Suppression of Ventilation-Induced Diaphragm Fibrosis through the Phosphoinositide 3-Kinase-γ in a Murine Bleomycin-Induced Acute Lung Injury Model.

Mechanical ventilation (MV), used in patients with acute lung injury (ALI), induces diaphragmatic myofiber atrophy and contractile inactivity, termed ventilator-induced diaphragm dysfunction. Phosphoinositide 3-kinase-γ (PI3K-γ) is crucial in modulating fibrogenesis during the reparative phase of ALI; however, the mechanisms regulating the interactions among MV, myofiber fibrosis, and PI3K-γ remain unclear. We hypothesized that MV with or without bleomycin treatment would increase diaphragm muscle fibrosis through the PI3K-γ pathway. Five days after receiving a single bolus of 0.075 units of bleomycin intratracheally, C57BL/6 mice were exposed to 6 or 10 mL/kg of MV for 8 h after receiving 5 mg/kg of AS605240 intraperitoneally. In wild-type mice, bleomycin exposure followed by MV 10 mL/kg prompted significant increases in disruptions of diaphragmatic myofibrillar organization, transforming growth factor-ß1, oxidative loads, Masson's trichrome staining, extracellular collagen levels, positive staining of α-smooth muscle actin, PI3K-γ expression, and myonuclear apoptosis (p < 0.05). Decreased diaphragm contractility and peroxisome proliferator-activated receptor-γ coactivator-1α levels were also observed (p < 0.05). MV-augmented bleomycin-induced diaphragm fibrosis and myonuclear apoptosis were attenuated in PI3K-γ-deficient mice and through AS605240-induced inhibition of PI3K-γ activity (p < 0.05). MV-augmented diaphragm fibrosis after bleomycin-induced ALI is partially mediated by PI3K-γ. Therapy targeting PI3K-γ may ameliorate MV-associated diaphragm fibrosis.

Validation of Downloadable Mobile Snore Applications by Polysomnography (PSG).

Purpose: Obstructive sleep apnea (OSA) is a common breathing disorder during sleep that is associated with symptoms such as snoring, excessive daytime sleepiness, and breathing interruptions. Polysomnography (PSG) is the most reliable diagnostic test for OSA; however, its high cost and lengthy testing duration make it difficult to access for many patients. With the availability of free snore applications for home-monitoring, this study aimed to validate the top three ranked snore applications, namely SnoreLab (SL), Anti Snore Solution (ASS), and Sleep Cycle Alarm (SCA), using PSG. Patients and Methods: Sixty participants underwent an overnight PSG while simultaneously using three identical smartphones with the tested apps to gather sleep and snoring data. Results: The study discovered that all three applications were significantly correlated with the total recording time and snore counts of PSG, with ASS showing good agreement with snore counts. Furthermore, the Snore Score, Time Snoring of SL, and Sleep Quality of SCA had a significant correlation with the natural logarithm of apnea hypopnea index (lnAHI) of PSG. The Snore Score of SL and the Sleep Quality of SCA were shown to be useful for evaluating snore severity and for pre-diagnosing or predicting OSA above moderate levels. Conclusion: These findings suggest that some parameters of free snore applications can be employed to monitor OSA progress, and future research could involve adjusted algorithms and larger-scale studies to further authenticate these downloadable snore and sleep applications.

Attenuation of Ventilation-Enhanced Epithelial-Mesenchymal Transition through the Phosphoinositide 3-Kinase-γ in a Murine Bleomycin-Induced Acute Lung Injury Model.

