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"Watkins, C"
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Trees in art
In this superbly illustrated book, Charles Watkins explores the myth and magic of arboreal art. Enter the groves of the classical world, from Daphne's metamorphosis into a laurel tree to the gardens of Pompeii. The tree in sacred art is represented in master works by Botticelli and Michelangelo. The oak as a symbol of nationhood and liberty across Europe is revealed. The mystery and drama of forest interiors, the formal beauty of avenues of trees, the representation of forestry over the ages and the world of `more than real' trees in the fantastic and surreal art of Arcimboldo, William Blake, Arthur Rackham and Salvador Dali are each illuminated in fascinating detail, coming right up to date with Giuseppe Penone and Ai Wei Wei. Watkins also elucidates the practice of genius in how artists learned to draw trees. 0Each thematic chapter takes a breathtaking journey through centuries of artists' engagement and fascination with a natural form that seems to allegorize or mirror the human journey through life. Drawing on the author's deep knowledge of the history and ecology of trees, Trees in Art shows that we can learn much about ourselves from the art of trees.
Book
Chemoptogenetic damage to mitochondria causes rapid telomere dysfunction
Reactive oxygen species (ROS) play important roles in aging, inflammation, and cancer. Mitochondria are an important source of ROS; however, the spatiotemporal ROS events underlying oxidative cellular damage from dysfunctional mitochondria remain unresolved. To this end, we have developed and validated a chemoptogenetic approach that uses a mitochondrially targeted fluorogen-activating peptide (Mito-FAP) to deliver a photosensitizer MG-2I dye exclusively to this organelle. Light-mediated activation (660 nm) of the Mito-FAP–MG-2I complex led to a rapid loss of mitochondrial respiration, decreased electron transport chain complex activity, and mitochondrial fragmentation. Importantly, one round of singlet oxygen produced a persistent secondary wave of mitochondrial superoxide and hydrogen peroxide lasting for over 48 h after the initial insult. By following ROS intermediates, we were able to detect hydrogen peroxide in the nucleus through ratiometric analysis of the oxidation of nuclear cysteine residues. Despite mitochondrial DNA (mtDNA) damage and nuclear oxidative stress induced by dysfunctional mitochondria, there was a lack of gross nuclear DNA strand breaks and apoptosis. Targeted telomere analysis revealed fragile telomeres and telomere loss as well as 53BP1-positive telomere dysfunction-induced foci (TIFs), indicating that DNA double-strand breaks occurred exclusively in telomeres as a direct consequence of mitochondrial dysfunction. These telomere defects activated ataxia-telangiectasia mutated (ATM)-mediated DNA damage repair signaling. Furthermore, ATM inhibition exacerbated the Mito-FAP–induced mitochondrial dysfunction and sensitized cells to apoptotic cell death. This profound sensitivity of telomeres through hydrogen peroxide induced by dysregulated mitochondria reveals a crucial mechanism of telomere–mitochondria communication underlying the pathophysiological role of mitochondrial ROS in human diseases.
Journal Article
The wiley international handbook of clinical supervision
This is the first handbook to examine the theory, research, and practice of clinical supervision from an international, multi-disciplinary perspective.
* Focuses on conceptual and research foundations, practice foundations, core skills, measuring competence, and supervision perspectives
* Includes original articles by contributors from around the world, including Australia, Finland, Hong Kong, Slovenia, South Africa, Sweden, the United Kingdom, and the United States
* Addresses key aspects of supervision, including competency frameworks, evidence-based practice, supervisory alliances, qualitative and quantitative assessment, diversity-sensitive supervision, and more
* Features timely and authoritative coverage of the latest research in the field and novel ideas for clinical practice
eBook
Gratitude and the good life : toward a psychology of appreciation
This book provides clear and sometimes surprising answers to why gratitude is important to living well. The science of gratitude has shown much growth in the last ten years, and there is now sufficient evidence to suggest that gratitude is one of the most important components of the good life. Both correlational and experimental studies have provided support for the theory that gratitude enhances well-being.
