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BackgroundIron (Fe) supplementation is a critical component of anemia therapy for patients with chronic kidney disease (CKD). However, serum Fe, ferritin, and transferrin saturation, used to guide Fe replacement, are far from optimal, as they can be influenced by malnutrition and inflammation. Currently, there is a trend of increasing Fe supplementation to target high ferritin levels, although the long-term risk has been overlooked.MethodsWe prospectively enrolled 28 patients with CKD on hemodialysis with high serum ferritin (> 1000 ng/ml) and tested the effects of 1-year deferoxamine treatment, accompanied by withdrawal of Fe administration, on laboratory parameters (Fe status, inflammatory and CKD-MBD markers), heart, liver, and iliac crest Fe deposition (quantitative magnetic resonance imaging [MRI]), and bone biopsy (histomorphometry and counting of the number of Fe positive cells in the bone marrow).ResultsMRI parameters showed that none of the patients had heart iron overload, but they all presented iron overload in the liver and bone marrow, which was confirmed by bone histology. After therapy, ferritin levels decreased, although neither hemoglobin levels nor erythropoietin dose was changed. A significant decrease in hepcidin and FGF-23 levels was observed. Fe accumulation was improved in the liver and bone marrow, reaching normal values only in the bone marrow. No significant changes in turnover, mineralization or volume were observed.ConclusionsOur data suggest that treatment with deferoxamine was safe and could improve Fe accumulation, as measured by MRI and histomorphometry. Whether MRI is considered a standard tool for investigating bone marrow Fe accumulation requires further investigation. Registry and the registration number of clinical trial: ReBEC (Registro Brasileiro de Ensaios Clinicos) under the identification RBR-3rnskcj available at: https://ensaiosclinicos.gov.br/pesquisador.

Gastrointestinal (GI) disturbances are a prevalent cause of marathon related complaints, and in extreme cases can promote life-threatening conditions such as exertional heat stroke. Our aim was to study intestinal cell injury [via intestinal fatty acid binding protein (I-FABP)] and perceived GI distress symptoms among marathon runners. We also examined potential risk factors (e.g., inadequate sleep) that could exacerbate GI disturbances in healthy, trained endurance runners. This was a parallel mixed-methods study design. 2019 Boston Marathon participants were recruited via email and subjects completed surveys before the race describing demographics and training history. Participants completed a GI questionnaire to assess presence and severity of symptoms, a survey regarding risk factors (e.g., recent illness, medications) that could promote GI disturbances, and provided a urine sample at three time points (immediately pre-race, post-race, and 24-h post-race). Due to weather, blood samples were only collected immediately and 24-h post-race. A total of 40 runners (males: n = 19, age = 44.9 ± 10.8 years; females: n = 21, age = 44.8 ± 10.6 years) completed this study. I-FABP significantly decreased from post-race (3367.5 ± 2633.5 pg/mL) to 24-h post-race (1657.3 ± 950.7 pg/mL, t (39) = −4.228, p < .001, d = −.669). There was a significant difference in overall GI symptom scores across the three time points (F (2, 39) = 41.37, p < .001). The highest average score occurred post-race (.84 ± .68), compared to pre-race (.09 ± .12) and 24-h post-race (.44 ± .28). Post-race I-FABP (r = .31, p = .048) and post-race urine specific gravity (r = .33, p = .041) were significantly correlated with post-race GI symptom scores. Our study provides further support to the individualized nature of GI disturbances, with participants experiencing a wide range of risk factors that can influence the extent of GI damage and perceived symptoms during and after exercise.

Exercise-associated hyponatremia (EAH) is commonly observed in endurance athletes, where prolonged physical exertion combined with being unaware of personal hydration needs can lead to excessive water consumption or inadequate sodium intake. Marching band (MB) is an emerging setting for sports medicine professionals. However, there is little research on non-musculoskeletal illnesses among these performing artists. This study is part of a larger cross-sectional study and seeks to examine whether MB artists have previously experienced EAH and the presence of known EAH risk factors (e.g., pre-existing medical conditions, medication use, nutritional behaviors). Active collegiate MB members (n = 1207; mean age = 19.6 ± 1.3 years) completed an online survey that characterized demographics, medical history, and nutrition behaviors. Statistical analyses included descriptives (mean, standard deviation) and frequencies for all data. Binomial logistic regressions analyzed the relationship and determined the odds ratio (OR) between previous EAH and EAH risk factors. Participants were from 23 different states, predominately White (82.9%), female (56.7%), and at NCAA Division I institutions (92%). A total of 74 (6.1%) participants reported previously experiencing EAH, 32 (43.2%) within the past year. Previous EAH occurrence was greatest among individuals who had kidney conditions (χ2(1) = 5.920, R2 = 0.013, OR = 15.708, p = 0.015); mood/neurological conditions (χ2(1) = 7.508, R2 = 0.017, OR = 2.154, p = 0.006), particularly anxiety (χ2(1) = 7.651, R2 = 0.017, OR = 3.590, p = 0.006); used mental health medications (χ2(1) = 7.512, R2 = 0.017, OR = 2.220, p = 0.006), particularly selective serotonin reuptake inhibitors (χ2(1) = 13.502, R2 = 0.030, OR = 3.297, p < 0.001); and who dieted (χ2(1) = 6.121, R2 = 0.014, OR = 1.913, p = 0.013) or perceived they had an eating disorder (χ2(1) = 9.502, R2 = 0.021, OR = 2.729, p = 0.002). Healthcare providers should be aware that MB artists may have pre-existing medication conditions, use medication, and have inadequate nutrition. Targeted hydration and nutritional education for MB artists is essential for effective prevention and early EAH recognition, improving health and performance for MB artists within demanding environments. [ABSTRACT FROM AUTHOR]

