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Among the existing applications of wireless body sensor networks (WBSNs), a wearable health monitoring system (WHMS) is the most important. In a typical WHMS, miniature wireless biosensors, attached to or implanted in the human body, collect bio-signals such as the electrocardiogram (ECG), blood pressure or electromyogram (EMG) to provide real time and continuous health monitoring. In this paper, we present a compressed sensing (CS)-based approach to compress and recover the sensed bio-signals from the wireless biosensors of a WBSN. The CS encoding process has a low computational complexity and is suitable for use in power-constrained systems such as WHMS. We propose a simple deterministic measurement matrix, which is easy to implement in hardware. We design a digital CS encoder implementing the proposed measurement matrix and use it to compress the bio-signals in EMG and ECG wireless biosensors. The simulations and experimental results have shown that the EMG and ECG signals are compressed and recovered without perceptible loss if the compression ratios are, respectively, less than or equal to 75 and 87.5%. The obtained results have also confirmed the simplicity of the proposed measurement matrix since the CS encoder does not affect the memory usage or the processing time of the microcontrollers embedded in the wireless biosensors. Additionally, the CS encoder decreases by up to 75 and 87.5% the energy consumption of the transceivers for the EMG and ECG wireless biosensors.

RationaleAcetazolamide and atomoxetine-plus-oxybutynin (‘AtoOxy’) can improve obstructive sleep apnoea (OSA) by stabilising ventilatory control and improving dilator muscle responsiveness respectively. Given the different pathophysiological mechanisms targeted by each intervention, we tested whether AtoOxy-plus-acetazolamide would be more efficacious than AtoOxy alone.MethodsIn a multicentre randomised crossover trial, 19 patients with moderate-to-severe OSA received AtoOxy (80/5 mg), acetazolamide (500 mg), combined AtoOxy-plus-acetazolamide or placebo at bedtime for three nights (half doses on first night) with a 4-day washout between conditions. Outcomes were assessed at baseline and night 3 of each treatment period. Mixed model analysis compared the reduction in Apnoea-Hypopnoea Index (AHI) from baseline between AtoOxy-plus-acetazolamide and AtoOxy (primary outcome). Secondary outcomes included hypoxic burden and arousal index.ResultsAlthough AtoOxy lowered AHI by 49 (33, 62)%baseline (estimate (95% CI)) vs placebo, and acetazolamide lowered AHI by+34 (14, 50)%baseline vs placebo, AtoOxy-plus-acetazolamide was not superior to AtoOxy alone (difference: −2 (−18, 11)%baseline, primary outcome p=0.8). Likewise, the hypoxic burden was lowered with AtoOxy (+58 (37, 71)%baseline) and acetazolamide (+37 (5, 58)%baseline), but no added benefit versus AtoOxy occurred when combined (difference: −13 (−5, 39)%baseline). Arousal index was also modestly reduced with each intervention (11%baseline–16%baseline). Mechanistic analyses revealed that similar traits (ie, higher baseline compensation, lower loop gain) were associated with both AtoOxy and acetazolamide efficacy.ConclusionsWhile AtoOxy halved AHI, and acetazolamide lowered AHI by a third, the combination of these leading experimental interventions provided no greater efficacy than AtoOxy alone. Failure of acetazolamide to further increase efficacy suggests overlapping physiological mechanisms.Trial registration number NCT03892772.

Abstract Introduction One third of patients with OSA have high loop gain. Acetazolamide (ACZ) and supplemental oxygen (O2) individually reduce loop gain (via different mechanisms) and the apnoea-hypopnoea-index (AHI). The current study aimed to explore the efficacy of combining both ACZ and O2 to maximally lower loop gain. Method Randomised single-blind cross-over trial. Participants took ACZ (500mg orally) or placebo for 7 days. Within each arm, participants completed two polysomnograms (PSGs) during which they slept with supplemental oxygen (3L/min) or sham-air. Sleep and respiratory events were scored by a (blinded) technologist. In addition to standard scoring, respiratory events were scored without SpO2 or arousal information to calculate a ‘flow-based AHI’ (fAHI). PSG data were then imported into Matlab for loop gain analysis. Results Nine participants (5 males, Age=52.4±9.1, BMI=32.0±4.9, AHI=39.9±22.0) have so far completed the trial. Loop gain was significantly reduced by ACZ (-22%, -0.15 CI95:-0.03 to -0.26, p=0.011), O2 (-25%, -0.19 CI95:-0.08 to -0.29, p=0.001) and combination ACZ+O2 (-33%, -0.23 CI95:-0.12 to -0.34, p<0.001) relative to placebo-sham-air condition. Similarly, fAHI was significantly reduced by ACZ (-34%, -15.7/hr CI95:-8.6 to -22.7, p<0.001), O2 (-21%, -10.2/hr CI95:-3.1 to -17.3, p<0.001) and ACZ+O2 (-45.2%, -21.3/hr CI95:-14.6 to -28.4, p<0.001). While fAHI was significantly lower on ACZ+O2 compared with O2 (p=0.003), the difference between ACZ+O2 and ACZ was not significant (-5.6/hr, p=0.12). ACZ+O2 induced a >50% reduction in fAHI in 4/9 participants. Discussion Our preliminary data demonstrate that ACZ+O2 may be an efficacious combination therapy for some OSA patients.

