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Seoul has experienced rapid economic growth and industrialization, and it has become the central city of South Korea. These densely populated urban spaces have undergone the urban heat island (UHI) phenomenon, wherein the temperature is higher than that of the surrounding areas. Green spaces constitute the primary response to this problem, yet Seoul has not yet taken measures to create small-scale green spaces, such as alley gardens. Therefore, this study analyses the case of alley gardens in Daegu and argues for the necessity of their introduction. Alley gardens in Daegu have proven effective in reducing heat and have influenced the residential satisfaction of residents in densely populated, old housing. After confirming that the concept of alley gardens can serve as a micro-urban planning tool to establish small-scale green spaces and alleviate the UHI effect in Seoul, we explored the target areas where alley gardens can be applied within Seoul. Through heat-related environmental indicators and social factor indicators, this study found that Mullae-dong is experiencing the UHI effect, and that the introduction of alley gardens would have a positive impact due to the concentration of small-scale, old residences. This paper establishes the rationale for applying alley gardens to Seoul, while also deriving the importance and implications for the dissemination and revitalization of micro-level urban environment policies.

Purpose: Appendectomy, which comprises most benign intra-abdominal surgeries, is currently assisted by laparoscopy in most cases. However, many patients complain of postoperative shoulder or subcostal pain after laparoscopic surgery. In some cases, the pain lasts even several weeks after surgery. This study aimed to analyze unmodifiable clinicopathological factors of patients who underwent laparoscopic appendectomy and to minimize preoperative and postoperative discomfort., Methods: Patients admitted for laparoscopic appendectomy for acute appendicitis with an American Society of Anesthesiology (ASA) grades I and II, and ages 12~70 years were enrolled in the study. Postoperative shoulder or subcostal pain was assessed using the visual analogue scale (VAS) for pain and analyzed with the clinicopathological factors of the patients, including age, sex, weight, height, body mass index (BMI), and abdominal circumference (AC) difference., Results: Of the 124 patients, 40 complained of postoperative shoulder or subcostal pain with a VAS score of ≥4. The risk of the postoperative shoulder or subcostal pain increased in women ( p =0.001). From a univariate analysis, the risk of postoperative shoulder or subcostal pain increased with lower height, weight and BMI ( p =0.002, p =0.001, p =0.012) and with greater AC difference ( p =0.012). However, a multivariate analysis showed that lower weight was the only risk factor of postoperative pain ( p =0.005)., Conclusion: The risk of postoperative shoulder or subcostal pain after laparoscopic appendectomy was significantly increased with lower weight., Competing Interests: CONFLICT OF INTEREST None., (Copyright © 2020 The Journal of Minimally Invasive Surgery. All rights reserved.)

Ahead of Print article withdrawn by publisher.

We previously reported that CDK2/Cyclin A can phosphorylate and activate the transcription factor NF-Y. In this study, we investigated a potential regulatory role for NF-Y in the transcription of Cyclin A and other cell cycle regulatory genes. Gel-shift assays demonstrate that NF-Y binds to CCAAT sequences in the Cyclin A promoter, as well as to those in the promoters of cell cycle G2 regulators such as CDC2, Cyclin B and CDC25C. Furthermore, expression of Cyclin A increases NF-Y's affinity for CCAAT sequences in the CDC2 promoter; however, Cyclin A's induction of CDC2 transcription is antagonized by p21, an inhibitor of CDK2/Cyclin A. These results suggest a model wherein NF-Y binds to and activates transcription from the Cyclin A promoter, increasing cellular levels of Cyclin A/CDK2 and potentiating NF-Y's capacity for transcriptional transactivation, and imply a positive feedback loop between NF-Y and Cyclin A/CDK2. Our findings are additionally indicative of a role for Cyclin A in activating Cyclin B/CDK1 through promoting NF-Y dependent transcription of Cyclin B and CDC2; NF-Y mediated crosstalk may therefore help to orchestrate cell-cycle progression.