bluuebunny/crossref_metadata_2025_split huggingface dataset:
Observer-based tools for non-technical skills assessment in simulated and real clinical environments in healthcare: a systematic review
Authors: Higham Helen , Greig Paul R , Rutherford John , Vincent Laura , Young Duncan , Vincent Charles 
Published: May 2019

BackgroundOver the past three decades multiple tools have been developed for the assessment of non-technical skills (NTS) in healthcare. This study was designed primarily to analyse how they have been designed and tested but also to consider guidance on how to select them.ObjectivesTo analyse the context of use, method of development, evidence of validity (including reliability) and usability of tools for the observer-based assessment of NTS in healthcare.DesignSystematic review.Data sourcesSearch of electronic resources, including PubMed, Embase, CINAHL, ERIC, PsycNet, Scopus, Google Scholar and Web of Science. Additional records identified through searching grey literature (OpenGrey, ProQuest, AHRQ, King’s Fund, Health Foundation).Study selectionStudies of observer-based tools for NTS assessment in healthcare professionals (or undergraduates) were included if they: were available in English; published between January 1990 and March 2018; assessed two or more NTS; were designed for simulated or real clinical settings and had provided evidence of validity plus or minus usability. 11,101 articles were identified. After limits were applied, 576 were retrieved for evaluation and 118 articles included in this review.ResultsOne hundred and eighteen studies describing 76 tools for assessment of NTS in healthcare met the eligibility criteria. There was substantial variation in the method of design of the tools and the extent of validity, and usability testing. There was considerable overlap in the skills assessed, and the contexts of use of the tools.ConclusionThis study suggests a need for rationalisation and standardisation of the way we assess NTS in healthcare and greater consistency in how tools are developed and deployed.
Drug-associated valvular heart diseases and serotonin-related pathways: a meta-analysis
Authors: Fortier Jacqueline H , Pizzarotti Beatrice , Shaw Richard E , Levy Robert J , Ferrari Giovanni , Grau Juan 
Published: May 2019

ObjectiveSerotonergic appetite suppressants and ergot-derived dopamine agonists have been associated with drug-induced valvular heart disease. The purpose of this meta-analysis is to synthesise the current evidence of a link between several medications affecting sertonergic pathways and valvular heart disease.MethodsPubMed was searched to identify studies evaluating an association between medications with serotonergic activity and cardiac valvular pathology. Case reports, uncontrolled studies and in vitro studies were excluded. Relevant studies were assessed for quality and potential bias; those of adequate quality were included in a quantitative synthesis. Sensitivity analyses were conducted, and potential publication bias was examined.ResultsThere was a consistent, significant relationship between certain medications and heart valve disease, including serotonergic medications (OR 3.30, 95% CI 1.99 to 5.49) and dopaminergic medications (OR 2.56, 95% CI 1.68 to 3.91). Subanalyses, including analyses that limited exposure to a single medication or effects to a single heart valve were also consistently significant. Most studies were retrospective or observational in nature, with a higher risk of selection and presentation biases. There was significant heterogeneity and variability between studies, particularly when it came to dose and duration of exposure.ConclusionsThere was a consistent, significant association between many medications that affect serotonergic pathways and valvular heart disease. Although many of these medications have been withdrawn from the market, some small studies suggest that recreational drug 3,4-methylenedioxy​methamphetamine and widely prescribed selective serotonin reuptake inhibitors may affect similar pathways.
Pathogenic variants in PLOD3 result in a Stickler syndrome-like connective tissue disorder with vascular complications
Authors: Ewans Lisa Jean , Colley Alison , Gaston-Massuet Carles , Gualtieri Angelica , Cowley Mark J , McCabe Mark James , Anand Deepti , Lachke Salil A , Scietti Luigi , Forneris Federico , Zhu Ying , Ying Kevin , Walsh Corrina , Kirk Edwin P , Miller David , Giunta Cecilia , Sillence David , Dinger Marcel , Buckley Michael , Roscioli Tony 
Published: May 2019

