Background: The effects of propofol, a commonly used intravenous anesthetic, on the breast cancer tumor microenvironment are not well understood. This study examined the influence of propofol on natural killer group 2, member D (NKG2D) ligand expression, matrix metalloproteinase (MMP)-mediated immune evasion, and natural killer (NK) cell-mediated cytotoxicity in breast cancer cells. Methods: We studied three human breast cancer cell lines representing distinct receptor subtypes: MCF-7 (estrogen receptor - and progesterone receptor-positive), MDA-MB-453 (human epidermal growth factor receptor 2-positive), and HCC-70 (triple-negative). Cells were treated with propofol at concentrations of 0 μg/ml (control; C), 4 μg/ml (P4), or 8 μg/ml (P8). Assessments included mRNA and protein expression of NKG2D ligands, NK cell cytotoxicity, protein levels of MMP-1 and MMP-2, and concentrations of soluble NKG2D ligands. Results: In MCF-7 and HCC-70 cell lines, propofol upregulated the mRNA and protein expression of NKG2D ligands in a dose-dependent manner, enhancing NK cell-mediated lysis. In contrast, in MDA-MB-453 cell lines, propofol downregulated the mRNA and protein expression of NKG2D ligands, resulting in diminished NK cell-mediated lysis. Across all receptor subtypes, propofol did not affect the expression of MMP-1 or MMP-2 or the concentration of soluble NKG2D ligands. Conclusions Our results demonstrate that propofol exerts receptor subtype-dependent effects on NK cell-mediated immunosurveillance in breast cancer cell lines, potentially mediated by changes in the transcription of NKG2D ligands rather than by alterations in MMP expression or their proteolytic activity.

Confounding and the healthy worker survivor effect (HWSE) represent major methodological challenges in epidemiology, particularly in studies of low-dose exposures, where effect sizes are small and risk estimates can be readily distorted by bias. This systematic review aimed to summarize the methods used to adjust for confounding and the HWSE in studies of medical radiation workers. We systematically searched PubMed and Embase for studies of medical radiation workers from inception through June 30, 2025. Studies reporting excess risk estimates for any health outcomes associated with occupational radiation exposure were included. Study selection followed the PECO (Population, Exposure, Comparator, Outcome) criteria, and data were synthesized descriptively. The review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and was registered in PROSPERO (CRD42024589851). Sixteen eligible studies from 3 countries were identified, all of which were rated as high quality. To control for confounding, regression was used in all studies, followed by stratification (62.5%) and restriction (18.8%). Age, sex, and birth year were adjusted for in all models, with smoking being the next most frequently controlled variable. To mitigate the HWSE, only a single approach, adjustment for employment characteristics, was identified, and it was applied in 3 studies (18.8%). No other approaches, including restriction or g-methods, were employed. Although confounding is generally addressed using conventional analytical approaches, the HWSE has rarely been considered in studies of medical radiation workers. More comprehensive strategies that explicitly account for the HWSE are needed to improve the validity of risk estimates, particularly in low-dose occupational studies.

The Korean Dementia Association (KDA) has been organizing biennial international academic conferences since 2019, with the International Conference of the KDA (IC-KDA) 2023 held in Busan under the theme ‘Beyond Boundaries: Advancing Global Dementia Solutions.’ The conference comprised 6 scientific sessions, 3 plenary lectures, and 4luncheon symposiums, drawing 804 participants from 35 countries. Notably, a Korea– Taiwan Joint Symposium addressed insights into Alzheimer’s disease (AD). Plenary lectures by renowned scholars explored topics such as microbiome-related AD pathogenesis, social cognition in neurodegenerative diseases, and genetic frontotemporal dementia (FTD). On the first day, specific presentations covered subjects like the gut–brain axis and neuroinflammation in dementia, blood-based biomarkers in AD, and updates in AD therapeutics. The second day’s presentations addressed recent issues in clinical neuropsychology, FTD cohort studies, and the pathogenesis of non-AD dementia. The Academic Committee of the KDA compiles lecture summaries to provide comprehensive understanding of the advanced dementia knowledge presented at IC-KDA 2023.

Ataxia is presented by various etiologies, including acquired, genetic and degenerative disorders. Although hereditary ataxia is suspected when typical symptom of ataxia with concurrent is identified, it is sometimes difficult to diagnose hereditary ataxia without genetic test. Clinically, next generation sequencing technology has been developed and widely used for diagnosis of hereditary disease. Hereby, we experienced cases of genetically confirmed OPA1 mutation, which are presented with various clinical manifestations including ataxic gait and decreased visual acuity.

