Role of UPF1-LIN28A interaction during early differentiation of pluripotent stem cells.

UPF1 and LIN28A are RNA-binding proteins involved in post-transcriptional regulation and stem cell differentiation. Most studies on UPF1 and LIN28A have focused on the molecular mechanisms of differentiated cells and stem cell differentiation, respectively. We reveal that LIN28A directly interacts with UPF1 before UPF1-UPF2 complexing, thereby reducing UPF1 phosphorylation and inhibiting nonsense-mediated mRNA decay (NMD). We identify the interacting domains of UPF1 and LIN28A; moreover, we develop a peptide that impairs UPF1-LIN28A interaction and augments NMD efficiency. Transcriptome analysis of human pluripotent stem cells (hPSCs) confirms that the levels of NMD targets are significantly regulated by both UPF1 and LIN28A. Inhibiting the UPF1-LIN28A interaction using a CPP-conjugated peptide promotes spontaneous differentiation by repressing the pluripotency of hPSCs during proliferation. Furthermore, the UPF1-LIN28A interaction specifically regulates transcripts involved in ectodermal differentiation. Our study reveals that transcriptome regulation via the UPF1-LIN28A interaction in hPSCs determines cell fate.

Expression of Major Histocompatibility Complex during Neuronal Differentiation of Somatic Cell Nuclear Transfer-Human Embryonic Stem Cells.

Human pluripotent stem cells (hPSCs) such as human embryonic stem cells (hESCs), induced pluripotent stem cells, and somatic cell nuclear transfer (SCNT)-hESCs can permanently self-renew while maintaining their capacity to differentiate into any type of somatic cells, thereby serving as an important cell source for cell therapy. However, there are persistent challenges in the application of hPSCs in clinical trials, where one of the most significant is graft rejection by the patient immune system in response to human leukocyte antigen (HLA) mismatch when transplants are obtained from an allogeneic (non-self) cell source. Homozygous SCNT-hESCs (homo-SCNT-hESCs) were used to simplify the clinical application and to reduce HLA mismatch. Here, we present a xeno-free protocol that confirms the efficient generation of neural precursor cells in hPSCs and also the differentiation of dopaminergic neurons. Additionally, there was no difference when comparing the HLA expression patterns of hESC, homo-SCNT-hESCs and hetero-SCNT-hESCs. We propose that there are no differences in the differentiation capacity and HLA expression among hPSCs that can be cultured in vitro. Thus, it is expected that homo-SCNT-hESCs will possess a wider range of applications when transplanted with neural precursor cells in the context of clinical trials.

Efficacy of GV1001 with gemcitabine/capecitabine in previously untreated patients with advanced pancreatic ductal adenocarcinoma having high serum eotaxin levels (KG4/2015): an open-label, randomised, Phase 3 trial.

BACKGROUND: The TeloVac study indicated GV1001 did not improve the survival of advanced pancreatic ductal adenocarcinoma (PDAC). However, the cytokine examinations suggested that high serum eotaxin levels may predict responses to GV1001. This Phase III trial assessed the efficacy of GV1001 with gemcitabine/capecitabine for eotaxin-high patients with untreated advanced PDAC. METHODS: Patients recruited from 16 hospitals received gemcitabine (1000 mg/m2, D 1, 8, and 15)/capecitabine (830 mg/m2 BID for 21 days) per month either with (GV1001 group) or without (control group) GV1001 (0.56 mg; D 1, 3, and 5, once on week 2-4, 6, then monthly thereafter) at random in a 1:1 ratio. The primary endpoint was overall survival (OS) and secondary end points included time to progression (TTP), objective response rate, and safety. RESULTS: Total 148 patients were randomly assigned to the GV1001 (n = 75) and control groups (n = 73). The GV1001 group showed improved median OS (11.3 vs. 7.5 months, P = 0.021) and TTP (7.3 vs. 4.5 months, P = 0.021) compared to the control group. Grade >3 adverse events were reported in 77.3% and 73.1% in the GV1001 and control groups (P = 0.562), respectively. CONCLUSIONS: GV1001 plus gemcitabine/capecitabine improved OS and TTP compared to gemcitabine/capecitabine alone in eotaxin-high patients with advanced PDAC. CLINICAL TRIAL REGISTRATION: NCT02854072.

CRISPR/Cas9-based genome-wide screening of the deubiquitinase subfamily identifies USP3 as a protein stabilizer of REST blocking neuronal differentiation and promotes neuroblastoma tumorigenesis.

