bluuebunny/crossref_metadata_2025_split huggingface dataset:
Erythropoietin does not have effects on the ventilatory and pulmonary vascular response to acute hypoxia in men and women
Authors: Berendsen Remco R. , Lindeman Rob C. , Boom Merel , Aarts Leon P. H. J. , van Dorp Eveline L. A. , Teppema Luc J. 
Published: July 2016

New Findings

What is the central question of this study?
Does a clinically relevant intravenous dose of erythropoeitin affect the hypoxic ventilatory response and/or hypoxic pulmonary vasoconstriction in healthy humans?

What is the main finding and its importance?
Erythropoeitin does not influence the ventilatory and pulmonary vascular responses to acute hypoxia in men or women.

Sustained and chronic hypoxia lead to an increase in pulmonary ventilation (hypoxic ventilatory response, HVR) and to an increase in pulmonary vascular resistance (hypoxic pulmonary vasoconstriction, HPV). In this study, we examined the effect of a clinical i.v. dose of recombinant human erythropoietin (50 IU kg−1) on the isocapnic HVR and HPV in seven male and seven female subjects by exposing them to hypoxia for 20 min (end‐tidal ∼50 mmHg) while measuring their ventilation and estimating pulmonary arterial pressure from the maximal velocity of the regurgitant jet over the tricuspid valve during systole (ΔPmax) with echocardiography. In the placebo session, after 5 and 20 min men responded with an increase in ventilation by 0.0056 and 0.0023 l min−1 kg−1 , respectively, indicating the presence of hypoxic ventilatory depression. In women, the increase in ventilation was 0.0067 and 0.0047 l min−1 kg−1 , respectively. In both sexes, erythropoietin did not alter these responses significantly. In the placebo session, mean ΔPmax increased by 6.1 ± 0.7 mmHg in men (P = 0.035) and by 8.4 ± 1.4 mmHg in women (P = 0.020) during the hypoxic exposure, whereby women had a ∼5 mmHg lower end‐tidal . Erythropoietin did not alter these responses; in men, ΔPmax increased by 7.5 ± 1.1 mmHg (n.s. versus placebo) and in women by 9.7 ± 2.2 mmHg (n.s. versus placebo). We conclude that women tended to have a greater HPV in placebo conditions and that a clinical dose of erythropoietin has no effect on the HVR and HPV in either sex.
Draft Whole-Genome Sequence of the Type Strain
Bacillus aquimaris
TF12
T
Authors: Hernández-González Ismael L. , Olmedo-Álvarez Gabriela 
Published: July 2016

ABSTRACT

Bacillus aquimaris
TF12 is a Gram-positive bacteria isolated from a tidal flat of the Yellow Sea in South Korea. We report the draft whole-genome sequence of
Bacillus aquimaris
TF12, the type strain of a set of bacteria typically associated with marine habitats and with a potentially high biotechnology value.
Complete Genome Sequence of a
Klebsiella pneumoniae
Strain Carrying
bla
NDM-1
on a Multidrug Resistance Plasmid
Authors: Conlan Sean , Lau Anna F. ,   NISC Comparative Sequencing Program, Palmore Tara N. , Frank Karen M. , Segre Julia A. 
Published: July 2016

ABSTRACT

Here, we report the genome sequence of a
bla
NDM-1
-positive
Klebsiella pneumoniae
AATZP isolate cultured from a perirectal surveillance swab collected upon admission of a patient to the NIH Clinical Center in 2014. Genome sequencing of this isolate revealed three plasmids, including one carrying the
bla
NDM-1
gene encoding resistance to carbapenems.
Interaction between Endothelial Protein C Receptor and Intercellular Adhesion Molecule 1 to Mediate Binding of Plasmodium falciparum-Infected Erythrocytes to Endothelial Cells
Authors: Avril Marion , Bernabeu Maria , Benjamin Maxwell , Brazier Andrew Jay , Smith Joseph D. 
Published: July 2016

