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Coronary high take-off-coronary origin above the sinotubular junction (STJ)-is clinically relevant for transcatheter interventions such as percutaneous coronary intervention (PCI). However, comprehensive morphometric data on coronary ostia in Koreans are limited. To determine the prevalence of coronary high take-off and measure coronary ostial height and diameter in Korean adults using cadaveric analysis. Ostial height was assessed in 128 hearts (83 males, 45 females) and ostial diameter in 45 hearts (25 males, 20 females) from cadavers donated between 2018 and 2024. After longitudinally opening the ascending aorta, ostial position was measured relative to the STJ with digital Vernier calipers. Diameter was measured along the vertical axis through the ostial center. Student's t-test (sex) and paired t-test (laterality) were used; Pearson correlation evaluated associations with age. Mean ostial heights were -1.70±3.81 mm (right coronary artery [RCA]) and -1.72 ± 3.78 mm (left coronary artery [LCA]). High take-off above the STJ was present in 19.5% (RCA) and 16.4% (LCA). Mean ostial diameters were 4.32±1.24 mm (RCA) and 4.61±0.98 mm (LCA); the LCA ostium was larger in 59.1% of specimens. No significant sex- or side-related differences were found for height or diameter. This study provides the first detailed coronary ostial morphometric data in a Korean population and demonstrates a relatively high prevalence of high take-off (19.5% RCA, 16.4% LCA). These findings may inform catheter-based procedures, particularly PCI, and support individualized preprocedural planning in Korean patients.
Background: Evidence linking fascia-oriented rhythmic movement to executive function and prefrontal hemodynamics in older adults remains limited. This pilot study examined the feasibility and preliminary within-subject associations of a four-week Fascial Circulation Exercise (FCE) program in older Korean women. Methods: Twelve cognitively screened women (74.3 ± 6.7 years) completed supervised FCE for four weeks. Pre-post assessments included body composition, grip strength, isokinetic knee performance, executive tasks (TMT-A/B, CDT), and task-evoked prefrontal activation measured via functional near-infrared spectroscopy (ΔHbO). Paired t-tests with effect sizes were reported. Results: Fat mass decreased (-0.71 kg, p = 0.016; dz = -0.74), whereas body weight and BMI were unchanged. Selective improvements were observed in knee flexor peak torque and extensor endurance (p < 0.05), with no change in grip strength. ΔHbO increased in the orbitofrontal, ventrolateral, and frontopolar regions during executive tasks. Behavioral performance improved in CDT and showed a trend toward improvement in TMT-B. Conclusions: Short-term FCE was feasible and was associated with reduced fat mass, selective neuromuscular gains, and increased task-evoked prefrontal oxygenation. The findings are exploratory and support future randomized controlled trials to determine clinical efficacy.
Postoperative bleeding requiring surgical re-exploration is a serious complication after cardiac surgery, yet its clinical impact in heart transplantation remains incompletely characterized. We assessed its clinical impact, predictors, and time-dependent risk profile. We retrospectively analyzed 813 adult recipients in the Korean Organ Transplantation Registry (2014 to 2021). The primary outcome was all-cause mortality and the secondary outcome was infection-related mortality. Between-group effects were estimated using multivariable Cox proportional hazards and Fine-Gray subdistribution hazard models. Time dependence was examined with smoothing splines and a prespecified 3-month landmark analysis. Predictors of re-exploration were identified with multivariable logistic regression; discrimination was assessed by receiver operating characteristic analysis and the area under the curve (AUC), and the final model was presented as a nomogram. Sixty-two patients (7.6%) underwent re-exploration. Early mortality at 30 days, 90 days, and 1 year was higher in the re-exploration group. Re-exploration was associated with increased all-cause mortality (adjusted hazard ratio [HR], 2.11; 95% confidence interval [CI], 1.28-3.48) and infection-related mortality (adjusted subdistribution HR, 2.33; 95% CI, 1.06-5.14). The excess mortality risk was confined to the first 3 months, as shown by time-varying hazard and 3-month landmark analyses; thereafter the hazards were comparable. Cardiopulmonary bypass (CPB) time and preoperative renal replacement therapy independently predicted re-exploration. The prediction model showed acceptable discrimination (AUC=0.77) and was implemented as a nomogram. Re-exploration for postoperative bleeding markedly increases early mortality after heart transplantation. CPB time and renal replacement therapy may aid perioperative risk stratification and targeted prevention.