Background: We investigated the effects of sevoflurane exposure on the expression of matrix metalloproteinase (MMP), expression and ablation of natural killer group 2, member D (NKG2D) ligands (UL16-binding proteins 1–3 and major histocompatibility complex class I chain-related molecules A/B), and natural killer (NK) cell-mediated cytotoxicity in breast cancer cells. Methods: Three human breast cancer cell lines (MCF-7, MDA-MB-453, and HCC-70) were incubated with 0 (control), 600 (S6), or 1200 μM (S12) sevoflurane for 4 h. The gene expression of NKG2D ligands and their protein expression on cancer cell surfaces were measured using multiplex polymerase chain reaction (PCR) and flow cytometry, respectively. Protein expression of MMP-1 and -2 and the concentration of soluble NKG2D ligands were analyzed using western blotting and enzyme-linked immunosorbent assays, respectively. Results: Sevoflurane downregulated the mRNA and protein expression of the NKG2D ligand in a dose-dependent manner in MCF-7, MDA-MB-453, and HCC-70 cells but did not affect the expression of MMP-1 or -2 or the concentration of soluble NKG2D ligands in the MCF-7, MDA-MB-453, and HCC-70 cells. Sevoflurane attenuated NK cell-mediated cancer cell lysis in a dose-dependent manner in MCF-7, MDA-MB-453, and HCC-70 cells (P = 0.040, P = 0.040, and P = 0.040, respectively). Conclusions Our results demonstrate that sevoflurane exposure attenuates NK cell-mediated cytotoxicity in breast cancer cells in a dose-dependent manner. This could be attributed to a sevoflurane-induced decrease in the transcription of NKG2D ligands rather than sevoflurane-induced changes in MMP expression and their proteolytic activity.

Neutrophil extracellular traps (NETs) exert a novel function of trapping pathogens. Released NETs can accumulate in inflamed tissues, be recognized by other immune cells for clearance, and lead to tissue toxicity. Therefore, the deleterious effect of NET is an etiological factor, causing several diseases directly or indirectly. NLR family pyrin domain containing 3 (NLRP3) in neutrophils is pivotal in signaling the innate immune response and is associated with several NET-related diseases. Despite these observations, the role of NLRP3 in NET formation in neuroinflammation remains elusive. Therefore, we aimed to explore NET formation promoted by NLRP3 in an LPS-induced inflamed brain. Wild-type and NLRP3 knockout mice were used to investigate the role of NLRP3 in NET formation. Brain inflammation was systemically induced by administering LPS. In such an environment, the NET formation was evaluated based on the expression of its characteristic indicators. DNA leakage and NET formation were analyzed in both mice through Western blot, flow cytometry, and in vitro live cell imaging as well as two-photon imaging. Our data revealed that NLRP3 promotes DNA leakage and facilitates NET formation accompanied by neutrophil death. Moreover, NLRP3 is not involved in neutrophil infiltration but is predisposed to boost NET formation, which is accompanied by neutrophil death in the LPS-induced inflamed brain. Furthermore, either NLRP3 deficiency or neutrophil depletion diminished pro-inflammatory cytokine, IL-1β, and alleviated blood-brain barrier damage. Overall, the results suggest that NLRP3 exacerbates NETosis in vitro and in the inflamed brain, aggravating neuroinflammation.These findings provide a clue that NLRP3 would be a potential therapeutic target to alleviate neuroinflammation.

