Objective: Sleep disturbances are common and debilitating nonmotor symptoms (NMS) in Parkinson’s disease (PD) patients and profoundly affect quality of life. Despite emerging evidence suggesting that monoamine oxidase B (MAO-B) and catechol-O-methyltransferase (COMT) inhibitors may alleviate NMS, their specific effects on sleep remain unclear. The aim of this network meta-analysis (NMA) was to compare the efficacy of these inhibitors related to sleep problems in PD patients. Methods: Following a systematic search of PubMed, Cochrane, and Embase, studies comparing MAO-B or COMT inhibitors and assessing sleep outcomes in PD patients were identified. An NMA was conducted using data from the seven studies that met our inclusion criteria. The outcomes included subjective sleep quality, daytime sleepiness, and objective polysomnography (PSG) parameters. Results: No statistically significant differences were found between the effects of the MAO-B and COMT inhibitors on improving subjective sleep quality or daytime sleepiness. However, analyses of objective PSG data revealed that, compared with rasagiline and placebo, safinamide significantly increased rapid eye movement sleep duration (mean difference, 5.70 min [95% CI, 2.26 to 9.14]) and decreased wake time after sleep onset (mean difference, -10.20 min [-19.38 to -1.02]). Conclusion These findings suggest that safinamide may offer additional value for managing sleep disruptions beyond its known motor benefits in patients with PD. Given the limited number and small scale of available trials, the overall evidence should be interpreted cautiously. Nonetheless, this analysis highlights the need for future high-quality trials focused on sleep outcomes to guide the personalized use of MAO-B and COMT inhibitors for sleep disturbances in PD patients.

Acute Respiratory Distress Syndrome (ARDS) is a severe condition characterized by extensive lung inflammation and increased alveolar-capillary permeability, often triggered by infections or systemic inflammatory responses. Mesenchymal stem cells (MSCs)-based therapy holds promise for treating ARDS, as MSCs manifest immunomodulatory and regenerative properties that mitigate inflammation and enhance tissue repair. Primed MSCs, modified to augment specific functionalities, demonstrate superior therapeutic efficacy in targeted therapies compared to naive MSCs. This study explored the immunomodulatory potential of MSCs using mixed lymphocyte reaction (MLR) assays and co-culture experiments with M1/M2 macrophages. Additionally, RNA sequencing was employed to identify alterations in immune and inflammation-related factors in primed MSCs. The therapeutic effects of primed MSCs were assessed in an LPS-induced ARDS mouse model, and the underlying mechanisms were investigated through spatial transcriptomics analysis. The study revealed that MSCs primed with IFN-γ and IL-1β significantly enhanced the suppression of T cell activity compared to naive MSCs, concurrently inhibiting TNF-α while increasing IL-10 production in macrophages. Notably, combined treatment with these two cytokines resulted in a significant upregulation of immune and inflammation-regulating factors. Furthermore, our analyses elucidated the mechanisms behind the therapeutic effects of primed MSCs, including the inhibition of inflammatory cell infiltration in lung tissue, modulation of immune and inflammatory responses, and enhancement of elastin fiber formation. Signaling pathway analysis confirmed that efficacy could be enhanced by modulating NFκB and TNF-α signaling. In conclusion, in early-phase ARDS, primed MSCs displayed enhanced homing capabilities, improved lung function, and reduced inflammation.

