ImportanceAcute respiratory infections (ARIs) account for most outpatient visits. Discriminating bacterial vs viral etiology is a diagnostic challenge with therapeutic implications.ObjectiveTo investigate whether FebriDx, a rapid, point-of-care immunoassay, can differentiate bacterial- from viral-associated host immune response in ARI through measurement of myxovirus resistance protein A (MxA) and C-reactive protein (CRP) from finger-stick blood.Design, Setting, and ParticipantsThis diagnostic study enrolled adults and children who were symptomatic for ARI and individuals in a control group who were asymptomatic between October 2019 and April 2021. Included participants were a convenience sample of patients in outpatient settings (ie, emergency department, urgent care, and primary care) who were symptomatic, aged 1 year or older, and had suspected ARI and fever within 72 hours. Individuals with immunocompromised state and recent vaccine, antibiotics, stroke, surgery, major burn, or myocardial infarction were excluded. Of 1685 individuals assessed for eligibility, 259 individuals declined participation, 718 individuals were excluded, and 708 individuals were enrolled (520 patients with ARI, 170 patients without ARI, and 18 individuals who dropped out).ExposuresBacterial and viral immunoassay testing was performed using finger-stick blood. Results were read at 10 minutes, and treating clinicians and adjudicators were blinded to results.Main Outcomes and MeasuresBacterial- or viral-associated systemic host response to an ARI as determined by a predefined comparator algorithm with adjudication classified infection etiology.ResultsAmong 520 participants with ARI (230 male patients [44.2%] and 290 female patients [55.8%]; mean [SD] age, 35.3 [17.7] years), 24 participants with missing laboratory information were classified as unknown (4.6%). Among 496 participants with a final diagnosis, 73 individuals (14.7%) were classified as having a bacterial-associated response, 296 individuals (59.7%) as having a viral-associated response, and 127 individuals (25.6%) as negative by the reference standard. The bacterial and viral test correctly classified 68 of 73 bacterial infections, demonstrating a sensitivity of 93.2% (95% CI, 84.9%-97.0%), specificity of 374 of 423 participants (88.4% [95% CI, 85.0%-91.1%]), positive predictive value (PPV) of 68 of 117 participants (58.1% [95% CI, 49.1%-66.7%), and negative predictive value (NPV) of 374 of 379 participants (98.7% [95% CI, 96.9%-99.4%]).The test correctly classified 208 of 296 viral infections, for a sensitivity of 70.3% (95% CI, 64.8%-75.2%), a specificity of 176 of 200 participants (88.0% [95% CI, 82.8%-91.8%]), a PPV of 208 of 232 participants (89.7% [95% CI, 85.1%-92.9%]), and an NPV of 176 of 264 participants (66.7% [95% CI, 60.8%-72.1%]).Conclusions and RelevanceIn this study, a rapid diagnostic test demonstrated diagnostic performance that may inform clinicians when assessing for bacterial or viral etiology of ARI symptoms.

Objective:Immersion induced hydrostatic pressure on thoracic cavity and limbs is one kind of cardiac overload model in simulating microgravity. We evaluated immersion hemodynamic parameters, investigated in vitro stretching induced aortic intact wall windkessel adaptations in whole-body immersion mice. Method: Kunming mice were divided into immersion group (n=20) and control group (n=10) randomize. In immersion group, mice further divided into immersion group (n=10) and immersion with weight-bearing group (5% of body weight, n=10). The immersion kept 20 min/day in warm water and continues for 1 week. The hemodynamic parameters were collected by left carotid artery cannulation and analyzed by biological signal acquisition system. Calculi of percussion wave were calculated with integral mode to determine left ventricle stroke volume. In vitro aortic wall were prepared to a vascular ring and mechanical stretching the preparation to 1 g as the initial load. The preparations were further stretched by a micro-adjusting tuner with the interval of 5 min which gradually increasing 1 mm in each step. The stretching induced passive tension, where after, stress relaxation duration and myogenic spontaneous contraction were analyzed. In a separated preparation, myogenic contraction changes investigated in 0.05% Nitrendipine treated preparation. Result: Mice carotid arterial pressure waveforms have significantly changed, however, mean arterial pressure were slightly increased but not significantly (immersion 9.14 ± 0.63 kPa, control 8.40 ± 0.97 kPa). The calculated stroke volume increased significantly (immersion 13.96 ± 0.12 µl/min, control 5.14 ± 0.69 μl/min, respectively). In vitro mechanical stretching induced less myogenic spontaneous contraction, stress relaxation period were shortening. Pre-treatment of 0.05% Nitrendipine induced more myogenic spontaneous contraction that revealed the spontaneous contraction was not solution Ca 2+ influenced. Conclusion: Immersion stress improved left ventricle functions that reflected in rapid ejection and isodiastolic period, suggested aortic windkessel properties were improved in microgravity simulation induced cardiac overload.

Toad urothelium barrier is the model to mimic and investigate urothelium permeability. Thiazide blocked ionic transportation in polarized membrane state. Jellyfish venom causes pores to be adjusted to urothelium permeability which improved polarization. This study aimed at CfTX-1 peptide in urothelium permeability evoked polarizations. Thiazide pretreated toad urothelium permeability to ions were investigated in modified Ussing chamber. Thiazide urothelium were further intervened by CfTX-1 peptide and treated with G-protein receptor agonists. 0.1 mol CaCl 2 activated transurothelium potential differences were recorded by unipolar lead and computerized by fast Fourier transform technique. Apical chamber was settled as anode. The amplitude of potential differences were evaluated to determine the urothelium polarizations. The results indicated that CaCl 2 activation induced a positive monophasic wave in thiazide urothelium, which suggested the urothelium was slightly polarized and significantly enhancive in adrenergic receptor treated urothelium. Furthermore, CfTX-1 peptide enhanced transurothelium potential difference in thiazide urothelium, therefore, urothelium were supra polarized. NPPB treatment significantly attenuated this supra polarization, which suggested that the Cl influx was the main stream ionic compound of this polarization. It is concluded that CfTX-1 peptide was considered to generate supra polarization in thiazide urothelium. This mechanism is useful to study the improvement of drug delivery crossing urothelium barrier.

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