There is poor agreement between the subjective and quantitative adjudication of aneurysm wall enhancement.

BACKGROUND AND PURPOSE: The determination of Aneurysm wall enhancement (AWE) by human readers on visual inspection alone is subjective and prone to error. A three-dimensional (3D) method for quantifying the aneurysm wall's signal intensity (SI) enables objective determination of AWE. Inter-reader agreement and agreement between subjective and objective determination of AWE were assessed in this study. MATERIALS AND METHODS: Patients with saccular intracranial aneurysms (IAs) were imaged with high-resolution MRI. Subjective assessment: Two internal adjudicators visually determined AWE if the degree of enhancement was equal to or higher than the pituitary stalk. An experienced internal neuroradiologist resolved disagreements. This internal adjudication was compared with an external adjudication to assess inter-rater agreement among centers. Objective assessment: The distribution of SI across the aneurysm wall after normalizing the SI to the corpus callosum was determined with an in-house code. The normalized mean SI on post-contrast T1 MRI was defined as 3D-circumferential AWE (3D-CAWE). If the 3D-CAWE value was higher than one, an IA was defined as objectively "enhancing." Inter-rater agreement was analyzed with kappa coefficients. Inter-technique agreement between subjective and objective assessment was performed using kappa statistics. Univariate regressions were performed to identify which morphological characteristics influenced subjective adjudication of enhancement. RESULTS: A total of 113 IAs were analyzed. The agreement of the internal assessment was moderate (k = 0.63), 49.5% of IAs (56) were classified as "enhancing" and 50.5% (57) as "non-enhancing" after consensus. Inter-rater agreement between internal and external adjudication was weak (k = 0.52) for the presence of AWE. There was no agreement between the subjective assessment of AWE and objective 3D-CAWE (k = 0.16, p 0.02). Subjective assessment was less likely to reliably adjudicate enhancement when assessing multiple aneurysms (OR 0.4, 95% CI 0.16 -0.97, p 0.04) and IAs larger than > 7 mm (OR 0.22, 95% CI 0.09 -0.55, p 0.002) despite being objectively "non-enhancing". CONCLUSIONS: Subjective adjudication of AWE has poor inter-rater agreement, and no agreement with an objective 3D method of determining AWE. It is also less likely than objective quantification to identify enhancement in aneurysms larger than 7 mm or when multiple aneurysms are present. Objective 3D quantification, such as the technique used in this study, should therefore be considered when assessing AWE, especially in patients with multiple aneurysms and aneurysms larger than 7 mm in size. ABBREVIATIONS: 3D, three-dimensional; 3D-CAWE, three-dimensional circumferential aneurysm wall enhancement; AWE, aneurysm wall enhancement; Gd, gadolinium; HR-MRI, high resolution MRI; HR 3D T1 VWI, high-resolution 3D T1 weighted black blood vessel wall imaging; IA, intracranial aneurysm; SI, signal intensity.

Study of the Properties of CdS:Al (R = [Al3+]/[Cd2+] = 0.30, 0.40, 0.50) Thin Films Grown by the CBD Method in an Ammonia-Free System.

CdS:Al thin films were fabricated on a glass substrate using the CBD method. The effect of aluminum incorporation on the structural, morphological, vibrational, and optical properties of CdS thin layers was investigated by X-ray diffraction (XRD), Raman spectroscopy (RS), atomic force microscopy (AFM), scanning electron microscopy (SEM), and UV-visible (UV-vis) and photoluminescence (PL) spectroscopies. XRD analysis of deposited thin films confirmed a hexagonal structure with a preferred (002) orientation in all samples. The crystallite size and surface morphology of the films are modified with aluminum content. Raman spectra exhibit fundamental longitudinal optical (LO) vibrational modes and their overtones. Optical properties were studied for each thin film. Here, it was observed that the optical properties of thin films are affected by the incorporation of aluminum into the CdS structure.

The C-Terminal Domain of LRRK2 with the G2019S Substitution Increases Mutant A53T α-Synuclein Toxicity in Dopaminergic Neurons In Vivo.

Alpha-synuclein (α-syn) and leucine-rich repeat kinase 2 (LRRK2) play crucial roles in Parkinson's disease (PD). They may functionally interact to induce the degeneration of dopaminergic (DA) neurons via mechanisms that are not yet fully understood. We previously showed that the C-terminal portion of LRRK2 (ΔLRRK2) with the G2019S mutation (ΔLRRK2G2019S) was sufficient to induce neurodegeneration of DA neurons in vivo, suggesting that mutated LRRK2 induces neurotoxicity through mechanisms that are (i) independent of the N-terminal domains and (ii) "cell-autonomous". Here, we explored whether ΔLRRK2G2019S could modify α-syn toxicity through these two mechanisms. We used a co-transduction approach in rats with AAV vectors encoding ΔLRRK2G2019S or its "dead" kinase form, ΔLRRK2DK, and human α-syn with the A53T mutation (AAV-α-synA53T). Behavioral and histological evaluations were performed at 6- and 15-weeks post-injection. Results showed that neither form of ΔLRRK2 alone induced the degeneration of neurons at these post-injection time points. By contrast, injection of AAV-α-synA53T alone resulted in motor signs and degeneration of DA neurons. Co-injection of AAV-α-synA53T with AAV-ΔLRRK2G2019S induced DA neuron degeneration that was significantly higher than that induced by AAV-α-synA53T alone or with AAV-ΔLRRK2DK. Thus, mutated α-syn neurotoxicity can be enhanced by the C-terminal domain of LRRK2G2019 alone, through cell-autonomous mechanisms.