Explore the vast range of titles available.

Background The impact of delaying atrial fibrillation catheter ablation (AFCA) for antiarrhythmic drug (AAD) management on the disease course remains unclear. This study investigated AFCA rhythm outcomes based on the diagnosis‐to‐ablation time (DAT) and AAD responsiveness in participants with persistent AF (PeAF). Methods We included data from 1038 AAD‐resistant PeAF participants, all of whom had a clear time point for AF diagnosis, especially PeAF at diagnosis time, and had undergone an AFCA for the first time. Participants who experienced recurrences of paroxysmal type on AAD therapy were analyzed as a cohort of AAD‐partial responders; those maintaining PeAF on AAD were AAD‐non‐responders. We determined the DAT cutoff for best discriminating long‐term rhythm outcomes using a maximum log‐likelihood estimation method based on the Cox proportional hazard regression model. Results Of the participants (79.8% male; median age 61), 806 (77.6%) were AAD‐non‐responders. AAD‐non‐responders had a higher body mass index and a larger left atrial diameter than AAD‐partial‐responders. They also had a higher incidence of AF recurrence after AFCA (adjusted hazard ratio 1.75, 95% confidence interval 1.33–2.30; log‐rank p < .001) compared to AAD‐partial‐responders. The maximum log‐likelihood estimation showed bimodal cutoffs at 22 and 40 months. The optimal DAT cutoff rhythm outcome was 22 months, which discriminated better in the AAD‐partial‐responders than in the AAD‐non‐responders. Conclusions Both DAT and AAD responsiveness influenced AFCA rhythm outcomes. Delaying AFCA to a DAT of longer than 22 months was inadvisable, particularly in the participants in whom PeAF was changed to paroxysmal AF during AAD therapy. AAD‐non‐responders had a higher incidence of AF recurrence after AFCA compared to AAD‐partial‐responders. The maximum log‐likelihood estimation showed bimodal cutoffs at 22 and 40 months. The optimal DAT cutoff rhythm outcome was 22 months, which discriminated better in the AAD‐partial‐responders than in the AAD‐non‐responders.

Spiraea prunifolia : var. simpliciflora (SP) is a known medical food that is used to treat emesis, malaria, and fever. This study investigated the therapeutic potential of SP leaf extract on oxidative stress and airway inflammation using a chronic obstructive pulmonary disease (COPD) mouse model induced by porcine pancreatic elastase (PPE) and lipopolysaccharide (LPS). Male C57BL/6N mice were treated intratracheal instillation of PPE (0.05 units/50 μL) and LPS (5 μg/50 μL), and administered positive control (dexamethasone; 3 mg/kg) and SP (50 and 100 mg/kg). SP treatment decreased T helper type 1 (Th-1) cytokines as well as counts of macrophage and neutrophil in bronchoalveolar lavage fluid of PPE/LPS-induced COPD. SP treatment reduced alveolar destruction, inflammatory cell infiltration, and collagen fiber with improvement of forced expiratory volume to forced vital capacity ratio and lung elastance in lung tissue. SP downregulated thioredoxin-interacting protein and NOD-like receptor pyrin domain-containing 3 inflammasome which inhibited caspase-1 and IL-1β expression. SP attenuated production of reactive oxygen and nitric oxide through enhancement of nuclear factor-erythroid 2-related factor translocation with elevation of heme oxygenase-1 and NAD(P)H quinone oxidoreductase 1 expression. Furthermore, SP attenuated the levels of reactive oxygen species and nitric oxide in mice with PPE/LPS-induced COPD. Thus, SP has the therapeutic potential for COPD treatment.

There are little direct comparative evidences of strategies between ≥50% and the absolute target goal of low-density lipoprotein cholesterol (LDL-C) level <55 mg/100 ml for the patients who underwent percutaneous coronary intervention (PCI). This study aimed to investigate the clinical impact of different strategies between 2 groups of patients who underwent PCI. A total of 3,104 patients with previous PCI were retrospectively enrolled from 2014 to 2020 at Yeungnam University Medical Center. The study population was stratified into 2 groups based on whether the LDL-C level was <55 mg/100 ml at the 1-year mark or not. Furthermore, the 50% reduction rate of LDL-C was also categorized based on whether it had decreased by ≥50% from the initial LDL-C level at the 1-year mark. The primary end point was 3-year major adverse cardiovascular events (MACEs) which were defined as a composite of cardiovascular death, nonfatal myocardial infarction, target lesion revascularization, hospitalization for heart failure, or nonfatal stroke. There was no significant difference between the LDL <55 mg/100 ml group and the LDL ≥55 mg/100 ml group in the risk of MACEs (hazard ratio 1.06, 95% confidence interval 0.81 to 1.38, p = 0.690) after propensity score matching. However, the group that achieved ≥50% reduction of LDL-C from baseline LDL-C level showed a significant reduction in the occurrence of MACEs in the subgroup of LDL-C level ≥55 mg/100 ml (hazard ratio 0.41, 95% confidence interval 0.19 to 0.89, p = 0.025) compared with the group with <50% reduction of LDL-C. In all patients, the achievement rate of target LDL-C <55 mg/100 ml and more than 50% reduction from baseline was 17.2%. In conclusion, guideline-directed management strategy of ≥50% reduction of LDL-C from the baseline will be needed to reduce the incidence of MACEs in patients with LDL-C ≥55 mg/100 ml who underwent PCI. Additional efforts to increase the target goal achievement rate of LDL-C are warranted.

