[A 47-year-old patient with longstanding nicotine abuse, increasing dyspnea on exertion and lower and peripheral lung predominant ground-glass opacities]. / 47-jähriger Patient mit langjährigem Nikotinabusus, zunehmender Belastungsdyspnoe und diffusen, peripher und basal betonten Milchglastrübungen in der Lunge.

The causal relationship between cigarette smoking and a number of interstitial lung diseases continues to evolve. These "smoking-related interstitial lung diseases" (SR-ILD) are a heterogeneous group of entities which have overlapping imaging findings and which can coexist. The presented case of a patient with smoking history and pulmonary ground-glass opacities demonstrates that thorough knowledge of the various manifestations of SR-ILD is essential for a confident diagnosis.

Iowa FICSIT trial: the feasibility of elderly wearing a hip joint protective garment to reduce hip fractures.

Hip fractures exact a heavy toll in the elderly population. While intervention strategies are being investigated to reduce the numbers of geriatric falls and to improve the body's resiliency, the geriatric population remains at risk for the mortality and morbidity associated with fractures. The Iowa FICSIT site is investigating the feasibility of passive protection of the proximal femur through the use of hip pads. The pad is designed to disperse throughout the pad the energy created in a fall. The focus of the Iowa trial is to determine if elderly will wear hip pads for the majority of their waking hours. Thirty subjects are being recruited from each of six elderly populations who are at high risk to fall and at increased risk of injury. To facilitate compliance, the following strategies are utilized: run-in period, graduated implementation, tailoring of wearing times, and self-report of compliance. Outcome measures include compliance rates and injuries sustained during falls.

Regulatory region of human amyloid precursor protein (APP) gene promotes neuron-specific gene expression in the CNS of transgenic mice.

The accumulation of beta-amyloid protein in specific brain regions is a central pathological feature of Alzheimer's disease (AD). The 4 kd beta-amyloid protein derives from a larger amyloid precursor protein (APP) by as yet unknown mechanisms. In the absence of a laboratory animal model of AD, transgenic mice expressing various APP gene products may provide new insights into the relationship between APP and beta-amyloid formation and the pathogenesis of AD. beta-amyloid accumulation in AD brain may result from interactions between APP and other molecules. Such interactions are likely to be developmentally regulated and tissue-specific. A transgenic mouse model of AD, therefore, would aim for APP transgene expression that mimics the endogenous APP gene. As an initial step in developing an animal model, we have identified a 4.5 kb DNA fragment from the 5' end of the human APP gene, which mediates neuron-specific gene expression in the CNS of transgenic mice, using E. coli lacZ as a reporter gene. Detectable levels of transgene expression are found in most neurons but not in glial and vascular endothelial cells. The expression pattern of this reporter gene closely resembles the distribution of endogenous APP mRNA in both the human and mouse CNS.

Map location of the gene for a 130,000-dalton glycoprotein of bovine herpesvirus 1.

A bovine herpesvirus 1 variant (mar6) containing a mutation in a viral glycoprotein with a molecular weight of 130,000 (g130) was isolated by selecting for resistance to a neutralizing monoclonal antibody (130-6) directed against g130. Mar6 was completely resistant to neutralization by monoclonal antibody 130-6 in the presence and absence of complement, but was neutralized by polyvalent immune sera. The mar6 mutant synthesized and processed g130, but produced plaques which failed to react with monoclonal antibody 130-6 in an in situ immunoassay (black plaque). However, monoclonal antibody 130-6 was capable of binding and immunoprecipitating g130 from infected-cell extracts produced by lysis of mar6-infected cells with nonionic detergents. The mutation in mar6 was mapped by marker rescue with cloned bovine herpesvirus 1 restriction enzyme fragments to a 3.8-kilobase fragment at approximate map units 0.405 to 0.432. In addition, it was found that a DNA probe containing the glycoprotein B gene of herpes simplex type 1 hybridized uniquely to the same 3.8-kilobase fragment which was shown by marker rescue to contain the mutation site in the gene for bovine herpesvirus 1 g130.