Background/Objectives: Out-of-hospital cardiac arrest (OHCA) remains associated with poor survival despite advances in resuscitation. Extracorporeal cardiopulmonary resuscitation (ECPR) is a potential salvage therapy for refractory OHCA, but optimal patient selection remains uncertain. Transient return of spontaneous circulation (ROSC) before ECPR has been proposed as a prognostic marker, although its clinical significance remains unclear. This study aimed to evaluate the impact of transient ROSC before ECPR initiation on survival and neurological outcomes. Methods: We conducted a nationwide retrospective cohort study based on the Korean Out-of-Hospital Cardiac Arrest Surveillance registry (2016-2022). The study population was divided according to the occurrence of transient ROSC prior to ECPR. The primary endpoint was survival to hospital discharge, while favorable neurological outcome served as the secondary endpoint. Propensity score matching (PSM) and multivariable logistic regression analyses were performed. Results: After PSM, survival to hospital discharge (16.7% vs. 17.6%; p = 1.000) and favorable neurological outcomes (10.8% vs. 8.8%; p = 0.814) did not differ between groups. In multivariable analysis, transient ROSC was not associated with survival before (AOR 1.179; 95% CI 0.564-2.464; p = 0.662) or after PSM (AOR 0.592; 95% CI 0.206-1.698; p = 0.329). Similarly, no association was observed for favorable neurological outcomes before (AOR 1.246; 95% CI 0.526-2.951; p = 0.617) or after PSM (AOR 1.094; 95% CI 0.307-3.900; p = 0.890). Conclusions: Transient ROSC before ECPR initiation was not associated with improved survival or neurological outcomes in patients with refractory OHCA.
Dabieshan tick virus (DBTV) is a recently identified phenuivirus transmitted by ticks and has been reported across East Asia, raising concerns regarding its epidemiological and public health significance. In South Korea, DBTV was first detected in 2021, yet its genetic and epidemiological characteristics remain poorly understood. Between 2024 and 2025, a total of 1039 ticks collected from vegetation across nine regions in South Korea were grouped into 287 pools and screened for phenuivirus infection. DBTV was detected in 34 tick pools, yielding an overall minimum infection rate of 3.3%, and was identified in all surveyed regions, indicating widespread circulation. Phylogenetic analyses of the L and N genes showed that South Korean DBTV strains clustered closely with strains from multiple provinces in China and from Japan, with high nucleotide sequence similarity. Selection pressure analyses indicated predominant purifying selection acting on both genes. However, several positively selected sites and potential recombination signals were detected in the L gene, suggesting limited but ongoing genetic diversification. Time-scaled Bayesian phylodynamic analyses estimated that the most recent common ancestor of the South Korean DBTV strains have emerged around 2015-2016. Phylogeographic reconstruction further supported the introduction of DBTV into South Korea from Hubei Province, followed by regional dissemination. Overall, this study provides molecular epidemiological evidence for the circulation and evolutionary history of DBTV in South Korea and highlights the need for continued surveillance.
Hyangsapyeongwi-san (HPS), known as Xiangsha Pingwei San in Chinese medicine, is a classical herbal formula composed of ten medicinal herbs that has been traditionally used in traditional Korean medicine and East Asian medicine for centuries to treat gastrointestinal disorders associated with digestive impairment, including functional dyspepsia and gastritis. In traditional Korean medicine theory, these conditions correspond to "dampness-heat accumulation" and "qi stagnation" patterns affecting the spleen and stomach. HPS is formulated to "eliminate dampness, strengthen the spleen, and regulate qi circulation"-a traditional rationale for which the present study provides molecular evidence by demonstrating suppression of key inflammatory signaling pathways underlying gastric mucosal injury. This study aimed to investigate the gastroprotective effects of HPS against acute gastric injury and to elucidate its underlying molecular mechanisms, with a focus on NLRP3 inflammasome activation. Male ICR mice were administered HPS (75 or 300 mg/kg) or ranitidine (40 mg/kg) orally once daily for 4 days prior to HCl/ethanol-induced gastric injury. Gastric damage, NLRP3 inflammasome components, inflammatory cytokines, signaling pathways, and apoptosis markers were assessed. Anti-inflammatory effects were further evaluated in TNF-α-stimulated MKN45 gastric epithelial cells. HPS dose-dependently reduced gastric damage scores and preserved mucosal architecture. High-dose HPS significantly suppressed IL-1β protein, IL-1β mRNA, and TNF-α mRNA expression. HPS inhibited NLRP3 inflammasome activation by reducing NLRP3 and caspase-1 levels, suppressed AKT and NF-κB p65 phosphorylation, and prevented apoptosis. In gastric epithelial cells, HPS attenuated IL-6 and IL-8 expression without cytotoxicity. HPS protects against acute gastric injury through NLRP3 inflammasome inhibition via the AKT/NF-κB pathway, providing molecular evidence that supports its traditional use for digestive disorders.
