Previously it was reported that Alzheimer's disease (AD) patients have reduced amyloid (Aβ 1-42 ) and elevated total tau (t-tau) and phosphorylated tau (p-tau 181p ) in the cerebrospinal fluid (CSF), suggesting that these same measures could be used to detect early AD pathology in healthy elderly (CN) and mild cognitive impairment (MCI). In this study, we tested the hypothesis that there would be an association among rates of regional brain atrophy, the CSF biomarkers Aβ 1-42 , t-tau, and ptau 181p and ApoE ε4 status, and that the pattern of this association would be diagnosis specific. Our findings primarily showed that lower CSF Aβ 1-42 and higher tau concentrations were associated with Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. increased rates of regional brain tissue loss and the patterns varied across the clinical groups. Taken together, these findings demonstrate that CSF biomarker concentrations are associated with the characteristic patterns of structural brain changes in CN and MCI that resemble to a large extent the pathology seen in AD. Therefore, the finding of faster progression of brain atrophy in the presence of lower Aβ 1-42 levels and higher p-tau levels supports the hypothesis that CSF Aβ 1-42 and tau are measures of early AD pathology. Moreover, the relationship among CSF biomarkers, ApoE ε4 status, and brain atrophy rates are regionally varying, supporting the view that the genetic predisposition of the brain to amyloid and tau mediated pathology is regional and disease stage specific. NIH Public Access

Effects were studied of population size, floor area, and feeder space per hen on variables associated with egg production and corticosterone level. A total of 408 White Leghorn-type laying hens was used in this study. Three treatments were observed: 5 hens per cage with 8.6 cm feeder space per hen, 5 hens per cage with 12 cm feeder space per hen, and 7 hens per cage with 8.6 cm feeder space per hen. Both 5-hen treatments had 420 cm2 of cage area per hen, while the 7-hen treatment had 300 cm2. Increased population size, reduced feeder space, and reduced floor area per hen resulted in a significant (P less than .01) decline in percent egg production. Restriction of feeder space was correlated with reduced feed consumption and mortality but not feed conversion, weight gain, and egg size. As cage space allowance increased, feed consumption and weight gain were higher, whereas mortality, feed conversion, and egg weight were lower. No significant (P greater than .05) differences in shell thickness, specific gravity, Haugh unit, throat skin ateromata, claw length, and corticosterone level were observed. Plumage condition and foot health were improved only when floor area allowances increased.

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The Technicon sequential multiple analysis system was used to measure plasma uric acid, lactate dehydrogenase, chloride, and total protein of 8 week old broilers exposed for 4 weeks and 9 week old broilers exposed for 4 hours to both 18-22°C. and 33-35°C.Broilers exposed for 4 weeks to 18-22°C. had a significant higher (P < 0.05) level of total ". protein than those exposed to 33-35°C. (3.6 vs. 3.3 gm. %). Plasma zinc analyzed by atomic • absorption spectrophotometry was found to be significantly higher (P < 0.05) in the broilers >~ exposed to 18-22°C. for 4 weeks (303 vs. 208 /ig./ml.) Broilers exposed for 4 hours to 33-35°C. had significantly (P < 0.05) higher plasma levels of uric acid (6.7 vs. 5.5 mg. %), lactate dehydrogenase (399 vs. 328 mU./ml.) and chloride (114 vs. Ill meq./L.) than sham treated broilers maintained at 18-22°C. Body temperature was significantly higher (P < 0.01) in the 33-35°C. 4-week exposed broilers than in the birds maintained at 18-22°C. (42 vs. 41°C. mean rectal temperature). In the 33-35°3. 4 hour exposed broilers body temperature was significantly higher (P < 0.05) than in the sham treated broilers (42 vs. 41°C).

The fat content and the concentrations of glucose and triglyceride in day-old chicks hatched from 27 and 60 wk-old broiler-breeder hens were determined from pooled samples of residual yolk and blood serum, respectively. Serum glucose and triglyceride levels were unaffected (P greater than .05) by breeder age, although there was a linear (P less than .001; r = .67) relationship between these characteristics and chick weight. Yolk fat, adjusted for chick weight, was on the average 13% greater (P less than .05) in chicks from old breeders than chicks from young breeder hens. Yolk wet weight was not affected (P greater than .05) by breeder age. Results indicate that breeder age may affect chick performance through alterations in the fat content of residual yolk.