We retrospectively reviewed the results of nine children who were less than sixteen years old and in whom partial or total arthroscopic meniscectomy was performed for symptomatic discoid meniscus in eleven knees between March 1991 and February 1997. On arthroscopic findings, there were two complete and eight incomplete type of lateral discoid menisci and one medial discoid meniscus. Among eleven cases, partial meniscectomy was performed in seven and total meniscectomy in four. The average duration of follow-up was two and a half years (range, one to five years). In this study, arthroscopic total meniscectomy was superior to partial meniscectomy for a symptomatic discoid meniscus including pain, click and locking in children. Therefore, arthroscopic meniscectomy may offer the best prognosis following accurate diagnosis in children.
Child* ; Diagnosis ; Follow-Up Studies ; Humans ; Knee ; Prognosis ; Retrospective Studies

Primary sclerosing cholangitis (PSC) is a progressive cholestatic, inflammatory, and fibrotic disease that is strongly associated with inflammatory bowel disease (IBD). PSC-IBD represents a unique disease entity and patients with this disease have an increased risk of malignancy development, such as colorectal cancer and cholangiocarcinoma. The pathogenesis of PSC-IBD involves genetic and environmental factors such as gut dysbiosis and bile acids alteration. However, despite the advancement of disease characteristics, no effective medical therapy has proven to have a significant impact on the prognosis of PSC. The treatment options for patients with PSC-IBD do not differ from those for patients with PSC alone. Potential candidate drugs have been developed based on the pathogenesis of PSC-IBD, such as those that target modulation of bile acids, inflammation, fibrosis, and gut dysbiosis. In this review, we summarize the current medical treatments for PSC-IBD and the status of new emerging therapeutic agents.

The intestine and liver share a unique regenerative property that sets them apart from other mammalian visceral organs. The intestinal epithelium exhibits rapid renewal, making it one of the fastest renewing tissues in humans. Under physiological conditions, intestinal stem cells within each intestinal crypt continuously differentiate into the different types of intestinal epithelial cells to maintain intestinal homeostasis. However, when exposed to tissue damage or stressful conditions such as inflammation, intestinal epithelial cells in the gastrointestinal tract exhibit plasticity, allowing fully differentiated cells to regain their stem cell properties. Likewise, hepatic epithelial cells possess a remarkable regenerative capacity to restore lost liver mass through proliferationmediated liver regeneration. When the proliferation-mediated regenerative capacity is impaired, hepatocytes and biliary epithelial cells (BECs) can undergo plasticity-mediated regeneration and replenish each other. The transition of mammalian liver progenitor cells to hepatocytes/BECs can be observed under tightly controlled experimental conditions such as severe hepatocyte injury accompanied by the loss of regenerative capacity. In this review, we will discuss the mechanism by which cellular plasticity contributes to the regeneration process and the potential therapeutic implications of understanding and harnessing cellular plasticity in the gut and liver.

The intestine and liver share a unique regenerative property that sets them apart from other mammalian visceral organs. The intestinal epithelium exhibits rapid renewal, making it one of the fastest renewing tissues in humans. Under physiological conditions, intestinal stem cells within each intestinal crypt continuously differentiate into the different types of intestinal epithelial cells to maintain intestinal homeostasis. However, when exposed to tissue damage or stressful conditions such as inflammation, intestinal epithelial cells in the gastrointestinal tract exhibit plasticity, allowing fully differentiated cells to regain their stem cell properties. Likewise, hepatic epithelial cells possess a remarkable regenerative capacity to restore lost liver mass through proliferationmediated liver regeneration. When the proliferation-mediated regenerative capacity is impaired, hepatocytes and biliary epithelial cells (BECs) can undergo plasticity-mediated regeneration and replenish each other. The transition of mammalian liver progenitor cells to hepatocytes/BECs can be observed under tightly controlled experimental conditions such as severe hepatocyte injury accompanied by the loss of regenerative capacity. In this review, we will discuss the mechanism by which cellular plasticity contributes to the regeneration process and the potential therapeutic implications of understanding and harnessing cellular plasticity in the gut and liver.

