BACKGROUND/AIMS: Few studies have evaluated the use of a smartphone application (app) for educating people undergoing colonoscopy and optimizing bowel preparation. Therefore, this study was designed to develop a smartphone app for people to use as a preparation guide and to evaluate the efficacy of this app when used prior to colonoscopy. METHODS: In total, 142 patients (male:female=84:58, mean age=43.5±9.3 years), who were scheduled to undergo a colonoscopy at Myongji Hospital, were enrolled in this study. Seventy-one patients were asked to use a smartphone app that we had recently developed to prepare for the colonoscopy, while the 71 patients of the sex and age-matched control group were educated via written and verbal instructions. RESULTS: The quality of bowel cleansing, evaluated using the Boston Bowel Preparation Scale, was significantly higher in the smartphone app group than in the control group (7.70±1.1 vs. 7.24±0.8, respectively, p=0.007 by t-test). No significant differences were found between the two groups regarding work-up time and the number of patients with polyps. CONCLUSIONS: In this study, targeting young adults (≤50 years), the bowel preparation achieved by patients using the smartphone app showed significantly better quality than that of the control group.
Colonic Neoplasms ; Colonoscopy* ; Enema ; Humans ; Mass Screening* ; Mobile Applications ; Patient Education as Topic* ; Polyps ; Smartphone* ; Young Adult

Hemostatic clips are widely used to treat gastrointestinal (GI) bleeding and closure of defects in the GI tract. Few data on retrieving hemostatic clips retained in the GI tract are available. Patients who had hemostatic clips retained in the stomach for more than 2 weeks after placement were enrolled. Clips were removed with grasping forceps during endoscopy. In 15 patients, a total of 45 clips were placed, and 31 clips (68.9%) were retained. The median periods of clip retention was 105 days (range, 39~1,383 days). Twenty-seven clips (87.1%) were successfully retrieved with grasping forceps, and four clips (12.9%) were not removed because they were fixed on the stomach wall. Adverse events occurred in two patients (13.3%): both involved immediate bleeding at the retrieval site; however, the bleeding was completely treated by replacing the clips. In conclusion, retrieving clips retained long-term was relatively safe and feasible. Complications were easily controlled by re-placement of clips.
Endoscopy ; Gastrointestinal Tract ; Hand Strength ; Hemorrhage ; Humans ; Magnetic Resonance Imaging ; Stomach* ; Surgical Instruments

Group 3 innate lymphoid cells (ILC3), which express IL-22 and IL-17A, has been introduced as one of pathologic cells in axial spondyloarthritis (axSpA). Dyslipidaemia should be managed in axSpA patients to reduce cardiovascular disease, and dyslipidaemia promotes inflammation. This study aimed to reveal the role of circulating ILC3 in axSpA and the impact of dyslipidaemia on axSpA pathogenesis. AxSpA patients with or without dyslipidaemia and healthy control were recruited. Peripheral blood samples were collected, and flow cytometry analysis of circulating ILC3 and CD4+ T cells was performed. The correlation between Ankylosing Spondylitis Disease Activity Score (ASDAS)-C-reactive protein (CRP) and circulating immune cells was evaluated. The effect of oxidized low-density lipoprotein cholesterol (oxLDL-C) on immune cell differentiation was confirmed. AxSpA human monocytes were cultured with with oxLDL-C, IL-22, or oxLDL-C plus IL-22 to evaluate osteoclastogenesis using tartrate-resistant acid phosphatase (TRAP) staining and realtime quantitative PCR of osteoclast-related gene expression. Total of 34 axSpA patients (13 with dyslipidaemia and 21 without) were included in the analysis. Circulating IL-22+ ILC3 and Th17 were significantly elevated in axSpA patients with dyslipidaemia (p=0.001 and p=0.034, respectively), and circulating IL-22+ ILC3 significantly correlated with ASDAS-CRP (Rho=0.4198 and p=0.0367). Stimulation with oxLDL-C significantly increased IL-22+ ILC3, NKp44 − ILC3, and Th17 cells, and these were reversed by CD36 blocking agent. IL-22 and oxLDL-C increased TRAP + cells and osteoclast-related gene expression. This study suggested potential role of circulating IL-22+ ILC3 as biomarker in axSpA. Furthermore, dyslipidaemia augmented IL-22+ ILC3 differentiation, and oxLDL-C and IL-22 markedly increased osteoclastogenesis of axSpA.