Acute Respiratory Distress Syndrome (ARDS) is a severe condition characterized by extensive lung inflammation and increased alveolar-capillary permeability, often triggered by infections or systemic inflammatory responses. Mesenchymal stem cells (MSCs)-based therapy holds promise for treating ARDS, as MSCs manifest immunomodulatory and regenerative properties that mitigate inflammation and enhance tissue repair. Primed MSCs, modified to augment specific functionalities, demonstrate superior therapeutic efficacy in targeted therapies compared to naive MSCs. This study explored the immunomodulatory potential of MSCs using mixed lymphocyte reaction (MLR) assays and co-culture experiments with M1/M2 macrophages. Additionally, RNA sequencing was employed to identify alterations in immune and inflammation-related factors in primed MSCs. The therapeutic effects of primed MSCs were assessed in an LPS-induced ARDS mouse model, and the underlying mechanisms were investigated through spatial transcriptomics analysis. The study revealed that MSCs primed with IFN-γ and IL-1β significantly enhanced the suppression of T cell activity compared to naive MSCs, concurrently inhibiting TNF-α while increasing IL-10 production in macrophages. Notably, combined treatment with these two cytokines resulted in a significant upregulation of immune and inflammation-regulating factors. Furthermore, our analyses elucidated the mechanisms behind the therapeutic effects of primed MSCs, including the inhibition of inflammatory cell infiltration in lung tissue, modulation of immune and inflammatory responses, and enhancement of elastin fiber formation. Signaling pathway analysis confirmed that efficacy could be enhanced by modulating NFκB and TNF-α signaling. In conclusion, in early-phase ARDS, primed MSCs displayed enhanced homing capabilities, improved lung function, and reduced inflammation.

Acute Respiratory Distress Syndrome (ARDS) is a severe condition characterized by extensive lung inflammation and increased alveolar-capillary permeability, often triggered by infections or systemic inflammatory responses. Mesenchymal stem cells (MSCs)-based therapy holds promise for treating ARDS, as MSCs manifest immunomodulatory and regenerative properties that mitigate inflammation and enhance tissue repair. Primed MSCs, modified to augment specific functionalities, demonstrate superior therapeutic efficacy in targeted therapies compared to naive MSCs. This study explored the immunomodulatory potential of MSCs using mixed lymphocyte reaction (MLR) assays and co-culture experiments with M1/M2 macrophages. Additionally, RNA sequencing was employed to identify alterations in immune and inflammation-related factors in primed MSCs. The therapeutic effects of primed MSCs were assessed in an LPS-induced ARDS mouse model, and the underlying mechanisms were investigated through spatial transcriptomics analysis. The study revealed that MSCs primed with IFN-γ and IL-1β significantly enhanced the suppression of T cell activity compared to naive MSCs, concurrently inhibiting TNF-α while increasing IL-10 production in macrophages. Notably, combined treatment with these two cytokines resulted in a significant upregulation of immune and inflammation-regulating factors. Furthermore, our analyses elucidated the mechanisms behind the therapeutic effects of primed MSCs, including the inhibition of inflammatory cell infiltration in lung tissue, modulation of immune and inflammatory responses, and enhancement of elastin fiber formation. Signaling pathway analysis confirmed that efficacy could be enhanced by modulating NFκB and TNF-α signaling. In conclusion, in early-phase ARDS, primed MSCs displayed enhanced homing capabilities, improved lung function, and reduced inflammation.

This retrospective study aims to evaluate the clinical outcomes of tracheal stent placement in dogs with tracheal collapse, identifying factors associated with success rates and adverse effects. Thirty-one dogs treated with intraluminal self-expanding nitinol stents for tracheal collapse at Smart Animal Hospital from 2018 to 2023 were analyzed. The investigation focused on median follow-up time (MFT), clinical outcomes, and factors affecting success and complications, including age at the time of stent placement, presence of stent-related complications, and concurrent bronchial collapse. The average follow-up time was 592 days, ranging from 35 to 2,189 days. As of December 31, 2023, 11 dogs were alive, 10 had died, and 10 were lost to follow-up. Excluding those lost to follow-up, 80% survived more than a year post-procedure. Yorkshire Terriers were the most common breed, followed by Pomeranians. The average age at the time of stent placement was around 9 years, with an average body weight of approximately 3 kg. There were no notable differences in MFT across age groups, indicating that age at the time of stent placement did not significantly affect survival outcomes. Postoperative outcomes were categorized as "Good" in 51.6% of cases, "Fair" in 32.3%, and "Poor" in 16.1%. Complications, including stent fracture, malposition, and migration, were observed in 23% of the dogs. The majority (83.9%) had concurrent bronchial collapse, which correlated with certain complications but did not significantly affect MFT. Overall, tracheal stent placement is a viable treatment option for canine tracheal collapse, demonstrating significant survival rates and manageable complications. This study underscores the importance of comprehensive postoperative monitoring and highlights the need for further research to optimize treatment strategies and improve patient outcomes in veterinary medicine.

