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"JENKINS, David"
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A solution to minimum sample size for regressions
Regressions and meta-regressions are widely used to estimate patterns and effect sizes in various disciplines. However, many biological and medical analyses use relatively low sample size (N), contributing to concerns on reproducibility. What is the minimum N to identify the most plausible data pattern using regressions? Statistical power analysis is often used to answer that question, but it has its own problems and logically should follow model selection to first identify the most plausible model. Here we make null, simple linear and quadratic data with different variances and effect sizes. We then sample and use information theoretic model selection to evaluate minimum N for regression models. We also evaluate the use of coefficient of determination (R2) for this purpose; it is widely used but not recommended. With very low variance, both false positives and false negatives occurred at N < 8, but data shape was always clearly identified at N ≥ 8. With high variance, accurate inference was stable at N ≥ 25. Those outcomes were consistent at different effect sizes. Akaike Information Criterion weights (AICc wi) were essential to clearly identify patterns (e.g., simple linear vs. null); R2 or adjusted R2 values were not useful. We conclude that a minimum N = 8 is informative given very little variance, but minimum N ≥ 25 is required for more variance. Alternative models are better compared using information theory indices such as AIC but not R2 or adjusted R2. Insufficient N and R2-based model selection apparently contribute to confusion and low reproducibility in various disciplines. To avoid those problems, we recommend that research based on regressions or meta-regressions use N ≥ 25.
Journal Article
Effect of Fructose on Glycemic Control in Diabetes: A systematic review and meta-analysis of controlled feeding trials
The effect of fructose on cardiometabolic risk in humans is controversial. We conducted a systematic review and meta-analysis of controlled feeding trials to clarify the effect of fructose on glycemic control in individuals with diabetes.
We searched MEDLINE, EMBASE, and the Cochrane Library (through 22 March 2012) for relevant trials lasting ≥7 days. Data were aggregated by the generic inverse variance method (random-effects models) and expressed as mean difference (MD) for fasting glucose and insulin and standardized MD (SMD) with 95% CI for glycated hemoglobin (HbA(1c)) and glycated albumin. Heterogeneity was assessed by the Cochran Q statistic and quantified by the I(2) statistic. Trial quality was assessed by the Heyland methodological quality score (MQS).
Eighteen trials (n = 209) met the eligibility criteria. Isocaloric exchange of fructose for carbohydrate reduced glycated blood proteins (SMD -0.25 [95% CI -0.46 to -0.04]; P = 0.02) with significant intertrial heterogeneity (I(2) = 63%; P = 0.001). This reduction is equivalent to a ~0.53% reduction in HbA(1c). Fructose consumption did not significantly affect fasting glucose or insulin. A priori subgroup analyses showed no evidence of effect modification on any end point.
Isocaloric exchange of fructose for other carbohydrate improves long-term glycemic control, as assessed by glycated blood proteins, without affecting insulin in people with diabetes. Generalizability may be limited because most of the trials were <12 weeks and had relatively low MQS (<8). To confirm these findings, larger and longer fructose feeding trials assessing both possible glycemic benefit and adverse metabolic effects are required.
Journal Article
Ingenious : how Canadian innovators made the world smarter, smaller, kinder, safer, healthier, wealthier, and happier
\"Successful innovation is always inspired by at least one of three forces--insight, necessity, and simple luck. Ingenious moves through history to explore what circumstances, incidents, coincidences, and collaborations motivated each great Canadian idea, and what twist of fate then brought that idea into public acceptance. Above all, the book explores what goes on in the mind of an innovator, and maps the incredible spectrum of personalities that have struggled to improve the lot of their neighbours, their fellow citizens, and their species. From the marvels of aboriginal invention such as the canoe, snowshoe, igloo, dogsled, lifejacket, and bunk bed to the latest pioneering advances in medicine, education, philanthropy, science, engineering, community development, business, the arts, and the media, Canadians have improvised and collaborated their way to international admiration. Ingenious tells you why they did it and how they made the world a better place.\"-- Provided by publisher.
Book
TRIM37 controls cancer-specific vulnerability to PLK4 inhibition
Centrosomes catalyse the formation of microtubules needed to assemble the mitotic spindle apparatus
1
. Centrosomes themselves duplicate once per cell cycle, in a process that is controlled by the serine/threonine protein kinase PLK4 (refs.
2
,
3
). When PLK4 is chemically inhibited, cell division proceeds without centrosome duplication, generating centrosome-less cells that exhibit delayed, acentrosomal spindle assembly
4
. Whether PLK4 inhibitors can be leveraged as a treatment for cancer is not yet clear. Here we show that acentrosomal spindle assembly following PLK4 inhibition depends on levels of the centrosomal ubiquitin ligase TRIM37. Low TRIM37 levels accelerate acentrosomal spindle assembly and improve proliferation following PLK4 inhibition, whereas high TRIM37 levels inhibit acentrosomal spindle assembly, leading to mitotic failure and cessation of proliferation. The Chr17q region containing the
TRIM37
gene is frequently amplified in neuroblastoma and in breast cancer
5
–
8
, rendering these cancer types highly sensitive to PLK4 inhibition. We find that inactivating TRIM37 improves acentrosomal mitosis because TRIM37 prevents PLK4 from self-assembling into centrosome-independent condensates that serve as ectopic microtubule-organizing centres. By contrast, elevated TRIM37 expression inhibits acentrosomal spindle assembly through a distinct mechanism that involves degradation of the centrosomal component CEP192. Thus, TRIM37 is an essential determinant of mitotic vulnerability to PLK4 inhibition. Linkage of
TRIM37
to prevalent cancer-associated genomic changes—including 17q gain in neuroblastoma and 17q23 amplification in breast cancer—may offer an opportunity to use PLK4 inhibition to trigger selective mitotic failure and provide new avenues to treatments for these cancers.
