Conservation threats and future prospects for the freshwater fishes of Ecuador: A hotspot of Neotropical fish diversity

Freshwater fish communities in Ecuador exhibit some of the highest levels of diversity and endemism in the Neotropics. Unfortunately, aquatic ecosystems in the country are under serious threat and conditions are deteriorating. In 2018–19, the government of Ecuador sponsored a series of workshops to examine the conservation status of Ecuador''s freshwater fishes. Concerns were identified for 35 species, most of which are native to the Amazon region, and overfishing of Amazonian pimelodid catfishes emerged as a major issue. However, much of the information needed to make decisions across fish groups and regions was not available, hindering the process and highlighting the need for a review of the conservation threats to Ecuador''s freshwater fishes. Here, we review how the physical alteration of rivers, deforestation, wetland and floodplain degradation, agricultural and urban water pollution, mining, oil extraction, dams, overfishing, introduced species and climate change are affecting freshwater fishes in Ecuador. Although many of these factors affect fishes throughout the Neotropics, the lack of data on Ecuadorian fish communities is staggering and highlights the urgent need for more research. We also make recommendations, including the need for proper enforcement of existing environmental laws, restoration of degraded aquatic ecosystems, establishment of a national monitoring system for freshwater ecosystems, investment in research to fill gaps in knowledge, and encouragement of public engagement in citizen science and conservation efforts. Freshwater fishes are an important component of the cultural and biological legacy of the Ecuadorian people. Conserving them for future generations is critical. © 2021 The Authors. Journal of Fish Biology published by John Wiley & Sons Ltd on behalf of Fisheries Society of the British Isles

T1 measurements identify extracellular volume expansion in hypertrophic cardiomyopathy sarcomere mutation carriers with and without left ventricular hypertrophy

Background—Myocardial fibrosis is a hallmark of hypertrophic cardiomyopathy (HCM) and a potential substrate for arrhythmias and heart failure. Sarcomere mutations seem to induce profibrotic changes before left ventricular hypertrophy (LVH) develops. To further evaluate these processes, we used cardiac magnetic resonance with T1 measurements on a genotyped HCM population to quantify myocardial extracellular volume (ECV). Methods and Results—Sarcomere mutation carriers with LVH (G+/LVH+, n=37) and without LVH (G+/LVH−, n=29), patients with HCM without mutations (sarcomere-negative HCM, n=11), and healthy controls (n=11) underwent contrast cardiac magnetic resonance, measuring T1 times pre- and postgadolinium infusion. Concurrent echocardiography and serum biomarkers of collagen synthesis, hemodynamic stress, and myocardial injury were also available in a subset. Compared with controls, ECV was increased in patients with overt HCM, as well as G+/LVH− mutation carriers (ECV=0.36±0.01, 0.33±0.01, 0.27±0.01 in G+/LVH+, G+/LVH−, controls, respectively; P≤0.001 for all comparisons). ECV correlated with N-terminal probrain natriuretic peptide levels (r=0.58; P60% of overt patients with HCM but absent from G+/LVH− subjects. Both ECV and late gadolinium enhancement were more extensive in sarcomeric HCM than sarcomere-negative HCM. Conclusions—Myocardial ECV is increased in HCM sarcomere mutation carriers even in the absence of LVH. These data provide additional support that fibrotic remodeling is triggered early in disease pathogenesis. Quantifying ECV may help characterize the development of myocardial fibrosis in HCM and ultimately assist in developing novel disease-modifying therapy, targeting interstitial fibrosis

Search for the Standard Model Higgs boson decaying into bb¯ produced in association with top quarks decaying hadronically in pp collisions at √s = 8 TeV with the ATLAS detector

A search for Higgs boson production in association with a pair of top quarks (tt¯ H) is performed, where the Higgs boson decays to bb¯, and both top quarks decay hadronically. The data used correspond to an integrated luminosity of 20.3 fb−1 of pp collisions at √s = 8 TeV collected with the ATLAS detector at the Large Hadron Collider. The search selects events with at least six energetic jets and uses a boosted decision tree algorithm to discriminate between signal and Standard Model background. The dominant multijet background is estimated using a dedicated data-driven technique. For a Higgs boson mass of 125 GeV, an upper limit of 6.4 (5.4) times the Standard Model cross section is observed (expected) at 95% confidence level. The best-fit value for the signal strength is μ = 1.6 ± 2.6 times the Standard Model expectation for mH = 125 GeV. Combining all tt¯ H searches carried out by ATLAS at √s = 8 and 7 TeV, an observed (expected) upper limit of 3.1 (1.4) times the Standard Model expectation is obtained at 95% confidence level, with a signal strength μ = 1.7 ± 0.8

Search for the Higgs boson produced in association with a W boson and decaying to four b-quarks via two spin-zero particles in pp collisions at 13 TeV with the ATLAS detector

