Abdominal tuberculous lymphadenopathy is a rare condition that can cause obstructive jaundice. The feature of tuberculosis lymphadenopathy may resemble those of cancer, metastasis, or lymphoma on computed tomography (CT) or magnetic resonance imaging; therefore, physicians must perform appropriate examinations, make correct diagnoses, and conduct suitable treatment. Herein, we report a case of obstructive jaundice caused by tuberculous lymphadenopathy. The patient was 27 years old, with an initial serum total bilirubin level of 6.76 mg/dL and a direct bilirubin level of 5.64 mg/dL. Aspartate transaminase and alanine transaminase levels were 466 and 801 IU/L, respectively. Abdominal CT revealed a mass-like effect and extraluminal compression accompanying bile duct obstruction. An abrupt bile duct stricture was observed on endoscopic retrograde cholangiopancreatography; thus, a biopsy was performed. However, the specimen which was taken by endoscopic retrograde cholangiopancreatography was confirmed to constitute superficially biopsied bile duct mucosa and benign-looking epithelial cell stripes. Positron emission tomography-CT showed a hypermetabolic lesion in the hepato-duodenal ligament with small lymph nodes in the aortocaval and retrocaval spaces. Additionally, it showed hypermetabolism of the neck lymph node at level II. The neck lymph node was biopsied. Granulomatous inflammation was observed and nested tuberculosis polymerase chain reaction was positive. The patient was treated with anti-tuberculosis medications and underwent endoscopic retrograde biliary drainage without surgery.

Abdominal tuberculous lymphadenopathy is a rare condition that can cause obstructive jaundice. The feature of tuberculosis lymphadenopathy may resemble those of cancer, metastasis, or lymphoma on computed tomography (CT) or magnetic resonance imaging; therefore, physicians must perform appropriate examinations, make correct diagnoses, and conduct suitable treatment. Herein, we report a case of obstructive jaundice caused by tuberculous lymphadenopathy. The patient was 27 years old, with an initial serum total bilirubin level of 6.76 mg/dL and a direct bilirubin level of 5.64 mg/dL. Aspartate transaminase and alanine transaminase levels were 466 and 801 IU/L, respectively. Abdominal CT revealed a mass-like effect and extraluminal compression accompanying bile duct obstruction. An abrupt bile duct stricture was observed on endoscopic retrograde cholangiopancreatography; thus, a biopsy was performed. However, the specimen which was taken by endoscopic retrograde cholangiopancreatography was confirmed to constitute superficially biopsied bile duct mucosa and benign-looking epithelial cell stripes. Positron emission tomography-CT showed a hypermetabolic lesion in the hepato-duodenal ligament with small lymph nodes in the aortocaval and retrocaval spaces. Additionally, it showed hypermetabolism of the neck lymph node at level II. The neck lymph node was biopsied. Granulomatous inflammation was observed and nested tuberculosis polymerase chain reaction was positive. The patient was treated with anti-tuberculosis medications and underwent endoscopic retrograde biliary drainage without surgery.

Abdominal tuberculous lymphadenopathy is a rare condition that can cause obstructive jaundice. The feature of tuberculosis lymphadenopathy may resemble those of cancer, metastasis, or lymphoma on computed tomography (CT) or magnetic resonance imaging; therefore, physicians must perform appropriate examinations, make correct diagnoses, and conduct suitable treatment. Herein, we report a case of obstructive jaundice caused by tuberculous lymphadenopathy. The patient was 27 years old, with an initial serum total bilirubin level of 6.76 mg/dL and a direct bilirubin level of 5.64 mg/dL. Aspartate transaminase and alanine transaminase levels were 466 and 801 IU/L, respectively. Abdominal CT revealed a mass-like effect and extraluminal compression accompanying bile duct obstruction. An abrupt bile duct stricture was observed on endoscopic retrograde cholangiopancreatography; thus, a biopsy was performed. However, the specimen which was taken by endoscopic retrograde cholangiopancreatography was confirmed to constitute superficially biopsied bile duct mucosa and benign-looking epithelial cell stripes. Positron emission tomography-CT showed a hypermetabolic lesion in the hepato-duodenal ligament with small lymph nodes in the aortocaval and retrocaval spaces. Additionally, it showed hypermetabolism of the neck lymph node at level II. The neck lymph node was biopsied. Granulomatous inflammation was observed and nested tuberculosis polymerase chain reaction was positive. The patient was treated with anti-tuberculosis medications and underwent endoscopic retrograde biliary drainage without surgery.

