Cigarette smoking and risk of non-Hodgkin's lymphoma--a population-based case-control study.

BACKGROUND: Epidemiologic evidence of an association between tobacco smoking and non-Hodgkin's lymphoma has been conflicting. This may reflect that non-Hodgkin's lymphoma comprises several distinct disease entities with different etiologies, as some studies have indicated an association between smoking and follicular lymphoma. OBJECTIVE: To investigate the association between cigarette smoking and non-Hodgkin's lymphoma risk, overall and by subtype. METHODS: As part of a nationwide Danish-Swedish population-based case-control study, we interviewed 3,055 incident non-Hodgkin's lymphoma patients and 3,187 population controls. All lymphomas were uniformly classified according to the WHO classification. We used unconditional logistic regression to estimate adjusted odds ratios (OR) and 95% confidence intervals (95% CI) for the association between cigarette smoking and risk of non-Hodgkin's lymphoma. RESULTS: Cigarette smoking was not associated with the risk of non-Hodgkin's lymphoma overall (OR, 0.97; 95% CI, 0.87-1.08) nor with the major subgroups such as diffuse large B-cell lymphoma (OR, 0.94; 95% CI, 0.79-1.10), chronic lymphocytic leukemia (OR, 0.86; 95% CI, 0.72-1.02), or follicular lymphoma (OR, 1.03; 95% CI, 0.85-1.24). Female smokers were at a marginally increased risk of follicular lymphoma (OR, 1.41; 95% CI, 1.04-1.92). Men who had ever smoked had a significantly increased risk of T-cell lymphoma (OR, 1.67; 95% CI, 1.11-2.51). No dose-response association with cigarette smoking could be established for any lymphoma subgroup. CONCLUSION: We found little evidence of an association between cigarette smoking and non-Hodgkin's lymphoma risk overall. Although increased risks of follicular lymphoma in female smokers and of T-cell lymphoma in male smokers were suggested, no dose-response relationship was observed, leaving limited support for causality.     

Distance from residence to power line and risk of childhood leukemia: a population-based case–control study in Denmark

Purpose

Epidemiological studies have found an association between exposure to extremely low-frequency magnetic fields (ELF-MF) and childhood leukemia. In 2005, a large British study showed an association between proximity of residence to high-voltage power lines and the risk of childhood leukemia. The association extended beyond distances at which the ‘power line’-induced magnetic fields exceed background levels, suggesting that the association was not explained by the magnetic field, but might be due to chance, bias, or other risk factors associated with proximity to power lines. Our aim was to conduct a comparable study in an independent setting (Denmark).

Methods

We included 1,698 cases aged <15, diagnosed with leukemia during 1968–2006, from the Danish Cancer Registry and 3,396 controls randomly selected from the Danish childhood population and individually matched by gender and year of birth. We used geographical information systems to determine the distance between residence at birth and the nearest 132–400 kV overhead power line.

Results

Odds ratios (ORs) were 0.76 [95 % confidence interval (CI) 0.40–1.45] for children who lived 0–199 m from the nearest power line and 0.92 (95 % CI 0.67–1.25) for those who lived 200–599 m away when compared with children who lived ≥600 m away. When restricting the analysis to 220 and 400 kV overhead power lines, the OR for children who lived 200–599 m from a power line was 1.76 (95 % CI 0.82–3.77) compared to children who lived ≥600 m away. However, chance is a likely explanation for this finding as the result was not significant, numbers were small, and there were no indications of an higher risk closer to the lines since no cases were observed within 200 m of these.

Conclusions

We found no higher risk of leukemia for children living 0–199 m or for children living 200–599 m of a 132–400 kV overhead power line. A slightly elevated OR for children living between 200 and 599 m of a 220–400 kV overhead power line is likely to be a chance finding.     

A cerebral glioma model for experimental therapy andin vivo invasion studies in syngeneic BD IX rats

Anin vivo glioma model was developed in syngeneic BD IX rats. The BT₄An tumor was derived from serialin vivo passages of the BT₄A tumor, originally induced from transformed fetal rat brain cells after transplacental exposure to ethylnitrosourea. The cell line was characterized for the presence of neuroglial differentiation markers, chromosome content and cell cycle distribution as determined by flowcytometry. A standardized method for i.c. tumor induction was developed, and the tumors were investigated by light and electron microscopy and for evidence of blood-brain barrier disruption. Tumor cell ability for phagocytosis was studied, as this property may be important for the invasion pattern of the tumors. We conclude that the model seems suitable for bothin vivo therapy and invasion studies. The tumor had 100% tumor take, yielded a predictable symptom-free life span after inoculation, had a characteristic histological picture of an aggressive glioma, and the blood-brain barrier within the tumor was in part disrupted. Compared to the parent cell line, there was loss of neuroglial differentiation markers, the chromosomal distribution was changed, and the ability for phagocytosis was practically lost.     