Mechanical ventilation (MV) used in patients with acute lung injury (ALI) induces lung inflammation and causes fibroblast proliferation and excessive collagen deposition-a process termed epithelial-mesenchymal transition (EMT). Phosphoinositide 3-kinase-γ (PI3K-γ) is crucial in modulating EMT during the reparative phase of ALI; however, the mechanisms regulating the interactions among MV, EMT, and PI3K-γ remain unclear. We hypothesized that MV with or without bleomycin treatment would increase EMT through the PI3K-γ pathway. C57BL/6 mice, either wild-type or PI3K-γ-deficient, were exposed to 6 or 30 mL/kg MV for 5 h after receiving 5 mg/kg AS605240 intraperitoneally 5 days after bleomycin administration. We found that, after bleomycin exposure in wild-type mice, high-tidal-volume MV induced substantial increases in inflammatory cytokine production, oxidative loads, Masson's trichrome staining level, positive staining of α-smooth muscle actin, PI3K-γ expression, and bronchial epithelial apoptosis (p < 0.05). Decreased respiratory function, antioxidants, and staining of the epithelial marker Zonula occludens-1 were also observed (p < 0.05). MV-augmented bleomycin-induced pulmonary fibrogenesis and epithelial apoptosis were attenuated in PI3K-γ-deficient mice, and we found pharmacological inhibition of PI3K-γ activity through AS605240 (p < 0.05). Our data suggest that MV augmented EMT after bleomycin-induced ALI, partially through the PI3K-γ pathway. Therapy targeting PI3K-γ may ameliorate MV-associated EMT.

Serial Increases in Human Leukocyte Antigen-DR Expression and Decreases in Interleukin-10 Expression in Alveolar Monocytes of Survivors of Pneumonia-Related Acute Respiratory Distress Syndrome.

ARDS is a potentially lethal syndrome. HLA-DR expression in monocytes reflects their activation and antigen-presenting capacity. However, the correlation between clinical outcomes and HLA-DR expression in alveolar monocytes/macrophages in patients with pneumonia-related ARDS remains unclear. Thus, we determined the trends of HLA-DR and cytokine expressions in alveolar monocytes using repeated measurements to answer this question. Thirty-one pneumonia patients with respiratory failure and ARDS without coronavirus disease 2019 between November 2019 and November 2021 were enrolled in our intensive care unit and three without complete data were excluded. Interleukin (IL)-10, IL-12, and HLA-DR expression in bronchoalveolar lavage (BAL) monocytes were determined on days one and eight. Monocyte HLA-DR expression (mHLA-DR) and CD4 T lymphocytes percentages in BAL cells of survivors increased remarkably after seven days. Monocyte IL-10 expression and monocytes percentages in BAL cells of survivors decreased substantially after seven days. The mHLA-DR was negatively correlated with disease severity scores on day one and eight. In conclusion, serial increases in HLA-DR expression and decreases in IL-10 expression were observed in BAL monocytes of survivors of pneumonia-related ARDS. More studies are needed to confirm this point of view, and then development of a therapeutic agent restoring mHLA-DR and preventing IL-10 production can be considered.

Decreased Monocyte HLA-DR Expression in Patients with Sepsis and Acute Kidney Injury.

Background and objectives: Acute kidney injury (AKI) is common in critically ill patients, especially those with sepsis. Persistently low human leukocyte antigen (HLA)-DR expression in monocytes reflects the decreased function of antigen-presenting cells, contributing to poor outcomes in sepsis. This study aimed to establish an association between AKI and HLA-DR expression in monocytes of patients with sepsis. Materials and Methods: We detected HLA-DR expression in monocytes and measured plasma levels of S100A12, high-mobility group box 1 (HMGB1), advanced glycation end products (AGE), and soluble receptor for AGE (sRAGE) from septic patients and healthy controls. Results: HLA-DR expression in monocytes was decreased in patients with AKI than in those without AKI (29.8 ± 5.0% vs. 53.1 ± 5.8%, p = 0.005). Compared with AKI patients, the mean monocyte HLA-DR expression in patients with end-stage renal disease was increased without statistical significance. There were no differences in the AGE/sRAGE ratio and plasma levels of S100A12, HMGB1, AGE, and sRAGE between patients with and without AKI. Conclusions: Compared with septic patients without AKI, patients with AKI had significantly lower HLA-DR expression in monocytes. The role of hemodialysis in monocyte HLA-DR expression needs further studies to explore.

