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\"Narrating History, Home, and Dyaspora: Critical Essays on Edwidge Danticat contains fifteen essays addressing how Edwidge Danticat's writing, anthologizing, and storytelling trace, (re)construct, and develop alternate histories, narratives of nation building, and conceptions of home and belonging. The prolific Danticat is renowned for novels, collections of short fiction, nonfiction, and editorial writing. As her experimentation in form expands, so does her force as a public intellectual. Danticat's literary representations, political commentary, and personal activism have proven vital to classroom and community work imagining radical futures. Among increasing anti-immigrant sentiment and containment and rampant ecological volatility, Danticat's contributions to public discourse, art, and culture deserve sustained critical attention. These essays offer essential perspectives to scholars, public intellectuals, and students interested in African diasporic, Haitian, Caribbean, and transnational American literary studies. This collection frames Danticat's work as an indictment of statelessness, racialized and gendered state violence, the persistence of political and economic margins, and the essential vitality of life in and as dyaspora. The first section of this volume, \"The Other Side of the Water,\" engages with Danticat's construction and negotiation of nation, both in Haiti and the United States; the broader dyaspora; and her own, her family's, and her fictional characters' places within them. The second section, \"Welcoming Ghosts,\" delves into the ever-present specter of history and memory, prominent themes found throughout Danticat's work. From origin stories to broader Haitian histories, this section addresses the underlying traumas involved when remembering the past and its relationship to the present. The third section, \"I Speak Out,\" explores the imperative to speak, paying particular attention to the narrative form with which such telling occurs. The fourth and final section, \"Create Dangerously,\" contends with Haitians' activism, community building, and the political and ecological climate of Haiti and its dyaspora\"-- Provided by publisher.

It is generally recognized that there are gender-related differences in children’s toy preferences. However, the magnitude of these differences has not been firmly established. Furthermore, not all studies of gender-related toy preferences find significant gender differences. These inconsistent findings could result from using different toys or methods to measure toy preferences or from studying children of different ages. Our systematic review and meta-analysis combined 113 effect sizes from 75 studies to estimate the magnitude of gender-related differences in toy preferences. We also assessed the impact of using different toys or methods to assess these differences, as well as the effect of age on gender-related toy preferences. Boys preferred boy-related toys more than girls did, and girls preferred girl-related toys more than boys did. These differences were large ( d  ≥ 1.60). Girls also preferred toys that researchers classified as neutral more than boys did ( d  = 0.29). Preferences for gender-typical over gender-atypical toys were also large and significant ( d  ≥ 1.20), and girls and boys showed gender-related differences of similar magnitude. When only dolls and vehicles were considered, within-sex differences were even larger and of comparable size for boys and girls. Researchers sometimes misclassified toys, perhaps contributing to an apparent gender difference in preference for neutral toys. Forced choice methods produced larger gender-related differences than other methods, and gender-related differences increased with age.

Aims/hypothesis Fenofibrate caused an acute, sustained plasma creatinine increase in the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) and Action to Control Cardiovascular Risk in Diabetes (ACCORD) studies. We assessed fenofibrate's renal effects overall and in a FIELD washout sub-study. Methods Type 2 diabetic patients (n = 9,795) aged 50 to 75 years were randomly assigned to fenofibrate (n = 4,895) or placebo (n = 4,900) for 5 years, after 6 weeks fenofibrate run-in. Albuminuria (urinary albumin/creatinine ratio measured at baseline, year 2 and close-out) and estimated GFR, measured four to six monthly according to the Modification of Diet in Renal Disease Study, were pre-specified endpoints. Plasma creatinine was re-measured 8 weeks after treatment cessation at close-out (washout sub-study, n = 661). Analysis was by intention-to-treat. Results During fenofibrate run-in, plasma creatinine increased by 10.0 μmol/l (p < 0.001), but quickly reversed on placebo assignment. It remained higher on fenofibrate than on placebo, but the chronic rise was slower (1.62 vs 1.89 μmol/l annually, p = 0.01), with less estimated GFR loss (1.19 vs 2.03 ml min⁻¹ 1.73 m⁻² annually, p < 0.001). After washout, estimated GFR had fallen less from baseline on fenofibrate (1.9 ml min⁻¹ 1.73 m⁻², p = 0.065) than on placebo (6.9 ml min⁻¹ 1.73 m⁻², p < 0.001), sparing 5.0 ml min⁻¹ 1.73 m⁻² (95% CI 2.3-7.7, p < 0.001). Greater preservation of estimated GFR with fenofibrate was observed with baseline hypertriacylglycerolaemia (n = 169 vs 491 without) alone, or combined with low HDL-cholesterol (n = 140 vs 520 without) and reductions of ≥0.48 mmol/l in triacylglycerol over the active run-in period (pre-randomisation) (n = 356 vs 303 without). Fenofibrate reduced urine albumin concentrations and hence albumin/creatinine ratio by 24% vs 11% (p < 0.001; mean difference 14% [95% CI 9-18]; p < 0.001), with 14% less progression and 18% more albuminuria regression (p < 0.001) than in participants on placebo. End-stage renal event frequency was similar (n = 21 vs 26, p = 0.48). Conclusions/interpretation Fenofibrate reduced albuminuria and slowed estimated GFR loss over 5 years, despite initially and reversibly increasing plasma creatinine. Fenofibrate may delay albuminuria and GFR impairment in type 2 diabetes patients. Confirmatory studies are merited. Trial registration ISRCTN64783481 Funding The study was funded by grants from Laboratoires Fournier SA (Dijon, France; now part of Abbott Pharmaceuticals) and the National Health and Medical Research Council, Australia