BackgroundPathogenic PLOD3 variants cause a connective tissue disorder (CTD) that has been described rarely. We further characterise this CTD and propose a clinical diagnostic label to improve recognition and diagnosis of PLOD3-related disease.MethodsReported PLOD3 phenotypes were compared with known CTDs utilising data from three further individuals from a consanguineous family with a homozygous PLOD3 c.809C>T; p.(Pro270Leu) variant. PLOD3 mRNA expression in the developing embryo was analysed for tissue-specific localisation. Mouse microarray expression data were assessed for phylogenetic gene expression similarities across CTDs with overlapping clinical features.ResultsKey clinical features included ocular abnormalities with risk for retinal detachment, sensorineural hearing loss, reduced palmar creases, finger contractures, prominent knees, scoliosis, low bone mineral density, recognisable craniofacial dysmorphisms, developmental delay and risk for vascular dissection. Collated clinical features showed most overlap with Stickler syndrome with variable features of Ehlers-Danlos syndrome (EDS) and epidermolysis bullosa (EB). Human lysyl hydroxylase 3/PLOD3 expression was localised to the developing cochlea, eyes, skin, forelimbs, heart and cartilage, mirroring the clinical phenotype of this disorder.ConclusionThese data are consistent with pathogenic variants in PLOD3 resulting in a clinically distinct Stickler-like syndrome with vascular complications and variable features of EDS and EB. Early identification of PLOD3 variants would improve monitoring for comorbidities and may avoid serious adverse ocular and vascular outcomes.
CD28 deficiency attenuates primary blast-induced renal injury in mice via the PI3K/Akt signalling pathway
Authors: Liu Ying , Liu Y E , Tong C C , Cong P F , Shi X Y , Shi L , Jin X H , Wang Q 
Published: May 2019

IntroductionPrimary blast affects the kidneys due to direct shock wave damage and the production of proinflammatory cytokines without effective treatment. CD28 has been reported to be involved in regulating T cell activation and secretion of inflammatory cytokines. The aim of this study was to investigate the influence of primary blast on the kidney and the effect of CD28 in mice.MethodsA mouse model of primary blast-induced kidney injury was established using a custom-made explosive device. The severity of kidney injury was investigated by H&E staining. ELISA was applied to study serum inflammation factors’ expression. Western blot assays were used to analyse the primary blast-induced inflammatory factors’ expression in the kidney. Immunofluorescence analysis was used to examine the PI3K/Akt signalling pathway.ResultsHistological examination demonstrated that compared with the primary blast group, CD28 deficiency caused a significant decrease in the severity of the primary blast-induced renal injury. Moreover, ELISA and western blotting revealed that CD28 deficiency significantly reduced the levels of interleukin (IL)-1β, IL-4 and IL-6, and increased the IL-10 level (p<0.05). Finally, immunofluorescence analysis indicated that PI3K/Akt expression also changed.ConclusionsCD28 deficiency had protective effects on primary blast-induced kidney injury via the PI3K/Akt signalling pathway. These findings improve the knowledge on primary blast injury and provide theoretical basis for primary blast injury treatment.
Reducing the severity of stroke
Authors: Meredith Georgina , Rudd Anthony 
Published: May 2019

AbstractStroke remains one of the most important causes of death and disability worldwide. Effective prevention could reduce the burden of stroke dramatically. The management of stroke has undergone a revolution over the last few decades, particularly with the development of techniques for revascularisation of patients with ischaemic stroke. Advanced imaging able to identify potentially salvageable brain is further increasing the potential for effective acute treatment. However, the majority of stroke patients won’t benefit from these treatments and will need effective specialist stroke care and ongoing rehabilitation to overcome impairments and adapt to living with a disability. There are still many unanswered questions about the most effective way of delivering rehabilitation. Likewise, research into how to manage primary intracerebral haemorrhage has yet to transform care.
Evaluation of acute myocardial infarction patients with mid-range ejection fraction after emergency percutaneous coronary intervention
Authors: Jiang Yufeng , Hu Shengda , Cao Mingqiang , Li Xiaobo , Zhou Jing , Ding Bing , Zhang Fangfang , Chen Tan , Zhou Yafeng 
Published: May 2019

AbstractBackgroundThere is currently no classification for acute myocardial infarction (AMI) according to left ventricular ejection fraction (LVEF). We aimed to perform a retrospective analysis of patients undergoing emergency percutaneous coronary intervention (PCI), comparing the clinical characteristics, in-hospital acute heart failure and all-cause death events of AMI patients with mid-range ejection fraction (mrEF), preserved ejection fraction (pEF) and reduced ejection fraction (rEF).Material and methodsTotally 1270 patients were stratified according to their LVEF immediately after emergency PCI into pEF group (LVEF 50% or higher), mrEF group (LVEF 40%–49%) and rEF group (LVEF &lt;40%). Kaplan-Meier curves and log rank tests were used to assess the effects of mrEF, rEF and pEF on the occurrence of acute heart failure and all-cause death during hospitalisation. The Cox proportional hazards model was used for multivariate correction.ResultsCompared with mrEF, rEF was an independent risk factor for acute heart failure events during hospitalisation (HR 5.01, 95% CI 3.53 to 7.11, p&lt;0.001), and it was also an independent risk factor for all-cause mortality during hospitalisation (HR 7.05, 95% CI 4.12 to 12.1, p&lt;0.001); Compared with mrEF, pEF was an independent protective factor for acute heart failure during hospitalisation (HR 0.49, 95% CI 0.30 to 0.82, p=0.01), and it was also an independent protective factor for all-cause death during hospitalisation (HR 0.33, 95% CI 0.11 to 0.96, p=0.04).ConclusionsmrEF patients with AMI undergoing emergency PCI share many similarities with pEF patients in terms of clinical features, but the prognosis is significantly worse than that of pEF patients, suggesting that we need to pay attention to the management of mrEF patients with AMI.
TnI and IL-18 levels are associated with prognosis of sepsis
Authors: Wu Qinghua , Xiao Zhaoyang , Pu Yanan , Zhou Jianwen , Wang Dehuai , Huang Zhiyong , Hou Dongnan 
Published: May 2019

