Background: L-Lactate has been used as a prognostic indicator for ill humans and animals. A portable analyzer that measures L-lactate could help veterinarians decide to proceed with correction of a displaced abomasum.Hypotheses: The likelihood of a dairy cow with a displaced abomasum remaining in the herd can be predicted by lactate concentration and other variables.Animals: Thirty-four healthy early-lactation dairy cows, and 131 cows with abomasal displacements (DA) presented to Cornell University, Ithaca, NY.Methods: Plasma L-lactate was measured using a commercial analyzer (i-STAT). A cow had a positive outcome (PO) if she remained in the herd 30 days after surgical correction of the displaced abomasum and a negative outcome (NO) if she was culled or died in that time. A multivariable model with physical examination and clinicopathologic variables for predicting NO for cows with right-sided abomasal displacements was constructed.Results: The median plasma L-lactate was 0.54 mM/L (interquartile range, 0.42-0.74) in healthy lactating Holstein cows. In cows with right-sided displaced abomasa, median plasma L-lactate concentrations were higher in cows with NO (5.88 mM/L) versus PO (3.23 mM/L) (P 5 .002). In a multivariable model, which identified chloride, heart rate, and L-lactate as the best fitting variables for cows with right-sided displacements, the probability of NO increased as L-lactate increased.Conclusions and Clinical Importance: Plasma L-lactate concentration might be a useful predictor of productive outcomes in cows with right-sided abomasal disorders.

No abstract

No abstract

Confirming the expression of TLRs in equine ocular tissues is an initial step in identifying how they play a role in infectious keratitis, particularly fungal. The results further support the use of equine ocular tissues as a model for human fungal keratitis. Studies of the TLR expression together with their cytokine profile induced during equine fungal keratitis may help further clarify the pathogenesis of the disease and possibly lead to the development of new treatment protocols for both equines and humans.

Dlx3, a homeodomain transcription factor, is essential for placental development in the mouse. The Dlx3(-/-) mouse embryo dies at embryonic d 9.5-10 putatively due to placental failure. To develop a more comprehensive understanding of the gene profile regulated by Dlx3, microarray analysis was used to determine differences in gene expression within the placenta of Dlx3(+/+) and Dlx3(-/-) mice. Array analysis revealed differential expression of 401 genes, 33 genes in which signal to log ratio values of null/wild-type were lower than -0.5 or higher than 0.5. To corroborate these findings, quantitative real-time PCR was used to confirm differential expression for 11 genes, nine of which displayed reduced expression and two with enhanced expression in the Dlx3(-/-) mouse. Loss of Dlx3 resulted in a marked reduction (>60%) in mRNA expression of placental growth factor (Pgf), a member of the vascular endothelial growth factor family. Consistent with these results, Pgf secretion from placental explants tended to be reduced in the Dlx3(-/-) mice, compared with wild type. To investigate mechanisms of Dlx3 regulation of Pgf gene transcription, we cloned 5.2 kb of the Pgf 5' flanking sequence for use in reporter gene assays. Expression of the Pgf promoter luciferase reporter containing at least three Dlx3 binding sites was increased markedly by overexpression of Dlx3 supporting the conclusion that Dlx3 may have a direct effect on Pgf promoter activity. These studies provide a novel view of the transcriptome regulated by Dlx3 in mouse placenta. Dlx3 is specifically required for full expression and secretion of Pgf in vivo. Moreover, in vitro studies support the conclusion that Dlx3 is sufficient to directly modulate expression of the Pgf gene promoter in placental cells.