All-Payer Claims Databases: State Initiatives to Improve Health Care Transparency

Examines states' efforts to support transparency and reform by developing claims databases with comprehensive information on disease incidence, utilization patterns, costs, and health outcomes. Outlines benefits, models, and implementation challenges

Model All-Payer Claims Database Legislation

With support from the Gary and Mary West Health Policy Center, the APCD Council has developed model legislation guidance for states to develop all-payer claims database legislation

All-Payer Claims Database Development Manual: Establishing a Foundation for Health Care Transparency and Informed Decision Making

With support from the Gary and Mary West Health Policy Center, the APCD Council has developed a manual for states to develop all-payer claims databases. Titled All-Payer Claims Database Development Manual: Establishing a Foundation for Health Care Transparency and Informed Decision Making, the manual is a first-of its-kind resource that provides states with detailed guidance on common data standards, collection, aggregation and analysis involved with establishing these databases

Learning to Teach in Mixed-Reality Simulated Virtual Environments at a Hispanic Serving Institution (HSI)

As a result of the COVID-19 pandemic, faculty at a Hispanic serving institution shifted from face-to-face to totally online teaching. The authors describe two assignments for teacher candidates that required them to design and deliver lessons that focused on practicing two high-leverage practices utilizing Mursion, a mixed-reality simulation (MRS) software and platform. MRS sessions were delivered through Zoom video conferencing and were delivered asynchronously. Benefits, challenges, and limitations of using MRS in conjunction with Zoom in online courses were identified and discussed. Detailed logistics for planning, preparing, and executing MRS effectively were provided. The authors describe implications for remote learning as it related to teaching at an HSI located in one of the poorest areas of the U.S., with one of the most vulnerable populations

Using TeachLivE to Foster the Development of High-Leverage Practices in a Teacher Education Program

During the Spring 2020 semester, a group of students (preservice teachers) in the elementary education program at a university in south Texas were required to deliver part of a lesson focusing on one particular high leverage practice, eliciting student thinking in a TeachLivE lab setting. The authors used the Instructional Coaching Model (Knight, 2007) to prepare students for the session and provide feedback immediately after the session. The participants were rated in several aspects of their ability to apply the high-leverage practice (HLP) and were asked to reflect on the process immediately after the TeachLivE session. Quantitative data was analyzed to assess change in the use of the HLP. Qualitative data, in turn, was examined in terms of how participants felt about their performance and what improvements they would like to make in the future

Catheter-Associated Urinary Tract Infection (CAUTI) Prevention Strategy Using Education in an Intensive Care Unit (ICU)

Purpose: To measure clinical impact of an evidence-based educational strategy on urinary tract infection (UTI) rates in a 900+ bed acute care facility located in a southwestern state in the United States (US). Clinical Question: Will a focu son staff education in the ICU on proper placement techniques, care, and early removal of urinary retention catheters reduce incidences of CAUTIs in an ICU setting

Role of Complement Activation in Obliterative Bronchiolitis Post Lung Transplantation

Obliterative bronchiolitis (OB) post lung transplantation involves IL-17 regulated autoimmunity to type V collagen and alloimmunity, which could be enhanced by complement activation. However, the specific role of complement activation in lung allograft pathology, IL-17 production, and OB are unknown. The current study examines the role of complement activation in OB. Complement regulatory protein (CRP) (CD55, CD46, Crry/CD46) expression was down regulated in human and murine OB; and C3a, a marker of complement activation, was up regulated locally. IL-17 differentially suppressed Crry expression in airway epithelial cells in vitro. Neutralizing IL-17 recovered CRP expression in murine lung allografts and decreased local C3a production. Exogenous C3a enhanced IL-17 production from alloantigen or autoantigen (type V collagen) reactive lymphocytes. Systemically neutralizing C5 abrogated the development of OB, reduced acute rejection severity, lowered systemic and local levels of C3a and C5a, recovered CRP expression, and diminished systemic IL-17 and IL-6 levels. These data indicated that OB induction is in part complement dependent due to IL-17 mediated down regulation of CRPs on airway epithelium. C3a and IL-17 are part of a feed forward loop that may enhance CRP down regulation, suggesting that complement blockade could be a therapeutic strategy for OB