Increased Production of Interleukin-10 and Tumor Necrosis Factor-Alpha in Stimulated Peripheral Blood Mononuclear Cells after Inhibition of S100A12.

Sepsis may induce immunosuppression and result in death. S100A12 can bind to the receptor for advanced glycation end-products (RAGE) and Toll-like receptor (TLR)4 following induction of various inflammatory responses. It is unclear whether S100A12 significantly influences the immune system, which may be associated with sepsis-related mortality. We measured plasma S100A12 levels and cytokine responses (mean ± standard error mean) of lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells (PBMCs) after S100A12 inhibition in healthy controls and patients with sepsis on days one and seven. Day one plasma soluble RAGE (sRAGE) and S100A12 levels in patients with sepsis were significantly higher than those in controls (2481.3 ± 295.0 vs. 1273.0 ± 108.2 pg/mL, p < 0.001; 530.3 ± 18.2 vs. 310.1 ± 28.1 pg/mL, p < 0.001, respectively). Day seven plasma S100A12 levels in non-survivors were significantly higher than those in survivors (593.1 ± 12.7 vs. 499.3 ± 23.8 pg/mL, p = 0.002, respectively). In survivors, plasma sRAGE levels were significantly decreased after 6 days (2297.3 ± 320.3 vs. 1530.1 ± 219.1 pg/mL, p = 0.009, respectively), but not in non-survivors. Inhibiting S100A12 increased the production of tumor necrosis factor (TNF)-α and interleukin (IL)-10 in stimulated PBMCs for both controls and patients. Therefore, S100A12 plays an important role in sepsis pathogenesis. S100A12 may competitively bind to TLR4 and RAGE, resulting in decreased IL-10 and TNF-α production.

Cellular analysis using label-free parallel array microscopy with Fourier ptychography.

Quantitative phase imaging (QPI) is an ideal method to non-invasively monitor cell populations and provide label-free imaging and analysis. QPI offers enhanced sample characterization and cell counting compared to conventional label-free techniques. We demonstrate this in the current study through a comparison of cell counting data from digital phase contrast (DPC) imaging and from QPI using a system based on Fourier ptychographic microscopy (FPM). Our FPM system offers multi-well, parallel imaging and a QPI-specific cell segmentation method to establish automated and reliable cell counting. Three cell types were studied and FPM showed improvement in the ability to resolve fine details and thin cells, despite limitations of the FPM system incurred by imaging artifacts. Relative to manually counted fluorescence ground-truth, cell counting results after automated segmentation showed improved accuracy with QPI over DPC.

Reduction in Ventilation-Induced Diaphragmatic Mitochondrial Injury through Hypoxia-Inducible Factor 1α in a Murine Endotoxemia Model.

Mechanical ventilation (MV) is essential for patients with sepsis-related respiratory failure but can cause ventilator-induced diaphragm dysfunction (VIDD), which involves diaphragmatic myofiber atrophy and contractile inactivity. Mitochondrial DNA, oxidative stress, mitochondrial dynamics, and biogenesis are associated with VIDD. Hypoxia-inducible factor 1α (HIF-1α) is crucial in the modulation of diaphragm immune responses. The mechanism through which HIF-1α and mitochondria affect sepsis-related diaphragm injury is unknown. We hypothesized that MV with or without endotoxin administration would aggravate diaphragmatic and mitochondrial injuries through HIF-1α. C57BL/6 mice, either wild-type or HIF-1α-deficient, were exposed to MV with or without endotoxemia for 8 h. MV with endotoxemia augmented VIDD and mitochondrial damage, which presented as increased oxidative loads, dynamin-related protein 1 level, mitochondrial DNA level, and the expressions of HIF-1α and light chain 3-II. Furthermore, disarrayed myofibrils; disorganized mitochondria; increased autophagosome numbers; and substantially decreased diaphragm contractility, electron transport chain activities, mitofusin 2, mitochondrial transcription factor A, peroxisome proliferator activated receptor-γ coactivator-1α, and prolyl hydroxylase domain 2 were observed (p < 0.05). Endotoxin-stimulated VIDD and mitochondrial injuries were alleviated in HIF-1α-deficient mice (p < 0.05). Our data revealed that endotoxin aggravated MV-induced diaphragmatic dysfunction and mitochondrial damages, partially through the HIF-1α signaling pathway.