Solute carrier family 23 member 1 (SLC23A1) encodes sodium-dependent vitamin C transporter 1, which mediates intestinal vitamin C absorption. Although SLC23A1 variants are associated with vitamin C bioavailability, their relationship with gut microbiome remains unexplored. We aimed to investigate the associations of SLC23A1 polymorphism with serum vitamin C status and gut microbial profiles in healthy Korean adults. We genotyped the SLC23A1 rs6596473 polymorphism in 257 healthy individuals (20-39 years) and measured their serum vitamin C concentrations, which were categorized as optimal (≥50 μM) or suboptimal (<50 μM). Logistic regression analysis was used to evaluate the association between genotypes and suboptimal serum vitamin C status after adjusting for covariates. A subset of 43 participants with suboptimal serum vitamin C status underwent gut microbiota analysis and serum short-chain fatty acid (SCFA) measurements. Microbial profiles and SCFA concentrations were compared across the genotypes. The genotype distributions were 92 CC, 131 CG, and 34 GG, with G as the minor allele. After covariate adjustment, GG carriers had higher odds of suboptimal serum vitamin C status than CC carriers (odds ratio = 2.65; p = 0.03). Among individuals with suboptimal serum vitamin C status, GG carriers (n = 7) exhibited distinct microbial community structures compared with CC (n = 13) and CG (n = 23) carriers, with elevated richness and evenness. GG carriers had higher abundances of Bifidobacterium (vs. CC, p < 0.01; vs. CG, p = 0.054) and Ruminococcaceae incertae sedis (all p < 0.05) compared with CC and CG carriers. In line with these microbial findings, GG carriers had higher propionate and butyrate concentrations than CC and CG carriers (all p < 0.05). The SLC23A1 rs6596473 variant was associated with reduced vitamin C absorption into systemic circulation in the overall population; however, among individuals with suboptimal serum vitamin C status, it was associated with beneficial gut microbial profiles. Our findings suggest that this genetic variant in the vitamin C transporter has complex health effects that extend beyond circulating vitamin C levels to gut microbial ecology, supporting the use of genotype-informed nutritional approaches. Clinical Research Information Services KCT0005074 (https://cris.nih.go.kr/cris/search/detailSearch.do?seq=16832&status=5&seq_group=16832&search_page=M) and KCT0004276 (https://cris.nih.go.kr/cris/search/detailSearch.do?seq=14590&status=5&seq_group=14590&search_page=M).
Low-density lipoprotein cholesterol (LDL-C) remains the principal therapeutic target in preventing atherosclerotic cardiovascular disease. Nevertheless, coronary artery disease (CAD) may develop even in patients whose LDL-C levels are at recommended targets. Using a contemporary Korean multicenter registry, we examined the association between lipid parameters and CAD in patients with suspected angina, considering statin use and LDL-C levels. We analyzed data from 2,410 adults with chest pain who underwent coronary angiography at 21 centers in South Korea (2012-2022). CAD was defined as ≥50% stenosis in major coronary arteries. To address multicollinearity among lipid parameters, principal component analysis-derived components were evaluated in multivariable logistic regression, with additional assessment of model discrimination using net reclassification improvement (NRI) and integrated discrimination improvement (IDI). Among the study population (60.1% women), 52.0% were on statins, and 36.5% were diagnosed with CAD, which was more frequent in statin users. The proportion of patients with LDL-C within target ranges was similar between statin users and non-users (p=0.695). Total cholesterol/high-density lipoprotein cholesterol (HDL-C) ratio, non-HDL-C/HDL-C ratio, and LDL-C/HDL-C ratio showed significant associations with CAD. These associations remained consistent regardless of statin use or LDL-C levels. Total cholesterol/HDL-C and non-HDL-C/HDL-C ratios moderately improved model performance (NRI: 0.413, IDI: 0.024); LDL-C/HDL-C ratio showed mild improvement (NRI: 0.373, IDI: 0.030). In this large, real-world Korean cohort, cholesterol ratios showed cross-sectional associations with CAD. These associations remained consistent regardless of statin use or LDL-C levels.
