Journal of investigative medicine : the official publication of the American Federation for Clinical Research
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Forty-one families with multiple cases of de novo acute myeloid leukemia (AML), B-cell acute lymphocytic leukemia (B-ALL), or both are presented. The families were randomly collected from physicians, genetic counselors, and other sources. Medical records were collected and reviewed for all families. ⋯ Curiously, this is not true of those in the AML-B-ALL group. Four of the 41 families had contributions to more than 1 family relationship category. Although inheritance in familial acute leukemia has usually been consistent with an autosomal dominant pattern, these data suggest that an X chromosome gene may be involved in some cases, perhaps in the pseudoautosomal region of the X chromosome as we have reported in familial Hodgkin lymphoma.
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The etiology of vascular problems in beta-thalassemia has been linked to endothelial damage. Antiangiogenic proteins such as soluble Fms-like tyrosine kinase-1 (sFLT-1) inhibit the signaling of vascular endothelial growth factor and placental growth factor, resulting in a decrease in the development of new blood vessels. Additionally, they promote the maturation of existing blood vessels and lead to endothelial dysfunction. ⋯ Regression analyses demonstrated a significant association between high sFLT-1 levels and the occurrence of PHT. Additionally, sFLT-1 (at a cutoff value of 8.84 pg/mL) demonstrated a sensitivity of 83.30% and a specificity of 80.0% in diagnosing thalassemic patients with PHT. In conclusion, beta-TM patients with elevated serum levels of sFLT-1 are at risk of developing endothelial dysfunction and subsequent development of PHT.
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There is little evidence of antimicrobial elimination via therapeutic plasma exchange (TPE) and no guidelines for antimicrobial optimal dosing in patients undergoing TPE. We aimed to assess current practices and knowledge regarding antimicrobial management during TPE. A structured online survey was conducted from May to November 2023, and physicians were invited to participate through national scientific platforms and professional societies. ⋯ The core questions regarding potential drug-, procedure-, and patient-related antimicrobial elimination factors via TPE were responded to accurately by less than half of the physicians. It was clear that they had a lack of clinical practices and knowledge regarding antimicrobial management during TPE. To ensure the therapeutic efficacy of antimicrobials and avoid treatment failure, physicians should improve their practice strategies and consider antimicrobial elimination factors with TPE in this data-poor setting.
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Some studies have indicated an association between serum magnesium and anemia, but these are primarily limited to research on serum magnesium. Few studies have explored the relationship between the bioavailability of magnesium and anemia. This study explores the association between the Magnesium Deficiency Score (MDS) and anemia among elderly Americans using data from the National Health and Nutrition Examination Survey (NHANES) 2009-2018. ⋯ The study suggests that improving the bioavailability of magnesium to reduce MDS may be a factor in preventing anemia in the elderly. This is the first study to explore the relationship between MDS and anemia in this population, highlighting the potential role of magnesium bioavailability in anemia prevention. Further prospective studies are needed to confirm these results and explore the underlying mechanisms.
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Atherosclerosis, a major cause of cardiovascular diseases, is characterized by the accumulation of oxidized lipoproteins (ox-LDL) within arterial walls, leading to inflammation and plaque formation. Hydrogen sulfide (H2S) has demonstrated anti-inflammatory and vascular protective properties, but its role in modulating macrophage endocytosis of ox-LDL and its impact on early atherosclerosis development remains unclear. Macrophage cultures were utilized for ox-LDL uptake experiments. ⋯ Furthermore, H2S down-regulated ox-LDL receptors CD36 and SR-A through the NF-κB signal pathway. H2S inhibits early atherosclerosis development by modulating macrophage uptake of ox-LDL through the down-regulation of CD36 and SR-A receptors via the NF-κB signaling pathway. These findings provide new evidence for the role of H2S in atherosclerosis and its potential therapeutic value.