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Areas of difficulties included the morphological boundaries of HG-BCL, not otherwise specified, cases with MYC and BCL2 or BCL6 translocations and TdT expression, which were categorized as B-lymphoblastic lymphoma/leukemia if most cells showed TdT positivity, and the clinico-pathologic overlap between intravascular large B-cell lymphoma, DLBCL CD5+ and DLBCL with primary presentation in BM, spleen and liver. This review summarizes our understanding of the main aggressive B-cell lymphoma categories with common primary BM presentation and potential problem areas, and makes suggestions for the immunophenotypic and genetic work-up, illustrated by the interesting and challenging cases submitted to the workshop. This article is protected by copyright. All rights reserved.PURPOSE To develop and validate a Monte Carlo model of the Varian TrueBeam to study electron collimation using the existing photon multi-leaf collimators (pMLC), instead of conventional electron applicators and apertures. selleck chemicals MATERIALS AND METHODS A complete Monte Carlo model of the Varian TrueBeam was developed using TOPAS (version 3.1.p3). Vendor-supplied information was used to model the treatment head components and the source parameters. A phase space plane was setup above the collimating jaws and captured particles were reused until a statistical uncertainty of 1% was achieved in the central axis. Electron energies 6, 9, 12, 16, and 20 MeV with a jaw-defined field of 20 x 20 cm2 at iso-center, pMLC-defined fields of 6.8 x 6.8 cm2 and 11.4 x 11.4 cm2 at 80 cm source-to-surface distance (SSD) and an applicator-defined field of 10 x 10 cm2 at iso-center were evaluated. All the measurements except the applicator-defined fields were measured using an ionization chamber in a water tank using 80 cm SSD. The dose d/1 mm for dose profiles. The simulation of clinically applicable cases demonstrated the clinical utility of pMLC-based electrons and the use of MC simulations for development of advanced radiation therapy techniques. This article is protected by copyright. All rights reserved.BACKGROUND AND OBJECTIVE Thyrotoxicosis is associated with accelerated bone turnover and increases the risk of fractures and osteoporosis. Graves' disease is the most common cause of hyperthyroidism. However, studies that examined risk factors associated with fragility fractures only in patients with Graves' disease are limited. Here we investigated whether the risk of vertebral fracture (VF) of postmenopausal Graves' disease patients is high and tried to identify the risk factors for VF in that population. DESIGN AND METHODS Forty-three postmenopausal women with Graves' disease were enrolled. Physical and biochemical indices, thyroid indices, and bone mineral density (BMD) were measured, and lateral X-rays were obtained to evaluate VFs. Age- and sex-matched healthy individuals were enrolled as the control group (n=86). RESULTS The prevalence of VFs (35% vs. 17%, p less then 0.05), osteoporosis (63% vs. 33%, p less then 0.01), and severe osteoporosis (40% vs. 17%, p less then 0.01) was significantly higher in the Graves' disease group. Although there was no significant difference in either thyroid hormone levels or the positive ratio of thyroid antibodies, the prevalence of thyroid stimulating antibody (TSAb) was significantly higher in Graves' disease patients with VF compared to without (100% vs. 68%, p less then 0.05). Multivariate logistic regression analyses adjusted for age identified Graves' disease as being associated with the presence of VFs (OR 2.72, 95% CI 1.13 - 6.54, p less then 0.05) in postmenopausal women. CONCLUSIONS Postmenopausal Graves' disease patients had high risks of VF and severe osteoporosis. TSAb could be involved as a risk factor for VF in postmenopausal Graves' disease. This article is protected by copyright. All rights reserved.Plants forage soil for water and nutrients, whose distribution is patchy and often dynamic. To improve their foraging activities, plants have evolved mechanisms to modify the physicochemical properties and microbial communities of the rhizosphere, i.e. the soil compartment under the influence of the roots. This dynamic interplay in root-soil-microbiome interactions creates emerging properties that impact plant nutrition and health. As a consequence, the rhizosphere can be considered an extended root phenotype, a manifestation of the effects of plant genes on their environment inside and/or outside of the organism. Here, we review current understanding of how plants shape the rhizosphere and the benefits it confers to plant fitness. We discuss future research challenges and how applying their solutions in crops will enable us to harvest the benefits of the extended root phenotype. This article is protected by copyright. All rights reserved.Context Acromegaly is usually a sporadic disease, but familial cases occur. Mutations in the aryl hydrocarbon receptor-interacting protein (AIP) gene are associated with familial pituitary adenoma predisposition. However, the pathogenicity of some AIP variants remains unclear and additional unknown genes may be involved. OBJECTIVE To explore the phenotype and genotype of a large kindred carrying the p.R304Q AIP variant. METHODS The family comprised 52 family members at risk of carrying the p.R304Q AIP variant including a case with gigantism and one with acromegaly and several family members with acromegalic features. Nine family members (three trios) underwent exome sequencing to identify putative pathogenic variants. RESULTS We identified 31 p.R304Q carriers and based on two cases with somatotropinomas the disease penetrance was 6%. We observed physical signs of acromegaly in several family members, which were independent of AIP status. Serum Insulin-like Growth Factor-I (IGF-I) levels in all family members were above the mean for age and sex [IGF-I SDS +0.6 (CI95% +0.4-0.9), p50 years) were screened for the PDE11A and ALG14 variant; both variants were present in five of ten persons. CONCLUSIONS This large family adds new information on the p.R304Q AIP variant and data suggest two new candidate genes could be associated with growth hormone excess. This article is protected by copyright. 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