Global cerebral ischemia remains a major cause of neurological morbidity and mortality, yet effective neuroprotective strategies have shown limited translational success. Experimental studies frequently rely on ischemic duration as a primary determinant of injury severity, implicitly assuming equivalence across global brain ischemia-reperfusion (IR) and cardiac arrest with return of spontaneous circulation (CA/ROSC) models. However, increasing experimental evidence indicates that identical ischemic durations can lead to substantially different neuronal outcomes depending on the physiological and systemic context of ischemia. In brain-restricted global IR models, partial preservation of systemic circulation allows residual metabolic activity, delayed stress responses, and region-specific neuronal vulnerability, most notably delayed neuronal death in the hippocampal cornu ammonis 1 region. By contrast, CA/ROSC is characterized by complete systemic circulatory arrest followed by a biologically hostile reperfusion phase that includes profound mitochondrial dysfunction, heterogeneous reperfusion, blood-brain barrier disruption, and amplification of systemic inflammatory responses. As a result, these qualitative differences shift ischemic injury thresholds toward earlier onset and broader neuronal damage in CA/ROSC, even when ischemic durations are nominally comparable. This review integrates experimental evidence from rat models to examine how energy failure, reperfusion biology, proteostasis disruption, and brain-body interactions collectively determine neuronal vulnerability beyond ischemic duration alone. Through direct comparison of global IR and CA/ROSC paradigms, we highlight limitations of duration-centric interpretations and outline implications for experimental design and translational neuroprotection. Recognition of context-dependent ischemic mechanisms is essential for improving model selection and advancing therapeutic strategies for global cerebral ischemia.
Nano-delivery has been largely focused on ligand-based navigational targeting, but several common limitations have been recognized. First, the same targeting ligand can be sporadically expressed by unintended cells and tissues across different temporal and spatial contexts. Second, clearance from blood circulation via the liver, kidney, lung, and spleen is largely uncontrollable, in addition to nonspecific uptake by immune cells during circulation or tissue accumulation. Accordingly, inherent characteristics of cells have recently been utilized as alternative strategic points for delivery. Cell-derived nanocarriers utilize plasma membranes as modulators of targeting and delivery mechanisms, including cell hitchhiking to alter carrier behavior, reprogram phenotypes, and enable drug hand-over. The membrane mediates contact with target cells in a manner analogous to cell-cell interactions, thereby enabling physical bridging between cells and natural homing to peer cells, in addition to user-specified molecular display through mother cell expression or chemical conjugation. Here, cell-derived nanocarriers for therapeutic delivery (CDNTD) are reviewed with emphasis on their mechanistic basis, distinctions from synthetic nanoparticles, and therapeutic potential. We recently introduced spleen-mediated delivery strategies that employ resident monocytes as second therapeutic carriers following uptake of primary nanocarriers. In this way, the natural targeting behavior of monocytes in response to inflammatory cues enhances payload delivery efficiency to ischemic sites. Future directions of CDNTD research are also discussed with respect to clinical translation.
Metformin, while central to diabetes management, functions as a highly pleiotropic agent with mechanisms that extend far beyond simple glycemic control. In age-related degenerative diseases, including neurodegenerative disorders, it may modulate mitochondrial function, reduce oxidative stress, and influence longevity-related pathways, suggesting possible anti-aging effects. Emerging evidence also points to anticancer activity, with studies reporting reduced incidence and improved outcomes across several malignancies, potentially through mammalian target of rapamycin (mTOR) inhibition, metabolic reprogramming, and suppression of inflammatory signaling. Furthermore, the 'intestinal glucotonic effect' has been proposed to involve glucose excretion from the circulation into the gut lumen through reactive oxygen species-dependent upregulation and membrane localization of glucose transporter type 1 (GLUT1), an adenosine monophosphate-activated protein kinase (AMPK)-independent process that may contribute to the reprogramming of systemic glucose flux and provides metabolic substrates for the microbiota. Metformin also alters the gut microbiome by increasing the abundance of multiple short-chain fatty acid-producing bacteria and enhancing intestinal barrier function, which may contribute to systemic metabolic and immunologic benefits. Collectively, metformin is a pleiotropic agent with broad effects on aging biology, cancer pathophysiology, host-microbiome interactions, and immunometabolic regulation. Despite decades of clinical use, important gaps remain in understanding how these mechanisms converge to influence outcomes in individuals with diabetes and beyond.
