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Background: A significant portion of cryptogenic stroke is hypothesized to be secondary to cardiac embolism. However, transthoracic echocardiogram is usually delayed after stroke, and more detailed cardiac imaging is not routinely done. Aims: This study aimed to determine whether non–ECG-gated cardiac CT angiography (cCTA) during hyperacute stroke would provide diagnostic quality images and act as an adjunct modality of cardiac imaging to detect sources of emboli. Methods: In this single-center prospective cohort study, modified Code Stroke imaging was implemented with a 64-slice CT scanner, where the longitudinal axis of CT angiography was extended from the carina to the diaphragm. The primary outcomes of image quality, recruitment feasibility, impact on hyperacute time metrics, and additional radiation dose were assessed. Secondary outcomes consisted of detection of high-risk cardiac sources of embolism, mediastinal or lung pathology, and impact on etiologic classification. Results: One hundred and twenty eligible patients were enrolled, of which 105 (87.5%) had good/moderate quality images for motion artifact and 119 (99.2%) for contrast opacification. Total CT time, door-to-needle time, and door-to-groin puncture time were unchanged with the addition of cCTA. Eighty-nine patients received a final diagnosis of ischemic stroke, of which 12/89 (13.5%) had high-risk cardioembolic findings on cCTA. Incidental findings, such as pulmonary embolism (PE) (7/89, 7.9%) and malignancy (6/89, 6.7%), were observed. cCTA led to changes in management for 19/120 (15.8%) of all patients, and reclassification of stroke etiology for 8/89 (9%) of patients. Conclusions: Non–ECG-gated cCTA can be feasibly incorporated into Code Stroke and provide diagnostic quality images without delays in hyperacute time metrics. It can detect high-risk cardiac sources, and other findings impacting patient care. This may help reclassify a subset of cryptogenic stroke cases and improve secondary prevention. [ABSTRACT FROM AUTHOR]

Rasamsonia argillacea (formerly known as Geosmithia argillacea) is a fungus recently recognized as a pathogen of immunocompromised patients. Here we report the first case of Rasamsonia infection in an immunocompetent host, presenting as a pulmonary and aortic graft infection. Its morphological similarity to nonpathogenic Penicillium species delayed the diagnosis and initiation of appropriate treatment.

To further investigate the role of MyoD during skeletal myogenesis, we backcrossed mdx mutant mice (lacking dystrophin) with MyoD knock-out mice to obtain viable mice with MyoD allele on a pure mdx background. However, after nine generations of backcrossing, it was not possible to obtain a viable mdx:MyoD-/- phenotype (designated as: mdx:MyoD[-/-.sup.9th]). The compound-mutant embryos were examined just before birth. Essentially normal Myf5-dependent and most of the MyoD-dependent musculature was observed. By contrast, the skeletal muscle compartment of the diaphragm was significantly reduced. The mesenchymal compartment of the diaphragm was intact and no herniations were observed. Other examined organs (e.g., liver, kidney, brain, etc.) showed no histological abnormalities. Pulmonary hypoplasia was determined as the cause of neonatal death. Therefore, using a different approach, our new data supplement our previous findings and suggest an essential role for MyoD in development of skeletal muscle of the diaphragm. The failure of mdx:MyoD[-/-.sup.9th] diaphragm to develop normally is not caused by a reduced number of satellite cells, but from the inability of stem cells to progress through the myogenic program. Our data also suggest that functions of MyoD and Myf5 (and the respective muscle precursor cell sub-populations) are not entirely redundant by term, as previously suggested, since Myf5 is not capable of fully substituting for MyoD in the diaphragm development. Keywords: Myf5; MyoD; Dystrophin; Mouse; Myogenesis; Diaphragm

To further investigate the role of MyoD during skeletal myogenesis, we backcrossed mdx mutant mice (lacking dystrophin) with MyoD knock-out mice to obtain viable mice with MyoD allele on a pure mdx background. However, after nine generations of backcrossing, it was not possible to obtain a viable mdx:MyoD−/− phenotype (designated as: mdx:MyoD−/−9th). The compound-mutant embryos were examined just before birth. Essentially normal Myf5-dependent and most of the MyoD-dependent musculature was observed. By contrast, the skeletal muscle compartment of the diaphragm was significantly reduced. The mesenchymal compartment of the diaphragm was intact and no herniations were observed. Other examined organs (e.g., liver, kidney, brain, etc.) showed no histological abnormalities. Pulmonary hypoplasia was determined as the cause of neonatal death. Therefore, using a different approach, our new data supplement our previous findings and suggest an essential role for MyoD in development of skeletal muscle of the diaphragm. The failure of mdx:MyoD−/−9th diaphragm to develop normally is not caused by a reduced number of satellite cells, but from the inability of stem cells to progress through the myogenic program. Our data also suggest that functions of MyoD and Myf5 (and the respective muscle precursor cell sub-populations) are not entirely redundant by term, as previously suggested, since Myf5 is not capable of fully substituting for MyoD in the diaphragm development. [Copyright &y& Elsevier]

To further investigate the role of MyoD during skeletal myogenesis, we backcrossed mdx mutant mice (lacking dystrophin) with MyoD knock-out mice to obtain viable mice with MyoD allele on a pure mdx background. However, after nine generations of backcrossing, it was not possible to obtain a viable mdx:MyoD-/- phenotype (designated as: mdx:MyoD-/-(9th)). The compound-mutant embryos were examined just before birth. Essentially normal Myf5-dependent and most of the MyoD-dependent musculature was observed. By contrast, the skeletal muscle compartment of the diaphragm was significantly reduced. The mesenchymal compartment of the diaphragm was intact and no herniations were observed. Other examined organs (e.g., liver, kidney, brain, etc.) showed no histological abnormalities. Pulmonary hypoplasia was determined as the cause of neonatal death. Therefore, using a different approach, our new data supplement our previous findings and suggest an essential role for MyoD in development of skeletal muscle of the diaphragm. The failure of mdx:MyoD-/-(9th) diaphragm to develop normally is not caused by a reduced number of satellite cells, but from the inability of stem cells to progress through the myogenic program. Our data also suggest that functions of MyoD and Myf5 (and the respective muscle precursor cell sub-populations) are not entirely redundant by term, as previously suggested, since Myf5 is not capable of fully substituting for MyoD in the diaphragm development.