Publications by authors named "Jane Howard"

There is increasing recognition in the field of health and social care research that community-engaged methods should include patients and the public throughout the research process. Therefore, individuals from all backgrounds should be involved in the research. We explored the public and patient engagement experience in research and how researchers and community groups can work together to make the research process more inclusive and sustainable.

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  • * Deleting the Mir142 gene leads to changes in intestinal ILC populations, notably missing T-bet cells and altering ILC3 characteristics, which is linked to reduced colitis severity and impaired development of gut-associated lymphoid tissues.
  • * The research identifies miR-142 as a key regulator in ILC3s, impacting their cellular behavior in the gut, while also increasing IL-17A production when Mir142 is absent, highlighting its critical role in intestinal immune responses.
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  • - The systematic review examines how type 2 diabetes mellitus (T2DM) raises the risk of late-onset Alzheimer's dementia (LOAD) by analyzing common metabolic mechanisms that connect the two conditions, including insulin signaling and inflammation.
  • - It consolidates findings from both human and animal studies, evaluating 923 publications for pathophysiological mechanisms and 357 for genomic associations and epigenetic modifications, ultimately identifying 138 gene loci linked to risk factors.
  • - The gathered evidence emphasizes the interplay between brain insulin resistance, neuroinflammation, and metabolic issues in T2DM and LOAD, suggesting pathways for future longitudinal research on their interconnected risks.
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  • Feline mammary adenocarcinomas (FMA) are aggressive tumors with few treatment options, and this study aimed to explore the role of specific miRNAs in these tumors as potential cancer biomarkers found in extracellular vesicles (EVs) from feline plasma.
  • Researchers examined tumor tissue and plasma from 10 felines, identifying 8 notable miRNAs through RT-qPCR analysis, with a focus on miR-20a and miR-15b, which showed increased expression in tumors but decreased in EVs from FMA compared to healthy controls.
  • The findings suggest that these miRNAs can be detected in both tissue and plasma EVs and may serve as non-invasive biomarkers for diagnosing FMA, indicating the need
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  • Extracellular vesicles (EVs) are tiny particles that transport biological materials in the body and have been extensively studied under the MISEV framework for standardizing research in this area since 2018.
  • Research has primarily focused on human EVs, but there's growing interest in applying the same standards to animal models, particularly felines, for comparative disease studies.
  • The study found that EVs isolated from healthy humans and felines shared similar characteristics, suggesting that the MISEV guidelines can be effectively applied to feline EV research, potentially benefiting our understanding of diseases in both species.
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Cardiovascular diseases (CVDs) are responsible for most pre-mature deaths worldwide, contributing significantly to the global burden of disease and its associated costs to individuals and healthcare systems. Obesity and associated metabolic inflammation underlie development of several major health conditions which act as direct risk factors for development of CVDs. Immune system responses contribute greatly to CVD development and progression, as well as disease resolution.

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  • Mammalian innate lymphoid cells (ILCs) are essential for maintaining mucosal surface integrity and play significant roles in both normal and diseased conditions like inflammatory bowel disease (IBD).
  • Key transcription factors like T-bet and RORγt are crucial for regulating different ILC subsets, impacting their development and function.
  • The review discusses the balance between mature ILC1 and ILC3 and suggests that understanding the interactions between these transcription factors and other molecular pathways could lead to new therapeutic options for treating human diseases.
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  • - T-bet is a key transcription factor for CD4 T 1 cells and is also present in other CD4 T cell types, but its role in their differentiation and function is not fully understood.
  • - To investigate T-bet expression, researchers tracked its presence using a special mouse model, revealing a unique subset of CD4 T cells that show naïve cell features while being distinct from traditional naïve and memory T cells.
  • - These T-bet-experienced cells are inclined to develop into T 1 cells, produce a specific cytokine called IFN-γ upon activation, and are less likely to change into other T cell types, indicating that lineage factors can influence T cell responses even without standard activation markers.
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Triple negative breast cancer (TNBC) is a rare, highly metastatic subtype of breast cancer that typically develops tumours of a high histological grade. As TNBC is negative for the oestrogen, progesterone and HER2 receptors it is also not eligible for targeted hormonal therapies. Therefore, those diagnosed with TNBC are faced with a very poor prognosis.

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Innate lymphoid cells (ILC) play a significant role in the intestinal immune response and T-bet CD127 group 1 cells (ILC1) have been linked to the pathogenesis of human inflammatory bowel disease (IBD). However, the functional importance of ILC1 in the context of an intact adaptive immune response has been controversial. In this report we demonstrate that induced depletion of T-bet using a Rosa26-Cre-ERT2 model resulted in the loss of intestinal ILC1, pointing to a post-developmental requirement of T-bet expression for these cells.

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Triple negative breast cancer (TNBC) is an aggressive cancer, particularly prone to metastasis and is associated with poor survival outcomes. The key to unravelling the aggressiveness of TNBC lies in decoding the mechanism by which it metastasises. Cofilin-1 is a well-studied member of the cofilin family, involved in actin depolymerisation.