AbstractAimTo evaluate the diagnostic value of interleukin-18 (IL-18) and troponin (TnI) in sepsis.MethodsThis retrospective analysis included 117 patients with sepsis (patient group) and 92 subjects who attended regular physical examinations (control group). We compared IL-18 and TnI expressions before treatment (T1) and on day 5 (T2), day 10 (T3) and day 15 (T4) of treatment. Acute Physiology and Chronic Health Evaluation II (APACHE II) guidelines were used to analyse the correlation between IL-18, TnI and APACHE II scores.ResultsAt T1, T2, T3 and T4, the IL-18 and TnI levels were all higher in the patient group than in the control group (p&lt;0.001). In the patient group, peak IL-18 and TnI levels were noted at T1, followed by T2, T3 and T4 (p&lt;0.001). The linear correlation analysis revealed positive correlations between IL-18 and TnI levels and APACHE II score (r =0.759, 0.866, p &lt;0.001). The 3-year survival rates of subjects with high IL-18 or TnI expression levels were all lower than of those with low expression levels (p=0.047, 0.048). In patients with sepsis, the expression of TnI and IL-18 is high and is positively correlated with APACHE II scores.ConclusionsMonitoring TnI and IL-18 levels can effectively evaluate the severity and recovery of patients with sepsis.
Lower Blood Pressure Is Not Associated With Decreased Arterial Spin Labeling Estimates of Perfusion in Intracerebral Hemorrhage
Authors: Klahr Ana C. , Kosior Jayme C. , Dowlatshahi Dariush , Buck Brian H. , Beaulieu Christian , Gioia Laura C. , Kalashyan Hayrapet , Wilman Alan H. , Jeerakathil Thomas , Emery Derek J. , Shuaib Ashfaq , Butcher Kenneth S. 
Published: May 2019

Background

Subacute ischemic lesions in intracerebral hemorrhage (
ICH
) have been hypothesized to result from hypoperfusion. Although studies of cerebral blood flow (
CBF
) indicate modest hypoperfusion in
ICH
, these investigations have been limited to early time points. Arterial spin labeling (
ASL
), a magnetic resonance imaging technique, can be used to measure
CBF
without a contrast agent. We assessed
CBF
in patients with ICH using
ASL
and tested the hypothesis that
CBF
is related to systolic blood pressure (
SBP
).

Methods and Results

In this cross‐sectional study, patients with ICH were assessed with
ASL
at 48 hours, 7 days, and/or 30 days after onset. Relative
CBF
(
rCBF
; ratio of ipsilateral/contralateral perfusion) was measured in the perihematomal regions, hemispheres, border zones, and the perilesional area in patients with diffusion‐weighted imaging hyperintensities. Twenty‐patients (65% men; mean±
SD
age, 68.5±12.7 years) underwent imaging with
ASL
at 48 hours (N=12), day 7 (N=6), and day 30 (N=11). Median (interquartile range) hematoma volume was 13.1 (6.3–19.3) mL. Mean±
SD
baseline
SBP
was 185.4±25.5 mm Hg. Mean perihematomal
rCBF
was 0.9±0.2 at 48 hours at all time points. Baseline
SBP
and other
SBP
measurements were not associated with a decrease in
rCBF
in any of the regions of interest (
P
≥0.111). r
CBF
did not differ among time points in any of the regions of interest (
P
≥0.097). Mean perilesional
rCBF
was 1.04±0.65 and was unrelated to baseline
SBP
(
P
=0.105).

Conclusions

ASL
can be used to measure
rCBF
in patients with acute and subacute
ICH
. Perihematomal
CBF
was not associated with
SBP
changes at any time point.