ABSTRACT

Intercellular adhesion molecule 1 (ICAM-1) and the endothelial protein C receptor (EPCR) are candidate receptors for the deadly complication cerebral malaria. However, it remains unclear if
Plasmodium falciparum
parasites with dual binding specificity are involved in cytoadhesion or different parasite subpopulations bind in brain microvessels. Here, we investigated this issue by studying different subtypes of ICAM-1-binding parasite lines. We show that two parasite lines expressing domain cassette 13 (DC13) of the
P. falciparum
erythrocyte membrane protein 1 (PfEMP1) family have dual binding specificity for EPCR and ICAM-1 and further mapped ICAM-1 binding to the first DBLβ domain following the PfEMP1 head structure in both proteins. As PfEMP1 head structures have diverged between group A (EPCR binders) and groups B and C (CD36 binders), we also investigated how ICAM-1-binding parasites with different coreceptor binding traits influence
P. falciparum
-infected erythrocyte binding to endothelial cells. Whereas levels of binding to tumor necrosis factor alpha (TNF-α)-stimulated endothelial cells from the lung and brain by all ICAM-1-binding parasite lines increased, group A (EPCR and ICAM-1) was less dependent than group B (CD36 and ICAM-1) on ICAM-1 upregulation. Furthermore, both group A DC13 parasite lines had higher binding levels to brain endothelial cells (a microvascular niche with limited CD36 expression). This study shows that ICAM-1 is a coreceptor for a subset of EPCR-binding parasites and provides the first evidence of how EPCR and ICAM-1 interact to mediate parasite binding to both resting and TNF-α-activated primary brain and lung endothelial cells.

IMPORTANCE
Cerebral malaria is a severe neurological complication of
P. falciparum
infection associated with infected erythrocyte (IE) binding in cerebral vessels. Yet little is known about the mechanisms by which parasites adhere in the brain or other microvascular sites. Here, we studied parasite lines expressing group A DC13-containing PfEMP1 variants, a subset that has previously been shown to have high brain cell- and other endothelial cell-binding activities. We show that DC13-containing PfEMP1 variants have dual EPCR- and ICAM-1-binding activities and that both receptors are involved in parasite adherence to lung and brain endothelial cells. As both EPCR and ICAM-1 are implicated in cerebral malaria, these findings suggest the possibility that parasites with dual binding activities are involved in parasite sequestration to microvascular beds with low CD36 expression, such as the brain, and we urge more research into the multiadhesive properties of PfEMP1 variants.
Plea for routinely presenting prediction intervals in meta-analysis
Authors: IntHout Joanna , Ioannidis John P A , Rovers Maroeska M , Goeman Jelle J 
Published: July 2016

ObjectivesEvaluating the variation in the strength of the effect across studies is a key feature of meta-analyses. This variability is reflected by measures like τ2or I2, but their clinical interpretation is not straightforward. A prediction interval is less complicated: it presents the expected range of true effects in similar studies. We aimed to show the advantages of having the prediction interval routinely reported in meta-analyses.DesignWe show how the prediction interval can help understand the uncertainty about whether an intervention works or not. To evaluate the implications of using this interval to interpret the results, we selected the first meta-analysis per intervention review of the Cochrane Database of Systematic Reviews Issues 2009–2013 with a dichotomous (n=2009) or continuous (n=1254) outcome, and generated 95% prediction intervals for them.ResultsIn 72.4% of 479 statistically significant (random-effects p<0.05) meta-analyses in the Cochrane Database 2009–2013 with heterogeneity (I2>0), the 95% prediction interval suggested that the intervention effect could be null or even be in the opposite direction. In 20.3% of those 479 meta-analyses, the prediction interval showed that the effect could be completely opposite to the point estimate of the meta-analysis. We demonstrate also how the prediction interval can be used to calculate the probability that a new trial will show a negative effect and to improve the calculations of the power of a new trial.ConclusionsThe prediction interval reflects the variation in treatment effects over different settings, including what effect is to be expected in future patients, such as the patients that a clinician is interested to treat. Prediction intervals should be routinely reported to allow more informative inferences in meta-analyses.
Research studies on patients' illness experience using the Narrative Medicine approach: a systematic review
Authors: Fioretti Chiara , Mazzocco Ketti , Riva Silvia , Oliveri Serena , Masiero Marianna , Pravettoni Gabriella 
Published: July 2016