Aims/hypothesis We investigated effects of renal function and albuminuria on cardiovascular outcomes in 9,795 low-risk patients with diabetes in the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study. Methods Baseline and year 2 renal status were examined in relation to clinical and biochemical characteristics. Outcomes included total cardiovascular disease (CVD), cardiac and non-cardiac death over 5 years. Results Lower estimated GFR (eGFR) vs eGFR ≥90 ml min⁻¹ 1.73 m⁻² was a risk factor for total CVD events: (HR [95% CI] 1.14 [1.01-1.29] for eGFR 60-89 ml min⁻¹ 1.73 m⁻²; 1.59 [1.28-1.98] for eGFR 30-59 ml min⁻¹ 1.73 m⁻²; p < 0.001; adjusted for other characteristics). Albuminuria increased CVD risk, with microalbuminuria and macroalbuminuria increasing total CVD (HR 1.25 [1.01-1.54] and 1.19 [0.76-1.85], respectively; p = 0.001 for trend) when eGFR ≥90 ml min⁻¹ 1.73 m⁻². CVD risk was further modified by renal status changes over the first 2 years. In multivariable analysis, 77% of the effect of eGFR and 81% of the effect of albumin:creatinine ratio were accounted for by other variables, principally low HDL-cholesterol and elevated blood pressure. Conclusions/interpretation Reduced eGFR and albuminuria are independent risk factors for cardiovascular events and mortality rates in a low-risk population of mainly European ancestry. While their independent contributions to CVD risk appear small when other risk factors are considered, they remain excellent surrogate markers in clinical practice because they capture risk related to a number of other characteristics. Therefore, both should be considered when assessing prognosis and treatment strategies in patients with diabetes, and both should be included in risk models.

Aims/hypothesis The aim of this study was to assess the relationships between lipid-lowering therapy and the prevalence and incidence of peripheral sensory neuropathy in type 2 diabetes mellitus. Methods We analysed data from an observational cohort study, the Fremantle Diabetes Study (FDS), specifically, (1) a cross-sectional sample comprising 1,237 FDS participants with type 2 diabetes mellitus, and (2) a longitudinal subgroup of 531 individuals who had attended six consecutive annual assessments. Neuropathy was identified using the clinical portion of the Michigan Neuropathy Screening Instrument. Results At entry, the cross-sectional sample had a mean ± SD age of 63.8 ± 11.3 years, 48.7% were men, median (interquartile range) diabetes duration was 4.0 (1.0-9.0) years, and 30.9% had peripheral neuropathy. Fibrates and statins were used by 3.5 and 6.8%, respectively. Multiple logistic regression analysis showed that older age, longer diabetes duration, central adiposity, increased height, higher fasting serum glucose, albuminuria and aboriginality were significant independent positive predictors of prevalent neuropathy, while systolic blood pressure and fibrate use (odds ratio 0.30, 95% CI 0.10-0.86; p = 0.025) were negatively associated. In the longitudinal subgroup, fibrate and statin use increased to 10.4 and 36.5%, respectively, over 5 years. In time-dependent Cox proportional hazards modelling, fibrate use [hazard ratio (HR) 0.52, 95% CI 0.27-0.98] and statin use (HR 0.65, 95% CI 0.46-0.93) were significant determinants of incident neuropathy (p <= 0.042). Conclusions/interpretation These preliminary observational data suggest that therapy with a statin or a fibrate may protect against the development of diabetic peripheral sensory neuropathy, but there is a need for additional confirmatory evidence, preferably from randomised clinical trials.