BACKGROUND: The repressor element-1 silencing transcription factor (REST), a master transcriptional repressor, is essential for maintenance, self-renewal, and differentiation in neuroblastoma. An elevated expression of REST is associated with impaired neuronal differentiation, which results in aggressive neuroblastoma formation. E3 ligases are known to regulate REST protein abundance through the 26 S proteasomal degradation pathway in neuroblastoma. However, deubiquitinating enzymes (DUBs), which counteract the function of E3 ligase-mediated REST protein degradation and their impact on neuroblastoma tumorigenesis have remained unexplored. METHODS: We employed a CRISPR/Cas9 system to perform a genome-wide knockout of ubiquitin-specific proteases (USPs) and used western blot analysis to screen for DUBs that regulate REST protein abundance. The interaction between USP3 and REST was confirmed by immunoprecipitation and Duolink in situ proximity assays. The deubiquitinating effect of USP3 on REST protein degradation, half-life, and neuronal differentiation was validated by immunoprecipitation, in vitro deubiquitination, protein-turnover, and immunostaining assays. The correlation between USP3 and REST expression was assessed using patient neuroblastoma datasets. The USP3 gene knockout in neuroblastoma cells was performed using CRISPR/Cas9, and the clinical relevance of USP3 regulating REST-mediated neuroblastoma tumorigenesis was confirmed by in vitro and in vivo oncogenic experiments. RESULTS: We identified a deubiquitinase USP3 that interacts with, stabilizes, and increases the half-life of REST protein by counteracting its ubiquitination in neuroblastoma. An in silico analysis showed a correlation between USP3 and REST in multiple neuroblastoma cell lines and identified USP3 as a prognostic marker for overall survival in neuroblastoma patients. Silencing of USP3 led to a decreased self-renewal capacity and promoted retinoic acid-induced differentiation in neuroblastoma. A loss of USP3 led to attenuation of REST-mediated neuroblastoma tumorigenesis in a mouse xenograft model. CONCLUSION: The findings of this study indicate that USP3 is a critical factor that blocks neuronal differentiation, which can lead to neuroblastoma. We envision that targeting USP3 in neuroblastoma tumors might provide an effective therapeutic differentiation strategy for improved survival rates of neuroblastoma patients.

Efficient Generation of Dopaminergic Neurons from Mouse Ventral Midbrain Astrocytes.

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by tremors, bradykinesia, and rigidity. PD is caused by loss of dopaminergic (DA) neurons in the midbrain substantia nigra (SN) and therefore, replenishment of DA neurons via stem cell-based therapy is a potential treatment option. Astrocytes are the most abundant non-neuronal cells in the central nervous system and are promising candidates for reprogramming into neuronal cells because they share a common origin with neurons. The ability of neural progenitor cells (NPCs) to proliferate and differentiate may overcome the limitations of the reduced viability and function of transplanted cells after cell replacement therapy. Achaete-scute complex homolog-like 1 (Ascl1) is a wellknown neuronal-specific factor that induces various cell types such as human and mouse astrocytes and fibroblasts to differentiate into neurons. Nurr1 is involved in the differentiation and maintenance of DA neurons, and decreased Nurr1 expression is known to be a major risk factor for PD. Previous studies have shown that direct conversion of astrocytes into DA neurons and NPCs can be induced by overexpression of Ascl1 and Nurr1 and additional transcription factors genes such as superoxide dismutase 1 and SRY-box 2. Here, we demonstrate that astrocytes isolated from the ventral midbrain, the origin of SN DA neurons, can be effectively converted into DA neurons and NPCs with enhanced viability. In addition, when these NPCs are inducted to differentiate, they exhibit key characteristics of DA neurons. Thus, direct conversion of midbrain astrocytes is a possible cell therapy strategy to treat neurodegenerative diseases.

Reduced Cytotoxicity by Repetitive mRNA Transfection in Differentiated Neurons.

Background and Objectives: mRNA-based protein expression technology has been used to express functional proteins. We have previously generated dopamine neurons from rat-embryo derived neural precursor cells (NPCs) through repeated transfection of synthetic transcription factor mRNA encoding dopamine-inducible genes. However, NPCs began to die approximately 10 d post-transfection. In this study, we examined a long-term transfection protocol that did not affect cell viability. Methods and Results: Experiments were performed in eight groups sorted according to the start date of mRNA transfection. mRNA was transfected into NPCs daily for 21 d and live cell images of each group were recorded. NPCs which were differentiated for more than five days showed sustained gene expression and appreciable viability despite daily mRNA transfection for 21 d. Conclusions: Repeated mRNA transfection requires cells with a sufficient differentiation period.