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Innate lymphoid cells are central to the regulation of immunity at mucosal barrier sites, with group 2 innate lymphoid cells (ILC2s) being particularly important in type 2 immunity. In this study, we demonstrate that microRNA(miR)-142 plays a critical, cell-intrinsic role in the homeostasis and function of ILC2s. Mice deficient for miR-142 expression demonstrate an ILC2 progenitor-biased development in the bone marrow, and along with peripheral ILC2s at mucosal sites, these cells display a greatly altered phenotype based on surface marker expression.

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Innate lymphoid cells (ILC) play a significant immunological role at mucosal surfaces such as the intestine. T-bet-expressing group 1 innate lymphoid cells (ILC1) are believed to play a substantial role in inflammatory bowel disease (IBD). However, a role of T-bet-negative ILC3 in driving colitis has also been suggested in mouse models questioning T-bet as a critical factor for IBD.

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Background: Glycosylation, one of the most fundamental post-translational modifications, is altered in cancer and is subject in part, to epigenetic regulation. As there are many epigenetic-targeted therapies currently in clinical trials for the treatment of a variety of cancers, it is important to understand the impact epi-therapeutics have on glycosylation.

Results: Ovarian and triple negative breast cancer cells were treated with the DNA methyltransferase inhibitor, 5-AZA-2-deoxycytidine (5-AZA-dC).

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  • * Von Willebrand factor (VWF), a protein in the blood involved in clotting, has been linked to tumor progression and the spread of breast cancer, showing significantly higher levels in patients with malignant tumors than those with benign conditions or healthy individuals.
  • * Patients with metastatic breast cancer display larger VWF structures due to decreased activity of a protein that normally regulates VWF size, potentially enhancing the interaction between platelets and tumor cells, contributing to the spread of cancer.
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  • * MicroRNAs (miRNAs) are important in regulating immune function and identity, with certain 'immuno-miRNAs' showing high expression in immune cells and affecting cellular pathways.
  • * The review discusses recent studies on how miRNAs influence immune responses and suggests that manipulating miRNA pathways, particularly in regulatory T cells, could offer new therapeutic strategies for treating CVD and its associated risks.
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Objectives: We hypothesised that maternal diet-induced-obesity has adverse consequences for offspring energy expenditure and susceptibility to obesity in adulthood, and that the prebiotic polydextrose (PDX) would prevent the consequences of programming by maternal obesity.

Methods: Female mice were fed a control (Con) or obesogenic diet (Ob) for 6 weeks prior to mating and throughout pregnancy and lactation. Half the obese dams were supplemented with 5% PDX (ObPDX) in drinking water throughout pregnancy and lactation.

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Comparative oncology is defined as the discipline that integrates naturally occurring cancers seen in veterinary medicine, into more general studies of cancer biology and therapy in humans, including the study of cancer-pathogenesis and new cancer treatments. While experimental studies in mice and rodents offer several advantages, including a wealth of genetic information, reduced variation and short generation intervals, their relevance in cancer biology is somewhat limited. Toward this end, as the biomedical research community works to make the promise of precision medicine a reality, more efficient animal cohort studies are critical.

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Organ transplantation is often lifesaving, but the long-term deleterious effects of combinatorial immunosuppression regimens and allograft failure cause significant morbidity and mortality. Long-term graft survival in the absence of continuing immunosuppression, defined as operational tolerance, has never been described in the context of multiple major histocompatibility complex (MHC) mismatches. Here, we show that miR-142 deficiency leads to indefinite allograft survival in a fully MHC mismatched murine cardiac transplant model in the absence of exogenous immunosuppression.

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Triple negative breast cancer (TNBC) is a breast cancer subtype which is particularly aggressive and invasive. The treatment of TNBC has been limited due to the lack of well-defined molecular targets. Exosomes are nano-sized extracellular vesicles that are released from virtually all cell types into the extracellular space.

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  • The objective of the study was to develop, improve, and assess a community health nurse (CHN) model to help individuals facing or at risk of homelessness access health and social care services.
  • Participants included clients and local service providers from a Melbourne suburb, with data collected through client records and feedback from stakeholders to refine the CHN model.
  • Results showed that after an average of seven CHN visits, clients improved their engagement with services, leading to better access to medical and housing support, and highlighted the positive impact of the CHN on both clients and other service providers.
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Background: Nurse practitioners (NPs) increasingly meet with families of young children who have been recently diagnosed with autism spectrum disorder (ASD). These families face a bewildering variety of treatment options and can benefit from working with NPs who can help them better understand those options and the likely outcomes for their children.

Purpose: This study describes outcomes for young children with autism, who were treated with either applied behavior analysis (ABA) or eclectic treatment.

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Tregs play a fundamental role in immune tolerance via control of self-reactive effector T cells (Teffs). This function is dependent on maintenance of a high intracellular cAMP concentration. A number of microRNAs are implicated in the maintenance of Tregs.

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  • Hereditary spastic paraplegia (HSP) is a neurologically varied disorder classified into pure and complex forms, with complex cases often having additional symptoms.
  • A report details a family affected by autosomal dominant (AD) complex HSP, presenting progressive spastic paraparesis and associated distal arthrogryposis, along with episodes of rhabdomyolysis.
  • Extensive genetic testing failed to find the gene responsible for this condition, suggesting it could represent a new genetic type of complex AD HSP, which may enhance our understanding of related neurological and skeletal issues.
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