Current factors affecting feeder cattle pricing in Kansas and Missouri cattle markets

Today’s tough economic environment for cattle producers makes each decision critically important, and increased knowledge of the link between pricing and genetic, management, and marketing decisions can increase an operation’s sustainability and profitability. Cow-calf producers and cattle feeders have long been interested in the impact of various physical and market characteristics on feeder cattle and calf prices. As demonstrated in many previous studies, significant relationships exist between feeder cattle prices and their physical and market characteristics. Weight, lot size, health, condition, fill, muscling, frame size, breed, time of sale, and horn status significantly affect feeder cattle auction prices. Historically, significant premiums and discounts have been associated with these particular feeder cattle physical characteristics. The purpose of this study was to gain knowledge of the current link between market pricing and genetic, management, and marketing decisions. Findings from this research will provide updated information regarding how the myriad of industry changes since the 1980s and 1990s has affected the characteristics that influence feeder cattle and calf prices

MN1 C-terminal truncation syndrome is a novel neurodevelopmental and craniofacial disorder with partial rhombencephalosynapsis

Contains fulltext : 218289.pdf (Publisher’s version ) (Closed access)MN1 encodes a transcriptional co-regulator without homology to other proteins, previously implicated in acute myeloid leukaemia and development of the palate. Large deletions encompassing MN1 have been reported in individuals with variable neurodevelopmental anomalies and non-specific facial features. We identified a cluster of de novo truncating mutations in MN1 in a cohort of 23 individuals with strikingly similar dysmorphic facial features, especially midface hypoplasia, and intellectual disability with severe expressive language delay. Imaging revealed an atypical form of rhombencephalosynapsis, a distinctive brain malformation characterized by partial or complete loss of the cerebellar vermis with fusion of the cerebellar hemispheres, in 8/10 individuals. Rhombencephalosynapsis has no previously known definitive genetic or environmental causes. Other frequent features included perisylvian polymicrogyria, abnormal posterior clinoid processes and persistent trigeminal artery. MN1 is encoded by only two exons. All mutations, including the recurrent variant p.Arg1295* observed in 8/21 probands, fall in the terminal exon or the extreme 3' region of exon 1, and are therefore predicted to result in escape from nonsense-mediated mRNA decay. This was confirmed in fibroblasts from three individuals. We propose that the condition described here, MN1 C-terminal truncation (MCTT) syndrome, is not due to MN1 haploinsufficiency but rather is the result of dominantly acting C-terminally truncated MN1 protein. Our data show that MN1 plays a critical role in human craniofacial and brain development, and opens the door to understanding the biological mechanisms underlying rhombencephalosynapsis