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Objectives: This was a pilot study to investigate the possibility of clinical analysis to support the lack of sample size of real data and to generate synthetic data. Since real data has many limitations, such as ethical issues and costly issues, there have been many attempts to create realistic synthetic data. The focus is on whether synthetic data can be used instead of real data. Methods: This study analyzed 11,978 lung cancer patients who used anticancer drug therapy using synthetic data as a quasi-experimental study. Clinically significant variables were extracted and some tables containing patient status and treatment records were preprocessed. This experiment was applied to the propensity score matching technique to prevent the bias of covariates. Then, the preprocessed data were analyzed using Kaplan-Meier estimation and Cox proportional hazards model. Results: When plotting the survival curves, the curves from the synthetic data did not match the curves for the actual data of the other covariates. In Cohort 1, Gen I had a better 5-year OS than Gen II (S1=0.973, S2=0.953, p1=0.990, S3=0.884, p< 0.05). In the exploratory sub-group analysis using the Cox regression model, the risk ratio was estimated. We found that Gen I had a better effect on hazard ratio than Gen II and III. However, those results were different from the actual trend. Conclusions: It was found that the analysis based on the DATA-FREE-BOX data was different from the trend of the survival analysis conducted with the real data. The trend of this analysis could be different from the real trend. It will be able to contribute to data-validation. Moreover, it is expected that the same methodology can be applied in clinical studies based on actual data by utilizing the technique used in this study.

Background: Catheter-related bladder discomfort (CRBD) is common in patients with a urinary catheter and is a risk factor for emergence agitation (EA). The mainstay of CRBD management is anticholinergics. Dexamethasone inhibits acetylcholine release. This study aimed to evaluate the effects of dexamethasone on postoperative CRBD and EA.Methods: In this prospective study, 90 patients undergoing urological surgery requiring urinary catheterization were allocated randomly to one of two groups (each n = 45). Before induction of anesthesia, the dexamethasone group received 10 mg (2 ml) of dexamethasone intravenously, while the control group received 2 ml of saline in the same manner. The incidence and severity of CRBD were assessed 0, 1, 2, and 6 h after the patient arrived in the post-anesthesia care unit (PACU) as the primary outcomes. The incidence and severity of EA were also compared during emergence and recovery from anesthesia as secondary outcomes.Results: The incidences of CRBD in the control group and dexamethasone group at 0, 1, 2, and 6 h postoperatively were 28.9% and 15.6%, 55.6% and 55.6%, 57.8% and 46.7%, and 53.3% and 51.1%, respectively. The incidence and severity of CRBD assessed at 0, 1, 2, and 6 h postoperatively did not show intergroup differences. The incidence and severity of EA in the operating room and PACU also showed no difference between the groups.Conclusions: Dexamethasone (10 mg) administered before induction of anesthesia did not further reduce the incidence or severity of CRBD or EA in patients undergoing urological surgery.

There are many epidemiological studies asserting that fine dust causes lung cancer, but the biological mechanism is not clear. This study was conducted to investigate the effect of PM10 (particulate matter less than 10 &mu, m) on single nucleotide variants through whole genome sequencing in lung epithelial cancer cell lines (HCC-827, NCI-H358) that have been exposed to PM10. The two cell lines were exposed to PM10 for 15 days. We performed experimental and next generation sequencing analyses on experimental group that had been exposed to PM10 as well as an unexposed control group. After exposure to PM10, 3005 single nucleotide variants were newly identified in the NCI-H358 group, and 4402 mutations were identified in the HCC-827 group. We analyzed these single nucleotide variants with the Mutalisk program. We observed kataegis in chromosome 1 in NCI-H358 and chromosome 7 in HCC-827. In mutational signatures analysis, the COSMIC mutational signature 5 was highest in both HCC-827 and NCI-H358 groups, and each cosine similarity was 0.964 in HCC-827 and 0.979 in the NCI-H358 group. The etiology of COSMIC mutational signature 5 is unknown at present. Well-designed studies are needed to determine whether environmental factors, such as PM10, cause COSMIC mutational signature 5.

