bluuebunny/crossref_metadata_2025_split huggingface dataset:
Present and Future Surveillance of Antimicrobial Resistance in Animals: Principles and Practices
Authors: Simjee S. , McDermott P. , Trott D.J. , Chuanchuen R. 
Published: July 2018

ABSTRACT

There is broad consensus internationally that surveillance of the levels of antimicrobial resistance (AMR) occurring in various systems underpins strategies to address the issue. The key reasons for surveillance of resistance are to determine (i) the size of the problem, (ii) whether resistance is increasing, (iii) whether previously unknown types of resistance are emerging, (iv) whether a particular type of resistance is spreading, and (v) whether a particular type of resistance is associated with a particular outbreak. The implications of acquiring and utilizing this information need to be considered in the design of a surveillance system. AMR surveillance provides a foundation for assessing the burden of AMR and for providing the necessary evidence for developing efficient and effective control and prevention strategies. The codevelopment of AMR surveillance programs in humans and animals is essential, but there remain several key elements that make data comparisons between AMR monitoring programs, and between regions, difficult. Currently, AMR surveillance relies on uncomplicated
in vitro
antimicrobial susceptibility methods. However, the lack of harmonization across programs and the limitation of genetic information of AMR remain the major drawbacks of these phenotypic methods. The future of AMR surveillance is moving toward genotypic detection, and molecular analysis methods are expected to yield a wealth of information. However, the expectation that these molecular techniques will surpass phenotypic susceptibility testing in routine diagnosis and monitoring of AMR remains a distant reality, and phenotypic testing remains necessary in the detection of emerging resistant bacteria, new resistance mechanisms, and trends of AMR.
Antimicrobial Resistance in
Mycoplasma
spp
Authors: Gautier-Bouchardon Anne V. 
Published: July 2018

ABSTRACT

Mycoplasmas are intrinsically resistant to antimicrobials targeting the cell wall (fosfomycin, glycopeptides, or β-lactam antibiotics) and to sulfonamides, first-generation quinolones, trimethoprim, polymixins, and rifampicin. The antibiotics most frequently used to control mycoplasmal infections in animals are macrolides and tetracyclines. Lincosamides, fluoroquinolones, pleuromutilins, phenicols, and aminoglycosides can also be active. Standardization of methods used for determination of susceptibility levels is difficult since no quality control strains are available and because of species-specific growth requirements. Reduced susceptibility levels or resistances to several families of antimicrobials have been reported in field isolates of pathogenic
Mycoplasma
species of major veterinary interest:
M. gallisepticum
and
M. synoviae
in poultry;
M. hyopneumoniae
,
M. hyorhinis
, and
M. hyosynoviae
in swine;
M. bovis
in cattle; and
M. agalactiae
in small ruminants. The highest resistances are observed for macrolides, followed by tetracyclines. Most strains remain susceptible to fluoroquinolones. Pleuromutilins are the most effective antibiotics
in vitro
. Resistance frequencies vary according to the
Mycoplasma
species but also according to the countries or groups of animals from which the samples were taken. Point mutations in the target genes of different antimicrobials have been identified in resistant field isolates,
in vitro
-selected mutants, or strains reisolated after an experimental infection followed by one or several treatments: DNA-gyrase and topoisomerase IV for fluoroquinolones; 23S rRNA for macrolides, lincosamides, pleuromutilins, and amphenicols; 16S rRNAs for tetracyclines and aminoglycosides. Further work should be carried out to determine and harmonize specific breakpoints for animal mycoplasmas so that
in vitro
information can be used to provide advice on selection of
in vivo
treatments.
Mechanisms of acute adductor longus injuries in male football players: a systematic visual video analysis
Authors: Serner Andreas , Mosler Andrea Britt , Tol Johannes L , Bahr Roald , Weir Adam 
Published: July 2018