Prospective evaluation of the comorbidity of obstructive sleep apnea in patients with glaucoma.

STUDY OBJECTIVES: This study aimed to identify prospectively the correlation between obstructive sleep apnea (OSA) severity, ocular microcirculation changes, and visual function changes in patients with glaucoma. METHODS: We prospectively enrolled patients with glaucoma who were willing to undergo overnight polysomnography. The enrolled patients were further divided into normal tension glaucoma, high-tension glaucoma, and control. Visual field progression was analyzed using sequential standard automated perimetry. Peripapillary and macular vessel density were assessed through optical coherence tomography angiography (OCT-angiography). The associations between polysomnography parameters, OCT-angiography parameters, and visual field progression were analyzed. RESULTS: A total of 22 patients with normal tension glaucoma, 30 patients with high-tension glaucoma, and 24 control patients were enrolled. Through regression analysis, glaucoma was found to be an independent predictor of moderate-to-severe OSA (P = .035); furthermore, moderate-to-severe OSA was significantly associated with visual field progression (P = .008 in the high-tension glaucoma subgroup and P = .008 in the overall glaucoma). Additionally, OSA severity was negatively correlated with the ganglion cell complex thinning rate in the normal tension glaucoma subgroup. CONCLUSIONS: Presence of glaucoma increased the risk of moderate-to-severe OSA compared with the control group. OSA severity was related to visual field deterioration in patients with glaucoma and further associated with structural progression in the normal tension glaucoma subgroup. Careful monitoring of the comorbid OSA status of patients with glaucoma is essential to prevent disease progression. CITATION: Chan Y-H, Chuang L-H, Yu C-C, et al. Prospective evaluation of the comorbidity of obstructive sleep apnea in patients with glaucoma. J Clin Sleep Med. 2022;18(1):47-56.

High-flow nasal cannula compared with continuous positive airway pressure in the treatment of obstructive sleep apnea.

PURPOSE: Continuous positive airway pressure (CPAP) is a standard treatment for obstructive sleep apnea (OSA). However, CPAP has limitations. High-flow nasal cannula (HFNC) is already in use for various types of respiratory diseases. As HFNC generates positive airway pressure, it may be a potential candidate for OSA treatment. This prospective study compared the therapeutic effects of HFNC to CPAP in patients with OSA. METHODS: Patients whose apnea-hypopnea index (AHI) was > 5 events/h were enrolled in this study. All participants were randomly divided into two groups. The first group underwent CPAP the first night and HFNC the second night. Conversely, the second group received HFNC the first night and CPAP the second night. Their respiratory events and sleep quality were compared using baseline polysomnography, CPAP, and HFNC. RESULTS: In total, 28 participants completed this study. Median [interquartile range] AHI (35.0 [20.0-48.6] vs. 10.8 [5.5-20.6] events/h; p < 0.001) was significantly improved by the HFNC. However, sleep quality was not improved. When CPAP was compared directly with HFNC, CPAP demonstrated a more favorable effect for respiratory events (AHI 5.0 [2.0-7.0] vs. 10.8 [5.5-20.6] events/h; p < 0.001) and sleep efficiency (88.1 [79.9-92.5] vs. 77.9 [69.2-86.6] %; p = 0.001). CONCLUSION: The efficacy of CPAP was superior to HFNC for both respiratory events and sleep quality. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT03843372; URL: www. CLINICALTRIALS: gov ; Date of registration: November 2, 2019.