ObjectiveSince its birth about 30 years ago, Narrative Medicine approach has increased in popularity in the medical context as well as in other disciplines. This paper aims to review Narrative Medicine research studies on patients' and their caregivers' illness experience.Setting and participantsMEDLINE, Psycinfo, EBSCO Psychological and Behavioural Science, The Cochrane Library and CINAHL databases were searched to identify all the research studies which focused on the Narrative Medicine approach reported in the title, in the abstract and in the keywords the words ‘Narrative Medicine’ or ‘Narrative-based Medicine’. Primary and secondary outcome measures: number of participants, type of disease, race and age of participants, type of study, dependent variables, intervention methods, assessment.ResultsOf the 325 titles screened, we identified 10 research articles fitting the inclusion criteria. Our systematic review showed that research on Narrative Medicine has no common specific methodology: narrative in Medicine is used as an intervention protocol as well as an assessment tool. Patients' characteristics, types of disease and data analysis procedures differ among the screened studies.ConclusionsNarrative Medicine research in medical practice needs to find clear and specific protocols to deepen the impact of narrative on medical practice and on patients' lives.
Healthcare professional and patient codesign and validation of a mechanism for service users to feedback patient safety experiences following a care transfer: a qualitative study
Authors: Scott Jason , Heavey Emily , Waring Justin , Jones Diana , Dawson Pamela 
Published: July 2016

ObjectiveTo develop and validate a mechanism for patients to provide feedback on safety experiences following a care transfer between organisations.DesignQualitative study using participatory methods (codesign workshops) and cognitive interviews. Workshop data were analysed concurrently with participants, and cognitive interviews were thematically analysed using a deductive approach based on the developed feedback mechanism.ParticipantsExpert patients (n=5) and healthcare professionals (n=11) were recruited purposively to develop the feedback mechanism in 2 workshops. Workshop 1 explored principles underpinning safety feedback mechanisms, and workshop 2 included the practical development of the feedback mechanism. Final design and content of the feedback mechanism (a safety survey) were verified by workshop participants, and cognitive interviews (n=28) were conducted with patients.ResultsWorkshop participants identified that safety feedback mechanisms should be patient-centred, short and concise with clear signposting on how to complete, with an option to be anonymous and balanced between positive (safe) and negative (unsafe) experiences. The agreed feedback mechanism consisted of a survey split across 3 stages of the care transfer: departure, journey and arrival. Care across organisational boundaries was recognised as being complex, with healthcare professionals acknowledging the difficulty implementing changes that impact other organisations. Cognitive interview participants agreed the content of the survey was relevant but identified barriers to completion relating to the survey formatting and understanding of a care transfer.ConclusionsParticipatory, codesign principles helped overcome differences in understandings of safety in the complex setting of care transfers when developing a safety survey. Practical barriers to the survey's usability and acceptability to patients were identified, resulting in a modified survey design. Further research is required to determine the usability and acceptability of the survey to patients and healthcare professionals, as well as identifying how governance structures should accommodate patient feedback when relating to multiple health or social care providers.
Mapping the progress and impacts of public health approaches to palliative care: a scoping review protocol
Authors: Archibald Daryll , Patterson Rebecca , Haraldsdottir Erna , Hazelwood Mark , Fife Shirley , Murray Scott A 
Published: July 2016

IntroductionPublic health palliative care is a term that can be used to encompass a variety of approaches that involve working with communities to improve people's experience of death, dying and bereavement. Recently, public health palliative care approaches have gained recognition and momentum within UK health policy and palliative care services. There is general consensus that public health palliative care approaches can complement and go beyond the scope of formal service models of palliative care. However, there is no clarity about how these approaches can be undertaken in practice or how evidence can be gathered relating to their effectiveness. Here we outline a scoping review protocol that will systematically map and categorise the variety of activities and programmes that could be classified under the umbrella term ‘public health palliative care’ and highlight the impact of these activities where measured.Methods and analysisThis review will be guided by Arksey and O'Malley's scoping review methodology and incorporate insights from more recent innovations in scoping review methodology. Sensitive searches of 9 electronic databases from 1999 to 2016 will be supplemented by grey literature searches. Eligible studies will be screened independently by two reviewers using a data charting tool developed for this scoping review.Ethics and disseminationThis scoping review will undertake a secondary analysis of data already collected and does not require ethical approval. The results will facilitate better understanding of the practical application of public health approaches to palliative care, the impacts these activities can have and how to build the evidence base for this work in future. The results will be disseminated through traditional academic routes such as conferences and journals and also policy and third sector seminars.
Review of the national external quality assessment (EQA) scheme for breast pathology in the UK
Authors: Rakha Emad A , Bennett Rachel L , Coleman Derek , Pinder Sarah E , Ellis Ian O 
Published: July 2016