This paper presents a dedicated search for exotic decays of the Higgs boson to a pair of new spin-zero particles, H → aa, where the particle a decays to b-quarks and has a mass in the range of 20–60 GeV. The search is performed in events where the Higgs boson is produced in association with a W boson, giving rise to a signature of a lepton (electron or muon), missing transverse momentum, and multiple jets from b-quark decays. The analysis is based on the full dataset of pp collisions at √s = 13 TeV recorded in 2015 by the ATLAS detector at the CERN Large Hadron Collider, corresponding to an integrated luminosity of 3.2 fb−1. No significant excess of events above the Standard Model prediction is observed, and a 95% confidence-level upper limit is derived for the product of the production cross section for pp → W H times the branching ratio for the decay H → aa → 4b. The upper limit ranges from 6.2 pb for an a-boson mass ma = 20 GeV to 1.5 pb for ma = 60 GeV

T1 measurements identify extracellular volume expansion in hypertrophic cardiomyopathy sarcomere mutation carriers with and without left ventricular hypertrophy

Background—Myocardial fibrosis is a hallmark of hypertrophic cardiomyopathy (HCM) and a potential substrate for arrhythmias and heart failure. Sarcomere mutations seem to induce profibrotic changes before left ventricular hypertrophy (LVH) develops. To further evaluate these processes, we used cardiac magnetic resonance with T1 measurements on a genotyped HCM population to quantify myocardial extracellular volume (ECV). Methods and Results—Sarcomere mutation carriers with LVH (G+/LVH+, n=37) and without LVH (G+/LVH−, n=29), patients with HCM without mutations (sarcomere-negative HCM, n=11), and healthy controls (n=11) underwent contrast cardiac magnetic resonance, measuring T1 times pre- and postgadolinium infusion. Concurrent echocardiography and serum biomarkers of collagen synthesis, hemodynamic stress, and myocardial injury were also available in a subset. Compared with controls, ECV was increased in patients with overt HCM, as well as G+/LVH− mutation carriers (ECV=0.36±0.01, 0.33±0.01, 0.27±0.01 in G+/LVH+, G+/LVH−, controls, respectively; P≤0.001 for all comparisons). ECV correlated with N-terminal probrain natriuretic peptide levels (r=0.58; P60% of overt patients with HCM but absent from G+/LVH− subjects. Both ECV and late gadolinium enhancement were more extensive in sarcomeric HCM than sarcomere-negative HCM. Conclusions—Myocardial ECV is increased in HCM sarcomere mutation carriers even in the absence of LVH. These data provide additional support that fibrotic remodeling is triggered early in disease pathogenesis. Quantifying ECV may help characterize the development of myocardial fibrosis in HCM and ultimately assist in developing novel disease-modifying therapy, targeting interstitial fibrosis

Multiresidue screening of milk withheld for sale at dairy farms in central New York State

Many of the drugs commonly used in lactating dairy cows result in residues in the milk, prohibiting its sale for human consumption. Milk withheld for sale because of drug treatment or from cows with high somatic cell counts is commonly called “waste milk.” One-third of dairy farms in the United States use waste milk to feed preweaned dairy calves. Limited information is currently available on the effect of this practice on the selection and dissemination of antibiotic-resistant bacteria. Pooled waste milk samples were collected from 34 dairy farms in central New York State with the objective of detecting the presence and quantity of drug residues in these samples. Samples were collected and refrigerated using ice packs and then stored at 4°C upon arrival at the Cornell laboratory (Ithaca, NY). Screening for β-lactam, tetracycline, and sulfonamide residues in the milk was performed using commercial enzyme-linked receptor-binding assay (SNAP) tests (Idexx Laboratories Inc., Westbrook, ME). Samples with a positive SNAP test were selected for screening using a multiresidue liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. The SNAP tests revealed that 75, 14.3, and 7.1% of waste milk samples (n = 34) contained β-lactam, tetracycline, and sulfamethazine residues, respectively. Of the samples sent for LC-MS/MS (n = 28), half had detectable quantities of drug residues. The most prevalent drugs detected by LC-MS/MS were ceftiofur (39.2%; mean ± SE concentration = 0.151 ± 0.042 μg/mL), penicillin G (14.2%; mean ± SE concentration = 0.008 ± 0.001 μg/mL), and ampicillin (7.1%; mean ± SE concentration = 0.472 ± 0.43 μg/mL). In addition, one sample had detectable concentrations of oxytetracycline and one sample had detectable concentrations of sulfadimethoxine. These results provide insight on drug residues present in waste milk from select farm in upstate New York, and additionally indicate the need for additional studies targeting on-farm treatments that could degrade drug residues present in waste milk and reduce the potential effects on the biosphere from the disposal and use of waste milk as a feed source