Effects of hydrogenated fat-spray-coated ß-carotene supplement on plasma ß-carotene concentration and conception rate after embryo transfer in Hanwoo beef cows.

We hypothesised that hydrogenated fat (HF)-spray-coated ß-carotene (ßC) supplement could be used to increase plasma ßC concentration and conception rates after embryo transfer (ET) in Hanwoo beef cows. In Experiment 1, 12 multiparous Hanwoo cows were fed one of four experimental diets in a triplicate 4 × 4 Latin square design for a 28-day period. Treatments included no ßC addition (control), HF-uncoated ßC (HFußC), HF-spray-coated ßC (HFßC), and HF-spray-coated ßC and vitamin A (HFßCA). The cows under ßC-supplemented treatments were fed 400 mg/day of ßC, and a daily intake for vitamin A of HFßCA treatment was 30 000 IU/day as retinyl acetate. Blood was collected on days 0, 26, 27, and 28 to analyse ßC and other metabolite concentrations. In Experiment 2, 199 Hanwoo cows with low fertility were randomly assigned to either control (n = 99) or HFßC treatments (n = 100) based on the results of Experiment 1. The oestrus of the cows was synchronised for ET. The HFßC group was fed from 4 weeks before to 4 weeks after ET with a daily intake of 400 mg ßC. Pregnancy for conception rates was diagnosed on day 60 after ET, and blood was collected for ßC concentrations on the day before ET. Supplementing ßC resulted in a high plasma ßC concentration (P < 0.001). Supplementing HFßC or HFßCA resulted in higher ßC concentrations than HFußC (P < 0.001); however, there was no difference between HFßC and HFßCA groups. Plasma retinol concentration was lower in the HFßCA treatment than in the control and HFßC groups (P < 0.05). Blood metabolites were unaffected by the treatments. The retinol:ßC ratio was lower in the ßC-supplemented treatments than in the controls, and was lower in HFßC and HFßCA than in HFußC groups (P < 0.001). Plasma ßC concentration was positively correlated with plasma high-density lipoprotein, low-density lipoprotein, and total cholesterol (P < 0.05). Plasma retinol concentration was negatively associated with plasma protein (P < 0.01), but positively associated with plasma creatinine (P < 0.001) and urea (P < 0.01). Supplementing HFßC to low-fertility cows resulted in higher plasma ßC concentration (P < 0.001) and conception rates (P = 0.024) than those in the controls. In conclusion, HFßC had a better bioavailability than HFußC, and an increase in conception rates by supplementing HFßC may be beneficial for producing more calves given the low pregnancy rates of bovine ET in Korea.

Muscle fiber type disproportion with an autosomal dominant inheritance.

Congenital muscle fiber type disproportion (CFTD) has been described as a form of congenital myopathy characterized by the smallness and marked predominance of type 1 fibers in a muscle biopsy. Clinical manifestations include hypotonia, nonprogressive muscle weakness, joint contractures, and skeletal deformities. However, it has also been noted that the same pathologic alterations appeared in clinically diverse conditions. Recently, we experienced a family, a mother and two children, in which a muscle biopsy showed the mother to have muscle fiber type disproportion. This case was unusual in that there was a significant progression of weakness, an absence of neonatal hypotonia, and other commonly associated musculo-skeletal deformities. In this report, we describe the clinicopathologic features of the family with a brief review about muscle fiber type disproportion.

Delayed movement disorders after carbon monoxide poisoning.

Of 242 patients with carbon monoxide (CO) poisoning examined between 1986 and 1996, delayed movement disorders were diagnosed in 32 (13. 2%). There were 15 men and 17 women. Ages at insult ranged from 9 to 69 years (mean 45.3 years). Of the 32 patients with delayed movement disorders, 23 (71.9%) had parkinsonism, 5 dystonia, 3 chorea and 1 myoclonus. All were associated with delayed CO encephalopathy. The median latency between CO poisoning and the onset of movement disorders was 4 weeks for parkinsonism, 51 weeks for dystonia, 4 weeks for chorea and 8 weeks for myoclonus. The latency of dystonia onset after CO poisoning was longer than that of other types of movement disorders. The CT findings in delayed movement disorders after CO poisoning were variable, and there was no correlation between the sites of imaging and the development of movement disorders. Abnormal dyskinesias disappeared within 8 weeks, and patients recovered from parkinsonism within 6 months. In conclusion, delayed movement disorders after CO poisoning are not rare, and usually appear as a part of delayed CO encephalopathy. The prognosis is good.