Receptor-interacting serine/threonine-protein kinase (RIPK) 3 is a member of the TNF receptor-I signaling complex and mediates necroptosis, an inflammatory cell death. Ulcerative colitis (UC) is an excessive inflammatory disease caused by uncontrolled T cell activation. The current study is aimed to determine whether RIPK3 inhibitor attenuates UC development inhibiting inflammation and necroptosis using experimental colitis mice model. Dextran sulfate sodium-induced colitis mice were administered RIPK3 inhibitor (3 mg/ml) 3 times and their tissues were analyzed by immunohistochemistry. RIPK3, mixed lineage kinase domain-like (MLKL), phosphorylated MLKL, IL-17, and CD4 in colitis patient colon tissues were detected using confocal microscopy. Protein levels were measured using immunohistochemistry and ELISA. The differentiation of Th17 cells was evaluated using flow cytometry. The expression of proinflammatory cytokines and necroptosis in peripheral blood mononuclear cells from UC patients was decreased markedly by RIPK3 inhibitor treatment. We also observed that the injection of RIPK3 inhibitor improves colitis severity and protects intestinal destruction. RIPK3 inhibitor reduced necroptosis factors and proinflammatory cytokines in the colon and consequently protected colon devastation. The expression of inflammatory mediators in experimental colitis mice splenocytes was decreased significantly by RIPK3 inhibitor treatment. These results suggest that RIPK3 inhibitor ameliorates severity of experimental colitis and reduces inflammation through the inhibition of inflammatory response and necroptosis and support RIPK3-targeting substances for treatment of UC.

A 73-year-old woman who has been suffering from ulcer pain on left lower leg of burn scars visited our clinic for prosthesis rehabilitation. Symptom has been developed since 12 months ago. She burned herself with oil at the age of 40. Biopsy on the skin lesion revealed squamous cell carcinoma. Marjolin's ulcer is a rare but highly aggressive squamous cell cancer that is most often associated with chronic burn wounds. Patient had undergone multiple prior split-thickness skin grafts for recurrent squamous cell carcinoma. She had undergone a trans-tibial amputation and subsequently given adjuvant chemotherapy for recurrent disease. After amputee training the patient was able to walk by herself and could perform all activities of daily living independently. Cancer induced amputees need prostheses with intensive rehabilitation training program for ambulation to prevent deterioration of physical function and mental health due to immobilization. However, she developed another recurrence and decided not to undergo further surgery and eventually died in hospice care due to progressive metastatic disease.
Activities of Daily Living ; Aged ; Amputation ; Amputees ; Biopsy ; Burns ; Carcinoma, Squamous Cell ; Chemotherapy, Adjuvant ; Cicatrix ; Female ; Hospice Care ; Humans ; Immobilization ; Leg ; Mental Health ; Neoplasms, Squamous Cell ; Prostheses and Implants ; Recurrence ; Skin ; Stress, Psychological ; Transplants ; Ulcer ; Walking

The protein encoded by the Gene Associated with Retinoid-Interferon-Induced Mortality-19 (GRIM-19) is located in the mitochondrial inner membrane and is homologous to the NADH dehydrogenase 1-alpha subcomplex subunit 13 of the electron transport chain.Multiple sclerosis (MS) is a demyelinating disease that damages the brain and spinal cord.Although both the cause and mechanism of MS progression remain unclear, it is accepted that an immune disorder is involved. We explored whether GRIM-19 ameliorated MS by increasing the levels of inflammatory cytokines and immune cells; we used a mouse model of experimental autoimmune encephalomyelitis (EAE) to this end. Six-to-eight-week-old male C57BL/6, IFNγ-knockout (KO), and GRIM-19 transgenic mice were used; EAE was induced in all strains. A GRIM-19 overexpression vector (GRIM19 OVN) was electrophoretically injected intravenously. The levels of Th1 and Th17 cells were measured via flow cytometry, immunofluorescence, and immunohistochemical analysis. IL-17A and IFNγ expression levels were assessed via ELISA and quantitative PCR. IL-17A expression decreased and IFNγ expression increased in EAE mice that received injections of the GRIM19 OVN. GRIM-19 transgenic mice expressed more IFNγ than did wild-type mice; this inhibited EAE development. However, the effect of GRIM-19 overexpression on the EAE of IFNγ-KO mice did not differ from that of the empty vector. GRIM-19 expression was therapeutic for EAE mice, elevating the IFNγ level. GRIM-19 regulated the Th17/Treg cell balance.