High concentrations of guar meal in broiler chicken diets reduce body weight and feed efficiency. The increased intestinal viscosity that is responsible for reduced measures of performance results from residual guar gum present in guar meal. Two experiments were designed to study the effects of 2 guar meal fractions at 3 different concentrations, germ (0, 5.0, and 7.5%) and hull (0, 2.5, and 5.0%), and the effectiveness of a beta-mannanase at three levels (0, 1x, and 4x; 1x = 1.09 x 10(5) units/ kg) on broiler growth and feed conversion. Growth and performance were measured as a function of intestinal viscosity. Addition of the germ fraction to rations did not reduce body weight, although feed conversion ratio was increased at 7.5% of the diet. Intestinal viscosity also increased significantly at this level. Enzyme addition significantly reduced intestinal viscosity. Due to an interaction that was present between hull and enzyme concentration, each treatment was compared separately. Inclusion of the hull fraction significantly reduced body weight at both levels of inclusion and increased feed conversion ratio at 5% inclusion. Addition of the enzyme significantly increased body weight and reduced feed conversion ratio in diets containing guar hull fractions. Supplementation of beta-mannanase to feeds containing either fraction of guar meal reduced intestinal viscosity and alleviated the deleterious effects associated with guar meal feeding.

Practising dentists were able to improve their detection of proximal-surface caries extending into the dentin, but not occlusal caries, using 3DX high-resolution cone beam CT images compared with CCD images.

High concentrations of guar meal in poultry diets deleteriously affect growth, feed intake, and digesta viscosity. These effects are attributed to residual gum in the meal. A 2 x 5 factorial experiment investigated the impacts of two guar meal fractions (germ and hull) at five inclusion levels (0, 2.5, 5.0, 7.5, and 10.0%) on intestinal viscosity, measures of growth, and feed conversion in broiler chickens fed to 20 d of age. Growth and feed conversion ratio were not affected by inclusion of as much as 7.5% of the germ fraction into poultry diets, while inclusion of the hull fraction reduced growth at all concentrations. The hull fraction increased intestinal viscosity at all inclusion levels fed, although feed conversion was not affected until the inclusion rate exceeded 5.0%. The germ fraction significantly increased intestinal viscosity at 7.5 and 10% inclusion rates. When germ fraction was fed, relative organ weights remained constant through all concentrations except for the ventriculus and duodenum at 7.5 and 10% inclusion levels. Relative pancreas weight was significantly increased at the 10% level of the hull fraction. Increases in intestinal viscosity corresponded with growth depression. These results suggest that residual gum was responsible for some deleterious effects seen when guar meal was fed. The germ fraction was a superior ingredient when compared with the hull fraction. The guar meal germ fraction constituting as much as 7.5% of the diet supported growth and feed conversion measures similar to those observed with a typical corn-soybean poultry ration.

The effects of deregulated Raf activation on the growth and differentiation of hematopoietic cells were investigated. The cytokine-dependent murine myeloid FDC-P1 and human erythroleukemic TF-1 cell lines were transformed to grow in response to deregulated Raf expression in the absence of exogenous cytokines. The conditionally active Raf proteins were regulated by ␤-estradiol as cDNAs containing the Raf catalytic, but lacking negative-regulatory domains, were ligated to the hormone binding domain of the estrogen receptor (⌬Raf:ER). Continuous ⌬Raf expression prevented apoptosis in the absence of exogenous cytokines and altered the morphology of the FD/⌬Raf:ER cells as they grew in large aggregated masses (Ͼ100 cells) whereas the parental cytokinedependent FDC-P1 cells grew in smaller grape-like clusters (Ͻ10 cells). FD/⌬Raf-1:ER cells growing in response to Raf activation displayed decreased levels of the Mac-2 and Mac-3 molecules on their cell surface. In contrast, when these cells were cultured in IL-3, higher levels of these adhesion molecules were detected. Expression of activated Raf oncoproteins also abrogated cytokine dependency and prevented apoptosis of TF-1 cells. Moreover, the differentiation status of these Raf-responsive cells was more immature upon Raf activation as culture with the differentiation-inducing agent phorbol 12 myristate 13-acetate (PMA) and ␤-estradiol resulted in decreased levels of the CD11b and CD18 integrin molecules on the cell surface. In contrast when the Raf-responsive cells were induced to differentiate with PMA and GM-CSF, in the absence of ⌬Raf:ER activation, increased levels of the CD11b and CD18 molecules were detected. Retinoic acid (RA) inhibited 3 H-thymidine incorporation in response to GM-CSF. Interestingly, Raf activation counterbalanced the inhibition of DNA synthesis caused by RA but not PMA. Thus deregulated Raf expression can alter cytokine dependency, integrin expression and the stage of differentiation. These Raf-responsive cell lines will be useful in elucidating the roles of the MAP kinase cascade on hematopoietic cell differentiation and malignant transformation. Leukemia

The Raf/MEK/ERK (MAPK) signal transduction cascade is a vital mediator of a number of cellular fates including growth, proliferation and survival, among others. The focus of this review centers on the MAPK signal transduction pathway, its mechanisms of activation, downstream mediators of signaling, and the transcription factors that ultimately alter gene expression. Furthermore, negative regulators of this cascade, including phosphatases, are discussed with an emphasis placed upon chemotherapeutic intervention at various points along the pathway. In addition, mounting evidence suggests that the PI3K/Akt pathway may play a role in the effects elicited via MAPK signaling; as such, potential interactions and their possible cellular ramifications are discussed.