Pneumonia rebound after stopping steroid in a patient with COVID-19: A case report.

Patients with severe coronavirus disease 2019 (COVID-19) can develop a systemic inflammatory response that can lead to lung injury and multisystem organ dysfunction. The current treatment guideline recommends the use of corticosteroids in patients who require supplemental oxygen or are mechanically ventilated. This study reports a patient with severe COVID-19 pneumonia. Initially, the patient was treated with dexamethasone for 10 days and remdesivir for 5 days. There was clinical improvement following the treatments. However, on day 15, the patient experienced rebound pneumonia and clinical deterioration. His clinical condition improved until dexamethasone was re-administered. This case demonstrates the rebound phenomenon after the steroid was discontinued. The duration and timing of steroids are crucial to reduce the risk of prolonged systemic inflammation and rebound pneumonia.

Increased Death of Peripheral Blood Mononuclear Cells after TLR4 Inhibition in Sepsis Is Not via TNF/TNF Receptor-Mediated Apoptotic Pathway.

BACKGROUND: Apoptosis is one of the causes of immune depression in sepsis. Pyroptosis also occurs in sepsis. The toll-like receptor (TLR) 4 and receptor for advanced glycation end products (RAGE) have been shown to play important roles in apoptosis and pyroptosis. However, it is still unknown whether TLR4 inhibition decreases apoptosis in sepsis. METHODS: Stimulated peripheral blood mononuclear cells (PBMCs) with or without lipopolysaccharides (LPS) and high-mobility group box 1 (HMGB1) were cultured with or without TLR4 inhibition using monoclonal antibodies from 20 patients with sepsis. Caspase-3, caspase-8, and caspase-9 activities were measured. The expression of B cell lymphoma 2 (Bcl2) and Bcl2-associated X (Bax) was measured. The cell death of PBMCs was detected using a flow cytofluorimeter. RESULTS: After TLR4 inhibition, Bcl2 to Bax ratio elevated both in LPS and HMGB1-stimulated PBMCs. The activities of caspase-3, caspase-8, and caspase-9 did not change in LPS or HMGB1-stimulated PBMCs. The cell death of LPS and HMGB1-stimulated CD8 lymphocytes and monocytes increased after TLR4 inhibition. The cell death of CD4 lymphocytes was unchanged. CONCLUSION: The apoptosis did not decrease, while TLR4 was inhibited. After TLR4 inhibition, there was an unknown mechanism to keep cell death in stimulated PBMCs in patients with sepsis.

Effect of compression stockings on overnight rostral fluid shift and obstructive sleep apnea: A meta-analysis.

OBJECTIVE: The overnight rostral fluid shift from the lower limbs is one of the causes of obstructive sleep apnea (OSA). Compression stockings (CS) prevent lower limb fluid retention and have been reported to decrease nighttime fluid shift. The aim of this study is to evaluate the effect of CS on fluid shift and the severity of OSA. METHODS: A systematic literature search was performed in the PubMed, EMBASE and Cochrane Library databases. The data were analyzed using Comprehensive Meta-Analysis software (Version 3; Biostat, Englewood, NJ). Studies evaluating the effect of CS on the overnight fluid shift and OSA severity were included in the analysis. RESULTS: A total of 4 studies were included in this meta-analysis. The pooled analysis showed that the apnea-hypopnea index (AHI) of the overall study group was significantly lower after using CS (SMD, -1.08; 95% CI, -1.49 to -0.67). Decreases in the AHI were also observed in the normal fluid status (SMD, -1.05; 95% CI, -1.73 to -0.37) and fluid overload status (SMD, -1.17; 95% CI, -1.76 to -0.58) populations. The overall study group had significant decreases in overnight changes in neck circumference (SMD, -1.05; 95% CI, -2.06 to -0.03) and leg fluid volume (SMD, -1.14; 95% CI, -1.88 to -0.41) after using CS. However, no significant differences in overnight changes in neck circumference and leg fluid volume were observed in normal fluid status patients. CONCLUSION: CS may help decrease overnight fluid shift and could be a treatment option for OSA.