Acentrosomal assembly of the mitotic spindle upon inhibition of the PLK4 protein is shown to depend on the ubiquitin ligase TRIM37, with implications for the use of PLK4 inhibitors to treat neuroblastoma and breast cancer.
Journal Article
Securing monetary and financial stability : why Canada needs a macroprudential policy framework
A newly created Macroprudential Policy Framework with clear objectives, tools and lines of responsibility could offer greater assurance of financial stability, while leaving the Bank of Canada to focus primarily on inflation and output stabilization.
Book
Effect of Tree Nuts on Glycemic Control in Diabetes: A Systematic Review and Meta-Analysis of Randomized Controlled Dietary Trials
Tree nut consumption has been associated with reduced diabetes risk, however, results from randomized trials on glycemic control have been inconsistent.
To provide better evidence for diabetes guidelines development, we conducted a systematic review and meta-analysis of randomized controlled trials to assess the effects of tree nuts on markers of glycemic control in individuals with diabetes.
MEDLINE, EMBASE, CINAHL, and Cochrane databases through 6 April 2014.
Randomized controlled trials ≥3 weeks conducted in individuals with diabetes that compare the effect of diets emphasizing tree nuts to isocaloric diets without tree nuts on HbA1c, fasting glucose, fasting insulin, and HOMA-IR.
Two independent reviewer's extracted relevant data and assessed study quality and risk of bias. Data were pooled by the generic inverse variance method and expressed as mean differences (MD) with 95% CI's. Heterogeneity was assessed (Cochran Q-statistic) and quantified (I2).
Twelve trials (n = 450) were included. Diets emphasizing tree nuts at a median dose of 56 g/d significantly lowered HbA1c (MD = -0.07% [95% CI:-0.10, -0.03%]; P = 0.0003) and fasting glucose (MD = -0.15 mmol/L [95% CI: -0.27, -0.02 mmol/L]; P = 0.03) compared with control diets. No significant treatment effects were observed for fasting insulin and HOMA-IR, however the direction of effect favoured tree nuts.
Majority of trials were of short duration and poor quality.
Pooled analyses show that tree nuts improve glycemic control in individuals with type 2 diabetes, supporting their inclusion in a healthy diet. Owing to the uncertainties in our analyses there is a need for longer, higher quality trials with a focus on using nuts to displace high-glycemic index carbohydrates.
ClinicalTrials.gov NCT01630980.
Journal Article
Modeling methods for marine science
This is a textbook on modelling, data analysis and numerical techniques for advanced students and researchers in chemical, biological, geological and physical oceanography.
Book
Relation of Total Sugars, Sucrose, Fructose, and Added Sugars With the Risk of Cardiovascular Disease: A Systematic Review and Dose-Response Meta-analysis of Prospective Cohort Studies
To determine the association of total and added fructose-containing sugars on cardiovascular (CVD) incidence and mortality.
MEDLINE, EMBASE and Cochrane Library were searched from January 1, 1980, to July 31, 2018. Prospective cohort studies assessing the association of reported intakes of total, sucrose, fructose and added sugars with CVD incidence and mortality in individuals free from disease at baseline were included. Risk estimates were pooled using the inverse variance method, and dose-response analysis was modeled.
Eligibility criteria were met by 24 prospective cohort comparisons (624,128 unique individuals; 11,856 CVD incidence cases and 12,224 CVD mortality cases). Total sugars, sucrose, and fructose were not associated with CVD incidence. Total sugars (risk ratio, 1.09 [95% confidence interval, 1.02 to 1.17]) and fructose (1.08 [1.01 to 1.15]) showed a harmful association for CVD mortality, there was no association for added sugars and a beneficial association for sucrose (0.94 [0.89 to 0.99]). Dose-response analyses showed a beneficial linear dose-response gradient for sucrose and nonlinear dose-response thresholds for harm for total sugars (133 grams, 26% energy), fructose (58 grams, 11% energy) and added sugars (65 grams, 13% energy) in relation to CVD mortality (P<.05). The certainty of the evidence using GRADE was very low for CVD incidence and low for CVD mortality for all sugar types.
Current evidence supports a threshold of harm for intakes of total sugars, added sugars, and fructose at higher exposures and lack of harm for sucrose independent of food form for CVD mortality. Further research of different food sources of sugars is needed to define better the relationship between sugars and CVD. REGISTRATION: clinicaltrials.gov, NCT01608620.
Journal Article