Integrated enhanced cognitive behavioural (I-CBTE) therapy significantly improves effectiveness of inpatient treatment of anorexia nervosa in real life settings.

Background: Inpatient treatment of anorexia nervosa can be lifesaving but is associated with high rates of relapse and poor outcomes. To address this, the Oxford service has adapted the enhanced cognitive behavioural treatment (CBTE) model, first developed for inpatients in Italy to a UK national health service (NHS) setting. In this study, we compared the outcomes from treatment as usual (TAU), integrated CBTE (I-CBTE), and alternative treatment models in routine UK clinical practice.

Risk, demand, capacity and outcomes in adult specialist eating disorder services in South-East of England before and since COVID-19.

Aims And Method: This is a longitudinal cohort study describing the demand, capacity and outcomes of adult specialist eating disorder in-patient services covering a population of 3.5 million in a South-East England provider collaborative before and since the COVID-19 pandemic, between July 2018 and March 2021.

Results: There were 351 referrals for admission; 97% were female, 95% had a diagnosis of anorexia nervosa and 19% had a body mass index (BMI) <13.

Applying Ethical Principles When Discussing Alcohol Use During Pregnancy.

Over the past 2 decades, more women in the United States are engaging in excessive alcohol use, including women of reproductive age. Consuming alcohol in amounts greater than recommended limits is associated with an increased risk for adverse health effects, such as breast cancer, hypertension stroke, spontaneous abortion, and infertility. No safe time, safe amount, or safe type of alcohol to consume during pregnancy has been identified.

Do safety briefings improve patient safety in the acute hospital setting? A systematic review.

Aims: To synthesize current knowledge about the impact of safety briefings as an intervention to improve patient safety.

Background: Improving safety in health care remains an ongoing challenge. There is a lack of evidence underpinning safety enhancing interventions.

Antenatal Vitamin D Preserves Placental Vascular and Fetal Growth in Experimental Chorioamnionitis Due to Intra-amniotic Endotoxin Exposure.

Background: Chorioamnionitis (CA) is associated with a high risk for the development of bronchopulmonary dysplasia (BPD) after preterm birth, but mechanisms that increase susceptibility for BPD and strategies to prevent BPD are uncertain. As a model of CA, antenatal intra-amniotic (IA) endotoxin (ETX) exposure alters placental structure, causes fetal growth restriction, increases perinatal mortality, and causes sustained cardiorespiratory abnormalities throughout infancy. Vitamin D (Vit D) has been shown to have both anti-inflammatory and proangiogenic properties.

Likelihood of cesarean delivery after applying leading active labor diagnostic guidelines.

Background: Friedman, the United Kingdom's National Institute for Health and Care Excellence (NICE), and the American College of Obstetricians and Gynecologists/Society for Maternal-Fetal Medicine (ACOG/SMFM) support different active labor diagnostic guidelines. Our aims were to compare likelihoods for cesarean delivery among women admitted before vs in active labor by diagnostic guideline (within-guideline comparisons) and between women admitted in active labor per one or more of the guidelines (between-guideline comparisons).

Design: Active labor diagnostic guidelines were retrospectively applied to cervical examination data from nulliparous women with spontaneous labor onset (n = 2573).

Hepatocyte growth factor as a downstream mediator of vascular endothelial growth factor-dependent preservation of growth in the developing lung.

Impaired vascular endothelial growth factor (VEGF) signaling contributes to the pathogenesis of bronchopulmonary dysplasia (BPD). We hypothesized that the effects of VEGF on lung structure during development may be mediated through its downstream effects on both endothelial nitric oxide synthase (eNOS) and hepatocyte growth factor (HGF) activity, and that, in the absence of eNOS, trophic effects of VEGF would be mediated through HGF signaling. To test this hypothesis, we performed an integrative series of in vitro (fetal rat lung explants and isolated fetal alveolar and endothelial cells) and in vivo studies with normal rat pups and eNOS(-/-) mice.

Labor Dystocia: A Common Approach to Diagnosis.

