Project description:Purpose: The goal of this study is to determine what genes are expressed, and at what level, in the developing diaphragm at a timepoint shown to be critical in the initiation of congenital diaphragmatic hernias in mice. Methods: PPFs were dissected from staged mouse embryos Methods: summary Purpose: The goal of this study is to determine what genes are expressed, and at what level, in the developing diaphragm at a timepoint shown to be critical in the initiation of congenital diaphragmatic hernias in mice. Methods: PPFs were dissected from staged mouse embryos
Project description:8 week old rats injected with streptozotocin or buffer alone at age of 8 weeks, diaphragm muscle obtained at age of 12 weeks (thus animals were diabetic for 4 weeks) Keywords: Disease state analysis (diabetes)
Project description:Mechanical ventilation contributes to diaphragm atrophy and muscle weakness, which is referred to as ventilator-induced diaphragmatic dysfunction (VIDD).Through snRNA seq, we demonstrated that diaphragm fibrosis resulting from FAP proliferation, EMT, immune cell infiltration, and diaphragm atrophy which are induced by phrenic nerve ending loss are the underlying causes of VIDD.
Project description:We sequenced more than 13000 cells of the pleuroperitoneal folds of a mouse embryo to better understand the mosaic nature of the developing diaphragm. We identified 18 different clusters, and 10 unique cell types. Through our analysis, we were able to determine that most of the developing diaphragm is comprised of mesenchymal cells, and that genes necessary for proper diaphragm development are expressed in these types of cells. These observations provide a strong basis for furhter studies about the development and physiology of the diaphragm.
Project description:Comparison of gene expression of heart (left vent) and diaphragm of normal Sprague Dawley rats, young adult Keywords: Cell type comparison
Project description:Interventions: R:PEEP=0;F:PEEP=5;P:Individualized PEEP
Primary outcome(s): Diaphragm mobility;End expiratory diaphragm thickness;Diaphragm thickness at the end of inspiration;Change rate of diaphragm thickness;Postoperative diaphragmatic dysfunction
Study Design: Parallel
Project description:Proteomic analysis of diaphragm tissue from rats subjected to chronic heart failure. Redox sensitive Cysteine residues from both adult and old diaphragm tissues examined
Project description:Type 2 diabetes differs from type 1 diabetes in its pathogenesis. Type 1 diabetic diaphragm has altered gene expression which includes lipid and carbohydrate metabolism, ubiquitination and oxidoreductase activity. The objectives of the present study were to assess respiratory muscle gene expression changes in type 2 diabetes and to determine whether they are greater for the diaphragm than an upper airway muscle. Diaphragm and sternohyoid muscle from Zucker diabetic fatty (ZDF) rats were analyzed with Affymetrix gene expression arrays. The two muscles had 97 and 102 genes, respectively, with at least ±1.5-fold significantly changed expression with diabetes, and these were assigned to gene ontology groups based on over-representation analysis. Several significantly changed groups were common to both muscles, including lipid metabolism, carbohydrate metabolism, muscle contraction, ion transport and collagen, although the number of genes and the specific genes involved differed considerably for the two muscles. In both muscles there was a shift in metabolism gene expression from carbohydrate metabolism toward lipid metabolism, but the shift was greater and involved more genes in diabetic diaphragm than diabetic sternohyoid muscle. Groups present in only diaphragm were blood circulation and oxidoreductase activity. Groups present in only sternohyoid were immune & inflammation and response to stress & wounding, with complement genes being a prominent component. In conclusion, type 2 diabetes-induced gene expression changes in respiratory muscles has both similarities and differences relative to previous data on type 1 diabetes gene expression. Furthermore, the diabetic alterations in gene expression differ between diaphragm and sternohyoid.
Project description:Embryonic mouse diaphragm is a primary model for studying myogenesis and neuro-muscular synaptogenesis, both of which represent processes regulated by spatially organized genetic programs of myonuclei located in distinct myodomains. However, a spatial gene expression pattern of embryonic mouse diaphragm has not been reported. Here we provide spatially resolved gene expression data for horizontally sectioned embryonic mouse diaphragms at E14.5 and E18.5. These data reveal gene signatures for specific muscle regions with distinct maturity and fiber type composition, as well as for a central neuromuscular junction and a peripheral myotendinous junction compartments. Comparing spatial expression patterns of wild type mice with those of mouse mutants lacking either the skeletal muscle calcium channel CaV1.1 or b-catenin, reveals curtailed muscle development and dysregulated expression of genes potentially involved in NMJ formation. Altogether, these datasets provide a powerful recourse for further studies of muscle development and NMJ formation in the mouse embryo.