BackgroundChange of direction and kicking have been described as the main actions resulting in adductor longus injury. Video descriptions of inciting events are lacking.ObjectivePerform a standardised visual video analysis of a series of acute adductor longus injuries in football.Study designCross-sectional.MethodsVideo footage was reviewed by players, and assessed independently by five sports medicine professionals. Inciting events were described and categorised using standardised scoring, including playing situation, player/opponent behaviour, movement and body positions.ResultsVideos of acute adductor longus injuries in 17 professional male football players were analysed. Most injuries occurred in non-contact situations (71%), following a quick reaction to a change in play (53%). Injury actions were: change of direction (35%), kicking (29%), reaching (24%) and jumping (12%). Change of direction and reaching injuries were categorised as closed chain movements (59%), characterised by hip extension and abduction with external rotation. Kicking and jumping injuries were categorised as open chain (41%), characterised by a change from hip extension to hip flexion, and hip abduction to adduction, with external rotation.ConclusionAcute adductor longus injuries in football occur in a variety of situations. Player actions can be categorised into closed (change of direction and reaching) and open (kicking and jumping) chain movements involving triplanar hip motion. A rapid muscle activation during a rapid muscle lengthening appears to be the fundamental injury mechanism for acute adductor longus injuries.
Cardiovascular mortality and oral antidiabetic drugs: protocol for a systematic review and network meta-analysis
Authors: Goyat Rashmi , Thornton James Douglas , Tan Xi , Kelley George A 
Published: July 2018

IntroductionCardiovascular diseases are the leading cause of morbidity and mortality among individuals with diabetes. Despite the beneficial effects of antidiabetic drugs (ADDs) in terms of lowering haemoglobin A1c, several ADDs have been shown to increase the risk of cardiovascular events. Given the high prevalence of cardiovascular disease among individuals with diabetes, it is important to weigh the benefits of ADDs against their cardiovascular safety. Therefore, the objective of the current study is to conduct a systematic review with network meta-analysis to compare the effects of different oral pharmacological classes of ADDs on cardiovascular safety.Methods and analysisRandomised clinical trials (RCTs) and observational studies published in English up to 31 January 2017, and which include direct and/or indirect evidence, will be included. Studies will be retrieved by searching four electronic databases and cross-referencing. Dual selection and abstraction of data will occur. The primary outcome will be cardiovascular mortality. Secondary outcomes will include all-cause mortality, new event of acute myocardial infarction, stroke (haemorrhagic and ischaemic), hospitalisation for acute coronary syndrome and urgent revascularisation procedures. Risk of bias will be assessed using the Cochrane Risk of Bias assessment instrument for RCTs and the Strengthening the Reporting of Observational Studies in Epidemiology instrument for observational studies. Network meta-analysis will be performed using multivariate random-effects meta-regression models. The surface under the cumulative ranking curve will be used to provide a hierarchy of ADDs that increase cardiovascular mortality.DisseminationThe results of this study will be presented at a professional conference and submitted to a peer-reviewed journal.PROSPERO registration numberCRD42017051220.
Speaking up about care concerns in the ICU: patient and family experiences, attitudes and perceived barriers
Authors: Bell Sigall K , Roche Stephanie D , Mueller Ariel , Dente Erica , O’Reilly Kristin , Sarnoff Lee Barbara , Sands Kenneth , Talmor Daniel , Brown Samuel M 
Published: July 2018

BackgroundLittle is known about patient/family comfort voicing care concerns in real time, especially in the intensive care unit (ICU) where stakes are high and time is compressed. Experts advocate patient and family engagement in safety, which will require that patients/families be able to voice concerns. Data on patient/family attitudes and experiences regarding speaking up are sparse, and mostly include reporting events retrospectively, rather than pre-emptively, to try to prevent harm. We aimed to (1) assess patient/family comfort speaking up about common ICU concerns; (2) identify patient/family-perceived barriers to speaking up; and (3) explore factors associated with patient/family comfort speaking up.MethodsIn collaboration with patients/families, we developed a survey to evaluate speaking up attitudes and behaviours. We surveyed current ICU families in person at an urban US academic medical centre, supplemented with a larger national internet sample of individuals with prior ICU experience.Results105/125 (84%) of current families and 1050 internet panel participants with ICU history completed the surveys. Among the current ICU families, 50%–70% expressed hesitancy to voice concerns about possible mistakes, mismatched care goals, confusing/conflicting information and inadequate hand hygiene. Results among prior ICU participants were similar. Half of all respondents reported at least one barrier to voicing concerns, most commonly not wanting to be a ‘troublemaker’, ‘team is too busy’ or ‘I don’t know how’. Older, female participants and those with personal or family employment in healthcare were more likely to report comfort speaking up.ConclusionSpeaking up may be challenging for ICU patients/families. Patient/family education about how to speak up and assurance that raising concerns will not create ‘trouble’ may help promote open discussions about care concerns and possible errors in the ICU.
Expression analysis of HLA-E and NKG2A and NKG2C receptors points at a role for natural killer function in ankylosing spondylitis
Authors: Cauli Alberto , Dessole Grazia , Piga Matteo , Angioni Maria Maddalena , Pinna Silvia , Floris Alberto , Congia Mattia , Mascia Enrico , Paladini Fabiana , Tedeschi Valentina , Sorrentino Rosa , Fiorillo Maria Teresa , Mathieu Alessandro 
Published: July 2018

