ABSTRACT
The recent pandemic of SARS-CoV-2 virus has made evident critical issues relating to virus sensing and the need for deployable tools for adequate, rapid, effective viral recognition on a large-scale. Although many conventional molecular and immuno-based techniques are widely used for these purposes, they still have some drawbacks concerning sensitivity, safety, laboriousness, long-term collection and data analysis. Therefore, new rapidly emerging approaches have been introduced such as terahertz (THz)-based technologies. In this contribution, we summarize the emerging THz radiation technology, its solutions and applications for high-sensitivity viral detection. © 2022 by the authors.
ABSTRACT
Rationale: Acute respiratory distress syndrome (ARDS), a disease of acute respiratory failure manifested by severe hypoxemia, is the leading cause of mortality and morbidity associated with coronavirus disease 2019 (COVID-19). Although hypoxemia is the key clinical feature of ARDS, acute alterations in pulmonary artery (PA) circulation and right ventricular (RV) function are also common prognostic determinants in typical ARDS as well as in COVID-19-induced ARDS. However, the effect of ARDS on cardiopulmonary hemodynamics, especially on RV function, remains understudied. Our objective is to investigate acute alterations in RV function in response to ARDS. Methods: ARDS was induced in Sprague-Dawley rats (n=3) by administrating a single 10-mg/kg dose of lipopolysaccharide (LPS;Escherichia coli, serotype O55:B5) instilled into the trachea using an angiocatheter. Control rats (n=3) were instilled with an equal volume of saline as that of LPS. At 16 hrs post-LPS instillation, terminal measurements including echocardiography and RV catheterization with pressure-volume measurements were performed. Micro-computed tomography (CT) scan was performed on one animal from each group. In select animals (2 ARDS, 2 controls), RV free wall (RVFW) myocardium was collected and subjected to biaxial stretching to characterize the mechanical adaptation of the RVFW. Results: Typical ARDS phenotype was confirmed by weight loss and pulmonary edema (WL;-5.77±3.01 vs. -0.53±1.38 percent;p=0.05). A significant increase in pulmonary vascular resistance (PVR) was observed (0.19±0.06 vs. 0.04±0.028 mmHg min/mL;p=0.03) that disturbed RV function, including a drop in cardiac output measured at both pre- and post-LPS instillation timepoints (pre;89.0±13.86 vs. 91.0±21.0, post;51.7±5.6 vs. 81.0±16.5 mL/min;p=0.01 for ARDS post vs. pre;p=0.04 for post ARDS vs. post Control). In contrast, ventriculararterial coupling, calculated by the ratio of end-systolic elastance to arterial elastance, increased (1.03±0.94 vs. 0.61±0.18) indicating resilience capacity of the RV to cope with acute changes in PVR. RV end-diastolic pressure also increased (5.1±1.00 vs. 2.9±0.96 mmHg;p=0.05) portending an acute impairment in diastolic function. Ex-vivo mechanical stretching of RVFW showed a stiffer response along the circumferential direction (max stress;12.6±3.6 vs. 8.0±2.1 kPa). Conclusion: Our study indicated both acute dysfunction and compensatory adaptation in RV's response to ARDS, with alterations ranging from moderate to comparable relative to typical RV dysfunctions observed in chronic pulmonary hypertension. Our findings highlight the significance of investigating the effect of pre-existing cardiopulmonary diseases on RV resilience and dysfunction in response to ARDS, including that induced by COVID-19.