Anti-Actin monoclonal antibody, clone IIG36

The aim of this study was to determine the changes of the biomarkers used for the diagnosis of necrotising enterocolitis of human neonates in premature calves with respiratory distress syndrome (RDS). Novel biomarkers including the intestinal fatty acid binding protein (IFABP), the liver-type FABP (LFABP), trefoil factor-3 (TFF3), actin gamma 2 smooth muscle (ACTG2), and Claudin-3 were investigated using bovine specific ELISA kits. Thirty premature calves with respiratory distress syndrome (the RDS group), seven premature calves without RDS (the non-RDS group), and seven healthy calves (control) were included in the study. Blood samples from all the groups were taken at 0 and 48 h for the blood gas and biomarker measurement. It was determined that IFABP (P < 0.05), LFABP (P < 0.05), TFF3 (P < 0.05), ACTG2 (P < 0.05), and Claudin-3 (P < 0.05) in the control group were significantly higher than those in the RDS and non-RDS groups at 0 hour. The LFABP and Claudin-3 concentrations in the control group were statistically higher (P < 0.05) than those in the RDS and non-RDS groups at 48 h, whereas the ACTG2 and TFF3 contents were significantly higher (P < 0.05) than the non-RDS group. A significant increase in the contents of IFABP (P <= 0.01), LFABP (P < 0.05), TFF3 (P < 0.05), ACTG2 (P < 0.05) at 48 h was detected in the RDS group only. In conclusion, the changes in the biomarkers support the suspicion of intestinal damage such as necrotising enterocolitis (NEC) after enteral feeding in premature calves with RDS. Intestinal damage biomarkers such as IFABP, LFABP, TFF3, and ACTG2 may be useful in the diagnosis of intestinal damage in premature calves. These results also indicate that the plasma concentrations of the intestinal biomarkers change in new born calves with their gestational age.

IntroductionVisceral myopathies remain difficult and frustrating clinical entities, a distinctive form of acquired degenerative visceral myopathy, African degenerative leiomyopathy, a myogenic functional intestinal obstruction without aganglionosis which affects smooth muscle of the intestine, in young indigenous African children. The Actin G2 gene is the main gene encoding smooth muscle actin found in enteric tissues. Recent research has identified Actin G2 alpha gene variation as an important causative biomarker in visceral myopathies and megacystis microcolon. This study of the Actin G2 gene (ACTG2) in an African population explores a possible molecular basis abnormal muscle function in a visceral myopathy.Patients and methodsFollowing ethical permission and informed consent, DNA was extracted from whole blood samples in five patients with histologically proven African degenerative leiomyopathy. PCR amplification of ACTG2 alpha gene products by semi-automated bi-directional sequencing analysis. Results were analysed using FinchTV Sequence Alignment Software and predicting bioinformatic investigation by PolyPhen 2 software.ResultsFive new patients with the ADL phenotypes were prospectively investigated for variation in the Actin G2 gamma gene (ACTG2). ACTG2 gene variation occurred in exon 5 (c.463 A>G K119R), in three (60%). In addition, intronic variation t>c-IVS3 was identified in three with the K119 mutation plus further g > c -IVS12 and t>c+IVS16(2), suggesting a possible haplotype. Bioinformatic modelling showed that these ACTG2 gene variations are highly non-conservative altering protein expression.ConclusionsRecurrent Actin G2 smooth muscle gene variation in African degenerative visceral leiomyopathy is associated with abnormal muscle actin development.