Aims/hypothesis The aim was to investigate the relationship between severe hypoglycaemia and cognitive impairment in older patients with diabetes. Methods A sample of 302 diabetic patients aged ≥70 years was assessed for dementia or cognitive impairment without dementia in 2001–2002 and a subsample of non-demented patients ( n  = 205) was followed to assess cognitive decline. A history of severe hypoglycaemia was determined from self-reports, physician assessments and records of health service use for hypoglycaemia (HSH). Prospective HSH was determined up to 2006. Data analysis, including multiple logistic and Cox regression models, was used to determine whether: (1) there were cross-sectional associations between hypoglycaemia and cognitive status, (2) historical hypoglycaemia predicted cognitive decline, and (3) baseline cognitive status predicted subsequent HSH. Results There were significant cross-sectional associations between both cognitive impairment and dementia and hypoglycaemia. Independent risk factors for future HSH included dementia (hazard ratio 3.00, 95% CI 1.06–8.48) and inability to self-manage medications (hazard ratio 4.17, 95% CI 1.43–12.13). However, there were no significant associations between historical hypoglycaemia, incident HSH and cognitive decline. Conclusions/interpretation Dementia is an important risk factor for hypoglycaemia requiring health service utilisation. We found no evidence that hypoglycaemia contributes to cognitive impairment in older patients with diabetes.

Background Type 2 Diabetes (T2D) is associated with increased risk of dementia. We aimed to determine the feasibility of a randomised controlled trial (RCT) examining the efficacy of exercise on cognition and brain structure in people with T2D. Methods A 6-month pilot parallel RCT of a progressive aerobic- and resistance-training program versus a gentle movement control group in people with T2D aged 50–75 years ( n  = 50) at the University of Tasmania, Australia. Assessors were blinded to group allocation. Brain volume (total, white matter, hippocampus), cortical thickness and white matter microstructure (fractional anisotrophy and mean diffusivity) were measured using magnetic resonance imaging, and cognition using a battery of neuropsychological tests. Study design was assessed by any changes (during the pilot or recommended) to the protocol, recruitment by numbers screened and time to enrol 50 participants; randomisation by similarity of characteristics in groups at baseline, adherence by exercise class attendance; safety by number and description of adverse events and retention by numbers withdrawn. Results The mean age of participants was 66.2 (SD 4.9) years and 48% were women. There were no changes to the design during the study. A total of 114 people were screened for eligibility, with 50 participants with T2D enrolled over 8 months. Forty-seven participants (94%) completed the study (23 of 24 controls; 24 of 26 in the intervention group). Baseline characteristics were reasonably balanced between groups. Exercise class attendance was 79% for the intervention and 75% for the control group. There were 6 serious adverse events assessed as not or unlikely to be due to the intervention. Effect sizes for each outcome variable are provided. Conclusion This study supports the feasibility of a large scale RCT to test the benefits of multi-modal exercise to prevent cognitive decline in people with T2D. Design changes to the future trial are provided. Trial registration ANZCTR 12614000222640 ; Registered 3/3/2014; First participant enrolled 26/6/2014, study screening commenced 1/9/2014; Australian and New Zealand Clinical Trial Registry.

Aims/hypothesis To determine whether serum uric acid: (1) is associated with cardiovascular disease (CVD) death and/or all-cause mortality in type 2 diabetes; and (2) consistent with published data, predicts these outcomes in older patients and those of southern European ethnicity. Methods We studied those 1,268 (98%) of 1,294 type 2 participants in the observational Fremantle Diabetes Study who had a fasting serum uric acid measured at baseline. Mortality data were collected over a mean (±SD) 10.3 ± 3.9 years. Cox proportional hazards modelling was used to determine independent baseline predictors of CVD and all-cause death including fasting serum uric acid as a continuous variable and quartiles. Results During follow up, 525 deaths occurred (41.4% of the cohort) of which 271 (51.6%) were attributed to CVD. In univariate analyses, patients in the highest uric acid quartile had the greatest CVD and all-cause mortality (p = 0.007 and p = 0.001). After adjustment for significant variables in the most parsimonious model, baseline serum uric acid was not an independent associate of CVD or all-cause mortality whether entered as a continuous variable (HR 1.11 [95% CI 0.96-1.27] and 1.10 [95% CI 0.98-1.22] for a 0.1 mmol/l increase, respectively) or as quartiles (p > 0.10). Analyses of 638 patients >65 years of age and 231 of southern European ethnicity produced similar results. Conclusions/interpretation Serum uric acid was not an independent predictor of CVD or all-cause mortality in our community-based type 2 patients. Fasting serum uric acid concentrations do not appear to be prognostically useful in type 2 diabetes.

