On the evolutionary ecology of symbioses between chemosynthetic bacteria and bivalves

Mutualistic associations between bacteria and eukaryotes occur ubiquitously in nature, forming the basis for key ecological and evolutionary innovations. Some of the most prominent examples of these symbioses are chemosynthetic bacteria and marine invertebrates living in the absence of sunlight at deep-sea hydrothermal vents and in sediments rich in reduced sulfur compounds. Here, chemosynthetic bacteria living in close association with their hosts convert CO2 or CH4 into organic compounds and provide the host with necessary nutrients. The dominant macrofauna of hydrothermal vent and cold seep ecosystems all depend on the metabolic activity of chemosynthetic bacteria, which accounts for almost all primary production in these complex ecosystems. Many of these enigmatic mutualistic associations are found within the molluscan class Bivalvia. Currently, chemosynthetic symbioses have been reported from five distinct bivalve families (Lucinidae, Mytilidae, Solemyidae, Thyasiridae, and Vesicomyidae). This brief review aims to provide an overview of the diverse physiological and genetic adaptations of symbiotic chemosynthetic bacteria and their bivalve hosts

Hypothesis for the evolution of three-helix Chl a/b and Chl a/c light-harvesting antenna proteins from two-helix and four-helix ancestors

The nuclear-encoded Chl a/b and Chl a/c antenna proteins of photosynthetic eukaryotes are part of an extended family of proteins that also includes the early light-induced proteins (ELIPs) and the 22 kDa intrinsic protein of PS II (encoded by psb S gene). All members of this family have three transmembrane helices except for the psb S protein, which has four. The amino acid sequences of these proteins are compared and related to the three-dimensional structure of pea LHC II Type I (Kühlbrandt and Wang, Nature 350: 130–134, 1991). The similarity of psb S to the three-helix members of the family suggests that the latter arose from a four-helix ancestor that lost its C-terminal helix by deletion. Strong internal similarity between the two halves of the psb S protein suggests that it in turn arose as the result of the duplication of a gene encoding a two-helix protein. Since psb S is reported to be present in at least one cyanobacterium, the ancestral four-helix protein may have been present prior to the endosymbiotic event or events that gave rise to the photosynthetic eukaryotes. The Chl a/b and Chl a/c antenna proteins, and the immunologically-related proteins in the rhodophytes may have had a common ancestor which was present in the early photosynthetic eukaryotes, and predated their division into rhodophyte, chromophyte and chlorophyte lineages. The LHC I-LHC II divergence probably occurred before the separation of higher plants from chlorophyte algae and euglenophytes, and the different Types of LHC I and LHC II proteins arose prior to the separation of angiosperms and gymnosperms.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/43538/1/11120_2004_Article_BF00029382.pd

Wildfire activity is driving summertime air quality degradation across the western US: a model-based attribution to smoke source regions

Over recent decades, wildfire activity across western North America has increased in concert with summertime air quality degradation in western US urban centers. Using a Lagrangian atmospheric modeling framework to simulate smoke transport for almost 20 years, we quantitatively link decadal scale air quality trends with regional wildfire activity. Modeled smoke concentrations correlate well with observed fine-mode aerosol (PM _2.5 ) concentrations (R > 0.8) at the urban centers most impacted by smoke, supporting attribution of observed trends to wildfire sources. Many western US urban centers (23 of 33 total) exhibit statistically significant trends toward enhanced, wildfire-driven, extreme (98th quantile) air quality episodes during the months of August and September for the years 2003–2020. In the most extreme cases, trends in 98th quantile PM _2.5 exceed 2 μ g m ^−3 yr ^−1 , with such large trends clustering in the Pacific Northwest and Northern/Central California. We find that the Pacific Northwest is uniquely impacted by smoke from wildfires in the mountainous Pacific Northwest, California, and British Columbia, leading to especially robust degradation of air quality. Summertime PM _2.5 trends in California and the Intermountain West are largely explained by wildfires in mountainous California and the American Rockies, respectively. These results may inform regional scale forest management efforts, and they present significant implications for understanding the wildfire—air quality connection in the context of climate driven trends toward enhanced wildfire activity and subsequent human exposure to degraded air quality

Fracture mechanisms of the Strombus gigas conch shell: implications for the design of brittle laminates

Flexural strength, crack-density evolution, work of fracture, and critical strain energy release rates were measured for wet and dry specimens of the Strombus gigas conch shell. This shell has a crossed-lamellar microarchitecture, which is layered at five distinct length scales and can be considered a form of ceramic plywood. The shell has a particularly high ceramic (mineral) content (99.9 wt%), yet achieves unusually good mechanical performance. Even though the strengths are modest (of the order 100 MPa), the laminated structure has a large strain to fracture, and a correspondingly large work of fracture, up to 13 kJ m–2. The large fracture resistance is correlated to the extensive microcracking that occurs along the numerous interfaces within the shell microstructure. Implications of this impressive work of fracture for design of brittle laminates are considered

