36 research outputs found

    Biola Hour Highlights, 1976 - 02

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    A New Year\u27s Message by Richard Chase Death-No Respecter of Humans by Charles Swindoll An Address to the Biola College Student Body by Clyde Narramore Facing the Law of God by Joseph Cooke Revelation by Lloyd Anderson Panel Discussions by Richard Chase, Charles Feinberg, and Samuel Sutherlandhttps://digitalcommons.biola.edu/bhhs/1024/thumbnail.jp

    Biola Hour Highlights, 1976 - 02

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    A New Year\u27s Message by Richard Chase Death-No Respecter of Humans by Charles Swindoll An Address to the Biola College Student Body by Clyde Narramore Facing the Law of God by Joseph Cooke Revelation by Lloyd Anderson Panel Discussions by Richard Chase, Charles Feinberg, and Samuel Sutherlandhttps://digitalcommons.biola.edu/bhhs/1024/thumbnail.jp

    Heterogeneity of cellular inflammatory responses in ageing white matter and relationship to Alzheimer’s and small vessel disease pathologies

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    Abstract: White matter lesions (WML) are common in the ageing brain, often arising in a field effect of diffuse white matter abnormality. Although WML are associated with cerebral small vessel disease (SVD) and Alzheimer’s disease (AD), their cause and pathogenesis remain unclear. The current study tested the hypothesis that different patterns of neuroinflammation are associated with SVD compared to AD neuropathology by assessing the immunoreactive profile of the microglial (CD68, IBA1 and MHC‐II) and astrocyte (GFAP) markers in ageing parietal white matter (PARWM) obtained from the Cognitive Function and Ageing Study (CFAS), an ageing population‐representative neuropathology cohort. Glial responses varied extensively across the PARWM with microglial markers significantly higher in the subventricular region compared to either the middle‐zone (CD68 p = 0.028, IBA1 p < 0.001, MHC‐II p < 0.001) or subcortical region (CD68 p = 0.002, IBA1 p < 0.001, MHC‐II p < 0.001). Clasmatodendritic (CD) GFAP+ astrocytes significantly increased from the subcortical to the subventricular region (p < 0.001), whilst GFAP+ stellate astrocytes significantly decreased (p < 0.001). Cellular reactions could be grouped into two distinct patterns: an immune response associated with MHC‐II/IBA1 expression and CD astrocytes; and a more innate response characterised by CD68 expression associated with WML. White matter neuroinflammation showed weak relationships to the measures of SVD, but not to the measures of AD neuropathology. In conclusion, glial responses vary extensively across the PARWM with diverse patterns of white matter neuroinflammation. Although these findings support a role for vascular factors in the pathogenesis of age‐related white matter neuroinflammation, additional factors other than SVD and AD pathology may drive this. Understanding the heterogeneity in white matter neuroinflammation will be important for the therapeutic targeting of age‐associated white matter damage

    Research and Science Today No. 2(4)/2012

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    THE KINETICS OF CALCITE DISSOLUTION PRECIPITATION

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    The channel-flow cell method is used to establish the dissolution/precipitation kinetics of calcite under wide ranges of bulk Ca1+ concentration (0-10 mM) and solution flow rate (10-30.3 cm3 s-1) for different bulk pH values. Detailed mathematical modeling of the heterogeneous reaction, and accompanying solution processes leads to the following rate equation based on a model in which Ca2+ and CO2- 3 undergo Langmuirian adsorption on the calcite surface: Dnet/mol cm-2s-1 = kbKCaKCO3 { KSP - [Ca2+]o[CO2- 3]O (1 + KCo[Ca2+]o(1 + KCO3 [CO3]o)} Here Dnet is the net flux of dissolving calcium ions, kb is a rate constant, Ksp, is the solubility product of calcite corrected for the ionic strength of the solution, KA (A = Ca2+ or CO2- 3) are Langmuirian adsorption constants, and [ ]o denotes the concentration at the Outer Helmholtz Plane. © 1993 Academic Press. All rights reserved

    Childhood Immunization Rates Before and After the Implementation of Medicaid Managed Care

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    Objective: To evaluate trends in childhood immunization coverage after implementation of Medicaid managed care in Tennessee (TennCare) in 1994. Design: Before-and-after study using the Tennessee Department of Health annual cross-sectional survey of children aged 24 months. Patients: A mean of 1663 children per year who were randomly sampled during 1986-1999. Main Outcome Measure: Completion rate for recommended immunizations by the age of 24 months or younger. Results: A total of 23 044 children were included. The proportion of children continuously enrolled in Medicaid from age 1 to 24 months increased slightly with TennCare. Among children enrolled, immunization rates increased considerably before TennCare (1986-1993) and continued to increase after TennCare (1994-1999), albeit less dramatically. Immunization coverage was significantly lower for children enrolled compared with children not enrolled in fee-for-service Medicaid. Among children enrolled in fee-for-service Medicaid, black children were more likely to be inadequately immunized than white children (40% vs 26%; relative risk [RR], 1.56; 95% confidence interval [CI], 1.40-1.73). These gaps were nearly eliminated after TennCare. An increased proportion of children enrolled in TennCare received immunizations in the private sector. Among children enrolled in fee-for-service Medicaid, those receiving immunizations entirely in the private sector were more likely to have incomplete immunization status than children immunized entirely in the public sector (27% vs 21%; RR, 1.28; 95% CI, 1.20-1.37). Under TennCare and after implementation of the Vaccines for Children program in Tennessee, the difference was not significant. Conclusions: Overall, TennCare had no discernible negative effect on immunization rates in Tennessee and perhaps contributed to decreasing the immunization gap between children enrolled and children not enrolled in Medicaid and between black and white children
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