Sepsis, characterized by an uncontrolled host inflammatory response to infections, remains a leading cause of death in critically ill patients worldwide. Sepsis-associated thrombocytopenia (SAT), a common disease in patients with sepsis, is an indicator of disease severity. Therefore, alleviating SAT is an important aspect of sepsis treatment; however, platelet transfusion is the only available treatment strategy for SAT. The pathogenesis of SAT involves increased platelet desialylation and activation. In this study, we investigated the effects of Myristica fragrans ethanol extract (MF) on sepsis and SAT. Desialylation and activation of platelets treated with sialidase and adenosine diphosphate (platelet agonist) were assessed using flow cytometry. The extract inhibited platelet desialylation and activation via inhibiting bacterial sialidase activity in washed platelets. Moreover, MF improved survival and reduced organ damage and inflammation in a mouse model of cecal ligation and puncture (CLP)-induced sepsis. It also prevented platelet desialylation and activation via inhibiting circulating sialidase activity, while maintaining platelet count. Inhibition of platelet desialylation reduces hepatic Ashwell–Morell receptor-mediated platelet clearance, thereby reducing hepatic JAK2/STAT3 phosphorylation and thrombopoietin mRNA expression. This study lays a foundation for the development of plant-derived therapeutics for sepsis and SAT and provides insights into sialidase-inhibition-based sepsis treatment strategies.

Alnus hirsuta (Spach) Rupr. (AH), a member of the Betulaceae family, is widely used in Eastern Asia of as a source of medicinal compounds for the treatment of hemorrhage, diarrhea, and alcoholism. In this study, we investigated the protective effects of a methanolic extract of AH branches against airway inflammation and mucus production in tumor necrosis factor (TNF)-α-stimulated NCI-H292 cells and in an ovalbumin (OVA)-challenged allergic asthma mouse model. Female BALB/c mice were injected with OVA (40 μg) and aluminum hydroxide (2 mg) on days 0 and 14 to induce allergic airway inflammation. The mice were then challenged with 1% OVA from days 21–23. Mice were treated with AH (50 and 100 mg/kg/day; 2% DMSO) or dexamethasone (positive control; 3 mg/kg/day) from days 18–23. AH treatment effectively attenuated airway resistance/hyperresponsiveness and reduced levels of T helper type 2 (Th2) cytokines, eotaxins, and number of inflammatory cells in bronchoalveolar lavage fluid, and immunoglobulin E in serums of OVA-challenged mice. In histological analysis, AH treatment significantly inhibited airway inflammation and mucus production in OVA-challenged mice. AH treatment downregulated the phosphorylation of I kappa B-alpha, p65 nuclear factor-kappa B (p65NF-κB), and mitogen-activated protein kinases with suppression of mucin 5AC (MUC5AC) in lung tissue. Moreover, AH treatment decreased the levels of pro-inflammatory cytokines and Th2 cytokines, as well as MUC5AC expression, and inhibited the phosphorylation of p65NF-κB in TNF-α-stimulated NCI-H292 cells. These results indicate that AH might represent a useful therapeutic agent for the treatment of allergic asthma.

Lindera obtusiloba is widespread in northeast Asia and used for treatment of improvement of blood circulation and anti-inflammation. In this study, we investigated anti-inflammatory and anti-oxidant effects of the methanolic extract of L. obtusiloba leaves (LOL) in an ovalbumin (OVA)-challenged allergic asthma model and tumor necrosis factor (TNF)-α-stimulated NCI-H292 cell. Female BALB/c mice were sensitized with OVA by intraperitoneal injection on days 0 and 14, and airway-challenged with OVA from days 21 to 23. Mice were administered 50 and 100 mg/kg of LOL by oral gavage 1 h before the challenge. LOL treatment effectively decreased airway hyper-responsiveness and inhibited inflammatory cell recruitment, Th2 cytokines, mucin 5AC (MUC5AC) in bronchoalveolar lavage fluid in OVA-challenged mice, which were accompanied by marked suppression of airway inflammation and mucus production in the lung tissue. LOL pretreatment inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB) with suppression of activator protein (AP)-1 and MUC5AC in the lung tissue. LOL also down-regulated expression of inflammatory cytokines, and inhibited the activation of NF-κB in TNF-α-stimulated NCI-H292 cells. LOL elevated the translocation of nuclear factor-erythroid 2-related factor (Nrf-2) into nucleus concurrent with increase of heme oxyngenase-1 (HO-1) and NAD(P)H quinine oxidoreductase 1 (NQO1). Moreover, LOL treatment exhibited a marked increase in the anti-oxidant enzymes activities, whereas effectively suppressed the production of reactive oxygen species and nitric oxide, as well as lipid peroxidation in lung tissue of OVA-challenged mice and TNF-α-stimulated NCI-H292 cells. These findings suggest that LOL might serve as a therapeutic agent for the treatment of allergic asthma.

