Histopathological assessment of radial artery calcification in patients with end-stage kidney disease.

BACKGROUND: A comprehensive understanding of vascular calcification pathology is significant for the development of cardiovascular disease therapy in high-risk populations. This cross-sectional study aimed to evaluate the prevalence and characteristics of radial artery calcification (RAC) and to identify the factors that are associated with RAC in end-stage kidney disease (ESKD). METHODS: Detailed medical histories of 180 patients with ESKD were recorded. Fragments of the radial artery obtained during the creation of arteriovenous fistula for hemodialysis access were stained with alizarin red S. RESULTS: Calcification was localized in the arterial media layer. The prevalence of positive calcification staining in the radial arteries was 21.1% (n = 38). Patients with RAC had a higher glycated hemoglobin level (p < 0.01), higher prevalence of dialysis duration >5 years (p = 0.022), and diabetes mellitus (p < 0.01) than those without RAC. Multiple logistic regression models showed dialysis duration >5 years (odds ratio [OR], 9.864; 95% confidence interval [CI], 2.666-36.502; p < 0.01) and diabetes mellitus (OR, 12.689; 95% CI, 2.796-34.597; p < 0.01) were independent risk factors for RAC in patients with ESKD. Patients with dialysis duration >5 years had a higher prevalence of RAC (p = 0.012) than those with dialysis duration ≤5 years. Patients with diabetes mellitus had a higher prevalence of RAC (p < 0.01) than those without diabetes mellitus. Patients with diabetes mellitus ≥15 years had a higher prevalence of RAC (p = 0.042) than those with diabetes mellitus <15 years. Radial artery calcification level showed a significantly positive correlation with dialysis duration (p < 0.05), diabetes mellitus duration (p < 0.01), HbA1c level (p < 0.01) and Calcium level (p < 0.01). CONCLUSIONS: In patients with ESKD, dialysis duration >5 years and diabetes predict RAC. Thus, the combination of prolonged dialysis and hyperglycemic conditions exerts a synergistic effect on RAC.

CD36 promotes the epithelial-mesenchymal transition and metastasis in cervical cancer by interacting with TGF-ß.

BACKGROUND: Accumulating evidence indicates that CD36 initiates metastasis and correlates with an unfavorable prognosis in cancers. However, there are few reports regarding the roles of CD36 in initiation and metastasis of cervical cancer. METHODS: Using immunohistochemistry, we analyzed 133 cervical cancer samples for CD36 protein expression levels, and then investigated the correlation between changes in its expression and clinicopathologic parameters. The effect of CD36 expression on the epithelial-mesenchymal transition (EMT) in cervical cancer cells was evaluated by Western immunoblotting analysis. In vitro invasion and in vivo metastasis assays were also used to evaluate the role of CD36 in cervical cancer metastasis. RESULTS: In the present study, we confirmed that CD36 was highly expressed in cervical cancer samples relative to normal cervical tissues. Moreover, overexpression of CD36 promoted invasiveness and metastasis of cervical cancer cells in vitro and in vivo, while CD36 knockdown suppressed proliferation, migration, and invasiveness. We demonstrated that TGF-ß treatment attenuated E-cadherin expression and enhanced the expression levels of CD36, vimentin, slug, snail, and twist in si-SiHa, si-HeLa, and C33a-CD36 cells, suggesting that TGF-ß synergized with CD36 on EMT via active CD36 expression. We also observed that the expression levels of TGF-ß in si-SiHa cells and si-HeLa cells were down-regulated, whereas the expression levels of TGF-ß were up-regulated in C33a-CD36 cells. These results imply that CD36 and TGF-ß interact with each other to promote the EMT in cervical cancer. CONCLUSIONS: Our findings suggest that CD36 is likely to be an effective target for guiding individualized clinical therapy of cervical cancer.

Comparison Between Injectable Platelet-rich Fibrin and Platelet-rich Plasma in Ameliorating UVA-induced Photoaging in Human Dermal Fibroblasts via the Activation of TGF-ß/Smad Signaling Pathway.

Early-stage photoaging is characterized by skin laxity and wrinkling, which are mainly attributable to the ultraviolet (UV) irradiation-mediated imbalance between matrix metalloproteinase (MMP) production and collagen degradation. Injectable platelet-rich fibrin (i-PRF) is a novel blood concentrate with potential effects on photoaging. Over the past few decades, platelet-rich plasma (PRP) has been widely researched and used in different clinical fields as a first-generation platelet concentrate. The aim of this study was to compare the antiphotoaging effects of i-PRF in UVA-irradiated human dermal fibroblasts with those of PRP by examining cell proliferation, migration and apoptosis, ROS generation, MMP-1 and collagen I levels. The activation of the TGF-ß/Smad signaling pathway by i-PRF and PRP was also investigated using western blotting. The results showed that i-PRF was more effective than PRP in promoting cell proliferation and migration. Moreover, i-PRF reduced ROS generation and cell apoptosis more effectively than PRP. With respect to the mechanism of collagen I upregulation, stronger stimulation of the TGF-ß/Smad signaling pathway and greater suppression of MMP-1 expression were achieved by i-PRF than by PRP. Our results suggest that i-PRF can be a promising substitute for PRP in alleviating UVA-induced photoaging and should be explored further for its anti-photoaging properties.

Learn to Estimate Genetic Mutation and Microsatellite Instability with Histopathology H&E Slides in Colon Carcinoma.

Colorectal cancer is one of the most common malignancies and the third leading cause of cancer-related mortality worldwide. Identifying KRAS, NRAS, and BRAF mutations and estimating MSI status is closely related to the individualized therapeutic judgment and oncologic prognosis of CRC patients. In this study, we introduce a cascaded network framework with an average voting ensemble strategy to sequentially identify the tumor regions and predict gene mutations & MSI status from whole-slide H&E images. Experiments on a colorectal cancer dataset indicate that the proposed method can achieve higher fidelity in both gene mutation prediction and MSI status estimation. In the testing set, our method achieves 0.792, 0.886, 0.897, and 0.764 AUCs for KRAS, NRAS, BRAF, and MSI, respectively. The results suggest that the deep convolutional networks have the potential to provide diagnostic insight and clinical guidance directly from pathological H&E slides.