Purpose: A proportion of patients who undergo kidney transplantation (KT) eventually experience graft failure and require dialysis. However, the characteristics of posttransplant patients differ from non-KT patients considering the long-term use of immunosuppressants, steroids, and associated complications. These differences may influence the outcomes of vascular access (VA). This study aims to compare the VA outcomes and infection rates between KT with allograft failures and non-KT patients. Methods: We retrospectively analyzed patients who underwent VA creation between January 2018 and November 2023.A propensity score-matched cohort was created based on age and sex, comparing 61 patients who received their first VA creation after KT to 222 patients who had never undergone KT before VA creation. Results: The median VA patency was 841 days. VA abandonment within 3 months occurred in 3.2% in the non-KT group and 1.6% in the KT with failed allograft group (P = 0.845). Infection rates were also similar (4.1% vs. 3.3%, P = 0.226). Cox regression indicated that KT was not a significant risk factor for VA patency, whereas low body mass index and diabetes mellitus were significant risk factors for long-term patency. In the KT group, steroid and mammalian target of rapamycin (mTOR) inhibitor use before VA formation were identified as risk factors for primary patency. Conclusion VA outcomes in KT patients with allograft failure were comparable to those of non-KT patients. While KT status itself does not adversely affect VA patency or infection rates, patients with low body mass index, diabetes mellitus, or who are receiving steroid or mTOR inhibitors should be carefully managed.

Janus kinase (JAK) inhibitors are an important treatment option for ulcerative colitis, providing rapid onset of action, oral administration, and efficacy even after biologic failure. The 3 approved agents—tofacitinib, filgotinib, and upadacitinib—differ in JAK isoform selectivity, leading to clinically meaningful differences in efficacy and safety. Evidence from network meta-analyses, clinical trials, and real-world studies consistently shows that upadacitinib provides the highest efficacy for induction and maintenance of remission, whereas filgotinib demonstrates the most favorable safety profile. The strong efficacy of upadacitinib and tofacitinib is particularly relevant in patients with severe disease, including acute severe ulcerative colitis, and upadacitinib maintains high efficacy regardless of prior advanced therapy exposure. JAK inhibitors also benefit extraintestinal manifestations. Although risks such as herpes zoster, serious infection, thromboembolism, and major cardiovascular events differ among agents, long-term data suggest generally acceptable safety when used appropriately. Intraclass JAK-to-JAK cycling is feasible, with about half of patients achieving steroid-free clinical remission in retrospective cohorts. Based on mechanistic, clinical, and real-world evidence, filgotinib may be a first-line option for patients with lower disease activity or when safety is a priority, whereas upadacitinib or tofacitinib may be preferred in higher disease activity. Strategically selecting agents may improve durability and outcomes.

Purpose: This study elucidates the mechanism of the physiological effect of cannabidiol (CBD) by assessing its impact on lipopolysaccharide (LPS)-induced inflammation in RWPE-1 cells and prostatitis-induced by 17β-estradiol and dihydrotestosterone in a rat model, focusing on its therapeutic potential for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Materials and Methods: RWPE-1 cells were stratified in vitro into three groups: (1) controls, (2) cells with LPS-induced inflammation, and (3) cells with LPS-induced inflammation and treated with CBD. Enzyme-linked immunosorbent assays and western blots were performed on cellular components and supernatants after administration of CBD. Five groups of six Sprague–Dawley male rats were assigned: (1) control, (2) CP/CPPS, (3) CP/CPPS and treated with 50 mg/kg CBD, (4) CP/CPPS and treated with 100 mg/kg CBD, and (5) CP/CPPS and treated with 150 mg/kg CBD. Prostatitis was induced through administration of 17β-estradiol and dihydrotestosterone. After four weeks of CBD treatment, a pain index was evaluated, and prostate tissue was collected for subsequent histologic examination and western blot analysis. Results: CBD demonstrated efficacy in vivo for CP/CPPS and in vitro for inflammation. It inhibited the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-κB) pathway by activating the CB2 receptor, reducing expression of interleukin-6, tumor necrosis factor-alpha, and cyclooxygenase-2 (COX2) (p<0.01). CBD exhibited analgesic effects by activating and desensitizing the TRPV1 receptor. Conclusions CBD inhibits the TLR4/NF-κB pathway by activating the CB2 receptor, desensitizes the TRPV1 receptor, and decreases the release of COX2. This results in relief of inflammation and pain in patients with CP/CPPS, indicating CBD as a potential treatment for CP/CPPS.

