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This book is autoethnographic account of one beginning teacher's struggle to transform his future teaching identity by unpacking the bruising encounters that shaped him as a student.

Key Points Across evolutionary time, inflammatory responses and depressive symptoms were part of an integrated adaptive response to pathogens that facilitated fighting infection, healing wounds and avoiding subsequent pathogen exposure in the pathogen-rich environments in which humans evolved. In the more sanitary environments of the modern world, the relationship between inflammatory pathways and the brain may drive depression and contribute to non-response to antidepressant medication. Increased levels of inflammatory cytokines and induction of their signalling pathways as well as activation of different immune cell subsets has been detected in the brain and peripheral blood of a subgroup of patients with depression. C-reactive protein (CRP), tumour necrosis factor, interleukin-1β (IL-1β) and IL-6 appear to be the most reliably elevated inflammatory markers in the peripheral blood of subjects with depression. Activation of the inflammasome by stress-induced, non-pathogenic stimuli, including damage-associated molecular patterns as well as microbial-associated molecular patterns elaborated from the gut microbiome, may drive peripheral inflammatory responses, which are then transmitted to the brain by trafficking of activated monocytes. Inflammation impacts several neurotransmitter systems in the brain, including serotonin, dopamine and glutamate pathways, as well as the kynurenine pathway, which generates the neurotoxic metabolite quinolinic acid. Neuroimaging studies have demonstrated that disruption of neurotransmitter pathways is associated with inflammation-induced alterations in brain circuits that mediate motivation and motor activity as well as anxiety, arousal and alarm. Activation of effector T cells during stress can prevent the development of depressive- and anxiety-like behaviour in mice. These effects may be mediated by the trafficking of effector T cells to the meningeal space where they produce IL-4, which supports anti-inflammatory responses while also stimulating the production of growth factors in the brain that support neural plasticity and resilience. Studies in depression suggest that inflammatory biomarkers, such as CRP, can be used to enrich samples for anti-inflammatory clinical trials for depression that target inflammation-related symptoms such as anhedonia and anxiety, thereby supporting intelligent trial design. Though still in development, imaging of neuroinflammation will help establish a 'target' in the brain to further facilitate the testing of anti-inflammatory therapies for depression. In this Review, the authors relate the growing appreciation of the neuroimmune circuits that link inflammatory and immune responses with depressive behaviours. They explore the evolutionary basis of this neuroimmune link and discuss how a better understanding of these pathways may lead to new therapies that treat depression by targeting the immune system. Crosstalk between inflammatory pathways and neurocircuits in the brain can lead to behavioural responses, such as avoidance and alarm, that are likely to have provided early humans with an evolutionary advantage in their interactions with pathogens and predators. However, in modern times, such interactions between inflammation and the brain appear to drive the development of depression and may contribute to non-responsiveness to current antidepressant therapies. Recent data have elucidated the mechanisms by which the innate and adaptive immune systems interact with neurotransmitters and neurocircuits to influence the risk for depression. Here, we detail our current understanding of these pathways and discuss the therapeutic potential of targeting the immune system to treat depression.

Engineer Jean-Baptiste Baratte is tasked with emptying an overflowing cemetery in Paris in 1785, work he considers noble until he begins to suspect that the destruction of the cemetery parallels his own fate and the demise of social order.

Increasing data indicate that inflammation and alterations in glutamate neurotransmission are two novel pathways to pathophysiology in mood disorders. The primary goal of this review is to illustrate how these two pathways may converge at the level of the glia to contribute to neuropsychiatric disease. We propose that a combination of failed clearance and exaggerated release of glutamate by glial cells during immune activation leads to glutamate increases and promotes aberrant extrasynaptic signaling through ionotropic and metabotropic glutamate receptors, ultimately resulting in synaptic dysfunction and loss. Furthermore, glutamate diffusion outside the synapse can lead to the loss of synaptic fidelity and specificity of neurotransmission, contributing to circuit dysfunction and behavioral pathology. This review examines the fundamental role of glia in the regulation of glutamate, followed by a description of the impact of inflammation on glial glutamate regulation at the cellular, molecular, and metabolic level. In addition, the role of these effects of inflammation on glia and glutamate in mood disorders will be discussed along with their translational implications.

