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This article discusses the role of Notch1 as a potential mechanosensor in the vascular system. Mechanosensors are responsible for detecting changes in hemodynamic forces and play a crucial role in maintaining vascular health. The article highlights the complex mechanisms of vascular mechanotransduction, including various techniques used to analyze mechanosignaling and the different mechanosensors involved. It also explores the Notch1 pathway and its interaction with other mechanosensory factors. The authors suggest that understanding the role of Notch1 in mechanosensing could have implications for vascular therapies. However, further research is needed to fully understand the extent of Notch1's role in vascular mechanotransduction. [Extracted from the article]

This paper proposes a novel data fusion technique for a wearable multi-sensory patch that integrates an accelerometer and a flexible resistive pressure sensor to accurately capture breathing patterns. It utilizes an accelerometer to detect breathing-related diaphragmatic motion and other body movements, and a flex sensor for muscle stretch detection. The proposed sensor data fusion technique combines inertial and pressure sensors to eliminate nonbreathing body motion-related artifacts, ensuring that the filtered signal exclusively conveys information pertaining to breathing. The fusion technique mitigates the limitations of relying solely on one sensor's data, providing a more robust and reliable solution for continuous breath monitoring in clinical and home environments. The sensing system was tested against gold-standard spirometry data from multiple participants for various breathing patterns. Experimental results demonstrate the effectiveness of the proposed approach in accurately monitoring breathing rates, even in the presence of nonbreathing-related body motion. The results also demonstrate that the multi-sensor patch presented in this paper can accurately distinguish between varying breathing patterns both at rest and during body movements. [ABSTRACT FROM AUTHOR]

Passive hyperthermia causes cerebral hypoperfusion primarily from heat‐induced respiratory alkalosis. However, despite the cerebral hypoperfusion, it is possible that the mild alkalosis might help to attenuate cerebral inflammation. In this study, the cerebral exchange of extracellular vesicles (microvesicles), which are known to elicit pro‐inflammatory responses when released in conditions of stress, were examined in hyperthermia with and without respiratory alkalosis. Ten healthy male adults were heated passively, using a warm water‐perfused suit, up to core temperature + 2°C. Blood samples were taken from the radial artery and internal jugular bulb. Microvesicle concentrations were determined in platelet‐poor plasma via cells expressing CD62E (activated endothelial cells), CD31+/CD42b− (apoptotic endothelial cells), CD14 (monocytes) and CD45 (pan‐leucocytes). Cerebral blood flow was measured via duplex ultrasound of the internal carotid and vertebral arteries to determine cerebral exchange kinetics. From baseline to poikilocapnic (alkalotic) hyperthermia, there was no change in microvesicle concentration from any cell origin measured (P‐values all >0.05). However, when blood CO2 tension was normalized to baseline levels in hyperthermia, there was a marked increase in cerebral uptake of microvesicles expressing CD62E (P = 0.028), CD31+/CD42b− (P = 0.003) and CD14 (P = 0.031) compared with baseline, corresponding to large increases in arterial but not jugular venous concentrations. In a subset of seven participants who underwent hypercapnia and hypocapnia in the absence of heating, there was no change in microvesicle concentrations or cerebral exchange, suggesting that hyperthermia potentiated the CO2/pH‐mediated cerebral uptake of microvesicles. These data provide insight into a potential beneficial role of respiratory alkalosis in heat stress. Key points: The hyperthermia‐induced hyperventilatory response is observed in most humans, despite causing potentially harmful reductions in cerebral blood flow.We tested the hypothesis that the respiratory‐induced alkalosis is associated with lower circulating microvesicle concentrations, specifically in the brain, despite the reductions in blood flow.At core temperature + 2°C with respiratory alkalosis, microvesicles derived from endothelial cells, monocytes and leucocytes were at concentrations similar to baseline in the arterial and cerebral venous circulation, with no changes in cross‐brain microvesicle kinetics.However, when core temperature was increased by 2°C with CO2/pH normalized to resting levels, there was a marked cerebral uptake of microvesicles derived from endothelial cells and monocytes. The CO2/pH‐mediated alteration in cerebral microvesicle uptake occurred only in hyperthermia.These new findings suggest that the heat‐induced hyperventilatory response might serve a beneficial role by preventing potentially inflammatory microvesicle uptake in the brain. [ABSTRACT FROM AUTHOR]