bluuebunny/crossref_metadata_2025_split huggingface dataset:
Opportunistic screening to detect atrial fibrillation in Aboriginal adults in Australia
Authors: Gwynne Kylie , Flaskas Yvonne , O'Brien Ciaran , Jeffries Thomas Lee , McCowen Debbie , Finlayson Heather , Martin Tanya , Neubeck Lis , Freedman Ben 
Published: November 2016

IntroductionThere is a 10-year gap in life expectancy between Aboriginal and non-Aboriginal Australians. The leading cause of death for Aboriginal Australians is cardiovascular disease, including myocardial infarction and stroke. Although atrial fibrillation (AF) is a known precursor to stroke there are no published studies about the prevalence of AF for Aboriginal people and limited evidence about AF in indigenous populations globally.Methods and analysisThis mixed methods study will recruit and train Aboriginal health workers to use an iECG device attached to a smartphone to consecutively screen 1500 Aboriginal people aged 45 years and older. The study will quantify the proportion of people who presented for follow-up assessment and/or treatment following a non-normal screening and then estimate the prevalence and age distribution of AF of the Australian Aboriginal population. The study includes semistructured interviews with the Aboriginal health workers about the effectiveness of the iECG device in their practice as well as their perceptions of the acceptability of the device for their patients. Thematic analysis will be undertaken on the qualitative data collected in the study. If the device and approach are acceptable to the Aboriginal people and widely adopted, it may help prevent the effects of untreated AF including ischaemic stroke and early deaths or impairment in Aboriginal people.Ethics and disseminationThis mixed methods study received ethics approval from the Aboriginal Health and Medical Research Council (1135/15) and the Australian Health Council of Western Australia (HREC706). Ethics approval is being sought in the Northern Territory. The findings of this study will be shared with Aboriginal communities, in peer reviewed publications and at conferences. There are Aboriginal investigators in each state/territory where the study is being conducted who have been actively involved in the study. They will also be involved in data analysis, dissemination and research translation.Trial registration numberACTRN12616000459426.
Systematic review of physical activity and exercise interventions to improve health, fitness and well-being of children and young people who use wheelchairs
Authors: O'Brien Thomas D , Noyes Jane , Spencer Llinos Haf , Kubis Hans-Peter , Hastings Richard P , Whitaker Rhiannon 
Published: November 2016

AimTo perform a systematic review establishing the current evidence base for physical activity and exercise interventions that promote health, fitness and well-being, rather than specific functional improvements, for children who use wheelchairs.DesignA systematic review using a mixed methods design.Data sourcesA wide range of databases, including Web of Science, PubMed, BMJ Best Practice, NHS EED, CINAHL, AMED, NICAN, PsychINFO, were searched for quantitative, qualitative and health economics evidence.Eligibilityparticipants: children/young people aged >25 years who use a wheelchair, or parents and therapists/carers. Intervention: home-based or community-based physical activity to improve health, fitness and well-being.ResultsThirty quantitative studies that measured indicators of health, fitness and well-being and one qualitative study were included. Studies were very heterogeneous preventing a meta-analysis, and the risk of bias was generally high. Most studies focused on children with cerebral palsy and used an outcome measure of walking or standing, indicating that they were generally designed for children with already good motor function and mobility. Improvements in health, fitness and well-being were found across the range of outcome types. There were no reports of negative changes. No economics evidence was found.ConclusionsIt was found that children who use wheelchairs can participate in physical activity interventions safely. The paucity of robust studies evaluating interventions to improve health and fitness is concerning. This hinders adequate policymaking and guidance for practitioners, and requires urgent attention. However, the evidence that does exist suggests that children who use wheelchairs are able to experience the positive benefits associated with appropriately designed exercise.Trial registration numberCRD42013003939.
Inflammation, but not recruitment, of adipose tissue macrophages requires signalling through Mac-1 (CD11b/CD18) in diet-induced obesity (DIO)
Authors: Wolf Dennis , Bukosza Nora , Engel David , Poggi Marjorie , Jehle Felix , Michel Nathaly Anto , Chen Yung-Chih , Colberg Christian , Hoppe Natalie , Dufner Bianca , Boon Louis , Blankenbach Hermann , Hilgendorf Ingo , zur Muhlen Constantin von , Reinöhl Jochen , Sommer Björn , Marchini Timoteo , Febbraio Mark A. , Weber Christian , Bode Christoph , Peter Karlheinz , Lutgens Esther , Zirlik Andreas 
Published: November 2016

