There is an urgent need for ultrarapid testing regimens to detect the severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2] infections in real-time within seconds to stop its spread. Current testing approaches for this RNA virus focus primarily on diagnosis by RT-qPCR, which is time-consuming, costly, often inaccurate, and impractical for general population rollout due to the need for laboratory processing. The latency until the test result arrives with the patient has led to further virus spread. Furthermore, latest antigen rapid tests still require 15–30 min processing time and are challenging to handle. Despite increased polymerase chain reaction (PCR)-test and antigen-test efforts, the pandemic continues to evolve worldwide. Herein, we developed a superfast, reagent-free, and nondestructive approach of attenuated total reflection Fourier-transform infrared (ATR-FTIR) spectroscopy with subsequent chemometric analysis toward the prescreening of virus-infected samples. Contrived saliva samples spiked with inactivated γ-irradiated COVID-19 virus particles at levels down to 1582 copies/mL generated infrared (IR) spectra with a good signal-to-noise ratio. Predominant virus spectral peaks are tentatively associated with nucleic acid bands, including RNA. At low copy numbers, the presence of a virus particle was found to be capable of modifying the IR spectral signature of saliva, again with discriminating wavenumbers primarily associated with RNA. Discrimination was also achievable following ATR-FTIR spectral analysis of swabs immersed in saliva variously spiked with virus. Next, we nested our test system in a clinical setting wherein participants were recruited to provide demographic details, symptoms, parallel RT-qPCR testing, and the acquisition of pharyngeal swabs for ATR-FTIR spectral analysis. Initial categorization of swab samples into negative versus positive COVID-19 infection was based on symptoms and PCR results ( n = 111 negatives and 70 positives). Following training and validation (using n = 61 negatives and 20 positives) of a genetic algorithm-linear discriminant analysis (GA-LDA) algorithm, a blind sensitivity of 95% and specificity of 89% was achieved. This prompt approach generates results within 2 min and is applicable in areas with increased people traffic that require sudden test results such as airports, events, or gate controls.

Fernandes T, Baraúna VG, Negrão CE, Phillips MI, Oliveira EM. Aerobic exercise training promotes physiological cardiac remodeling involving a set of microRNAs. Am J Physiol Heart Circ Physiol 309: H543-H552, 2015. First published June 12, 2015 doi:10.1152/ajpheart.00899.2014 hypertrophy is an important physiological compensatory mechanism in response to chronic increase in hemodynamic overload. There are two different forms of LV hypertrophy, one physiological and another pathological. Aerobic exercise induces beneficial physiological LV remodeling. The molecular/cellular mechanisms for this effect are not totally known, and here we review various mechanisms including the role of microRNA (miRNA). Studies in the heart, have identified antihypertrophic . Four miRNAs are recognized as cardiacspecific: miRNA-1, -133a/b, -208a/b, and -499 and called myomiRs. In our studies we have shown that miRNAs respond to swimming aerobic exercise by 1) decreasing cardiac fibrosis through miRNA-29 increasing and inhibiting collagen, 2) increasing angiogenesis through miRNA-126 by inhibiting negative regulators of the VEGF pathway, and 3) modulating the renin-angiotensin system through the miRNAs-27a/b and -143. Exercise training also increases cardiomyocyte growth and survival by swimming-regulated miRNA-1, -21, -27a/b, -29a/c, -30e, -99b, -100, -124, -126, -133a/b, -143, -144, -145, -208a, and -222 and running-regulated miRNA-1, -26, -27a, -133, -143, -150, and -222, which influence genes associated with the heart remodeling and angiogenesis. We conclude that there is a potential role of these miRNAs in promoting cardioprotective effects on physiological growth. cardiac hypertrophy; angiogenesis; swimming training; running training; microRNA THIS ARTICLE is part of a collection on Exercise Training in Cardiovascular Disease: Cell, Molecular, and Integrative Perspectives. Other articles appearing in this collection, as well as a full archive of all collections, can be found online at http://ajpheart.physiology.org/.EXERCISE TRAINING IS the most effective nonpharmacological intervention to reduce cardiovascular disease (CVD). Its prescription is recommended by the guidelines of the most important entities, such as the American College of Sport Medicine and the American Heart Association (39).Exercise training is well known to promote beneficial adaptations in the cardiovascular system which can vary according to type, intensity, and duration of exercise (32). Exercise training induces marked beneficial systemic effects on metabolism control, skeletal muscle, cognitive function, and cardiovascular function (30, 39). Among them, the set of adaptations induced in the myocardium are collectively referred to as "athlete's heart" and includes increased cardiac mass, formations of new blood vessels, and decreased collagen content (15a, 17, 20, 23, 77, 91). Individuals with high levels of physical activity have a lower prevalence and lower death rates from CVD (32, 86). Thus exercise training has been established not only as a way to ma...

