3 research outputs found
Milk fatty acid profile from grazing buffaloes fed a blend of soybean and linseed oils
Milk fatty acid profile from grazing buffaloes fed a blend of soybean and linseed oils
The aim of the study was to examine the changes in milk fatty acid (FA) profile of grazing buffaloes fed either low (L, 276g/d) or high (H, 572g/d) doses of a blend (70:30, wt/wt) of soybean and linseed oils. Fourteen multiparous Mediterranean buffaloes grazing on a native pasture were fed 4 kg/day of a commercial concentrate containing no supplemental oil over a pre-experimental period of ten days. The baseline milk production and composition and milk FA profile were measured over the last three days. After this pre-experimental period the animals received the same concentrate added with either the L or H oil doses for 26 additional days. Milk yield (g/animal/day) did not differ at the start (1776 ± 522 and 1662 ± 291 for L and H, respectively, P<0.622) or at the end of the trial (4590 ± 991 and 4847 ± 447 in L and H, respectively, P<0.543). Baseline milk fat content (g/kg) averaged 77.1 (±20.5) in L and 74.3 (±9.9) in H (P<0.10) and was reduced (P<0.031) to 60.7 (±23.6) and 49.4 (±11.2) (P<0.0031) respectively after L and H with no differences between treatments (P<0.277). Baseline milk protein content (L=43.2 ± 3.4 and H= 44.3 ± 6.9g/kg) increased after oil supplementation (P<0.0001) in both L (73.2 ± 6.0g/kg) and H (68.4 ± 4.9g/kg) without differences between oil doses (P<0.123). Milk fat content of 14:0 decreased after oil supplementation only in the H treatment (5.29 to 4.03, P<0.007) whereas that of 16:0 was reduced (P<0.001) at both L (24.49 to 19.75g/100g FA) and H (25.92 to 19.17g/100g FA) doses. The reduction of total content of 12:0 to 16:0 was higher (P<0.052) in H (32.02 to 23.93g/100g FA) than L (30.17 to 25.45g/100g FA). Vaccenic acid content increased (P<0.001) from 5.70 to 13.24g/100g FA in L and from 5.25 to 16.77 in H, with higher results in the in H treatment (P<0.001). Baseline rumenic acid was sharply increased (P<0.001) in L (1.80 to 4.09g/100g FA, +127%) and H (1.60 to 4.61g/100g FA, +187%) with no differences between L and H (P<0.19). Overall, these results indicate a pronounced improvement in the nutritional value of milk fat from grazing buffaloes fed little amounts (0.276g/day) of a blend of soybean and linseed oils
Clinical and molecular delineation of the 17q21.31 microdeletion syndrome.
The chromosome 17q21.31 microdeletion syndrome is a novel genomic disorder that has originally been identified using high-resolution genome analyses in patients with unexplained mental retardation. Here we report the molecular and/or clinical characterization of 22 individuals with the 17q21.31 microdeletion syndrome. We estimate the prevalence of the syndrome to be 1 in 16,000 and show that it is highly underdiagnosed. Extensive clinical examination, reveals that developmental delay, hypotonia, facial dysmorphisms including a long face, a tubular or pear-shaped nose and a bulbous nasal tip, and a friendly/amiable behavior are the most characteristic features. Other clinically important features include epilepsy, heart defects (ASD, VSD), and kidney/ urologic anomalies. Using high-resolution oligonucleotide arrays, we narrow the 17q21.31 critical region to a 424-kb genomic segment (chr17: 41046729-41470954, hg17), encompassing at least six genes, among which the gene encoding microtubule-associated protein tau (MAPT). Mutation screening of MAPT in 122 individuals with a phenotype suggestive of 17q21.31 deletion carriers, but who do not carry the recurrent deletion, failed to identify any disease-associated variants. In five deletion carriers, we identify a <500-bp rearrangement hotspot at the proximal breakpoint contained within an L2 LINE motif and show that in every case examined, the parent originating the deletion carries a common 900-kb 17q21.31 inversion polymorphism, indicating that this inversion is a necessary factor for deletion to occur (p<10-5). Our data establishes the 17q21.31 microdeletion syndrome as a clinically and molecularly well recognizable genomic disorder