BackgroundAnkylosing spondylitis (AS) is a complex chronic inflammatory disease strongly associated with the majority of human leucocyte antigen (HLA)-B27 alleles. HLA-E molecules are non-classical major histocompatibility complex (MHC) class I molecules that specifically interact with the natural killer receptors NKG2A (inhibitory) and NKG2C (activating), and have been recently proposed to be involved in AS pathogenesis.‘’ObjectiveTo analyse the expression of HLA-E and the CD94/NKG2 pair of receptors in HLA-B27-positive patients with AS and healthy controls (HC) bearing the AS-associated B*2705 and the non-AS-associated B*2709 alleles.MethodsThe level of surface expression of HLA-E molecules on CD14+ peripheral blood mononuclear cell was evaluated in 21 HLA-B*2705 patients with AS, 12 HLA-B*2705 HC, 12 HLA-B*2709 HC and 6 HLA-B27-negative HC using the monoclonal antibody MEM-E/08 by quantitative cytofluorimetric analysis. The percentage and density of expression of HLA-E ligands NKG2A and NKG2C were also measured on CD3−CD56+ NK cells.ResultsHLA-E expression in CD14+ cells was significantly higher in patients with AS (587.0, IQR 424–830) compared with B*2705 HC (389, IQR 251.3–440.5; p=0.0007), B*2709 HC (294.5, IQR 209.5–422; p=0.0004) and HLA-B27-negative HC (380, IQR 197.3–515.0; p=0.01). A higher number of NK cells expressing NKG2A compared with NKG2C were found in all cohorts analysed, as well as a higher cell surface density.ConclusionThe higher surface level of HLA-E molecules in patients with AS compared with HC, concurrently with a prevalent expression of NKG2A, suggests that the crosstalk between these two molecules might play a role in AS pathogenesis, accounting for the previously reported association between HLA-E and AS.
Noninvasive wave intensity analysis predicts functional worsening in children with pulmonary arterial hypertension
Authors: Schäfer Michal , Wilson Neil , Ivy D. Dunbar , Ing Richard , Abman Steven , Browne Lorna P. , Morgan Gareth , Ross Michael , McLennan Daniel , Barker Alex J. , Fonseca Brian , Di Maria Michael , Hunter Kendall S. , Truong Uyen 
Published: July 2018

The purpose of the present study was to characterize pulmonary vascular stiffness using wave intensity analysis (WIA) in children with pulmonary arterial hypertension (PAH), compare the WIA indexes with catheterization- and MRI-derived hemodynamics, and assess the prognostic ability of WIA-derived biomarkers to predict the functional worsening. WIA was performed in children with PAH ( n = 40) and healthy control subjects ( n = 15) from phase-contrast MRI-derived flow and area waveforms in the main pulmonary artery (MPA). From comprehensive WIA spectra, we collected and compared with healthy control subjects forward compression waves (FCW), backward compression waves (BCW), forward decompression waves (FDW), and wave propagation speed ( c-MPA). There was no difference in the magnitude of FCW between PAH and control groups (88 vs. 108 mm5·s−1·ml−1, P = 0.239). The magnitude of BCW was increased in patients with PAH (32 vs. 5 mm5·s−1·ml−1, P < 0.001). There was no difference in magnitude of indexed FDW (32 vs. 28 mm5·s−1·ml−1, P = 0.856). c-MPA was increased in patients with PAH (3.2 vs. 1.6 m/s, P < 0.001). BCW and FCW correlated with mean pulmonary arterial pressure, right ventricular volumes, and ejection fraction. Elevated indexed BCW [heart rate (HR) = 2.91, confidence interval (CI): 1.18–7.55, P = 0.019], reduced indexed FDW (HR = 0.34, CI: 0.11–0.90, P = 0.030), and increased c-MPA (HR = 3.67, CI: 1.47–10.20, P = 0.004) were strongly associated with functional worsening of disease severity. Our results suggest that noninvasively derived biomarkers of pulmonary vascular resistance and stiffness may be helpful for determining prognosis and monitoring disease progression in children with PAH. NEW & NOTEWORTHY Wave intensity analysis (WIA) studies are lacking in children with pulmonary arterial hypertension (PAH) partially because WIA, which is necessary to assess vascular stiffness, requires an invasive pressure-derived waveform along with simultaneous flow measurements. We analyzed vascular stiffness using WIA in children with PAH who underwent phase-contrast MRI and observed significant differences in WIA indexes between patients with PAH and control subjects. Furthermore, WIA indexes were predictive of functional worsening and were associated with standard catheterization measures.
Characterization of a mouse model of obesity-related fibrotic cardiomyopathy that recapitulates features of human heart failure with preserved ejection fraction
Authors: Alex Linda , Russo Ilaria , Holoborodko Volodymir , Frangogiannis Nikolaos G 
Published: July 2018