The prevalence and prognostic value of concomitant eosinophilia in chronic graft-versus-host disease after allogeneic stem cell transplantation

The prognostic significance of eosinophilia after myeloablative allogeneic stem cell transplantation (ASCT) remains to be established. Patients, whom developed chronic graft-versus-host disease (cGVHD) after ASCT, were included (n = 142). Eosinophil count was analyzed at cGVHD onset. We observed no significant association between EO and the grade of cGVHD, thrombocytopenia, nor extensive skin involvement. Importantly, we observed no significant association between cGVHD with concomitant eosinophilia and long-term clinical outcomes, and subgroup analyses revealed a considerable confounding effect of ongoing steroid treatment. In conclusion, we advocate that prognostic conclusions regarding cGVHD with concomitant eosinophilia after ASCT should be interpreted with caution.     

Influence of intensive lipid‐lowering on CT derived fractional flow reserve in patients with stable chest pain: Rationale and design of the FLOWPROMOTE study

IntroductionCoronary CT angiography (CTA) derived fractional flow reserve (FFR_CT) shows high diagnostic performance when compared to invasively measured FFR. Presence and extent of low attenuation plaque density have been shown to be associated with abnormal physiology by measured FFR. Moreover, it is well established that statin therapy reduces the rate of plaque progression and results in morphology alterations underlying atherosclerosis. However, the interplay between lipid lowering treatment, plaque regression, and the coronary physiology has not previously been investigated.AimTo test whether lipid lowering therapy is associated with significant improvement in FFR_CT, and whether there is a dose–response relationship between lipid lowering intensity, plaque regression, and coronary flow recovery.MethodsInvestigator driven, prospective, multicenter, randomized study of patients with stable angina, coronary stenosis ≥50% determined by clinically indicated first‐line CTA, and FFR_CT ≤ 0.80 in whom coronary revascularization was deferred. Patients are randomized to standard (atorvastatin 40 mg daily) or intensive (rosuvastatin 40 mg + ezetimibe 10 mg daily) lipid lowering therapy for 18 months. Coronary CTA scans with blinded coronary plaque and FFR_CT analyses will be repeated after 9 and 18 months. The primary endpoint is the 18‐month difference in FFR_CT using (1) the FFR_CT value 2 cm distal to stenosis and (2) the lowest distal value in the vessel of interest. A total of 104 patients will be included in the study.ConclusionThe results of this study will provide novel insights into the interplay between lipid lowering, and the pathophysiology in coronary artery disease.     

Attitudes among parents of persons with autism spectrum disorder towards information about genetic risk and future health

Clinical relevance of genetic testing is increasing in autism spectrum disorder (ASD). Information about genetic risk may contribute to improved diagnostics, treatment and family planning, but may also be perceived as a burden. Knowledge about the families’ preferences with regard to genetic risk information is important for both health care professionals and policy makers. We investigated attitudes towards sharing information about genetic risk of ASD and knowledge about future health among parent members of the Norwegian Autism Association (N = 1455) using a questionnaire, and the relationships with parent and child characteristics, such as age, gender and ASD severity. Most preferred autonomy in deciding whom to inform about genetic risk of ASD (74.4%) and a minority supported extensive intra-familial disclosure of the genetic risk (41.1%). The majority agreed that it is an obligation to know as much as possible relevant for future health (58.0%) and only 51.7% agreed to a principle of a ‘right not to know’. In regression models, the attitudes were associated with opinions about benefits and harms of genetic testing (e.g., treatment, family planning, understanding of ASD pathology, insurance discrimination and family conflict). In sum, the findings show that most parents want to know as much as possible relevant for their children’s future health and keep their autonomy and intra-familial confidentiality about genetic risk information. Nearly half of the parents were not concerned with a “right not to know”. These attitudes can inform development of guidelines and bioethics in the age of genomic precision medicine.Subject terms: Genetic counselling, Ethics, Medical ethics     

Experimental Tests and Numerical Simulations on the Ballistic Impact Response of a Highly Inhomogeneous Aluminium Foam

A sandwich structure is a composite material consisting of thin skins encapsulating a cellular core. Such structures have proven to be excellent energy absorbents and are frequently found in various types of protection. Even so, few studies exist in the open literature on the response of the core material itself under extreme loadings such as blast and impact. Since a blast load is usually accompanied by numerous fragments, it is important to understand and be able to predict the ballistic impact resistance of the often highly inhomogeneous cellular core materials in design. In this study, the ballistic impact response of an aluminium foam with a complex cell structure has been investigated both experimentally and numerically. First, an extensive material test program involving compression tests on cubic specimens loaded in the thickness direction of the foam was carried out to reveal the mechanical properties of the material. In addition, several of the specimens were scanned before testing using X-ray Micro Computed Tomography (XRMCT) to map the multi-scale topology and morphology of the material. These data were later analysed to extract density-variation plots in many different material orientations. Second, ballistic impact tests were conducted using a gas gun where rigid spheres were launched towards aluminium foam plates, and the ballistic limit velocity and curve of the foam material were established. Finally, numerical simulations of both the material tests and the ballistic impact tests were carried out using LS-DYNA and different modelling approaches based on the XRMCT data. It will be shown that, independent of the modelling strategy applied, good agreement between the experimental impact tests and the numerical predictions can be obtained. However, XRMCT data are important if the final goal is to numerically optimise and improve the behaviour of inhomogeneous foams with respect to energy absorption, thermal isolation, or similar properties.