Sustaining the Use of Evidence-Based Tier 1 Literacy Practices That Benefit Students With Disabilities.

The adoption and sustainability of evidence-based Tier 1 literacy practices in secondary content-area classes is important to improve reading success for students with learning disabilities. We conducted an exploratory multiple-case study investigating teachers' adoption and sustained use of evidence-based Tier 1 literacy practices that benefit students with learning disabilities. The study was conducted within the context of an adolescent literacy model demonstration project funded by the U.S. Office of Special Education Programs (i.e., Promoting Adolescents' Comprehension of Text [PACT] Plus). Interviews were conducted with two administrators and seven teachers who sustained implementation of the PACT practices beyond 1 year of researcher support. Analyses revealed practice and school-level factors that influenced teachers' sustained use of the practices. We used findings from this study to propose a model of sustainability of Tier 1 evidence-based literacy practices used to improve outcomes for students with learning disabilities. Limitations and implications for future research are provided.

Delayed Diagnosis of Paget-Schroetter Syndrome in a Patient with COVID-19.

Paget-Schroetter Syndrome (PSS), a subtype of thoracic outlet syndrome, is a rare condition defined as thrombosis of the axillosubclavian vein secondary to anatomical abnormalities or repetitive injury to vessel endothelium from exertion. In the setting of the COVID-19 pandemic, venous thrombosis in COVID-positive patients may be attributed to the well-described hypercoagulability associated with the viral syndrome, increasing the rate of misdiagnosis of PSS and delaying definitive treatment. We report a case of PSS in a 19-year-old male who presented to multiple health care providers with an upper extremity thrombus and was found to be SARS-CoV-2 positive on hospitalization. In his case, his COVID status likely contributed to a delay in diagnosis of Paget- Schroetter syndrome, with the patient missing the window for the standard treatment protocol.

The Pathophysiological Sequence of Glucocorticoid-Induced Osteonecrosis of the Femoral Head in Male Mice.

In search of the sequence of pathogenic events leading to glucocorticoid-induced osteonecrosis, we determined the molecular, biomechanical, cellular, and vascular changes in the femur of C57BL/6 mice receiving prednisolone for 14, 28, or 42 days. The femoral head, but not the distal femur, of mice treated for 14 days showed a decrease in the expression of the hypoxia-inducible factor (Hif)-1α and vascular endothelial growth factor (VEGF), the number of osteoblasts, and bone formation rate and strength and showed an increase in osteoclasts. These changes were accompanied by conversion of the normal dendritic vasculature to pools of edema as detected by magnetic resonance imaging, providing robust diagnostic evidence of early osteonecrosis. At that time point, there were no detectable changes in bone density, cortical or cancellous bone architecture, midshaft or distal cancellous bone, or osteocyte apoptosis. In mice treated for 28 days, femoral head cancellous density, cortical width, and trabecular thickness decreased, and by 42 days the femoral heads had full-depth cortical penetrations and cancellous tissue osteonecrosis. These results indicate that the femoral head is a particularly sensitive anatomical site to the adverse effects of glucocorticoid excess on bone and that decreases of Hif-1α and VEGF expression, bone vascularity, and strength precede the loss of bone mass and microarchitectural deterioration, thus rendering the femoral head vulnerable to collapse.

Mitochondrial catalase overexpressed transgenic mice are protected against lung fibrosis in part via preventing alveolar epithelial cell mitochondrial DNA damage.

RATIONALE: Alveolar epithelial cell (AEC) injury and mitochondrial dysfunction are important in the development of lung fibrosis. Our group has shown that in the asbestos exposed lung, the generation of mitochondrial reactive oxygen species (ROS) in AEC mediate mitochondrial DNA (mtDNA) damage and apoptosis which are necessary for lung fibrosis. These data suggest that mitochondrial-targeted antioxidants should ameliorate asbestos-induced lung. OBJECTIVE: To determine whether transgenic mice that express mitochondrial-targeted catalase (MCAT) have reduced lung fibrosis following exposure to asbestos or bleomycin and, if so, whether this occurs in association with reduced AEC mtDNA damage and apoptosis. METHODS: Crocidolite asbestos (100µg/50µL), TiO2 (negative control), bleomycin (0.025 units/50µL), or PBS was instilled intratracheally in 8-10 week-old wild-type (WT - C57Bl/6J) or MCAT mice. The lungs were harvested at 21d. Lung fibrosis was quantified by collagen levels (Sircol) and lung fibrosis scores. AEC apoptosis was assessed by cleaved caspase-3 (CC-3)/Surfactant protein C (SFTPC) immunohistochemistry (IHC) and semi-quantitative analysis. AEC (primary AT2 cells from WT and MCAT mice and MLE-12 cells) mtDNA damage was assessed by a quantitative PCR-based assay, apoptosis was assessed by DNA fragmentation, and ROS production was assessed by a Mito-Sox assay. RESULTS: Compared to WT, crocidolite-exposed MCAT mice exhibit reduced pulmonary fibrosis as measured by lung collagen levels and lung fibrosis score. The protective effects in MCAT mice were accompanied by reduced AEC mtDNA damage and apoptosis. Similar findings were noted following bleomycin exposure. Euk-134, a mitochondrial SOD/catalase mimetic, attenuated MLE-12 cell DNA damage and apoptosis. Finally, compared to WT, asbestos-induced MCAT AT2 cell ROS production was reduced. CONCLUSIONS: Our finding that MCAT mice have reduced pulmonary fibrosis, AEC mtDNA damage and apoptosis following exposure to asbestos or bleomycin suggests an important role for AEC mitochondrial H2O2-induced mtDNA damage in promoting lung fibrosis. We reason that strategies aimed at limiting AEC mtDNA damage arising from excess mitochondrial H2O2 production may be a novel therapeutic target for mitigating pulmonary fibrosis.