A smart mask integrated with a remote, noncontact multiplexed sensor system, or
“Lab-on-Mask” (LOM) is designed for monitoring respiratory diseases, such
as the COVID-19. This LOM can monitor the heart rate, blood oxygen saturation, blood
pressure, and body temperature associated with symptoms of pneumonia caused by
coronaviruses in real time. Because of this remote monitoring system, frontline
healthcare staff can minimize the exposure they face from close contact with the
patients and reduce the risks of being infected.
Hydrogen sulfide (H 2 S) is a neuromodulator in the central nervous system. However, the physiological role of H 2 S in the nucleus ambiguus (NA) has rarely been reported. This research aimed to elucidate the role of H 2 S in the regulation of gastrointestinal motility in rats. Male Wistar rats were randomly assigned to sodium hydrosulfide (NaHS; 4 and 8 nmol) groups, physiological saline (PS) group, capsazepine (10 pmol) + NaHS (4 nmol) group, L703606 (4 nmol) + NaHS (4 nmol) group, and pyrrolidine dithiocarbamate (PDTC, 4 nmol) + NaHS (4 nmol) group. Gastrointestinal motility curves before and after the injection were recorded using a latex balloon attached with a pressure transducer, which was introduced into the pylorus through gastric fundus. The results demonstrated that NaHS (4 and 8 nmol), an exogenous H 2 S donor, remarkably suppressed gastrointestinal motility in the NA of rats (P < 0.01). The suppressive effect of NaHS on gastrointestinal motility could be prevented by capsazepine, a transient receptor potential vanilloid 1 (TRPV1) antagonist, and PDTC, a NF-κB inhibitor. However, the same amount of PS did not induce significant changes in gastrointestinal motility (P > 0.05). Our findings indicate that NaHS within the NA can remarkably suppress gastrointestinal motility in rats, possibly through TRPV1 channels and NF-κB-dependent mechanism.
We observed that both low and high doses of H2O2 (100 microM and 1 mM, respectively) caused significant and irreversible injury to cardiac contractile function in the isolated perfused heart model. Using 31P-nuclear magnetic resonance spectroscopy, we observed marked metabolic changes following exposure to H2O2, especially at the 1 mM dose. Most remarkable were the increases in the intensity of the phosphomonoester resonance that occurred immediately after exposure to H2O2. The major phosphomonoester species accumulating in hearts exposed to 1 mM H2O2 appears to be AMP. Exposure of hearts to H2O2 in the setting of metabolic acidosis did not significantly alter the functional response of isolated hearts to H2O2. However, the increases in phosphomonoester peak intensity following both doses of H2O2 and the decreases in tissue ATP and total phosphates following 1 mM H2O2 were attenuated by metabolic acidosis.
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