We investigated the stress-induced changes in the lipid and hormonal concentrations in plasma, including cytochrome P450 (CYP)-derived oxidative stress in the liver, and the anti-stresseffect of Korean Red Ginseng (KRG) water extract in mice. Stress induction using restraint increased the levels of corticosterone (CORT), glucose, total cholesterol (TC), and low-den-sity lipoprotein-cholesterol (LDL-C) while decreasing in the levels of insulin and high-density lipoprotein-cholesterol (HDL-C), compared with those of unstressed mice. Restraint-stress also increased the generation of reactive oxygen species (ROS) in plasma by 5.4-fold. More-over, the stress resulted in a 2.8-fold higher production of C-reactive protein (CRP) than the control group. In addition, the catalytic activities of CYP1A2 and CYP3A4 in the liver micro-somes were stimulated by 5.5- and 3.8-fold, respectively, and concomitant ROS formation was elevated by 4.3-fold in the liver extract, compared to the normal group. In contrast, the KRG treatment (5, 20, or 50 mg/kg/day) to stress-exposed 3 groups alleviated the increased CORT, TC, LDL-C, ROS, and CRP levels and restored the decreased insulin concentrations.The enhanced each ROS in the plasma and liver, and the CYP enzyme activities were also attenuated in KRG-treated mice in a concentration-dependent manner. In conclusion, these results suggest that KRG ameliorates stress-induced detrimental effects on the plasma and liver of treated mice.

Background: The incidence of epistaxis during nasotracheal intubation via the left nostril is more frequent than that during intubation via the right nostril. This study evaluated the effect of the reverse bevel and tip direction of the nasotracheal tube on the incidence of epistaxis during nasotracheal intubation via the left nostril. Methods: Patients undergoing right-sided maxillofacial surgery requiring left nasotracheal intubation were randomly allocated to the control (tracheal tube in the conventional direction) or reverse (a 180˚ reverse direction, with the tube bevel facing the nasal septum and the leading edge (i.e., the tip) of the bevel pointing away from the nasal septum) groups (n = 37 for both). The primary outcome was the incidence of epistaxis evaluated using videolaryngoscopy. Results: The incidence of epistaxis in the reverse group was significantly lower than that in the control group (9 [24.3%] vs. 20 [54.1%], P = 0.009; relative risk: 0.45, 95% CI [0.24, 0.85], absolute risk reduction: 29.8%, number needed to treat: 3). The severity of epistaxis was significantly lower in the reverse group (P = 0.002). The first attempt nasal passage (P = 0.027) was significantly higher in the reverse group. Postoperative nasal pain was lower (P < 0.001), and patient satisfaction was higher (P < 0.001) in the reverse group. Nasotracheal tube-related complications did not occur in either group. Conclusions The reverse bevel and tip direction of the nasotracheal tube reduced the incidence and severity of epistaxis and increased patient satisfaction among patients undergoing left nasotracheal intubation.