Purpose: This study was based on the Korean Foot and Ankle Society (KFAS) member survey and aimed to report the current trends in the management of syndesmotic injuries over the last few decades. Materials and Methods: A web-based questionnaire containing 36 questions was sent to all KFAS members in September 2021. The questions were mainly related to the preferred techniques and clinical experiences in the treatment of patients with syndesmotic injuries. Answers with a prevalence ≥50% of respondents were considered a tendency. Results: Seventy-six (13.8%) of the 550 members responded to the survey. The results showed that the most preferred method to diagnose a syndesmotic injury was magnetic resonance imaging (MRI). Intraoperatively, the external rotation stress test and the Cotton test were most frequently used to confirm syndesmotic diastasis. The reduction was usually done by a reduction clamp. One 3.5-mm screw was used most frequently over three cortices at 2~4 cm above the ankle joint. The preferred ankle position during fixation was 0° dorsiflexion. Removal of the syndesmotic screw was routinely done by most surgeons, mainly because of the limitation of movement and risk of screw breakage. Factors that affect suture button selection included non-rigid fixation which enables adequate fixation, early weight-bearing, and an infrequent need to remove the hardware. Inadequate reduction was considered the main factor that affects poor prognosis. Conclusion This study proposes updated information about the current trends in the management of syndesmotic injuries in Korea. Consensuses in both the diagnostic and therapeutic approach to patients with syndesmotic injury were identified in this survey study. This study may raise the awareness of the various possible approaches toward the injury and should be used to further establish a standard protocol for the management of syndesmotic injuries.

GuillainBarré syndrome (GBS) is the inflammatory neuropathy that affects the myelin and nodal or paranodal areas of peripheral nerves. Immunoglobulin G GM1 antibody is well known as the cause of GBS associated with Campylobacter jejuni infection. However, the relationship between other specific infectious agents and autoantibodies is not yet well elucidated in patients with GBS. Recently we have experienced a case with GBS associated with antiGM1 and phosphatidic acid complex antibody that occurred after Shiga toxinproducing and enterotoxigenic Escherichia coli enteritis.

Purpose: This study proposed the optimal definition of biochemical recurrence (BCR) after salvage radiotherapy (SRT) following radical prostatectomy for prostate cancer. Materials and Methods: Among 1,117 patients who had received SRT, data from 205 hormone-naïve patients who experienced post-SRT prostate-specific antigen (PSA) elevation were included in a multi-institutional database. The primary endpoint was to determine the PSA parameters predictive of distant metastasis (DM). Absolute serum PSA levels and the prostate-specific antigen doubling time (PSA-DT) were adopted as PSA parameters. Results: When BCR was defined based on serum PSA levels ranging from 0.4 ng/mL to nadir+2.0 ng/mL, the 5-year probability of DM was 27.6%-33.7%. The difference in the 5-year probability of DM became significant when BCR was defined as a serum PSA level of 0.8 ng/ml or higher (1.0-2.0 ng/mL). Application of a serum PSA level of ≥ 0.8 ng/mL yielded a c-index value of 0.589. When BCR was defined based on the PSA-DT, the 5-year probability was 22.7%-39.4%. The difference was significant when BCR was defined as a PSA-DT ≤ 3 months and ≤ 6 months. Application of a PSA-DT ≤ 6 months yielded the highest c-index (0.660). These two parameters complemented each other; for patients meeting both PSA parameters, the probability of DM was 39.5%-44.5%; for those not meeting either parameter, the probability was 0.0%-3.1%. Conclusion A serum PSA level > 0.8 ng/mL was a reasonable threshold for the definition of BCR after SRT. In addition, a PSA-DT ≤ 6 months was significantly predictive of subsequent DM, and combined application of both parameters enhanced predictability.

This study was aimed to evaluate the prophylactic anti-glaucoma effect of topical 5% betaxolol (BTX) and 2% dorzolamide (DRZ) on the second eye in dogs with unilateral primary angle closure glaucoma (PACG). Medical records of 60 dogs with unilateral PACG who received prophylactic anti-glaucoma eyedrops in the second eye, from 2016 to 2021, were reviewed. The duration of prophylactic effects of BTX only and DRZ after BTX failure was calculated. The prophylactic effects of BTX were maintained on 28/60 (46.7%) eyes until last visit and BTX failure was observed on median 510 (range, 53-1,927) days in 32/60 (53.3%) eyes. After DRZ instillation in BTX failure eyes, the prophylactic effects were extended at median 610 (range, 157-2,270) days in 21/32 (65.6%) eyes. DRZ failure eyes (17/21, 81.0%) eyes required chemical ablation or surgical intervention due to uncontrolled intraocular pressure. The duration of prophylactic effects was decreased with aging (R² = 0.334, p = 0.006). The predominant breeds were Shih-Tzu (41.9%) and American Cocker Spaniel (30.6%) with no significant differences in survival curves (p = 0.210). The average prophylactic effects of BTX persisted more than 1.5 year and could be selected the first prophylactic eye drop in unilateral PACG. Also, early surgical intervention should be considered in prophylactic medications failure cases.