Objective:The definition of drug-resistant epilepsy (DRE) affects case identification and treatment, and impacts prevalence or incidence estimates and health burden estimation in epidemiology. The objective of this systematic review is to evaluate the consistency between definitions of DRE in the literature and the official definition in the International League Against Epilepsy (ILAE) guidelines, and to estimate the incidence, prevalence, and risk factors for DRE. Methods: MEDLINE and EMBASE were searched for observational studies of DRE published between January 1980 and July 2015. The definitions of DRE in these studies were compared with the definition in the ILAE guidelines. Randomeffect model meta-analyses were used to generate pooled estimates of prevalence or incidence and pooled odds ratios of the association with risk factors. Results: Thirty-five studies met inclusion criteria, including 13 080 epilepsy patients and 3941 patients with DRE. The definition of DRE varied widely across studies, with only 12% meeting the requirements of the ILAE definition. The pooled prevalence proportion of DRE among epilepsy patients was 0.30 (95% confidence interval [CI] 0.19-0.42), and the pooled incidence proportion was 0.15 (95% CI 0.11-0.19). Age at onset, symptomatic epilepsy, abnormal neuroimaging findings, abnormal electroencephalography results, history of mental retardation, neuropsychiatric disorders, febrile seizure, and status epilepticus increased risk for DRE. Significance: There are limited high-quality data available on DRE. Lack of consistency in definitions limits the ability to obtain robust estimates on the burden of DRE. More data based on the ILAE definition from well-designed epidemiologic studies are needed to generate accurate and reliable results. K E Y W O R D Sdrug resistant, epidemiology, epilepsy, frequency, review, risk
Multigene assays highlight racial disparities in tumor subtype distribution that persist even in clinically defined subgroups. Differences in tumor biology (eg, HER2-enriched status) may be targetable to reduce disparities among clinically ER+/HER2- cases.
OBJECTIVEThe Dietary Approaches to Stop Hypertension (DASH) diet has been widely promoted; however, little is known about its impact on type 2 diabetes.RESEARCH DESIGN AND METHODSWe evaluated the association of the DASH diet with incidence of type 2 diabetes among 862 participants of the Insulin Resistance Atherosclerosis Study (IRAS) who completed a 1-year food frequency questionnaire at baseline. Type 2 diabetes odds ratios (ORs) were estimated at tertiles of the DASH score.RESULTSAn inverse association was observed in whites (tertile 2 vs. tertile 1, OR 0.66 [95% CI 0.29–1.48]) that became significant for the most extreme contrast (tertile 3 vs. tertile 1, 0.31 [0.13–0.75]), with adjustment for covariates. No association was observed in blacks or Hispanics (tertile 2 vs. tertile 1, 1.16 [0.61–2.18 ]; tertile 3 vs. tertile 1, 1.34 [0.70–2.58 ]).CONCLUSIONSAdherence to the DASH dietary pattern, which is rich in vegetables, fruit, and low-fat dairy products, may have the potential to prevent type 2 diabetes.
Background Activation of inflammatory pathways is one plausible mechanism underlying the association between obesity and increased breast cancer risk. However, macrophage infiltration and local biomarkers of inflammation in breast adipose tissue have seldom been studied in association with obesity. Experiment Design Gene expression profiles of normal breast tissue from reduction mammoplasty patients. were evaluated by whole genome microarrays to identify patterns associated with obesity status (normal-weight, body mass index (BMI) < 25; overweight, BMI 25-29.9; obese, BMI ≥ 30). The presence of macrophage-enriched inflammatory loci with immunopositivity for CD68 protein was evaluated by immunohistochemistry (IHC). Results After adjusting for confounding by age, 760 genes were differentially expressed (203 up and 557 down; FDR=0.026) between normal-weight and obese women. Gene ontology analysis suggested significant enrichment for pathways involving IL-6, IL-8, CCR5 signaling in macrophages and RXRα and PPARα activation, consistent with a pro-inflammatory state and suggestive of macrophage infiltration. Gene Set Enrichment Analysis (GSEA) also demonstrated that the genomic signatures of monocytes and macrophages were overrepresented in the obese group with FDR of 0.08 and 0.13 respectively. Increased macrophage infiltration was confirmed by IHC, which showed that the breast adipose tissue of obese women had higher average macrophage counts (mean=8.96 vs 3.56 in normal-weight women) and inflammatory foci counts (mean=4.91 vs 2.67 in normal-weight women). Conclusion Obesity is associated with local inflammation and macrophage infiltration in normal human breast adipose tissues. Given the role of macrophages in carcinogenesis, these findings have important implications for breast cancer etiology and progression.
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