Platelet transfusions are essential for managing thrombocytopenia but have critical limitations, including a 5-7-day shelf-life causing wastage, alloimmune refractoriness in chronically transfused patients, and vulnerability to supply disruptions. Ex vivo platelet production from stem cells represents a transformative solution, evolving from initial hematopoietic stem cell approaches to induced pluripotent stem cell platforms with unlimited expansion and genetic tractability for universal platelet products. We critically reviewed the state and future trajectory of ex vivo platelet production, focusing on stem cell sources, manufacturing innovations, QC methods, and progression from laboratory concept to clinical reality. Key advances include immortalized megakaryocyte progenitor cell lines for scalable manufacturing; turbulence-based bioreactors that harness physiological shear stress to produce over 100 billion platelets/run; and comprehensive quality frameworks spanning cellular and molecular characterization, functional assays, and in vivo validation. We comparatively analyzed pioneering first-in-human clinical trials that collectively established the safety of iPSC-derived platelet transfusion and highlighted the translational challenges of achieving donor-comparable efficacy. We also highlighted the evolving corporate landscape, wherein companies pursue commercialization alongside national initiatives, including Korea's 15-yr artificial blood program. Convergence between biological insight, engineering innovation, and sustained investment suggests that ex vivo platelet production can transform transfusion medicine. Remaining challenges include reducing costs and optimizing in vivo circulation of platelet products. Initial implementation will likely focus on high-value applications, such as transfusion for alloimmunized patients, before broader adoption. The long-term goal is to replace the vulnerable donor-dependent system with on-demand production of standardized, pathogen-free, and universally compatible platelets.
Patients with type 2 diabetes mellitus (T2DM) have an elevated risk of adverse cardiovascular events due to accelerated atherosclerosis and a higher burden of multivessel coronary artery disease (CAD). However, the optimal initial noninvasive test for CAD in T2DM remains unclear. This study compared coronary computed tomographic angiography (CCTA) vs. functional testing for the initial evaluation of suspected CAD in newly diagnosed T2DM. Using data from the Korean National Health Insurance Service, we identified patients with newly diagnosed T2DM from 2007 to 2019. Among 93,152 patients, 34,694 underwent noninvasive testing for suspected CAD. After propensity score matching, 14,895 patients were included in each group. The primary outcome was a composite of acute myocardial infarction or death from CAD. Secondary outcomes included rates of invasive coronary angiography (ICA) and coronary revascularization. The primary outcome was lower in the CCTA group compared with the functional testing group (1.0% vs. 1.4%; adjusted hazard ratio [HR], 0.72; 95% confidence interval [CI], 0.58-0.89; p=0.002). The ICA rate was also lower in the CCTA group (10.6% vs. 16.0%; adjusted HR, 0.67; 95% CI, 0.63-0.71; p<0.001). Coronary revascularization rates were similar (5.4% vs. 6.2%; adjusted HR, 0.92; 95% CI, 0.83-1.01; p=0.069). In patients with newly diagnosed T2DM and suspected CAD, CCTA as an initial test was associated with better cardiovascular outcomes compared with functional testing. Although these findings cannot establish causality due to residual confounding and selection bias, they remain clinically relevant.
