Response of UK interventional radiologists to the COVID-19 pandemic - survey findings.

Background: The COVID-19 pandemic has had an unprecedented effect upon the National Health Service (NHS). Like other specialties, Interventional Radiology (IR) rapidly adapted to the evolving situation. Members of BSIR were surveyed to obtain a snapshot of the experiences of UK IRs in response to COVID-19.

Management of blunt splenic injury in a UK major trauma centre and predicting the failure of non-operative management: a retrospective, cross-sectional study.

Purpose: To review the management of patients >16 years with blunt splenic injury in a single, UK, major trauma centre and identify whether the following are associated with success or failure of non-operative management with selective use of arterial embolization (NOM ± AE): age, Injury Severity Score (ISS), head injury, haemodynamic instability, massive transfusion, radiological hard signs [contrast extravasation or pseudoaneurysm on the initial computed tomography (CT) scan], grade, and presence of intraparenchymal haematoma or splenic laceration.

Methods: Retrospective, cross-sectional study undertaken between April 2012 and October 2015. Paediatric patients, penetrating splenic trauma, and iatrogenic injuries were excluded.

Hypoxic proliferation requires EGFR-mediated ERK activation in human pulmonary microvascular endothelial cells.

We have previously shown that hypoxic proliferation of human pulmonary microvascular endothelial cells (hPMVECs) depends on epidermal growth factor receptor (EGFR) activation. To determine downstream signaling leading to proliferation, we tested the hypothesis that hypoxia-induced proliferation in hPMVECs would require EGFR-mediated activation of extracellular signal-regulated kinase (ERK) leading to arginase II induction. To test this hypothesis, hPMVECs were incubated in either normoxia (21% O, 5% CO) or hypoxia (1% O, 5% CO) and Western blotting was performed for EGFR, arginase II, phosphorylated-ERK (pERK), and total ERK (ERK).

Non-invasive assessment of portal hypertension using quantitative magnetic resonance imaging.

Background & Aims: Hepatic venous pressure gradient (HVPG) measurement is currently the only validated technique to accurately evaluate changes in portal pressure. In this study, we evaluate the use of non-contrast quantitative magnetic resonance imaging (MRI) as a surrogate measure of portal pressure.

Methods: Thirty patients undergoing HVPG measurement were prospectively recruited.

The Src family tyrosine kinases src and yes have differential effects on inflammation-induced apoptosis in human pulmonary microvascular endothelial cells.

Endothelial cells are essential for normal lung function: they sense and respond to circulating factors and hemodynamic alterations. In inflammatory lung diseases such as acute respiratory distress syndrome, endothelial cell apoptosis is an inciting event in pathogenesis and a prominent pathological feature. Endothelial cell apoptosis is mediated by circulating inflammatory factors, which bind to receptors on the cell surface, activating signal transduction pathways, leading to caspase-3-mediated apoptosis.

Disparities by race, ethnicity, and sex in treating acute coronary syndromes.

Background: Disparities in the management of coronary artery disease were consistently documented in blacks and women in the 1980s and 1990s. Our objective was to determine if racial/ethnic and sex differences in the use of coronary revascularization persist in a more recent cohort.

Methods: We examined all 20,604 Medicare beneficiaries admitted for acute coronary syndrome in 2001 from a random sample of 750,000 enrollees that was oversampled for black and Hispanic subjects to assess any cardiac revascularization.

Tracking abnormal cervical cancer screening: evaluation of an EMR-based intervention.

Introduction: System level barriers have been associated with inadequate follow-up of abnormal cervical cytology.

Objective: The aim of this study was to develop and evaluate an electronic tracking system to improve follow-up of abnormal Pap tests.

Program Description: We implemented an electronic medical record (EMR)-based Pap test tracking system at two clinical practices at an inner-city academic health center.

Progress and priorities in the health of women and girls: a decade of advances and challenges.

Objective: Following the initial wave of federal support to address women's health, there is a need to assess successes and determine the next priorities to advance the health of women. The objective of this study was to systematically collect expert opinion on the major advances in women's health in the past decade and priorities for women's health research and service in the coming decade.

Methods: We utilized a Delphi method to query the leadership from academic and community Centers of Excellence in Women's Health, as designated by the Department of Health and Human Services.