Background: and Purpose This study was an open-label, dose-escalation, phase 1 clinical trial to determine the safety and dose of EN001 for patients with Duchenne muscular dystrophy (DMD). EN001, developed by ENCell, are allogeneic early-passage Wharton’s jelly-derived mesenchymal stem cells that originate at the umbilical cord, with preclinical studies demonstrating their high therapeutic efficacy for DMD. Methods: This phase 1 clinical trial explored the safety and tolerability of EN001 as a potential treatment option for patients with DMD. Six pediatric participants with DMD were divided into two subgroups of equal size: low-dose EN001 (5.0×105 cells/kg) and high-dose EN001 (2.5×106 cells/kg). All participants were monitored for 12 weeks after EN001 administration to assess its safety. Dose-limiting toxicity (DLT) was evaluated across 2 weeks post administration. Exploratory efficacy was evaluated by measuring serum creatine kinase levels, and functional evaluations—including spirometry, myometry, the North Star Ambulatory Assessment, and the 6-minute walk test—were conducted at week 12 and compared with the baseline values. Results: No participants experienced serious adverse events related to EN001 injection during the 12-week follow-up period. Mild adverse events included injection-related local erythema, edema, parosmia, and headache, but DLT was not observed. Functional evaluations at week 12 revealed no significant changes from baseline. Conclusions These results demonstrated that EN001 are safe and well tolerated for patients with DMD, and did not cause serious adverse events. The efficacy of EN001 could be confirmed through larger-scale future studies that incorporate repeated dosing and have a randomized controlled trial design.

Background: and Purpose This study was an open-label, dose-escalation, phase 1 clinical trial to determine the safety and dose of EN001 for patients with Duchenne muscular dystrophy (DMD). EN001, developed by ENCell, are allogeneic early-passage Wharton’s jelly-derived mesenchymal stem cells that originate at the umbilical cord, with preclinical studies demonstrating their high therapeutic efficacy for DMD. Methods: This phase 1 clinical trial explored the safety and tolerability of EN001 as a potential treatment option for patients with DMD. Six pediatric participants with DMD were divided into two subgroups of equal size: low-dose EN001 (5.0×105 cells/kg) and high-dose EN001 (2.5×106 cells/kg). All participants were monitored for 12 weeks after EN001 administration to assess its safety. Dose-limiting toxicity (DLT) was evaluated across 2 weeks post administration. Exploratory efficacy was evaluated by measuring serum creatine kinase levels, and functional evaluations—including spirometry, myometry, the North Star Ambulatory Assessment, and the 6-minute walk test—were conducted at week 12 and compared with the baseline values. Results: No participants experienced serious adverse events related to EN001 injection during the 12-week follow-up period. Mild adverse events included injection-related local erythema, edema, parosmia, and headache, but DLT was not observed. Functional evaluations at week 12 revealed no significant changes from baseline. Conclusions These results demonstrated that EN001 are safe and well tolerated for patients with DMD, and did not cause serious adverse events. The efficacy of EN001 could be confirmed through larger-scale future studies that incorporate repeated dosing and have a randomized controlled trial design.

Abdominal tuberculous lymphadenopathy is a rare condition that can cause obstructive jaundice. The feature of tuberculosis lymphadenopathy may resemble those of cancer, metastasis, or lymphoma on computed tomography (CT) or magnetic resonance imaging; therefore, physicians must perform appropriate examinations, make correct diagnoses, and conduct suitable treatment. Herein, we report a case of obstructive jaundice caused by tuberculous lymphadenopathy. The patient was 27 years old, with an initial serum total bilirubin level of 6.76 mg/dL and a direct bilirubin level of 5.64 mg/dL. Aspartate transaminase and alanine transaminase levels were 466 and 801 IU/L, respectively. Abdominal CT revealed a mass-like effect and extraluminal compression accompanying bile duct obstruction. An abrupt bile duct stricture was observed on endoscopic retrograde cholangiopancreatography; thus, a biopsy was performed. However, the specimen which was taken by endoscopic retrograde cholangiopancreatography was confirmed to constitute superficially biopsied bile duct mucosa and benign-looking epithelial cell stripes. Positron emission tomography-CT showed a hypermetabolic lesion in the hepato-duodenal ligament with small lymph nodes in the aortocaval and retrocaval spaces. Additionally, it showed hypermetabolism of the neck lymph node at level II. The neck lymph node was biopsied. Granulomatous inflammation was observed and nested tuberculosis polymerase chain reaction was positive. The patient was treated with anti-tuberculosis medications and underwent endoscopic retrograde biliary drainage without surgery.