Resistance training is accompanied by cardiac hypertrophy, but the role of the renin-angiotensin system (RAS) in this response is elusive. We evaluated this question in 36 male Wistar rats divided into six groups: control (n=6); trained (n=6); control+losartan (10 mg.kg(-1).day(-1), n=6); trained+losartan (n=6); control+high-salt diet (1%, n=6); and trained+high-salt diet (1%, n=6). High salt was used to inhibit the systemic RAS and losartan to block the AT1 receptor. The exercise protocol consisted of: 4x12 bouts, 5x/wk during 8 wk, with 65-75% of one repetition maximum. Left ventricle weight-to-body weight ratio increased only in trained and trained+high-salt diet groups (8.5% and 10.6%, P<0.05) compared with control. Also, none of the pathological cardiac hypertrophy markers, atrial natriuretic peptide, and alphaMHC (alpha-myosin heavy chain)-to-betaMHC ratio, were changed. ACE activity was analyzed by fluorometric assay (systemic and cardiac) and plasma renin activity (PRA) by RIA and remained unchanged upon resistance training, whereas PRA decreased significantly with the high-salt diet. Interestingly, using Western blot analysis and RT-PRC, no changes were observed in cardiac AT2 receptor levels, whereas the AT1 receptor gene (56%, P<0.05) and protein (31%, P<0.05) expressions were upregulated in the trained group. Also, cardiac ANG II concentration evaluated by ELISA remained unchanged (23.27+/-2.4 vs. 22.01+/-0.8 pg/mg, P>0.05). Administration of a subhypotensive dose of losartan prevented left ventricle hypertrophy in response to the resistance training. Altogether, we provide evidence that resistance training-induced cardiac hypertrophy is accompanied by induction of AT1 receptor expression with no changes in cardiac ANG II, which suggests a local activation of the RAS consistent with the hypertrophic response.

1. The present study sought to evaluate cardiovascular adaptations, such as blood pressure (BP), heart rate (HR) and cardiac hypertrophy, to resistance training (RT) in a rat model. 2. The training protocol consisted of four sets of 10-12 repetitions of the squat exercise performed at 65-75% of one repetition maximum (1RM) over 4 weeks. Animals were randomly divided into three groups: control (n = 8, CO), electrically stimulated (n = 8, ES) and trained (n = 8, TR; also electrically stimulated). Blood pressure and HR were measured by a direct method in conscious rats after the training period. 3. All groups began with similar 1RM and 1RM/bodyweight (BW) ratio, however, at the end of the protocol only the TR group was different from the beginning (56% and 50%, respectively; both P < 0.01). The CO and ES groups had similar values for cardiac chambers weight/BW ratio, HR and diastolic, systolic and mean BP. Left ventricular hypertrophy (LVH) determined by the left ventricle (LV) weight/BW ratio was increased in the TR group (12%) when compared to CO (P < 0.01) or ES groups (P < 0.01). No changes were found in the weights of the atrium or right ventricle. Diastolic (14%) and mean BP (13%) were lower in the TR group (P < 0.05), whereas systolic BP and HR remained unchanged. 4. Collectively these results demonstrate that the rat RT model used is associated with significant development of cardiac hypertrophy and lowering of resting BP. These cardiovascular adaptations seem to a result of the training exercise and not influenced by stress since circulating catecholamine levels and adrenal gland weights remained unchanged in all groups.

To evaluate the effects of heat acclimation on sweat rate redistribution and thermodynamic parameters, 9 tropical native volunteers were submitted to 11 days of exercise-heat exposures (40Ϯ0°C and 45.1Ϯ0.2% relative humidity). Sudomotor function was evaluated by measuring total and local (forehead, chest, arm, forearm, and thigh) sweat rates, local sweat sodium concentration, and mean skin and rectal temperatures. We also calculated heat production (H), heat storage (S), heat exchange by radiation (R) and by convection (C), evaporated sweat (E sw ), sweating efficiency (h sw ), skin wettedness (w sk ), and the ratio between the heat storage and the sum of heat production and heat gains by radiation and convection (S/(HϩRϩC)). The heat acclimation increased the whole-body sweat rate and reduced the mean skin temperature. There were changes in the local sweat rate patterns: on the arm, forearm, and thigh it increased significantly from day 1 to day 11 (all pϽ0.05) and the sweat rates from the forehead and the chest showed a small nonsignificant increase (pϭ0.34 and 0.17, respectively). The relative increase of local sweat rates on day 11 was not different among the sites; however, when comparing the limbs (arm, forearm, and thigh) with the trunk (forehead and chest), there was a significant higher increase in the limbs (32Ϯ5%) in comparison to the trunk (11Ϯ2%, pϭ0.001). After the heat acclimation period we observed higher w sk and E sw and reduced S/(HϩRϩC), meaning greater thermoregulatory efficiency. The increase in the limb sweat rate, but not the increase in the trunk sweat rate, correlated with the increased w sk , E sw , and reduced S/(HϩRϩC) (pϽ0.05 to all). Altogether, it can be concluded that heat acclimation increased the limbs' sweat rates in tropical natives and that this increase led to increased loss of heat through evaporation of sweat and this higher sweat evaporation was related to higher thermoregulatory efficiency.