Search

This study described the developmental and behavioral characteristics of children identified with idiopathic sensory processing disorder (SPD) as well as the relations among specific types of SPD as proposed by the nosology presented by Miller et al. (2007), adaptive behavior profiles, and behaviors associated with mental functioning. A retrospective, non-experimental design applying descriptive and correlational analyses was used. Data were obtained from clinic medical records of 78 children ages 2 to 7 years who were identified with sensory processing problems affecting daily life, but who did not meet criteria for any other neurodevelopmental or mental disorders following a comprehensive diagnostic evaluation. Results revealed that all SPD types as described by current typologies were well represented with the most common being the over-responsivity sensory modulation subtype. Within the sample, 53% of the children displayed more than one SPD type. Atypical externalizing and internalizing behavior scores associated with various mental disorders as measured by the child behavior checklist (CBCL) fell in the borderline dysfunctional range. Adaptive behavior for all developmental domains was below average, and the severity of SPD symptoms moderately and positively correlated with behaviors associated with mental disorders, and with lower adaptive behavior performance. It was concluded that symptoms characteristic of the various types of idiopathic SPD overlap substantially suggesting that current typologies may include more types/subtypes than are necessary or clinically useful. Children with SPD share similar, but often less severe pathological behaviors associated with other mental or related neurodevelopmental disorders. Psychometrically sound measures of SPD are needed, and further study of the neural mechanisms involved in sensory processing deficits is vital for validating idiopathic SPD as its own diagnostic entity. [ABSTRACT FROM AUTHOR]

The equine hoof inner epithelium is folded into primary and secondary epidermal lamellae which increase the dermo-epidermal junction surface area of the hoof and can be affected by laminitis, a common disease of equids. Two keratin proteins (K), K42 and K124, are the most abundant keratins in the hoof lamellar tissue of Equus caballus. We hypothesize that these keratins are lamellar tissue-specific and could serve as differentiation- and disease-specific markers. Our objective was to characterize the expression of K42 and K124 in equine stratified epithelia and to generate monoclonal antibodies against K42 and K124. By RT-PCR analysis, keratin gene (KRT) KRT42 and KRT124 expression was present in lamellar tissue, but not cornea, haired skin, or hoof coronet. In situ hybridization studies showed that KRT124 localized to the suprabasal and, to a lesser extent, basal cells of the lamellae, was absent from haired skin and hoof coronet, and abruptly transitions from KRT124-negative coronet to KRT124-positive proximal lamellae. A monoclonal antibody generated against full-length recombinant equine K42 detected a lamellar keratin of the appropriate size, but also cross-reacted with other epidermal keratins. Three monoclonal antibodies generated against N- and C-terminal K124 peptides detected a band of the appropriate size in lamellar tissue and did not cross-react with proteins from haired skin, corneal limbus, hoof coronet, tongue, glabrous skin, oral mucosa, or chestnut on immunoblots. K124 localized to lamellar cells by indirect immunofluorescence. This is the first study to demonstrate the localization and expression of a hoof lamellar-specific keratin, K124, and to validate anti-K124 monoclonal antibodies. [ABSTRACT FROM AUTHOR]

[Display omitted] The euglycemic hyperinsulinemic clamp model (EHC) of equine endocrinopathic laminitis induces rapid loss of lamellar tissue integrity, disrupts keratinocyte functions, and induces inflammation similar to natural disease. Continuous digital hypothermia (CDH) blocks tissue damage in this experimental model, allowing identification of specific genes or molecular pathways contributing to disease initiation or early progression. Archived lamellar tissues (8 horses, 48 h EHC treatment, including CDH-treated front limbs) were used to measure relative expression levels of genes encoding keratin 17 (KRT17), a stress-induced intermediate filament protein, and genes upregulated downstream of keratin 17 and/or interleukin 17A (IL-17A), as mediators of inflammation. Compared to front or hind limbs at ambient temperature, CDH resulted in significantly lower expression of KRT17 , CCL2 , CxCL8 , PTGS2 (encoding COX2), IL6 , TNFα , S100A8 and MMP1. By immunofluorescence, COX2 was robustly expressed in lamellar keratinocytes from ambient limbs, but not in CDH-treated limbs. Genes not significantly reduced by CDH were IL17A , DEFB4B , S100A9 and MMP9. Overall, 8 of 12 genes were expressed at lower levels in the CDH-treated limb. These 8 genes are expressed by wounded or stress-activated keratinocytes in human disease or mouse models, highlighting the role of keratinocytes in equine laminitis. [ABSTRACT FROM AUTHOR]