Clinical Trial Registration

URL:
http://www.clinicaltrials.gov
. Unique identifier: NCT00963976.
O‐GlcNAc Transferase Promotes Compensated Cardiac Function and Protein Kinase A O‐GlcNAcylation During Early and Established Pathological Hypertrophy From Pressure Overload
Authors: Zhu Wei‐Zhong , El‐Nachef Danny , Yang Xiulan , Ledee Dolena , Olson Aaron K. 
Published: May 2019

Background

Protein posttranslational modifications by
O
‐linked β‐N‐acetylglucosamine (O‐GlcNAc) increase with cardiac hypertrophy, yet the functional effects of these changes are incompletely understood. In other organs, O‐GlcNAc promotes adaptation to acute physiological stressors; however, prolonged O‐GlcNAc elevations are believed to be detrimental. We hypothesize that early O‐GlcNAcylation improves cardiac function during initial response to pressure overload hypertrophy, but that sustained elevations during established pathological hypertrophy negatively impact cardiac function by adversely affecting calcium handling proteins.

Methods and Results
Transverse aortic constriction or sham surgeries were performed on littermate controls or cardiac‐specific, inducible O‐GlcNAc transferase knockout (OGTKO) mice to reduce O‐GlcNAc levels. O‐GlcNAc transferase deficiency was induced at different times. To evaluate the initial response to pressure overload, OGTKO was completed preoperatively and mice were followed for 2 weeks post‐surgery. To assess prolonged O‐GlcNAcylation during established hypertrophy, OGTKO was performed starting 18 days after surgery and mice were followed until 6 weeks post‐surgery. In both groups, OGTKO with transverse aortic constriction caused significant left ventricular dysfunction. OGTKO did not affect levels of the calcium handling protein SERCA2a. OGTKO reduced phosphorylation of phospholamban and cardiac troponin I, which would negatively impact cardiac function. O‐GlcNAcylation of protein kinase A catalytic subunit, a kinase for phospholamban, decreased with OGTKO.

Conclusions
O‐GlcNAcylation promotes compensated cardiac function in both early and established pathological hypertrophy. We identified a novel O‐GlcNAcylation of protein kinase A catalytic subunit, which may regulate calcium handling and cardiac function.
Long‐Term Outcomes in Patients With Turner Syndrome: A 68‐Year Follow‐Up
Authors: Fuchs Margaret M. , Attenhofer Jost Christine , Babovic‐Vuksanovic Dusica , Connolly Heidi M. , Egbe Alexander 
Published: May 2019

Background

Turner syndrome (
TS
) is the most common sex chromosome abnormality in women and is associated with increased morbidity and mortality. We describe long‐term outcomes in a large cohort of patients with
TS
.

Methods and Results

Retrospective review of patients with
TS
followed at Mayo Clinic Rochester from 1950 to 2017 was performed. Clinical, imaging, surgical, and genetic data were analyzed. Survival analysis was performed with the Kaplan–Meier method using age‐ and sex‐matched Olmsted County residents as the reference group. The study cohort comprised 317 patients with
TS
. Average age at diagnosis was 9 (range, 2–12) years, genetic testing was performed in 202 (64%), and pure monosomy X was present in 75 (37%). Congenital heart disease occurred in 131 (41%), with the most frequent lesions being bicuspid aortic valve (n=102, 32%) and coarctation of the aorta (n=43, 14%). Ascending aortic dilation was common, with mean aortic root size index 2 cm/m
2
, and aortic dissection occurred in 6 (2%) patients. The average follow‐up was 11 (range, 2–26) years, yielding 3898 patient‐years, and during this period 46 (14%) patients died; mean age at the time of death was 53±17 years. Patients
with TS
had reduced survival compared with the control group (82% versus 94% at 30 years;
P
<0.001), and the leading causes of death were cardiovascular disease, liver disease, and malignancy.

Conclusions

Patients with
TS
have reduced survival compared with age‐matched controls, and cardiovascular disease is the major cause of death. Further studies are required to determine if targeted cardiovascular risk factor modification will result in improved survival in this population.
Cumulative Rheumatic Inflammation Modulates the Bone–Vascular Axis and Risk of Coronary Calcification
Authors: Chan Yap‐Hang , Ngai Michael Cheong , Chen Yan , Wu Mei‐Zhen , Yu Yu‐Juan , Zhen Zhe , Lai Kevin , Cheung Tommy , Ho Lai‐Ming , Chung Ho‐Yin , Lau Chak‐Sing , Tse Hung‐Fat , Yiu Kai‐Hang 
Published: May 2019

Background
Rheumatic diseases are related to both abnormal bone turnover and atherogenesis, but a mechanistic link was missing.

