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"Richard, L."
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Olfactory dysfunction in neurodegenerative diseases: is there a common pathological substrate?
In patients with neurodegenerative diseases, there is a spectrum of smell dysfunction ranging from severe loss, as seen in Alzheimer's disease and Parkinson's disease, to relatively little loss, as seen in progressive supranuclear palsy. Given the ubiquitous but varying degrees of olfactory dysfunction among such diseases, it is conceivable that differential disruption of a common primordial neuropathological substrate causes these differences in olfactory function. For example, the amount of damage to forebrain neurotransmitter and neuromodulator circuits, most notably those involving cholinergic transmission, appears to be correlated with quantitative smell test scores across a wide range of neurodegenerative diseases. Thus, a key question is whether damage to such a substrate is the basis for the perceptual differences in olfaction or whether disease-specific or other entities, such as respiratory infections or pollution, are responsible. In light of the early preclinical onset of smell deficits in many neurodegenerative diseases, the answer to this question might provide crucial insight into the cause of disease pathology at its earliest stages of development.
Journal Article
Pathologies of the mind/body interface : exploring the curious domain of the psychosomatic disorders
\"Unlike other texts on the subject, this book aims to provide a well-integrated approach to the diagnosis and treatment of the pervasive effects of the mind/body splitting that lead to somatoform disorders. Kradin explores the spectrum of currently recognized disorders with reference to the DSM-V formulations, as well as the medical, psychobiological, psychodynamic, and cognitive-behavioral approaches to these disorders. Additionally, he explores the role of developmental trauma in pathogenesis, and how stress, modulation, body-oriented therapies, Jungian-oriented embodied imaginal work, and psychopharmacological interventions can be integrated in the treatment of these disorders\"--Provided by publisher.
Book
Maturation of Induced Pluripotent Stem Cell Derived Hepatocytes by 3D-Culture
Induced pluripotent stem cell derived hepatocytes (IPSC-Heps) have the potential to reduce the demand for a dwindling number of primary cells used in applications ranging from therapeutic cell infusions to in vitro toxicology studies. However, current differentiation protocols and culture methods produce cells with reduced functionality and fetal-like properties compared to adult hepatocytes. We report a culture method for the maturation of IPSC-Heps using 3-Dimensional (3D) collagen matrices compatible with high throughput screening. This culture method significantly increases functional maturation of IPSC-Heps towards an adult phenotype when compared to conventional 2D systems. Additionally, this approach spontaneously results in the presence of polarized structures necessary for drug metabolism and improves functional longevity to over 75 days. Overall, this research reveals a method to shift the phenotype of existing IPSC-Heps towards primary adult hepatocytes allowing such cells to be a more relevant replacement for the current primary standard.
Journal Article
Emerging biology of sphingosine-1-phosphate: its role in pathogenesis and therapy
Membrane sphingolipids are metabolized to sphingosine-1-phosphate (S1P), a bioactive lipid mediator that regulates many processes in vertebrate development, physiology, and pathology. Once exported out of cells by cell-specific transporters, chaperone-bound S1P is spatially compartmentalized in the circulatory system. Extracellular S1P interacts with five GPCRs that are widely expressed and transduce intracellular signals to regulate cellular behavior, such as migration, adhesion, survival, and proliferation. While many organ systems are affected, S1P signaling is essential for vascular development, neurogenesis, and lymphocyte trafficking. Recently, a pharmacological S1P receptor antagonist has won approval to control autoimmune neuroinflammation in multiple sclerosis. The availability of pharmacological tools as well as mouse genetic models has revealed several physiological actions of S1P and begun to shed light on its pathological roles. The unique mode of signaling of this lysophospholipid mediator is providing novel opportunities for therapeutic intervention, with possibilities to target not only GPCRs but also transporters, metabolic enzymes, and chaperones.
Journal Article
Immune modulation by bacterial outer membrane vesicles
Key Points
Outer membrane vesicles (OMVs) are bacterial nanoparticles that are naturally produced during bacterial growth both
in vitro
and
in vivo
. OMVs can interact with many host cell types — including mucosal epithelial cells, myeloid cells and cells distal to the site of OMV entry — and thus have a range of inflammatory outcomes.
