Background: The efficacy of high-flow nasal oxygenation (HFNO) in improving oxygenation is influenced by several factors, and its effectiveness is not always guaranteed. Therefore, we aimed to compare the effects of HFNO and standard low-flow nasal oxygenation during rigid bronchoscopy in the apneic patients. Methods: All patients were administered general anesthesia with full muscle relaxation and were randomly assigned to receive either HFNO (HFNO group) or standard low-flow oxygenation (Standard group). The study endpoints included the lowest peripheral oxygen saturation (SpO2), hypoxemia-related surgical interruptions (SpO2 ≤ 94%), and changes in arterial oxygen tension (PaO2) and carbon dioxide tension (PaCO2) during the apnea period for rigid bronchoscopy. Results: A total of 53 patients completed the study. No significant differences were found between the HFNO and the Standard groups in the lowest SpO2 levels (median [Q1, Q3]; 99 [98, 100]% vs. 98 [94, 100]%, P = 0.059) and in the increase rate of PaCO2 (mean ± standard deviation [SD]; 1.6 ± 0.7 mmHg/min vs. 2.0 ± 0.8 mmHg/min, P = 0.064). However, the HFNO group had fewer patients with hypoxemia-related surgical interruptions than the Standard group (1 [3.8%] vs. 8 [29.6%], P = 0.024) and exhibited an attenuated decline rate in PaO2 (median [Q1, Q3]: 4.6 [0.0, 7.9] mmHg/min vs. 10.5 [6.4, 12.9] mmHg/min, P = 0.005). Conclusions While HFNO did not enhance the lowest SpO2 levels in comparison with standard low-flow oxygenation, it did reduce hypoxemia-related surgical interruptions with an attenuated decline in PaO2. Therefore, HFNO has considerable clinical efficacy for rigid bronchoscopy.

Background: The efficacy of high-flow nasal oxygenation (HFNO) in improving oxygenation is influenced by several factors, and its effectiveness is not always guaranteed. Therefore, we aimed to compare the effects of HFNO and standard low-flow nasal oxygenation during rigid bronchoscopy in the apneic patients. Methods: All patients were administered general anesthesia with full muscle relaxation and were randomly assigned to receive either HFNO (HFNO group) or standard low-flow oxygenation (Standard group). The study endpoints included the lowest peripheral oxygen saturation (SpO2), hypoxemia-related surgical interruptions (SpO2 ≤ 94%), and changes in arterial oxygen tension (PaO2) and carbon dioxide tension (PaCO2) during the apnea period for rigid bronchoscopy. Results: A total of 53 patients completed the study. No significant differences were found between the HFNO and the Standard groups in the lowest SpO2 levels (median [Q1, Q3]; 99 [98, 100]% vs. 98 [94, 100]%, P = 0.059) and in the increase rate of PaCO2 (mean ± standard deviation [SD]; 1.6 ± 0.7 mmHg/min vs. 2.0 ± 0.8 mmHg/min, P = 0.064). However, the HFNO group had fewer patients with hypoxemia-related surgical interruptions than the Standard group (1 [3.8%] vs. 8 [29.6%], P = 0.024) and exhibited an attenuated decline rate in PaO2 (median [Q1, Q3]: 4.6 [0.0, 7.9] mmHg/min vs. 10.5 [6.4, 12.9] mmHg/min, P = 0.005). Conclusions While HFNO did not enhance the lowest SpO2 levels in comparison with standard low-flow oxygenation, it did reduce hypoxemia-related surgical interruptions with an attenuated decline in PaO2. Therefore, HFNO has considerable clinical efficacy for rigid bronchoscopy.

