ObjectivesAs much as 50%–90% of research is estimated to be irreproducible, costing upwards of $28 billion in USA alone. Reproducible research practices are essential to improving the reproducibility and transparency of biomedical research, such as including preregistering studies, publishing a protocol, making research data and metadata publicly available, and publishing in open access journals. Here we report an investigation of key reproducible or transparent research practices in the published oncology literature.DesignWe performed a cross-sectional analysis of a random sample of 300 oncology publications published from 2014 to 2018. We extracted key reproducibility and transparency characteristics in a duplicative fashion by blinded investigators using a pilot tested Google Form.Primary outcome measuresThe primary outcome of this investigation is the frequency of key reproducible or transparent research practices followed in published biomedical and clinical oncology literature.ResultsOf the 300 publications randomly sampled, 296 were analysed for reproducibility characteristics. Of these 296 publications, 194 contained empirical data that could be analysed for reproducible and transparent research practices. Raw data were available for nine studies (4.6%). Five publications (2.6%) provided a protocol. Despite our sample including 15 clinical trials and 7 systematic reviews/meta-analyses, only 7 included a preregistration statement. Less than 25% (65/194) of publications provided an author conflict of interest statement.ConclusionWe found that key reproducibility and transparency characteristics were absent from a random sample of published oncology publications. We recommend required preregistration for all eligible trials and systematic reviews, published protocols for all manuscripts, and deposition of raw data and metadata in public repositories.
Improved survival among HIV-1 infected individuals with the advent of antiretroviral therapy has clearly led to a greater prevalence of non-infectious complications. One of the most devastating sequelae in these individuals is the development of pulmonary arterial hypertension (PAH). Various epidemiological studies suggest a worse survival of HIV-PAH patients when compared to other forms of PAH. Given that only a subset and not all HIV-infected individuals develop HIV-PAH, suggests that an additional second hit of genetic or environmental triggers is needed for the development of PAH. In this context, it has been well documented that HIV patients who abuse illicit drugs such as stimulants, opioids etc. are more susceptible to develop PAH. In this review, we highlight the studies that support the significance of a double hit of HIV and drug abuse in the incidence of PAH and focus on the research that has been undertaken to unravel the pathobiology and vascular remodeling mechanisms underlying the deleterious synergy between HIV infection and drugs of abuse in orchestrating the development of PAH.
BackgroundRandomised controlled trials (RCTs) provide the highest-level of evidence among primary research in cardiovascular medicine. Yet, even the best trial may be less useful if it fails to provide an accurate means of reproducibility. Unfortunately, discrepancies in the standards of trial reporting have been persistent in previous trials. The Template for Intervention Description and Replication (TIDieR) checklist aims to improve research efficacy by setting standards for quality intervention reporting and reproducibility. The goal of this study was to assess adherence to the TIDieR checklist among RCTs published in cardiovascular health journals. We also compared the quality of intervention reporting before and after the publication of TIDieR.MethodsThis cross-sectional, methodological study analysed 101 trials published within high-impact cardiology journals. Our primary objective was to assess overall adherence to the TIDieR checklist. Our secondary objective was to use an interrupted time-series analysis to determine if intervention reporting increased following the publication of TIDieR in March 2014. Additionally, we used generalised estimating equations to identify trial characteristics associated with intervention reporting.ResultsTrials in our sample reported 8.6/12 TIDieR checklist items, on average. The most under-reported items were those for describing the expertise of the interventionists and for describing the location of the intervention.ConclusionImproved outcome reporting and intervention reproducibility among RCTs are greatly needed in cardiovascular medicine. Clinicians and researchers should advocate for the ethical publication of complete, translatable and replicable clinical research results.
Pulmonary arterial hypertension is a fatal disease associated with pulmonary vascular remodeling and right ventricular hypertrophy. Pre-clinical animal models that reproduce the human pulmonary arterial hypertension process and pharmacological response to available therapies are critical for future drug development. The most prevalent animal model reproducing many aspects of angioobliterative forms of pulmonary arterial hypertension is the rat Sugen/hypoxia model in which Sugen, a vascular endothelial growth factor receptor antagonist, primarily causes initiation of endothelial injury and later in the presence of hypoxia promotes proliferation of apoptosis-resistant endothelial cells. We previously demonstrated that exposure of human pulmonary microvascular endothelium to morphine and HIV-proteins results in initial apoptosis followed by increased proliferation. Here, we demonstrate that the double-hit of morphine and Sugen 5416 (Sugen-morphine) in rats leads to the development of pulmonary arterial hypertension with significant medial hypertrophy of pre-acinar pulmonary arteries along with neo-intimal thickening of intra-acinar vessels. In addition, the pulmonary smooth muscle and endothelial cells isolated from Sugen-morphine rats showed hyperproliferation and apoptotic resistance, respectively, in response to serum starvation. Our findings support that the dual hit model of Sugen 5416 and morphine provides another experimental strategy to induce significant pulmonary vascular remodeling and development of severe pulmonary arterial hypertension pathology in rats without exposure to hypoxia.
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