Contemporary labor and birth population norms should be the basis for evaluating labor progression and determining slow progress that may benefit from intervention. The aim of this article is to present guidelines for a common, evidence-based approach for determination of active labor onset and diagnosis of labor dystocia based on a synthesis of existing professional guidelines and relevant contemporary publications. A 3-point approach for diagnosing active labor onset and classifying labor dystocia-related labor aberrations into well-defined, mutually exclusive categories that can be used clinically and validated by researchers is proposed.

Labor Dystocia: Uses of Related Nomenclature.

Introduction: Labor dystocia (slow or difficult labor or birth) is the most commonly diagnosed aberration of labor and the most frequently documented indication for primary cesarean birth. Yet, dystocia remains a poorly specified diagnostic category, with determinations often varying widely among clinicians. The primary aims of this review are to 1) summarize definitions of active labor and dystocia, as put forth by leading professional obstetric and midwifery organizations in world regions wherein English is the majority language and 2) describe the use of dystocia and related terms in contemporary research studies.

Antenatal endotoxin disrupts lung vitamin D receptor and 25-hydroxyvitamin D 1α-hydroxylase expression in the developing rat.

Vitamin D [vit D; 1,25-(OH)2D] treatment improves survival and lung alveolar and vascular growth in an experimental model of bronchopulmonary dysplasia (BPD) after antenatal exposure to endotoxin (ETX). However, little is known about lung-specific 1,25-(OH)2D3 regulation during development, especially regarding maturational changes in lung-specific expression of the vitamin D receptor (VDR), 1α-hydroxylase (1α-OHase), and CYP24A1 during late gestation and the effects of antenatal ETX exposure on 1,25-(OH)2D3 metabolism in the lung. We hypothesized that vit D regulatory proteins undergo maturation regulation in the late fetal and early neonatal lung and that prenatal exposure to ETX impairs lung growth partly through abnormal endogenous vit D metabolism.

Outcomes of nulliparous women with spontaneous labor onset admitted to hospitals in preactive versus active labor.

Introduction: The timing of when a woman is admitted to the hospital for labor care following spontaneous contraction onset may be among the most important decisions that labor attendants make because it can influence care patterns and birth outcomes. The aims of this study were to estimate the percentage of low-risk, nulliparous women at term who are admitted to labor units prior to active labor and to evaluate the effects of the timing of admission (ie, preactive vs active labor) on labor interventions and mode of birth.

Methods: Data from low-risk, nulliparous women with spontaneous labor onset at term gestation were merged from 2 prospective studies conducted at 3 large Midwestern hospitals.

Cord blood endothelial colony-forming cells from newborns with congenital diaphragmatic hernia.

Endothelial colony-forming cells (ECFCs) are decreased in the cord blood of preterm infants with moderate-to-severe bronchopulmonary dysplasia. We quantified ECFCs from infants with congenital diaphragmatic hernia, a neonatal disorder with severe lung hypoplasia. Unlike newborns who develop bronchopulmonary dysplasia, those with congenital diaphragmatic hernia had increased and highly-proliferative cord blood ECFCs.

Endothelial colony-forming cell conditioned media promote angiogenesis in vitro and prevent pulmonary hypertension in experimental bronchopulmonary dysplasia.

Late-outgrowth endothelial colony-forming cells (ECFCs), a type of circulating endothelial progenitor cell (EPC), may contribute to pulmonary angiogenesis during development. Cord blood ECFCs from preterm newborns proliferate more rapidly than term ECFCs but are more susceptible to the adverse effects of hyperoxia. Recent studies suggest that bone marrow-derived EPCs protect against experimental lung injury via paracrine mechanisms independent of vascular engraftment.

Cord blood angiogenic progenitor cells are decreased in bronchopulmonary dysplasia.

Bronchopulmonary dysplasia (BPD), the chronic lung disease of prematurity, is associated with impaired vascular and alveolar growth. Antenatal factors contribute to the risk for developing BPD by unclear mechanisms. Endothelial progenitor cells, such as angiogenic circulating progenitor cells (CPCs) and late-outgrowth endothelial colony-forming cells (ECFCs), may contribute to angiogenesis in the developing lung.

Bone marrow-derived angiogenic cells restore lung alveolar and vascular structure after neonatal hyperoxia in infant mice.

