Interest in spatial ability has grown over the past few decades following the emergence of correlational evidence associating spatial aptitude with educational performance in the fields of science, technology, engineering, and mathematics. The research field at large and the anatomy education literature on this topic are mixed. In an attempt to generate consensus, a meta‐analysis was performed to objectively summarize the effects of spatial ability on anatomy assessment performance across multiple studies and populations. Relevant studies published within the past 50 years (1969–2019) were retrieved from eight databases. Study eligibility screening was followed by a full‐text review and data extraction. Use of the Mental Rotations Test (MRT) was required for study inclusion. Out of 2,450 screened records, 15 studies were meta‐analyzed. Seventy‐three percent of studies (11 of 15) were from the United States and Canada, and the majority (9 of 15) studied professional students. Across 15 studies and 1,245 participants, spatial ability was weakly associated with anatomy performance (rpooled = 0.240; CI at 95% = 0.09, 0.38; P = 0.002). Performance on spatial and relationship‐based assessments (i.e., practical assessments and drawing tasks) was correlated with spatial ability, while performance on assessments utilizing non‐spatial multiple‐choice items was not correlated with spatial ability. A significant sex difference was also observed, wherein males outperformed females on spatial ability tasks. Given the role of spatial reasoning in learning anatomy, educators are encouraged to consider curriculum delivery modifications and a comprehensive assessment strategy so as not to disadvantage individuals with low spatial ability.

Ischemicstroke is a leading cause of death and disability in the United States, but recent advances in treatments [i.e., endovascular thrombectomy and tissue plasminogen activator (t-PA)] that target the stroke-causing blood clot, while improving overall stroke mortality rates, have had much less of an impact on overall stroke morbidity. This may in part be attributed to the lack of therapeutics targeting reperfusion-induced injury after the blood clot has been removed, which, if left unchecked, can expand injury from its core into the surrounding at risk tissue (penumbra). This occurs in two phases of increased permeability of the blood-brain barrier, a physical barrier that under physiologic conditions regulates brain influx and efflux of substances and consists of tight junction forming endothelial cells (and transporter proteins), astrocytes, pericytes, extracellular matrix, and their integrin cellular receptors. During, embryonic development, maturity, and following stroke reperfusion, cerebral vasculature undergoes significant changes including changes in expression of integrins and degradation of surrounding extracellular matrix. Integrins, heterodimers with α and β subunits, and their extracellular matrix ligands, a collection of proteoglycans, glycoproteins, and collagens, have been modestly studied in the context of stroke compared with other diseases (e.g., cancer). In this review, we describe the effect that various integrins and extracellular matrix components have in embryonic brain development, and how this changes in both maturity and in the poststroke environment. Particular focus will be on how these changes in integrins and the extracellular matrix affect blood-brain barrier components and their potential as diagnostic and therapeutic targets for ischemic stroke.

Stroke remains a leading cause of death and disability with limited therapeutic options. Endothelial cell β1 integrin receptors play a direct role in blood-brain barrier (BBB) dysfunction through regulation of tight junction proteins and infiltrating leukocytes, potentially mediated by β1 integrins. Following tandem transient common carotid artery/middle cerebral artery occlusion on wild-type mice, we administered the integrin a5b1 inhibitor, ATN-161, intraperitoneal (IP) injection at 1 mg/kg acutely after reperfusion, on post-stroke day (PSD)1 and PSD2. Systemic changes (heart rate, pulse distension, and body temperature) were determined. Additionally, infarct volume and edema were determined by 2,3-triphenyltetrazolium chloride and magnetic resonance imaging, while neurological changes were evaluated using an 11-point Neuroscore. Brain immunohistochemistry was performed for claudin-5, α5β1, IgG, and CD45 + cells, and quantitative polymerase chain reaction (qPCR) was performed for matrix metalloproteinase-9 (MMP-9), interleukin (IL)-1β, collagen IV, and CXCL12. ATN-161 significantly reduced integrin α5β1 expression in the surrounding peri-infarct region with no systemic changes. Infarct volume, edema, and functional deficit were significantly reduced in ATN-161-treated mice. Furthermore, ATN-161 treatment reduced IgG extravasation into the parenchyma through conserved claudin-5, collagen IV, CXCL12 while reducing MMP-9 transcription. Additionally, IL-1β and CD45 + cells were reduced in the ipsilateral cortex following ATN-161 administration. Collectively, ATN-161 may be a promising novel stroke therapy by reducing post-stroke inflammation and BBB permeability.

We have developed a novel tissue banking protocol using mechanical thrombectomy to capture thrombus along with arterial blood proximal and distal to it. The protocol provides high-quality specimens, facilitating analysis of the initial molecular response to ischemic stroke in the human condition for the first time. This approach will permit reverse translation to animal models for treatment development.

