Curcumin has shown protective potential on osteoarthritis. However, its effect on treatment of osteoarthritis remains elusive so far. This study aimed to determine whether curcumin could ameliorate osteoarthritis in vivo and the underline mechanisms. The mice subjected to destabilization of the medial meniscus (DMM) surgery were administered curcumin. Cartilage integrity was evaluated by immunohistological staining. Expression levels of inflammatory cytokines from mice arthrodial cartilage were detected. THP-1 cells were primed by lipopolysaccharide (LPS)/ATP to induce inflammation, followed by the addition of curcumin. The expression of proinflammatory cytokines was also detected. Moreover, the expression of pro-caspase-1, cleaved caspase-1, and NLRP3 inflammasome was examined. Administration of curcumin significantly reduced osteoarthritis disease progression in DMM model of osteoarthritis. Curcumin suppressed mRNA expression of proinflammatory mediators in arthrodial cartilage of mice subjected to surgery. In LPS- and ATP-induced THP-1 macrophage cells, curcumin significantly suppressed the expression of interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) at both RNA and protein levels. Compared to vehicle-treated controls, curcumin also showed remarkably increased pro-caspase-1 and decreased cleaved caspase-1. This study provides the first evidence that curcumin exerts protection on osteoarthritis by inhibition to the release of inflammasome NLRP3, leading to the downregulation of inflammatory cytokines.

Questionnaires from 493 participants aged from 16 to 26 years were included in the final database. The seven ethnic groups included in the final analysis were Han, Korean, Mongolian, Uyghur, Tibetan, Hui, and Tujia. Compared to the Han Chinese, the members of the other six ethnic groups had lower cervical cancer knowledge levels. The knowledge scores of Mongolian and Korean students were significantly lower than those of the Han Chinese. The willingness to accept cervical cancer prevention efforts also differed across different ethnic groups. After adjusting for age and place of residence, the acceptance of cervical cancer screening among the Tibetan, Uyghur, and Korean groups was significantly lower than among the Han Chinese, with different related decision-making factors in each group. Cervical cancer prevention-related public education is an urgent need in China. Extra consideration of ethnic differences should be taken into account when designing and improving new current cervical cancer prevention programs.

The objective of this study is to evaluate the diagnostic value of combination of artificial neural networks (ANN) and support vector machine (SVM)-based CAD systems in differentiating malignant from benign thyroid nodes with gray-scale ultrasound images. Two morphological and 65 texture features extracted from regions of interest in 610 2D-ultrasound thyroid node images from 543 patients (207 malignant, 403 benign) were used to develop the ANN and SVM models. Tenfold cross validation evaluated their performance; the best models showed accuracy of 99% for ANN and 100% for SVM. From 50 thyroid node ultrasound images from 45 prospectively enrolled patients, the ANN model showed sensitivity, specificity, positive and negative predictive values, Youden index, and accuracy of 88.24, 90.91, 83.33, 93.75, 79.14, and 90.00%, respectively, the SVM model 76.47, 90.91, 81.25, 88.24, 67.38, and 86.00%, respectively, and in combination 100.00, 87.88, 80.95, 100.00, 87.88, and 92.00%, respectively. Both ANN and SVM had high value in classifying thyroid nodes. In combination, the sensitivity increased but specificity decreased. This combination might provide a second opinion for radiologists dealing with difficult to diagnose thyroid node ultrasound images.

In inflamed joints, enhanced hyaluronic acid (HA) degradation is closely related to the pathogenesis of rheumatoid arthritis (RA). KIAA1199 has been identified as a hyaladherin that mediates the intracellular degradation of HA, but its extracellular function remains unclear. In this study, we found that the serum and synovial levels of secreted KIAA1199 (sKIAA1199) and low-molecular-weight HA (LMW-HA, MW < 100 kDa) in RA patients were significantly increased, and the positive correlation between them was shown for the first time. Of note, treatment with anti-KIAA1199 mAb effectively alleviated the severity of arthritis and reduced serum LMW-HA levels and cytokine secretion in collagen-induced arthritis (CIA) mice. In vitro, sKIAA1199 was shown to mediate exogenous HA degradation by attaching to the cell membrane of RA fibroblast-like synoviosytes (RA FLS). Furthermore, the HA-degrading activity of sKIAA1199 depended largely on its adhesion to the membrane, which was achieved by its G8 domain binding to ANXA1. In vivo, kiaa1199-KO mice exhibited greater resistance to collagen-induced arthritis. Interestingly, this resistance could be partially reversed by intra-articular injection of vectors encoding full-length KIAA1199 instead of G8-deleted KIAA119 mutant, which further confirmed the indispensable role of G8 domain in KIAA1199 involvement in RA pathological processes. Mechanically, the activation of NF-κB by interleukin-6 (IL-6) through PI3K/Akt signaling is suggested to be the main pathway to induce KIAA1199 expression in RA FLS. In conclusion, our study supported the contribution of sKIAA1199 to RA pathogenesis, providing a new therapeutic target for RA by blocking sKIAA1199-mediated HA degradation.