SummaryCell accumulation is a prerequisite for adipose tissue inflammation. The leukocyte integrin Mac-1 (CD11b/CD18, αMβ2) is a classic adhesion receptor critically regulating inflammatory cell recruitment. Here, we tested the hypothesis that a genetic deficiency and a therapeutic modulation of Mac-1 regulate adipose tissue inflammation in a mouse model of diet-induced obesity (DIO). C57Bl6/J mice genetically deficient (Mac-1-/-) or competent for Mac-1 (WT) consumed a high fat diet for 20 weeks. Surprisingly, Mac-1-/- mice presented with increased diet-induced weight gain, decreased insulin sensitivity in skeletal muscle and in the liver in insulin-clamps, insulin secretion deficiency and elevated glucose levels in fasting animals, and dyslipidaemia. Unexpectedly, accumulation of adipose tissue macrophages (ATMs) was unaffected, while gene expression indicated less inflamed adipose tissue and macrophages in Mac-1-/- mice. In contrast, inflammatory gene expression at distant locations, such as in skeletal muscle, was not changed. Treatment of ATMs with an agonistic anti-Mac-1 antibody, M1/70, induced pro-inflammatory genes in cell culture. In vivo, treatment with M1/70 induced a hyper-inflammatory phenotype with increased expression of IL-6 and MCP-1, whereas accumulation of ATMs did not change. Finally, inhibition of Mac-1’s adhesive interaction to CD40L by the peptide inhibitor cM7 did not affect myeloid cell accumulation in adipose tissue. We present the surprising finding that adhesive properties of the leukocyte integrin Mac-1 are not required for macrophage accumulation in adipose tissue. Instead, Mac-1 modulates inflammatory gene expression in macrophages. These findings question the net effect of integrin blockade in cardio-metabolic disease.D. W., N. B., and D. E. equally contributed to this work.K. P., E. L., and A. Z. share senior authorship.Note: The review process for this manuscript was fully handled by Gregory Y. H. Lip, Editor in Chief.Supplementary Material to this article is available online at www.thrombosis-online.com.
Neuroprotective Effects of the Glucagon-Like Peptide-1 Analog Exenatide After Out-of-Hospital Cardiac Arrest
Authors: Wiberg Sebastian , Hassager Christian , Schmidt Henrik , Thomsen Jakob Hartvig , Frydland Martin , Lindholm Matias Greve , Høfsten Dan Eik , Engstrøm Thomas , Køber Lars , Møller Jacob Eifer , Kjaergaard Jesper 
Published: November 2016

Background:
In-hospital mortality in comatose patients resuscitated from out-of-hospital cardiac arrest (OHCA) is ≈50%. In OHCA patients, the leading cause of death is neurological injury secondary to ischemia and reperfusion. Glucagon-like peptide-1 analogs are approved for type 2 diabetes mellitus; preclinical and clinical data have suggested their organ-protective effects in patients with ischemia and reperfusion injury. The aim of this trial was to investigate the neuroprotective effects of the glucagon-like peptide-1 analog exenatide in resuscitated OHCA patients.

Methods:
We randomly assigned 120 consecutive comatose patients resuscitated from OHCA in a double-blind, 2-center trial. They were administered 17.4 μg exenatide (Byetta) or placebo over a 6-hour and 15-minute infusion, in addition to standardized intensive care including targeted temperature management. The coprimary end points were feasibility, defined as initiation of the study drug in >90% patients within 240 minutes of return of spontaneous circulation, and efficacy, defined as the geometric area under the neuron-specific enolase curve from 24 to 72 hours after admission. The main secondary end points included a composite end point of death and poor neurological function, defined as a Cerebral Performance Category score of 3 to 5 assessed at 30 and 180 days.

