Explore the vast range of titles available.

Body composition, bone mineral density, and cardiopulmonary exercise testing (CPET) are commonly used to assess aerobic fitness in athletes, but their interrelationships remain unclear. This study compared these parameters by sex and examined their associations in elite athletes. Our study included 145 youth water polo players (age: 15.7 ± 1.6 years; male: 75). Body composition was measured by DEXA, and treadmill CPET was performed using a sport-specific protocol. We analysed the correlations between the following factors by multivariate linear regression: lean body mass (LBM, LBMindex); body fat mass (BFM); percent body fat (PBF); bone mineral content (BMC); lumbar, femoral, and radial bone mineral density (LBMD, FNBMD, FTBMD, RBMD); exercise time; absolute and relative maximal oxygen uptake (VO2absmax, VO2relmax); maximal ventilation (VEmax). Exercise time was found to be negatively correlated with BFM, while VO2relmax was found to be negatively correlated with BFM and PBF. VO2absmax was found to be positively correlated with BFM, LBM, BMC, FNBMD, and RBMD. VEmax was found to be positively correlated with LBM and LBMindex. In males, VO2absmax and VEmax were found to be positively correlated with LBMD and FTBMD. Correlations between bone density and CPET proved to be stronger in males. Our results indicate that body composition and bone density parameters influence CPET parameters, and their complex evaluation can support personalized diagnostics and athletes’ health.

Rapidly evolving clinical data suggest that the novel coronavirus (SARS-CoV-2) and vaccination against COVID-19 might be associated with thyroid disturbances. However, studies remain limited among the pediatric population . Our aim was to assess the prevalence and permanence of thyroid autoimmunity (TA) and dysfunction in children after an acute infection and its potential association with vaccination. A prospective, multicenter registry analysis was performed among 458 children (mean age: 12.4 ± 3,8 years, 45.4% male) with preceding COVID-19. Patient inclusion lasted from 24 th March, 2021 to 23 rd March, 2022 at three pediatric outpatient facilities at Semmelweis University, Budapest. Primary outcomes were the rate of thyroid disturbances assessed by laboratory parameters (thyroid function tests, antithyroglobulin [ATG] and anti-thyroid peroxidase [ATPO] antibodies) and thyroid ultrasound. TA rate among vaccinated and unvaccinated children was determined. Children with newly diagnosed thyroid alterations were followed up for 12.7 ± 4.3 months. Six children had previous thyroid disease. Out of 452 children, 30 cases (6.6%) of newly diagnosed TA (six of them had abnormal thyroid-stimulating hormone [TSH] levels) and eight cases (1.8%) of isolated TSH elevation were observed. Ultrasound-proven autoimmune thyroiditis (AIT) was 4.0%. No association was found between COVID-19 vaccination and thyroid autoimmunity (χ 2 (1,N = 452) = 0.138, p  = 0.815). Among children with TA, 73.3% had long-lasting alterations.   Conclusion : Vaccination had no effect on the prevalence of TA. Until further controlled studies state otherwise, children with preceding COVID-19 might benefit from thyroid screening. What is Known: • Numerous case reports implicate that coronavirus disease-2019 (COVID-19) and vaccination against SARS-CoV-2 can be responsible for thyroid disturbances. • Thyroid alterations discovered during acute COVID-19 tend to cease by time and only incidental thyroid autoimmunity (TA) is diagnosed after COVID-19. In adults, no increase in vaccine-related hyper- or hypothyroidism was found. What is New: • TA rate after COVID-19 vaccination among children was not increased. TA had no role in long COVID syndrome. • We discovered a considerable rate of TA (6.6%) and ultrasound-proven autoimmune thyroiditis (AIT) (4.0%) after SARS-CoV-2 infection, and the majority of these alterations remained positive after 6 months.

Body composition and cardiopulmonary exercise testing (CPET) are vital for optimizing sports performance, but the correlations between them are still underexplored. Our study aimed to investigate the relationships between body composition and specific CPET variables describing physical fitness in young athletes, also adjusting for age and height, in a less-studied, female population. Seventy players participated in our study (age: 16.10 ± 1.63 y). After determining body composition using dual-energy X-ray absorptiometry, we conducted treadmill-based maximal-intensity CPET. Data were analyzed in R using multivariate linear regression, accounting for age and height as confounders. Lean body mass (LBM), body fat mass (BFM), and bone mineral content (BMC) showed no effect on resting, maximum, or recovery heart rates and no correlation with resting or maximal lactate values. LBM positively correlated with maximum ventilation (VE-max) (Est: 1.3 × 10−3; SE: 6.1 × 10−4; p < 0.05) and maximum absolute oxygen consumption (VO2abs-max) (Est: 7.710−5; SE: 6.9 × 10−6; p < 0.001)—with age as an influencing factor for VE-max and height as an influencing factor for VO2abs-max. Conversely, BFM showed a negative correlation with maximum relative oxygen consumption (VO2rel-max) (Est: −4.8 × 10−4; SE: 1.2 × 10−4; p < 0.001). Moreover, BFM and BMC were also negatively correlated with maximal exercise duration (Est: −2.2 × 10−4; SE: 8.0 × 10−5; p < 0.01; Est: −3.2 × 10−3; SE: 1.4 × 10−3; p < 0.05) with height as an influencing factor. Our findings indicate complex correlations between body composition and CPET parameters, providing important information for the analysis of individual ergospirometric data. Our results draw attention to the fact that body composition is more precise than weight and height in the evaluation of athletes’ physical fitness.