BackgroundStroke remains a leading cause of death and disability worldwide despite recent treatment breakthroughs. A primary event in stroke pathogenesis is the development of a potent and deleterious local and peripheral inflammatory response regulated by the pro-inflammatory cytokine interleukin-1 (IL-1). While the role of IL-1β (main released isoform) has been well studied in stroke, the role of the IL-1α isoform remains largely unknown. With increasing utilization of intravenous tissue plasminogen activator (t-PA) or thrombectomy to pharmacologically or mechanically remove ischemic stroke causing blood clots, respectively, there is interest in pairing successful cerebrovascular recanalization with neurotherapeutic pharmacological interventions (Fraser et al., J Cereb Blood Flow Metab 37:3531–3543, 2017; Hill et al., Lancet Neurol 11:942–950, 2012; Amaro et al., Stroke 47:2874–2876, 2016).MethodsTransient stroke was induced in mice via one of two methods. One group of mice were subjected to tandem ipsilateral common carotid artery and middle cerebral artery occlusion, while another group underwent the filament-based middle cerebral artery occlusion. We have recently developed an animal model of intra-arterial (IA) drug administration after recanalization (Maniskas et al., J Neurosci Met 240:22–27, 2015). Sub groups of the mice were treated with either saline or Il-1α, wherein the drug was administered either acutely (immediately after surgery) or subacutely (on the third day after stroke). This was followed by behavioral and histological analyses.ResultsWe now show in the above-mentioned mouse stroke models (transient tandem ipsilateral common carotid artery (CCA) and middle cerebral artery occlusion (MCA) occlusion, MCA suture occlusion) that IL-1α is neuroprotective when acutely given either intravenously (IV) or IA at low sub-pathologic doses. Furthermore, while IV administration induces transient hemodynamic side effects without affecting systemic markers of inflammation, IA delivery further improves overall outcomes while eliminating these side effects. Additionally, we show that delayed/subacute IV IL-1α administration ameliorates functional deficit and promotes neurorepair.ConclusionsTaken together, our present study suggests for the first time that IL-1α could, unexpectedly, be an effective ischemic stroke therapy with a broad therapeutic window.

The well-known vapor-liquid-solid (VLS) mechanism results in high-purity, single-crystalline wires with few defects and controllable diameters, and is the method of choice for the growth of nanowires for a vast array of nanoelectronic devices. It is of utmost importance, therefore, to understand how such wires interact with metallic interconnects-an understanding which relies on comprehensive knowledge of the initial growth process, in which a crystalline wire is ejected from a metallic particle. Though ubiquitous, even in the case of single elemental nanowires the VLS mechanism is complicated by competing processes at multiple heterogeneous interfaces, and despite decades of study, there are still aspects of the mechanism which are not well understood. Recent breakthroughs in studying the mechanism and kinetics of VLS growth have been strongly aided by the use of in situ techniques, and would have been impossible through other means. As well as several systematic studies of nanowire growth, reports which focus on the role and the nature of the catalyst tip reveal that the stability of the droplet is a crucial factor in determining nanowire morphology and crystallinity. Additionally, a reverse of the VLS process dubbed solid-liquid-vapor (SLV) has been found to result in the formation of cavities, or "negative nanowires". Here, we present a series of heating studies conducted in situ in the transmission electron microscope (TEM), in which we observe the complete dissolution of metal oxide nanowires into the metal catalyst particles at their tips. We are able to consistently explain our observations using a solid-liquid-vapor (SLV) type mechanism in which both evaporation at the liquid-vapor interface and adhesion of the catalyst droplet to the substrate surface contribute to the overall rate.

Medical education has reported a shortage of anatomy educators since the 1960s. While the faculty pipeline has recently been explored, insights into retirement intentions, a key driver of faculty turnover, have yet to be investigated. With the mean age of anatomists rising, knowledge of retirement intentions among current educators is essential to understanding the anatomy educator shortage. This study explored the retirement intentions of current anatomy educators and their likely effects on the workforce. Surveys were distributed to department heads and the American Association for Anatomy (AAA) membership to inquire about job postings from 2018–2020 and retirement intentions, respectively. Department heads sought to fill open positions due to faculty retirements (36%, 15 of 42), faculty relocations/sabbaticals/new responsibilities (31%), and brand new positions (24%). The retirement intentions survey revealed that 61% (23 of 38) of faculty ‘55 and older’ intend to retire within five years. Based on the extrapolation of AAA membership data, estimates suggest that almost twice as many anatomy faculty could retire per year (n = 40) over the next five years compared to the estimated number of annual PhD graduates (n = 22) likely to enter the workforce. Factors driving retirement intentions were overwhelmingly age and finances, followed by job satisfaction and family. The creation of new anatomy educator positions to address increased student enrollments and new health sciences programs is likely to place even greater strain on workforce demands.

Ischemic stroke is a leading cause of death and disability with limited therapeutic options. Resulting inflammatory mechanisms after reperfusion (removal of the thrombus) result in cytokine activation, calcium influx, and leukocytic infiltration to the area of ischemia. In particular, leukocytes migrate toward areas of inflammation by use of integrins, particularly integrins β 1 and β 2 . Integrins have been shown to be necessary for leukocyte adhesion and migration, and thus are of immediate interest in many inflammatory diseases, including ischemic stroke. In this review, we identify the main integrins involved in leukocytic migration following stroke (α L β 2 , α D β 2 , α 4 β 1 , and α 5 β 1 ) and targeted clinical therapeutic interventions.