ObjectiveTo evaluate the impact of the adaptive iterative dose reduction (AIDR) three-dimensional (3D) algorithm in CT on noise reduction and the image quality compared to the filtered back projection (FBP) algorithm and to compare the effectiveness of AIDR 3D on noise reduction according to the body habitus using phantoms with different sizes.Materials and MethodsThree different-sized phantoms with diameters of 24 cm, 30 cm, and 40 cm were built up using the American College of Radiology CT accreditation phantom and layers of pork belly fat. Each phantom was scanned eight times using different mAs. Images were reconstructed using the FBP and three different strengths of the AIDR 3D. The image noise, the contrast-to-noise ratio (CNR) and the signal-to-noise ratio (SNR) of the phantom were assessed. Two radiologists assessed the image quality of the 4 image sets in consensus. The effectiveness of AIDR 3D on noise reduction compared with FBP were also compared according to the phantom sizes.ResultsAdaptive iterative dose reduction 3D significantly reduced the image noise compared with FBP and enhanced the SNR and CNR (p < 0.05) with improved image quality (p < 0.05). When a stronger reconstruction algorithm was used, greater increase of SNR and CNR as well as noise reduction was achieved (p < 0.05). The noise reduction effect of AIDR 3D was significantly greater in the 40-cm phantom than in the 24-cm or 30-cm phantoms (p < 0.05).ConclusionThe AIDR 3D algorithm is effective to reduce the image noise as well as to improve the image-quality parameters compared by FBP algorithm, and its effectiveness may increase as the phantom size increases.
Background Thymectomy is required for the treatment of thymoma‐associated myasthenia gravis (MG). However, MG may develop only after thymectomy, a condition known as post‐thymectomy MG. This study aimed to investigate the risk factors for post‐thymectomy MG in patients with thymoma. Methods We retrospectively identified 235 patients with thymoma who underwent thymectomy at a single hospital from January 2008 to December 2017: 44 with preoperatively diagnosed MG were excluded, leaving 191 patients in the final analysis. Univariable survival analyses using Cox proportional hazards regression model and Kaplan‐Meier estimate were conducted to identify risk factors for post‐thymectomy MG. Results Post‐thymectomy MG developed in 4.2% (8/191) of the patients with thymoma between 18 days and 108 mo after surgery. Hazard ratios (HRs) of pre‐ and postoperative anti‐acetylcholine receptor antibody (AChR‐Ab) titers were 2.267 (P = .002) and 1.506 (P < .001), respectively. Patients with extended thymectomy had a low chance of post‐thymectomy MG (HR 0.035, P = .007). Larger thymoma (HR, 1.359; P = .005) and type A or AB thymoma according to World Health Organization histological classification (HR, 11.92; P = .021) were associated with higher chances of post‐thymectomy MG. Within the subgroup of preoperatively AChR‐Ab seropositive patients, post‐thymectomy MG developed in 22.2% (6/27). Conclusions Pre‐ and postoperative AChR‐Ab levels should be measured in patients with thymoma. A large thymoma and partial thymectomy appear to be associated with a higher probability of post‐thymectomy MG.
Progressive myoclonic epilepsy (PME) is a heterogeneous neurogenetic disorder manifesting as progressive myoclonus, seizure, and ataxia. We report a case of PME caused by a novel DHDDS variant. Additionally, by reviewing the literature on DHDDS mutations, we compared the phenotype of our patient with previously reported phenotypes. We identified DHDDS (c.638G>A, p. Ser213-Asn) as a likely pathogenic variant. The literature review revealed 15 PME patients with DHDDS mutations from 13 unrelated families. According to previous studies, late-onset patients tend to have a slow-progressive disease course. Although his myoclonus and ataxia were adult onset, our patient experienced rapid disease aggravation.
Circular RNAs (circRNAs) involve in the epigenetic regulation and its major mechanism is the sequestration of the target micro RNAs (miRNAs). We hypothesized that circRNAs might be related with the pathophysiology of chronic epilepsy and evaluated the altered cir-cRNA expressions and their possible regulatory effects on their target miRNAs and mRNAs in a mouse epilepsy model. The circRNA expression profile in the hippocampus of the pilocarpine mice was analyzed and compared with control. The correlation between the expression of miRNA binding sites (miRNA response elements, MRE) in the dysregulated circRNAs and the expression of their target miRNAs was evaluated. As miRNAs also inhibit their target mRNAs, circRNA-miRNA-mRNA regulatory network, comprised of dysregulated RNAs that targets one another were searched. For the identified networks, bioinformatics analyses were performed. As the result, Forty-three circRNAs were dysregulated in the hippocampus (up-regulated, 26; down-regulated, 17). The change in the expression of MRE in those circRNAs negatively correlated with the change in the relevant target miRNA expression (r = -0.461, P<0.001), supporting that circRNAs inhibit their target miRNA. 333 dysregulated circRNA-miRNA-mRNA networks were identified. Gene ontology and pathway analyses demonstrated that the up-regulated mRNAs in those networks were closely related to the major processes in epilepsy. Among them, STRING analysis identified 37 key mRNAs with abundant (�4) interactions with other dysregulated target mRNAs. The dysregulation of the circRNAs which had multiple interactions with key mRNAs were validated by PCR. We concluded that dysregulated circRNAs might have a pathophysiologic role in chronic epilepsy by regulating multiple disease relevant mRNAs via circRNA−miRNA −mRNA interactions.
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