Laser treatment for diabetic retinopathy is often associated with visual field reduction and other ocular side-effects. Our aim was to assess whether long-term lipid-lowering therapy with fenofibrate could reduce the progression of retinopathy and the need for laser treatment in patients with type 2 diabetes mellitus. The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study was a multinational randomised trial of 9795 patients aged 50–75 years with type 2 diabetes mellitus. Eligible patients were randomly assigned to receive fenofibrate 200 mg/day (n=4895) or matching placebo (n=4900). At each clinic visit, information concerning laser treatment for diabetic retinopathy—a prespecified tertiary endpoint of the main study—was gathered. Adjudication by ophthalmologists masked to treatment allocation defined instances of laser treatment for macular oedema, proliferative retinopathy, or other eye conditions. In a substudy of 1012 patients, standardised retinal photography was done and photographs graded with Early Treatment Diabetic Retinopathy Study (ETDRS) criteria to determine the cumulative incidence of diabetic retinopathy and its component lesions. Analyses were by intention to treat. This study is registered as an International Standard Randomised Controlled Trial, number ISRCTN64783481. Laser treatment was needed more frequently in participants with poorer glycaemic or blood pressure control than in those with good control of these factors, and in those with a greater burden of clinical microvascular disease, but the need for such treatment was not affected by plasma lipid concentrations. The requirement for first laser treatment for all retinopathy was significantly lower in the fenofibrate group than in the placebo group (164 [3·4%] patients on fenofibrate vs 238 [4·9%] on placebo; hazard ratio [HR] 0·69, 95% CI 0·56–0·84; p=0·0002; absolute risk reduction 1·5% [0·7–2·3]). In the ophthalmology substudy, the primary endpoint of 2-step progression of retinopathy grade did not differ significantly between the two groups overall (46 [9·6%] patients on fenofibrate vs 57 [12·3%] on placebo; p=0·19) or in the subset of patients without pre-existing retinopathy (43 [11·4%] vs 43 [11·7%]; p=0·87). By contrast, in patients with pre-existing retinopathy, significantly fewer patients on fenofibrate had a 2-step progression than did those on placebo (three [3·1%] patients vs 14 [14·6%]; p=0·004). An exploratory composite endpoint of 2-step progression of retinopathy grade, macular oedema, or laser treatments was significantly lower in the fenofibrate group than in the placebo group (HR 0·66, 95% CI 0·47–0·94; p=0·022). Treatment with fenofibrate in individuals with type 2 diabetes mellitus reduces the need for laser treatment for diabetic retinopathy, although the mechanism of this effect does not seem to be related to plasma concentrations of lipids.

Aims/hypothesis Diabetes is associated with an increased risk of dementia but the reasons for this association are unclear because there are many potential mechanisms. We explored the relative contribution of diabetes-related variables as predictors of dementia in older individuals with diabetes. Methods Survivors, aged >=70 or more, were recruited from an existing observational cohort study 7.6 ± 1.0 years after baseline, when they underwent a comprehensive assessment of diabetes, complications and cardiovascular risk factors. Dementia, probable Alzheimer's disease and cognitive impairment without dementia were diagnosed clinically. Logistic regression modelling determined independent predictors of cognitive diagnoses. Results Of 302 participants, aged 75.7 ± 4.6 years, 28 (9.3%) had dementia (16 with probable Alzheimer's disease) and 60 (19.9%) had cognitive impairment without dementia. The major independent longitudinal predictors of dementia were older age (per decade; odds ratio 4.0, 95% CI 1.59-10.10), diabetes duration (for each 5 years; odds ratio 1.69, 95% CI 1.24-2.32), peripheral arterial disease (odds ratio 5.35, 95% CI 2.08-13.72) and exercise (which was protective; odds ratio 0.26, 95% CI 0.09-0.73). For Alzheimer's disease, diabetes duration was an independent predictor in addition to age and diastolic blood pressure. The results of the cross-sectional analyses were similar with respect to diabetes duration and peripheral arterial disease. Conclusions/interpretation Peripheral arterial disease is a strong independent risk factor for dementia in diabetes. After adjustment for a wide range of potential risk factors, diabetes duration remains independently associated with dementia and probable Alzheimer's disease, indicating that factors not measured in this study may be important in the pathogenesis of dementia in diabetes.