BackgroundThe National Health Service Breast Screening Programme (NHSBSP; pathology) external quality assurance (EQA) scheme aims to provide a mechanism for examination and monitoring of concordance of pathology reporting within the UK. This study aims to review the breast EQA scheme performance data collected over a 24-year period following its introduction.MethodsData on circulations, number of cases and diagnosis were collected. Detailed analyses with and without combinations of certain diagnostic entities, and over different time periods were performed.ResultsOverall, of 576 cases (172 benign, 11 atypical hyperplasia, 98 ductal carcinoma in situ/microinvasive and 295 invasive disease), consistency of assessment of diagnostic parameters was very high (overall k=0.80; k for benign diagnosis=0.79; k for invasive disease=0.91). For distinguishing benign versus malignant lesions, no further improvement is considered possible in view of the limitations of the scheme methodology. Although diagnostic consistency of atypical hyperplasia remains at a low level, combining it with the benign category results in a high level of agreement (k=0.93). The level of consistency of reporting prognostic information is variable and some items such as lymphovascular invasion and tumour size measurement may need further intervention to improve their reporting consistency. Although the level of consistency of reporting of histological grade remained at a moderate level overall (k=0.48), it was variable among cases and appears to have levelled off; no further significant improvement is expected and no significant impact of the previous publication of guidelines is observed.ConclusionsThese results provide further evidence to indicate the value of the breast EQA scheme in monitoring performance and the identification of specific areas where improvement or new approaches are required. For most parameters, the concordance of reporting reached a plateaux a few years after the introduction of the EQA scheme. It is important to maintain this high level and also to tackle specific low-performance areas innovatively.
Associations of socioeconomic position in childhood and young adulthood with cardiometabolic risk factors: the Jerusalem Perinatal Family Follow-Up Study
Authors: Savitsky B , Manor O , Friedlander Y , Burger A , Lawrence G , Calderon-Margalit R , Siscovick D S , Enquobahrie D A , Williams M A , Hochner H 
Published: July 2016

BackgroundSeveral stages in the life course have been identified as important to the development of cardiovascular disease. This study aimed to assess the associations of childhood and adulthood socioeconomic position (SEP) and social mobility with cardiometabolic risk factors (CMRs) later in life.MethodsWe conducted follow-up examinations of 1132 offspring, aged 32, within a population-based cohort of all births in Jerusalem from 1974 to 1976. SEP was indicated by parents’ occupation and education, and adulthood SEP was based on offspring's occupation and education recorded at age 32. Linear regression models were used to investigate the associations of SEP and social mobility with CMRs.ResultsChildhood-occupational SEP was negatively associated with body mass index (BMI; β=−0.29, p=0.031), fat percentage (fat%; β=−0.58, p=0.005), insulin (β=−0.01, p=0.031), triglycerides (β=−0.02, p=0.024) and low-density lipoprotein cholesterol (LDL-C; β=−1.91, p=0.015), independent of adulthood SEP. Adulthood-occupational SEP was negatively associated with waist-to-hip ratio (WHR; β=−0.01, p=0.002), and positively with high-density lipoprotein cholesterol (HDL-C; β=0.87, p=0.030). Results remained similar after adjustment for smoking and inactivity. Childhood-educational SEP was associated with decreased WHR and LDL-C level (p=0.0002), and adulthood-educational SEP was inversely associated with BMI (p=0.001), waist circumference (p=0.008), WHR (p=0.001) and fat% (p=0.0002) and positively associated with HDL-C (p=0.030). Additionally, social mobility (mainly upward) was shown to have adverse cardiometabolic outcomes.ConclusionsBoth childhood and adulthood SEP contribute independently to CMR. The match–mismatch hypothesis may explain the elevated CMRs among participants experiencing social mobility. Identification of life-course SEP-related aspects that translate into social inequality in cardiovascular risk may facilitate efforts for improving health and for reducing disparities in cardiovascular disease.
Local renin-angiotensin system mediates endothelial dilator dysfunction in aging arteries
Authors: Flavahan Sheila , Chang Fumin , Flavahan Nicholas A. 
Published: July 2016

