Systems genetic analysis of binge-like eating in a C57BL/6J x DBA/2J-F2 cross

Binge eating is a heritable trait associated with eating disorders and refers to the rapid consumption of a large quantity of energy-dense food that is, associated with loss of control and negative affect. Binge eating disorder is the most common eating disorder in the United States; however, the genetic basis is unknown. We previously identified robust mouse inbred strain differences between C57BL/6J and DBA/2J in binge-like eating of sweetened palatable food in an intermittent access, conditioned place preference paradigm. To map the genetic basis of changes in body weight and binge-like eating (BLE) and to identify candidate genes, we conducted quantitative trait locus (QTL) analysis in 128 C57BL/6J x DBA/2J-F2 mice combined with PheQTL and trait covariance analysis in GeneNetwork2 using legacy BXD-RI trait datasets. We identified a QTL on Chromosome 18 influencing changes in body weight across days in females (log of the odds [LOD] = 6.3; 1.5-LOD: 3–12 cM) that contains the candidate gene Zeb1. We also identified a sex-combined QTL influencing initial palatable food intake on Chromosome 5 (LOD = 5.8; 1.5-LOD: 21–28 cM) that contains the candidate gene Lcorl and a second QTL influencing escalated palatable food intake on Chromosome 6 in males (LOD = 5.4; 1.5-LOD: 50–59 cM) that contains the candidate genes Adipor2 and Plxnd1. Finally, we identified a suggestive QTL in females for slope of BLE on distal Chromosome 18 (LOD = 4.1; p = 0.055; 1.5-LOD: 23–35 cM). Future studies will use BXD-RI strains to fine map loci and support candidate gene nomination for gene editing.     

Lumbar vertebral morphology and isthmic spondylolysis in a British medieval population

The British medieval population from Wharram Percy, England, has a greater prevalence of isthmic spondylolysis (11.9% of skeletons, 8.5% at the L5 level) than in modern populations (3%–6%). This may in part be due to differences in activity patterns between groups. However, Ward and Latimer (Spine 30 [2005] 1808–1814) proposed that the likelihood of developing and maintaining spondylolytic defects is also influenced by a lack of sufficient increase in mediolateral separation between articular processes in the lowest lumbar segments, given the human lumbar lordosis. Here, we demonstrate that spondylolytic individuals from Wharram Percy tend to have a less pronounced difference between mediolateral facet joint spacing of adjacent segments in the lowest lumbar region than do unaffected individuals, as seen in modern clinical and skeletal populations. These comparisons suggest that regardless of lifestyle, insufficient mediolateral increase in facet spacing predisposes people to spondylolytic defects, and so interfacet spacing patterns may have predictive utility in a clinical context. We also compare the Wharram Percy sample to a modern sample from the Hamann Todd collection with a typically modern prevalence rate. Data do not support the hypothesis that the Wharram Percy individuals had a less pronounced interfacet increase than the Hamann Todd, although they do have narrower lumbar facet spacing at the lowest three levels. Further investigation of anatomical variation underlying population‐specific prevalence rates needs to be conducted. Am J Phys Anthropol 2010. © 2009 Wiley‐Liss, Inc.     

Verminous mastitis in a mare caused by a free-living nematode

Verminous mastitis was the reason for euthanasia of a 22-yr-old Paso Fino mare from Miami, Florida. The etiologic agent was a species of Cephalobus (Rhabditida: Cephalobidae), a genus of soil-inhabiting nematodes that were obviously multiplying in the mammary gland. Only females and larvae were detected in the tissues by histologic section or by teasing the tissue to liberate the worms. At least 12,900 individuals were present per gram of tissue. This is the first case of Cephalobus infecting horses and it indicates that not all histiotropic infections of horses by rhabditoid nematodes are by Halicephalobus deletrix ( = Micronema deletrix).     

Age-related changes in function of transfer ribonucleic acid of rat livers.

Changes in transfer ribonucleic acids during aging could be caused by alterations in regulation or mutation and give rise to slower and less accurate protein synthesis. Rodent liver parenchymal cells, purified from disaggregated livers, do decrease in ability to incorporate labeled amino acids during aging. Moreover, old rodents have a rapidly degraded fraction of liver soluble RNA which is absent from middle-aged animals. In addition, tRNAs purified from old unfractionated liver cannot be acylated as well as from young. High speed supernatant tRNAs from old and young liver are quite similar in acylation capacity. Analysis indicates that a defective subfraction of tRNA may be bound to the ribosomal fraction of the liver cell. Some evidence indicates that base modification levels differ in young and old rodent liver. Shifts in the proportions of lysine and serine isoacceptors during aging are consistent with this idea. One isoacceptor change is an increase in tRNAlys4, which is correlated with cell division capacity in other systems.