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Ticks are not only bloodsucking ectoparasites but also important vectors of tick‐borne diseases (TBDs), posing significant threats to public and animal health. Domesticated animals serve as critical hosts for numerous ticks, highlighting the importance of understanding tick infestations in Taiwan. To address this knowledge gap, we conducted a nationwide survey to identify ticks on domesticated animals and associated environments in 2018 and 2019. A total of 6,205 ticks were collected from 1,337 host animals, revealing the presence of seven tick species, with Rhipicephalus microplus, and Rhipicephalus sanguineus being the dominant species. High infestation rates and widespread distribution of ticks were observed on domesticated animals, especially on dogs and cattle (yellow cattle and angus cattle), and the neighbouring grassland of yellow cattle. While this study has certain limitations, it provides valuable insights into the distribution and prevalence of ticks on domesticated animals in Taiwan and their implications for controlling TBDs. Further research is needed to comprehensively understand the complex interactions among ticks, hosts and pathogens. [ABSTRACT FROM AUTHOR]

Passive stiffness of the heart is determined largely by extracellular matrix and titin, which functions as a molecular spring within sarcomeres. Titin stiffening is associated with the development of diastolic dysfunction (DD), while augmented titin compliance appears to impair systolic performance in dilated cardiomyopathy. We found that myofibril stiffness was elevated in mice lacking histone deacetylase 6 (HDAC6). Cultured adult murine ventricular myocytes treated with a selective HDAC6 inhibitor also exhibited increased myofibril stiffness. Conversely, HDAC6 overexpression in cardiomyocytes led to decreased myofibril stiffness, as did ex vivo treatment of mouse, rat, and human myofibrils with recombinant HDAC6. Modulation of myofibril stiffness by HDAC6 was dependent on 282 amino acids encompassing a portion of the PEVK element of titin. HDAC6 colocalized with Z-disks, and proteomics analysis suggested that HDAC6 functions as a sarcomeric protein deacetylase. Finally, increased myofibril stiffness in HDAC6-deficient mice was associated with exacerbated DD in response to hypertension or aging. These findings define a role for a deacetylase in the control of myofibril function and myocardial passive stiffness, suggest that reversible acetylation alters titin compliance, and reveal the potential of targeting HDAC6 to manipulate the elastic properties of the heart to treat cardiac diseases., Introduction Stiffness of the heart is categorized as either active or passive. Active stiffness is dependent on actomyosin cross-bridge interactions, while passive stiffness is determined by myocardial extracellular matrix and [...]

Much diseased human myocardial tissue is fibrotic and stiff, which increases the work that the ventricular myocytes must perform to maintain cardiac output. The hypothesis tested is that the increased load due to greater stiffness of the substrata drives sarcomere assembly of cells, thus strengthening them. Neonatal rat ventricular myocytes (NRVM) were cultured on polyacrylamide or polydimethylsiloxane substrates with stiffness of 10 kPa, 100 kPa, or 400 kPa, or glass with stiffness of 61.9 GPa. Cell size increased with stiffness. Two signaling pathways were explored, phosphorylation of focal adhesion kinase (p-FAK) and lipids by phosphatidylinositol 4,5-bisphosphate (PIP2). Subcellular distributions of both were determined in the sarcomeric fraction by antibody localization, and total amounts were measured by Western or dot blotting, respectively. More p-FAK and PIP2 distributed to the sarcomeres of NRVM grown on stiffer substrates. Actin assembly involves the actin capping protein Z (CapZ). Both actin and CapZ dynamic exchange were significantly increased on stiffer substrates when assessed by fluorescence recovery after photobleaching (FRAP) of green fluorescent protein tags. Blunting of actin FRAP by FAK inhibition implicates linkage from mechano-signalling pathways to cell growth. Thus, increased stiffness of cardiac disease can be modeled with polymeric materials to understand how the microenvironment regulates cardiac hypertrophy. Key words: mechano-transduction, focal adhesion kinase, lipid signaling, actin assembly, substrate stiffness. Une bonne partie du tissu myocardique pathologique chez l'homme est fibrotique et rigide, ce qui augmente le travail impose aux myocytes ventriculaires pour maintenir le debit cardiaque. Nous avons teste l'hypothese selon laquelle l'augmentation de la charge provoquee par l'augmentation de la rigidite des substrats commande l'assemblage des cellules en sarcomeres, ce qui les fortifie. Nous avons mis des myocytes ventriculaires de rats nouveau-nes (MVRN) en culture sur un substrat de polyacrylamide ou de polydimethylsiloxane avec des rigidites de 10 kPa, de 100 kPa ou de 400 kPa, ou sur du verre dont la rigidite etait de 61,9 GPa. La taille des cellules augmentait en fonction de la rigidite. Nous avons etudie 2 voies de signalisation : celle de la phosphorylation de la p-FAK (<< focal adhesion kinase >>) et celle des lipides par le PIP2 (phosphatidylinositol 4,5-bisphosphate). Nous avons etabli la repartition subcellulaire de chacune d'elles dans la fraction sarcomerique a l'aide de la technique de localisation d'anticorps et nous avons mesure leur quantite totale a l'aide des techniques de buvardage de western et << en point >> (<< dot blot >>), respectivement. Plus de p-FAK et de PIP2 etaient repartis dans les sarcomeres de MVRN sur des substrats plus rigides. L'assemblage de l'actine met en jeu la proteine de coiffage de l'actine CapZ (pour << actin capping protein Z >>). L'evaluation de la recuperation de la fluorescence apres photoblanchiment (FRAP pour << fluorescence recovery after photobleaching >>) de marqueurs proteiques verts fluorescents nous a permis d'observer que les echanges dynamiques de l'actine comme de la CapZ augmentaient de facon marquee sur des substrats plus rigides. L'attenuation de la FRAP de l'actine par l'inhibition de la FAK trace un lien entre les voies de signalisation mecaniques et la croissance des cellules. Par consequent, l'augmentation de la rigidite observee en cas de maladie cardiaque peut etre modelisee a l'aide de materiaux polymeres en vue de comprendre comment le microenvironnement assure la regulation de l'hypertrophie cardiaque. [Traduit par la Redaction] Mots-cles : mecano-transduction, << focal adhesion kinase >>, signalisation lipidique, assemblage de l'actine, rigidite du substrat., Introduction The mechanical properties of the local microenvironment influence the function of cells (Yang et al. 2014). This is particularly critical following a myocardial infarction, in which stiff, fibrotic scar [...]