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L R Jacobs

Publications and source records attributed to L R Jacobs.

44 records · Page 3Linked to original sources
PubMed1982

Dietary wheat bran lowers colonic pH in rats.

The effect of chronic dietary wheat bran supplementation on the pH of gastrointestinal contents was examined in thirty-one Sprague-Dawley rats. Ten control rats received a fiber-free diet while twenty-one rats were fed the same diet plus a 20% wheat bran supplement. The fiber-fed rats developed a greater acidity of intestinal contents: cecal pH was 6.30 +/- 0.33 in the controls (P less than 0.01). These changes in gastrointestinal pH may be of relevance to the nutrient modulation of gastric and colonic tumor development.

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PubMed1981

Intestinal diffusion barrier: unstirred water layer or membrane surface mucous coat?

The dimensions of the small intestinal diffusion barrier interposed between luminal nutrients and their membrane receptors were determined from kinetic analysis of substrate hydrolysis by integral surface membrane enzymes. The calculated equivalent thickness of the unstirred water layer was too large to be compatible with the known dimensions of rat intestine. The discrepancy could be reconciled by consideration of the mucous coat overlying the intestinal surface membrane. Integral surface membrane proteins could not be labeled by an iodine-125 probe unless the surface coat was first removed. The mucoprotein surface coat appears to constitute an important diffusion barrier for nutrients seeking their digestive and transport sites on the outer intestinal membrane.

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PubMed1981

Alterations in labeling of cell-surface glycoproteins from normal and diabetic rat intestinal microvillous membranes.

The effect of chronic streptozotocin-induced diabetes was studied on intestinal microvillous membrane surface carbohydrate groups. After 7 weeks of diabetes, purified microvillous membranes were prepared from rat small intestine and surface galactoproteins identified by labeling with galactose oxidase/sodium boro[3H]hydride. Membrane surface sialic acid residues were labeled using the sodium metaperiodate/sodium boro[3H]hydride technique. Membranes were solubilized in SDS and protein labeling analyzed by acrylamide electrophoresis. Membranes from diabetic rats showed an 81% increase in galactoprotein labeling (P less than 0.02) while labeling of sialic acid residues was unchanged. The greatest increase in galactoprotein labeling occurred in protein monomers of Mr 116,000-200,000, where there was a 155% increase in labeling (P less than 0.005). These results indicate that intestinal microvillous membrane protein glycosylation is altered in chronic diabetes. This increase in surface membrane carbohydrates could explain the decreased rates of proteolytic degradation previously described for at least one microvillous protein. An increase in membrane galactose groups has also been noted in hepatocyte and kidney glomerular basement membranes, which suggests the presence of a systematic change in membrane protein glycosylation occurring as a result of the diabetic state.

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PubMed1981

Alterations in surface ultrastructure and anionic sites of rat dimethylhydrazine-induced intestinal tumors.

The relative roles of cell surface shedding and electronegative charge as determinants of metastatic capacity were studied in experimentally produced intestinal tumors. The ultrastructural organization and distribution of anionic sites on the luminal plasma membrane surface components were examined in small intestinal and colonic tumors induced in male Sprague-Dawley rats with 1,2-dimethylhydrazine. The overall distribution of negatively charged groups was demonstrated with ruthenium red staining. Compared to normal epithelial cells, neoplastic cells revealed evidence of decreased cell surface shedding as manifested by decreased numbers of membrane-bound bodies, and an increased quantity of glycocalyx. Malignant cell surfaces were directly exposed to the intestinal lumen as a result of losing the enteric surface coat covering. The exposed microvilli appeared damaged with shortening and blunting. The glycocalyx and surface coat both reacted strongly with ruthenium red indicating the presence of anionic sites. As a result of surface coat loss, the malignant cell surface components revealed an overall decrease in net negative charge. These alterations in cell surface component ultrastructure and electronegative charge appear to be consistent with the low capacity for chemically induced rat intestinal tumors to metastasize.

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PubMed1981

Effects of dietary wheat bran on rat colonic structure and mucosal cell growth.

The effects of dietary wheat bran on colonic morphology and mucosal cell growth were examined in male Wistar rats. Two groups of rats were fed defined diets for 2 weeks. The control group was fed a fiber-free diet while the experimental group received the same diet plus a 20% wheat bran supplement. Nutrient intake and body weight gain were similar in the two groups of rats. The bran-fed group developed an increase in proximal (cecum) and distal colonic weights (P less than 0.02 0.02) but mucosal weight was only increased in the distal colon when compared to the control group (P less than 0.005). Histological measurements revealed deeper colonic crypts (P less than 0.001) and mucosal cell hyperplasia in the bran-fed group in addition to an increase in muscle thickness (P less than 0.001). Mucosal cell hyperplasia, as measured by the increases in mucosal protein (P less than 0.01), DNA (P less than 0.01) and RNA (P less than 0.005) was most marked in the distal colon. Proximal colon showed no significant change in mucosal cell mass. Cell RNA content was decreased only in the proximal colonic mucosa (P less than 0.01). These results demonstrate that dietary wheat bran regulates colonic mucosal cell growth according to the anatomical region of the colon, producing distal mucosal hyperplasia and decreasing proximal colonic cell RNA.

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PubMed1976

Oxygen tension and the selective tropism of K-virus for mouse pulmonary endothelium.

This study focused on the unique nature of K-virus pneumonitis in suckling mice. This process, rather than being a conventional pneumonitis, is characterized by viral replication and cytopathic effects restricted exclusively to pulmonary endothelium. The selective viral attack on this air-blood interface suggests that K-virus is an endotheliotrope that requires a richly oxygenated intracellular milieu for replication. This possibility has been explored by studies of the course of K-virus infection in suckling mice under conditions of normal (21 per cent), increased (40 per cent), and decreased (10 per cent) 02 content of inspired air. The absence of critical modulating influences of these varied environmental conditions rules out a significant role of tissue 02 concentrations as determinants of the selective tropism of K-virus.

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