Abstract Background Marching band artists are a physically active population, composed of approximately 27,000 people in the United States. University marching band artists face many of the same physically active demands and mental stressors as student athletes, potentially predisposing them to injury, illness, and risk for eating disorders (EDs). The purpose of this study was to examine ED risk across sex in university marching band artists, and to determine the type of risk based on the Eating Disorder Inventory-3 (EDI-3) and Eating Disorder Inventory-3 Symptom Check List (EDI-3 SC). A secondary aim examined marching band artists and pathogenic weight control behavior use across sex. Methods This was a cross-sectional study. A total of 150 marching band artists (female: n = 84, male: n = 66, age = 19.9 ± 1.1 years) from three National Collegiate Athletic Association Division I university marching bands participated in the study. We screened for ED risk using the EDI-3, and the EDI-3 SC. Results Overall, marching band artists were at risk for EDs, using only the EDI-3, 45.3% (n = 68) were at risk, with females at significant higher risk than males [χ2 = 5.228, p = .022]; using only the EDI-3 SC, 54% (n = 81) were at risk and no significant differences were found across sex. Overall, 48% of all participants reported dieting and 20.7% engaged in excessive exercise to control weight. Significant differences were found between sex and purging to control weight [χ2 = 3.94, p = .047] and laxative use [χ2 = 4.064, p = .044], with females engaging in behavior more than males. Conclusions Eating disorder risk was prevalent for both female and male marching band artists, with females displaying higher risk for EDs than males. Furthermore, marching band artists are engaging in pathogenic behaviors to control their weight. Healthcare providers (e.g., physicians, athletic trainers, physical therapist, dietitians, etc.) working in this setting should be aware of the risk factors displayed in marching band artists, and be able to provide education, prevention, and clinical interventions to this population. Additionally, marching band administrators should be aware of all medical risk factors and the benefit of having a healthcare provider (e.g., athletic trainer) to oversee the healthcare and wellness of marching band artists.

The purpose of our field study was to investigate the effects of running the Boston Marathon on acute kidney injury (AKI) biomarkers. We hypothesized that biomarker values would be elevated immediately post-marathon but would resolve in the 24-h post-marathon. Secondarily, we sought to identify sex differences related to renal stress. Participants were 65 runners who completed the Boston Marathon (46 ± 9 years, 65.4 ± 10.8 kg). Urine samples were collected at three different time points (pre-marathon, post-marathon, and 24-h post-marathon). Blood samples were collected post-marathon and 24-h post-marathon. Urine specific gravity (USG) and AKI biomarkers were evaluated. Pre-marathon USG (1.012 ± 0.007) was significantly less than post-marathon (1.018 ± 0.008) and 24-h post-marathon (1.020 ± 0.009; P < 0.001). Male USG (1.024 ± 0.009) was significantly greater 24-h post-marathon than females (1.017 ± 0.008; P = 0.019). Urinary neutrophil gelatinase-associated lipocalin values were significantly greater over time (P < 0.001), and there was a main effect of sex with female urinary creatinine (UCr) greater than males at all three time points (P = 0.040). Post-marathonUCr (366.24 ± 295.16 mg/dl) was significantly greater than pre-marathon (206.65 ± 145.28.56 mg/dl; p < 0.001) and 24-h post-marathon was significantly lower than other time-points (93.90 ± 125.07 mg/dl; P < 0.001). FemaleUCr values were significantly greater than males 24-h post-marathon (P < 0.001). There was no difference in serum cystatin C (SCys) values post- or 24-h post-marathon (P = 0.178). Serum creatinine (SCr) significantly decreased between post-marathon and 24-h post-marathon, (P < 0.001). We can infer that the characteristics unique to the Boston Marathon may have attributed to prolonged elevations in AKI biomarkers. Sex differences were observed during the Boston Marathon warranting further investigation.

