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The lateral parietal lobe, such as right inferior parietal lobe (IPL) and supramarginal gyrus (SMG), was detected as the discriminative features exclusively in Slow-4. Our findings, at the first time, indicated that the ML approach is a promising choice for detecting abnormal regions in PD, and a multi-frequency scheme would provide us more specific information. Genetic neurodevelopmental disorders - that often include epilepsy as part of their phenotype - are a heterogeneous and clinically challenging spectrum of disorders in children. Although seizures often contribute significantly to morbidity in these affected populations, the mechanisms of epileptogenesis in these conditions remain poorly understood. Different model systems have been developed to aid in unraveling these mechanisms, which include a number of specific mutant mouse lines which genocopy specific general types of mutations present in patients. These mouse models have not only allowed for assessments of behavioral and electrographic seizure phenotypes to be ascertained, but also have allowed effects on the neurodevelopmental alterations and cognitive impairments associated with these disorders to be examined. In addition, these models play a role in advancing our understanding of these epileptic processes and developing preclinical therapeutics. TTI 101 clinical trial The concordance of seizure phenotypes - in a select group of rare, genetic, neurodevelopmental disorders and epileptic encephalopathies - found between human patients and their model counterparts will be summarized. This review aims to assess whether models of Rett syndrome, CDKL5 deficiency disorder, Fragile-X syndrome, Dravet syndrome, and Ohtahara syndrome phenocopy the seizures seen in human patients. Non-alcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD) are worldwide public health problems, affecting up to 25-30% (NAFLD), and up to 10-15% (CKD) of the general population. Recently, it has also been established that there is a strong association between NAFLD and CKD, regardless of the presence of potential confounding diseases such as obesity, hypertension and type 2 diabetes. Since NAFLD and CKD are both common diseases that often occur alongside other metabolic conditions, such as type 2 diabetes or metabolic syndrome, elucidating the relative impact of NAFLD on the risk of incident CKD presents a substantial challenge for investigators working in this research field. A growing body of epidemiological evidence suggests that NAFLD is an independent risk factor for CKD and recent evidence also suggests that associated factors such as metabolic syndrome, dysbiosis, unhealthy diets, platelet activation and processes associated with ageing could also contribute mechanisms linking NAFLD and CKD. This narrative review provides an overview of the literature on a) the evidence for an association and causal link between NAFLD and CKD and b) the underlying mechanisms by which NAFLD (and factors strongly linked with NAFLD) may increase the risk of developing CKD. PURPOSE To apply in vivo corneal confocal microscopy (IVCM) to study the pathogenesis of keratitis (keratoendotheliitis) fugax hereditaria, an autosomal dominant cryopyrin-associated periodic keratitis, associated with the c.61G>C pathogenic variant in the NLRP3 gene, in its acute and chronic phase, and to report histopathological findings after penetrating keratoplasty. DESIGN Observational case series METHODS Study population Six patients during an acute attack, 18 patients in the chronic phase, and one patient who underwent penetrating keratoplasty. INTERVENTION Sanger sequencing for the NLRP3 variant c.61C>G. Clinical examination, corneal photography, IVCM, light microscopy and immunohistochemistry. MAIN OUTCOME MEASURES IVCM and histopathological findings. RESULTS During the acute attack, hyperreflective cellular structures consistent with inflammatory cells transiently occupied the anterior to middle layers of the corneal stroma. Other corneal layers were unremarkable. With recurring attacks, central oval stromal opacities accumulated. IVCM revealed that they contained long hyperreflective needle-shaped structures in extracellular matrix. By light microscopy, the anterior half of the stroma displayed thin and finely vacuolated lamellae, and keratocytes throughout the stroma were immunopositive for syndecan. CONCLUSIONS The acute attacks and chronic stromal deposits mainly involve the anterior to middle layers of the corneal stroma, and the disease is primarily a keratitis rather than a keratoendotheliitis. IVCM shows that inflammatory cells invade only the stroma during an acute attack. IVCM and light microscopic findings suggest that the central corneal opacities represent gradual deposition of extracellular lipids. The disease could make a good in vivo model to study activation of the NLRP3 inflammasome in cryopyrin-associated periodic syndromes. PURPOSE To demonstrate the proper use of the Phansalkar's local thresholding method (Phansalkar method) in choriocapillaris (CC) quantification with optical coherence tomography angiography (OCTA). DESIGN Retrospective, observational case series. METHODS Swept source OCTA imaging was performed using 3x3 mm and 6x6 mm scanning patterns. The CC slab was extracted following semi-automatic segmentation of the retinal pigment epithelium/Bruch's membrane complex. Retinal projection artifacts were removed before further analysis, and CC OCTA images from drusen eyes were compensated using a previously published strategy. CC flow deficits (FDs) were segmented with two previously published algorithms fuzzy C-means approach (FCM method) and Phansalkar method. With the Phansalkar method, different parameters were tested and a local window radius of 1-15 pixels was used. FD density (FDD), mean FD size (MFDS) and FD number (FDN) were calculated for comparison. RESULTS Six normal eyes from six subjects and six eyes with drusen secondary to age-related macular degeneration from six subjects were analyzed. With both 3x3 mm and 6x6 mm scans from all eyes, the FD metrics were highly dependent on the selection of the local window radius when using the Phansalkar method. Larger window radii resulted in higher FDD values. FDN increased with the increase in the window radius but then decreased, with an inflection point at about 1 - 2 inter-capillary distances (ICDs). MFDS decreased then increased with increasing window radii. CONCLUSIONS Multiple parameters, especially the local window radius, should be optimized before using the Phansalkar method for the quantification of CC FDs with OCTA imaging. It is recommended that the proper use of the Phansalkar method should include the selection of the window radius that is related to the expected ICD in normal eyes.
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