Frank M. Tomas

The site of magnesium absorption from the ruminant stomach

1. A low-magnesium diet was fed to four sheep, each of which had been surgically prepared with a rumen fistula, a tube into the cranial one-third of the omasum, a tube to the cranial one-third of the abomasum and a re-entrant duodenal cannula. Mg, as gluconate or acate or acetate, was continuously infused for 12-14 d in turn into (1) the caudal duodenal cannula, (2) the abomasum, (3) the omasum, (4) the rumen. A continuous infusion of the chromium-ethylenediaminetetraacetic acid complex (CrEDTA) was maintained to the rumen. The abomasal effluent which flowed through the cranial duodenal cannula was continually sampled and the flow of Mg calculated from the concentrations of Mg and CrEDTA. Blood and rumen fluid samples were taken and urine and faeces collected during each period of Mg infusion. 2. The Mg infused to either the abomasum or omasum was completely recovered at the duodenum, indicating a lack of net absorption of Mg from these stomach compartments. In contrast, 13-7-18-7 mmol (36-61%) of the Mg infused to the rumen was not recovered at the duodenum which suggested that a substantial net absorption of the infused Mg occurred from the reticulo-rumen. Absorption of Mg caudal to the pylorus was not related to the site of Mg infusion and averaged 3-28 +/- 0-56 (SEM) mmol/d. 3. Compared with the intraruminal infusion, the post-ruminal infusion of Mg was associated with decreased plasma and rumen fluid Mg concentrations, decreased urinary Mg exretion, decreased Mg balance and increased faecal Mg excretion. 4. It is concluded that no significant absorption of Mg occurs from either the omasum or abomasum in sheep and that the reticulo-rumen is the principal site of Mg absorption before the pylorus. Absorption of Mg post-ruminally is insufficient to maintain normal Mg status in the animal.

Inhibition of cell migration from tendon explants into fibrin clots by extracts derived from cheese whey is largely due to transforming growth factor‐beta

Whey‐derived growth factor extract (WGFE) and the acid‐activated form (WGFE‐a) were tested for their ability to influence the migration of cells from chicken flexor tendon biopsies into fibrin clots. When added to the medium surrounding clots, both extracts significantly inhibited migration relative to controls (P < 0.05) in a dose‐dependent manner when measurements were made after seven days of incubation. WGFE‐a was approximately ten times more potent than WGFE. Since transforming growth factor (TGF)‐β1 and ‐β2 activity of WGFE‐a is much higher than in WGFE we hypothesized that TGF‐β was responsible for the inhibition of tendon cell migration. Neutralizing anti‐TGF‐β monoclonal antibody was added to the medium bathing tendon biopsies in fibrin clots along with WGFE‐a. WGFE‐a alone inhibited migration by 51% and this was reversed by the antibody in a dose‐dependent manner. Furthermore, recombinant human TGF‐β1 and ‐β2 significantly inhibited tendon cell migration with similar dose‐dependent potency when tested in the assay. These results indicate that TGF‐β is largely responsible for the inhibition of tendon cell migration by WGFE‐a. This sheds further light on the functions of this growth factor during the early events in tendon repair.