Heart failure with preserved ejection fraction (HFpEF) is caused, or exacerbated by, a wide range of extracardiac conditions. Diabetes, obesity, and metabolic dysfunction are associated with a unique HFpEF phenotype, characterized by inflammation, cardiac fibrosis, and microvascular dysfunction. Development of new therapies for HFpEF is hampered by the absence of reliable animal models. The leptin-resistant db/ db mouse has been extensively studied as a model of diabetes-associated cardiomyopathy; however, data on the functional and morphological alterations in db/ db hearts are conflicting. In the present study, we report a systematic characterization of the cardiac phenotype in db/ db mice, focusing on the time course of functional and histopathological alterations and on the identification of sex-specific cellular events. Although both male and female db/ db mice developed severe obesity, increased adiposity, and hyperglycemia, female mice had more impressive weight gain and exhibited a modest but significant increase in blood pressure. db/ db mice had hypertrophic ventricular remodeling and diastolic dysfunction with preserved ejection fraction; the increase in left ventricular mass was accentuated in female mice. Histological analysis showed that both male and female db/ db mice had cardiomyocyte hypertrophy and interstitial fibrosis, associated with marked thickening of the perimysial collagen, and expansion of the periarteriolar collagen network, in the absence of replacement fibrosis. In vivo and in vitro experiments showed that fibrotic changes in db/ db hearts were associated with increased collagen synthesis by cardiac fibroblasts, in the absence of periostin, α-smooth muscle actin, or fibroblast activation protein overexpression. Male db/ db mice exhibited microvascular rarefaction. In conclusion, the db/ db mouse model recapitulates functional and histological features of human HFpEF associated with metabolic dysfunction. Development of fibrosis in db/ db hearts, in the absence of myofibroblast conversion, suggests that metabolic dysfunction may activate an alternative profibrotic pathway associated with accentuated extracellular matrix protein synthesis. NEW & NOTEWORTHY We provide a systematic analysis of the sex-specific functional and structural myocardial alterations in db/ db mice. Obese diabetic C57BL6J db/ db mice exhibit diastolic dysfunction with preserved ejection fraction, associated with cardiomyocyte hypertrophy, interstitial/perivascular fibrosis, and microvascular rarefaction, thus recapitulating aspects of human obesity-related heart failure with preserved ejection fraction. Myocardial fibrosis in db/ db mice is associated with a matrix-producing fibroblast phenotype, in the absence of myofibroblast conversion, suggesting an alternative mechanism of activation.
Regional and temporal changes in left ventricular strain and stiffness in a porcine model of myocardial infarction
Authors: Torres William M. , Jacobs Julia , Doviak Heather , Barlow Shayne C. , Zile Michael R. , Shazly Tarek , Spinale Francis G. 
Published: July 2018

