Pancreatic ductal adenocarcinoma (PDAC) exhibits an altered metabolic profile compared to normal pancreatic tissue. However, studies on actual pancreatic tissues are limited. Untargeted metabolomics analysis was conducted on 54 pairs of tumor and matched normal tissues. Taurine levels were validated via immunohistochemistry (IHC) on separate PDAC and normal tissues.Bioinformatics analysis of transcriptomics and proteomics data evaluated genes associated with taurine metabolism. Identified taurine-associated gene was validated through gene modulation. Clinical implications were evaluated using patient data. Metabolomics analysis showed a 2.51-fold increase in taurine in PDAC compared to normal tissues (n=54). IHC confirmed this in independent samples (n=99 PDAC, 19 normal). Bioinformatics identified 2-aminoethanethiol dioxygenase (ADO) as a key gene modulating taurine metabolism. IHC on a tissue microarray (39 PDAC, 10 normal) confirmed elevated ADO in PDAC. The ADOTaurine axis correlated with PDAC recurrence and disease-free survival. ADO knockdown reduced cancer cell proliferation and tumor growth in a mouse xenograft model. The MEK-related signaling pathway is suggested to be modulated by ADO-Taurine metabolism. Our multi-omics investigation revealed elevated taurine synthesis mediated by ADO upregulation in PDAC. The ADOTaurine axis may serve as a biomarker for PDAC prognosis and a therapeutic target.

Purpose: This study aimed to develop a Korean version of the frailty model that reflects a holistic perspective. There were three phases of the study: a literature review, a two-round Delphi study, and a public hearing. Methods: The model was developed based on the middle-range theory generation approach proposed by Roy. A literature search was conducted, and a review of 36 studies on frailty involving Koreans led to the development of an initial frailty model. A two-round Delphi study was then conducted with nine experts to evaluate the appropriateness of the model. The revised model was presented at a public hearing to achieve consensus. Based on feedback indicating the need for improved visualization, a finalized diagrammatic model was developed. Results: The final frailty model comprised four domains, seven subdomains, and 30 items. It included specific items reflecting the distinctive characteristics of Korean culture, such as relationships with adult children (filial piety), nutritional status (consumption of red meat), and type of residential building. Conclusion The final frailty model provides a comprehensive perspective on the factors contributing to frailty, their interactions, and the potential interventions that healthcare providers can implement to prevent frailty.

Pancreatic ductal adenocarcinoma (PDAC) exhibits an altered metabolic profile compared to normal pancreatic tissue. However, studies on actual pancreatic tissues are limited. Untargeted metabolomics analysis was conducted on 54 pairs of tumor and matched normal tissues. Taurine levels were validated via immunohistochemistry (IHC) on separate PDAC and normal tissues.Bioinformatics analysis of transcriptomics and proteomics data evaluated genes associated with taurine metabolism. Identified taurine-associated gene was validated through gene modulation. Clinical implications were evaluated using patient data. Metabolomics analysis showed a 2.51-fold increase in taurine in PDAC compared to normal tissues (n=54). IHC confirmed this in independent samples (n=99 PDAC, 19 normal). Bioinformatics identified 2-aminoethanethiol dioxygenase (ADO) as a key gene modulating taurine metabolism. IHC on a tissue microarray (39 PDAC, 10 normal) confirmed elevated ADO in PDAC. The ADOTaurine axis correlated with PDAC recurrence and disease-free survival. ADO knockdown reduced cancer cell proliferation and tumor growth in a mouse xenograft model. The MEK-related signaling pathway is suggested to be modulated by ADO-Taurine metabolism. Our multi-omics investigation revealed elevated taurine synthesis mediated by ADO upregulation in PDAC. The ADOTaurine axis may serve as a biomarker for PDAC prognosis and a therapeutic target.