Background: The incidence of epistaxis during nasotracheal intubation via the left nostril is more frequent than that during intubation via the right nostril. This study evaluated the effect of the reverse bevel and tip direction of the nasotracheal tube on the incidence of epistaxis during nasotracheal intubation via the left nostril. Methods: Patients undergoing right-sided maxillofacial surgery requiring left nasotracheal intubation were randomly allocated to the control (tracheal tube in the conventional direction) or reverse (a 180˚ reverse direction, with the tube bevel facing the nasal septum and the leading edge (i.e., the tip) of the bevel pointing away from the nasal septum) groups (n = 37 for both). The primary outcome was the incidence of epistaxis evaluated using videolaryngoscopy. Results: The incidence of epistaxis in the reverse group was significantly lower than that in the control group (9 [24.3%] vs. 20 [54.1%], P = 0.009; relative risk: 0.45, 95% CI [0.24, 0.85], absolute risk reduction: 29.8%, number needed to treat: 3). The severity of epistaxis was significantly lower in the reverse group (P = 0.002). The first attempt nasal passage (P = 0.027) was significantly higher in the reverse group. Postoperative nasal pain was lower (P < 0.001), and patient satisfaction was higher (P < 0.001) in the reverse group. Nasotracheal tube-related complications did not occur in either group. Conclusions The reverse bevel and tip direction of the nasotracheal tube reduced the incidence and severity of epistaxis and increased patient satisfaction among patients undergoing left nasotracheal intubation.

We investigated the stress-induced changes in the lipid and hormonal concentrations in plasma, including cytochrome P450 (CYP)-derived oxidative stress in the liver, and the anti-stresseffect of Korean Red Ginseng (KRG) water extract in mice. Stress induction using restraint increased the levels of corticosterone (CORT), glucose, total cholesterol (TC), and low-den-sity lipoprotein-cholesterol (LDL-C) while decreasing in the levels of insulin and high-density lipoprotein-cholesterol (HDL-C), compared with those of unstressed mice. Restraint-stress also increased the generation of reactive oxygen species (ROS) in plasma by 5.4-fold. More-over, the stress resulted in a 2.8-fold higher production of C-reactive protein (CRP) than the control group. In addition, the catalytic activities of CYP1A2 and CYP3A4 in the liver micro-somes were stimulated by 5.5- and 3.8-fold, respectively, and concomitant ROS formation was elevated by 4.3-fold in the liver extract, compared to the normal group. In contrast, the KRG treatment (5, 20, or 50 mg/kg/day) to stress-exposed 3 groups alleviated the increased CORT, TC, LDL-C, ROS, and CRP levels and restored the decreased insulin concentrations.The enhanced each ROS in the plasma and liver, and the CYP enzyme activities were also attenuated in KRG-treated mice in a concentration-dependent manner. In conclusion, these results suggest that KRG ameliorates stress-induced detrimental effects on the plasma and liver of treated mice.

We investigated the stress-induced changes in the lipid and hormonal concentrations in plasma, including cytochrome P450 (CYP)-derived oxidative stress in the liver, and the anti-stresseffect of Korean Red Ginseng (KRG) water extract in mice. Stress induction using restraint increased the levels of corticosterone (CORT), glucose, total cholesterol (TC), and low-den-sity lipoprotein-cholesterol (LDL-C) while decreasing in the levels of insulin and high-density lipoprotein-cholesterol (HDL-C), compared with those of unstressed mice. Restraint-stress also increased the generation of reactive oxygen species (ROS) in plasma by 5.4-fold. More-over, the stress resulted in a 2.8-fold higher production of C-reactive protein (CRP) than the control group. In addition, the catalytic activities of CYP1A2 and CYP3A4 in the liver micro-somes were stimulated by 5.5- and 3.8-fold, respectively, and concomitant ROS formation was elevated by 4.3-fold in the liver extract, compared to the normal group. In contrast, the KRG treatment (5, 20, or 50 mg/kg/day) to stress-exposed 3 groups alleviated the increased CORT, TC, LDL-C, ROS, and CRP levels and restored the decreased insulin concentrations.The enhanced each ROS in the plasma and liver, and the CYP enzyme activities were also attenuated in KRG-treated mice in a concentration-dependent manner. In conclusion, these results suggest that KRG ameliorates stress-induced detrimental effects on the plasma and liver of treated mice.