Primary astrocytic mitochondrial transplantation ameliorates ischemic stroke.

Mitochondria are important organelles that regulate adenosine triphosphate production, intracellular calcium buffering, cell survival, and apoptosis. They play therapeutic roles in injured cells via transcellular transfer through extracellular vesicles, gap junctions, and tunneling nanotubes. Astrocytes can secrete numerous factors known to promote neuronal survival, synaptic formation, and plasticity. Recent studies have demonstrated that astrocytes can transfer mitochondria to damaged neurons to enhance their viability and recovery. In this study, we observed that treatment with mitochondria isolated from rat primary astrocytes enhanced cell viability and ameliorated hydrogen peroxide-damaged neurons. Interestingly, isolated astrocytic mitochondria increased the number of cells under damaged neuronal conditions, but not under normal conditions, although the mitochondrial transfer efficiency did not differ between the two conditions. This effect was also observed after transplanting astrocytic mitochondria in a rat middle cerebral artery occlusion model. These findings suggest that mitochondria transfer therapy can be used to treat acute ischemic stroke and other diseases. [BMB Reports 2023; 56(2): 90-95].

Natural Course of Asymptomatic Upper Gastrointestinal Subepithelial Lesion of 2 cm or Less in Size.

There is limited evidence of a natural course of an upper gastrointestinal (UGI)-subepithelial lesion (SEL) of 2 cm or less in size. This study aims to determine the natural course of UGI-SELs and find the risk factors of the endoscopic and endoscopic ultrasonography (EUS) findings associated with an increase in size. The medical records of 2539 patients with UGI-SELs between 2004 and 2016 were reviewed retrospectively. A total of 672 SELs of 2 cm or less in size were analyzed through EUS and followed up for at least 36 months. The mean follow-up duration was 68 months (range: 36-190 months), and 97 SELs (14.4%) showed an increase in size with a mean increase rate of 1.2 mm/year. Initial size (aOR 1.03, 95% confidence interval (CI) 1.01-1.06), an endoscopic finding of a hemorrhagic spot (aOR 3.13, 95% CI 1.14-8.60), and an EUS finding of a lesion in the fourth layer (aOR 1.87, 95% CI (1.21-2.88) were related to an increase in size. An endoscopic finding of translucidity (aOR 0.28, 95% CI (0.10-0.76) and an EUS finding of calcification (aOR 0.30, 95% CI 0.09-0.95) were inversely related to an increase in size. There was no death related to UGI-SELs during the follow-up. While most UGI-SELs of 2 cm or less in size showed no significant size change and favorable prognosis, an individualized follow-up strategy needs to be considered in case of the presence of hemorrhagic spots and lesions in the fourth layer.

Single balloon enteroscopy-guided endoscopic retrograde pancreatography for the treatment of a symptomatic pancreatic pseudocyst complicated by pancreaticojejunostomy stricture: A case report.

RATIONALE: Endoscopic treatment of a pancreatic pseudocyst complicated by pancreaticojejunostomy (PJ) stricture is challenging. PATIENT CONCERNS: A 76-year-old woman presented with worsening abdominal pain and dyspepsia. She had been receiving adjuvant chemotherapy (capecitabine and cisplatin) for 4 months after pylorus-preserving pancreaticoduodenectomy (PPPD) for the treatment of extrahepatic cholangiocarcinoma. DIAGNOSES: Laboratory findings included elevated serum amylase (145 U/L) and lipase (437 U/L) levels. Abdominal computed tomography (CT) showed a pancreatic pseudocyst of approximately 3 cm in size and pancreatic duct dilatation in the remnant pancreas. According to the Response Evaluation Criteria in Solid Tumors, cholangiocarcinoma is a stable disease. INTERVENTIONS AND OUTCOMES: Endoscopic drainage of the pancreatic pseudocyst was planned. Single-balloon enteroscopy (SBE)-guided endoscopic retrograde pancreatography (ERP) with endoscopic ultrasonography (EUS) using a mini probe demonstrated a membranous PJ stricture and a pancreatic pseudocyst. Endoscopic pseudocyst drainage using a 7-Fr plastic stent was successfully performed after needle-knife incision of the PJ stricture. Follow-up abdominal CT after 3 weeks showed complete resolution of the pseudocyst. Chemotherapy was resumed. LESSONS: SBE-guided ERP with EUS using a mini probe may be an effective and safe treatment in a patient with a pancreatic pseudocyst complicated by membranous PJ stricture after PPPD.

