BACKGROUND/OBJECTIVES: Inflammatory responses are key pathological factors in various canine diseases, making the control of inflammatory responses vital for canine health.This study examined the anti-inflammatory effects of rutin on DH82 cells, a type of canine macrophage, against lipopolysaccharide (LPS)-induced inflammatory responses.MATERIALS/METHODS: The inflammatory in vitro experimental model was established by stimulating canine macrophage DH82 cells with LPS. To evaluate the inflammationpreventative effects of rutin, analyses were conducted using enzyme-linked immunosorbent assay, western blot, and real-time quantitative reverse transcription polymerase chain reaction. RESULTS: Rutin inhibited the LPS-induced increase in the protein and gene levels of proinflammatory cytokines (interleukin [IL]-1β, IL-6, tumor necrosis factor-α), while antiinflammatory cytokines (IL-10, transforming growth factor-β1) levels remained unchanged.Furthermore, rutin suppressed the LPS-induced activation of phosphorylated extracellular signal-regulated kinase, Jun N-terminal kinase, inhibitor of nuclear factor kappa B, and nuclear factor kappa B (NF-κB) in DH82 cells. CONCLUSION Rutin exerts anti-inflammatory effects by inhibiting the mitogen-activated protein kinase-NF-κB signaling pathway and reducing the production of pro-inflammatory cytokines in DH82 cells.

BACKGROUND/OBJECTIVES: Inflammatory responses are key pathological factors in various canine diseases, making the control of inflammatory responses vital for canine health.This study examined the anti-inflammatory effects of rutin on DH82 cells, a type of canine macrophage, against lipopolysaccharide (LPS)-induced inflammatory responses.MATERIALS/METHODS: The inflammatory in vitro experimental model was established by stimulating canine macrophage DH82 cells with LPS. To evaluate the inflammationpreventative effects of rutin, analyses were conducted using enzyme-linked immunosorbent assay, western blot, and real-time quantitative reverse transcription polymerase chain reaction. RESULTS: Rutin inhibited the LPS-induced increase in the protein and gene levels of proinflammatory cytokines (interleukin [IL]-1β, IL-6, tumor necrosis factor-α), while antiinflammatory cytokines (IL-10, transforming growth factor-β1) levels remained unchanged.Furthermore, rutin suppressed the LPS-induced activation of phosphorylated extracellular signal-regulated kinase, Jun N-terminal kinase, inhibitor of nuclear factor kappa B, and nuclear factor kappa B (NF-κB) in DH82 cells. CONCLUSION Rutin exerts anti-inflammatory effects by inhibiting the mitogen-activated protein kinase-NF-κB signaling pathway and reducing the production of pro-inflammatory cytokines in DH82 cells.

BACKGROUND/OBJECTIVES: Inflammatory responses are key pathological factors in various canine diseases, making the control of inflammatory responses vital for canine health.This study examined the anti-inflammatory effects of rutin on DH82 cells, a type of canine macrophage, against lipopolysaccharide (LPS)-induced inflammatory responses.MATERIALS/METHODS: The inflammatory in vitro experimental model was established by stimulating canine macrophage DH82 cells with LPS. To evaluate the inflammationpreventative effects of rutin, analyses were conducted using enzyme-linked immunosorbent assay, western blot, and real-time quantitative reverse transcription polymerase chain reaction. RESULTS: Rutin inhibited the LPS-induced increase in the protein and gene levels of proinflammatory cytokines (interleukin [IL]-1β, IL-6, tumor necrosis factor-α), while antiinflammatory cytokines (IL-10, transforming growth factor-β1) levels remained unchanged.Furthermore, rutin suppressed the LPS-induced activation of phosphorylated extracellular signal-regulated kinase, Jun N-terminal kinase, inhibitor of nuclear factor kappa B, and nuclear factor kappa B (NF-κB) in DH82 cells. CONCLUSION Rutin exerts anti-inflammatory effects by inhibiting the mitogen-activated protein kinase-NF-κB signaling pathway and reducing the production of pro-inflammatory cytokines in DH82 cells.

