Tuning of shortening speed in coleoid cephalopod muscle: no evidence for tissue-specific muscle myosin heavy chain isoforms

The contractile protein myosin II is ubiquitous in muscle. It is widely accepted that animals express tissue-specific myosin isoforms that differ in amino acid sequence and ATPase activity in order to tune muscle contractile velocities. Recent studies, however, suggested that the squid Doryteuthis pealeii might be an exception; members of this species do not express muscle-specific myosin isoforms, but instead alter sarcomeric ultrastructure to adjust contractile velocities. We investigated whether this alternative mechanism of tuning muscle contractile velocity is found in other coleoid cephalopods. We analyzed myosin heavy chain transcript sequences and expression profiles from muscular tissues of a cuttlefish, Sepia officinalis, and an octopus, Octopus bimaculoides, in order to determine if these cephalopods express tissue-specific myosin heavy chain isoforms. We identified transcripts of four and six different myosin heavy chain isoforms in S. officinalis and O. bimaculoides muscular tissues, respectively. Transcripts of all isoforms were expressed in all muscular tissues studied, and thus S. officinalis and O. bimaculoides do not appear to express tissue-specific muscle myosin isoforms. We also examined the sarcomeric ultrastructure in the transverse muscle fibers of the arms of O. bimaculoides and the arms and tentacles of S. officinalis using transmission electron microscopy and found that the fast contracting fibers of the prey capture tentacles of S. officinalis have shorter thick filaments than those found in the slower transverse muscle fibers of the arms of both species. It thus appears that coleoid cephalopods, including the cuttlefish and octopus, may use ultrastructural modifications rather than tissue-specific myosin isoforms to adjust contractile velocities

Muscular tissues of the squid Doryteuthis pealeii express identical myosin heavy chain isoforms: an alternative mechanism for tuning contractile speed

The speed of muscle contraction is largely controlled at the sarcomere level by the ATPase activity of the motor protein myosin. Differences in amino acid sequence in catalytically important regions of myosin yield different myosin isoforms with varying ATPase activities and resulting differences in cross-bridge cycling rates and interfilamentary sliding velocities. Modulation of whole-muscle performance by changes in myosin isoform ATPase activity is regarded as a universal mechanism to tune contractile properties, especially in vertebrate muscles. Invertebrates such as squid, however, may exhibit an alternative mechanism to tune contractile properties that is based on differences in muscle ultrastructure, including variable myofilament and sarcomere lengths. To determine definitively whether contractile properties of squid muscles are regulated via different myosin isoforms (i.e. different ATPase activities), the nucleotide and amino acid sequences of the myosin heavy chain from the squid Doryteuthis pealeii were determined from the mantle, arm, tentacle, fin and funnel retractor musculature. We identified three myosin heavy chain isoforms in squid muscular tissues, with differences arising at surface loop 1 and the carboxy terminus. All three isoforms were detected in all five tissues studied. These results suggest that the muscular tissues of D. pealeii express identical myosin isoforms, and it is likely that differences in muscle ultrastructure, not myosin ATPase activity, represent the most important mechanism for tuning contractile speeds

Chlorido{N-[2-(diphenylphosphanyl)benz­ylidene]-2-(2-thienyl)ethanamine-κ2 N,P}methylpalladium(II) dichloromethane hemisolvate

In the title compound, [Pd(CH3)Cl(C25H22NPS)]·0.5C2H2Cl2, the PdII atom is coordinated by the N,P-bidentate ligand, a methyl group and a chloride ion, generating a distorted square-planar PdCClNS coordination geometry, with the N and Cl atoms trans. The thio­phene ring is equally disordered over two orientations and the dichloro­methane solvent mol­ecule is disordered about an inversion centre

Long-term Outcomes of Enhanced Depression Treatment in Patients with Acute Coronary Syndromes

