BACKGROUND: Neointimal hyperplasia, as the most important mechanism of restenosis after intracoronary artery stenting, its severity is closely correlated with the degree of local inflammatory reaction initiated by vasular injury during stenting procedure. So, we proceeded this study to determine whether inflammatory markers such as CD11b/CD18 (Mac-1) adehsion molecules of neutrophils, sICAM-1 (soluble intercellular adhesion molecule-1), ESR, and CRP increase or not in the peripheral circulation after coronary artery stenting, and whether there is any association between these findings and the degree of later restenosis. METHOD: 32 patients (chronic stable angina 4, unstable angina 17, acute myocardial infarction 11) underwent single vessel coronary artery stenting were enrolled in our study. Blood samples were obtained from peripheral vein just before coronary artery stenting and 48 hours thereafter. The degrees of CD11b/CD18 expression on the surface of neutrophils were analyzed by flow cytometry with monoclonal antibodies, and sICAM-1 by ELISA method. At each times, ESR and CRP were also measured. Follow-up coronary artery angiography was performed with QCA analysis at least 6 months later. We compared the each 48 hours values with the baseline (just before procedure) values. Percentage increments (as a ratio 48 hours values to baseline) of CD11b/CD18 expression, sICAM-1, ESR, and CRP levels were also compared with the results of follow-up QCA analysis. RESULTS: Restenosis (diameter stenosis > or = 50%) occurred in 6 patients (19%) at follow up angiography. 48 hours values of CD11b/CD18 expression, sICAM-1, ESR, and CRP were significantly elevated from the baseline values (each p values, CD11b : < 0.0001, CD18 : 0.01, sICAM-1 : < 0.0001, ESR : 0.005, and CRP : 0.001). The percentage increments of CD11b/CD18 expression were more elevated in restenosis group than nonrestenosis group (CD11b : 341+/-215%/74+/-95%, CD18 : 84+/-60%/17+/-37%, each p < 0.001, 0.001). There was some positive correlation between the percentage increments in the expression of CD11b and the late loss index at the follow up angiography (r=.43, p<0.05). CONCLUSIONS: Through this study, we found that the activation of neutrophils was occurred, and that sICAM-1 level was increased after coronary artery stenting in the peripheral blood. There was some correlations between the degree of CD11b expression on the surface of neutrophils and the severity of late lumen loss of inserted stents. The measurements of increased neutrophil adhesion molecules of CD11b/CD18 levels at 48hrs after coronary stenting may have a value as the predictor of subsequent late restenosis.
Angina, Stable ; Angina, Unstable ; Angiography ; Antibodies, Monoclonal ; Arteries ; Constriction, Pathologic ; Coronary Vessels* ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Follow-Up Studies ; Humans ; Hyperplasia ; Myocardial Infarction ; Neutrophils* ; Stents* ; Veins

PURPOSE: To report two cases of temporary severe neurogenic blepharoptosis after successful reconstruction of orbital medial wall fracture. CASE SUMMARY: A 36-year-old woman and a 52-year-old man received orbital medial wall reconstruction with Medpor(R) for large fractures. Before the operation, the patients had only moderate swelling of the lid and periorbital ecchymosis. There were no limitations of extraocular muscles or ptosis. The operations were successful, although the patients developed unilateral complete ptosis with totally impaired levetor muscle function immediately after recovering from anesthesia. There were no anisocoria or limitations of the extraocular muscles. After oral steroid therapy, the patients began to improve on postoperative day 4 and after one month, respectively, and recovered to normal lid height and levator function after two months. CONCLUSIONS: Blepharoptosis after orbital medial wall reconstruction may result from ischemic damage at the end of the superior branch of the oculomotor nerve in the orbit due to compressive and tractional manipulation. Although very rare and temporary, this complication should be considered important because the occurrence can be unpredictable and may cause dissatisfaction to the surgeon and the patient after a successful operation.
Adult ; Anesthesia ; Anisocoria ; Blepharoptosis ; Ecchymosis ; Female ; Humans ; Middle Aged ; Muscles ; Oculomotor Nerve ; Orbit ; Traction