BACKGROUND/OBJECTIVES: Inflammatory responses are key pathological factors in various canine diseases, making the control of inflammatory responses vital for canine health.This study examined the anti-inflammatory effects of rutin on DH82 cells, a type of canine macrophage, against lipopolysaccharide (LPS)-induced inflammatory responses.MATERIALS/METHODS: The inflammatory in vitro experimental model was established by stimulating canine macrophage DH82 cells with LPS. To evaluate the inflammationpreventative effects of rutin, analyses were conducted using enzyme-linked immunosorbent assay, western blot, and real-time quantitative reverse transcription polymerase chain reaction. RESULTS: Rutin inhibited the LPS-induced increase in the protein and gene levels of proinflammatory cytokines (interleukin [IL]-1β, IL-6, tumor necrosis factor-α), while antiinflammatory cytokines (IL-10, transforming growth factor-β1) levels remained unchanged.Furthermore, rutin suppressed the LPS-induced activation of phosphorylated extracellular signal-regulated kinase, Jun N-terminal kinase, inhibitor of nuclear factor kappa B, and nuclear factor kappa B (NF-κB) in DH82 cells. CONCLUSION Rutin exerts anti-inflammatory effects by inhibiting the mitogen-activated protein kinase-NF-κB signaling pathway and reducing the production of pro-inflammatory cytokines in DH82 cells.

BACKGROUND/OBJECTIVES: Inflammatory responses are key pathological factors in various canine diseases, making the control of inflammatory responses vital for canine health.This study examined the anti-inflammatory effects of rutin on DH82 cells, a type of canine macrophage, against lipopolysaccharide (LPS)-induced inflammatory responses.MATERIALS/METHODS: The inflammatory in vitro experimental model was established by stimulating canine macrophage DH82 cells with LPS. To evaluate the inflammationpreventative effects of rutin, analyses were conducted using enzyme-linked immunosorbent assay, western blot, and real-time quantitative reverse transcription polymerase chain reaction. RESULTS: Rutin inhibited the LPS-induced increase in the protein and gene levels of proinflammatory cytokines (interleukin [IL]-1β, IL-6, tumor necrosis factor-α), while antiinflammatory cytokines (IL-10, transforming growth factor-β1) levels remained unchanged.Furthermore, rutin suppressed the LPS-induced activation of phosphorylated extracellular signal-regulated kinase, Jun N-terminal kinase, inhibitor of nuclear factor kappa B, and nuclear factor kappa B (NF-κB) in DH82 cells. CONCLUSION Rutin exerts anti-inflammatory effects by inhibiting the mitogen-activated protein kinase-NF-κB signaling pathway and reducing the production of pro-inflammatory cytokines in DH82 cells.

Purpose: In high-risk non-muscle-invasive bladder cancer (NMIBC), intravesical Bacillus Calmette-Guérin (BCG) is the standard adjuvant therapy post-transurethral resection of bladder tumor (TURBT). Intravesical gemcitabine, used as an alternative or second-line therapy amid BCG shortages, lacks outcome studies in the Korean population. Materials and Methods: Patients who received weekly intravesical gemcitabine for 6 weeks after TURBT from 2019 to 2022 were retrospectively investigated. Based on the American Urological Association risk classification, patients with high- or very high-risk NMIBC who refused cystectomy were included. Maintenance treatment was performed depending on their risk. Recurrence was defined as histologic confirmation on subsequent cystoscopic biopsies or TURBT. Disease free survival (DFS) was evaluated by the Kaplan–Meier method. Results: The study included 60 patients, comprising 45 high-risk (group 1) patients with a median age of 76 years and 15 very high-risk (group 2) patients with a median age of 68 years. Among them, 28 patients had previously received intravesical BCG.Over a median follow-up of 22 months, recurrence occurred in 31 patients in group 1 and 11 in group 2. The DFS rates of the highrisk group and the very high-risk group were 57.8% versus 40% at 1 year, 20.7% versus 21.3% at 2 years and 20.7% versus 21.3% at 3 years, respectively (p=0.831). Tis stage (p=0.042) and prostatic urethra invasion (p=0.028) were significant predictors of DFS.Cancer-specific mortality rates were 2.2% in group 1 and 6.7% in group 2 (p=0.441). Conclusions Similar DFS outcome between high-risk and very high-risk patients were observed based on short-term results in Korea. This finding is crucial for clinical practice; however, studies analyzing more patients and long-term outcomes are needed.