Abstract Background Weight loss improves upper airway collapsibility in people with obstructive sleep apnoea (OSA). However, it’s unclear how weight loss affects the other endotypes responsible for OSA (loop gain, arousal threshold and muscle compensation). We investigated the effect surgical weight loss has on the OSA endotypes and whether the baseline endotypes predict response to surgery. Methods Endotypes were measured using non-invasive methods in 43 OSA patients who had a clinical polysomnogram before and after (~6-18 months) receiving weight loss surgery. Linear regression was used to assess whether the baseline endotypes predicted improvement in OSA severity defined by the apnoea-hypopnoea index (AHI). Results Weight loss surgery was associated with significant improvements in AHI (43.4[28.6-64.8]events/hr vs. 16.9[11.6-33.3]events/hr, p<0.001), body mass index (42.1 ±5.5kg/m2 vs. 32.8 ±4.5kg/m2, p<0.001), upper airway collapsibility (73.8[65.2-78.5]%eupnea vs. 77.1[71.7-81.3]%eupnea, p=0.034) and loop gain (0.62[0.53-0.71] vs. 0.54[0.44-0.72], p=0.012). Weight loss surgery was also associated with a reduced arousal threshold (144.5[130.1-160.5] vs.136.9[121.9-156.4], p=0.007). A greater reduction in OSA severity was associated with greater improvements in upper airway collapsibility (p=0.001, r2 =0.23) and reductions in the arousal threshold (p<0.001, r2=0.27). Poor upper airway collapsibility at baseline was weakly predictive of a greater improvement in OSA severity (p=0.018, r2 =0.13). No other endotype was predictive of OSA improvement. Discussion Weight loss surgery is associated with improvements in weight, OSA severity, upper airway collapsibility and loop gain. There was a paradoxical worsening of arousal threshold. Furthermore, weight loss surgery may be particularly effective in improving OSA in those with poor upper airway collapsibility.

Monitoring vaccine safety is a complex and shared responsibility. It can be carried out in many ways, one of which is the reporting of individual cases of adverse reactions thought to be due to vaccination. The task is difficult because ascribing causality to an individual case report is fraught with challenges. A standardized evaluation instrument – known as the causality assessment form – was therefore developed for use by an expert advisory committee to facilitate the process. By following the several sections in this form, the members of the committee are taken through a series of points to establish causality. These points include the basic criteria for causation such as biological plausibility, the time elapsed between the vaccine administration and the onset of the adverse event, and whether other factors (drugs, chemicals or underlying disease) could account for the adverse symptoms. The form concludes with a consensus assessment of causality, a commentary about the assessment, and advice for further study or follow-up. This method of assessing the more serious cases of adverse reaction reported to vaccination has proven useful in evaluating ongoing safety of vaccines in Canada. Through analyses such as this, new signals can be identified and investigated further.

Abstract Introduction Currently two leading experimental pharmacological interventions are under investigation for obstructive sleep apnea (OSA). Acetazolamide, which acts to stabilise ventilatory control, lowers the apnea-hypopnea index (AHI) by ∼38%. More recently, atomoxetine-plus-oxybutynin (“AtoOxy”), acting via improvements to dilator muscle responsiveness and baseline tone, was found to lower AHI by >50%. Given that each potential therapy targets a different pathophysiology, we tested whether combined AtoOxy-plus-acetazolamide would be more efficacious than AtoOxy alone. Methods In a multicenter randomised crossover trial, 19 patients with moderate-to-severe OSA received AtoOxy (80/5mg respectively), acetazolamide (500mg), AtoOxy-plus-acetazolamide, or placebo at bedtime for 3 nights (half-dose on first night); outcomes were assessed at baseline and night 3 of each treatment period. Primary outcome: mixed model analysis compared the reduction in AHI(3% desaturation or arousal criterion) from baseline between AtoOxy-plus-acetazolamide and AtoOxy. Secondary outcomes included hypoxic burden, arousal index, and visual analog scale for sleep quality. Results Compared with placebo, AHI was lowered with AtoOxy by +49 [33, 62] %baseline (estimate [95%CI]), AtoOxy-plus-acetazolamide by +47 [31, 61]%baseline, and acetazolamide by +34 [14, 50]%baseline. However, there was no effect of AtoOxy-plus-acetazolamide vs. AtoOxy alone (−3 [−33, 20]%baseline, P=0.8). Secondary outcomes: AtoOxy, acetazolamide and combined AtoOxy-plus-acetazolamide each lowered hypoxic burden and arousal index, but no differential effect of combination therapy was observed. There was no impact on the visual analog scale for sleep quality. Conclusions While AtoOxy halved AHI, and acetazolamide lowered AHI by a third, the combination of these leading experimental interventions provided no greater efficacy than AtoOxy alone.