Purpose: This study aimed to evaluate the cumulative recurrence rate and risk factors for recurrent abdominal wall endometriosis (AWE) after surgical treatment. Materials and Methods: A retrospective cohort study was conducted at a single gynecological surgery center between January 2004 and December 2020. Patients who were surgically treated and followed up for at least 6 months after surgery were selected. Results: Eighteen patients with pathologically diagnosed AWE were included in this study. The median follow-up duration was 22.5 months (range, 6–106). The median age was 37 years (range, 22–48), and 33.3% of the patients were nulliparous. Among the patients included in our study, 55.6% complained of a mass with cyclic pain, and 27.8% had a palpable mass. In addition, 22.2% of patients experienced recurrence with 17.5±9.7 months of mean time to recurrence. The cumulative recurrence rates at 24 and 60 months after surgical treatment of AWE were 23.8% and 39.1%, respectively. There were no statistically significant risk factors for the recurrence of AWE, including postoperative medical treatment. Conclusion The recurrence rate of AWE appears to be correlated with the follow-up duration. There was no statistically significant risk factor for the recurrence of AWE. Unlike ovarian endometriosis, postoperative hormonal treatment does not seem to lower the recurrence of AWE. The findings of the current study may help healthcare providers in counselling and managing patients with AWE.

The technique of endoscopic submucosal dissection is occasionally used for resection of myogenic tumors originating from muscularis mucosa or muscularis propria of stomach and esophagus. However, endoscopic treatments for esophageal myogenic tumors >2 cm have rarely been reported. Herein, we report a case of large leiomyoma originating from muscularis propria in the upper esophagus. A 59-year-old woman presented with dysphagia. Esophagoscopy and endoscopic ultrasonography revealed an esophageal subepithelial tumor which measured 25x20 mm in size, originated from muscularis propria, and was located at 20 cm from the central incisors. The tumor was successfully removed by endoscopic submucosal dissection and there were no complications after en bloc resection. Pathologic examination was compatible with leiomyoma.
Esophageal Neoplasms/*diagnosis/pathology/surgery ; Esophagus/surgery/ultrasonography ; Female ; Gastroscopy ; Humans ; Leiomyoma/*diagnosis/pathology/surgery ; Middle Aged ; Mucous Membrane/pathology ; Stents ; Tomography, X-Ray Computed

Osteoarthritis (OA) is a degenerative joint disease characterized by a progressive loss of cartilage. And, increased oxidative stress plays a relevant role in the pathogenesis of OA. Ursodeoxycholic acid (UDCA) is a used drug for liver diseases known for its free radical-scavenging property. The objectives of this study were to investigate the in vivo effects of UDCA on pain severity and cartilage degeneration using an experimental OA model and to explore its mode of actions. OA was induced in rats by intra-articular injection of monosodium iodoacetate (MIA) to the knee. Oral administration UDCA was initiated on the day of MIA injection. Limb nociception was assessed by measuring the paw withdrawal latency and threshold. Samples were analyzed macroscopically and histologically. Immunohistochemistry was used to investigate the expression of interleukin-1beta (IL-1beta), IL-6, nitrotyrosine and inducible nitric oxide synthase (iNOS) in knee joints. UDCA showed an antinociceptive property and attenuated cartilage degeneration. OA rats given oral UDCA significantly exhibited a decreased number of osteoclasts in subchondral bone legion compared with the vehicle-treated OA group. UDCA reduced the expression of IL-1beta, IL-6, nitrotyrosine and iNOS in articular cartilage. UDCA treatment significantly attenuated the mRNA expression of matrix metalloproteinase-3 (MMP-3), -13, and ADAMTS5 in IL-1beta-stimulated human OA chondrocytes. These results show the inhibitory effects of UDCA on pain production and cartilage degeneration in experimentally induced OA. The chondroprotective properties of UDCA were achieved by suppressing oxidative damage and inhibiting catabolic factors that are implicated in the pathogenesis of cartilage damage in OA.
Administration, Oral ; Animals ; Cartilage* ; Cartilage, Articular ; Chondrocytes ; Extremities ; Humans ; Immunohistochemistry ; Injections, Intra-Articular ; Interleukin-1beta ; Interleukin-6 ; Joint Diseases ; Knee ; Knee Joint ; Liver Diseases ; Nitric Oxide Synthase Type II ; Nociception ; Osteoarthritis* ; Osteoclasts ; Oxidative Stress ; Rats* ; RNA, Messenger ; Ursodeoxycholic Acid*