Results:

The study drug was initiated within 240 minutes of return of spontaneous circulation in 96% patients. The median blood glucose 8 hours after admission in patients receiving exenatide was lower than that in patients receiving placebo (5.8 [5.2–6.7] mmol/L versus 7.3 [6.2–8.7] mmol/L,
P
<0.0001). However, there were no significant differences in the area under the neuron-specific enolase curve, or a composite end point of death and poor neurological function between groups. Adverse events were rare with no significant difference between groups.

Conclusions:
Acute administration of exenatide to comatose patients in the intensive care unit after OHCA is feasible and safe. Exenatide did not reduce neuron-specific enolase levels and did not significantly improve a composite end point of death and poor neurological function after 180 days.

Clinical Trial Registration:

URL:
http://www.clinicaltrials.gov
. Unique identifier: NCT02442791.
Relationship Between β‐Blocker Therapy at Discharge and Clinical Outcomes in Patients With Acute Coronary Syndrome Undergoing Percutaneous Coronary Intervention
Authors: Li Chenze , Sun Yang , Shen Xiaoqing , Yu Ting , Li Qing , Ruan Guoran , Zhang Lina , Huang Qiang , Zhuang Hang , Huang Jingqiu , Ni Li , Wang Luyun , Jiang Jiangang , Wang Yan , Wang Dao Wen 
Published: November 2016

Background
The evidence supporting the use of β‐blockers in patients with acute coronary syndrome after successful percutaneous coronary intervention has been inconsistent and scarce.

Methods and Results

Between March 1, 2009, and December 30, 2014, a total of 3180 eligible patients with acute coronary syndrome undergoing percutaneous coronary intervention were consecutively enrolled. The primary end point was all‐cause death and the secondary end point was a composite of all‐cause death, nonfatal myocardial infarction, heart failure readmission, and cardiogenic hospitalization. Patients were compared according to the use of β‐blockers at discharge. Compared with the no β‐blocker group, the risk of all‐cause death was significantly lower in the β‐blocker group (hazard ratio [
HR
], 0.33; 95%
CI
, 0.17–0.65 [
P
=0.001]). A consistent result was obtained in multiple adjusted model and propensity score–matched analysis. The use of β‐blockers was also associated with decreased risk of composite of adverse cardiovascular events (
HR
, 0.47; 95%
CI
, 0.28–0.81 [
P
=0.006]), although statistical significance disappeared after multivariable adjustment and propensity score matching. Furthermore, we performed post hoc analysis for the subsets of patients and the results revealed that patients with non–ST‐segment elevation myocardial infarction benefited the most from β‐blocker therapy at discharge (
HR
, 0.04; 95%
CI
, 0.00–0.27 [
P
=0.001]), and the use of <50% of target dose was significantly associated with better outcome compared with no β‐blocker use, rather than ≥50% of target dose.

Conclusions
The administration of relatively low β‐blocker dose is associated with improved clinical outcomes among patients with acute coronary syndrome after successful percutaneous coronary intervention, especially for patients with non‐ST‐segment elevation myocardial infarction.
Correlation between apparent diffusion coefficient and histopathology subtypes of osteosarcoma after neoadjuvant chemotherapy
Authors: Wang Jifei , Sun Meili , Liu Dawei , Hu Xiaoshu , Pui Margaret H , Meng Quanfei , Gao Zhenhua 
Published: November 2016