There is abundant evidence that bone mineral content is highly heritable, while the heritability of bone quality (i.e. trabecular bone score [TBS] and quantitative ultrasound index [QUI]) is rarely investigated. We aimed to disentangle the role of genetic, shared and unique environmental factors on TBS and QUI among Hungarian twins. Our study includes 82 twin (48 monozygotic, 33 same-sex dizygotic) pairs from the Hungarian Twin Registry. TBS was determined by DXA, QUI by calcaneal bone ultrasound. To estimate the genetic and environmental effects, we utilized ACE-variance decomposition. For the unadjusted model of TBS, an AE model provided the best fit with > 80% additive genetic heritability. Adjustment for age, sex, BMI and smoking status improved model fit with 48.0% of total variance explained by independent variables. Furthermore, there was a strong dominant genetic effect (73.7%). In contrast, unadjusted and adjusted models for QUI showed an AE structure. Adjustments improved model fit and 25.7% of the total variance was explained by independent variables. Altogether 70–90% of the variance in QUI was related to additive genetic influences. We found a strong genetic heritability of bone quality in unadjusted models. Half of the variance of TBS was explained by age, sex and BMI. Furthermore, the adjusted model suggested that the genetic component of TBS could be dominant or an epistasis could be present. In contrast, independent variables explained only a quarter of the variance of QUI and the additive heritability explained more than half of all the variance.

Children with osteogenesis imperfecta are often treated with intravenous bisphosphonates. We aimed to assess the safety and efficacy of risedronate, an orally administered third-generation bisphosphonate, in children with the disease. In this multicentre, randomised, parallel, double-blind, placebo-controlled trial, children aged 4–15 years with osteogenesis imperfecta and increased fracture risk were randomly assigned by telephone randomisation system in a 2:1 ratio to receive either daily risedronate (2·5 or 5 mg) or placebo for 1 year. Study treatment was masked from patients, investigators, and study centre personnel. Thereafter, all children received risedronate for 2 additional years in an open-label extension. The primary efficacy endpoint was percentage change in lumbar spine areal bone mineral density (BMD) at 1 year. The primary efficacy analysis was done by ANCOVA, with treatment, age group, and pooled centre as fixed effects, and baseline as covariate. Analyses were based on the intention-to-treat population, which included all patients who were randomly assigned and took at least one dose of assigned study treatment. The trial is registered with ClinicalTrials.gov, number NCT00106028. Of 147 patients, 97 were randomly assigned to the risedronate group and 50 to the placebo group. Three patients from the risedronate group and one from the placebo group did not receive study treatment, leaving 94 and 49 in the intention-to-treat population, respectively. The mean increase in lumbar spine areal BMD after 1 year was 16·3% in the risedronate group and 7·6% in the placebo group (difference 8·7%, 95% CI 5·7–11·7; p<0·0001). After 1 year, clinical fractures had occurred in 29 (31%) of 94 patients in the risedronate group and 24 (49%) of 49 patients in the placebo group (p=0·0446). During years 2 and 3 (open-label phase), clinical fractures were reported in 46 (53%) of 87 patients in the group that had received risedronate since the start of the study, and 32 (65%) of 49 patients in the group that had been given placebo during the first year. Adverse event profiles were otherwise similar between the two groups, including frequencies of reported upper-gastrointestinal and selected musculoskeletal adverse events. Oral risedronate increased areal BMD and reduced the risk of first and recurrent clinical fractures in children with osteogenesis imperfecta, and the drug was generally well tolerated. Risedronate should be regarded as a treatment option for children with osteogenesis imperfecta. Alliance for Better Bone Health (Warner Chilcott and Sanofi).

Abstract Context Glucocorticoids (GCs) prescribed for chronic pediatric illnesses are associated with osteoporotic fractures. Objective This study aims to determine the efficacy and safety of intravenous (IV) zoledronic acid (ZA) compared with placebo to treat pediatric GC-induced osteoporosis (GIO). Methods Children aged 5 to 17 years with GIO were enrolled in this multinational, randomized, double-blind, placebo-controlled phase 3 trial (ClinicalTrials.gov NCT 00799266). Eligible children were randomly assigned 1:1 to 6 monthly IV ZA 0.05 mg/kg or IV placebo. The primary end point was the change in lumbar spine bone mineral density z score (LSBMDZ) from baseline to month 12. Incident fractures and safety were assessed. Results Thirty-four children were enrolled (mean age 12.6 ± 3.4 years [18 on ZA, 16 on placebo]), all with low-trauma vertebral fractures (VFs). LSBMDZ increased from −2.13 ± 0.79 to −1.49 ± 1.05 on ZA, compared with −2.38 ± 0.90 to −2.27 ± 1.03 on placebo (least squares means difference 0.41 [95% CI, 0.02-0.81; P = .04]); when corrected for height z score, the least squares means difference in LBMDZ was 0.75 [95% CI, 0.27-1.22; P = .004]. Two children on placebo had new low-trauma VF vs none on ZA. Adverse events (AEs) were reported in 15 of 18 children (83%) on ZA, and in 12 of 16 (75%) on placebo, most frequently within 10 days after the first infusion. There were no deaths or treatment discontinuations due to treatment-emergent AEs. Conclusion LSBMDZ increased significantly on ZA compared with placebo over 1 year in children with GIO. Most AEs occurred after the first infusion.