Background: The Coronary Psychosocial Evaluation Studies trial demonstrated promising results for enhanced depression treatment to reduce cardiovascular risk of patients with acute coronary syndrome and comorbid depression, but the long-term effectiveness of this intervention is unclear. Methods: A total of 157 participants with persistent depression after hospitalization for acute coronary syndromes were enrolled in the Coronary Psychosocial Evaluation Studies trial. A total of 80 participants were allocated to 6 months of enhanced depression treatment, and 77 participants were allocated to usual care. We report on an additional 12 months of observational follow-up for the composite outcome of death or first hospitalization for myocardial infarction or unstable angina. Results: Although the intervention was previously shown to have favorable cardiovascular effects during the treatment period, we observed a significant time-by-treatment group interaction during extended follow-up (P = .008). Specifically, during the 6-month treatment period, death or hospitalization for myocardial infarction/unstable angina occurred in 3 participants (4%) in the treatment group compared with 11 participants (14%) in the usual care group (hazard ratio, 0.25; 95% confidence interval, 0.07-0.90; P = .03). In contrast, during 12 months of additional observational follow-up, 11 participants (14%) in the treatment group experienced the composite outcome of death or hospitalization for myocardial infarction/unstable angina compared with 3 participants (4%) in the usual care group (hazard ratio, 2.91; 95% confidence interval, 0.80-10.56; P = .10). Conclusions: Enhanced depression treatment was associated with a reduced risk of death or hospitalization for myocardial infarction/unstable angina during active treatment, but this effect did not persist after treatment ceased. Future research is needed to confirm our findings and to determine the optimal duration of depression treatment in patients with depression after acute coronary syndromes

The ‘Perfect Storm’ and Acute Coronary Syndrome Onset: Do Psychosocial Factors Play a Role?

The revolution in cardiac care over the past two decades, characterized by emergent revascularization, drug eluting stents, anti-platelet medications, and advanced imaging has had little impact on overall ACS recurrence, or ACS prevention. The “Perfect Storm” refers to a confluence of events and processes, including atherosclerotic plaque, coronary flow dynamics, hemostatic and fibrinolytic function, metabolic and inflammatory conditions, neurohormonal dysregulation, and environmental events that give rise to, and result in an ACS event. In this article we illustrate the limits of the traditional main effect research model, giving a brief description of the current state of knowledge regarding the development of atherosclerotic plaque and the rupturing of these plaques that defines an ACS event. We then apply the Perfect Storm conceptualization to describe a program of research concerning a psychosocial vulnerability factor that contributes to increased risk of recurrent ACS and early mortality, and that has defied our efforts to identify underlying pathophysiology and successfully mount efforts to fully mitigate this risk

Optimizing management of invasions in an uncertain world using dynamic spatial models

Dispersal drives invasion dynamics of nonnative species and pathogens. Applying knowledge of dispersal to optimize the management of invasions can mean the difference between a failed and a successful control program and dramatically improve the return on investment of control efforts. A common approach to identifying optimal management solutions for invasions is to optimize dynamic spatial models that incorporate dispersal. Optimizing these spatial models can be very challenging because the interaction of time, space, and uncertainty rapidly amplifies the number of dimensions being considered. Addressing such problems requires advances in and the integration of techniques from multiple fields, including ecology, decision analysis, bioeconomics, natural resource management, and optimization. By synthesizing recent advances from these diverse fields, we provide a workflow for applying ecological theory to advance optimal management science and highlight priorities for optimizing the control of invasions. One of the striking gaps we identify is the extremely limited consideration of dispersal uncertainty in optimal management frameworks, even though dispersal estimates are highly uncertain and greatly influence invasion outcomes. In addition, optimization frameworks rarely consider multiple types of uncertainty (we describe five major types) and their interrelationships. Thus, feedbacks from management or other sources that could magnify uncertainty in dispersal are rarely considered. Incorporating uncertainty is crucial for improving transparency in decision risks and identifying optimal management strategies. We discuss gaps and solutions to the challenges of optimization using dynamic spatial models to increase the practical application of these important tools and improve the consistency and robustness of management recommendations for invasions

Trait anxiety and trait anger measured by ecological momentary assessment and their correspondence with traditional trait questionnaires

Ecological momentary assessments (EMA) of anxiety and anger/hostility were obtained every 25–30 min over two 24-h periods, separated by a median of 6 months, from 165 employees at a university in the Northeast. We used a multilevel trait-state-error structural equation model to estimate: (1) the proportion of variance in EMA anxiety and anger/hostility attributable to stable trait-like individual differences; (2) the correspondence between these trait-like components of EMA anxiety and anger/hostility and traditional questionnaire measures of each construct; and (3) the test–retest correlation between two 24-h averages obtained several months apart. After adjustment for measurement error, more than half the total variance in EMA reports of anxiety and anger/hostility is attributable to stable trait-like individual differences; however, the trait-like component of each construct is only modestly correlated with questionnaire measures of that construct. The 6-month “test–retest” correlations of latent variables representing the true 24-h EMA average anxiety and average anger are quite high (r ≥ 0.83). This study represents the longest follow-up period over which EMA-based estimates of traits have been examined. The results suggest that although the trait component (individual differences) of EMA momentary ratings of anxiety and anger is larger than the state component, traditional self-report questionnaires of trait anxiety and anger correspond only weakly with EMA-defined traits