Spiraea prunifolia var. simpliciflora (SP) is traditionally used as an herbal remedy to treat fever, malaria, and emesis. This study aimed to evaluate the anti-oxidative and anti-inflammatory properties of the methanol extract of SP leaves in tumor necrosis factor (TNF)-α-stimulated NCI-H292 cells and in a lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse model. SP decreased the number of inflammatory cells and the levels of TNF-α, interleukin (IL)-1β, and IL-6 in the bronchoalveolar lavage fluid, and inflammatory cell infiltration in the lung tissues of SP-treated mice. In addition, SP significantly suppressed the mRNA and protein levels of TNF-α, IL-1β, and IL-6 in TNF-α-stimulated NCI-H292 cells. SP significantly suppressed the phosphorylation of the mitogen-activated protein kinases (MAPKs) and p65-nuclear factor-kappa B (NF-κB) in LPS-induced ALI mice and TNF-α-stimulated NCI-H292 cells. SP treatment enhanced the nuclear translocation of nuclear factor erythroid 2-related factor (Nrf2) with upregulated antioxidant enzymes and suppressed reactive oxygen species (ROS)-mediated oxidative stress in the lung tissues of LPS-induced ALI model and TNF-α-stimulated NCI-H292 cells. Collectively, SP effectively inhibited airway inflammation and ROS-mediated oxidative stress, which was closely related to its ability to induce activation of Nrf2 and inhibit the phosphorylation of MAPKs and NF-κB. These findings suggest that SP has therapeutic potential for the treatment of ALI.

In order to improve the reliability of robotic systems, various fault detection and isolation (FDI) algorithms have been proposed. However, most of these algorithms are model-based and thus, an accurate model of the robot is required although it is hard to obtain and often time-varying. Acceleration estimation is an additional challenge in dynamic model-based algorithms as it is hard to measure accurately in practice. In this study, a neural network based fault detection algorithm that does not require the use of physical robot model and acceleration is proposed. By utilizing neural network, the fault torque can be estimated, which allows effective fault detection and diagnosis. The feasibility of the proposed fault detection algorithm is validated through various simulations and experiments.

The smoothness and continuity of the tool path are crucial in high-quality machining. However, many tool paths are described using only line segments (G01), which inevitably cause discontinuities between blocks. Such discontinuity leads to vibration and feed rate fluctuation, which ultimately leads to a poor surface finish. This study proposes a novel input shaping-based corner rounding algorithm that ensure machining accuracy and vibration suppression. Input shaping is a model-based, robust vibration suppression solution, and it has been widely used in many applications. However, input shaping also distorts the original trajectory, which limits its usage in multiaxis systems. To ensure position accuracy, the corner rounding algorithm proposed in this study includes the position deviation regulation module and the distortion compensation module. The position deviation regulation module limits the position deviation due to corner rounding within the threshold while the distortion compensation scheme compensates for the distortion due to input shaping. The proposed algorithm has been verified via simulations and experiments using a two-degrees of freedom (DOF) Cartesian machine.

There is, currently, no consensus with regard to the role of endoscopy in the etiologic investigation of asymptomatic pemenopausal women suffering from iron deficiency anemia (IDA). We conducted a retrospective case-control study to evaluate the contribution of esophagogastroduodenoscopy (EGD) and colonoscopy to the etiologic diagnosis of a group of asymptomatic premenopausal women suffering from IDA. One hundred eight consecutive asymptomatic premenopausal women who fulfilled our entry criteria were included in our patient group between January 1998 and December 2004. One hundred thirty-five age-matched asymptomatic premenopausal women without anemia who had undergone EGD and colonoscopy for medical checkups were included in the control group. Clinically relevant lesions were detected in 7 of 108 (6.5%) of the patients and in 8 of 135 (5.9%) of the controls. There were no differences with regard to the frequency of clinically relevant lesions between the two groups (P > 0.05). Concomitant upper and lower GI lesions were not detected in any patients. In the upper GI tract, the only lesion found to be potentially causative of IDA anemia was a severe erosive gastritis, which was found in both the patient and the control groups. A source consistent with chronic bleeding was detected in the lower GI tract in 6 (5.6%) of the patients and 7 (5.2%) of the controls. Bleeding hemorrhoids represented the most frequently detected lesions in both the patient and control groups. Only one case of colon cancer was detected in the patient group. As IDA in the premenopausal women could not be attributed consistently to GI blood loss in this study, prospective studies should be conducted to validate our findings and to identify which subgroup of asymptomatic premenopausal women would benefit from a diagnostic endoscopic evaluation.