Purpose: This study aimed to develop a Korean version of the frailty model that reflects a holistic perspective. There were three phases of the study: a literature review, a two-round Delphi study, and a public hearing. Methods: The model was developed based on the middle-range theory generation approach proposed by Roy. A literature search was conducted, and a review of 36 studies on frailty involving Koreans led to the development of an initial frailty model. A two-round Delphi study was then conducted with nine experts to evaluate the appropriateness of the model. The revised model was presented at a public hearing to achieve consensus. Based on feedback indicating the need for improved visualization, a finalized diagrammatic model was developed. Results: The final frailty model comprised four domains, seven subdomains, and 30 items. It included specific items reflecting the distinctive characteristics of Korean culture, such as relationships with adult children (filial piety), nutritional status (consumption of red meat), and type of residential building. Conclusion The final frailty model provides a comprehensive perspective on the factors contributing to frailty, their interactions, and the potential interventions that healthcare providers can implement to prevent frailty.

Pancreatic ductal adenocarcinoma (PDAC) exhibits an altered metabolic profile compared to normal pancreatic tissue. However, studies on actual pancreatic tissues are limited. Untargeted metabolomics analysis was conducted on 54 pairs of tumor and matched normal tissues. Taurine levels were validated via immunohistochemistry (IHC) on separate PDAC and normal tissues.Bioinformatics analysis of transcriptomics and proteomics data evaluated genes associated with taurine metabolism. Identified taurine-associated gene was validated through gene modulation. Clinical implications were evaluated using patient data. Metabolomics analysis showed a 2.51-fold increase in taurine in PDAC compared to normal tissues (n=54). IHC confirmed this in independent samples (n=99 PDAC, 19 normal). Bioinformatics identified 2-aminoethanethiol dioxygenase (ADO) as a key gene modulating taurine metabolism. IHC on a tissue microarray (39 PDAC, 10 normal) confirmed elevated ADO in PDAC. The ADOTaurine axis correlated with PDAC recurrence and disease-free survival. ADO knockdown reduced cancer cell proliferation and tumor growth in a mouse xenograft model. The MEK-related signaling pathway is suggested to be modulated by ADO-Taurine metabolism. Our multi-omics investigation revealed elevated taurine synthesis mediated by ADO upregulation in PDAC. The ADOTaurine axis may serve as a biomarker for PDAC prognosis and a therapeutic target.

Purpose: This study aimed to develop a Korean version of the frailty model that reflects a holistic perspective. There were three phases of the study: a literature review, a two-round Delphi study, and a public hearing. Methods: The model was developed based on the middle-range theory generation approach proposed by Roy. A literature search was conducted, and a review of 36 studies on frailty involving Koreans led to the development of an initial frailty model. A two-round Delphi study was then conducted with nine experts to evaluate the appropriateness of the model. The revised model was presented at a public hearing to achieve consensus. Based on feedback indicating the need for improved visualization, a finalized diagrammatic model was developed. Results: The final frailty model comprised four domains, seven subdomains, and 30 items. It included specific items reflecting the distinctive characteristics of Korean culture, such as relationships with adult children (filial piety), nutritional status (consumption of red meat), and type of residential building. Conclusion The final frailty model provides a comprehensive perspective on the factors contributing to frailty, their interactions, and the potential interventions that healthcare providers can implement to prevent frailty.

Replacement of the retrohepatic inferior vena cava (IVC) after concurrent resection of IVC and tumor-bearing liver is regarded as a feasible living donor liver transplantation (LDLT) technique to cope with tumors around the IVC. This method can make the resection extent of LDLT comparable to that of deceased-donor liver transplantation. We present one pediatric LDLT case with IVC replacement using an enlarged iliac vein conduit to treat advanced hepatoblastoma. The patient was a 33-monthold and 12 kg-weighing girl suffering from large multiple hepatoblastomas invading the retrohepatic IVC. At 2-month waiting after deciding LDLT, we obtained a coldstored iliac vein graft and LDLT was performed with the father’s left lateral section graft. A 1.3 cm-wide and 10 cm-long iliac vein was transformed to be a 2 cm-wide and 5 cm-long vein graft through a double-barrel unification venoplasty. The left lateral section graft was implanted along the standard procedure of LDLT. The patient recovered uneventfully and is undergoing scheduled adjuvant chemotherapy. IVC replacement with vein homograft is a feasible option for LDLT in pediatric patients with advanced liver malignancy.