Background: The efficacy of high-flow nasal oxygenation (HFNO) in improving oxygenation is influenced by several factors, and its effectiveness is not always guaranteed. Therefore, we aimed to compare the effects of HFNO and standard low-flow nasal oxygenation during rigid bronchoscopy in the apneic patients. Methods: All patients were administered general anesthesia with full muscle relaxation and were randomly assigned to receive either HFNO (HFNO group) or standard low-flow oxygenation (Standard group). The study endpoints included the lowest peripheral oxygen saturation (SpO2), hypoxemia-related surgical interruptions (SpO2 ≤ 94%), and changes in arterial oxygen tension (PaO2) and carbon dioxide tension (PaCO2) during the apnea period for rigid bronchoscopy. Results: A total of 53 patients completed the study. No significant differences were found between the HFNO and the Standard groups in the lowest SpO2 levels (median [Q1, Q3]; 99 [98, 100]% vs. 98 [94, 100]%, P = 0.059) and in the increase rate of PaCO2 (mean ± standard deviation [SD]; 1.6 ± 0.7 mmHg/min vs. 2.0 ± 0.8 mmHg/min, P = 0.064). However, the HFNO group had fewer patients with hypoxemia-related surgical interruptions than the Standard group (1 [3.8%] vs. 8 [29.6%], P = 0.024) and exhibited an attenuated decline rate in PaO2 (median [Q1, Q3]: 4.6 [0.0, 7.9] mmHg/min vs. 10.5 [6.4, 12.9] mmHg/min, P = 0.005). Conclusions While HFNO did not enhance the lowest SpO2 levels in comparison with standard low-flow oxygenation, it did reduce hypoxemia-related surgical interruptions with an attenuated decline in PaO2. Therefore, HFNO has considerable clinical efficacy for rigid bronchoscopy.

Background: The efficacy of high-flow nasal oxygenation (HFNO) in improving oxygenation is influenced by several factors, and its effectiveness is not always guaranteed. Therefore, we aimed to compare the effects of HFNO and standard low-flow nasal oxygenation during rigid bronchoscopy in the apneic patients. Methods: All patients were administered general anesthesia with full muscle relaxation and were randomly assigned to receive either HFNO (HFNO group) or standard low-flow oxygenation (Standard group). The study endpoints included the lowest peripheral oxygen saturation (SpO2), hypoxemia-related surgical interruptions (SpO2 ≤ 94%), and changes in arterial oxygen tension (PaO2) and carbon dioxide tension (PaCO2) during the apnea period for rigid bronchoscopy. Results: A total of 53 patients completed the study. No significant differences were found between the HFNO and the Standard groups in the lowest SpO2 levels (median [Q1, Q3]; 99 [98, 100]% vs. 98 [94, 100]%, P = 0.059) and in the increase rate of PaCO2 (mean ± standard deviation [SD]; 1.6 ± 0.7 mmHg/min vs. 2.0 ± 0.8 mmHg/min, P = 0.064). However, the HFNO group had fewer patients with hypoxemia-related surgical interruptions than the Standard group (1 [3.8%] vs. 8 [29.6%], P = 0.024) and exhibited an attenuated decline rate in PaO2 (median [Q1, Q3]: 4.6 [0.0, 7.9] mmHg/min vs. 10.5 [6.4, 12.9] mmHg/min, P = 0.005). Conclusions While HFNO did not enhance the lowest SpO2 levels in comparison with standard low-flow oxygenation, it did reduce hypoxemia-related surgical interruptions with an attenuated decline in PaO2. Therefore, HFNO has considerable clinical efficacy for rigid bronchoscopy.

Background: Ischemia-reperfusion (I/R) injury is inevitable during the perioperative period. The pancreas is susceptible to I/R injury. Autophagy, a self-digestion process, is upregulated during I/R injury and strongly induced by hypoxia. This study aims to determine whether dexmedetomidine can decrease pancreatic β-cell damage by regulating autophagy under hypoxia. Methods: INS-1 rat insulinoma cells were cultured in dexmedetomidine before being exposed to cobalt chloride (CoCl2)-induced hypoxia. Cell viability and the expression of autophagy-related proteins (light chain 3B [LC3B]-II, p62, and ATGs) were assessed. The expression of apoptosis-related proteins (BCL-2 and P-BAD) were also evaluated. CoCl2-treated INS-1 cells were pretreated with the autophagosome formation inhibitor, 3-methyladenine (3-MA), to compare its effects with those of dexmedetomidine. Bafilomycin-A1 (Baf-A1) that inhibits autophagosome degradation was used to confirm the changes in autophagosome formation induced by dexmedetomidine. Results: Dexmedetomidine attenuated the increased expression of autophagic proteins (LC3B-II, p62, and ATGs) and reversed the CoCl2-induced reduction in the proliferation of INS-1 cells after hypoxia. Dexmedetomidine also alleviated the decreased expression of the anti-apoptotic protein (BCL-2) and the increased expression of apoptotic protein (BAX). Dexmedetomidine reduces the activation of autophagy through inhibiting autophagosome formation, as confirmed by a decrease in LC3B-II/I ratio, a marker of autophagosome formation, in LC3B turnover assay combined with Baf-A1. Conclusions Dexmedetomidine alleviates the degree of cellular damage in INS-1 cells against CoCl2-induced hypoxia by regulating autophagosome formation. These results provide a basis for further studies to confirm these effects in clinical practice.

