Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019270 (hernia)
 15,856 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study examines the relationship between the migration of mesenchyme and associated cutaneous nerves that are involved in the closure of the anterior body wall in embryonic mice and rats by light and electron microscopy. The sternum is formed by the migration of condensations of mesenchyme originating in the dorsolateral body wall known as sternal bands. In the course of analyzing this process in rodent embryos we have identified similar paired caudal extensions of the sternal bands that are responsible for the closure of the abdominal wall following resolution of the umbilical hernia, and we suggest these bands of mesoderm should be referred to as the abdominal bands. Both the sternal and abdominal bands are associated with the development of the segmental spinal nerves and their cutaneous terminal branches. The first cutaneous nerve to reach the skin surface in rats is the later cutaneous nerve (PCN and ACN) at E13.5 days. The ACN co-migrates with the sternal and abdominal bands, and terminal branches of axons from the ACN approach the epidermis during this migration. Differentiation of the epidermis could be recognized as a change in shape of epidermal cells from squamous to cuboidal, and this initial differentiation coincides with the onset of cutaneous innervation, beginning at the site of the LCN and following the extent of innervation of the PCN as well as the migration of the mesodermal bands and associated ACN. The paired ACN's meet in the ventral midline at E16.5 in rats as the sternal bands fuse, and terminal axons from both nerves densely innervate the midline skin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differentiation of the anterior body wall and truncal epidermis and associated co-migration of cutaneous nerves and mesenchyme. 183 19

Nitrofen induces in rats diaphragmatic hernia (CDH) with heart and lung hypoplasia by a mechanism involving oxidation. The aim of this study was to examine if prenatal administration of the anti-oxidant agent vitamin E (VitE) prevents to some extent heart and lung hypoplasia. Pregnant rats received on E9.5 either 100 mg of nitrofen alone or followed by 150 IU of VitE on E16.5-E20.5. Control animals received either vehicle or VitE alone. The fetuses were recovered on E21. The hearts and lungs were weighed and DNA and proteins were measured. Sections of the heart and lung were immunohistochemically stained for ki-67, Tunel and TTF-1, and the proportions of proliferating, apoptotic and TTF-1-expressing cells were determined. Cultured human pneumocytes were exposed to the same agents and similarly processed. TTF-1 expression and the proportion of proliferating cells were quantitated. The ANOVA or Kruskall-Wallis tests were used for comparison with p<0.05 as threshold of significance. Nitrofen-exposed rats had decreased lung and heart weight/body weight ratios, lung and heart DNA and protein, lung TTF-1 expression and proportion of proliferating cells in lung and heart. Additional treatment with VitE ameliorated these decreases except for lung TTF-1 and heart weight. In cultured pneumocytes, TTF-1 expression was decreased by nitrofen and rescued by VitE. Cell proliferation followed the same pattern. Antioxidant VitE partially reverses the effects of nitrofen on the heart and lungs of exposed rats. The same effects are observed in cultured human pneumocytes. These results further substantiate the oxidative nature of the effects of nitrofen and suggest that anti-oxidant agents could have a potential clinical application.
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PMID:Prenatal vitamin E improves lung and heart hypoplasia in experimental diaphragmatic [correction of diaphragamatic] hernia. 1289 60

Congenital diaphragmatic hernia (CDH) is a common (1 in 3,000 live births) major congenital malformation that results in significant morbidity and mortality. The discovery of CDH loci using standard genetic approaches has been hindered by its genetic heterogeneity. We hypothesized that gene expression profiling of developing embryonic diaphragms would help identify genes likely to be associated with diaphragm defects. We generated a time series of whole-transcriptome expression profiles from laser captured embryonic mouse diaphragms at embryonic day (E)11.5 and E12.5 when experimental perturbations lead to CDH phenotypes, and E16.5 when the diaphragm is fully formed. Gene sets defining biologically relevant pathways and temporal expression trends were identified by using a series of bioinformatic algorithms. These developmental sets were then compared with a manually curated list of genes previously shown to cause diaphragm defects in humans and in mouse models. Our integrative filtering strategy identified 27 candidates for CDH. We examined the diaphragms of knockout mice for one of the candidate genes, pre-B-cell leukemia transcription factor 1 (Pbx1), and identified a range of previously undetected diaphragmatic defects. Our study demonstrates the utility of genetic characterization of normal development as an integral part of a disease gene identification and prioritization strategy for CDH, an approach that can be extended to other diseases and developmental anomalies.
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PMID:Congenital diaphragmatic hernia candidate genes derived from embryonic transcriptomes. 2231 23