24 research outputs found

    Brain age as a surrogate marker for cognitive performance in multiple sclerosis

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    Background: Data from neuro-imaging techniques allow us to estimate a brain's age. Brain age is easily interpretable as "how old the brain looks", and could therefore be an attractive communication tool for brain health in clinical practice. This study aimed to investigate its clinical utility by investigating the relationship between brain age and cognitive performance in multiple sclerosis (MS). Methods: A linear regression model was trained to predict age from brain MRI volumetric features and sex in a healthy control dataset (HC_train, n=1673). This model was used to predict brain age in two test sets: HC_test (n=50) and MS_test (n=201). Brain-Predicted Age Difference (BPAD) was calculated as BPAD=brain age minus chronological age. Cognitive performance was assessed by the Symbol Digit Modalities Test (SDMT). Results: Brain age was significantly related to SDMT scores in the MS_test dataset (r=-0.46, p<.001), and contributed uniquely to variance in SDMT beyond chronological age, reflected by a significant correlation between BPAD and SDMT (r=-0.24, p<.001) and a significant weight (-0.25, p=0.002) in a multivariate regression equation with age. Conclusions: Brain age is a candidate biomarker for cognitive dysfunction in MS and an easy to grasp metric for brain health

    Immobilization of animal rennet.

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    Rennet was immobilized on porous glass beads (50-100 mesh) using diazotization [Paquot et al., DSA 38, 5851], TiCl4 [Barker et al., Process Biochemistry (1971) 5, 11], glutaraldehyde [Stanley & Olson, Journal of Food Science (1974) 39, 660] or glutaraldehyde followed by reduction of aldehyde groups by NaBH4 [Cheryan et al., DSA 38, 6728]. Residual enzyme activity was low using all 4 methods, being highest using TiCl4 (24.4%). After 13 days storage, loss of enzyme activity using diazotization and TiCl4 was resp. 82 and 58%. Activity of rennet immobilized using TiCl4 decreased with time during the passage of milk through the column, this being due to release of enzyme rather than denaturation. Ca2+ ions were responsible for the release; loss of enzyme activity during four 15-min passages of whey, casein solution (pH 7) and casein solution + EDTA was resp. 87, 57 and 4.5%. Precoating the glass beads with serum albumin resulted in significant increases in residual activity of rennet, particularly when immobilized using glutaraldehyde/NaBH4. This improvement diminished on storage

    Characterization of a protein serine kinase from yeast plasma membrane.

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    A casein kinase activity, which copurifies with the H+-ATPase activity during isolation of plasma membranes Saccharomyces cerevisiae and during centrifugation of the solubilized membrane extract through a sucrose gradient, is separated from the Mr = 100,000 ATPase catalytic polypeptide by subsequent DEAE-cellulose chromatography. The purified casein kinase activity exhibits a low Km of 12 microM MgATP, is maximally stimulated by 6 mM free Mg2+, and is 50% inhibited by 300 microM Zn2+, by 7.5 micrograms of heparin/ml, and by 300 microM orthovanadate. It phosphorylates only seryl residues. The purified casein kinase contains two polypeptides of Mr = 45,000 and 39,000 which yield antibodies which do not cross-react to each other. The two polypeptides seem to originate from a precursor of Mr = 85,000 which is detected by both antibodies in partly purified fractions. In the absence of casein, a zinc and heparin-sensitive phosphorylation of the ATPase polypeptide is observed in partly purified ATPase fractions, and a peptide of similar mobility is phosphorylated, among others, in isolated plasma membranes. The purified ATPase activity is markedly inhibited by incubation in the presence of acid phosphatase. In agreement with a recent report that the purified active ATPase molecule is largely phosphorylated (Yanagita, Y., Abdel-Ghany, M., Raden, D., Nelson, N., and Racker, E. (1987) Proc. Natl. Acad. Sci. U. S. A. 894, 925-929) this data suggests that dephosphorylation leads to deactivation of ATPase activity

    A mass sensor based on 3-DOF mode localized coupled resonator under atmospheric pressure

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    In this paper, for the first time, the mass sensitivity of a 3-DoF mode localized electrostatically coupled resonator is investigated and characterized under atmospheric pressure. A reversible method is used in which nanoparticles are added on and removed from one resonator of the 3-DOF coupled resonator system. Furthermore, a comparison of three mass sensitivity characterization methods was carried out: resonance frequency shift, resonance vibration amplitude change and resonance vibration amplitude ratio. MATLAB/SIMULINK and COMSOL Multiphysics models for the 3-DoF coupled resonator system are presented. The simulation results and theoretical calculations are in good agreement with the experimental data. The results show that a 3-DOF mode localized coupled resonator has potential to be employed for biosensing applications

    The role of hippocampal theta oscillations in working memory impairment in multiple sclerosis

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    Working memory (WM) problems are frequently present in people with multiple sclerosis (MS). Even though hippocampal damage has been repeatedly shown to play an important role, the underlying neurophysiological mechanisms remain unclear. This study aimed to investigate the neurophysiological underpinnings of WM impairment in MS using magnetoencephalography (MEG) data from a visual‐verbal 2‐back task. We analysed MEG recordings of 79 MS patients and 38 healthy subjects through event‐related fields and theta (4–8 Hz) and alpha (8–13 Hz) oscillatory processes. Data was source reconstructed and parcellated based on previous findings in the healthy subject sample. MS patients showed a smaller maximum theta power increase in the right hippocampus between 0 and 400 ms than healthy subjects (p = .014). This theta power increase value correlated negatively with reaction time on the task in MS (r = −.32, p = .029). Evidence was provided that this relationship could not be explained by a ‘common cause’ confounding relationship with MS‐related neuronal damage. This study provides the first neurophysiological evidence of the influence of hippocampal dysfunction on WM performance in MS
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