A randomised controlled trial of cognitive behavioural treatment for obsessive compulsive disorder in children and adolescents.

Cognitive behaviour therapy (CBT) for young people with obsessive compulsive disorder (OCD) has become the treatment of first choice. However, the literature is largely based on studies emphasising exposure and response prevention. In this study, we report on a randomised controlled trial of CBT for young people carried out in typical outpatient clinic conditions which focused on cognitions.

Human CD34+AC133+VEGFR-2+ cells are not endothelial progenitor cells but distinct, primitive hematopoietic progenitors.

Objective: Endothelial progenitor cells (EPCs) are used for angiogenic therapies or as biomarkers to assess cardiovascular disease risk. However, there is no uniform definition of an EPC, which confounds EPC studies. EPCs are widely described as cells that coexpress the cell-surface antigens CD34, AC133, and vascular endothelial growth factor receptor-2 (VEGFR-2).

K-ras is critical for modulating multiple c-kit-mediated cellular functions in wild-type and Nf1+/- mast cells.

p21(ras) (Ras) proteins and GTPase-activating proteins (GAPs) tightly modulate extracellular growth factor signals and control multiple cellular functions. The specific function of each Ras isoform (H, N, and K) in regulating distinct effector pathways, and the role of each GAP in negatively modulating the activity of each Ras isoform in myeloid cells and, particularly, mast cells is incompletely understood. In this study, we use murine models of K-ras- and Nf1-deficient mice to examine the role of K-ras in modulating mast cell functions and to identify the role of neurofibromin as a GAP for K-ras in this lineage.

Neurofibroma-associated growth factors activate a distinct signaling network to alter the function of neurofibromin-deficient endothelial cells.

Genetic inactivation of tumor suppressor genes initiates human cancers. However, interaction of accessory cells with the tumor-initiating cell within the microenvironment is often required for tumor progression. This paradigm is relevant to understanding neurofibroma development in neurofibromatosis type I patients.

Neurofibromin is a novel regulator of RAS-induced signals in primary vascular smooth muscle cells.

Neurofibromatosis type I (NF1) is a genetic disorder caused by mutations in the NF1 tumor suppressor gene. Neurofibromin is encoded by NF1 and functions as a negative regulator of Ras activity. NF1 patients develop renal artery stenosis and arterial occlusions resulting in cerebral and visceral infarcts.

Genetic reduction of class IA PI-3 kinase activity alters fetal hematopoiesis and competitive repopulating ability of hematopoietic stem cells in vivo.

Class I(A) phosphatidylinositol-3 kinase (PI-3K) is a lipid kinase, which is activated in blood cells by hematopoietic growth factors. In vitro experiments using chemical inhibitors of PI-3K suggest that this kinase is potentially important for hematopoietic stem and progenitor cell (HSC/P) function, and recent studies identify PI-3K as a therapeutic target in treating different leukemias and lymphomas. However, the role of PI-3K in regulating fetal liver or adult hematopoiesis in vivo is unknown.

K-Ras is essential for normal fetal liver erythropoiesis.

In vitro studies suggest that Ras activation is necessary for erythroid cell development. However, genetic inactivation of the Ras isoforms H-Ras, N-Ras, and K-Ras in mice reportedly did not affect adult or fetal erythropoiesis, though K-Ras(-/-) embryos were anemic. Given these discrepancies, we performed a more detailed analysis of fetal erythropoiesis in K-Ras(-/-) embryos.

Neurofibromin-deficient Schwann cells secrete a potent migratory stimulus for Nf1+/- mast cells.

The NF1 tumor suppressor gene encodes a GTPase-activating protein called neurofibromin that negatively regulates Ras signaling. Mutations in NF1 cause neurofibromatosis type 1 (NF1). The development of neurofibromas, which are complex tumors composed of multiple cell types, is a hallmark of NF1.

Functional p85alpha gene is required for normal murine fetal erythropoiesis.

In vitro studies suggest that activation of class IA phosphatidylinositol 3 (PI-3) kinase is necessary for normal erythroid cell development. However, when class IA PI-3 kinase-deficient mice were generated by a targeted deletion of the p85alpha regulatory subunit, fetal erythropoiesis was reportedly unaffected. Given the discrepancies between these studies, we performed a more detailed in vivo analysis of class IA PI-3 kinase-deficient embryos.