Serine/threonine acetylation of TGFbeta-activated kinase (TAK1) by Yersinia pestis YopJ inhibits innate immune signaling

The Gram-negative bacteria Yersinia pestis, causative agent of plague, is extremely virulent. One mechanism contributing to Y. pestis virulence is the presence of a type-three secretion system, which injects effector proteins, Yops, directly into immune cells of the infected host. One of these Yop proteins, YopJ, is proapoptotic and inhibits mammalian NF-kappaB and MAP-kinase signal transduction pathways. Although the molecular mechanism remained elusive for some time, recent work has shown that YopJ acts as a serine/threonine acetyl-transferase targeting MAP2 kinases. Using Drosophila as a model system, we find that YopJ inhibits one innate immune NF-kappaB signaling pathway (IMD) but not the other (Toll). In fact, we show YopJ mediated serine/threonine acetylation and inhibition of dTAK1, the critical MAP3 kinase in the IMD pathway. Acetylation of critical serine/threonine residues in the activation loop of Drosophila TAK1 blocks phosphorylation of the protein and subsequent kinase activation. In addition, studies in mammalian cells show similar modification and inhibition of hTAK1. These data present evidence that TAK1 is a target for YopJ-mediated inhibition

Directionality of the Relationship Between Depressive Symptom Dimensions and C-Reactive Protein in Patients With Acute Coronary Syndromes

Objective: Previous theoretical models predict that elevated inflammation may predict later depressive symptoms, but bidirectional associations are possible. We examined whether depressive symptoms or inflammation predicts change in the other for a 3-month period in a sample of adults with acute coronary syndromes (ACS). Methods: During hospitalization for their index ACS event (baseline) and then again 1 and 3 months later, 163 post-ACS patients completed the Beck Depression Inventory, a measure of depressive symptom severity with cognitive-affective and somatic-affective subscales. C-reactive protein (CRP) was also assessed at each visit; known correlates of depression and CRP were assessed at baseline. Path analyses were conducted to evaluate prospective associations between depressive symptoms and log-transformed CRP values and whether strength and/or directionality varied by specific depressive symptom dimensions. Results: Baseline total depressive symptom severity predicted a smaller decrease in CRP from baseline to 1 month (unstandardized parameter estimates [B] = 0.04, p < .001) controlling for all covariates, as did baseline cognitive-affective depressive symptom severity (B = 0.10, p = .02). Baseline somatic-affective depressive symptom severity did not predict change in CRP (B = −0.002, p = .94). CRP did not predict 1- or 3-month change in total, cognitive-affective, or somatic-affective depressive symptom severity. The results did not differ for men and women. Conclusions: Greater cognitive-affective and total depressive symptom severity at the time of a cardiac event predicts a smaller decrease in CRP 1 month later, but there was no evidence in this study that CRP predicts change in depressive symptoms

Revisando el papel de los buitres en al interfaz de enfermedades que afectan a humanos, animales salvajes y ganado : una perspectiva africana

Vultures are a key component of an effective scavenger guild and have evolved a number of adaptations that allow them to locate and dispose of carcasses quickly and efficiently. The continuing decline of African vultures is threatening the stability of the African scavenger guild, which may result in increased carcass decomposition times and thus, more rapid development of pathogenic bacteria. The absence of competitive regulation by these apex scavengers may also result in changes in the composition of the vertebrate scavenger guild, with an increase in mammalian scavengers giving rise to increased contact rates at carcasses, which may increase the risk of viral disease transmission to humans, livestock, and other wildlife. Although the economic value of vultures in terms of the sanitation services they provide has been evaluated, their contribution to the economics of human health and veterinary care remains to be quantified. Efforts to do so are hampered by lack of data, as well as a number of confounding factors that may mask causality, such as improved disease prevention and surveillance systems. However, the circumstantial nature of the link between vultures and disease prevention should not deter efforts to conserve them, as their regulation of mammalian scavengers and the sanitation services they provide place them firmly within the sphere of One Health, thereby warranting their urgent protection. The restoration of vulture populations and the ecosystem services they provide will benefit the welfare of all humans, but particularly those who are most vulnerable to economic instability and the spillover of disease at the human-wildlife-livestock interface.This review article is a product of an investigation entitled ‘‘There is still time to save Africa’s vultures,’’ hosted and funded by the National Socio-Environmental Synthesis Center (SESYNC) in Annapolis, MD USA.https://bioone.org/journals/journal-of-raptor-researcham2022Zoology and Entomolog