Eight lactating Holstein cows were fed four diets in a replicated 4 x 4 Latin square design to determine how hydrogenation affects fats as supplements for dairy rations. Four isonitrogenous diets contained either no added fat, 5% yellow grease, or 3 or 5% hydrogenated yellow grease. Only yellow grease reduced DM intake compared with DM intake of the control diet. Diets supplemented with fat had lower digestibilities of fiber, nitrogen, energy, and fatty acids than the control diet did. Ruminal acetate concentration and acetate to propionate ratio were higher for the hydrogenated fat than for yellow grease. However, fatty acid digestibilities were lower for diets containing hydrogenated fat. Milk yields of fat-supplemented diets, whether actual or 4% FCM, did not exceed the control diet except for 5% hydrogenated yellow grease. This study shows that hydrogenated fats have fewer negative effects on food intake, milk fat content, and ruminal fermentation but have lower digestibilities than other fats. Hydrogenation improved milk yield compared with yellow grease fed at the same amount of supplementation.
Eighteen Holstein (experiment 1) and 15 Jersey (experiment 2) heifer calves were fed milk replacer once or twice daily to determine effects of feeding frequency on weight gain, starter intake, and glucose metabolism. Body weights were measured weekly from birth to 8 wk. Blood samples were collected at wk 1 through 6 from all calves before and at 30, 60, 90, 120 and 180 min after the morning feeding. Plasma was analyzed for glucose, insulin, glucagon, and nonesterified fatty acids (NEFA). Urine was collected 90 min postfeeding to measure glucose concentration. Treatment did not affect mean starter intake or body weight. In experiments 1 and 2 mean plasma glucagon, glucose, NEFA, and insulin and urinary glucose concentrations were not affected by treatment. There was an interaction of sampling time and treatment for plasma insulin concentrations but not for glucose concentrations in both experiments. Following feeding, calves fed milk replacer once daily had higher insulin concentrations than those fed twice daily. There was an interaction of sampling time and treatment for plasma NEFA concentrations in Jersey calves only. Jersey calves fed milk replacer once daily had higher plasma NEFA concentrations before the morning milk replacer feeding. At wk 3 and 6, frequently sampled intravenous glucose tolerance tests were performed to assess glucose effectiveness, insulin sensitivity, and acute insulin response. In experiments 1 and 2 glucose effectiveness and insulin sensitivity were similar regardless of milk replacer feeding frequency. In Holstein and Jersey calves fed milk replacer twice daily, acute insulin response was greater than in calves fed once daily. However, insulin sensitivity decreased with age, while acute insulin response increased with age. These data suggest that feeding calves milk replacer once daily did not deleteriously affect performance or glucose metabolism regardless of breed.
Eighty-four Holstein calves were assigned at 2 d of age to one of three treatments: 1) control with no additives; 2) 10 g of a mixed microbial concentrate containing Lactobacillus acidophilus, Lactobacillus lactis, and Bacillus subtilis; or 3) 10 g of a B. subtilis concentrate. The microbial concentrates were mixed with milk replacer during the a.m. feeding. The milk replacer was offered twice daily at 5% BW per feeding; the reconstituted replacer contained 12.5% DM. Volume of replacer fed was based on initial weight of calf and held constant until weaning. Water and starter ration were offered for ad libitum intake throughout the trial. Calves were weaned abruptly at 30 d of age and received only water and starter from d 31 to 44. General health and performance of all calves were good. Although differences in weight gain and feed efficiency were not significant, the B. subtilis concentrate tended to have a positive effect on feed efficiency during wk 1 to 4 and on immediate postweaning gain. A higher fecal bacilli count at 6 wk in calves fed the microbial concentrates may be related to their tendency for improved gain during d 31 to 44, the immediate postweaning period.
Primary human brain tumours account for approximately 2% of all cancers. High levels of expression of vascular endothelial growth factor-A (VEGF-A), a potent angiogenic factor, are linked to poor prognosis. In contrast, the potential role in human brain tumour biology of newer VEGF family members, VEGF-C and VEGF-D, both of which are lymphangiogenic factors, is poorly understood. In the present study, the expression of all VEGFs (VEGF-A, -B, -C, and -D) and their receptors (VEGFR-1, -2, and -3) has been assessed in 39 primary human brain tumours. The well-established findings were confirmed with VEGF-A. Surprisingly, however, VEGF-C and VEGF-D, as well as VEGFR-3, were expressed in some tumour types such as haemangioblastomas and glioblastomas, despite their lack of lymphatic vessels. VEGF-C and VEGFR-3 transcripts were localized to the tumour palisade around necrotic areas in glioblastomas and were evenly distributed throughout haemangioblastomas. VEGF-C protein was localized by immunohistochemistry to the palisade layer in glioblastomas. More than 50% of VEGF-C-positive cells also expressed the intermediate-stage inflammatory macrophage marker CD163; however, a significant proportion of VEGF-C-positive cells were CD163-negative. These data demonstrate the presence of molecules, primarily described as regulators of lymphangiogenesis, in normal human brain and brain tumours that are devoid of lymphatics. Their localization in macrophages points to a role in tumour-associated inflammation.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.