Aging impairs endothelium-dependent NO-mediated dilatation, which results from increased production of reactive oxygen species (ROS). The local generation of angiotensin II (ANG II) is increased in aging arteries and contributes to inflammatory and fibrotic activity of smooth muscle cells and arterial wall remodeling. Although prolonged in vivo ANG II inhibition improves the impaired endothelial dilatation of aging arteries, it is unclear whether this reflects inhibition of intravascular or systemic ANG II systems. Experiments were therefore performed on isolated tail arteries from young (3–4 mo) and old (22–24 mo) F344 rats to determine if a local renin-angiotensin system contributes to the endothelial dilator dysfunction of aging. Aging impaired dilatation to the endothelial agonist acetylcholine but did not influence responses to a nitric oxide (NO) donor (DEA NONOate). Dilatation to acetylcholine was greatly reduced by NO synthase inhibition [nitro-l-arginine methyl ester (l-NAME)] in young and old arteries. In isolated arteries, acute inhibition of angiotensin-converting enzyme (ACE) (perindoprilat), renin (aliskiren), or AT1 receptors (valsartan, losartan) did not influence dilatation to acetylcholine in young arteries but increased responses in old arteries. After ANG II inhibition, the dilator response to acetylcholine was similar in young and old arteries. ROS activity, which was increased in endothelium of aging arteries, was also reduced by inhibiting ANG II (perindoprilat, losartan). Renin expression was increased by 5.6 fold and immunofluorescent levels of ANG II were confirmed to be increased in aging compared with young arteries. Exogenous ANG II inhibited acetylcholine-induced dilatation. Therefore, aging-induced impairment of endothelium-dependent dilatation in aging is caused by a local intravascular renin-angiotensin system. Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/angii-and-aging-induced-endothelial-dysfunction/ .
Contributions of HIV to Non-Hodgkin Lymphoma Mortality Trends in the United States
Authors: Howlader Nadia , Shiels Meredith S. , Mariotto Angela B. , Engels Eric A. 
Published: July 2016

Abstract
Background: The human immunodeficiency virus (HIV) epidemic has strongly influenced non-Hodgkin lymphoma (NHL) incidence in the U.S. general population, but its effects on NHL mortality trends are unknown.
Methods: Using SEER cancer registry data, we assessed NHL mortality rates in the United States (2005–2012) and mapped NHL deaths to prior incident cases. Data included HIV status at NHL diagnosis. We describe the proportion of NHL deaths linked to an HIV-infected case, for 3 AIDS-defining subtypes [diffuse large B-cell lymphoma (DLBCL), Burkitt lymphoma, and central nervous system (CNS) lymphoma] and within demographic categories. We also present incidence-based mortality (IBM) rates showing the impact of HIV on mortality trends and describe survival after NHL diagnosis by calendar year.
Results: Of 11,071 NHL deaths, 517 (4.6%) were in HIV-infected persons. This proportion was higher in deaths mapped to DLBCL (7.3% with HIV), Burkitt lymphoma (33.3%), and CNS lymphoma (17.6%), and among deaths from these subtypes, for people aged 20–49 years (46.6%), males (15.2%), and blacks (39.3%). IBM rates declined steeply during 2005–2012 for HIV-infected NHL cases (−7.6% per year, P = 0.001). This trend reflects a steep decline in incident NHL among HIV-infected people after 1996, when highly active antiretroviral therapy was introduced. Five-year cancer-specific survival improved more markedly among HIV-infected cases (9%–54%) than HIV-uninfected cases (62%–76%) during 1990–2008.
Conclusions: The HIV epidemic has strongly contributed to NHL deaths, especially for AIDS-defining NHL subtypes and groups with high HIV prevalence.
Impact: Declining NHL mortality rates for HIV-infected cases reflect both declining incidence and improving survival. Cancer Epidemiol Biomarkers Prev; 25(9); 1289–96. ©2016 AACR.