How will multifaceted trust impact domestic travel during the COVID-19 pandemic and subjective well-being? A comparison between Korea and the US.

This study examines the impact of extended tourist trust constructs on domestic travel experiences, subjective well-being, and future travel intention in the pandemic. Data was obtained through a survey conducted on 1181 Korean and American domestic tourists. The results show that policy trust and destination trust have positive effects on travel frequency and satisfaction. Moreover, interactional trust positively impacted travel satisfaction. While both travel frequency and travel satisfaction have positive impacts on subjective well-being of travelers, travel satisfaction has a stronger impact on subjective well-being than travel frequency. However, certain relationships were influenced by national backgrounds (U·S vs. Korea).

Endoscopist-Driven Sedation Practices in South Korea: Re-evaluation Considering the Nationwide Survey in 2019.

Background/Aims: This study aimed to determine changes in endoscopist-driven sedation practices 5 years after the first nationwide survey in 2014 by the Korean Society of Gastrointestinal Endoscopy (KSGE). Methods: A 59-item survey covering current practices was electronically mailed to all members of the KSGE in 2019. Results: In total, 955 (12.8%) out of 7,486 questionnaires were returned. A total of 738 (77.7%) out of 955 respondents attended dedicated sedation education programs. The American Society of Anesthesiologists class was recorded by 464 (51.2%) out of 907 respondents. The recording rate was higher in respondents who completed sedation education (p=0.014) and worked in general or tertiary hospitals (p<0.001). Compared to that reported in the previous survey, the reported use of propofol was higher in 2019. The respondents had higher satisfaction scores for propofol-based sedation compared with midazolam monotherapy (p<0.001). The rates of oxygen supplementation (p<0.001) and oxygen saturation level monitoring (p<0.001) during sedative endoscopy were higher in 2019 than in the previous survey. A total of 876 (98.4%) out of 890 respondents reported a separate recovery bay, and 615 (70.5%) out of 872 respondents reported that personnel were assigned solely to the recovery bay. Conclusions: Endoscopist-driven sedation and monitoring practices in 2019 were significantly different than those in 2014. The respondents favored propofol-based sedation and utilized oxygen supplementation and monitoring of O2 saturation more frequently in 2019 than in 2014.

CRISPR/Cas9-based genome-wide screening for deubiquitinase subfamily identifies USP1 regulating MAST1-driven cisplatin-resistance in cancer cells.

Background: Cisplatin is one of the frontline anticancer agents. However, development of cisplatin-resistance limits the therapeutic efficacy of cisplatin-based treatment. The expression of microtubule-associated serine/threonine kinase 1 (MAST1) is a primary factor driving cisplatin-resistance in cancers by rewiring the MEK pathway. However, the mechanisms responsible for MAST1 regulation in conferring drug resistance is unknown. Methods: We implemented a CRISPR/Cas9-based, genome-wide, dual screening system to identify deubiquitinating enzymes (DUBs) that govern cisplatin resistance and regulate MAST1 protein level. We analyzed K48- and K63-linked polyubiquitination of MAST1 protein and mapped the interacting domain between USP1 and MAST1 by immunoprecipitation assay. The deubiquitinating effect of USP1 on MAST1 protein was validated using rescue experiments, in vitro deubiquitination assay, immunoprecipitation assays, and half-life analysis. Furthermore, USP1-knockout A549 lung cancer cells were generated to validate the deubiquitinating activity of USP1 on MAST1 abundance. The USP1-MAST1 correlation was evaluated using bioinformatics tool and in different human clinical tissues. The potential role of USP1 in regulating MAST1-mediated cisplatin resistance was confirmed using a series of in vitro and in vivo experiments. Finally, the clinical relevance of the USP1-MAST1 axis was validated by application of small-molecule inhibitors in a lung cancer xenograft model in NSG mice. Results: The CRISPR/Cas9-based dual screening system identified USP1 as a novel deubiquitinase that interacts, stabilizes, and extends the half-life of MAST1 by preventing its K48-linked polyubiquitination. The expression analysis across human clinical tissues revealed a positive correlation between USP1 and MAST1. USP1 promotes MAST1-mediated MEK1 activation as an underlying mechanism that contributes to cisplatin-resistance in cancers. Loss of USP1 led to attenuation of MAST1-mediated cisplatin-resistance both in vitro and in vivo. The combined pharmacological inhibition of USP1 and MAST1 using small-molecule inhibitors further abrogated MAST1 level and synergistically enhanced cisplatin efficacy in a mouse xenograft model. Conclusions: Overall, our study highlights the role of USP1 in the development of cisplatin resistance and uncovers the regulatory mechanism of MAST1-mediated cisplatin resistance in cancers. Co-treatment with USP1 and MAST1 inhibitors abrogated tumor growth and synergistically enhanced cisplatin efficacy, suggesting a novel alternative combinatorial therapeutic strategy that could further improve MAST1-based therapy in patients with cisplatin-resistant tumors.