PURPOSE: Distribution and survival of sarcoma in Korea are not well described, after the changing of sarcoma classification on 2013. The researchers investigated the distribution and survival in single center 2017 cases of sarcoma.METHODS: Patients with primary sarcoma, who underwent surgery, were investigated. All cases were collected during a 20 year period (1995–2015) from Samsung Medical Center in Korea. Histopathologic types were classified by World Health Organization (WHO) classification (2013). And overall survival rates were analyzed.RESULTS: Between 1995 and 2015, 2017 patients were collected. The most frequent type of sarcoma was gastrointestinal tumor (15%), followed by liposarcoma (12%), leiomyosarcoma (9%), dermatofibrosarcoma (6%), giant cell sarcoma (6%). The most common primary site of sarcoma was the intra-abdominal area (45%, including visceral area). Extremities accounted for 26% of all cases. Sixteen percent of sarcoma were located in retroperitoneal area. The overall survival rate was 70.4% (median follow-up time, 36.8 months; range, 0.1–261.3 months). The best prognosis was dermatofibrosarcoma (100%, 5-year survival rate). The worst prognosis was angiosarcoma (39.3%). Survival analysis by the primary site demonstrated favor prognosis in extremities than head & neck, chest lesion.CONCLUSION: The researchers reported Korean sarcoma characteristics with using the new WHO classification.
Classification ; Dermatofibrosarcoma ; Epidemiology ; Extremities ; Follow-Up Studies ; Giant Cells ; Head ; Hemangiosarcoma ; Humans ; Korea ; Leiomyosarcoma ; Liposarcoma ; Neck ; Prognosis ; Sarcoma ; Survival Rate ; Thorax ; World Health Organization

Interleukin (IL)-27 is a novel cytokine of the IL-6/IL-12 family that has been reported to be involved in the pathogenesis of autoimmune diseases and has a pivotal role as both a pro- and anti-inflammatory cytokine. We investigated the in vivo effects of IL-27 on arthritis severity in a murine collagen-induced arthritis (CIA) model and its mechanism of action regarding control of regulatory T (Tregs) and IL-17-producing T helper 17 (Th17) cells. IL-27-Fc-treated CIA mice showed a lower severity of arthritis. IL-17 expression in the spleens was significantly decreased in IL-27-Fc-treated CIA mice compared with that in the CIA model. The Th17 population was decreased in the spleens of IL-27-Fc-treated CIA mice, whereas the CD4+CD25+Foxp3+ Treg population increased. In vitro studies revealed that IL-27 inhibited IL-17 production in murine CD4+ T cells, and the effect was associated with retinoic acid-related orphan receptor gammaT and signal transducer and activator of transcription 3 inhibition. In contrast, fluorescein isothiocyanate-labeled forkhead box P3 (Foxp3) and IL-10 were profoundly augmented by IL-27 treatment. Regarding the suppressive capacity of Treg cells, the proportions of CTLA-4+ (cytotoxic T-lymphocyte antigen 4), PD-1+ (programmed cell death protein 1) and GITR+ (glucocorticoid-induced tumor necrosis factor receptor) Tregs increased in the spleens of IL-27-Fc-treated CIA mice. Furthermore, in vitro differentiated Treg cells with IL-27 exerted a more suppressive capacity on T-cell proliferation. We found that IL-27 acts as a reciprocal regulator of the Th17 and Treg populations in CD4+ cells isolated from healthy human peripheral blood mononuclear cells (PBMCs), as well as from humans with rheumatoid arthritis (RA) PBMCs. Our study suggests that IL-27 has the potential to ameliorate overwhelming inflammation in patients with RA through a reciprocal regulation of Th17 and Treg cells.
Animals ; Arthritis, Experimental/*drug therapy/immunology ; Cells, Cultured ; Humans ; Interleukins/immunology/*therapeutic use ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; T-Lymphocytes, Regulatory/*immunology ; Th17 Cells/*immunology

