Development of the Entorhinal Cortex Occurs via Parallel Lamination During Neurogenesis.

The entorhinal cortex (EC) is the spatial processing center of the brain and structurally is an interface between the three layered paleocortex and six layered neocortex, known as the periarchicortex. Limited studies indicate peculiarities in the formation of the EC such as early emergence of cells in layers (L) II and late deposition of LIII, as well as divergence in the timing of maturation of cell types in the superficial layers. In this study, we examine developmental events in the entorhinal cortex using an understudied model in neuroanatomy and development, the pig and supplement the research with BrdU labeling in the developing mouse EC. We determine the pig serves as an excellent anatomical model for studying human neurogenesis, given its long gestational length, presence of a moderate sized outer subventricular zone and early cessation of neurogenesis during gestation. Immunohistochemistry identified prominent clusters of OLIG2+ oligoprogenitor-like cells in the superficial layers of the lateral EC (LEC) that are sparser in the medial EC (MEC). These are first detected in the subplate during the early second trimester. MRI analyses reveal an acceleration of EC growth at the end of the second trimester. BrdU labeling of the developing MEC, shows the deeper layers form first and prior to the superficial layers, but the LV/VI emerges in parallel and the LII/III emerges later, but also in parallel. We coin this lamination pattern parallel lamination. The early born Reln+ stellate cells in the superficial layers express the classic LV marker, Bcl11b (Ctip2) and arise from a common progenitor that forms the late deep layer LV neurons. In summary, we characterize the developing EC in a novel animal model and outline in detail the formation of the EC. We further provide insight into how the periarchicortex forms in the brain, which differs remarkably to the inside-out lamination of the neocortex.

Risk factors for gastric ulceration in nursery pigs.

Pars oesophageal gastric ulceration is a prevalent condition in swine production and often observed in finisher pigs at slaughter, with reported prevalence ranging from 32 % to 65 %. Although feeding practices in nursery and finisher pigs are similar, little is known about the prevalence and risk factors associated with this condition in nursery pigs. This prospective cohort study aimed to identify risk factors for gastric ulceration in nursery pigs. The objectives were: (1) to estimate the association of inherent pig characteristics (birth weight, sex, parity of sow, litter size, and pen fouling behavior) and management characteristics (antibiotic treatment during suckling and post weaning, piglet rotation during lactation, weaning age and weight) with pars oesophageal lesions; (2) to assess differences in gastric dry matter content, pH, and percentage of solid particles in the sediment in relation to pars oesophageal lesions. A total of 58 piglets tracked from birth to 20 days of age and 210 nursery pigs from birth to 10 weeks of age were euthanized and assessed for pars oesophageal gastric lesions. All nursery pigs were fed finely ground pelleted feed ad libitum. Based on a macroscopic assessment, the pigs' stomachs were categorized as either LPO "lesions in the Pars oesophagea" or NLPO "no lesions in the Pars oesophagea". We observed an overall prevalence of 26.2 % (CI 95 % 0.67 - 0.79) for LPO in nursery pigs at 10 weeks of age, while no lesion were observed in piglets at 20 days of age. A mixed multivariable logistic regression model showed that piglets with a birthweight ≤ 1.11 kg had a 2.11 times higher odds of LPO (CI 95 % 1.02-4.37, p = 0.04) than their heavier counterparts. There was a weak association of LPO in nursery pigs from pens with pen fouling with a 2.14 times higher odds (CI 95 % 0.97-4.72 p = 0.05). Nursery pigs with LPO presented an increased gastric content fluidity with a reduced (p ≤ 0.01) gastric dry matter content (18.7 %), solid phase (74.7 %), and pH (3.22) compared to NLPO nursery pigs (20.5 %, 85.09 %, 3.56, respectively). We have demonstrated that LPO are present in nursery pigs as early as 10 weeks of age. We observed that low birth weight is associated with higher odds for LPO in nursery pigs. These observations might help explain differences between individual pigs in terms of LPO development when groups are exposed to similar environments, management, and feeding conditions.

Association between gastric content fluidity and pars oesophageal ulcers in nursery pigs: a cross-sectional study of high-risk Danish herds using commercial feed.

BACKGROUND: The objective of this cross-sectional study was to assess the within-herd prevalence of pars oesophageal ulcers (POU) in high-risk Danish herds using commercial diets. Furthermore, we aimed to estimate the association between gastric content fluidity and POU using a generalised additive model (GAM). The study included 200 clinically healthy nursery pigs randomly selected from ten farms (20 pigs from each farm). The 10 farms were selected based on a suspected high prevalence of gastric ulcers. Post-mortem gastric ulcer assessment was based on macroscopic lesions, and gastric content fluidity was assessed based on the solid particle sedimentation percentage (solid phase). RESULTS: We observed an overall prevalence of 35.5% for POU in nursery pigs. Within-herd prevalence varied considerably among farms, with values ranging from 0% in Farm 1 to 84% in Farm 4. Our model showed strong associations between POU and gastric content fluidity (P < 0.001), as well as between POU and farm of origin (P < 0.001). In addition, we observed that the risk of POU decreased non-linearly as the gastric content solid phase percentage increased, i.e. as the gastric content became more solid. CONCLUSION: We have demonstrated that pars oesophageal ulcers are present in Danish herds with nursery pigs fed commercial diets. Furthermore, we have established that gastric content fluidity is strongly associated with POU in nursery pigs. Even so, we cannot conclude that gastric content fluidity is solely responsible for POU. Future research should look into the association between pars oesophageal ulcers and both farm management activities and individual pig factors.