Rationale and Objectives: To retrospectively analyze the chest imaging findings in patients with coronavirus disease 2019 (COVID-19) on thin-section CT.Materials and Methods: Fifty-three patients with confirmed COVID-19 infection underwent thin-section CT examination. Two chest radiologists independently evaluated the imaging in terms of distribution, ground-glass opacity (GGO), consolidation, air bronchogram, stripe, enlarged mediastinal lymph node, and pleural effusion.Results: Fourty-seven cases (88.7%) had findings of COVID-19 infection, and the other six (11.3%) were normal. Among the 47 cases, 78.7% involved both lungs, and 93.6% had peripheral infiltrates distributed along the subpleural area. All cases showed GGO, 59.6% of which were round and 40.4% patchy. Other imaging features included "crazy-paving pattern" (89.4%), consolidation (63.8%), and air bronchogram (76.6%). Air bronchograms were observed within GGO (61.7%) and consolidation (70.3%). Neither enlarged mediastinal lymph nodes nor pleural effusion were present. Thirty-three patients (62.3%) were followed an average interval of 6.2 § 2.9 days. The lesions increased in 75.8% and resorbed in 24.2% of patients.Conclusion: COVID-19 showed the pulmonary lesions in patients infected with COVID-19 were predominantly distributed peripherally in the subpleural area.

Background and PurposeStroke of large-artery atherosclerosis and small-artery occlusion are two main subtypes of stroke according to TOAST classification. The underlying mechanisms of how these two subtypes affect dynamic cerebral autoregulation (dCA) might be heterogeneous, resulting in varied clinical conditions and outcomes. We therefore studied the pattern of dCA in these two subtypes.MethodsForty-one patients with acute unilateral middle cerebral artery (MCA) territory stroke (15 with ipsilateral large-artery atherosclerosis and 26 with small-artery occlusion) and 20 healthy volunteers were enrolled. Non-invasive continuous cerebral blood flow velocity and arterial blood pressure were recorded simultaneously from each subject in supine position using transcranial Doppler on MCA bilaterally and servo-controlled plethysmograph on the middle finger, respectively. Transfer function analysis was applied to derive autoregulatory parameters, gain, phase difference (PD), and slope of step response.ResultsIn the large-artery atherosclerosis group, PD in affected hemisphere was 42.9±18.5 degree, which is significantly lower than the unaffected hemisphere (72.4±29.9 degree, P<0.01), and the healthy group (P<0.01). However, PD is similar in the unaffected hemisphere and healthy group (P>0.1). In the small-artery occlusion group, PD in the affected hemisphere was similar to that in the contralateral hemisphere (33.8±17.9 vs. 32.6±21.1 degree, P>0.1), both sides were significantly lower than the healthy group (all P<0.001).The results of the slope of step response agree with the findings in PD.ConclusionsDCA in different subtypes of acute ischemic stroke is heterogeneous, which might be attributed to the varied pathologic changes of cerebral blood vessels.

In response to a number of stresses, including nutrient deprivation, General Control Nonderepressible 2 kinase (GCN2) attenuates mRNA translation by phosphorylating eukaryotic initiation factor 2 alpha (eIF2αSer51). Energy starvation is known to exacerbate congestive heart failure (CHF) and eIF2αSer51 phosphorylation is increased in the failing heart. However, the impact of GCN2 during the evolution of CHF has not been tested. In this study we examined the influence of GCN2 expression in response to a cardiac stress by inducing chronic pressure overload with Transverse Aortic Constriction (TAC) in Wild Type (WT) and GCN2 knockout (GCN2−/−) mice. Under basal conditions, GCN2−/− had normal LV structure or function but following TAC, demonstrated less contractile dysfunction, less increase of lung weight, less increase of lung inflammation and vascular remodeling, and less myocardial apoptosis and fibrosis compared with WT mice, despite an equivalent degree of LV hypertrophy. As expected, GCN2−/− attenuated TAC induced cardiac eif2αSer51 phosphorylation and preserved Sarcoplasmic reticulum Ca2+ ATPase (Serca2a) expression compared with WT mice. Interestingly, expression of the anti-apoptotic protein Bcl-2 was significantly elevated in GCN2−/− hearts, while in isolated neonatal cardiomyocytes, selective knockdown of GCN2 increased Bcl-2 protein expression and enhanced myocyte resistance to an apoptotic stress. Collectively, our data support the notion that GCN2 impairs the ventricular adaptation to chronic pressure overload by reducing Bcl-2 expression and increasing cardiomyocyte susceptibility to apoptotic stimuli. Our findings suggest that strategies to reduce GCN2 activity in cardiac tissue may be a novel approach to attenuate congestive heart failure development.