Methods and Results

We investigated the effect of cumulative rheumatic inflammation (
CRI
) on risk of coronary calcification in a retrospective cohort of 145 rheumatoid arthritis patients. A time‐adjusted aggregate
CRI
score was derived by conglomerating all quarterly biomarker encounters of serum C‐reactive protein over 60 months immediately preceding computed tomography coronary angiography. Flow cytometry was performed to measure the osteocalcin‐positive (
OCN
+
)
CD
34
+
KDR
+
and
OCN
+
CD
34
+
circulating endothelial progenitor cells (
EPCs
). Conventional early circulating
EPCs CD
34
+
CD
133
+
KDR
+
was determined. Coronary calcification was defined as any Agatston score >0. 50% of patients (n=72/145) had coronary calcification.
CRI
score was associated with presence of coronary calcification (
P
=0.004) (multivariable‐adjusted: highest versus lowest quartile: odds ratio=5.6 [95%
CI
1.1–28.9],
P
=0.041). Receiver operating characteristics curve revealed divergent behavior of
OCN
‐expressing circulating
EPCs
(
OCN
+
CD
34
+
EPCs
: area under the curve=0.60,
P
=0.034;
OCN
+
CD
34
+
KDR
+
EPCs
: area under the curve=0.59,
P
=0.053, positive predictors) versus conventional early
EPCs
(
CD
34
+
CD
133
+
KDR
+
: area under the curve=0.60,
P
=0.034, negative predictor) for coronary calcification, which persisted after multivariable adjustments (
OCN
+
CD
34
+
KDR
+
[>75th percentile]: odds ratio=7.2 [95%
CI
1.8–27.9],
P
=0.005;
OCN
+
CD
34
+
EPCs
[>75th percentile]: odds ratio=6.0 [95%
CI
1.5–23.3],
P
=0.010;
CD
34
+
CD
133
+
KDR
+
[>75th percentile: odds ratio=0.3 [95%
CI
0.1–1.0],
P
=0.053). Intriguingly, the
CRI
score was associated with increased
OCN
+
CD
34
+
EPCs
(highest versus lowest quartile: B=+25.6 [95%
CI
0.8–50.5] [×10
3
/mL peripheral blood],
P
=0.043), but reduced
CD
34
+
CD
133
+
KDR
+
EPCs
(highest versus lowest quartile: B=−16.2 [95%
CI
−31.5 to −0.9],
P
=0.038).

Conclusions

Preceding 60 months of
CRI
is associated with increased risk of coronary calcification and altered
OCN
expression in circulating
EPCs
.
Assessment of cytocompatibility and mechanical properties of detergent-decellularized ovine pericardial tissue
Authors: Mogaldea Alexandru , Theodoridis Karolina , Goecke Tobias , Tudorache Igor , Haverich Axel , Cebotari Serghei , Hilfiker Andres 
Published: May 2019

Background: Autologous pericardium is widely used for the repair of different sized cardiovascular defects. However, its use is limited especially in redo cardiac surgery. We developed an engineered tissue based on decellularized pericardium reseeded with blood-derived endothelial cells. Materials and Methods: Decellularization of ovine pericardium was performed using detergent treatment. Ovine outgrowth blood-derived and green fluorescent protein–labeled endothelial cells were used to reseed the decellularized ovine pericardium on the mesothelial side. The cell adhesion was assessed using fluorescent microscopy up to 15 days of in vitro cultivation. The mechanical properties of the pericardium were evaluated using suturability, burst pressure, and suture retention strength tests. Results: After decellularization the pericardial sheets appeared cell-free and repopulation using ovine blood-derived endothelial cells was successful by forming a robust monolayer. Detergent treatment did not affect the extracellular matrix. The thickness of decellularized tissue was similar to native ovine pericardium (285.3 ± 28.2 µm, respective 276.9 ± 23.8 µm, p = 0.48). Decellularized patch showed similar suturability comparable to the native ovine pericardium. Resulted burst pressure was not significantly different (native/decellularized: 312.5 ± 13.6/304.2 ± 16, p = 0.35). The suture retention strength of native pericardium was 638.33 ± 90.2 gr and comparable to decellularized tissue (622.2 ± 89.9 gr, p = 0.76). No differences were observed concerning elongation of native and decellularized pericardium (8.33 ± 1.5 and 8.5 ± 0.84 mm, respectively; p = 0.82). Conclusion: Mesothelial surface of decellularized ovine pericardium is suitable for reseeding with ovine blood-derived endothelial cells. The mechanical properties of detergent-treated pericardium were comparable to native tissue.