Quality of Literature Searches Published in Leading Neurosurgical Journals: A Review of Reviews.

BACKGROUND: There is mounting evidence that the search strategies upon which systematic reviews (SRs) are based frequently contain errors are incompletely reported or insensitive. OBJECTIVE: To appraise the quality of search strategies in the 10 leading specialty neurosurgical journals and identify factors associated with superior searches. METHODS: This research-on-research study systematically surveyed SRs published in the 10 leading neurosurgical journals between 01/10/2017 and 31/10/2019. All SRs were eligible for assessment using a predefined coding manual that was adapted from the preferred reporting items for systematic reviews and meta-analyses (PRISMA), a measurement tool to assess systematic reviews (AMSTAR), and Cochrane Collaboration guidelines. The PubMed interface was used to search the MEDLINE database, which was supplemented by individual journal searches. Descriptive statistics were utilized to identify factors associated with improved search strategies. RESULTS: A total of 633 articles were included and contained a median of 19.00 (2.00-1654.00) studies. Less than half (45.97%) of included search strategies were considered to be reproducible. Aggregated reporting score was positively associated with in-text reference to reporting guideline adherence (τb = 0.156, P < .01). The number of articles retrieved by a search (τb = 0.11, P < .01) was also associated with the reporting of a reproducible search strategy. CONCLUSION: This study demonstrates that the search strategies used in neurosurgical SRs require improvement. In addition to increasing awareness of reporting standards, we propose that this be achieved by the incorporation of PRISMA and other guidelines into article submission and peer-review processes. This may lead to the conduct of more informative SRs, which may result in improved clinician decision-making and patient outcomes.

Reporting Quality of Systematic Review Abstracts Published in Leading Neurosurgical Journals: A Research on Research Study.

BACKGROUND: Systematic review (SR) abstracts are frequently relied upon to guide clinical decision-making. However, there is mounting evidence that the quality of abstract reporting in the medical literature is suboptimal. OBJECTIVE: To appraise SR abstract reporting quality in neurosurgical journals and identify factors associated with improved reporting. METHODS: This study systematically surveyed SR abstracts published in 8 leading neurosurgical journals between 8 April 2007 and 21 August 2017. Abstracts were identified through a search of the MEDLINE database and their reporting quality was determined in duplicate using a tool derived from the Preferred Reporting Items for Systematic Reviews and Meta-analyses for Abstracts (PRISMA-A) statement. All SR abstracts that provided comparison between treatment strategies were eligible for inclusion. Descriptive statistics were utilized to identify factors associated with improved reporting. RESULTS: A total of 257 abstracts were included in the analysis, with a mean of 22.8 (±25.3) included studies. The overall quality of reporting in included abstracts was suboptimal, with a mean score of 53.05% (±11.18). Reporting scores were higher among abstracts published after the release of the PRISMA-A guidelines (M = 56.52; 21.74-73.91) compared with those published beforehand (M = 47.83; 8.70-69.57; U = 4346.00, z = -4.61, P < .001). Similarly, both word count (r = 0.338, P < .001) and journal impact factor (r = 0.199, P = .001) were associated with an improved reporting score. CONCLUSION: This study demonstrates that the overall reporting quality of abstracts in leading neurosurgical journals requires improvement. Strengths include the large number abstracts assessed, and its weaknesses include the fact that only neurosurgery-specific journals were surveyed. We recommend that attention be turned toward strengthening abstract submission and peer-review processes.

Anti-mycobacterial function of macrophages is impaired in a diet induced model of type 2 diabetes.

Type 2 diabetes (T2D) is one of the major risk factors for tuberculosis (TB). In this study, a diet induced murine model of T2D (DIMT2D) was developed and characterized in the context of metabolic, biochemical and histopathological features following diet intervention. Mycobacterial susceptibility was investigated using Mycobacterium fortuitum as a surrogate. Phagocytic capability of alveolar macrophages and resident peritoneal macrophages were determined by in vitro assays using mycolic acid coated beads and M. fortuitum. Results demonstrated that bacillary loads were significantly higher in liver, spleen, and lungs of diabetic mice compared to controls. Higher inflammatory lesions and impaired cytokine kinetics (TNF-α, MCP-1, IL-12, IFN-γ) were also observed in diabetic mice. Macrophages isolated from diabetic mice had lower uptake of mycolic acid coated beads, reduced bacterial internalization and killing and altered cytokine responses (TNF-α, IL-6, MCP-1). This model will be useful to further investigate different facets of host-pathogen interactions in TB-T2D.

Development of a diet-induced murine model of diabetes featuring cardinal metabolic and pathophysiological abnormalities of type 2 diabetes.

The persistent rise in global incidence of type 2 diabetes (T2D) continues to have significant public health and economic implications. The availability of relevant animal models of T2D is critical to elucidating the complexity of the pathogenic mechanisms underlying this disease and the implications this has on susceptibility to T2D complications. Whilst many high-fat diet-induced rodent models of obesity and diabetes exist, growing appreciation of the contribution of high glycaemic index diets on the development of hyperglycaemia and insulin resistance highlight the requirement for animal models that more closely represent global dietary patterns reflective of modern society. To that end, we sought to develop and validate a murine model of T2D based on consumption of an energy-dense diet containing moderate levels of fat and a high glycaemic index to better reflect the aetiopathogenesis of T2D. Male C57BL/6 mice were fed an energy-dense (ED) diet and the development of pathological features used in the clinical diagnosis of T2D was assessed over a 30-week period. Compared with control mice, 87% of mice fed an ED diet developed pathognomonic signs of T2D including glucose intolerance, hyperglycaemia, glycosylated haemoglobin (HbA1c) and glycosuria within 30 weeks. Furthermore, dyslipidaemia, chronic inflammation, alterations in circulating leucocytes and renal impairment were also evident in ED diet-fed mice compared with mice receiving standard rodent chow. Longitudinal profiling of metabolic and biochemical parameters provide support of an aetiologically and clinically relevant model of T2D that will serve as a valuable tool for mechanistic and therapeutic studies investigating the pathogenic complications of T2D.

The double burden: a new-age pandemic meets an ancient infection.

Tuberculosis is responsible for significant morbidity and mortality in the tropics. Active TB develops when host defences are impaired. Epidemiological evidence and studies addressing the double burden of communicable and non-communicable diseases demonstrate a clear association between diabetes and susceptibility to TB, treatment failure and complications. The immune mechanisms involved in host-pathogen interactions in co-morbid TB-diabetes are not well defined and require further investigation. This combined with the increase in diabetes predominately in low- and middle-income countries where TB is prevalent has major health implications.