In traditional Combinatorial Group Testing the problem is to identify up to d defective items from a set of n items on the basis of group tests. In this paper we describe a variant of the group testing problem above, which we call parity group testing. The problem is to identify up to d defective items from a set of n items as in the classical group test problem. The main difference is that we check the parity of the defective items in a subset. The test can be applied to an arbitrary subset of the n items with two possible outcomes. The test is positive if the number of defective items in the subset is odd, otherwise it is negative. In this paper we extend Hirschberg et al.’s method to the parity group testing scenario.

In recent years, following the deployment of wavelength division multiplexing networks, fault detection and localisation has become a challenging issue in networks with high reliability. Optical layer monitoring schemes based on monitoring trails (m-trail) are considered an efficient way to localise a single fault unambiguously in all-optical networks. In spite of the extensive work on the m-trail concept, the issue has not been validated from the feasibility point of view. Previous works on the m-trail monitoring scheme have focused mainly on algorithm design for minimising the number of monitors, however, none of them have observed that length limitations should be considered as well. The authors investigate the physical constraints of launching m-trails, mainly focusing on the maximum length that each m-trail may have and describe an algorithm that solves the length constrained m-trail formulation problem. Numerous simulations were implemented in a physical layer simulator for observing qualitative parameters in different m-trail lengths. The authors propose 15 000 km as a length limit for each m-trail for out-of-band monitoring. Finally, an algorithmic solution is provided for monitoring trail design problem satisfying these physical constraints.

Multiple endocrine neoplasia syndromes (MEN) are genetic disorders with glandular hyperplasia and consecutive malignant neoplasia. MEN type 2B is the least common form of these tumor syndromes. It presents with typical dysmorphic features, mucosal neuromas, ganglioneuromatosis, medullary thyroid carcinoma (MTC) and phaeochromocytoma. The prognosis depends on the presence of MTC. We have surprisingly found two unrelated patients with this syndrome at our department within two weeks. In the medical history of a 17-year-old boy, Crohn’s disease had been considered because of abdominal pain and distention. He had marfanoid appearance and previously undergone minor surgeries for a large tongue with neuromas and hypertrophic gums. Two weeks later, a 10-year-old girl presented with a hard palpable mass on her neck. She had thickened lips, neuromas on the tongue and a solitary thyroid nodule. Genetic analysis was carried out in both patients and a heterozygous M918T mutation of the RET proto-oncogene was found. Laboratory tests and imaging studies were consistent with MTC. Phaeochromocytoma was not present. Both patients underwent total thyroidectomy and lymph node dissection. Histological examination confirmed the diagnosis of MTC. In conclusion, the initial diagnosis of MEN 2B should be suspected on the presence of typical facial/oral signs and gastrointestinal symptoms. Hormonal tests and imaging techniques of the thyroid and the adrenals can confirm the clinical diagnosis of MEN 2B and genetic analysis can prove its germline origin.

We examined the vasoactive effect of estradiol in a rat model of early PCOS and the influence of vitamin D deficiency (VDD). We created a model of chronic hyperandrogenism and VDD in adolescent female Wistar rats (N = 46) with four experimental groups: vitamin D supplemented (T-D+), VDD (T-D-), hyperandrogenic and vitamin D supplemented (T+D+), and hyperandrogenic and VDD (T+D-). T+ groups received an 8-week-long transdermal Androgel treatment, D-animals were on vitamin D-reduced diet and D+ rats were supplemented orally with vitamin D3. Estrogen-induced vasorelaxation of thoracic aorta segments were measured with a wire myograph system with or without the inhibition of endothelial nitric oxide synthase (eNOS) or cyclooxygenase-2 (COX-2). The distribution of estrogen receptor (ER), eNOS and COX-2 in the aortic wall was assessed by immunohistochemistry. VDD aortas showed significantly lower estradiol-induced relaxation independently of androgenic status that was further decreased by COX-2 inhibition. COX-2 inhibition failed to alter vessel function in D+ rats. Inhibition of eNOS abolished the estradiol-induced relaxation in all groups. Changes in vascular function in VDD were accompanied by significantly decreased ER and eNOS staining. Short-term chronic hyperandrogenism failed to, but VDD induced vascular dysfunction, compromised estrogen-dependent vasodilatation and changes in ER and eNOS immunostaining.