Clinical studies have demonstrated the presence of OMVs in host tissues, suggesting that they have potentially pathogenic roles in various infectious diseases, particularly in those of a chronic nature. OMVs may also be important as previously unrecognized mediators of the inflammatory pathologies that accompany certain infectious diseases of idiopathic origin.
OMVs can enter non-phagocytic human epithelial cells via multiple mechanisms including lipid raft-dependent and lipid raft-independent endocytosis, in addition to dynamin-dependent and dynamin-independent mechanisms. When they are present inside cells, OMVs migrate to early endosomes and are detected by the host intracellular immune receptor nucleotide-binding oligomerization domain-containing protein 1 (NOD1), which results in the induction of autophagy and the generation of a pro-inflammatory response.
When OMVs are within epithelial cells, their protein cargo is processed and OMV peptides are released in exosomes. These peptide-laden exosomes can then be taken up by professional antigen-presenting cells and presented to T cells, resulting in the generation of antigen-specific adaptive immune responses.
In addition to their pro-inflammatory effects, OMVs can modulate or even suppress immune cell responses through their direct effects on host cells. Evidence is also emerging that OMVs produced by commensal bacteria may have roles in immune tolerance and other physiological functions of benefit to the host.
OMVs are highly stable, non-infectious and genetically tractable nanoparticles that contain the major immunogenic proteins of the parent bacterium and are able to elicit responses from both arms of the immune system, thus making them highly suited as vaccines and adjuvants.
Outer membrane vesicles (OMVs) are produced by bacteria and can interact with leukocytes and other host cells to shape the immune response during infection. OMVs can have both pro-inflammatory and anti-inflammatory effects; in this Review, the authors discuss how they may contribute to human diseases and also their potential as vaccine adjuvants.
Gram-negative bacteria shed extracellular outer membrane vesicles (OMVs) during their normal growth both
in vitro
and
in vivo
. OMVs are spherical, bilayered membrane nanostructures that contain many components found within the parent bacterium. Until recently, OMVs were dismissed as a by-product of bacterial growth; however, findings within the past decade have revealed that both pathogenic and commensal bacteria can use OMVs to manipulate the host immune response. In this Review, we describe the mechanisms through which OMVs induce host pathology or immune tolerance, and we discuss the development of OMVs as innovative nanotechnologies.
Journal Article
An Official American Thoracic Society/European Respiratory Society Policy Statement: Enhancing Implementation, Use, and Delivery of Pulmonary Rehabilitation
Pulmonary rehabilitation (PR) has demonstrated physiological, symptom-reducing, psychosocial, and health economic benefits for patients with chronic respiratory diseases, yet it is underutilized worldwide. Insufficient funding, resources, and reimbursement; lack of healthcare professional, payer, and patient awareness and knowledge; and additional patient-related barriers all contribute to the gap between the knowledge of the science and benefits of PR and the actual delivery of PR services to suitable patients.
The objectives of this document are to enhance implementation, use, and delivery of pulmonary rehabilitation to suitable individuals worldwide.
Members of the American Thoracic Society (ATS) Pulmonary Rehabilitation Assembly and the European Respiratory Society (ERS) Rehabilitation and Chronic Care Group established a Task Force and writing committee to develop a policy statement on PR. The document was modified based on feedback from expert peer reviewers. After cycles of review and revisions, the statement was reviewed and formally approved by the Board of Directors of the ATS and the Science Council and Executive Committee of the ERS.
This document articulates policy recommendations for advancing healthcare professional, payer, and patient awareness and knowledge of PR, increasing patient access to PR, and ensuring quality of PR programs. It also recommends areas of future research to establish evidence to support the development of an updated funding and reimbursement policy regarding PR.
The ATS and ERS commit to undertake actions that will improve access to and delivery of PR services for suitable patients. They call on their members and other health professional societies, payers, patients, and patient advocacy groups to join in this commitment.
Journal Article