Suppression of Hypoxia-Inducible Factor 1α by Low-Molecular-Weight Heparin Mitigates Ventilation-Induced Diaphragm Dysfunction in a Murine Endotoxemia Model.

Mechanical ventilation (MV) is required to maintain life for patients with sepsis-related acute lung injury but can cause diaphragmatic myotrauma with muscle damage and weakness, known as ventilator-induced diaphragm dysfunction (VIDD). Hypoxia-inducible factor 1α (HIF-1α) plays a crucial role in inducing inflammation and apoptosis. Low-molecular-weight heparin (LMWH) was proven to have anti-inflammatory properties. However, HIF-1α and LMWH affect sepsis-related diaphragm injury has not been investigated. We hypothesized that LMWH would reduce endotoxin-augmented VIDD through HIF-1α. C57BL/6 mice, either wild-type or HIF-1α-deficient, were exposed to MV with or without endotoxemia for 8 h. Enoxaparin (4 mg/kg) was administered subcutaneously 30 min before MV. MV with endotoxemia aggravated VIDD, as demonstrated by increased interleukin-6 and macrophage inflammatory protein-2 levels, oxidative loads, and the expression of HIF-1α, calpain, caspase-3, atrogin-1, muscle ring finger-1, and microtubule-associated protein light chain 3-II. Disorganized myofibrils, disrupted mitochondria, increased numbers of autophagic and apoptotic mediators, substantial apoptosis of diaphragm muscle fibers, and decreased diaphragm function were also observed (p < 0.05). Endotoxin-exacerbated VIDD and myonuclear apoptosis were attenuated by pharmacologic inhibition by LMWH and in HIF-1α-deficient mice (p < 0.05). Our data indicate that enoxaparin reduces endotoxin-augmented MV-induced diaphragmatic injury, partially through HIF-1α pathway inhibition.

Trazodone improves obstructive sleep apnea after ischemic stroke: a randomized, double-blind, placebo-controlled, crossover pilot study.

BACKGROUND: Low arousal threshold plays a part in the pathogenesis of obstructive sleep apnea (OSA) and may be improved by sedatives. Sedative antidepressants are frequently prescribed for stroke patients due to their high prevalence of insomnia and depression. However, the effect of sedative antidepressants on the severity of OSA in stroke patients has not been studied well. METHODS: In a double-blinded randomized crossover pilot study, 22 post-acute ischemic stroke patients (mean age, 61.7 ± 10.6 y) with OSA received 100 mg of trazodone or a placebo just before polysomnography, with approximately 1 week between measures. The study also measured baseline heart rate variability and 24-h ambulatory blood pressure. RESULTS: Administration of trazodone significantly increased the percentage time of slow-wave sleep (31.5 ± 13.2 vs. 18.4 ± 8.7%; P < 0.001) and improved almost all the parameters of OSA severity, including the apnea-hypopnea index (AHI, 25.4 ± 15.4 vs. 39.1 ± 18.4 events/h; P < 0.001), the respiratory arousal index (9.8 (5.8-11.95) vs. 14.1 (11.3-18.7) events/h; P < 0.001), and the minimum oxygen saturation (80.2 ± 9.1 vs. 77.1 ± 9.6%; P = 0.016). Responders to therapy (AHI reduced by > 50%; n = 7/22) had predominant OSA during rapid-eye-movement sleep and decreased sympathetic tone, as reflected in significantly lower mean blood pressure, diastolic blood pressure, and normalized low-frequency power. CONCLUSIONS: Obstructive sleep apnea with comorbid ischemic stroke may be a distinctive phenotype which responds quite well to trazodone, decreasing OSA severity without increasing nocturnal hypoxia. TRIAL REGISTRATION: Clinicaltrials.gov: NCT04162743, 2019/11/10.

