We propose an equation to predict the probability of malignancy in thyroid nodules based on 12 features of thyroid nodules as noted on TUS. This equation, and the stratification of its results into categories, should be useful in reporting the findings of US for thyroid nodules and in guiding management decisions.
ObjectiveThis study aimed to investigate the differences in brain morphology according to handedness.Materials and MethodsForty‐two healthy subjects were enrolled (21 right‐handers and 21 nonright‐handers). The two groups were classified according to the Edinburgh Handedness Inventory. Measures of cortical morphology, such as thickness, surface area, volume, and curvature, and the volumes of subcortical structures, such as the amygdala, caudate, hippocampus, globus pallidus, putamen, and thalamus, were compared between the groups according to handedness using whole‐brain 3D T1‐weighted MRI. In addition, we investigated the white matter differences between the groups using diffusion tensor imaging. Moreover, we quantified correlations between the handedness scales of the Edinburgh Handedness Inventory and each measure of different brain morphologies.ResultsThe volumes of the right putamen and left globus pallidus in nonright‐handed participants were significantly larger than those who were right‐handed (0.3559 vs. 0.3155%, p = .0028; 0.1101 vs. 0.0975%, p = .0025; respectively). Moreover, the volumes of the right putamen and left globus pallidus were negatively correlated with the handedness scales of the Edinburgh Handedness Inventory (r = −.392, p = .0101; r = −.361, p = .0189; respectively). However, the cortex morphology and the other subcortical volumes were not significantly different between the two groups. In addition, we did not find any white matter differences between the groups.ConclusionsWe demonstrated that there were significant differences in brain morphology between right‐handers and nonright‐handers, especially in the basal ganglia, which could produce differences in motor control according to handedness.
Based on lumbosacral radiculography through 3D MR rendering, important findings related to the diagnosis of symptomatic extraforaminal disc herniation include swelling of DRG and/or nerve roots and DRG indentation. Ultimately, 3D MR lumbosacral radiculography is a very useful method in the diagnosis of the symptomatic extraforaminal disc herniation.
The synthesis and characterization of [Ru(tpy)(Rbpy)(L)](X) complexes (tpy = 2,2':6',2''-terpyridine, Rbpy = 4,4'-dimethyl-2,2'-bipyridine (dmbpy), or 4,4'-bis(trifluoromethyl)-2,2'-bipyridine (tfmbpy), X = Cl or PF, and n = 1 or 2) are described. The dmbpy and tfmbpy bidentate ligands allow for investigating the effects of electron-donating and electron-withdrawing ligands, respectively, on the frontier orbital energetics as well as the photoreactivity of these ruthenium polypyridyl complexes for five prototypical monodentate ligands L = Cl, HO, CHCN, 2-(methylthio)ethanol (Hmte), or pyridine. According to spectroscopic and electrochemical studies, the dmbpy analogues displayed a singlet metal-to-ligand charge transfer (MLCT) transition at higher energy than the tfmbpy analogues. The shift of the MLCT to higher energy results from the lowest unoccupied molecular orbital (LUMO) for the dmbpy analogues being tpy-based, whereas for the tfmbpy analogues orbital inversion occurs resulting in a tfmbpy-based LUMO. The energy level of the highest occupied molecular orbital (HOMO) was considerably affected by the nature of the monodentate ligand. Visible light irradiation of the complexes demonstrated that the tfmbpy analogue increased the rate and quantum yields of photosubstitution reactions, compared to the dmbpy analogue, suggesting that the electron-withdrawing substituents allowed better thermal accessibility of the triplet metal-centered (MC) state from the photochemically generated triplet metal-to-ligand charge transfer (MLCT) excited state. A correlation between the photolability of the monodentate ligands and the electrochemical reversibility of the metal-based oxidation is also reported.
ObjectiveWe wished to report on the MRI findings of non-infectious ischiogluteal bursitis.Materials and MethodsThe MRI findings of 17 confirmed cases of non-infectious ischiogluteal bursitis were analyzed: four out of the 17 cases were confirmed with surgery, and the remaining 13 cases were confirmed with MRI plus the clinical data.ResultsThe enlarged bursae were located deep to the gluteus muscles and postero-inferior to the ischial tuberosity. The superior ends of the bursal sacs abutted to the infero-medial aspect of the ischial tuberosity. The signal intensity within the enlarged bursa on T1-weighted image (WI) was hypo-intense in three cases (3/17, 17.6%), iso-intense in 10 cases (10/17, 58.9%), and hyper-intense in four cases (4/17, 23.5%) in comparison to that of surrounding muscles. The bursal sac appeared homogeneous in 13 patients (13/17, 76.5%) and heterogeneous in the remaining four patients (4/17, 23.5%) on T1-WI. On T2-WI, the bursa was hyper-intense in all cases (17/17, 100%); it was heterogeneous in 10 cases and homogeneous in seven cases. The heterogeneity was variable depending on the degree of the blood-fluid levels and the septae within the bursae. With contrast enhancement, the inner wall of the bursae was smooth (5/17 cases), and irregular (12/17 cases) because of the synovial proliferation and septation.ConclusionIschiogluteal bursitis can be diagnosed with MRI by its characteristic location and cystic appearance.
The aberrant pyramidal tract (APT) refers to the collateral pathway of the pyramidal tract through the medial lemniscus in the brainstem. We showed the presence of an APT in the normal human brain using diffusion tensor tractography. Diffusion tensor tractography showed that the motor tracts of the 28 hemispheres in 14 healthy normal individuals originated from the primary sensori-motor cortex and descended through the known pathway of the pyramidal tract. However, in five (17.9%) of the 28 hemispheres, we observed that the APT descended through the medial lemniscus from the midbrain to the pons, and then entered into the pyramidal tract at the upper medulla, after which it descended through the pyramidal tract to the lower medulla.
SummaryInduced pluripotent stem cells (iPSCs), generated from somatic cells by overexpression of transcription factors Oct4, Sox2, Klf4 and cMyc have the same characteristics as pluripotent embryonic stem cells (ESCs). iPSCs reprogrammed from differentiated cells undergo epigenetic modification during reprogramming, and ultimately acquire a similar epigenetic state to that of ESCs. In this study, these epigenetic changes were observed in reprogramming of uniparental parthenogenetic somatic cells. The parthenogenetic pattern of imprinted genes changes during the generation of parthenogenetic maternal iPSCs (miPSCs), a process referred to as pluripotent reprogramming. We determined whether altered imprinted genes are maintained or revert to the parthenogenetic state when the reprogrammed cells are redifferentiated into specialized cell types. To address this question, we redifferentiated miPSCs into neural stem cells (miPS-NSCs) and compared them with biparental female NSCs (fNSCs) and parthenogenetic NSCs (pNSCs). We found that pluripotent reprogramming of parthenogenetic somatic cells could reset parthenogenetic DNA methylation patterns in imprinted genes, and that alterations in DNA methylation were maintained even after miPSCs were redifferentiated into miPS-NSCs. Notably, maternally methylated imprinted genes (Peg1, Peg3, Igf2r, Snrpn and Ndn), whose differentially methylated regions were fully methylated in pNSCs, were demethylated and their expression levels were found to be close to the levels in normal biparental fNSCs after reprogramming and redifferentiation. Our findings suggest that pluripotent reprogramming of parthenogenetic somatic cells followed by redifferentiation leads to changes in DNA methylation of imprinted genes and the reestablishment of gene expression levels to those of normal biparental cells.
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