The intestine and liver share a unique regenerative property that sets them apart from other mammalian visceral organs. The intestinal epithelium exhibits rapid renewal, making it one of the fastest renewing tissues in humans. Under physiological conditions, intestinal stem cells within each intestinal crypt continuously differentiate into the different types of intestinal epithelial cells to maintain intestinal homeostasis. However, when exposed to tissue damage or stressful conditions such as inflammation, intestinal epithelial cells in the gastrointestinal tract exhibit plasticity, allowing fully differentiated cells to regain their stem cell properties. Likewise, hepatic epithelial cells possess a remarkable regenerative capacity to restore lost liver mass through proliferationmediated liver regeneration. When the proliferation-mediated regenerative capacity is impaired, hepatocytes and biliary epithelial cells (BECs) can undergo plasticity-mediated regeneration and replenish each other. The transition of mammalian liver progenitor cells to hepatocytes/BECs can be observed under tightly controlled experimental conditions such as severe hepatocyte injury accompanied by the loss of regenerative capacity. In this review, we will discuss the mechanism by which cellular plasticity contributes to the regeneration process and the potential therapeutic implications of understanding and harnessing cellular plasticity in the gut and liver.

The intestine and liver share a unique regenerative property that sets them apart from other mammalian visceral organs. The intestinal epithelium exhibits rapid renewal, making it one of the fastest renewing tissues in humans. Under physiological conditions, intestinal stem cells within each intestinal crypt continuously differentiate into the different types of intestinal epithelial cells to maintain intestinal homeostasis. However, when exposed to tissue damage or stressful conditions such as inflammation, intestinal epithelial cells in the gastrointestinal tract exhibit plasticity, allowing fully differentiated cells to regain their stem cell properties. Likewise, hepatic epithelial cells possess a remarkable regenerative capacity to restore lost liver mass through proliferationmediated liver regeneration. When the proliferation-mediated regenerative capacity is impaired, hepatocytes and biliary epithelial cells (BECs) can undergo plasticity-mediated regeneration and replenish each other. The transition of mammalian liver progenitor cells to hepatocytes/BECs can be observed under tightly controlled experimental conditions such as severe hepatocyte injury accompanied by the loss of regenerative capacity. In this review, we will discuss the mechanism by which cellular plasticity contributes to the regeneration process and the potential therapeutic implications of understanding and harnessing cellular plasticity in the gut and liver.

PURPOSE: To investigate the underlying causes and clinical characteristics of patients referred with intraocular pressure (IOP) elevation. METHODS: We retrospectively reviewed the medical records of patients who were referred with IOP elevation from July 2016 to July 2017. Patients with baseline IOP ≥ 22 mmHg and those who were treated and followed up for 6 months were included. The prevalence rates of the underlying diseases that caused IOP elevation were evaluated and the clinical characteristics were compared between patients with primary and secondary glaucoma. RESULTS: A total of 127 patients were included (mean age, 59.3 ± 16.8 years; baseline IOP, 31.7 ± 10.5 mmHg). Among the study participants, 22.0%, 31.5%, and 46.5% had been diagnosed with ocular hypertension, primary glaucoma, and secondary glaucoma, respectively. Among the causes of IOP elevation, open-angle glaucoma (20.5%) had the highest prevalence rate among those with primary glaucoma and inflammation-related glaucoma (12.6%) was the most prevalent cause among those with secondary glaucoma. In a comparison between patients with primary and secondary glaucoma, the percentage of IOP reduction was not significantly different at 6 months after treatment (52.1% vs. 53.9%, p = 0.603). However, the rate of patients treated with drugs other than IOP lowering agents or who underwent surgery was significantly higher in the secondary glaucoma group compared with the primary glaucoma group (all p < 0.05). At 6-month follow-up, the secondary glaucoma group showed significantly higher improvement rates of visual acuity (p = 0.004), but had a larger proportion of patients with a visual acuity of less than or equal to finger count (p = 0.027). CONCLUSIONS: Treatment and visual outcome can vary depending on the underlying cause of IOP elevation. Therefore, a thorough examination for determining the cause of IOP elevation is recommended at the initial stage.
Fingers ; Follow-Up Studies ; Glaucoma ; Glaucoma, Open-Angle ; Humans ; Intraocular Pressure ; Medical Records ; Ocular Hypertension ; Prevalence ; Retrospective Studies ; Visual Acuity

