Publications by authors named "Pattison J"

Article Synopsis
  • Scientists have created a new way to turn special stem cells into brain cells (neurons) that behave like real neurons in humans, which helps study brain diseases.
  • They can make a lot of these neurons that stay healthy and grow for at least 150 days, showing that they are developing properly.
  • The research also shows that these neurons can express genes related to brain diseases, which makes them useful for scientists trying to understand and test treatments for these disorders.
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Background: The COVID-19 pandemic necessitated rapid implementation of continuous glucose monitoring (CGM) in the intensive care unit (ICU). Although rarely reported, perceptions from nursing staff who used the systems are critical for successful implementation and future expanded use of CGM in the inpatient setting.

Methods: A 22-item survey focused on CGM use was distributed to ICU nurses at two large academic medical centers in the United States in 2022.

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Background: There has been a spate of recent cases of human alveolar echinococcosis (AE) in Alberta, Canada. Alveolar echinococcosis is caused by , which is prevalent among coyote populations and present in domestic dogs in Alberta.

Methods And Results: Using qPCR, we estimated the seasonal fecal prevalence of in coyotes and dogs in a multiuse recreation area close to Edmonton, Alberta, where we also setup remote cameras to model seasonal changes in the overlap in temporal activity and the spatial intensity of use among coyotes, humans, and dogs, as a proxy of potential transmission.

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Ectodermal dysplasias including skin abnormalities and cleft lip/palate result from improper surface ectoderm (SE) patterning. However, the connection between SE gene regulatory networks and disease remains poorly understood. Here, we dissect human SE differentiation with multiomics and establish GRHL2 as a key mediator of early SE commitment, which acts by skewing cell fate away from the neural lineage.

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Tight regulation of protein degradation pathways is essential for maintaining cardiac homeostasis. The goal of this work was to define the role of chaperone-mediated autophagy (CMA), in cardiomyocytes. CMA acts as a selective degradation pathway of proteins using a cytosolic and lysosomal co-chaperone, HSPA8/HSC70, and the CMA-specific LAMP2A (lysosomal-associated membrane protein 2A) receptor.

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The use of diabetes technology, including insulin pumps, continuous glucose monitoring devices, and automated insulin delivery systems, has increased significantly in recent years. As more people with diabetes adopt technology in the outpatient setting, we are seeing these devices more frequently in the inpatient setting. This review offers best-practice guidelines for the continuation of personal diabetes technology use in the inpatient setting.

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Proper ectodermal patterning during human development requires previously identified transcription factors such as GATA3 and p63, as well as positional signalling from regional mesoderm. However, the mechanism by which ectoderm and mesoderm factors act to stably pattern gene expression and lineage commitment remains unclear. Here we identify the protein Gibbin, encoded by the Xia-Gibbs AT-hook DNA-binding-motif-containing 1 (AHDC1) disease gene, as a key regulator of early epithelial morphogenesis.

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Chaperone-mediated autophagy (CMA) is a chaperone-dependent process of selective cytosolic protein turnover that targets specific proteins to lysosomes for degradation. Enhancing protein degradation mechanisms has been shown to be beneficial in multiple models of cardiac disease, including myocardial infarction (MI) and ischemia-reperfusion (I/R) injury. However, the causal role of CMA in cardiomyocyte injury and death is largely unknown.

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This article presents findings collected in 2016-2017 from a multi-method ethnographic study of Shirebrook, Derbyshire in the English East Midlands, examining the narratives used by the local authority (LA) and local residents that construct immigration as a social problem. In doing so, it contributes to the literature on race and migration by extending analysis beyond metropolitan localities with long histories of multi-ethnic settlement, to consider a relatively small, peripheral former colliery town. The paper demonstrates how migration is framed as a social problem by central government funding streams with consequences for localities, and the influence this has on local narratives of social change.

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With the rise in popularity of media pieces depicting alternative sexual/relationship preferences, there has been a rise in interest in kink and BDSM (Sprott & Berkey, 2015), which corresponds with research suggesting that approximately 20% of Americans have been in a consensually non-monogamous relationship (Haupert et al., 2016). Despite this growing popularity, these populations are often stigmatized and misunderstood (Bettinger, 2002).

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Defects in the activity of the proteasome or its regulators are linked to several pathologies, including neurodegenerative diseases. We hypothesize that proteasome heterogeneity and its selective partners vary across brain regions and have a significant impact on proteasomal catalytic activities. Using neuronal cell cultures and brain tissues obtained from mice, we compared proteasomal activities from two distinct brain regions affected in neurodegenerative diseases, the striatum and the hippocampus.

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If the resources used to wage wars could be spent elsewhere and save more lives, does this mean that wars are unjustified? This article considers this question, which has been largely overlooked by Just War Theorists and pacifists. It focuses on whether the opportunity costs of war lead to a form of pacifism, which it calls 'Opportunity Costs Pacifism'. The article argues that Opportunity Costs Pacifism is, at the more ideal level, compelling.