Dual role of deubiquitinating enzyme USP19 regulates mitotic progression and tumorigenesis by stabilizing survivin.

Survivin is a component of the chromosomal passenger complex, which includes Aurora B, INCENP, and Borealin, and is required for chromosome segregation and cytokinesis. We performed a genome-wide screen of deubiquitinating enzymes for survivin. For the first time, we report that USP19 has a dual role in the modulation of mitosis and tumorigenesis by regulating survivin expression. Our results found that USP19 stabilizes and interacts with survivin in HCT116 cells. USP19 deubiquitinates survivin protein and extends its half-life. We also found that USP19 functions as a mitotic regulator by controlling the downstream signaling of survivin protein. Targeted genome knockout verified that USP19 depletion leads to several mitotic defects, including cytokinesis failure. In addition, USP19 depletion results in significant enrichment of apoptosis and reduces the growth of tumors in the mouse xenograft. We envision that simultaneous targeting of USP19 and survivin in oncologic drug development would increase therapeutic value and minimize redundancy.

[The Latest Knowledge on Endoscopic Retrograde Cholangiopancreatography-related Pancreatitis].

ERCP has been established as a golden diagnostic and therapeutic modality in various pancreatobiliary diseases, including gallstones and malignancy. On the other hand, ERCP is a relatively invasive procedure with radiation hazards and major complications. Among the major complications, ERCP-related pancreatitis has been reported in more than 14.7% of high-risk patients, which might lead to extended hospitalization and a substantial burden for both patients and physicians. Recent guidelines have defined the high-risk factors for ERCP-related pancreatitis. In addition, several outstanding studies have shown that rectal non-steroidal anti-inflammatory drugs, aggressive hydration with lactated Ringer's solution, and pancreatic stents can reduce ERCP-related pancreatitis in high-risk patients or all patients. A prevention algorithm for ERCP-related pancreatitis was provided based on advanced research.

Current trends in the management of pancreatic cystic neoplasms in Korea: a national survey.

BACKGROUND/AIMS: The study aimed to investigate the current practice patterns in the management of pancreatic cystic neoplasms in Korea. METHODS: An electronic survey was systematically distributed by email to members of the Korean Pancreatobiliary Association from December 2019 to February 2020. RESULTS: In total, 115 (110 gastroenterologists, five surgeons) completed the survey, 72.2% of whom worked in a tertiary/academic medical center. Most (65.2%) followed the 2012/2017 International Association of Pancreatology guidelines for the management of pancreatic cystic neoplasms. A gadolinium-enhanced magnetic resonance imaging/magnetic resonance cholangiopancreatography was the most common first-line diagnostic modality (42.1%), but a contrast-enhanced computed tomography scan was preferred as a subsequent surveillance tool (58.3%). Seventy-four percent of respondents routinely performed endoscopic ultrasound-guided fine needle aspiration for pancreatic cystic neoplasms with suspicious mural nodules. Endoscopic ultrasound-guided fine needle aspiration cytology (94.8%) and cystic fluid carcinoembryonic antigen (95.7%) were used for cystic fluid analysis. Most (94%) typically recommended surgery in patients with high-risk stigmata, but 18.3% also considered proceeding with surgery in patients with worrisome features. Most (96.5%) would continue surveillance of pancreatic cystic neoplasms for more than 5 years. CONCLUSION: According to this survey, there was variability in the management of pancreatic cystic neoplasms among the respondents. These results suggest that the development of evidence-based guidelines for pancreatic cystic neoplasms that fit the Korean practice is needed to create an optimal approach to the management of pancreatic cystic neoplasms.

USP32 confers cancer cell resistance to YM155 via promoting ER-associated degradation of solute carrier protein SLC35F2.

