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Foster, R. R.

Publications and source records attributed to Foster, R. R..

2 recordsLinked to original sources

Time-series models can forecast long periods of human temporalEEG responses to randomly alternating visual stimuli

Visual stimuli with constant temporal frequency input is known to induce peaks in the driving frequency of the power spectrum of the electroencephalogram (EEG) over the visual cortex. While EEG responses with random temporal frequencies (m-sequences) have been studied, the underlying mechanisms that shape these responses are not fully understood. We analyze our new EEG data from a controlled experiment with m-sequence inputs and model the EEG using statistical time series models: an autoregressive (AR) model, adding exogenous input to AR (ARX), adding moving average terms (ARMAX), and finally adding a seasonality term (SARMAX). We implement computational methods to robustly handle model instabilities induced by this data, fitting these models with the Box-Jenkins methodology and assessing prediction accuracy for long periods of several seconds out-of-sample. We find in-sample fits are good in all models despite the complexities of the visual pathway, and that all models can predict aspects of EEG: including the distribution of point-wise values in time, the point-wise Pearsons correlation of EEG and model, and the frequency content. Surprisingly, we find little variation in the performance among these models, with the most sophisticated model (SARMAX) performing comparatively poorly in some instances. Our results suggest the simplest AR model is viable and can out perform more complicated models. Since these models are relatively simple and more transparent than contemporary models with numerous parameters, our study could inform future mechanistic studies of the temporal dynamics of human EEG responses to visual stimuli.

neuroscience↗

Inhibition of MMP 2 protects the endothelial glycocalyx and improves diastolic function in diabetic cardiomyopathy

The coronary microvascular endothelial glycocalyx (EGlx) is a vital regulator of vascular permeability and EGlx damage contributes to the development of diabetic cardiomyopathy. Matrix metalloproteinases 2 and 9 (MMP2/9) have been identified as key enzymes in the degradation of EGlx components, notably syndecan 4 (SDC4), and are upregulated in diabetes. We tested the hypothesis that inhibition of MMP2/9 can protect the EGlx and improve diastolic function in diabetic cardiomyopathy. Type 1 diabetes was induced in FVB mice by streptozotocin (STZ) injections. Mice were treated with daily injections of the MMP2/9 inhibitor, SB-3CT, for 2 weeks from 7 weeks post STZ. Echocardiography was utilised to assess heart function and lectin staining for the measurement of EGlx depth. Immunolabelling of heart sections for albumin provided an indication of albumin extravasation. A mechanism of EGlx shedding was investigated in vitro in human coronary microvascular endothelial cells treated with TNF- and SB-3CT. Diabetic mice developed diastolic dysfunction from 6 weeks post STZ. MMP2/9 inhibition reversed diastolic dysfunction, EGlx thinning and albumin extravasation in diabetic animals. In vitro, TNF- caused an increase in MMP9 activity and SDC4 shedding from human coronary microvascular endothelial cells. Treatment with SB-3CT reduced MMP9 activity and prevented SDC4 shedding. Knockdown of MMP9 expression prevented TNF- induced SDC4 shedding. This study demonstrates MMP2/9 inhibition as a strategy to protect the EGlx and improve diastolic function in diabetic cardiomyopathy. Our findings suggest new avenues for therapeutic interventions in cardiovascular complications associated with diabetes. Statements and DeclarationsO_ST_ABSCompeting interestsC_ST_ABSThe authors have no competing interests to declare that are relevant to the content of this article.

physiology↗