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Preeclampsia complicates 2-8% of pregnancies and is associated with prematurity and intrauterine growth restriction. Cholesterol and sterol transport is a key function of the placenta and it is elicited through ATP binding cassette (ABC) transporters. ABCA1 expression changes during trophoblast cell fusion, a process required to form the placental syncytium that enables maternal-fetal nutrient transfer. ABCA1 expression is dysregulated in preeclamptic placentas. But whether ABC transporters expression during trophoblast fusion is disrupted in preeclampsia remains unknown. We investigated if cholesterol and sterol ABC transporters are altered in term and preterm preeclampsia placentas and during human cytotrophoblast syncytialization. Human placental biopsies were collected from healthy term (≥37 weeks; n = 11) and term preeclamptic (≥36 6/7 weeks; n = 8) and pre-term preeclamptic (28-35 weeks; n = 8) pregnancies. Both, protein and mRNA expression for ABCA1, ABCG1, ABCG5, and ABCG8 were evaluated. Primary cytotrophoblasts isolated from a subset of placentas were induced to syncytialize for 96 h and ABCA1, ABCG1 and ABCG8 mRNA expression evaluated at 0 h and 96 h. Protein and gene expression of ABC transporters were not altered in preeclamptic placentas. In the healthy Term group, ABCA1 expression was similar before and after syncytialization. After 96 h of syncytialization, mRNA expression of ABCA1 and ABCG1 increased significantly, while ABCG8 decreased significantly in term-preeclampsia, but not pre-term preeclampsia. While placental expression of ABCA1 and ABCG1 remained unaltered in term preeclampsia, the disruption in their dynamic expression pattern during cytotrophoblast syncytialization suggests that cholesterol transport may contribute to the pathophysiologic role of the placenta in preeclampsia. [ABSTRACT FROM AUTHOR]

Abstract: The survival and growth of oak advance regeneration is often limited by shade-tolerant species that are abundant in the understory of oak stands. Evidence of historic burning has prompted the use of prescribed fire as a tool to improve the competitive status of oak regeneration in mature stands. A primary shortfall of fire effects research in oak forests has been a lack of long-term studies on the effects of multiple fires. Here we describe the effects of repeated fires on stand structure and tree regeneration over a 13-year period in mature mixed-oak forests located in southern Ohio, USA. Three stands were burned 3–5 times from 1996 to 2005 with low-intensity dormant-season fires, and two stands remained unburned. Woody vegetation was sampled periodically on nine 0.125ha plots per stand. Plots were located across the upland landscape and were characterized by an Integrated Moisture Index. Fire altered stand structure by reducing the density of large saplings (3.0–9.9cm DBH) and midstory trees (10–25cm DBH) by 76% and 34%, respectively. Fire had little impact on trees >25cm DBH. Small saplings (1.4m tall to 2.9cm DBH) were dynamic over time on dry plots that were burned. After being repeatedly topkilled from year 1–8, the small sapling layer had redeveloped on dry burned plots by year 13 and species composition had shifted from dominance by shade-tolerant species to a more equal distribution of shade-tolerants, oaks+hickories, and sassafras. The density of oak+hickory and sassafras advance regeneration (stems 30cm tall to 2.9cm DBH) was significantly greater on burned plots than on unburned plots in year 13, though variability among plots was high. Advance regeneration of shade-tolerant species was equally abundant on burned and unburned plots. Density of oak+hickory advance regeneration in year 13 was positively related to its weighted frequency (a surrogate for size and abundance) in year 0 (r 2 =0.67, p <0.0001) and inversely related to stand density (r 2 =0.33, p <0.0001) and canopy cover (r 2 =0.31, p <0.0001), both of which were reduced by fire. Although oak+hickory advance regeneration was more abundant on burned plots, we conclude that other methods (e.g., herbicide, partial cutting) are necessary to further reduce stand density and promote the development of larger oak+hickory regeneration, particularly on mesic sites. [Copyright &y& Elsevier]