Background: The most commonly preferred chemotherapeutic agents to treat cancers are small-molecule drugs. However, the differential sensitivity of various cancer cells to small molecules and untargeted delivery narrow the range of potential therapeutic applications. The mechanisms responsible for drug resistance in a variety of cancer cells are also largely unknown. Several deubiquitinating enzymes (DUBs) are the main determinants of drug resistance in cancer cells. Methods: We used CRISPR-Cas9 to perform genome-scale knockout of the entire set of genes encoding ubiquitin-specific proteases (USPs) and systematically screened for DUBs resistant to the clinically evaluated anticancer compound YM155. A series of in vitro and in vivo experiments were conducted to reveal the relationship between USP32 and SLC35F2 on YM155-mediated DNA damage in cancer cells. Results: CRISPR-based dual-screening method identified USP32 as a novel DUB that governs resistance for uptake of YM155 by destabilizing protein levels of SLC35F2, a solute-carrier protein essential for the uptake of YM155. The expression of USP32 and SLC35F2 was negatively correlated across a panel of tested cancer cell lines. YM155-resistant cancer cells in particular exhibited elevated expression of USP32 and low expression of SLC35F2. Conclusion: Collectively, our DUB-screening strategy revealed a resistance mechanism governed by USP32 associated with YM155 resistance in breast cancers, one that presents an attractive molecular target for anti-cancer therapies. Targeted genome knockout verified that USP32 is the main determinant of SLC35F2 protein stability in vitro and in vivo, suggesting a novel way to treat tumors resistant to small-molecule drugs.

Spontaneous resolution of gallbladder hematoma in blunt traumatic injury: A case report.

BACKGROUND: We report a case of intragallbladder hematoma and biliary tract obstruction caused by blunt gallbladder injury. We report that the patient was safely treated by conservative treatment after the obstruction was resolved by endoscopic retrograde cholangiopancreatography (ERCP). CASE SUMMARY: A 67-year-old man was admitted via the emergency department due to complaints of right-sided abdominal pain that started 2 d prior. Four days prior to presentation, the patient had slipped, fallen and struck his abdomen on a motorcycle handle. His initial vital signs were stable. On physical examination, he showed right upper quadrant pain and Murphy's sign, with decreased bowel sounds. Additionally, he had had a poor appetite for 4 d. He had been on aspirin for 2 years due to underlying hypertension. Initial simple radiography revealed a slight ileus. The laboratory findings were as follows: white blood cell count, 15.5 × 103/µL (normal range 4.8 × 103-10.8 × 103); hemoglobin, 9.4 g/dL; aspartate aminotransferase/alanine transferase, 423/348 U/L; total bilirubin/direct bilirubin, 4.45/3.26 mg/dL; -GTP , 639 U/L (normal range 5-61 U/L); and C-reactive protein, 12.32 mg/dL (0-0.3). Abdominal computed tomography showed a distended gallbladder with edematous wall change and a 55 mm × 40 mm hematoma. Dilatation was observed in both the intrahepatic and common bile duct areas. Antibiotic treatment was initiated, and ERCP was performed, with hemobilia found during treatment. After cannulation, the patient's symptoms were relieved, and after conservative management, the patient was discharged with no further complications. After 1-month follow-up, the gallbladder hematoma was completely resolved. CONCLUSION: In the case of traumatic injury to the gallbladder, conservative treatment is feasible even in the presence of hematoma.

A Nationwide Survey on the Facilities and Personnel for Endoscopic Sedation: Results from 50 Qualified Endoscopy Units of Teaching Hospitals Accredited by the Korean Society of Gastrointestinal Endoscopy (KSGE).

BACKGROUND/AIMS: This study aimed to determine the current status of facilities, equipment, and personnel for endoscopic sedation from endoscopy units of representative hospitals in South Korea. METHODS: A questionnaire survey was conducted on 50 qualified endoscopy units accredited by the Korean Society of Gastrointestinal Endoscopy. RESULTS: All included endoscopy units had regulations and educational programs regarding sedation training for endoscopists and nursing personnel. There present one assisting nurse during endoscopy in 35 units (70%) and at least two nurses in 12 units (24.0%). All endoscopy units had examination rooms equipped with oxygen supply and suction systems. Endoscopist-directed sedation was performed in 48 units (96.0%). Propofol-based sedation was the most used sedation method. All units had a separate recovery bay. The daily number of patients per bed was greater than 10 in 17 units (34.0%). In 26 (52.0%) units, a single nurse cared for ≥10 patients per day. All the units fulfilled the discharge criteria. CONCLUSION: This study presents data regarding endoscopic sedation clinical practice in 50 endoscopy units in South Korea. This study presents the current status of endoscopic sedation clinical practice in 50 qualified endoscopy units accredited by the KSGE, which provide excellent quality management.