BACKGROUND/AIMS: Angiogenesis, which is a critical step in the initiation and progression of rheumatoid arthritis (RA), involves pro-angiogenic factors, including interleukin (IL)-8 and vascular endothelial growth factor (VEGF). We investigated the role of Toll-like receptor 3 (TLR3) in the regulation of pro-angiogenic factors in RA fibroblast-like synoviocytes (FLS). METHODS: FLS were isolated from RA synovial tissues and stimulated with the TLR3 ligand, poly (I:C). The levels of VEGF and IL-8 in the culture supernatants were measured using enzyme-linked immunosorbent assays, and the mRNA levels were assessed by semiquantitative reverse transcription-polymerase chain reaction. The expression patterns of VEGF and IL-8 in the RA synovium and osteoarthritis (OA) synovium were compared using immunohistochemistry. RESULTS: The expression levels of TLR3, VEGF, and IL-8 were significantly higher in the RA synovium than in the OA synovium. VEGF and IL-8 production were increased in the culture supernatants of RA FLS stimulated with poly (I:C), and the genes for these proteins were up-regulated at the transcriptional level after poly (I:C) treatment. Treatment with inhibitors of nuclear factor-kappaB (NF-kappaB), i.e., pyrrolidine dithiocarbamate and parthenolide, abrogated the stimulatory effect of poly (I:C) on the production of VEGF and IL-8 in RA FLS. CONCLUSIONS: Our results suggest that the activation of TLR3 in RA FLS promotes the production of proangiogenic factors, in a process that is mediated by the NF-kappaB signaling pathway. Therefore, targeting the TLR3 pathway may be a promising approach to preventing pathologic angiogenesis in RA.
Arthritis, Rheumatoid/drug therapy/*etiology/metabolism ; Cells, Cultured ; Fibroblasts/metabolism ; Humans ; Interleukin-8/analysis/*biosynthesis/genetics ; NF-kappa B/physiology ; Neovascularization, Pathologic/etiology ; RNA, Messenger/analysis ; Synovial Membrane/cytology/*metabolism ; Toll-Like Receptor 3/analysis/*physiology ; Vascular Endothelial Growth Factor A/analysis/*biosynthesis/genetics

Osteoarthritis (OA) is a common degenerative joint disease characterized by breakdown of joint cartilage. Mitochondrial dysfunction of the chondrocyte is a risk factor for OA progression. We examined the therapeutic potential of mitochondrial transplantation for OA. Mitochondria were injected into the knee joint of monosodium iodoacetateinduced OA rats. Chondrocytes from OA rats or patients with OA were cultured to examine mitochondrial function in cellular pathophysiology. Pain, cartilage destruction, and bone loss were improved in mitochondrial transplanted-OA rats. The transcript levels of IL-1β, TNF-α, matrix metallopeptidase 13, and MCP-1 in cartilage were markedly decreased by mitochondrial transplantation. Mitochondrial function, as indicated by membrane potential and oxygen consumption rate, in chondrocytes from OA rats was improved by mitochondrial transplantation. Likewise, the mitochondrial function of chondrocytes from OA patients was improved by coculture with mitochondria. Furthermore, inflammatory cell death was significantly decreased by coculture with mitochondria. Mitochondrial transplantation ameliorated OA progression, which is caused by mitochondrial dysfunction. These results suggest the therapeutic potential of mitochondrial transplantation for OA.

Osteoarthritis (OA) is the most common form of arthritis associated with ageing. Vitamin D has diverse biological effect on bone and cartilage, and observational studies have suggested it potential benefit in OA progression and inflammation process. However, the effect of vitamin D on OA is still contradictory. Here, we investigated the therapeutic potential of vitamin D in OA. Six-week-old male Wistar rats were injected with monosodium iodoacetate (MIA) to induce OA. Pain severity, cartilage destruction, and inflammation were measured in MIA-induced OA rats. Autophagy activity and mitochondrial function were also measured. Vitamin-D (1,25(OH) 2 D3) and celecoxib were used to treat MIAinduced OA rats and OA chondrocytes. Oral supplementation of vitamin D resulted in significant attenuations in OA pain, inflammation, and cartilage destruction. Interestingly, the expressions of MMP-13, IL-1β, and MCP-1 in synovial tissues were remarkably attenuated by vitamin D treatment, suggesting its potential to attenuate synovitis in OA.Vitamin D treatment in OA chondrocytes resulted in autophagy induction in human OA chondrocytes and increased expression of TFEB, but not LC3B, caspase-1 and -3, in inflamed synovium. Vitamin D and celecoxib showed a synergistic effect on antinociceptive and chondroprotective properties in vivo. Vitamin D showed the chondroprotective and antinociceptive property in OA rats. Autophagy induction by vitamin D treatment may be a promising treatment strategy in OA patients especially presenting vitamin D deficiency.Autophagy promoting strategy may attenuate OA progression through protecting cells from damage and inflammatory cell death.