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Background And Objectives: Minimal change disease is an important cause of nephrotic syndrome in adults. Corticosteroids are first-line therapy for minimal change disease, but a prolonged course of treatment is often required and relapse rates are high. Patients with minimal change disease are therefore often exposed to high cumulative corticosteroid doses and are at risk of associated adverse effects.

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Anthracnose fruit rot and anthracnose crown rot (ACR) caused by two species complexes of the fungus referred to as and , respectively, are major pathogens of strawberry in North Carolina. Anthracnose epidemics are common when susceptible cultivars and asymptomatic planting stocks carrying quiescent infection or hemibiotrophic infection (HBI) are planted. The main objective of this study was to assess resistance to HBI and ACR in strawberry.

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Tissue development results from lineage-specific transcription factors (TFs) programming a dynamic chromatin landscape through progressive cell fate transitions. Here, we define epigenomic landscape during epidermal differentiation of human pluripotent stem cells (PSCs) and create inference networks that integrate gene expression, chromatin accessibility, and TF binding to define regulatory mechanisms during keratinocyte specification. We found two critical chromatin networks during surface ectoderm initiation and keratinocyte maturation, which are driven by TFAP2C and p63, respectively.

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Objective: Atherosclerosis is a major cause of cardiovascular disease. Monocyte-endothelial cell interactions are partly mediated by expression of monocyte CX3CR1 and endothelial cell fractalkine (CX3CL1). Interrupting the interaction between this ligand-receptor pair should reduce monocyte binding to the endothelial wall and reduce atherosclerosis.

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Human embryonic stem cell (hESC) differentiation promises advances in regenerative medicine, yet conversion of hESCs into transplantable cells or tissues remains poorly understood. Using our keratinocyte differentiation system, we employ a multi-dimensional genomics approach to interrogate the contributions of inductive morphogens retinoic acid and bone morphogenetic protein 4 (BMP4) and the epidermal master regulator p63 (encoded by TP63) during surface ectoderm commitment. In contrast to other master regulators, p63 effects major transcriptional changes only after morphogens alter chromatin accessibility, establishing an epigenetic landscape for p63 to modify.

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Information on the inheritance of resistance to Colletotrichum gloeosporioides and C. acutatum hemibiotrophic infections (HBI) in strawberry leaf tissue and the genetic control of anthracnose crown rot (ACR) in crown tissue are relatively unknown. Six parental genotypes were crossed in a half-diallel mating design to generate 15 full-sib families.

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In this Letter, affiliation number 1 was originally missing from the HTML; the affiliations were missing for author Ming-Yow Hung in the HTML; and the Fig. 4 legend erroneously referred to panels a-h, instead of a-g. These errors have been corrected online.

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Oxidized phospholipids (OxPL) are ubiquitous, are formed in many inflammatory tissues, including atherosclerotic lesions, and frequently mediate proinflammatory changes . Because OxPL are mostly the products of non-enzymatic lipid peroxidation, mechanisms to specifically neutralize them are unavailable and their roles in vivo are largely unknown. We previously cloned the IgM natural antibody E06, which binds to the phosphocholine headgroup of OxPL, and blocks the uptake of oxidized low-density lipoprotein (OxLDL) by macrophages and inhibits the proinflammatory properties of OxPL.

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Ischemic preconditioning (IPC), which involves intermittent periods of ischemia followed by reperfusion, is an effective clinical intervention that reduces the risk of myocardial injury and confers ischemic tolerance to skeletal muscle. Repeated bouts of IPC have been shown to stimulate long-term changes vascular function, however, it is unclear what metabolic adaptations may occur locally in the muscle. Therefore, we investigated 7 days of bilateral lower limb IPC (4 × 5 min) above limb occlusion pressure (220 mmHg; = 10), or sham (20 mmHg; = 10), on local muscle oxidative capacity and microvascular blood flow.

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Cardiac diseases including hypertrophic and ischemic cardiomyopathies are increasingly being reported to accumulate misfolded proteins and damaged organelles. These findings have led to an increasing interest in protein degradation pathways, like autophagy, which are essential not only for normal protein turnover but also in the removal of misfolded and damaged proteins. Emerging evidence suggests a previously unprecedented role for autophagic processes in cardiac physiology and pathology.

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Apolipoprotein A-I binding protein (AIBP) has been shown to augment cholesterol efflux from endothelial cells and macrophages. In zebrafish and mice, AIBP-mediated regulation of cholesterol levels in the plasma membrane of endothelial cells controls angiogenesis. The goal of this work was to evaluate metabolic changes and atherosclerosis in AIBP loss-of-function and gain-of-function animal studies.

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Patients with traumatic intracranial hemorrhage (ICH) with a clinical indication for antithrombotic medication present a clinical dilemma, burdened by the task of weighing the risks of hemorrhage expansion against the risk of thrombosis. We sought to determine the effect of subdural hemorrhage on the risk of hemorrhage expansion after administration of antithrombotic medication. Medical records of 1626 trauma patients admitted with traumatic ICH between March 1, 2008, and March 31, 2013, to a Level I trauma center were retrospectively reviewed.

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