Valsartan in early-stage hypertrophic cardiomyopathy:a randomized phase 2 trial

Hypertrophic cardiomyopathy (HCM) is often caused by pathogenic variants in sarcomeric genes and characterized by left ventricular (LV) hypertrophy, myocardial fibrosis and increased risk of heart failure and arrhythmias. There are no existing therapies to modify disease progression. In this study, we conducted a multi-center, double-blind, placebo-controlled phase 2 clinical trial to assess the safety and efficacy of the angiotensin II receptor blocker valsartan in attenuating disease evolution in early HCM. In total, 178 participants with early-stage sarcomeric HCM were randomized (1:1) to receive valsartan (320 mg daily in adults; 80–160 mg daily in children) or placebo for 2 years (NCT01912534). Standardized changes from baseline to year 2 in LV wall thickness, mass and volumes; left atrial volume; tissue Doppler diastolic and systolic velocities; and serum levels of high-sensitivity troponin T and N-terminal pro-B-type natriuretic protein were integrated into a single composite z-score as the primary outcome. Valsartan (n = 88) improved cardiac structure and function compared to placebo (n = 90), as reflected by an increase in the composite z-score (between-group difference +0.231, 95% confidence interval (+0.098, +0.364); P = 0.001), which met the primary endpoint of the study. Treatment was well-tolerated. These results indicate a key opportunity to attenuate disease progression in early-stage sarcomeric HCM with an accessible and safe medication

Cardiac remodeling in subclinical hypertrophic cardiomyopathy: the VANISH randomized clinical trial

Importance: Valsartan has shown promise in attenuating cardiac remodeling in patients with early-stage sarcomeric hypertrophic cardiomyopathy (HCM). Genetic testing can identify individuals at risk of HCM in a subclinical stage who could benefit from therapies that prevent disease progression. Objective: To explore the potential for valsartan to modify disease development, and to characterize short-term phenotypic progression in subclinical HCM. Design, Setting, and Participants: The multicenter, double-blind, placebo-controlled Valsartan for Attenuating Disease Evolution in Early Sarcomeric Hypertrophic Cardiomyopathy (VANISH) randomized clinical trial was conducted from April 2014 to July 2019 at 17 sites in 4 countries (Brazil, Canada, Denmark, and the US), with 2 years of follow-up. The prespecified exploratory VANISH cohort studied here included sarcomere variant carriers with subclinical HCM and early phenotypic manifestations (reduced E′ velocity, electrocardiographic abnormalities, or an increased left ventricular [LV] wall thickness [LVWT] to cavity diameter ratio) but no LV hypertrophy (LVH). Data were analyzed between March and December 2022. Interventions: Treatment with placebo or valsartan (80 mg/d for children weighing <35 kg, 160 mg/d for children weighing ≥35 kg, or 320 mg/d for adults aged ≥18 years). Main Outcomes and Measures: The primary outcome was a composite z score incorporating changes in 9 parameters of cardiac remodeling (LV cavity volume, LVWT, and LV mass; left atrial [LA] volume; E′ velocity and S′ velocity; and serum troponin and N-terminal prohormone of brain natriuretic peptide levels). Results: This study included 34 participants, with a mean (SD) age of 16 (5) years (all were White). A total of 18 participants (8 female [44%] and 10 male [56%]) were randomized to valsartan and 16 (9 female [56%] and 7 male [44%]) were randomized to placebo. No statistically significant effects of valsartan on cardiac remodeling were detected (mean change in composite z score compared with placebo: −0.01 [95% CI, −0.29 to 0.26]; P = .92). Overall, 2-year phenotypic progression was modest, with only a mild increase in LA volume detected (increased by 3.5 mL/m2 [95% CI, 1.4-6.0 mL/m2]; P = .002). Nine participants (26%) had increased LVWT, including 6 (18%) who developed clinically overt HCM. Baseline LA volume index (LAVI; 35 vs 28 mL/m2; P = .01) and average interventricular septum thickness (8.5 vs 7.0 mm; P = .009) were higher in participants who developed HCM. Conclusions and Relevance: In this exploratory cohort, valsartan was not proven to slow progression of subclinical HCM. Minimal changes in markers of cardiac remodeling were observed, although nearly one-fifth of patients developed clinically overt HCM. Transition to disease was associated with greater baseline interventricular septum thickness and LAVI. These findings highlight the importance of following sarcomere variant carriers longitudinally and the critical need to improve understanding of factors that drive disease penetrance and progression. Trial Registration: ClinicalTrials.gov Identifier: NCT0191253

Using Magnetic Helicity, Topology, and Geometry to Investigate Complex Magnetic Fields

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