The dried pericarp of Zanthoxylum bungeanum Maxim. (Rutaceae), widely recognized as Sichuan pepper (Hua Jiao), is a prominent herb within the Traditional Chinese Medicine (TCM), boasting a long and well-documented history of ethnopharmacological application. Its traditional uses primarily involve the internal management of gastrointestinal ailments, such as stomachaches, alongside promoting systemic blood circulation. Building on this traditional foundation, modern pharmacological studies have confirmed and extended its therapeutic profile, revealing potent anti-inflammatory and antitumor biological activities. We examined the anticoronaviral effects and the mechanism of action of the 30% ethanol extract of Z. bungeanum against human coronavirus (HCoV)-OC43 infection. Antiviral activity was measured using the virus-induced cytopathic effect (CPE) reduction assay, qRT-PCR was performed to calculate viral RNA copy numbers, and western blotting and immunofluorescence staining were performed to detect viral proteins. To evaluate the mode of action of Z. bungeanum, time-of-addition, attachment, penetration, and virucidal assays were performed. The effect of the extract on virus-induced autophagic flux was examined by measuring LC3 protein expression via western blotting, and autophagy, lysosomes, and lysosomal degradation were assessed using CYTO-ID® Green, LysoTracker™ Deep Red, and DQ™ Red BSA, respectively. Ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry was used to identify the active components in the extract. Z. bungeanum extract protected against HCoV-OC43-induced CPEs with IC50 of 284.1 ± 44.0 µg/mL. The extract reduced the number of intracellular and extracellular viral RNA copy and viral protein expression. Z. bungeanum mainly affected the early phase of the virus life cycle by inhibiting viral entry. Additionally, Z. bungeanum inhibited HCoV-OC43 replication by inducing autolysosome accumulation, thereby blocking virus-induced autophagic flux. Hydroxy-α-sanshool and p-coumaric acid were identified as the active antiviral components. This study suggested the potential of Z. bungeanum as a novel anticoronaviral agent.
Collateral perfusion and neurovascular stability critically influence outcomes after ischemic stroke; however, no pharmacological agent is currently approved to enhance these processes. Chunghyul-dan (CHD), a standardized multi-botanical ethanol extract with reported vascular and anti-inflammatory properties, was evaluated for its neurovascular protective effects in a permanent middle cerebral artery occlusion (pMCAO) mouse model. Male ICR mice subjected to pMCAO received oral Chunghyul-dan (30-120 mg/kg). Cortical infarct volume, anterior cerebral artery perfusion, angiogenesis-related signaling, neuroinflammation, and endothelial barrier integrity were assessed using histological analysis, laser Doppler flowmetry, immunohistochemistry, and complementary in vitro studies in BV2 microglia and bEND.3 endothelial cells. CHD significantly reduced cortical infarct volume, with maximal protection observed at 60 mg/kg. Laser Doppler analysis demonstrated enhanced ACA perfusion at 30 mg/kg during early ischemia. CHD upregulated VEGF expression in ischemic cortex and endothelial cells, supporting vascular remodeling. Neuroinflammation was attenuated, as CHD reduced Iba-1-positive microglial activation and suppressed iNOS, IL-6, and TNF-α expression. Endothelial barrier integrity was preserved through reduced PECAM-1 expression, restoration of claudin-5 and occludin, and selective inhibition of STAT3 phosphorylation, whereas TLR4/MAPK signaling remained unchanged. CHD confers multi-level neurovascular protection by promoting collateral perfusion, facilitating VEGF-associated vascular adaptation, suppressing neuroinflammation, and stabilizing endothelial junctional architecture. These findings support further translational evaluation of CHD as a pharmacological modulator of collateral circulation in ischemic stroke.
Antibody-drug conjugates (ADCs), which integrate a cytotoxic drug known as the payload into a tumor-targeting monoclonal antibody via a linker, have emerged as promising candidates for cancer therapy and are a new avenue for targeted cancer therapy. The pharmacokinetic (PK) profiles of ADCs are distinctive due to their unique distribution, catabolism, and elimination. Their deconjugation in circulation and variations in the drug-to-antibody ratio increase the complexity of their PK profiles. Pharmacometric models depicting the PK properties and exposure-response (E-R) relationships of ADCs are important for optimizing dosing regimens and supporting decisions during ADC development. This review considers the PK profiles of ADCs, physiologically based PK models, semi-mechanistic and mechanistic PK models, population PK models, and E-R analyses for dose optimization. The prospects and challenges for ADCs, especially the urgent need for advanced analytical technology and modeling approaches, are also outlined.