Purpose: This study elucidates the mechanism of the physiological effect of cannabidiol (CBD) by assessing its impact on lipopolysaccharide (LPS)-induced inflammation in RWPE-1 cells and prostatitis-induced by 17β-estradiol and dihydrotestosterone in a rat model, focusing on its therapeutic potential for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Materials and Methods: RWPE-1 cells were stratified in vitro into three groups: (1) controls, (2) cells with LPS-induced inflammation, and (3) cells with LPS-induced inflammation and treated with CBD. Enzyme-linked immunosorbent assays and western blots were performed on cellular components and supernatants after administration of CBD. Five groups of six Sprague–Dawley male rats were assigned: (1) control, (2) CP/CPPS, (3) CP/CPPS and treated with 50 mg/kg CBD, (4) CP/CPPS and treated with 100 mg/kg CBD, and (5) CP/CPPS and treated with 150 mg/kg CBD. Prostatitis was induced through administration of 17β-estradiol and dihydrotestosterone. After four weeks of CBD treatment, a pain index was evaluated, and prostate tissue was collected for subsequent histologic examination and western blot analysis. Results: CBD demonstrated efficacy in vivo for CP/CPPS and in vitro for inflammation. It inhibited the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-κB) pathway by activating the CB2 receptor, reducing expression of interleukin-6, tumor necrosis factor-alpha, and cyclooxygenase-2 (COX2) (p<0.01). CBD exhibited analgesic effects by activating and desensitizing the TRPV1 receptor. Conclusions CBD inhibits the TLR4/NF-κB pathway by activating the CB2 receptor, desensitizes the TRPV1 receptor, and decreases the release of COX2. This results in relief of inflammation and pain in patients with CP/CPPS, indicating CBD as a potential treatment for CP/CPPS.

Background: and Purpose: Empathy comprises cognitive and emotional components.However, the impairments in empathy among individuals with mild cognitive impairment (MCI) and dementia of the Alzheimer’s type (DAT) are not well understood, particularly in the context of depression, which may exacerbate these deficits. This study aimed to evaluate the effects of neurodegeneration and depression on empathetic abilities. Methods: The study included 31 healthy elderly (HE) individuals, 30 patients with amnestic multi-domain MCI (amMCI), and 30 patients with DAT. Empathy was assessed using the Korean-Multifaceted Empathy Test (K-MET), and the Interpersonal Response Index (IRI).Participants were classified as depressed or non-depressed using the Geriatric Depression Scale. A two-way MANOVA was conducted to examine differences in empathy based on group and depressive status. Results: A significant interaction between group and depressive status was found for both cognitive and emotional empathy on the K-MET, but not on the IRI. In the depressed group, cognitive empathy scores were lower in the order of HE, amMCI, and DAT. Similarly, in the non-depressed group, the HE group performed better than both amMCI and DAT, with no significant difference between the latter two. Regarding emotional empathy, the depressed HE group scored higher than both amMCI and DAT, with no significant difference between these groups. In the non-depressed group, emotional empathy declined in the order of HE, amMCI, and DAT. Conclusions These findings indicate that both neurodegeneration and depression significantly impair empathetic abilities, with declines in cognitive and emotional empathy evident at the MCI stage, regardless of depressive status.