Background: Cancer stem cells (CSCs) identified in lung cancer exhibit resistance to chemotherapy, radiotherapy, and targeted therapy. Therefore, a technology to control of CSCs is needed to overcome such resistance to cancer therapy. Various evidences about the association between epithelial-mesenchymal transition related transcriptomic alteration and acquisition of CSC phenotype have been proposed recently. In our previous research, down-regulated miR-26a-5p is closely related to mesenchymal-like lung cancer cell lines. These findings suggest that miR-26a-5p might be involved in lung cancer stemness. Methods: RNA polymerase III subunit G (POLR3G) was selected as a candidate target of miR-26a-5p related to cancer stemness. its quantitative relationship was investigated by polymerase chain reaction, western blot after transfection of miR-26a-5p. luciferase assay were done for investigating the direct regulation of miR-26a-5p on POLR3G expression. After transfection of miR-26a-5p, colony formation assay and sphere formation assay were performed to evaluate the effect on cancer stemness. By treating cancer cell by miR-26a-5p and paclitaxel, cell viability was checked by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay and Muse cell analyzer. Expression level of each gene and its impact on survival were revealed by the cancer genome atlas pancancer database. Results: miR-26a-5p regulated the expression of POLR3G directly. Overexpression of miR-26a-5p induced down regulation of POLR3G and a marked reduction of colony formation and sphere formation. Co-treatment of miR-26a-5p with paclitaxel decreased cell growth, suggesting that miR-26a-5p might play a role as a chemotherapy sensitizer. In the cancer genome atlas data, down-regulated miR-26a-5p and up-regulated POLR3G were shown compared to adjacent normal tissue. High miR-26a-5p and low POLR3G expression were also related to higher survival rate of patients with lung adenocarcinoma. Conclusions: Overexpression of miR-26a-5p can suppress lung cancer stemness and make cancer cell become sensitive to chemotherapy. This finding provides a novel insight into a potential lung cancer treatment by regulating stemness. Citation Format: Daeun Kang, Chang Ryul Park, Minhyeok Lee, Su Yel Lee, Se Jin Park, Wan Jin Hwang, Gwan Woo Ku, Seong Lan Yu, In Beom Jeong, Sun Jung Kwon, Jaeku Kang, Eung Bae Lee, Ji Woong Son. microRNA-26a-5p is a prognostic factor that regulates cancer stemness [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 817.

Aneurysm and pseudoaneurysm of the dorsalis pedis artery (DPA) are rare vascular entities. Pseudoaneurysms of the DPA are commonly due to blunt trauma, sharp penetrating injury, fracture, or iatrogenic injury. Herein, we report the case of a patient with a rare iatrogenic pseudoaneurysm that occurred after blood sampling. The diagnosis was suspected based on palpitation of a pulsatile mass on the dorsal foot and confirmed by color Doppler ultrasound and computed tomography angiography. Surgical treatment was successfully performed by reconstruction with an autologous venous graft. The patient recovered well, with no ischemic complications.

An arteriovenous fistula (AVF) from the renal artery following a penetrating abdominal trauma is not common. We report the case of a 19-year-old male who presented with a knife stab wound in the right upper quadrant. Due to unstable vital signs and to the protrusion of the mesentery through the stab...

Background Although parenchyma-saving resection makes it possible to preserve the lung parenchyma, most surgeons are reluctant to perform it for congenital cystic adenomatoid malformation (CCAM) because it could also result in recurrent pulmonary infection or residual lesion. This study compared the early and late postoperative outcomes according to the extent of resection in CCAM patients to determine if the extent of resection would influence the short- and long-term results. Methods Between 1995 and 2006, 45 patients underwent surgical resection for CCAM. Ten patients received a segmentectomy and 2 a wedge resection (the parenchyma-saving group), and 32 received a lobectomy and 1 a pneumonectomy (the lobectomy group). A retrospective analysis was done to compare the early and late postoperative outcomes between two groups. Results No significant differences were observed for severity and duration of preoperative symptoms. No in-hospital or late deaths occurred. There were no significant differences in the incidence of early postoperative complications and late morbidities between the two groups. No significant differences were observed between the two groups for hospital length of stay and duration of chest tube placement. Conclusions The early and late outcomes were excellent even after parenchyma-saving resection in patients with CCAM. We suggest that parenchyma-saving resection can be safely performed in selected patients with a well-confined CCAM lesion and thereby avoiding pneumonectomy in children.