The aim of this study was to determine the effect of feeding frequency and route of administration on abomasal luminal pH in suckling calves. Six male dairy calves with cannulae in the abomasal body were administered the following six treatments in a randomized crossover design: 24 h fasting, suckling of a high-quality milk replacer (all-milk protein; 12% of body weight [BW]/d) at 12-h (2x), 8-h (3x), 6-h (4x), and 3-h (8x) intervals, and ruminal intubation of milk replacer (12% of body weight/day) at a 12-h (2x) interval. Abomasal luminal pH was measured every second for 24 h with miniature glass pH electrodes. Least squares mean 24-h fasting abomasal luminal pH was 1.73, whereas mean 24-h pH after suckling and intubation of milk replacer every 12 h were higher at 3.44 and 3.17, respectively. Increasing the frequency of milk replacer suckling to 3x, 4x, and 8x increased mean 24-h abomasal luminal pH; however, there was no difference in mean 24-h pH between 3x (3.69), 4x (3.64), and 8x (3.67) suckling. The percentage of the 24-h recording period that abomasal luminal pH was > 3.0 was 0, 49, 53, 61, 61, and 71% for fasting, 2x intubation of milk replacer, and 2x, 3x, 4x, and 8x suckling of milk replacer, respectively. Increasing the frequency of milk replacer suckling may be efficacious in the prophylaxis of abomasal ulceration in milk-fed calves.

The aim of this study was to investigate a cell delivery system for repair of severe chronic osteochondral defects using magnetically labeled mesenchymal stem cells (m-MSCs), with the aid of an external magnetic device, through the accumulation of a small number of m-MSCs into a desired area and to detect the suitable number of autologous m-MSCs needed for repair of the defect. Twenty-six male Japanese white rabbits aged 6 months were used. An osteochondral defect was created bilaterally at the weight-bearing surface of the medial femoral condyle of the rabbits' knees (3 mm diameter; 4 mm depth). At 4 weeks after creation of the defect, autogenic transplantation of the m-MSCs into the defect area was performed, followed by 10-min exposure to an external magnetic device, where animals were divided into four groups: high (1 × 10 6 m-MSCs), medium (2 × 10 5 m-MSCs), low (4 × 10 4 m-MSCs), and control (PBS injection). At 4 and 12 weeks posttransplantation of m-MSCs, repaired tissue was assessed histologically using the Fortier score with toluidine blue staining. Transplantation of a low number of m-MSCs was not enough to improve osteogenesis and chondrogenesis, but the medium and high groups improved repair of the chronic defect with chondrogenic tissues and showed histologically significantly better results than the control and low groups. The use of a magnetic targeting system for delivering m-MSCs has the potential to overcome the clinical hurdles for repair of the severe chronic osteochondral defect. Furthermore, this system is predicted to produce good clinical outcomes for humans, not only to repair osteochondral defects but also to repair a variety of damaged tissues.

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Abomasal acid secretion in milk-fed calves is mediated in part by histamine type-2 receptors. Cimetidine and ranitidine may be efficacious in the treatment of abomasal ulcers in milk-fed calves.

Abomasal ulceration occurs commonly in suckling calves, and the cause for the high prevalence of abomasal ulceration is unknown. We hypothesized that diet may play a role in the etiopathogenesis of abomasal ulceration. Six male dairy calves with an abomasal body cannula suckled fresh Holstein cow's milk, all milk-protein milk replacer, or combined milk- and soy-protein milk replacer twice daily at 12% of body weight/d. Abomasal luminal pH was measured every second for 24 hours by using a miniature glass pH electrode. Mean 24-hour abomasal luminal pH for all milk-protein milk replacer (3.22) and combined milk- and soy-protein milk replacer (3.27) were similar but significantly (P < .05) higher than that for cow's milk (2.77; standard error = 0.08). Both milk-replacer formulations failed to clot after the addition of chymosin, whereas cow's milk clotted within 2 minutes. The in vitro titration curve of cow's milk and all milk-protein milk replacer were similar, but different to that of combined milk- and soy-protein milk replacer. The osmolalities of all milk-protein milk replacer (375 mOsm/kg) and combined milk- and soy-protein milk replacer (410 mOsm/kg) were greater than that of cow's milk (278 mOsm/kg). The slightly lower mean abomasal luminal pH in calves suckling cow's milk, compared to milk replacer, was probably due to clotting of cow's milk, with extrusion of low pH whey, and a slower rate of abomasal emptying caused by the hyperosmolality of milk replacer. Examination of our results suggests that suckling cow's milk may increase the prevalence of abomasal ulceration by decreasing mean luminal pH, although this remains to be determined.