Background Neoadjuvant chemotherapy has made limb-salvage surgery possible for the patients with osteosarcoma. Diffusion-weighted magnetic resonance imaging (DWI) has been used to monitor chemotherapy response. Purpose To correlate the apparent diffusion coefficient (ADC) values with histopathology subtypes of osteosarcoma after neoadjuvant chemotherapy. Material and Methods Twelve patients with osteoblastic (n = 7), chondroblastic (n = 4), and fibroblastic (n = 1) osteosarcomas underwent post-chemotherapy DWI before limb-salvage surgery. ADCs corresponding to 127 histological tissue samples from the 12 resected specimens were compared to histological features. Results The mean ADC value of non-cartilaginous viable tumor (38/91, ADC = 1.22 ± 0.03 × 10−3 mm2/s) was significantly ( P < 0.001) lower than that of non-cartilaginous tumor cell necrosis without stroma disintegration (25/91, ADC =1.77 ± 0.03 × 10−3 mm2/s), cartilaginous viable tumor (14/91, ADC = 2.19 ± 0.04 × 10−3 mm2/s), and cystic areas including liquefied necrosis, blood space, and secondary aneurysmal bone cyst (14/91, ADC = 2.29 ± 0.05 × 10−3 mm2/s). The mean ADC value of non-cartilaginous tumor cell necrosis was also significantly ( P < 0.001) smaller than those of viable cartilaginous tumor and cystic/hemorrhagic necrosis whereas the mean ADC values were not significantly ( P > 0.05) different between viable cartilaginous tumor and cystic/hemorrhagic necrosis. Conclusion DWI allows assessment of tumor necrosis after neoadjuvant chemotherapy by ADC differences between viable tumor and necrosis in fibroblastic and osteoblastic osteosarcomas whereas viable chondroblastic osteosarcoma has high ADC and cannot be distinguished reliably from necrosis.
Hip Strength as an Intrinsic Risk Factor for Lateral Ankle Sprains in Youth Soccer Players: A 3-Season Prospective Study
Authors: De Ridder Roel , Witvrouw Erik , Dolphens Mieke , Roosen Philip , Van Ginckel Ans 
Published: November 2016

Background: Numerous epidemiological studies have emphasized the burden of lateral ankle sprains in youth soccer players. However, no prospective study has identified intrinsic physical and modifiable risk factors for these injuries in this particular population. Although injury prevention programs in soccer incorporate proximal hip and core stability exercises, it is striking that the relationship between impaired proximal hip function and ankle sprains has not yet been prospectively investigated in youth soccer players. Hypothesis: This prospective study aimed to examine whether hip muscle strength is a risk factor for sustaining a lateral ankle sprain in youth soccer players. We hypothesized that decreased hip muscle strength would predispose youth soccer players to an increased risk of lateral ankle sprains. Study Design: Case-control study; Level of evidence, 3. Methods: This study included a total of 133 male youth soccer players (age divisions U11-U17) for analysis. At the beginning of the season, anthropometric characteristics were collected and hip muscle strength was assessed using a handheld dynamometer. Injury registration was performed by the team medical staff during 3 consecutive seasons. A principal-component, multivariate Cox regression analysis was performed to identify potential risk factors for sustaining a lateral ankle sprain. Results: Twelve participants (18% of all reported injuries) sustained a lateral ankle sprain (0.36 per 1000 athletic-exposure hours). After adjustment for body size dependencies and other hip muscle forces, an increase in hip muscle extension force was associated with a significant decrease in the hazard of the injury (hazard ratio, 0.3; 95% confidence interval, 0.1-0.9; P = .028). No other study variable could be identified as a risk factor for lateral ankle sprains. Conclusion: Reduced hip extension muscle strength is an independent risk factor for lateral ankle sprains in male youth soccer players. Other hip muscle strength outcomes were not identified as risk factors. Replication in larger samples with more injured cases is warranted to further ascertain the importance of this risk factor.
Economic evaluation of home-based telebehavioural health care compared to in-person treatment delivery for depression
Authors: Bounthavong Mark , Pruitt Larry D , Smolenski Derek J , Gahm Gregory A , Bansal Aasthaa , Hansen Ryan N 
Published: November 2016

Introduction Home-based telebehavioural healthcare improves access to mental health care for patients restricted by travel burden. However, there is limited evidence assessing the economic value of home-based telebehavioural health care compared to in-person care. We sought to compare the economic impact of home-based telebehavioural health care and in-person care for depression among current and former US service members. Methods We performed trial-based cost-minimisation and cost-utility analyses to assess the economic impact of home-based telebehavioural health care versus in-person behavioural care for depression. Our analyses focused on the payer perspective (Department of Defense and Department of Veterans Affairs) at three months. We also performed a scenario analysis where all patients possessed video-conferencing technology that was approved by these agencies. The cost-utility analysis evaluated the impact of different depression categories on the incremental cost-effectiveness ratio. One-way and probabilistic sensitivity analyses were performed to test the robustness of the model assumptions. Results In the base case analysis the total direct cost of home-based telebehavioural health care was higher than in-person care (US$71,974 versus US$20,322). Assuming that patients possessed government-approved video-conferencing technology, home-based telebehavioural health care was less costly compared to in-person care (US$19,177 versus US$20,322). In one-way sensitivity analyses, the proportion of patients possessing personal computers was a major driver of direct costs. In the cost-utility analysis, home-based telebehavioural health care was dominant when patients possessed video-conferencing technology. Results from probabilistic sensitivity analyses did not differ substantially from base case results. Discussion Home-based telebehavioural health care is dependent on the cost of supplying video-conferencing technology to patients but offers the opportunity to increase access to care. Health-care policies centred on implementation of home-based telebehavioural health care should ensure that these technologies are able to be successfully deployed on patients’ existing technology.
Spinal astrocytic activation contributes to mechanical allodynia in a rat model of cyclophosphamide-induced cystitis
Authors: Liu Bolong , Su Minzhi , Tang ShaoJun , Zhou Xiangfu , Zhan Hailun , Yang Fei , Li Wenbiao , Li Tengcheng , Xie Juncong 
Published: November 2016