Systemic infection modifies the neuroinflammatory response in late stage Alzheimer's disease

Abstract Clinical studies indicate that systemic infections accelerate cognitive decline in Alzheimer’s disease. Animal models suggest that this may be due to enhanced pro-inflammatory changes in the brain. We have performed a post-mortem human study to determine whether systemic infection modifies the neuropathology and in particular, neuroinflammation, in the late-stage of the disease. Sections of cerebral cortex and underlying white matter from controls and Alzheimer's patients who died with or without a terminal systemic infection were immunolabelled and quantified for: (i) Αβ and phosphorylated-tau; (ii) the inflammation-related proteins Iba1, CD68, HLA-DR, FcγRs (CD64, CD32a, CD32b, CD16), CHIL3L1, IL4R and CCR2; and (iii) T-cell marker CD3. In Alzheimer's disease, the synaptic proteins synaptophysin and PSD-95 were quantified by ELISA, and the inflammatory proteins and mRNAs by MesoScale Discovery Multiplex Assays and qPCR, respectively. Systemic infection in Alzheimer's disease was associated with decreased CD16 (p = 0.027, grey matter) and CD68 (p = 0.015, white matter); increased CD64 (p = 0.017, white matter) as well as increased protein expression of IL6 (p = 0.047) and decreased IL5 (p = 0.007), IL7 (p = 0.002), IL12/IL23p40 (p = 0.001), IL15 (p = 0.008), IL16 (p < 0.001) and IL17A (p < 0.001). Increased expression of anti-inflammatory genes CHI3L1 (p = 0.012) and IL4R (p = 0.004) were detected in this group. T-cell recruitment to the brain was reduced when systemic infection was present. However, exposure to systemic infection did not modify the pathology. In Alzheimer's disease, CD68 (p = 0.026), CD64 (p = 0.002), CHI3L1 (p = 0.016), IL4R (p = 0.005) and CCR2 (p = 0.010) were increased independently of systemic infection. Our findings suggest that systemic infections modify neuroinflammatory processes in Alzheimer's disease. However, rather than promoting pro-inflammatory changes, as observed in experimental models, they seem to promote an anti-inflammatory, potentially immunosuppressive, environment in the human brain

MRI-derived g-ratio and lesion severity in newly diagnosed multiple sclerosis

Myelin loss is associated with axonal damage in established multiple sclerosis. This relationship is challenging to study in vivo in early disease. Here, we ask whether myelin loss is associated with axonal damage at diagnosis, by combining non-invasive neuroimaging and blood biomarkers. We performed quantitative microstructural MRI and single molecule ELISA plasma neurofilament measurement in 73 patients with newly diagnosed, immunotherapy naïve relapsing-remitting multiple sclerosis. Myelin integrity was evaluated using aggregate g-ratios, derived from magnetization transfer saturation (MTsat) and neurite orientation dispersion and density imaging (NODDI) diffusion data. We found significantly higher g-ratios within cerebral white matter lesions (suggesting myelin loss) compared with normal-appearing white matter (0.61 vs 0.57, difference 0.036, 95% CI 0.029 to 0.043, p &amp;lt; 0.001). Lesion volume (Spearman’s rho rs= 0.38, p &amp;lt; 0.001) and g-ratio (rs= 0.24 p &amp;lt; 0.05) correlated independently with plasma neurofilament. In patients with substantial lesion load (n = 38), those with higher g-ratio (defined as greater than median) were more likely to have abnormally elevated plasma neurofilament than those with normal g-ratio (defined as less than median) (11/23 [48%] versus 2/15 [13%] p &amp;lt; 0.05). These data suggest that, even at multiple sclerosis diagnosis, reduced myelin integrity is associated with axonal damage. MRI-derived g-ratio may provide useful additional information regarding lesion severity, and help to identify individuals with a high degree of axonal damage at disease onset. York, Martin et al. simultaneously measured g-ratio and plasma neurofilament in 73 relapsing-remitting multiple sclerosis patients at diagnosis using advanced MRI and single molecule ELISA. They demonstrate that g-ratio of cerebral white matter lesions varies at diagnosis, and show that high g-ratio of lesions is associated with elevated plasma neurofilament