Neonatal hyperoxia impairs vascular and alveolar growth in mice and decreases endothelial progenitor cells. To determine the role of bone marrow-derived cells in restoration of neonatal lung structure after injury, we studied a novel bone marrow myeloid progenitor cell population from Tie2-green fluorescent protein (GFP) transgenic mice (bone marrow-derived angiogenic cells; BMDAC). We hypothesized that treatment with BMDAC would restore normal lung structure in infant mice during recovery from neonatal hyperoxia.

Hyperoxia disrupts vascular endothelial growth factor-nitric oxide signaling and decreases growth of endothelial colony-forming cells from preterm infants.

Exposure of preterm infants to hyperoxia impairs vascular growth, contributing to the development of bronchopulmonary dysplasia and retinopathy of prematurity. Disruption of vascular endothelial growth factor (VEGF)-nitric oxide (NO) signaling impairs vascular growth. Endothelial progenitor cells (EPCs) may play an important role in vascular growth.

Treatment of nausea and vomiting in terminally ill cancer patients.

Nausea and vomiting is a common and distressing symptom complex in patients with far-advanced cancer, affecting up to 60% of individuals at some stage of their illness. The current approach to the palliative care of patients with nausea and vomiting is based on identifying the cause, understanding its pathophysiology and knowing the pharmacology of the drugs available for its amelioration. The following six main syndromes are identified: gastric stasis, biochemical, raised intracranial pressure, vestibular, mechanical bowel obstruction and ileus.

The interaction of adenovirus E1A with p300 family members modulates cellular gene expression to reduce tumorigenicity.

The use of adenovirus serotype 2 or 5 (Ad2/5) E1A as therapy for human malignancy requires an understanding of the mechanisms involved in E1A-induced tumor suppression. The prevailing use of E1A in the treatment of human malignancy stresses the non-immunologically mediated, anti-tumorigenic activities of E1A. However, the capacity of E1A to elicit a NK-cell and T-cell anti-tumor immune response and to sensitize tumor cells to lysis by immune effector molecules utilized by NK cells and T cells is also an important component of the anti-tumorigenic activity of E1A.

Adenovirus serotype 5 E1A sensitizes tumor cells to NKG2D-dependent NK cell lysis and tumor rejection.

The expression of the Adenovirus serotype 5 (Ad5) E1A oncogene sensitizes tumor cells to natural killer (NK) cell-mediated killing and tumor rejection in vivo. These effects are dependent on the ability of E1A to bind the transcriptional coadaptor protein p300. To test the hypothesis that E1A up-regulates ligands recognized by the NKG2D-activating receptor, we stably transfected the highly tumorigenic mouse fibrosarcoma cell line MCA-205 with Ad5-E1A or a mutant form of E1A that does not interact with p300 (E1A-Deltap300).

Macrophages kill human papillomavirus type 16 E6-expressing tumor cells by tumor necrosis factor alpha- and nitric oxide-dependent mechanisms.

The expression of adenovirus serotype 2 or 5 (Ad2/5) E1A sensitizes cells to killing by NK cells and activated macrophages, a property that correlates with the ability of E1A to bind the transcriptional coadaptor proteins p300-CBP. The E6 oncoproteins derived from the high-risk human papillomaviruses (HPV) interact with p300 and can complement mutant forms of E1A that cannot interact with p300 to induce cellular immortalization. Therefore, we determined if HPV type 16 (HPV16) E6 could sensitize cells to killing by macrophages and NK cells.

Expression of an E1A/E7 chimeric protein sensitizes tumor cells to killing by activated macrophages but not NK cells.

Adenovirus (Ad) E1A and human papillomavirus (HPV) E7 express homologous conserved regions (CRs) that mediate their shared biological functions. Despite their similarities, the expression of E1A sensitizes tumor cells to killing by NK cells and macrophages but the expression of E7 does not, a factor that may contribute to the dissimilar oncogenicities of Ad and HPV. This study was undertaken to define molecular differences between E1A and E7 that are responsible for the ability of E1A and the inability of E7 to sensitize cells to killing by NK cells and macrophages.