Background: Ischemia-reperfusion (I/R) injury is inevitable during the perioperative period. The pancreas is susceptible to I/R injury. Autophagy, a self-digestion process, is upregulated during I/R injury and strongly induced by hypoxia. This study aims to determine whether dexmedetomidine can decrease pancreatic β-cell damage by regulating autophagy under hypoxia. Methods: INS-1 rat insulinoma cells were cultured in dexmedetomidine before being exposed to cobalt chloride (CoCl2)-induced hypoxia. Cell viability and the expression of autophagy-related proteins (light chain 3B [LC3B]-II, p62, and ATGs) were assessed. The expression of apoptosis-related proteins (BCL-2 and P-BAD) were also evaluated. CoCl2-treated INS-1 cells were pretreated with the autophagosome formation inhibitor, 3-methyladenine (3-MA), to compare its effects with those of dexmedetomidine. Bafilomycin-A1 (Baf-A1) that inhibits autophagosome degradation was used to confirm the changes in autophagosome formation induced by dexmedetomidine. Results: Dexmedetomidine attenuated the increased expression of autophagic proteins (LC3B-II, p62, and ATGs) and reversed the CoCl2-induced reduction in the proliferation of INS-1 cells after hypoxia. Dexmedetomidine also alleviated the decreased expression of the anti-apoptotic protein (BCL-2) and the increased expression of apoptotic protein (BAX). Dexmedetomidine reduces the activation of autophagy through inhibiting autophagosome formation, as confirmed by a decrease in LC3B-II/I ratio, a marker of autophagosome formation, in LC3B turnover assay combined with Baf-A1. Conclusions Dexmedetomidine alleviates the degree of cellular damage in INS-1 cells against CoCl2-induced hypoxia by regulating autophagosome formation. These results provide a basis for further studies to confirm these effects in clinical practice.

Background: Ischemia-reperfusion (I/R) injury is inevitable during the perioperative period. The pancreas is susceptible to I/R injury. Autophagy, a self-digestion process, is upregulated during I/R injury and strongly induced by hypoxia. This study aims to determine whether dexmedetomidine can decrease pancreatic β-cell damage by regulating autophagy under hypoxia. Methods: INS-1 rat insulinoma cells were cultured in dexmedetomidine before being exposed to cobalt chloride (CoCl2)-induced hypoxia. Cell viability and the expression of autophagy-related proteins (light chain 3B [LC3B]-II, p62, and ATGs) were assessed. The expression of apoptosis-related proteins (BCL-2 and P-BAD) were also evaluated. CoCl2-treated INS-1 cells were pretreated with the autophagosome formation inhibitor, 3-methyladenine (3-MA), to compare its effects with those of dexmedetomidine. Bafilomycin-A1 (Baf-A1) that inhibits autophagosome degradation was used to confirm the changes in autophagosome formation induced by dexmedetomidine. Results: Dexmedetomidine attenuated the increased expression of autophagic proteins (LC3B-II, p62, and ATGs) and reversed the CoCl2-induced reduction in the proliferation of INS-1 cells after hypoxia. Dexmedetomidine also alleviated the decreased expression of the anti-apoptotic protein (BCL-2) and the increased expression of apoptotic protein (BAX). Dexmedetomidine reduces the activation of autophagy through inhibiting autophagosome formation, as confirmed by a decrease in LC3B-II/I ratio, a marker of autophagosome formation, in LC3B turnover assay combined with Baf-A1. Conclusions Dexmedetomidine alleviates the degree of cellular damage in INS-1 cells against CoCl2-induced hypoxia by regulating autophagosome formation. These results provide a basis for further studies to confirm these effects in clinical practice.

