anti-VEGFs as potential therapy for HA and their impact on prevention and treatment of HA.Dystonin (Dst) is a causative gene for Dystonia musculorum (dt) mice, which is an inherited disorder exhibiting dystonia-like movement and ataxia with sensory degeneration. Apoptosis inhibitor Dst is expressed in a variety of tissues, including the central nervous system and the peripheral nervous system (PNS), muscles, and skin. However, the Dst-expressing cell type(s) for dt phenotypes have not been well characterized. To address the questions whether the disruption of Dst in Schwann cells induces movement disorders and how much impact does it have on dt phenotypes, we generated Dst conditional knockout (cKO) mice using P0-Cre transgenic mice and Dst gene trap mice. First, we assessed the P0-Cre transgene-dependent Cre recombination using tdTomato reporter mice and then confirmed the preferential tdTomato expression in Schwann cells. In the Dst cKO mice, Dst mRNA expression was significantly decreased in Schwann cells, but it was intact in most of the sensory neurons in the dorsal root ganglion. Next, we analyzed the phenotype of Dst cKO mice. They exhibited a normal motor phenotype during juvenile periods, and thereafter, started exhibiting an ataxia. Behavioral tests and electrophysiological analyses demonstrated impaired motor abilities and slowed motor nerve conduction velocity in Dst cKO mice, but these mice did not manifest dystonic movements. Electron microscopic observation of the PNS of Dst cKO mice revealed significant numbers of hypomyelinated axons and numerous infiltrating macrophages engulfing myelin debris. These results indicate that Dst is important for normal PNS myelin organization and Dst disruption in Schwann cells induces late-onset neuropathy and sensory ataxia. MAIN POINTS Dystonin (Dst) disruption in Schwann cells results in late-onset neuropathy and sensory ataxia. Dst in Schwann cells is important for normal myelin organization in the peripheral nervous system.Chemical exchange saturation transfer of glycosaminoglycans, gagCEST, is a quantitative MR technique that has potential for assessing cartilage proteoglycan content at field strengths of 7 T and higher. However, its utility at 3 T remains unclear. The objective of this work was to implement a rapid volumetric gagCEST sequence with higher gagCEST asymmetry at 3 T to evaluate its sensitivity to osteoarthritic changes in knee articular cartilage and in comparison with T2 and T1ρ measures. We hypothesize that gagCEST asymmetry at 3 T decreases with increasing severity of osteoarthritis (OA). Forty-two human volunteers, including 10 healthy subjects and 32 subjects with medial OA, were included in the study. Knee Injury and Osteoarthritis Outcome Scores (KOOS) were assessed for all subjects, and Kellgren-Lawrence grading was performed for OA volunteers. Healthy subjects were scanned consecutively at 3 T to assess the repeatability of the volumetric gagCEST sequence at 3 T. For healthy and OA subjects, gagCEST asymmetry and T2 and T1ρ relaxation times were calculated for the femoral articular cartilage to assess sensitivity to OA severity. Volumetric gagCEST imaging had higher gagCEST asymmetry than single-slice acquisitions (p = 0.015). The average scan-rescan coefficient of variation was 6.8%. There were no significant differences in average gagCEST asymmetry between younger and older healthy controls (p = 0.655) or between healthy controls and OA subjects (p = 0.310). T2 and T1ρ relaxation times were elevated in OA subjects (p less then 0.001 for both) compared with healthy controls and both were moderately correlated with total KOOS scores (rho = -0.181 and rho = -0.332 respectively). The gagCEST technique developed here, with volumetric scan times under 10 min and high gagCEST asymmetry at 3 T, did not vary significantly between healthy subjects and those with mild-moderate OA. This further supports a limited utility for gagCEST imaging at 3 T for assessment of early changes in cartilage composition in OA.Acute kidney injury (AKI) in premature neonates is common due to the administration of life-saving therapies. The impact of AKI on renal morphology and susceptibility to further renal damage is poorly understood. Recent advances in radiological imaging have allowed integration of soft tissue morphology in the intact organ, facilitating a more complete understanding of changes in tissue microstructure associated with pathology. Here, we applied magnetic resonance imaging (MRI) to detect both glomerular and vascular changes in a rabbit model of neonatal AKI, induced by indomethacin and gentamicin. Using combined spin-echo MRI and cationic ferritin enhanced gradient-echo MRI (CFE-MRI), we observed 1) an increased cortical arterial diameter in the AKI cohort compared to healthy controls, and 2) focal loss of vascular density and glomerular loss in a circumferential band ~1 mm from the cortical surface. This combined use of vascular and glomerular imaging may give insight into the etiology of AKI and its impact on renal health later in life. This article is protected by copyright. All rights reserved.Background Work on Swedish petroleum tankers before the late 1980s has been associated with an increased risk of hematologic malignancy (HM). Since then, ship modernizations have decreased occupational exposure to gases, including the carcinogen benzene. We explored the risk of HMs in Swedish seafarers who had worked on newer types of tankers. Methods A case-referent study in male seafarers from a cohort of all Swedish seafarers was set up by record linkage with the Swedish Cancer Registry using the subjects’ personal identification number. For each case (N = 315), five referents were randomly chosen from within the cohort, matched by birth year and three different periods of first sea service ( less then 1985, 1985-1991, and ≥1992). Information on the type of ship and dates of service was retrieved from the Swedish Seafarers’ Registry. Odds ratios (OR) were calculated by conditional logistic regression together with 95% confidence intervals (CI). Results The OR of HM was 1.07 (95% CI, 0.80-1.42) for work on tankers.