18 research outputs found
Pulmonary 18F-FDG uptake helps refine current risk stratification in idiopathic pulmonary fibrosis (IPF)
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A preliminary investigation of the structure of southern Yucca Flat, Massachusetts Mountain, and CP basin, Nevada Test Site, Nevada, based on geophysical modeling.
New gravity and magnetic data collected in the vicinity of Massachusetts Mountain and CP basin (Nevada Test Site, NV) provides a more complex view of the structural relationships present in the vicinity of CP basin than previous geologic models, helps define the position and extent of structures in southern Yucca Flat and CP basin, and better constrains the configuration of the basement structure separating CP basin and Frenchman Flat. The density and gravity modeling indicates that CP basin is a shallow, oval-shaped basin which trends north-northeast and contains ~800 m of basin-filling rocks and sediment at its deepest point in the northeast. CP basin is separated from the deeper Frenchman Flat basin by a subsurface ridge that may represent a Tertiary erosion surface at the top of the Paleozoic strata. The magnetic modeling indicates that the Cane Spring fault appears to merge with faults in northwest Massachusetts Mountain, rather than cut through to Yucca Flat basin and that the basin is downed-dropped relative to Massachusetts Mountain. The magnetic modeling indicates volcanic units within Yucca Flat basin are down-dropped on the west and supports the interpretations of Phelps and KcKee (1999). The magnetic data indicate that the only faults that appear to be through-going from Yucca Flat into either Frenchman Flat or CP basin are the faults that bound the CP hogback. In general, the north-trending faults present along the length of Yucca Flat bend, merge, and disappear before reaching CP hogback and Massachusetts Mountain or French Peak
Incidence et pronostic des sous-types et co-mutations de KRAS dans le Cancer Bronchique Non à Petites Cellules métastatique : étude rétrospective au CHU de Caen entre 2016 et 2020.
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Belimumab in refractory organizing pneumonia associated with systemic lupus erythematosus: a case report
Loss of β Epithelial Sodium Channel Function in Meibomian Glands Produces Pseudohypoaldosteronism 1–Like Ocular Disease in Mice
Human subjects with pseudohypoaldosteronism-1 because of loss-of-function mutations in epithelial sodium channel (ENaC) subunits exhibit meibomian gland (MG) dysfunction. A conditional βENaC MG knockout (KO) mouse model was generated to elucidate the pathogenesis of absent ENaC function in the MG and associated ocular surface disease. βENaC MG KO mice exhibited a striking age-dependent, female-predominant MG dysfunction phenotype, with white toothpaste-like secretions observed obstructing MG orifices at 7 weeks of age. There were compensatory increases in tear production but higher tear sodium and indexes of mucin concentration in βENaC MG KO mice. Histologically, MG acinar atrophy was observed with ductal enlargement and ductal epithelial hyperstratification. Inflammatory cell infiltration was observed in both MG and conjunctiva of βENaC MG KO mice. In older βENaC MG KO mice (5 to 11 months), significant ocular surface pathologies were noted, including corneal opacification, ulceration, neovascularization, and ectasia. Inflammation in MG and conjunctiva was confirmed by increased cytokine gene and protein expression and positive Ly-6B.2 immunostaining. Cell proliferation assays revealed lower proliferation rates of MG cells derived from βENaC MG KO than control mice, suggesting that βENaC plays a role in cell renewal of mouse MG. Loss of βENaC function resulted in MG disease and severe ocular surface damage that phenocopied aspects of human pseudohypoaldosteronism-1 MG disease and was sex dependent