Background: Ischemia-reperfusion (I/R) injury is inevitable during the perioperative period. The pancreas is susceptible to I/R injury. Autophagy, a self-digestion process, is upregulated during I/R injury and strongly induced by hypoxia. This study aims to determine whether dexmedetomidine can decrease pancreatic β-cell damage by regulating autophagy under hypoxia. Methods: INS-1 rat insulinoma cells were cultured in dexmedetomidine before being exposed to cobalt chloride (CoCl2)-induced hypoxia. Cell viability and the expression of autophagy-related proteins (light chain 3B [LC3B]-II, p62, and ATGs) were assessed. The expression of apoptosis-related proteins (BCL-2 and P-BAD) were also evaluated. CoCl2-treated INS-1 cells were pretreated with the autophagosome formation inhibitor, 3-methyladenine (3-MA), to compare its effects with those of dexmedetomidine. Bafilomycin-A1 (Baf-A1) that inhibits autophagosome degradation was used to confirm the changes in autophagosome formation induced by dexmedetomidine. Results: Dexmedetomidine attenuated the increased expression of autophagic proteins (LC3B-II, p62, and ATGs) and reversed the CoCl2-induced reduction in the proliferation of INS-1 cells after hypoxia. Dexmedetomidine also alleviated the decreased expression of the anti-apoptotic protein (BCL-2) and the increased expression of apoptotic protein (BAX). Dexmedetomidine reduces the activation of autophagy through inhibiting autophagosome formation, as confirmed by a decrease in LC3B-II/I ratio, a marker of autophagosome formation, in LC3B turnover assay combined with Baf-A1. Conclusions Dexmedetomidine alleviates the degree of cellular damage in INS-1 cells against CoCl2-induced hypoxia by regulating autophagosome formation. These results provide a basis for further studies to confirm these effects in clinical practice.

Objective: To systematically review the efficacy of e-Health interventions on physical performance, activity and quality of life in older adults with sarcopenia or frailty. Methods: A systematic review was conducted by searching the MEDLINE, Embase, Cochrane Library, CINHAL, Web of Science, and the Physiotherapy Evidence Database for experimental studies published in English from 1990 to 2021. E-Health studies investigating physical activity, physical performance, quality of life, and activity of daily living assessment in adults aged ≥65 years with sarcopenia or frailty were selected. Results: Among the 3,164 identified articles screened, a total of 4 studies complied with the inclusion criteria. The studies were heterogeneous by participant characteristics, type of e-Health intervention, and outcome measurement. Age criteria for participant selection and sex distribution were different between studies. Each study used different criteria for frailty, and no study used sarcopenia as a selection criteria. E-Health interventions were various across studies. Two studies used frailty status as an outcome measure and showed conflicting results. Muscle strength was assessed in 2 studies, and meta-analysis showed statistically significant improvement after intervention (standardized mean difference, 0.51; 95% confidence interval, 0.07–0.94; p=0.80, I2=0%). Conclusion This systematic review found insufficient evidence to support the efficacy of e-Health interventions. Nevertheless, the studies included in this review showed positive effects of e-Health interventions on improving muscle strength, physical activity, and quality of life in older adults with frailty.

We report an extremely severe case of dysphagia in an elderly patient. Tracheostomy alone was found to be the cause of severe upper esophageal opening dysfunction. An 84-year-old woman was admitted with dyspnea. During hospitalization, she had respiratory failure and underwent a tracheostomy. On day 41 in the hospital, she complained of dysphagia and was a swallowing evaluation was done at the rehabilitation department. We ruled out other etiologies of upper esophageal dysfunction through a brain magnetic resonance imaging (MRI) and endoscopic evaluation. Through follow-up tests, it was found retrospectively that extreme dysphagia could have occurred through the following mechanism: the airway was not protected at the time of the tracheostomy because the movement of the epiglottis did not appear to be normal. This was due to the reduction in laryngeal function affecting the upper esophageal opening after the tracheostomy, and at the same time, the power to push the bolus was weak. After 6 months, at the third test, she had improved enough to ingest a soft diet and fluid with thickeners, so she was able to start an oral diet without decannulation. It is thus important to recognize that tracheostomy alone can cause extremely severe aspiration. If these findings are observed in patients undergoing tracheostomy, it is necessary to check the movements of the epiglottis properly and evaluate whether the condition can be improved by rehabilitation treatment.