had other contributing factors to ill‐thrift. A range of other conditions were noted in 40 case control falcons. This first report of Lawsonia infection in falcons suggests that the agent may have a limited contribution to clinical disease in these birds, including ill‐thrift syndromes. This lack of clinical disease association mimics that noted among Lawsonia infections recorded in other avian families.

Spotty Liver Disease (SLD) is a serious infectious disease which occurs mainly in laying chickens in free range production systems. SLD outbreaks can increase mortality and decrease egg production of chickens, adversely impact welfare and cause economic hardship for poultry producers. The bacterium Campylobacter hepaticus is the primary cause of the disease. This study aimed to identify the effects of C. hepaticus on chicken gut microbiota and gut structure. Three C. hepaticus strains (HV10T, NSW44L and QLD19L), isolated from different states of Australia, were used in the study. Chickens at 26-weeks post-hatch were orally dosed with one of the C. hepaticus strains (challenged groups) or Brucella broth (unchallenged or control group). Six days after the challenge, birds were necropsied to assess liver damage, and caecal content and tissue samples were collected for histology, microbiology, and 16S rRNA gene amplicon sequencing to characterize the composition of the bacterial microbiota. Strain C. hepaticus NSW44L produced significantly more disease compared to the other C. hepaticus strains and this coincided with more adverse changes observed in the caecal microbiota of the birds challenged with this strain compared to the control group. Microbial diversity determined by Shannon and Simpson alpha diversity indices was lower in the NSW44L challenged groups compared to the control group (p = 0.009 and 0.0233 respectively, at genus level). Short-chain fatty acids (SCFAs) producing bacteria Faecalibacterium, Bifidobacterium and Megamonas were significantly reduced in the challenged groups compared to the unchallenged control group. Although SLD-induction affected the gut microbiota of chickens, their small intestine morphology was not noticeably affected as there were no significant differences in the villus height or ratio of villus height and crypt depth. As gut health plays a pivotal role in the overall health and productivity of chickens, approaches to improve the gut health of the birds during SLD outbreaks such as through diet and keeping the causes of stress to a minimum, may represent significant ways to alleviate the impact of SLD.

Acetylcholine plays a major role in brain cognitive and motor functions with regional cholinergic terminal loss common in several neurodegenerative disorders. We describe age-related declines of regional cholinergic neuron terminal density in vivo using the positron emission tomography (PET) ligand [18F](–)5-Fluoroethoxybenzovesamicol ([18F]FEOBV), a vesamicol analogue selectively binding to the vesicular acetylcholine transporter (VAChT). A total of 42 subjects without clinical evidence of neurologic disease (mean 50.55 [range 20–80] years, 24 Male/18 Female) underwent [18F]FEOBV brain PET imaging. We used SPM based voxel-wise statistical analysis to perform whole brain voxel-based parametric analysis (family-wise error corrected, FWE) and to also extract the most significant clusters of regions correlating with aging with gender as nuisance variable. Age-related VAChT binding reductions were found in primary sensorimotor cortex, visual cortex, caudate nucleus, anterior to mid-cingulum, bilateral insula, para-hippocampus, hippocampus, anterior temporal lobes/amygdala, dorsomedial thalamus, metathalamus, and cerebellum (gender and FWE-corrected, P

Background Left circumflex culprit is often missed by the standard 12‐lead ECG. Extended lead systems (body surface potential map [BSPM]) should improve the diagnosis of culprit left circumflex stenosis with myocardial infarction. Methods and Results Retrospective analysis of a hospital research registry (August 2000–August 2010) comprising consecutive patients with (1) ischemic‐type chest pain at rest; (2) 12‐lead ECG and 80‐lead BSPM at first medical contact; and (3) cardiac troponin‐T 12 hours after symptom onset and/or creatine kinase MB fraction, were undertaken. Enrolled in the cohort were patients with culprit left circumflex stenosis (thrombolysis in myocardial infarction flow grade 0/1) at angiography. Acute myocardial infarction AMI was defined as cardiac troponin‐T ≥0.1 μg/L and/or creatine kinase MB fraction >2 upper limits of normal. Enrolled were 482 patients: 168 had exclusion criteria. Of the remaining 314 (age 64±11 years; 62% male), 254 (81%) had AMI: of these, 231 had BSPM STE—sensitivity 0.91, specificity 0.72, positive predictive value 0.93, negative predictive value 0.65, and c‐statistic 0.803 for AMI (P