56 research outputs found

    Factors leading to disparity in lung cancer diagnosis among black/African American communities in the USA: a qualitative study

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    This is the final version. Available on open access from BMJ Publishing Group via the DOI in this recordData availability statement: Data are available upon reasonable request. The authors confirm that the data supporting the findings of this study are available within the article and its supplementary materials. The data will become available immediately after publication, with no end date for anyone who wishes access.OBJECTIVE: This study has two objectives: first, to explore the diagnostic experiences of black/African American (BAA) patients with lung cancer to pinpoint pitfalls, suboptimal experiences and instances of discrimination leading to disparities in outcomes compared with patients of other ethnic backgrounds, especially white patients. The second objective is to identify the underlying causes contributing to health disparities in the diagnosis of lung cancer among BAA patients. METHODS: We employed a phenomenological research approach, guiding in-depth interviews with patients self-identifying as BAA diagnosed with lung cancer, as well as caregivers, healthcare professionals and community advocates knowledgeable about BAA experiences with lung cancer. We performed thematic analysis to identify experiences at patient, primary care and specialist levels. Contributing factors were identified using the National Institute of Minority Health and Health Disparities (NIMHD) health disparity model. RESULTS: From March to November 2021, we conducted individual interviews with 19 participants, including 9 patients/caregivers and 10 providers/advocates. Participants reported recurring and increased pain before seeking treatment, treatment for non-cancer illnesses, delays in diagnostic tests and referrals, poor communication and bias when dealing with specialists and primary care providers. Factors contributing to suboptimal experiences included reluctance by insurers to cover costs, provider unwillingness to conduct comprehensive testing, provider bias in recommending treatment, high healthcare costs, and lack of healthcare facilities and qualified staff to provide necessary support. However, some participants reported positive experiences due to their insurance, availability of services and having an empowered support structure. CONCLUSIONS: BAA patients and caregivers encountered suboptimal experiences during their care. The NIMHD model is a useful framework to organise factors contributing to these experiences that may be leading to health disparities. Additional research is needed to fully capture the extent of these experiences and identify ways to improve BAA patient experiences in the lung cancer diagnosis pathway.Cancer Research UKLUNGevity Foundatio

    Recurrence of Type 1 Diabetes After Simultaneous Pancreas-Kidney Transplantation, Despite Immunosuppression, Is Associated With Autoantibodies and Pathogenic Autoreactive CD4 T-Cells

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    ObjectiveTo investigate if recurrent autoimmunity explained hyperglycemia and C-peptide loss in three immunosuppressed simultaneous pancreas-kidney (SPK) transplant recipients.Research design and methodsWe monitored autoantibodies and autoreactive T-cells (using tetramers) and performed biopsy. The function of autoreactive T-cells was studied with in vitro and in vivo assays.ResultsAutoantibodies were present pretransplant and persisted on follow-up in one patient. They appeared years after transplantation but before the development of hyperglycemia in the remaining patients. Pancreas transplant biopsies were taken within approximately 1 year from hyperglycemia recurrence and revealed beta-cell loss and insulitis. We studied autoreactive T-cells from the time of biopsy and repeatedly demonstrated their presence on further follow-up, together with autoantibodies. Treatment with T-cell-directed therapies (thymoglobulin and daclizumab, all patients), alone or with the addition of B-cell-directed therapy (rituximab, two patients), nonspecifically depleted T-cells and was associated with C-peptide secretion for >1 year. Autoreactive T-cells with the same autoantigen specificity and conserved T-cell receptor later reappeared with further C-peptide loss over the next 2 years. Purified autoreactive CD4 T-cells from two patients were cotransplanted with HLA-mismatched human islets into immunodeficient mice. Grafts showed beta-cell loss in mice receiving autoreactive T-cells but not control T-cells.ConclusionsWe demonstrate the cardinal features of recurrent autoimmunity in three such patients, including the reappearance of CD4 T-cells capable of mediating beta-cell destruction. Markers of autoimmunity can help diagnose this underappreciated cause of graft loss. Immune monitoring during therapy showed that autoimmunity was not resolved by the immunosuppressive agents used

    Investigating the Role of T-Cell Avidity and Killing Efficacy in Relation to Type 1 Diabetes Prediction

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    During the progression of the clinical onset of Type 1 Diabetes (T1D), high-risk individuals exhibit multiple islet autoantibodies and high-avidity T cells which progressively destroy beta cells causing overt T1D. In particular, novel autoantibodies, such as those against IA-2 epitopes (aa1-577), had a predictive rate of 100% in a 10-year follow up (rapid progressors), unlike conventional autoantibodies that required 15 years of follow up for a 74% predictive rate (slow progressors). The discrepancy between these two groups is thought to be associated with T-cell avidity, including CD8 and/or CD4 T cells. For this purpose, we build a series of mathematical models incorporating first one clone then multiple clones of islet-specific and pathogenic CD8 and/or CD4 T cells, together with B lymphocytes, to investigate the interaction of T-cell avidity with autoantibodies in predicting disease onset. These models are instrumental in examining several experimental observations associated with T-cell avidity, including the phenomenon of avidity maturation (increased average T-cell avidity over time), based on intra- and cross-clonal competition between T cells in high-risk human subjects. The model shows that the level and persistence of autoantibodies depends not only on the avidity of T cells, but also on the killing efficacy of these cells. Quantification and modeling of autoreactive T-cell avidities can thus determine the level of risk associated with each type of autoantibodies and the timing of T1D disease onset in individuals that have been tested positive for these autoantibodies. Such studies may lead to early diagnosis of the disease in high-risk individuals and thus potentially serve as a means of staging patients for clinical trials of preventive or interventional therapies far before disease onset

    Supplemental Feeding of Honey Bee Colonies

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    This publication discusses the general food requirements of honey bees, Apis mellifera L., and presents formulas for supplementary diets and methods for feeding such foods to bee colonies. In early spring, before pollen and nectar are available or at other times of the year when these materials are not available for bees in the field or in the hive, supplementary feeding may help the colony survive or sustain brood rearing and colony development. None of the protein supplemental foods fed to honey bees is a complete replacement for natural pollen; however, several brewer's yeast products, Wheast, and soybean flour, fed singly or in combination, can be used to improve the nutrition of colonies when natural pollen is scarce. Cane or beet sugar and isomerized corn sirup can be used to supplement the bees' diet of nectar or honey
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