Tobacco policies in Austria during the Third Reich.

BACKGROUND: The anti-smoking stance taken by Adolf Hitler, coupled with Nazi support for research on smoking and lung cancer and campaigns to discourage smoking, have encouraged pro-smoking groups to equate tobacco control activities with totalitarianism. Previous work has described the situation in Germany. OBJECTIVE: To examine the situation in Austria, also part of the Reich after 1938. DESIGN: Iterative analysis of documents and reports about the situation in Austria in the 1930s and 1940s, supplemented by a review of Reich legal ordinances, party newspapers, health behaviour guidelines issued by Nazi party organisations and interviews with expert informants. RESULTS: In contrast to the situation in Germany where, albeit to a much lesser degree than is commonly believed, some anti-smoking policies were adopted, the Nazi authorities in Austria made almost no attempt to discourage smoking and the Austrian tobacco company worked closely with the Nazi authorities to ensure that supplies were maintained. CONCLUSION: Especially when looked at in the Austrian context, the much-cited link between anti-smoking policies and Nazism is a gross over-simplification. This purported link should not be used to justify the continued failure to act effectively against smoking in Germany and Austria.     

LHRH-A对孕中期大鼠抗妊娠作用的研究

本文观察了[D-Ala⁶,Pro⁹-Ethylamide¹⁰]-LHRH(LHRH-A)对孕中期大鼠的抗妊娠作用。结果显示:在孕9～11d sc 200μg/d LHRH-A,血浆孕酮水平自第二次给药后明显下降(P<0.05),给药大鼠均流产终止妊娠;LHRH-A的抗妊娠作用可被醋酸甲地孕酮所拮抗;LHRH-A对体外培养的假孕大鼠和孕d 9大鼠黄体细胞分泌孕酮有明显的直接抑制作用。     

Mortality league tables: do they inform or mislead?

OBJECTIVE--To examine certain methodological issues related to the publication of mortality league tables, with particular reference to severity adjustment and sample size. DESIGN--Retrospective analysis of inpatient hospital records. SETTING--22 hospitals in North West Thames health region for the fiscal year 1992-3. SUBJECTS--All admissions with a principal diagnosis of aortic aneurysm, carcinoma of the colon, cervical cancer, cholecystectomy, fractured neck of femur, head injury, ischaemic heart disease, and peptic ulcer. MAIN MEASURES--In hospital mortality rates adjusted by disease severity and calculated on the basis of both admissions and episodes. RESULTS--The numbers of deaths from specific conditions were often small and the corresponding confidence intervals wide. Rankings of hospitals by death rate are sensitive to adjustment for severity of disease. There are some differences that cannot be explained using routine data. CONCLUSIONS--Comparison of crude death rates may be misleading. Some adjustment for differences in severity is possible, but current systems are unsatisfactory. Differences in death rates should be studied, but because of the scope for manipulating data, this should be undertaken in a collaborative rather than a confrontational way. Any decision to publish league tables of death rates will be on political rather than scientific grounds.     

GGA1 acts as a spatial switch altering amyloid precursor protein trafficking and processing

The beta-amyloid (Abeta) precursor protein (APP) is cleaved sequentially by beta-site of APP-cleaving enzyme (BACE) and gamma-secretase to release the Abeta peptides that accumulate in plaques in Alzheimer's disease (AD). GGA1, a member of the Golgi-localized gamma-ear-containing ARF-binding (GGA) protein family, interacts with BACE and influences its subcellular distribution. We now report that overexpression of GGA1 in cells increased the APP C-terminal fragment resulting from beta-cleavage but surprisingly reduced Abeta. GGA1 confined APP to the Golgi, in which fluorescence resonance energy transfer analyses suggest that the proteins come into close proximity. GGA1 blunted only APP but not notch intracellular domain release. These results suggest that GGA1 prevented APP beta-cleavage products from becoming substrates for gamma-secretase. Direct binding of GGA1 to BACE was not required for these effects, but the integrity of the GAT (GGA1 and TOM) domain of GGA1 was. GGA1 may act as a specific spatial switch influencing APP trafficking and processing, so that APP-GGA1 interactions may have pathophysiological relevance in AD.