1233 CRITICAL APPRAISAL OF MACHINE LEARNING PROGNOSTIC MODELS FOR ACUTE PANCREATITIS: A SYSTEMATIC REVIEW
Ila LahootiBrian CritelliAmier HassanAli LahootiNathan MatzkoJan Niklas AdamsLukas LißJustin QuionDavid RestrepoMelica NikahdStacey CulpLydia NohJoon Seong ParkKathleen TongVenkata S. AkshintalaJohn A. WindsorNikhil K. MullGeorgios PapachristouSomashekar G. KrishnaSamuel HanMitchell L. RamseyPhil A. HartLeo Anthony CeliPeter Lee
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Preface Contributors The history of chronic pancreatitis Molecular pathogenesis and gentic alterations in chronic pancreatitis Pathogenesis of chronic pancreatitis: Current state and trends Chronic pancreatitis: The role of nerves and neuroimmune interaction Diagnosis of chronic pancreatitis: Function tests Chronic pancreatitis: Diagnostic imaging Chronic pancreatitis: An attempt to classify Difficult decision-making in chronic pancreatitis: An interactive workshop Chronic pancreatitis diabetes mellitus and nutrition Conservative treatment of chronic pancreatitis 100th anniversary of pancreatic enzyme treatment Endoscopic treatment of chronic pancreatitis: Impact on long-term outcome Surgical treatment of chronic pancreatitis: Standard procedures Surgical treatment of chronic pancreatitis: Long-term results Index
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This chapter on critical appraisal provides an essential guide to students and researchers on the what, why and how of an increasingly important set of skills in health research. Indeed, critical appraisal is now a key tenet of academic writing and scholarship. This chapter covers: what critical appraisal is; why critical appraisal is important; critical appraisal tools and checklists, including an overview of how to find and select them for different research designs; and useful practical guidance on how to assess methodological quality – what, why, when and how.
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In Brief Critical appraisal is the assessment of research studies' worth to clinical practice. Critical appraisal—the heart of evidence-based practice—involves four phases: rapid critical appraisal, evaluation, synthesis, and recommendation. This article reviews each phase and provides examples, tips, and caveats to help evidence appraisers successfully determine what is known about a clinical issue. Patient outcomes are improved when clinicians apply a body of evidence to daily practice. How do nurses assess the quality of clinical research? This article outlines a stepwise approach to critical appraisal of research studies' worth to clinical practice: rapid critical appraisal, evaluation, synthesis, and recommendation. When critical care nurses apply a body of valid, reliable, and applicable evidence to daily practice, patient outcomes are improved.
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Corticosterone (CORT) and other glucocorticoids cause peripheral insulin resistance and compensatory increases in β-cell mass. A prolonged high-fat diet (HFD) induces insulin resistance and impairs β-cell insulin secretion. This study examined islet adaptive capacity in rats treated with CORT and a HFD. Male Sprague-Dawley rats (age ∼6 weeks) were given exogenous CORT (400 mg/rat) or wax (placebo) implants and placed on a HFD (60% calories from fat) or standard diet (SD) for 2 weeks (N = 10 per group). CORT-HFD rats developed fasting hyperglycemia (>11 mM) and hyperinsulinemia (∼5-fold higher than controls) and were 15-fold more insulin resistant than placebo-SD rats by the end of ∼2 weeks (Homeostatic Model Assessment for Insulin Resistance [HOMA-IR] levels, 15.08 ± 1.64 vs 1.0 ± 0.12, P < .05). Pancreatic β-cell function, as measured by HOMA-β, was lower in the CORT-HFD group as compared to the CORT-SD group (1.64 ± 0.22 vs 3.72 ± 0.64, P < .001) as well as acute insulin response (0.25 ± 0.22 vs 1.68 ± 0.41, P < .05). Moreover, β- and α-cell mass were 2.6- and 1.6-fold higher, respectively, in CORT-HFD animals compared to controls (both P < .05). CORT treatment increased p-protein kinase C-α content in SD but not HFD-fed rats, suggesting that a HFD may lower insulin secretory capacity via impaired glucose sensing. Isolated islets from CORT-HFD animals secreted more insulin in both low and high glucose conditions; however, total insulin content was relatively depleted after glucose challenge. Thus, CORT and HFD, synergistically not independently, act to promote severe insulin resistance, which overwhelms islet adaptive capacity, thereby resulting in overt hyperglycemia.
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This appendix contains sections titled: JBI Critical Appraisal Checklist for Experimental Studies JBI QARI Critical Appraisal Checklist for Interpretive and Critical Research JBI NOTARI Critical Appraisal Checklist for Narrative, Opinion and Textual Papers JBI Critical Appraisal Checklist for Observational Studies Checklist for Assessing the Validity of Cohort Studies Checklist for Assessing the Validity of Case Control Studies
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The effect of 48 h of fasting in C57B1/6J-ob/ob and +/+ mice on body weight (BW), blood glucose (BG), serum immunreactive insulin (IRI), plasma immunoreactive glucagon (IRG) and on tissue levels of cyclic adenosine monophosphate (cAMP) were studied. Both groups of mice lost weight and demonstrated a decrease in BG and IRI with fasting. However, the BG and IRI of the ob/ob animals were initially highter and remained higher than those of the 2% of their initial weight while the +/+ lost 14 %. The +/+ mice exhibited an increase in cAMP levels in skeletal muscle, fat and liver with fasting, while the ob/ob mice had increased levels of cAMP in fat, but not in muscle. They also had a paradoxical decrease in liver cAMP levels with fasting, and associated with this was the lack of stimulation of glycogenolysis. Glycogenolysis was significant in the livers of fasted +/+ mice. The plasma IRG levels of the fed ob/ob mice were significantly higher (1.8) times) than those of the fed +/+ mice. Islet cAMP levels were decreased with fasting in ob/ob mice. However, the levels were significantly higher in 48-h faster ob/ob mice compared to the fasted +/+ group. The apparent paradoxical response to fasting observed in the livers of the ob/ob mice remains unexplained.
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Critical appraisal
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Empirical Research
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The majority of content indexed in healthcare databases has not undergone additional critical appraisal. The papers indexed on these databases are not appraised by the indexers, and consequently their quality is variable. This chapter contains some resources for appraising documents. The critical appraisal process should entail a fair assessment of the research, weighing up the strengths and weaknesses, benefits and limitations. The purpose of critical appraisal is to find out the answers to the following three questions: (i) what are the results (ii) are the results valid, and (iii) how will these results help? The chapter provides a list of checklists and tools available to help support critical appraisal such as Centre for Evidence-Based Medicine – checklists and tools, and Critical Appraisal Skills Programme (CASP) – tools.
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Critical appraisal is used to evaluate research and determine whether it should be incorporated into the reader's area of practice. Checklists are used in critical appraisal to provide a useful framework for the systematic analysis of research studies. Critical appraisal skills can be acquired in a number of ways, and can even be self-taught.
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