No abstract

Inverse associations between dairy consumption and CVD have been reported in several epidemiological studies. Our objective was to conduct a meta-analysis of prospective cohort studies of dairy intake and CVD. A comprehensive literature search was conducted to identify studies that reported risk estimates for total dairy intake, individual dairy products, low/full-fat dairy intake, Ca from dairy sources and CVD, CHD and stroke. Random-effects meta-analyses were used to generate summary relative risk estimates (SRRE) for high v. low intake and stratified intake dose-response analyses. Additional dose-response analyses were performed. Heterogeneity was examined in sub-group and sensitivity analyses. In total, thirty-one unique cohort studies were identified and included in the meta-analysis. Several statistically significant SRRE below 1.0 were observed, namely for total dairy intake and stroke (SRRE = 0·91; 95 % CI 0·83, 0·99), cheese intake and CHD (SRRE = 0·82; 95 % CI 0·72, 0·93) and stroke (SRRE = 0·87; 95 % CI 0·77, 0·99), and Ca from dairy sources and stroke (SRRE = 0·69; 95 % CI 0·60, 0·81). However, there was little evidence for inverse dose-response relationships between the dairy variables and CHD and stroke after adjusting for within-study covariance. The results of this meta-analysis of prospective cohort studies have shown that dairy consumption may be associated with reduced risks of CVD, although additional data are needed to more comprehensively examine potential dose-response patterns.

This study attempts to evaluate the clinicopathologic features of mixed subtype adenocarcinomas and the prognostic implications of histopathology classifications. Surgical specimens from 141 patients with clinical stage I or II lung adenocarcinoma during the period 1992-2004 were included. These cases were classified into four groups defined by the extent of the bronchioloalveolar carcinoma component: group I: pure bronchioloalveolar carcinoma; group II: mixed subtype with predominant bronchioloalveolar carcinoma component and r5 mm invasive component; group III: mixed subtype with bronchioloalveolar carcinoma component and 45 mm invasive component; group IV: invasive carcinoma with no bronchioloalveolar carcinoma component. Descriptive statistics were used to examine the groups with respect to age, tumor size, lymph node metastasis, and Ki-67 and p53 expression levels. Death rate for the groups was obtained by patient's charts and from the National Death Index database. The population was similar in age, tumor size and lymph node metastasis. Immunohistochemical results showed that the mean Ki-67 labeling and the amount of p53 overexpression had the same trend of increasing mean values or positive results from groups I to IV. The reported proportion of deaths ranged from 0% for groups I and II, 20% in patients with predominant invasive component with bronchioloalveolar carcinoma (group III), and 18% in patients with invasive carcinomas and no bronchioloalveolar carcinoma component (group IV). The difference between the proportion of patients with reported deaths in the time period of this study in the combined greater than 5 mm þ pure invasive groups (groups III, IV), and the o5 mm þ noninvasive groups (groups I, II) is statistically significant. These results suggest that histological features may be useful in defining categories of lung adenocarcinomas with differing survival and prognostic features. These results are helpful in defining a subcategory of 'minimally invasive adenocarcinoma', which has features similar to bronchioloalveolar carcinoma. Noguchi et al 2 looked at small lung adenocarcinomas measuring o2 cm, and defined six different categories including pure bronchioloalveolar carcinoma, bronchioloalveolar carcinoma with areas of fibroblastic foci due to structural collapse, bronchioloalveolar carcinoma with active fibroblastic proliferation, and different categories of invasive carcinoma. They showed that patients with tumors with a pure bronchioloalveolar carcinoma pattern had a 100% 5-year survival, patients with adenocarcinomas of mixed subtype with bronchioloalveolar carcinoma and invasive components had a 75% 5-year survival, while those patients with a purely invasive carcinoma had a 52% 5-year survival.

Object This retrospective analysis of Medicare administrative data was performed to evaluate the risk of infection following instrumented lumbar fusion over a 10-year follow-up period in the Medicare population. Although infection can be a devastating complication, due to its rarity it is difficult to characterize infection risk except in large patient populations. Methods Using ICD-9-CM and CPT4 procedure codes, the Medicare 5% analytical research files for inpatient, outpatient, and physician carrier claims were checked to identify patients who were treated between 1997 and 2009 with lumbar spine fusion in which cages or posterior instrumentation were used. Patients younger than 65 years old were excluded. Patients were followed continuously by using the matching denominator file until they withdrew from Medicare or died. The authors identified 15,069 patients with primary fusion procedures and 605 with revision of instrumented lumbar fusion. Infections were identified by the related ICD-9 codes (998.59 or 996.67) after fusion. Kaplan-Meier survival analysis and Cox regression were performed to determine adjusted infection risk for each type of spine procedure (primary vs revision) and surgical approach (anterior, posterior, combined anteroposterior), accounting for patient (for example, age, sex, comorbidities/Charlson Comorbidity Index [CCI], and state buy-in) and hospital (census region) characteristics. Results At 10 years, the overall infection incidence, including superficial and deep infections, was 8.5% in primary procedures and 12.2% in revisions. Among the factors considered, infection risk within 10 years was most influenced by comorbidities: for a CCI of 5 versus 0, the adjusted hazard ratio (AHR) was 2.48 (95% CI 1.93–3.19, p < 0.001); for ≥ 9 versus 2–3 fused vertebrae, the AHR was 2.39 (95% CI 1.20–4.76, p < 0.001); for revision versus primary fusion procedures, the AHR was 1.66 (95% CI 1.28–2.15, p < 0.001). Other significant predictors of 10-year infection risk included diagnosis of obesity (p < 0.001); state buy-in—a proxy for socioeconomic status (p = 0.02); age (p = 0.003); surgical approach (p = 0.03); census region (p = 0.02); and the year of the index procedure (p = 0.03). Conclusions Patient comorbidities were the greatest predictor of infection risk for the Medicare population. The high incidence of infection following instrumented fusion warrants increased focus on infection risk mitigation, especially for patients with comorbid conditions.