Thermal energy-based catheter ablation techniques, including cryoballoon ablation (CBA) and radiofrequency ablation (RFA), are widely utilized for rhythm control in patients with atrial fibrillation. However, direct comparisons of CBA and RFA using real-world data are limited. This study aims to evaluate the short- and long-term outcomes of CBA and RFA. A total of 4,868 patients who underwent procedures between January 2018 and July 2022 were selected from the Korean CBA Registry and a multicenter RFA cohort. The primary outcome was the atrial tachyarrhythmia recurrence. To reduce selection bias, 1:1 propensity score matching (PSM) was performed, yielding 1,843 patients in each group. After PSM, RFA demonstrated significantly lower recurrence rates compared with CBA at both 1 year (20.9% vs. 27.9%; hazard ratio [HR], 0.69; 95% confidence interval [CI], 0.61-0.79) and 3 years (31.9% vs. 35.2%; HR, 0.72; 95% CI, 0.65-0.81). In multivariable Cox regression analysis, RFA was independently associated with lower recurrence risk, with a 30% relative risk reduction at 1 year (HR, 0.70; 95% CI, 0.61-0.80) and a 27% relative risk reduction at 3 years (HR, 0.73; 95% CI, 0.65-0.81). When cavotricuspid isthmus (CTI) ablation was performed in addition to pulmonary vein isolation (PVI), recurrence rates were comparable between RFA and CBA. In this large, multicenter real-world cohort, RFA consistently demonstrated more favorable short- and long-term outcomes than CBA, even after PSM and multivariable adjustment. However, outcomes were comparable when CTI ablation was additionally performed, underscoring the importance of procedural strategies beyond PVI.
Gastric cancer (GC) is one of the most aggressive malignancies with a dismal prognosis, late diagnosis, and limited therapy efficacy. Biologically, GC is associated with multiple barriers to therapeutic response including gastric mucosal layer, acidic tumor microenvironment (TME), high accumulation of extracellular matrix (ECM) components, and limited penetration depth of anticancer drugs into tumor tissue. Furthermore, inherent or acquired drug resistance associated with drug efflux transporters, deregulated autophagy, tumor heterogeneity, and cell survival pathways severely compromise treatment response. Nanotechnology has been widely used to develop next-generation nanotherapeutic delivery systems to overcome these biological barriers. Currently available nanoplatforms such as liposomes, polymeric nanoparticles, dendrimers, and inorganic nanocarriers have improved drug loading capacity, aqueous solubility, circulation time stability, tumor-targeted delivery, and sustained release of chemotherapeutics. Smart and stimuli-responsive nanocarriers can also take advantage of pathological hallmarks of tumors including low pH, redox potential, and overexpressed enzymes for enhanced selective delivery to the tumor site. Nanotherapeutics have also shown promise for co-delivery of multiple therapeutic agents to overcome drug resistance, manipulation of TME, and suppression of autophagy and apoptosis signaling pathways associated with drug resistance. This review discusses recent advances in nanotherapeutics for GC including approaches to overcome biological barriers and drug resistance and highlights translational gaps for clinical development.
In traditional Chinese medicine, benign prostatic hyperplasia (BPH) is attributed to qi deficiency caused by blood stasis, and Glycyrrhiza species (licorice) have long been used to enhance qi, relieve congestion, and promote blood circulation. Wongam (WG), a newly developed licorice cultivar generated through hybridization and cultivated in the Republic of Korea, has not yet been evaluated for its anti-BPH properties. This study investigated the pharmacological potential of WG against BPH using an integrated approach combining network pharmacology with experimental validation. Network pharmacology was applied to identify potential molecular targets and pathways, and the predicted mechanisms were experimentally validated in BPH-1 cells and in rats with testosterone propionate (TP)-induced BPH. WG alleviated prostate enlargement in rats with TP-induced BPH. Network pharmacology predicted that WG could modulate key regulators of cell cycle progression and apoptosis. Consistently, WG suppressed androgen receptor (AR) signaling in both BPH-1 cells and rats with TP-induced BPH. WG also inhibited G1/S checkpoint regulators and induced apoptosis by reducing B-cell lymphoma (Bcl)-2 and Bcl-xL/Bcl-2 associated X protein ratios, leading to the activation of caspase-9 and -3. Through these actions, WG prevented the activation of the AR signaling pathway, promoted cell cycle arrest, and triggered apoptosis, thereby mitigating BPH progression. These findings, supported by both network pharmacology predictions and experimental data, suggest that WG has promising therapeutic potential for the treatment of BPH.