Myosin heavy chain profiles and body composition are different in old versus young Standardbred mares

There are limited data on age-related changes in body composition or skeletal muscle in the horse. Therefore, the purpose of this study was to investigate any differences in muscle myosin heavy chain (MHC) and body composition associated with aging. Twenty-three young (4-8 years) and eight old (20+ years) unfit Standardbred mares were evaluated. Rump fat thickness was measured using B-mode ultrasound and per cent body fat (% fat) was calculated. Needle muscle biopsies were obtained from right gluteus medius muscle. MHC composition was determined via sodium dodecyl sulphate-polyacrylamide gel electrophoresis. Three MHC isoforms were subsequently identified as type I, type IIA, and type IIX and quantified using a scanning and densometric system. There were no significant differences (p>0.05) between old and young mares in fat (%) (19.0+/-6.4 vs 20.5+/-5.4), fat mass (kg) (102.3+/-39.9 vs 106.9+/-37.1), or body weight (kg) (529.4+/-34.9 vs 512.7+/-57.7). However, the old mares had significantly (p<0.05) greater lean body mass than the young mares (427.1+/-24.5 vs 405.7+/-37.9). Aged mares had significantly (p<0.05) less type I (7.8+/-2.9% vs 12.1+/-4.4%) and IIA (27.8+/-7.1% vs 36.1+/-9.5%) fibres than the young group but more type IIX (64.6+/-4.7% vs 51.8+/-11.1%). The MHC data are consistent with the age-related changes seen in other species.     

Measurement of genetic and environmental variation in barley (Hordeum vulgare) grain hardness

In this study, we assessed a broad range of barley breeding lines and commercial varieties by three hardness methods (two particle size methods and one crush resistance method (SKCS—Single-Kernel Characterization System), grown at multiple sites to see if there was variation in barley hardness and if that variation was genetic or environmentally controlled. We also developed near-infrared reflectance (NIR) calibrations for these three hardness methods to ascertain if NIR technology was suitable for rapid screening of breeding lines or specific populations. In addition, we used this data to identify genetic regions that may be associated with hardness. There were significant (p<0.05) genetic effects for the three hardness methods. There were also environmental effects, possibly linked to the effect of protein on hardness, i.e. increasing protein resulted in harder grain. Heritability values were calculated at >85% for all methods. The NIR calibrations, with R² values of >90%, had Standard Error of Prediction values of 0.90, 72 and 4.0, respectively, for the three hardness methods. These equations were used to predict hardness values of a mapping population which resulted in genetic markers being identified on all chromosomes but chromosomes 2H, 3H, 5H, 6H and 7H had markers with significant LOD scores. The two regions on 5H were on the distal end of both the long and short arms. The region that showed significant LOD score was on the long arm. However, the region on the short arm associated with the hardness (hordoindoline) genes did not have significant LOD scores. The results indicate that barley hardness is influenced by both genotype and environment and that the trait is heritable, which would allow breeders to develop very hard or soft varieties if required. In addition, NIR was shown to be a reliable tool for screening for hardness. While the data set used in this study has a relatively low variation in hardness, the tools developed could be applied to breeding populations that have large variation in barley grain hardness.     

Ciguatera Fish Poisoning: Treatment,Prevention and Management

Ciguatera Fish Poisoning (CFP) is the most frequently reported seafood-toxin illness in the world, and it causes substantial physical and functional impact. It produces a myriad of gastrointestinal, neurologic and/or cardiovascular symptoms which last days to weeks, or even months. Although there are reports of symptom amelioration with some interventions (e.g. IV mannitol), the appropriate treatment for CFP remains unclear to many physicians. We review the literature on the treatments for CFP, including randomized controlled studies and anecdotal reports. The article is intended to clarify treatment options, and provide information about management and prevention of CFP, for emergency room physicians, poison control information providers, other health care providers, and patients.     

White fat progenitor cells reside in the adipose vasculature

White adipose (fat) tissues regulate metabolism, reproduction, and life span. Adipocytes form throughout life, with the most marked expansion of the lineage occurring during the postnatal period. Adipocytes develop in coordination with the vasculature, but the identity and location of white adipocyte progenitor cells in vivo are unknown. We used genetically marked mice to isolate proliferating and renewing adipogenic progenitors. We found that most adipocytes descend from a pool of these proliferating progenitors that are already committed, either prenatally or early in postnatal life. These progenitors reside in the mural cell compartment of the adipose vasculature, but not in the vasculature of other tissues. Thus, the adipose vasculature appears to function as a progenitor niche and may provide signals for adipocyte development.