Time delays between physiological signals in interpreting the body's responses to intermittent hypoxia in obstructive sleep apnea.

Objective.Intermittent hypoxia, the primary pathology of obstructive sleep apnea (OSA), causes cardiovascular responses resulting in changes in hemodynamic parameters such as stroke volume (SV), blood pressure (BP), and heart rate (HR). However, previous studies have produced very different conclusions, such as suggesting that SV increases or decreases during apnea. A key reason for drawing contrary conclusions from similar measurements may be due to ignoring the time delay in acquiring response signals. By analyzing the signals collected during hypoxia, we aim to establish criteria for determining the delay time between the onset of apnea and the onset of physiological parameter response.Approach.We monitored oxygen saturation (SpO2), transcutaneous oxygen pressure (TcPO2), and hemodynamic parameters SV, HR, and BP, during sleep in 66 patients with different OSA severity to observe body's response to hypoxia and determine the delay time of above parameters. Data were analyzed using the Kruskal-Wallis test, Quade test, and Spearman test.Main results.We found that simultaneous acquisition of various parameters inevitably involved varying degrees of response delay (7.12-25.60 s). The delay time of hemodynamic parameters was significantly shorter than that of SpO2and TcPO2(p< 0.01). OSA severity affected the response delay of SpO2, TcPO2, SV, mean BP, and HR (p< 0.05). SV delay time was negatively correlated with the apnea-hypopnea index (r= -0.4831,p< 0.0001).Significance.The real body response should be determined after removing the effect of delay time, which is the key to solve the problem of drawing contradictory conclusions from similar studies. The methods and important findings presented in this study provide key information for revealing the true response of the cardiovascular system during hypoxia, indicating the importance of proper signal analysis for correctly interpreting the cardiovascular hemodynamic response phenomena and exploring their physiological and pathophysiological mechanisms.

[Time-dependent injury of mouse cerebral cortex and hippocampus by acute hypoxia].

The aim of this study was to investigate the harmful effects of acute hypoxia on mouse cerebral cortex and hippocampus and the underlying mechanism. Mouse model of acute hypoxia was constructed by using a sealed glass jar. Laser speckle contrast imaging was used to detect the changes of cerebral blood flow after different time duration of hypoxia. Total superoxide dismutase (T-SOD) and malondialdehyde (MDA) assay kits were used to detect oxidative stress in cerebral cortex and hippocampus. Immunofluorescent staining was used to detect neuroinflammatory response of microglia in the cerebral cortex and hippocampus. One-step TUNEL method was used to detect neuronal apoptosis. The results showed that, compared with non-hypoxia (0 min hypoxia) group, 30 min hypoxia group exhibited decreased cerebral blood flow, higher percentage of CD68+/Iba1+ microglia, and increased neural apoptosis in the cerebral cortex and hippocampus. Compared with 30 min group, 60 min hypoxia group showed significantly decreased cerebral blood flow, increased MDA content in the cortex, as well as greater percentage of CD68+/Iba1+ microglia and neuronal apoptosis in the cerebral cortex and hippocampus. These results suggest that acute hypoxia damages brain tissue in a time-dependent manner and the oxidative stress and neuroinflammation are important mechanisms.

Light emitting properties of Si+ self-ion implanted silicon-on-insulator from visible to infrared band.

The photoluminescence (PL) properties of silicon-on-insulator (SOI) samples, modified by the Si+ self-ion-implantation (SII) into Si thin film followed by annealing, have been well investigated. The well-known W-line can also be observed in SII SOI samples, its emitting behavior and structural evolution have been discussed in this article. The parallel PL pattern trend and the similar changes of temperature-dependent intensity suggest that luminescence center of I1 and I2 peaks located in the near-infrared band originates from the same interstitial-clusters (InCs). The PL peak at 1.762 eV can be ascribed to the quantum confinement (QC) from small-sized Si nanocrystals. Based on the electron spin resonance (ESR) experiments and the variation of normalized PL intensities at different annealing temperature (TA), the neutral oxygen vacancy (NOV) [O3≡Si-Si≡O3] is proposed to be responsible for the blue emission of P2 and P3 peaks, whose intensity can be restrained by the existence of the paramagnetic E1' defects [O3≡Si+]. The density of E1' defect is found to reduce with the increase of annealing temperature (TA). Our results provide a useful method to identify the origin of luminescence centers and pave a way for the application of new type optical defects on silicon based light emitting devices (LEDs).