Book
Magnify is a universal molecular anchoring strategy for expansion microscopy
Expansion microscopy enables nanoimaging with conventional microscopes by physically and isotropically magnifying preserved biological specimens embedded in a crosslinked water-swellable hydrogel. Current expansion microscopy protocols require prior treatment with reactive anchoring chemicals to link specific labels and biomolecule classes to the gel. We describe a strategy called Magnify, which uses a mechanically sturdy gel that retains nucleic acids, proteins and lipids without the need for a separate anchoring step. Magnify expands biological specimens up to 11 times and facilitates imaging of cells and tissues with effectively around 25-nm resolution using a diffraction-limited objective lens of about 280 nm on conventional optical microscopes or with around 15 nm effective resolution if combined with super-resolution optical fluctuation imaging. We demonstrate Magnify on a broad range of biological specimens, providing insight into nanoscopic subcellular structures, including synaptic proteins from mouse brain, podocyte foot processes in formalin-fixed paraffin-embedded human kidney and defects in cilia and basal bodies in drug-treated human lung organoids.
Expansion microscopy with gel-anchored molecules enables simultaneous retention of nucleic acids, proteins and lipids in diverse tissue types.
Journal Article
Infiltration of inflammatory macrophages and neutrophils and widespread pyroptosis in lung drive influenza lethality in nonhuman primates
Severe influenza kills tens of thousands of individuals each year, yet the mechanisms driving lethality in humans are poorly understood. Here we used a unique translational model of lethal H5N1 influenza in cynomolgus macaques that utilizes inhalation of small-particle virus aerosols to define mechanisms driving lethal disease. RNA sequencing of lung tissue revealed an intense interferon response within two days of infection that resulted in widespread expression of interferon-stimulated genes, including inflammatory cytokines and chemokines. Macaques with lethal disease had rapid and profound loss of alveolar macrophages (AMs) and infiltration of activated CCR2 + CX3CR1 + interstitial macrophages (IMs) and neutrophils into lungs. Parallel changes of AMs and neutrophils in bronchoalveolar lavage (BAL) correlated with virus load when compared to macaques with mild influenza. Both AMs and IMs in lethal influenza were M1-type inflammatory macrophages which expressed neutrophil chemotactic factors, while neutrophils expressed genes associated with activation and generation of neutrophil extracellular traps (NETs). NETs were prominent in lung and were found in alveolar spaces as well as lung parenchyma. Genes associated with pyroptosis but not apoptosis were increased in lung, and activated inflammatory caspases, IL-1β and cleaved gasdermin D (GSDMD) were present in bronchoalveolar lavage fluid and lung homogenates. Cleaved GSDMD was expressed by lung macrophages and alveolar epithelial cells which were present in large numbers in alveolar spaces, consistent with loss of epithelial integrity. Cleaved GSDMD colocalized with viral NP-expressing cells in alveoli, reflecting pyroptosis of infected cells. These novel findings reveal that a potent interferon and inflammatory cascade in lung associated with infiltration of inflammatory macrophages and neutrophils, elaboration of NETs and cell death by pyroptosis mediates lethal H5N1 influenza in nonhuman primates, and by extension humans. These innate pathways represent promising therapeutic targets to prevent severe influenza and potentially other primary viral pneumonias in humans.
Journal Article
Taos Society of Artists
\"\"A lavishly illustrated two-volume study of the Taos Society of Artists. Essays on the TSA and its founding plus scholarly biographical and art historical essays on twelve TSA artists with exemplary works of the artists studied\"-Provided by publisher\"-- Provided by publisher.
BOOK
Mesenchymal stem cells use extracellular vesicles to outsource mitophagy and shuttle microRNAs
Mesenchymal stem cells (MSCs) and macrophages are fundamental components of the stem cell niche and function coordinately to regulate haematopoietic stem cell self-renewal and mobilization. Recent studies indicate that mitophagy and healthy mitochondrial function are critical to the survival of stem cells, but how these processes are regulated in MSCs is unknown. Here we show that MSCs manage intracellular oxidative stress by targeting depolarized mitochondria to the plasma membrane via arrestin domain-containing protein 1-mediated microvesicles. The vesicles are then engulfed and re-utilized via a process involving fusion by macrophages, resulting in enhanced bioenergetics. Furthermore, we show that MSCs simultaneously shed micro RNA-containing exosomes that inhibit macrophage activation by suppressing Toll-like receptor signalling, thereby de-sensitizing macrophages to the ingested mitochondria. Collectively, these studies mechanistically link mitophagy and MSC survival with macrophage function, thereby providing a physiologically relevant context for the innate immunomodulatory activity of MSCs.
The physiological role of crosstalk between mesenchymal stem cells (MSC) and macrophages is unclear. Here, Phinney
et al
. show that MSCs transfer mitochondria to macrophages under oxidative stress, and desensitize macrophages to mitochondria by using microvesicles to repress Toll receptor signalling.
Journal Article