Background and Objectives: This study aimed to evaluate the factors that influence deep sleep restoration in patients with obstructive sleep apnea (OSA) following positive airway pressure (PAP) therapy. Methods: In total, 363 patients diagnosed with OSA who received PAP therapy over at least 3 months were enrolled in the study. Polysomnographic parameters, anatomical characteristics, and subjective sleep-related parameters were evaluated according to the presence of daytime sleepiness and morning headache before and after 3 months of PAP treatment. Results: Age was significantly different according to whether excessive daytime sleepiness (EDS) was alleviated (average: 49.35 years) or persisted (average: 52.82 years) (p=0.001). Age was also significantly associated with morning headache (p=0.037). Body mass index (BMI) was higher in the alleviated EDS group (28.70 kg/m2) than in the persistent EDS group (27.13 kg/m2; p=0.002). The apnea-hypopnea index (AHI) was correlated with the EDS outcome (p=0.011). The group with alleviated EDS had a longer mandibular plane to hyoid distance (MPH) than the group with persistent EDS (17.95 mm vs. 15.38 mm; p<0.001). However, BMI, AHI, and MPH showed no significant associations with morning headache. Epworth Sleepiness Scale scores were higher in the alleviated EDS and alleviated morning headache groups (EDS: p<0.001, morning headache: p=0.001). Self-Efficacy Measure for Sleep Apnea (SEMSA) values differed significantly between the EDS groups (p<0.001), but not between the morning headache groups (p=0.122). After 3 months of PAP therapy, the MPH was negatively correlated with EDS in univariate (odds ratio [OR]=0.921, p<0.001) and multivariate analyses (OR=0.937, p=0.028). The SEMSA score was also negatively correlated with EDS in univariate (OR=0.961, p<0.001) and multivariate (OR=0.973, p=0.019) analyses. Conclusion Age, polysomnographic metrics, and anatomical considerations were important for sleep quality-associated daytime symptoms. In addition, anatomical characteristics and the patient’s self-efficacy were significantly associated with the effect of PAP treatment on sleep quality.

Fixed drug eruption (FDE) is a well-defined hyperpigmented patch that recurs in a fixed location each time a particular drug is taken. Common causative agents of FDE are nonsteroidal anti-inflammatory drugs, non-narcotic analgesics, sedatives, anticonvulsants, sulfonamides, and tetracycline. We report a 33-year-old male who presented with a recurrent, localized, brownish-to-erythematous macule and papules on the peri-philtrum area two hours after taking valacyclovir. Three episodes of valacyclovir ingestion for treatment of Herpes simplex virus infection provoked a similar skin rash at the same site. Histopathology results showed vacuolar degeneration in the basal layer of the epidermis, pigmentary incontinence, and perivascular inflammatory cell infiltration in the papillary dermis. Although patch test and skin prick test showed negative responses to acyclovir and valacyclovir, an intradermal test showed a positive reaction only to valacyclovir. The oral provocation test to acyclovir and valacyclovir showed a positive reaction only to valacyclovir. Through drug history, histopathological examination, patch test, intradermal test, and oral provocation test, we established a final diagnosis of FDE due to valacyclovir without cross-reactivity to acyclovir. To find alternative therapeutic drugs, we suggest diagnostic tests with not only the suspected drugs, but also other drugs in the same class.