Background Previous studies have demonstrated that glial cells play an important role in the generation and maintenance of neuropathic pain. Activated glial cells produce numerous mediators such as proinflammatory cytokines that facilitate neuronal activity and synaptic plasticity. Similarly, bladder pain syndrome/interstitial cystitis shares many characteristics of neuropathic pain. However, related report on the involvement of spinal glia in bladder pain syndrome/interstitial cystitis-associated pathological pain and the underlying mechanisms are still lacking. The present study investigated spinal glial activation and underlying molecular mechanisms in a rat model of bladder pain syndrome/interstitial cystitis. Results A rat model of bladder pain syndrome/interstitial cystitis was established via systemic injection with cyclophosphamide. Mechanical allodynia was tested with von Frey monofilaments and up-down method. Moreover, Western blots and double immunofluorescence were used to detect the expression and location of glial fibrillary acidic protein, OX42/Iba1, P-P38, NeuN, interleukin (IL)-1β, phosphorylation of N-methyl-D-aspartate receptor 1 (P-NR1), and IL-1 receptor I (IL-1RI) in the L6-S1 spinal cord. We found that glial fibrillary acidic protein rather than OX42/Iba1 or P-P38 was significantly increased in the spinal cord of cyclophosphamide-induced cystitis. L-alpha-aminoadipate but not minocycline markedly attenuated the allodynia. Furthermore, we found that spinal IL-1β was dramatically increased in cyclophosphamide-induced cystitis, and activated astrocytes were the only source of IL-1β release, which contributed to allodynia in cystitis rats. Besides, spinal P-NR1 was statistically increased in cyclophosphamide-induced cystitis and only localized in IL-1RI positive neurons in spinal dorsal horn. Additionally, NR antagonist significantly attenuated the cystitis-induced pain. Interestingly, the time course of the P-NR1 expression paralleled to that of IL-1β or glial fibrillary acidic protein. Conclusions Our results demonstrated that astrocytic activation but not microglial activation contributed to the allodynia in cyclophosphamide-induced cystitis and IL-1β released from astrocytes might bind to its endogenous receptor on the neurons inducing the phosphorylation of NR1 subunit, leading to sensory neuronal hyperexcitability and pathological pain.
Skeletal muscle mitochondrial capacity in people with multiple sclerosis
Authors: Harp Mary Ann , McCully Kevin K , Moldavskiy Marina , Backus Deborah 
Published: November 2016

Background People with multiple sclerosis (MS) have functional disability and may have reduced muscle mitochondrial capacity. Objective The objective of this paper is to measure muscle mitochondrial capacity of leg muscles using near-infrared spectroscopy (NIRS) and compare to functional status. Materials and methods People with MS ( n = 16) and a control (CON) group ( n = 9) were evaluated for 25-ft walk time. Mitochondrial capacity of both gastrocnemius muscles were measured with NIRS as the rate of recovery of oxygen consumption in after exercise. Results Mitochondrial capacity was lower in the MS group compared to the CON group (rate constants: 1.13 ± 0.29 vs. 1.68 ± 0.37 min−1, p < 0.05). There was a tendency for people with MS who used assistive devices to have lower mitochondrial capacity in the weaker leg ( p = 0.07). Conclusion NIRS measurements of mitochondrial capacity suggest a 40% deficit in people with MS compared to CONs and this may contribute to walking disability.