Background: Iron (Fe) supplementation is a critical component of anemia therapy for patients with chronic kidney disease (CKD). However, serum Fe, ferritin, and transferrin saturation, used to guide Fe replacement, are far from optimal, as they can be influenced by malnutrition and inflammation. Currently, there is a trend of increasing Fe supplementation to target high ferritin levels, although the long-term risk has been overlooked. Methods: We prospectively enrolled 28 patients with CKD on hemodialysis with high serum ferritin (> 1000 ng/ml) and tested the effects of 1-year deferoxamine treatment, accompanied by withdrawal of Fe administration, on laboratory parameters (Fe status, inflammatory and CKD-MBD markers), heart, liver, and iliac crest Fe deposition (quantitative magnetic resonance imaging [MRI]), and bone biopsy (histomorphometry and counting of the number of Fe positive cells in the bone marrow). Results: MRI parameters showed that none of the patients had heart iron overload, but they all presented iron overload in the liver and bone marrow, which was confirmed by bone histology. After therapy, ferritin levels decreased, although neither hemoglobin levels nor erythropoietin dose was changed. A significant decrease in hepcidin and FGF-23 levels was observed. Fe accumulation was improved in the liver and bone marrow, reaching normal values only in the bone marrow. No significant changes in turnover, mineralization or volume were observed. Conclusions: Our data suggest that treatment with deferoxamine was safe and could improve Fe accumulation, as measured by MRI and histomorphometry. Whether MRI is considered a standard tool for investigating bone marrow Fe accumulation requires further investigation. Registry and the registration number of clinical trial: ReBEC (Registro Brasileiro de Ensaios Clinicos) under the identification RBR-3rnskcj available at: https://ensaiosclinicos.gov.br/pesquisador. [ABSTRACT FROM AUTHOR]

Colon cancer is a malignancy in gastrointestinal tract. It causes high mortality rate in global cancer population. However, chemotherapy as its first option therapy is still controversial due to its effectiveness and its adverse effects. Finding supportive and alternative drugs to cure cancer is one of focus in cancer research. A drug which also has anticancer effects is metformin. Metformin is a biguanide antidiabetic which show its potential anticancer benefit in metabolic-related cancers including colon cancer. To investigate anticancer potency of metformin in targeting p53-related molecules. Metformin treatment were divided into 4 groups by 0, 5, 10 and 20 mM concentrations and incubated in 37o C and 5 % CO2 condition for 48 hours. Immunohistochemistry were conducted to asses level of expression of Bax, p21, cyclin D1 and E2F1, respectively. Level of expression were measured by H-SCORE using percentage and intensity calculation. Comparisons of H-SCORE between groups were performed by ANOVA for parametrical data and Kruskal-Wallis for non-parametrical data. Growth inhibition were observed after metformin treatment. Metformin increases Bax expression significantly at all concentrations. p21 expression was also increased after metformin treatment but is not statistically significant. Subsequently, metformin decreases cyclin D1 expression at 10 and 20 mM concentration thus decreased E2F1 expression at 5 and 10 mM concentration. These data suggest that metformin may have potential therapeutic effects in mutant p53 colon cancer cell line by targeting p53-related molecules. Keywords: Colon cancer; p53; Biguanide; Metformin; p53-mutant cell line

PURPOSE:Osteoblasts and adipocytes are derived from mesenchymal stem cells. An imbalance in the differentiation of these lineages could affect the preservation of bone integrity. Several studies have suggested the importance of this imbalance in the pathogenesis of osteoporosis after kidney transplant (KT), but the role of bone marrow adiposity in this process is not well known, and if the treatment with the anti-absorptive (zoledronic acid-ZA) drugs could attenuate bone loss. Thus, our objective was compare bone marrow adiposity, osteoblasts and osteocytes before and after KT, verify an association between bone remodeling process (Turnover, Volume, and Mineralization-TMV classification), the osteocyte sclerostin expression to evaluate if there is a role of Wnt pathway, as well as the effect of ZA on these cells. METHODS:We studied 29 new living-donor KT patients. One group received ZA at the time of KT plus cholecalciferol for twelve months, and the other group received only cholecalciferol. Bone biopsies were performed at baseline and after 12 months of treatment. Histomorphometric evaluation was performed in bone and bone marrow adipocytes. Sclerostin (Scl) expression in osteocytes was evaluated by immunohistochemistry. RESULTS:Some bone marrow adiposity parameters were increased before KT. After KT, some of them remained increased and they worsened with the use of ZA. In the baseline, lower bone Volume and Turnover, were associated with increased bone marrow adiposity parameters (some of them). After KT, both groups showed the same associations. Osteocyte Scl expression after KT decreased with the use of ZA. We observed also an inverse association between bone adiposity parameters and lower osteocyte sclerostin expression 12 months after KT. CONCLUSION:In conclusion, the present study suggests that KT fails to normalize bone marrow adiposity, and it even gets worse with the use of ZA. Moreover, bone marrow adiposity is inversely associated with bone Volume and Turnover, which seems to be accentuated by the antiresorptive therapy.