Totally Implanted Port May Be an Alternative to Centrally Inserted Central Catheter for Measurement of Central Venous Pressure.

Background: A conventional centrally inserted central catheter (CICC) is frequently used to measure central venous pressure (CVP) to monitor the cardiocirculatory status of patients. The tip of the totally implanted port (TIP) is inserted at the same location in the superior vena cava as that of a CICC, and the TIP has been implanted in many patients with cancer. Measurements of CVP using CICC (CICCP) and TIP (TIPP) may be closely related. Material and Methods. Ten patients with TIPs in an intensive care unit were prospectively studied, and 121 records of 4536 paired CICCP and TIPP measurements were collected. A bench test in a static or dynamic setting was performed, and 598 paired measurements taken using CICC and TIP were recorded. Results: The measurement of TIPP was highly correlated with that of CICCP in patients with cancer, especially those in a calm state. Patients with a calm state and ≥3 consecutive identical TIPP were recorded (≥30 seconds), and 90% of the mean difference between CICCP and TIPP was ≤2 mmHg. The pressure measurements recorded using CICC and TIP were identical in both the static and dynamic bench tests. Conclusions: TIP may be an alternative to CICC for measuring CVP.

High-flow nasal cannula ventilation therapy for obstructive sleep apnea in ischemic stroke patients requiring nasogastric tube feeding: a preliminary study.

Obstructive sleep apnea (OSA) is associated with increasing risk of recurrent stroke and mortality. Nasogastric tubes used by dysphagic stroke patients may interfere with nasal continuous positive airway pressure (CPAP) due to air leakage. This study was evaluated the effects and short-term tolerability of high-flow nasal cannula (HFNC) therapy for OSA in stroke patients with nasogastric intubation. The HFNC titration study was performed in post-acute ischemic stroke patients with nasogastric intubation and OSA. Then, participants were treated with HFNC therapy in the ward for one week. Eleven participants (eight males) who were all elderly with a median age of 72 (IQR 67-82) years and a body mass index of 23.5 (IQR 22.0-26.6) completed the titration study. The HFNC therapy at a flow rate up to 50~60 L/min significantly decreased the apnea-hypopnea index from 52.0 events/h (IQR 29.9-61.9) to 26.5 events/h (IQR 3.3-34.6) and the total arousal index from 34.6 (IQR 18.6-42.3) to 15.0 (IQR 10.3-25.4). The oxygen desaturation index was also significantly decreased from 53.0 events/h (IQR 37.0-72.8) to 16.2 events/h (IQR 0.8-20.1), accompanied by a significant improvement in the minimum SpO2 level. Finally, only three participants tolerated flow rates of 50~60 L/minute in one-week treatment period. Conclusively, HFNC therapy at therapeutic flow rate is effective at reducing the OSA severity in post-acute ischemic stroke patients with nasogastric intubation. Owing to the suboptimal acceptance, HFNC might be a temporary treatment option, and CPAP therapy is suggested after the nasogastric tube is removed.

Normal tension glaucoma in obstructive sleep apnea syndrome: A structural and functional study.

This study characterized and evaluated normal tension glaucoma (NTG) in obstructive sleep apnea syndrome (OSAS).In this retrospective, cross-sectional study, all participants were examined with polysomnography (PSG). Functional parameters of standard automated perimetry (SAP) were recorded. Structural parameters in optical coherence tomography angiography (OCTA) included peripapillary superficial vessel density (VD RPC), peripapillary whole-layer (VD NH), and superficial and deep macular area VD. Participants were categorized into perimetric and nonperimetric groups by SAP result. Low reliability of SAP and signal strength index <50 in OCTA were excluded.Severity of OSAS was graded by apnea-hypopnea index (AHI) in PSG. Those with moderate/severe OSAS (AHI ≥ 15, n = 39) had longer neck circumference and shorter ocular axial length than mild OSAS (AHI < 15, n = 14). Furthermore, there was significantly higher AHI and larger neck circumference in the NTG perimetric group (n = 27) than in the control group (n = 26; p < 0.001 and p = 0.047, respectively). Superficial and deep-layer peripapillary and macular area VD significantly decreased in the perimetric group. Overall, structural and functional parameters show that VF PSD was negatively correlated with VD NH and VD RPC (p = 0.007, p = 0.015); and VF MD was positively correlated with VD NH (p = 0.029), but not significantly to VD RPC (p = 0.106).OSAS is a risk factor of NTG. With aid of OCTA, whole-layer retinal capillary dropout supports that the vascular dysregulation of OSAS leads to NTG.