Gastric cancer is one of the most common cancers in both Korea and worldwide. Since 2004, the Korean Practice Guidelines for Gastric Cancer have been regularly updated, with the 4th edition published in 2022. The 4th edition was the result of a collaborative work by an interdisciplinary team, including experts in gastric surgery, gastroenterology, endoscopy, medical oncology, abdominal radiology, pathology, nuclear medicine, radiation oncology, and guideline development methodology. The current guideline is the 5th version, an updated version of the 4th edition. In this guideline, 6 key questions (KQs) were updated or proposed after a collaborative review by the working group, and 7 statements were developed, or revised, or discussed based on a systematic review using the MEDLINE, Embase, Cochrane Library, and KoreaMed database. Over the past 2 years, there have been significant changes in systemic treatment, leading to major updates and revisions focused on this area.Additionally, minor modifications have been made in other sections, incorporating recent research findings. The level of evidence and grading of recommendations were categorized according to the Grading of Recommendations, Assessment, Development and Evaluation system. Key factors for recommendation included the level of evidence, benefit, harm, and clinical applicability. The working group reviewed and discussed the recommendations to reach a consensus. The structure of this guideline remains similar to the 2022 version.Earlier sections cover general considerations, such as screening, diagnosis, and staging of endoscopy, pathology, radiology, and nuclear medicine. In the latter sections, statements are provided for each KQ based on clinical evidence, with flowcharts supporting these statements through meta-analysis and references. This multidisciplinary, evidence-based gastric cancer guideline aims to support clinicians in providing optimal care for gastric cancer patients.

Purpose: This study elucidates the mechanism of the physiological effect of cannabidiol (CBD) by assessing its impact on lipopolysaccharide (LPS)-induced inflammation in RWPE-1 cells and prostatitis-induced by 17β-estradiol and dihydrotestosterone in a rat model, focusing on its therapeutic potential for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Materials and Methods: RWPE-1 cells were stratified in vitro into three groups: (1) controls, (2) cells with LPS-induced inflammation, and (3) cells with LPS-induced inflammation and treated with CBD. Enzyme-linked immunosorbent assays and western blots were performed on cellular components and supernatants after administration of CBD. Five groups of six Sprague–Dawley male rats were assigned: (1) control, (2) CP/CPPS, (3) CP/CPPS and treated with 50 mg/kg CBD, (4) CP/CPPS and treated with 100 mg/kg CBD, and (5) CP/CPPS and treated with 150 mg/kg CBD. Prostatitis was induced through administration of 17β-estradiol and dihydrotestosterone. After four weeks of CBD treatment, a pain index was evaluated, and prostate tissue was collected for subsequent histologic examination and western blot analysis. Results: CBD demonstrated efficacy in vivo for CP/CPPS and in vitro for inflammation. It inhibited the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-κB) pathway by activating the CB2 receptor, reducing expression of interleukin-6, tumor necrosis factor-alpha, and cyclooxygenase-2 (COX2) (p<0.01). CBD exhibited analgesic effects by activating and desensitizing the TRPV1 receptor. Conclusions CBD inhibits the TLR4/NF-κB pathway by activating the CB2 receptor, desensitizes the TRPV1 receptor, and decreases the release of COX2. This results in relief of inflammation and pain in patients with CP/CPPS, indicating CBD as a potential treatment for CP/CPPS.

Background: and Purpose: Empathy comprises cognitive and emotional components.However, the impairments in empathy among individuals with mild cognitive impairment (MCI) and dementia of the Alzheimer’s type (DAT) are not well understood, particularly in the context of depression, which may exacerbate these deficits. This study aimed to evaluate the effects of neurodegeneration and depression on empathetic abilities. Methods: The study included 31 healthy elderly (HE) individuals, 30 patients with amnestic multi-domain MCI (amMCI), and 30 patients with DAT. Empathy was assessed using the Korean-Multifaceted Empathy Test (K-MET), and the Interpersonal Response Index (IRI).Participants were classified as depressed or non-depressed using the Geriatric Depression Scale. A two-way MANOVA was conducted to examine differences in empathy based on group and depressive status. Results: A significant interaction between group and depressive status was found for both cognitive and emotional empathy on the K-MET, but not on the IRI. In the depressed group, cognitive empathy scores were lower in the order of HE, amMCI, and DAT. Similarly, in the non-depressed group, the HE group performed better than both amMCI and DAT, with no significant difference between the latter two. Regarding emotional empathy, the depressed HE group scored higher than both amMCI and DAT, with no significant difference between these groups. In the non-depressed group, emotional empathy declined in the order of HE, amMCI, and DAT. Conclusions These findings indicate that both neurodegeneration and depression significantly impair empathetic abilities, with declines in cognitive and emotional empathy evident at the MCI stage, regardless of depressive status.