PURPOSE: Antithrombotic therapy could be related with nuisance bleeding. This study investigated whether vitreous hemorrhage (VH) is associated with specific types of antithrombotic medication in patients with atrial fibrillation (AF). MATERIALS AND METHODS: In the Korean National Health Insurance Service National Sample Cohort, we identified 9352 antiplatelet/anticoagulant-treated AF patients. The occurrence of VH was compared between warfarin (n=1493) and a propensity score (PS)-matched antiplatelet group (n=1493) and between warfarin (n=1493) and a PS-matched warfarin+antiplatelet group (n=1493). RESULTS: The outcomes of VH were lower in the warfarin than in the matched antiplatelet (1.45 vs. 3.72 events/1000 patient-years) and matched warfarin+antiplatelet groups (1.45 vs. 6.87 events/1000 patient-years). Compared with warfarin, the risk of VH increased with antiplatelet [adjusted hazard ratio (aHR) 3.90; 95% confidence interval (CI) 1.22–12.4, p=0.022] and warfarin+antiplatelet agents (aHR 4.39, 95% CI 1.74–11.2, p=0.002). Compared with warfarin only, warfarin+antiplatelet agents increased the risk of VH in patients ≥65 years, regardless of gender and hypertension. The risk of VH was significantly higher with dual antiplatelet therapy (aHR: 5.02, 95% CI: 1.56–16.2, p=0.007) or in dual (aHR: 5.02, 95% CI: 1.74–14.5, p=0.003) or triple therapy using warfarin and antiplatelet agents than with warfarin monotherapy (aHR: 6.12, 95% CI: 1.76–21.3, p=0.004). CONCLUSION: Dual antiplatelet or triple therapy increased the risk of VH significantly, compared to warfarin monotherapy. Considering the low efficacy of preventing ischemic stroke and high risk of bleeding, dual or triple therapy using warfarin and antiplatelet agents should be avoided to prevent VH in AF patients.
Atrial Fibrillation* ; Cohort Studies* ; Hemorrhage ; Humans ; Hypertension ; National Health Programs* ; Platelet Aggregation Inhibitors ; Propensity Score ; Stroke ; Vitreous Hemorrhage* ; Warfarin

Outer membrane proteins (OMPs) of Gram-negative bacteria constitute the first line of defense protecting cells against environmental stresses including chemical, biophysical, and biological attacks. Although the 43-kDa OMP (OMP43) is major porin protein among Bartonella henselae-derived OMPs, its function remains unreported. In this study, OMP43-deficient mutant B. henselae (Δomp43) was generated to investigate OMP43 function. Interestingly, Δomp43 exhibited weaker proliferative ability than that of wild-type (WT) B. henselae. To study the differences in proteomic expression between WT and Δomp43, two-dimensional gel electrophoresis-based proteomic analysis was performed. Based on Clusters of Orthologus Groups functional assignments, 12 proteins were associated with metabolism, 7 proteins associated with information storage and processing, and 3 proteins associated with cellular processing and signaling. By semi-quantitative reverse transcriptase polymerase chain reaction, increases in tldD, efp, ntrX, pdhA, purB, and ATPA mRNA expression and decreases in Rho and yfeA mRNA expression were confirmed in Δomp43. In conclusion, this is the first report showing that a loss of OMP43 expression in B. henselae leads to retarded proliferation. Furthermore, our proteomic data provide useful information for the further investigation of mechanisms related to the growth of B. henselae.
Bartonella henselae ; Bartonella ; Gram-Negative Bacteria ; Information Storage and Retrieval ; Membrane Proteins ; Membranes ; Metabolism ; Proteomics ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger

The natural flavonoid macakurzin C (1) exhibited adiponectin biosynthesis-inducing activity during adipogenesis in human bone marrow mesenchymal stem cells and its molecular mechanism was directly associated with a pan-peroxisome proliferator-activated receptor (PPAR) modulator affecting all three PPAR subtypes α, γ, and δ. In this study, increases in adiponectin biosynthesisinducing activity by macakurzin C derivatives (2–7) were studied. The most potent adiponectin biosynthesis-inducing compound 6, macakurzin C 3,5-dimethylether, was elucidated as a dual PPARα/γ modulator. Compound 6 may exhibit the most potent activity because of the antagonistic relationship between PPARδ and PPARγ. Docking studies revealed that the O-methylation of macakurzin C to generate compound 6 significantly disrupted PPARδ binding. Compound 6 has therapeutic potential in hypoadiponectinemia-related metabolic diseases.