Development and validation of a Chinese version of the Sleep Apnea Quality of Life Index.

OBJECTIVE: A Chinese version of the Sleep Apnea Quality of Life Index (SAQLI) for patients with obstructive sleep apnea (OSA) undergoing treatment with continuous positive airway pressure (CPAP) was developed and validated. No Chinese versions of the SAQLI have been previously validated. METHODS: A convenience sample of 78 patients with OSA who received CPAP therapy at a Taiwanese teaching hospital was enrolled. The SAQLI is organized into four domains: daily functioning, social interactions, emotional functioning, and symptoms. This study evaluated the equivalence (forward translation and back translation), validity, and reliability of a Chinese version of the SAQLI. RESULTS: The content validity index (CVI) values of the daily functioning, social interactions, emotional functioning, and symptom domains were .93, .93, .96, and 1.00, respectively. Construct validity of one factor was generated by exploratory factor analysis, and the factor explained the following: (A) daily functioning 54%, (B) social interactions 59%, (C) emotional functioning 64%, and (D) symptoms 75% of total explained variance. The Cronbach's α internal consistency values for the daily functioning, social interactions, emotional functioning, and symptom domains were 0.68, 0.94, 0.93, and 0.92, respectively. The repeatability of the SAQLI at 7 days and 30 days after the first administration showed reliability coefficients of .94 and .93 (p = 0.001), respectively. CONCLUSIONS: The results indicate that the Chinese version of the SAQLI has good reliability and validity, as well as refined indicators for assessing the tool's accuracy. Clinicians may thus use the scale to examine the quality of life in Chinese-speaking patients with OSA undergoing CPAP therapy.

The cancer control status and APACHE II score are prognostic factors for critically ill patients with cancer and sepsis.

BACKGROUND/PURPOSE: Patients with cancer are eligible for hospice care when their life expectancy is 180 days or shorter. This study investigated the prognostic factors of patients with cancer and sepsis who were admitted to an intensive care unit (ICU) to assist with clinical decisions of hospice care. METHODS: A series of 279 patients admitted to the medical ICU with cancer and sepsis were included. Another series of 109 patients with cancer and sepsis admitted to the other medical ICU in the different branch of our hospital was included to verify the results. RESULTS: Among 279 patients, the 30-, 90-, and 180-day mortality rates were 47.3%, 72.0%, and 81.0%, respectively. APACHE II score and the cancer control status (controlled or remission (CR), active newly diagnosed (AND) and active recurrent or progressive (ARP)) were significant predictors of 30- and 90-day mortality(30-day: AND(odds ratio: 5.66; 95% confidence interval: 2.12-15.15), ARP(6.24; 2.92-13.33), APACHE II( 1.07; 1.03-1.11); 90-day: AND(4.78; 1.91-11.99), ARP( 24.03; 11.11-51.99), APACHE II( 1.07; 1.02-1.19)) and were associated with a poor 180-day outcome. The 180-day mortality were significantly different among the patients with different cancer control status in the series of 279 patients (CR: 29.8%; AND: 69.4%; and ARP: 98.9 %) and that of 109 patients (46.4%; 96.8%; and 94.0%). CONCLUSION: APACHE II score and the cancer control status may be the prognostic factors for critically ill patients with cancer and sepsis, and they may be helpful for evaluating hospice care.