The development of pulmonary lesions in beagle dogs was studied following chronic inhalation exposures to radon (at 105 % 20 nCi/l), radon daughters (at 605 k 169 WL), uranium ore dust (at 12.9 5 6.7 mglm') and cigarette smoke. Chronic exposures to mixtures of these agents caused significant lifespan shortening when compared with controls. Survival times of controls and smoke-exposed dogs were equivalent during the 4 to 5-yr mean survival time of the dogs exposed to radon-daughter and ore-dust mixtures (with or without added cigarette smoke).Animals with tumors of the respiratory tract generally had cumulative radon-daughter exposures exceeding 13,000 WLM, and their survival time was longer than the survival time of nontumor-bearing animals. Under the conditions of the experiment, exposure to cigarette smoke was found to have a mitigating effect on radon daughter-induced tumors. It is uncertain whether this would be a general finding applicable to other levels of exposure to radon daughters, uranium ore dust and cigarette smoke. tract lesions. However, exposure to 20 cigarettedd, 7 d/wk resulted in pulmonary emphysema, fibrosis and chronic bronchitis and bronchiolitis.Emphysema and fibrosis were much more prevalent and severe in the dogs exposed to mixtures which included radon daughters and uranium ore dust. These dogs also had adenomatous lesions which progressed to squamous metaplasia of aleveolar epithelium, epidermoid carcinoma and bronchioloalveolar carcinoma. Pathologic changes in the airways of these dogs were most prominent in the nasal mucosa, and included a few squamous carcinomas in the nasal cavity.We conclude that the beagle dog is a useful animal for modeling pulmonary lesions produced by uranium mine air contaminants. Tumors were produced at levels that did not greatly exceed some exposures reported for uranium miners. These tumors, found after approx. 50mo of exposure, might partially account for the absence of tumors in experiments where exposures terminated before 50 mo.
words) 66Objective: Global factors have been identified in measures of cognitive performance 67 (i.e., Spearman's g) and psychopathology (i.e., "General Psychopathology", "p"). 68Dementia is also strongly determined by the latent phenotype "δ", derived from g. We 69 wondered if the Behavior and Psychological Symptoms of Dementia (BPSD) might arise 70 from an association between δ and p.71 Methods: δ and p were constructed by confirmatory factor analyses in data from the 72 Alzheimer's Disease Neuroimaging Initiative (ADNI).δ and orthogonal factors 73 representing "domain-specific" variance in memory (MEM) and executive function (EF) 74 were regressed onto p and orthogonal factors representing "domain-specific" variance in 75 positive (+) and negative (-) symptoms rated by the Neuropsychiatric Inventory Nursing 76 Home Questionnaire (NPI-Q) by multiple regression in a structural equation model 77 (SAM) framework.78 Results: Model fit was excellent (CFI = 0.98, RMSEA = 0.03).δ was strongly associated 79 with p, (+) and (-) and strongly associated with p (r = -0.57, p<0.001). All three 80 associations were inverse (adverse). Independently of δ , MEM was uniquely associated 81 with (+), while ECF was associated with (-). Both associations were moderately strong. 82ECF was also weakly associated with p. 83 Conclusions: Dementia severity (δ) derived from general intelligence (g) is specifically 84 associated with general psychopathology (p). This is p's first demonstration in an elderly 85 sample and the first to distinguish the global behavioral and psychological symptoms 86 specific to dementia (BPSSD) from behavioral disturbances arising by way of non-87 dementing, albeit likely disease-specific, processes affecting domain-specific cognitive 88 and behavioral constructs. Our findings call into question the utility of proposed regional 89 interventions in BPSSD, and point to the need to explore global interventions against 90 dementia-specific behavioral features. 91 92 93 94 Introduction: 95 96 The so-called Behavioral and Psychological Symptoms of Dementia (BPSD) are a major 97 source of comorbidity and caregiver burden (1). BPSD increase exposure to 98 psychopharmacological agents and their associated adverse drug reactions (ADR) (2). 99They are a major factor in caregiver stress (3)(4), increase the risk of institutionalization 100 (5) and inflate the costs associated with dementia care (3). 102Regardless, surprisingly little is known about the biological substrates of BPSD, their 103 natural history or risk factors. It is widely assumed that BPSD arise from the regional 104 neuropathology(ies) specific to the disease(s) in which they develop. Some investigators 105 have attempted to use to BPSD to develop etiologically precise BPSD signatures. 106However, in young adults, a global "general psychpathology" factor "p" has been 107 proposed to influence all psychopathological behavioral domains (6-7) and is 108 demonstrable in a wide range of conditions (8).
Gompertz growth curves were fitted to both skeletal growth and skeletal accumulation data from miniature swine ingesting from 1 to 125 pCi 90Sr/day from birth to nearly 8 yr of age. Normalized 90Sr accumulation data from the animals ingesting 1 , 5, or 25 pCi per day were adequately described by a single equation. Those from the 125 pCi/day animals, however, required a different equation to reflect their increased absorption and/or retention of that apparently resulted from radiation damage. Derived equations expressing 90Sr concentration in skeleton vs. age peaked at about 9 months of age and then decreased to a plateau. This resulted from the 90Sr content of the skeleton plateauing earlier in life than did skeletal weight. Utilization of these equations and appropriate factors permitted calculation of the cumulative ionizing radiation dose delivered to bone over the lifetime of the animals. Two complimentary studies were conducted to better define the radiation dose to bone surfaces and fetuses of these animals.
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