Background: The coronavirus disease 2019 (COVID-19) pandemic has increased burden on healthcare systems with subsequent reductions in non-emergent hospitalizations and procedures. While there are widespread reports of intentional reductions in elective hospitalizations, trends in urgent or emergent hospitalizations including heart failure (HF) hospitalizations have not been adequately characterized.Methods: We evaluated trends of HF hospitalizations before and during the COVID-19 pandemic at the University of Mississippi Medical Center using electronic health records and discharge database. We also compared HF hospitalization trends during the same time frame in 2019 to account for seasonal variation in HF presentations.Results: Prior to the COVID-19 pandemic in our medical center, a mean of 30 patients per week were admitted with a principal diagnosis of HF. After the first case of COVID-19 was diagnosed in Mississippi, there was a sharp 50% decline in the number of HF hospitalizations that declined even further after a "state of emergency" was declared in Mississippi.Conclusions: Based on observations from a large academic medical center, there has been a significant reduction in the number of patients hospitalized for HF during the COVID-19 pandemic. Further investigation of these trends is warranted to determine the effects of the COVID-19 pandemic on long-term HF outcomes. [ABSTRACT FROM AUTHOR]

Introduction: A new orthodontic bracket bonding method or material invariably spawns bond strength studies examining the efficacy of the innovation. The primary purpose of this project was to ascertain whether the mode of in-vitro bracket debonding used in a study affects the measured bond strength. The secondary aim was to compare the bond strengths of 2 different bonding systems. Methods: Flattened stainless steel orthodontic brackets were bonded to flattened bovine enamel with a resin composite bonding agent (Transbond XT, 3M Unitek, Monrovia, Calif). The enamel was prepared with traditional acid etching and priming (37% phosphoric acid gel and Transbond XT Primer, 3M Unitek) or a single-step method (Transbond Plus, 3M Unitek) that combined etching and priming. Cement thickness was kept constant, and bonding was done under controlled temperature and humidity. Brackets were debonded in shear-peel, tension, or torsion. Results: When tested in shear-peel mode, traditional etching and priming produced a stronger bond than the single-step self-etch system. When tested in tension, the traditional bond was weaker than the single-step bond, and when tested in torsion, the bond strengths were similar. Conclusions: Bond strength can vary depending on the method of testing. Claims of clinical efficacy might not be valid. [Copyright &y& Elsevier]

An exostosis or osteochondroma is an aberrant bony growth occurring next to the growth plate either as an isolated growth abnormality or as part of the Hereditary Multiple Exostosis (HME) syndrome. Mutations in either exostosin 1 (EXT1) or exostosin 2 (EXT2) gene cause the HME syndrome and also some isolated osteochondromas. The EXT1 and EXT2 genes are glycosyltransferases that function as hetero-oligomers in the Golgi to add repeating glycosaminoglycans (GAGs) to heparan sulfate (HS) chains. Previously, we demonstrated that HS is markedly diminished in the exostosis cartilage cap and that the HS proteoglycan, perlecan, has an abnormal distribution in these caps. The present studies were undertaken to evaluate which chondrocyte-specific functions are associated with diminished HS synthesis in human chondrocytes harboring either EXT1 or EXT2 mutations. Systematic evaluation of exostosis cartilage caps and chondrocytes, both in vitro and in vivo, suggests that chondrocyte-specific cell functions account for diminished HS levels. In addition, we provide evidence that perichondrial cells give rise to chondrocytes that clonally expand and develop into an exostosis. Undifferentiated EXT chondrocytes synthesized amounts of HS similar to control chondrocytes; however, EXT chondrocytes displayed very poor survival in vitro under conditions that promote normal chondrocyte differentiation with high efficiency. Collectively, these observations suggest that loss of one copy of either the EXT1 or EXT2 gene product compromises the perichondrial chondrocytes' ability to differentiate normally and to survive in a differentiated state in vitro. In vivo, these compromised responses may lead to abnormal chondrocyte growth, perhaps from a perichondrial stem cell reserve. [ABSTRACT FROM AUTHOR]