Tim, an affable young man with modest ambition, is infatuated with Maud the moment they meet in the University Sailing Club. Who else could have entered Tim's life the way Maud did? The beautiful girl who fell past him, lay seemingly dead on the ground, than stood and walked. That is how it began. A career scientist who betrays little of herself, Maud is found by some to be enchanting, by others distant, and there is little to suggest that she has any need of anyone. Tim ties his life to hers, but slowly the marriage unravels as she quietly refuses to conform to the conventional demands of wife and mother. What begins as a story of a mismatched relationship accelerates into unforgiving judgment when a sudden tragedy forces Tim and Maud to confront the harsh reality of their life together. Walking away from her marriage, Maud sets out to sea alone, challenging nature with her own mind and body to protect her. Equal parts bold exploration of the unknowable in others and a brilliant critique of love and motherhood, The Crossing is a thrilling tale of one woman's resolute quest to seize control of her life and fate. - From inside cover.

The term ‘fibroblast’ often serves as a catch-all for a diverse array of mesenchymal cells, including perivascular cells, stromal progenitor cells and bona fide fibroblasts. Although phenotypically similar, these subpopulations are functionally distinct, maintaining tissue integrity and serving as local progenitor reservoirs. In response to tissue injury, these cells undergo a dynamic fibroblast–myofibroblast transition, marked by extracellular matrix secretion and contraction of actomyosin-based stress fibres. Importantly, whereas transient activation into myofibroblasts aids in tissue repair, persistent activation triggers pathological fibrosis. In this Review, we discuss the roles of mechanical cues, such as tissue stiffness and strain, alongside cell signalling pathways and extracellular matrix ligands in modulating myofibroblast activation and survival. We also highlight the role of epigenetic modifications and myofibroblast memory in physiological and pathological processes. Finally, we discuss potential strategies for therapeutically interfering with these factors and the associated signal transduction pathways to improve the outcome of dysregulated healing.Fibroblasts undergo transient activation into myofibroblasts to restore homeostasis to injured tissues. This Review explores the influence of mechanical cues and epigenetic modifications on (myo)fibroblast activation and memory and discusses potential therapeutic prevention of persistent myofibroblast activation in fibrosis.

One rain-swept February night in 1809, an unconscious man is carried into a house in Somerset. He is Captain John Lacroix, home from Britain's disastrous campaign against Napoleon's forces in Spain. Gradually Lacroix recovers his health, but not his peace of mind - he cannot talk about the war or face the memory of what happened in a village on the gruelling retreat to Corunna. After the command comes to return to his regiment, he sets out instead for the Hebrides, with the vague intent of reviving his musical interests and collecting local folksongs. Lacroix sails north incognito, unaware that he has far worse to fear than being dragged back to the army: a vicious English corporal and a Spanish officer are on his trail, with orders to kill. The haven he finds on a remote island with a family of free-thinkers and the sister he falls for are not safe, at all.--Provided by publisher.

Although intermittent increases in inflammation are critical for survival during physical injury and infection, recent research has revealed that certain social, environmental and lifestyle factors can promote systemic chronic inflammation (SCI) that can, in turn, lead to several diseases that collectively represent the leading causes of disability and mortality worldwide, such as cardiovascular disease, cancer, diabetes mellitus, chronic kidney disease, non-alcoholic fatty liver disease and autoimmune and neurodegenerative disorders. In the present Perspective we describe the multi-level mechanisms underlying SCI and several risk factors that promote this health-damaging phenotype, including infections, physical inactivity, poor diet, environmental and industrial toxicants and psychological stress. Furthermore, we suggest potential strategies for advancing the early diagnosis, prevention and treatment of SCI. Systemic chronic inflammation increases with age and is linked to the development of several diseases, as presented in this Perspective.

Ecotourism Development in Costa Rica: The Search for Oro Verde, by Andrew P. Miller, examines the use of ecotourism as a development strategy in Costa Rica and its applicability to other Central American states. Ecotourism provides an important environmental check on industry, giving the environment a voice by making its preservation an economic necessity due to the number of people who derive their income from it. The move away from agriculture to ecotourism is a natural fit because many of those who are engaged in agriculture have extensive knowledge of plants and animals that can be utilized by the ecotourism industry.

The muscarinic receptor agonist xanomeline has antipsychotic properties without dopamine blockade. Cholinergic adverse events limit its use. When xanomeline was combined with trospium to limit peripheral effects, scores were better on measures of schizophrenia than were scores with placebo over a period of 5 weeks.