An exosome (30–150 nm size) is a cell-derived vesicle. Exosome-induced regulation in inflammatory bowel disease (IBD) is becoming increasingly popular due to their potential functions of exosomal pathways. Exosomes, which are involved in the regulation of IBD, can be released from various cell types, or found in many physiological fluids, and plants. The specific functions of exosomes in IBD primarily depend on the internal functional components, including RNAs, proteins, and other substances. However, exosome-induced transport mechanisms involving cell-cell communications or cell-environment interactions are also very important. Recent studies have revealed that exosome crosstalk mechanisms may influence major IBD-related pathways, such as immune responses, barrier functions, and intestinal flora. This review highlights the advancements in the biology of exosome secretions and their regulation in IBD. The functional roles of exosomal components, including nucleic acids, proteins, and some other components, are the main focus of this review. More animal and clinical research is needed to study the functions of exosomes on IBD. Designing new drug dosage form using exosome-like-structure may provide new insights into IBD treatment. This review suggests a potential significance for exosomes in IBD diagnosis and treatment.
The lymphocyte-to-monocyte ratio (LMR), as a surrogate marker of systemic inflammation, has been found to be a novel prognostic indicator in various malignancies. Data from 672 advanced epithelial ovarian cancer (EOC) patients treated with neoadjuvant chemotherapy (NAC) followed by debulking surgery were analyzed, and the prognostic value of LMR were evaluated. The optimal cutoff point of LMR in prediction of survival was defined as 3.45 through receiver operating characteristics curve analysis. Patients with low LMR (≤3.45) at diagnosis tended to have more adverse clinical features, such as higher histological grade, chemotherapy resistance, and residual tumor >1cm after debulking surgery. No significant correlation was found between LMR level and age and histological type. Moreover, after NAC, the complete remission (CR) rate for the low-LMR group was lower than those for the high-LMR group (P<0.05). Patients with low LMR had poorer progression-free survival (PFS; P<0.001) and overall survival (OS; P<0.001). Multivariate analysis revealed that low LMR was an independent adverse predictor for PFS and OS. Results indicated that low LMR at diagnosis is a novel independent prognostic factor for advanced EOC. However, prospective study is needed to validate this prognostic factor and biological studies should further investigate the mechanisms underlying the correlation between low LMR and poor prognosis in advanced EOC.
Activation of phosphatase and tensin homolog (PTEN) is known to induce cell apoptosis. MicroRNA-374a (miR-374a), which can suppress PTEN expression, has been found abnormally expressed in inflammatory bowel disease (IBD). Fortunellin is a citrus flavonoid that is a potential anti-inflammation agent in inflammatory diseases. The present study investigated the effects and mechanisms underlying fortunellin-induced inhibition of PTEN in IBD. Colitis was established in rats by the intracolonic administration of 2,4,6-trinitrobenzene sulfonic acid to mimic human ulcerative colitis, which is the main type of IBD. miR-374a expression was measured by quantitative real-time polymerase chain reaction, and the regulation of PTEN by miR-374a was evaluated by dual luciferase reporter assay. Western blotting was used to measure the corresponding protein expression. Fortunellin ameliorated colitis symptoms, including excessive inflammation and oxidative stress. Fortunellin decreased epithelial cell apoptosis through inhibiting PTEN expression in colitis. Fortunellin-induced downregulation of PTEN could be counteracted by miR-374a depletion. Moreover, knockdown of miR-374a in vivo partly inhibited the effects of fortunellin on rat colitis. In conclusion, PTEN inhibition contributes to the amelioration effects of fortunellin on colitis. It was confirmed that fortunellin targets miR-374a, which is a negative regulator of PTEN. This study provides novel insights into the pathological mechanisms and treatment alternatives of colitis.
BackgroundAccording to renal M type phospholipase A2 receptor (PLA2R) immunohistochemistry, idiopathic membranous nephropathy (IMN) could be categorized into PLA2R-associated and non-PLA2R-associated IMN. We conducted a retrospective, multicenter cohort study with 91 patients to compare the effect of immunosuppressive therapy between PLA2R-associated and non-PLA2R-associated IMN patients.MethodsA total of 91 biopsy-proven IMN patients from Huashan hospital and People’s Hospital of Wuxi in past 5 years were collected into this study. IMN with positive PLA2R immunohistochemistry in kidney biopsies were designated as PLA2R-associated IMN. Seventy-eight of the 91 IMN patients was PLA2R-associated IMN and 13 were non-PLA2R-associated IMN. Forty-five patients were treated with prednisone plus cyclophosphamide (CTX), and 46 with prednisone plus calcineurin inhibitors (CNIs). The follow-up duration was 15 months.ResultsThe total remission rate (76.9% versus 44.9%, p = 0.032) and complete remission rate (30.8% versus 2.6%, p = 0.003) were both significantly higher in the non-PLA2R-associated group than in the PLA2R-associated group at the 3rd month visit point, and at the 6th month time point, the complete remission rate was still significantly higher in the non-PLA2R-associated group (46.2% versus 11.5%,p = 0.007). But similar remission rates were found after the 9th month. Relapses were observed in 8 patients in PLA2R-associated group and none in non-PLA2R-associated group, although there was no significant difference between these two groups.ConclusionCompared with the PLA2R-associated IMN, the non-PLA2R-associated IMN responded quicker to the immunosuppressive therapy.
BackgroundEarly gastric cancer (EGC) is invasive gastric cancer that invades no deeper than the submucosa, regardless of lymph node metastasis (LNM). It is mainly treated by surgery. Recently, the resection range of EGC has been minimized, but cancer recurrence and overall survival in some patients should be given high status. LNM is an important indicator of prognosis and treatment in gastric cancer. The law of the number and location of metastatic lymph nodes in EGC is not yet clear. Therefore, we aimed to identify the risk factors of LNM in radically resected EGC and guide treatment.MethodsThe clinicopathological factors of 611 patients with EGC were retrospectively analyzed in six hospitals between January 2010 and December 2016. The relationship between clinicopathological factors and LNM, as well as their prognostic significance, were analyzed by univariate and multivariate analyses.ResultsThe rate of LNM was 20.0% in the 611 EGC patients. The depth of invasion, differentiation type, tumor diameter, morphological ulceration, and lymphovascular invasion were independent risk factors for LNM (P<0.05) by logistic regression analysis. Tumor location in the proximal third of the stomach and morphological ulceration were significant factors for group 2 LNM. Moreover, the 5-year survival rate was 94.9% for patients with no positive nodes, 88.5% for patients with 1-2 positive nodes, 64.3% for patients with 3-6 positive nodes, and 41.8% for patients with >6 metastatic nodes. Interestingly, the 7-year risk of relapse diminished for patients with no LNM or retrieved no less than 15 lymph nodes.ConclusionsFifteen lymph node dissection and D2 radical operation are the surgical options in case of high risk factors for LNM. Extended lymph node dissection (D2+) is recommended for morphological ulceration or disease located in the proximal third of the stomach due to their high rate of group 2 LNM. Furthermore, LNM is a significant prognostic factor of EGC. Moreover, lymph nodes can also play a significant role in the chemotherapeutic and radiotherapy approach for non-surgical patients with EGC.
Cystatin C and NGAL both appear to be useful biomarkers of renal injury. Studies with larger numbers are needed, however. Also, allopurinol does exhibit renoprotective effects against ischemic injury.
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