No abstract

Increased D-serine in the aqueous and vitreous humour was found in patients with PDR compared with control subjects.

Retroperitoneal desmoid-type fibromatosis (RPDF) is a rare mesenchymal neoplasm, and it covers a broad spectrum of aggressive monoclonal, fibroblastic proliferation. There is no evidence-based or established optimal treatment available for this intriguing disease yet. Therefore, we here investigated the clinicopathological characteristics, surgical, and survival outcomes in RPDF among Chinese patients. Patients with histologically confirmed RPDF were retrospectively studied from 2010 to 2018 within the West China Hospital of Sichuan University. Demographics, clinicopathological characteristics, treatment, and survival outcome data were collected. Of the 29 cases of RPDF, 19 were females. Tumor diameter ranged from 4 to 40 cm, with a median of 10 cm. Of these patients, surgical resection was the primary treatment adopted for RPDF in 26 cases; while 3 patients underwent watchful waiting. In surgical group, complete and incomplete macroscopic resection was achieved in 21 (80.77%) and 6 (19.23%) cases, respectively. Totally, 21 (80.77%) cases underwent multi-visceral resection. With a median follow-up duration of 48 months, 11 patients experienced tumor progression for the entire cohort. Tumor progression was observed for those patients with incomplete and complete macroscopic resection in 2/5 (40.0%) and 6/21 (28.6%) cases, respectively. In the watchful waiting group, there were no documented cases of RPDF regression. The progression-free survival rate was 86.1%, 71.5%, and 62.3% at 1-, 2-, and 3-years, respectively. RPDFs are rare types of tumor, which have characteristically varied natural histories. Surgical resection had a relative favorable outcome, but some patients were associated with burden of significant surgical complications.

About 10-16 mouse pups were used per group, and both eyes were removed for experimental Background/aim: Erythropoietin (EPO) has been proven recently to be a critical mediator in retinal neovascularization (RNV). Previous studies have indicated that the use of recombinant human EPO (rEPO) is a high risk factor in the development of retinopathy of prematurity. In this study, we aimed to investigate the effect of rEPO administration on RNV and its underlying mechanism in a mouse model of oxygen-induced retinopathy (OIR). Materials and methods:A murine model of OIR was used to generate RNV. After daily intraperitoneal injection of rEPO from postnatal day 12 (P12), mice were euthanized at P17. Whole-mount retina staining was used to indicate the nonperfused area and neovascularization tufts. Preretinal neovascular cells were calculated through hematoxylin and eosin staining. The expression levels of vascular endothelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS) were detected via western blot analysis. Results:We found that injection of rEPO promoted the severity of RNV. The areas of neovascular tufts and preretinal neovascular cells were increased after administration of rEPO. When mice were injected with rEPO, a dose-dependent upregulation in VEGF and iNOS was observed. Conclusion:The study indicates the proangiogenic role of EPO, suggesting that rEPO contributes to the pathogenesis of RNV.

No abstract

Ankylosing spondylitis (AS) is a chronic progressive autoimmune disease with insidious onset, high rates of disability among patients, unknown pathogenesis, and no effective treatment. Ferroptosis is a novel type of regulated cell death that is associated with various cancers and diseases. However, its relation to AS is not clear. In the present study, we identified two potential therapeutic targets for AS based on genes associated with ferroptosis and explored their association with immune cells and immune cell infiltration (ICI). We studied gene expression profiles of two cohorts of patients with AS (GSE25101 and GSE41038) derived from the gene expression omnibus database, and ferroptosis-associated genes (FRGs) were obtained from the FerrDb database. LASSO regression analysis was performed to build predictive models for AS based on FRGs, and the ferroptosis level in each sample was assessed via single-sample gene set enrichment analysis. Weighted gene co-expression network and protein-protein interaction network analyses were performed for screening; two key genes, DDIT3 and HSPB1, were identified in patients with AS. The relationship between key genes and ICI levels was assessed using the CIBERSORT algorithm, followed by gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses. Finally, DDIT3 and HSPB1 were identified as diagnostic markers and potential therapeutic targets for AS. DDIT3 was highly positively correlated with the infiltration levels of various immune cells, while HSPB1 was negatively correlated with the infiltration levels of several different types of immune cells. In conclusion, DDIT3 and HSPB1 may induce ferroptosis in the cells of patients with AS via changes in the inflammatory response in the immune microenvironment, and these genes could serve as molecular targets for AS therapy.

No abstract

Chronic kidney disease (CKD) has a significant negative impact on bone health. However, the mechanisms of cortical bone deterioration and cortical porosity enlargement caused by CKD have not been fully described. We therefore examined the association of CKD stages with cortical porosity index (PI), and explored potential mediators of this association. Double-echo ultrashort echo-time magnetic resonance imaging (UTE MRI) provides the possibility of quantifying cortical porosity in vivo. A total of 95 patients with CKD stages 2-5 underwent 3D double-echo UTE-Cones MRI (3.0T) of the midshaft tibia to obtain the PI. PI was defined as the ratio of the image signal intensity of a sufficiently long echo time (TE) to the shortest achievable TE. Parathyroid hormone (PTH), β-CrossLaps (β-CTX), total procollagen type I amino-terminal propeptide (T-P1NP), osteocalcin (OC), 25-hydroxyvitamin D (25OHD), and lumbar bone mineral density (BMD) were measured within one week of the MRI. Partial correlation analysis was performed to address associations between PI, eGFR and potential mediators (PTH, β-CTX, T-P1NP, OC, 25OHD, BMD, and T-score). Multiple linear regression models were used to assess the association between CKD stages and PI value. Then, a separate exploratory mediation analysis was carried out to explore the impact of CKD stages and mediators on the PI value. The increasing CKD stages were associated with a higher PI value (Ptrend < 0.001). The association of CKD stages and PI mediated 34.4% and 30.8% of the total effect by increased PTH and β-CTX, respectively. Our study provides a new idea to monitor bone health in patients with CKD, and reveals the internal mechanism of bone deterioration caused by CKD to some extent.