Background: and Purpose This study was an open-label, dose-escalation, phase 1 clinical trial to determine the safety and dose of EN001 for patients with Duchenne muscular dystrophy (DMD). EN001, developed by ENCell, are allogeneic early-passage Wharton’s jelly-derived mesenchymal stem cells that originate at the umbilical cord, with preclinical studies demonstrating their high therapeutic efficacy for DMD. Methods: This phase 1 clinical trial explored the safety and tolerability of EN001 as a potential treatment option for patients with DMD. Six pediatric participants with DMD were divided into two subgroups of equal size: low-dose EN001 (5.0×105 cells/kg) and high-dose EN001 (2.5×106 cells/kg). All participants were monitored for 12 weeks after EN001 administration to assess its safety. Dose-limiting toxicity (DLT) was evaluated across 2 weeks post administration. Exploratory efficacy was evaluated by measuring serum creatine kinase levels, and functional evaluations—including spirometry, myometry, the North Star Ambulatory Assessment, and the 6-minute walk test—were conducted at week 12 and compared with the baseline values. Results: No participants experienced serious adverse events related to EN001 injection during the 12-week follow-up period. Mild adverse events included injection-related local erythema, edema, parosmia, and headache, but DLT was not observed. Functional evaluations at week 12 revealed no significant changes from baseline. Conclusions These results demonstrated that EN001 are safe and well tolerated for patients with DMD, and did not cause serious adverse events. The efficacy of EN001 could be confirmed through larger-scale future studies that incorporate repeated dosing and have a randomized controlled trial design.

Abdominal tuberculous lymphadenopathy is a rare condition that can cause obstructive jaundice. The feature of tuberculosis lymphadenopathy may resemble those of cancer, metastasis, or lymphoma on computed tomography (CT) or magnetic resonance imaging; therefore, physicians must perform appropriate examinations, make correct diagnoses, and conduct suitable treatment. Herein, we report a case of obstructive jaundice caused by tuberculous lymphadenopathy. The patient was 27 years old, with an initial serum total bilirubin level of 6.76 mg/dL and a direct bilirubin level of 5.64 mg/dL. Aspartate transaminase and alanine transaminase levels were 466 and 801 IU/L, respectively. Abdominal CT revealed a mass-like effect and extraluminal compression accompanying bile duct obstruction. An abrupt bile duct stricture was observed on endoscopic retrograde cholangiopancreatography; thus, a biopsy was performed. However, the specimen which was taken by endoscopic retrograde cholangiopancreatography was confirmed to constitute superficially biopsied bile duct mucosa and benign-looking epithelial cell stripes. Positron emission tomography-CT showed a hypermetabolic lesion in the hepato-duodenal ligament with small lymph nodes in the aortocaval and retrocaval spaces. Additionally, it showed hypermetabolism of the neck lymph node at level II. The neck lymph node was biopsied. Granulomatous inflammation was observed and nested tuberculosis polymerase chain reaction was positive. The patient was treated with anti-tuberculosis medications and underwent endoscopic retrograde biliary drainage without surgery.

Cellular senescence causes cell cycle arrest and promotes permanent cessation of proliferation. Since the senescence of mesenchymal stem cells (MSCs) reduces proliferation and multipotency and increases immunogenicity, aged MSCs are not suitable for cell therapy. Therefore, it is important to inhibit cellular senescence in MSCs. It has recently been reported that metabolites can control aging diseases. Therefore, we aimed to identify novel metabolites that regulate the replicative senescence in MSCs. Using a fecal metabolites library, we identified nervonic acid (NA) as a candidate metabolite for replicative senescence regulation. In replicative senescent MSCs, NA reduced senescence-associated β-galactosidase positive cells, the expression of senescence-related genes, as well as increased stemness and adipogenesis. Moreover, in non-senescent MSCs, NA treatment delayed senescence caused by sequential subculture and promoted proliferation. We confirmed, for the first time, that NA delayed and inhibited cellular senescence.Considering optimal concentration, duration, and timing of drug treatment, NA is a novel potential metabolite that can be used in the development of technologies that regulate cellular senescence.

Background: The benefits of transradial access (TRA) over transfemoral access (TFA) for bifurcation percutaneous coronary intervention (PCI) are uncertain because of the limited availability of device selection. This study aimed to compare the procedural differences and the in-hospital and long-term outcomes of TRA and TFA for bifurcation PCI using secondgeneration drug-eluting stents (DESs). Methods: Based on data from the Coronary Bifurcation Stenting Registry III, a retrospective registry of 2,648 patients undergoing bifurcation PCI with second-generation DES from 21 centers in South Korea, patients were categorized into the TRA group (n = 1,507) or the TFA group (n = 1,141). After propensity score matching (PSM), procedural differences, in-hospital outcomes, and device-oriented composite outcomes (DOCOs; a composite of cardiac death, target vessel-related myocardial infarction, and target lesion revascularization) were compared between the two groups (772 matched patients each group). Results: Despite well-balanced baseline clinical and lesion characteristics after PSM, the use of the two-stent strategy (14.2% vs. 23.7%, P = 0.001) and the incidence of in-hospital adverse outcomes, primarily driven by access site complications (2.2% vs. 4.4%, P = 0.015), were significantly lower in the TRA group than in the TFA group. At the 5-year follow-up, the incidence of DOCOs was similar between the groups (6.3% vs. 7.1%, P = 0.639). Conclusion The findings suggested that TRA may be safer than TFA for bifurcation PCI using second-generation DESs. Despite differences in treatment strategy, TRA was associated with similar long-term clinical outcomes as those of TFA. Therefore, TRA might be the preferred access for bifurcation PCI using second-generation DES.