The aim of the present study was to serially track how myocardial infarction (MI) impacts regional myocardial strain and mechanical properties of the left ventricle (LV) in a large animal model. Post-MI remodeling has distinct regional effects throughout the LV myocardium. Regional quantification of LV biomechanical behavior could help explain changes in global function and thus advance clinical assessment of post-MI remodeling. The present study is based on a porcine MI model to characterize LV biomechanics over 28 days post-MI via speckle-tracking echocardiography (STE). Regional myocardial strain and strain rate were recorded in the circumferential, radial, and longitudinal directions at baseline and at 3, 14, and 28 days post-MI. Regional myocardial wall stress was calculated using standard echocardiographic metrics of geometry and Doppler-derived hemodynamic measurements. Regional diastolic myocardial stiffness was calculated from the resultant stress-strain relations. Peak strain and phasic strain rates were nonuniformly reduced throughout the myocardium post-MI, whereas time to peak strain was increased to a similar degree in the MI region and border zone by 28 days post-MI. Elevations in diastolic myocardial stiffness in the MI region plateaued at 14 days post-MI, after which a significant reduction in MI regional stiffness in the longitudinal direction occurred between 14 and 28 days post-MI. Post-MI biomechanical changes in the LV myocardium were initially limited to the MI region but nonuniformly extended into the neighboring border zone and remote myocardium over 28 days post-MI. STE enabled quantification of regional and temporal differences in myocardial strain and diastolic stiffness, underscoring the potential of this technique for clinical assessment of post-MI remodeling. NEW & NOTEWORTHY For the first time, speckle-tracking echocardiography was used to serially track regional biomechanical behavior and mechanical properties postmyocardial infarction (post-MI). We found that changes initially confined to the MI region extended throughout the myocardium in a nonuniform fashion over 28 days post-MI. Speckle-tracking echocardiography-based evaluation of regional changes in left ventricular biomechanics could advance both clinical assessment of left ventricular remodeling and therapeutic strategies that target aberrant biomechanical behavior post-MI.
Proteomic analysis of aortic smooth muscle cell secretions reveals an association of myosin heavy chain 11 with abdominal aortic aneurysm
Authors: Yokoyama Utako , Arakawa Noriaki , Ishiwata Ryo , Yasuda Shota , Minami Tomoyuki , Goda Motohiko , Uchida Keiji , Suzuki Shinichi , Matsumoto Masataka , Koizumi Nobusato , Taguri Masataka , Hirano Hisashi , Yoshimura Koichi , Ogino Hitoshi , Masuda Munetaka , Ishikawa Yoshihiro 
Published: July 2018

Abdominal aortic aneurysm (AAA) is a life-threatening disease, and no disease-specific circulating biomarkers for AAA screening are currently available. We have identified a smooth muscle cell (SMC)-specific biomarker for AAA. We cultured aneurysmal tunica media that were collected from eight patients undergoing elective open-repair surgeries. Secreted proteins in culture medium were subjected to liquid chromatography/tandem mass spectrometry. Myosin heavy chain 11 (myosin-11) was identified as a SMC-specific protein in the tunica media-derived secretions of all patients. We then examined myosin-11 protein concentrations by ELISA in plasma samples from patients with AAA ( n = 35) and age-matched healthy control subjects ( n = 34). Circulating myosin-11 levels were significantly higher in patients with AAA than control subjects. The area under the receiver-operating characteristic curve (AUC) of myosin-11 was 0.77, with a specificity of 65% at a sensitivity of 91%. Multivariate logistic regression analysis showed a significant association between the myosin-11 level and presence of AAA. When the myosin-11 level was combined with hypertension, it improved the prediction of AAA (AUC 0.88) more than hypertension per se. We then investigated the correlation between aortic diameter and circulating myosin-11 levels using AAA serum samples from patients undergoing endovascular aneurysm repair ( n = 20). Circulating myosin-11 levels were significantly correlated with maximum aortic diameter. Furthermore, changes in myosin-11 concentrations from the baseline 12 mo after endovascular aneurysm repair were associated with those in aortic diameter. These data suggest that circulating levels of myosin-11, which is a SMC-specific myosin isoform, may be useful as a biomarker for AAA.NEW & NOTEWORTHY Extensive studies have revealed that inflammation- or proteolysis-related proteins are proposed as biomarkers for abdominal aortic aneurysm (AAA). Changes in these protein concentrations are not specific for smooth muscle, which is a major part of AAA pathologies. Hence, no disease-specific circulating markers for AAA are currently available. We found, using secretome-based proteomic analysis on human AAA tunica media, that myosin heavy chain 11 was associated with AAA. Circulating myosin heavy chain 11 may be a new tissue-specific AAA marker.