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Intervertebral disc degeneration (IVDD) is a common chronic musculoskeletal disease that causes chronic low back pain and imposes an immense financial strain on patients. The pathological mechanisms underlying IVDD have not been fully elucidated. The development of IVDD is closely associated with abnormal epigenetic changes, suggesting that IVDD progression may be controlled by epigenetic mechanisms. Consequently, this study aimed to investigate the role of epigenetic regulation, including DNA methyltransferase 3a (DNMT3a)‐mediated methylation and peroxisome proliferator‐activated receptor γ (PPARγ) inhibition, in IVDD development. The expression of DNMT3a and PPARγ in early and late IVDD of nucleus pulposus (NP) tissues was detected using immunohistochemistry and western blotting analyses. Cellularly, DNMT3a inhibition significantly inhibited IL‐1β‐induced apoptosis and extracellular matrix (ECM) degradation in rat NP cells. Pretreatment with T0070907, a specific inhibitor of PPARγ, significantly reversed the anti‐apoptotic and ECM degradation effects of DNMT3a inhibition. Mechanistically, DNMT3a modified PPARγ promoter hypermethylation to activate the nuclear factor‐κB (NF‐κB) pathway. DNMT3a inhibition alleviated IVDD progression. Conclusively, the results of this study show that DNMT3a activates the NF‐κB pathway by modifying PPARγ promoter hypermethylation to promote apoptosis and ECM degradation. Therefore, we believe that the ability of DNMT3a to mediate the PPARγ/NF‐κB axis may provide new ideas for the potential pathogenesis of IVDD and may become an attractive target for the treatment of IVDD. [ABSTRACT FROM AUTHOR]

Intervertebral disc degeneration (IDD), an important cause of chronic low back pain (LBP), is considered the pathological basis for various spinal degenerative diseases. A series of factors, including inflammatory response, oxidative stress, autophagy, abnormal mechanical stress, nutritional deficiency, and genetics, lead to reduced extracellular matrix (ECM) synthesis by intervertebral disc (IVD) cells and accelerate IDD progression. Mammalian target of rapamycin (mTOR) is an evolutionarily conserved serine/threonine kinase that plays a vital role in diverse degenerative diseases. Recent studies have shown that mTOR signalling is involved in the regulation of autophagy, oxidative stress, inflammatory responses, ECM homeostasis, cellular senescence, and apoptosis in IVD cells. Accordingly, we reviewed the mechanism of mTOR signalling in the pathogenesis of IDD to provide innovative ideas for future research and IDD treatment. [ABSTRACT FROM AUTHOR]

Recently, 'Liquid crystal display (LCD) vs. organic light-emitting diode (OLED) display: who wins?' has become a topic of heated debate. In this review, we perform a systematic and comparative study of these two flat panel display technologies. First, we review recent advances in LCDs and OLEDs, including material development, device configuration and system integration. Next we analyze and compare their performances by six key display metrics: response time, contrast ratio, color gamut, lifetime, power efficiency, and panel flexibility. In this section, we focus on two key parameters: motion picture response time (MPRT) and ambient contrast ratio (ACR), which dramatically affect image quality in practical application scenarios. MPRT determines the image blur of a moving picture, and ACR governs the perceived image contrast under ambient lighting conditions. It is intriguing that LCD can achieve comparable or even slightly better MPRT and ACR than OLED, although its response time and contrast ratio are generally perceived to be much inferior to those of OLED. Finally, three future trends are highlighted, including high dynamic range, virtual reality/augmented reality and smart displays with versatile functions., Competing Interests: The authors declare no conflict of interest.

Objective To explore the safety and effectiveness of Shenkang Injection (SI) for con- trast-induced nephropathy (CIN) in elderly patients with chronic kidney disease (CKD). Methods Totally 206 elderly CKD patients who were scheduled to undergo coronary angiography (CAG) were assigned to three groups according to random digit table, i.e., the rehydration therapy group (67 cases) , the SI group (71 cases) , and the control group (68 cases). Patients in the rehydration therapy group received intrave- nous dripping of normal saline 12 h before and after CAG. Patients in the SI group received intravenous drip- ping of SI, while those in the control group received intravenous dripping of 5% glucose injection. SI and 5% glucose injection was respectively used 3 days before CAG and 4 days after CAG, once per day. The inci- dence rate of CIN, and levels of creatinine, blood urea nitrogen (BUN) , serum cystatin C (CysC), kidney injury molecule-1 (KIM-1), and P2-microglobulin (P2-MG) were detected before CAG, 24 h and 96 h after CAG, respectively. Age, sex, SI, contrast dose, pre-CAG indicators of renal function were compared. Their correlations with changed 24-h creatinine value (the difference between the value at post-CAG 24 h and pre-CAG) and CIN incidence rate were analyzed using Sperman correlation and Logistic regression analy- ses. Results Compared with the rehydration therapy group and the control group, the incidence rate of CIN was significantly lower in the SI group (x2 = 5. 32, P <0. 05). Compared with before treatment in the same group, levels of creatinine and CysC were all elevated in the 3 groups after 24-and 96-h treatment (P <0. 05) ; the KIM-1 level increased in rehydration therapy group and the control group (P <0. 05) ; P2-MG level increased in the SI group (P <0.05). Compared with the control group, post-CAG P2-MG level in- creased in the SI group (P <0. 05). There was no statistical difference in other index (P >0. 05). SI was neg- atively with the incidence rate of CIN and changed 24-h creatinine value (r = -0. 612, -0. 517, P <0. 05). The contrast dose was positively with the incidence rate of CIN and changed 24-h creatinine value (r = 0. 644, 0. 562, P <0. 05). Increased contrast dose could elevate the incidence rate of CIN (P <0. 05). SI could obviously lower the incidence rate of CIN (P <0. 05). Conclusion SI could lower the incidence rate of CIN in elder CKD patients by playing certain roles in prevention and treatment.

Objective: To observe the effect of simvastatin on the expression of high mobility group box-1 protein (HMGB1) and morphology of atherosclerotic plaques in atherosclerotic rats, to ascertain whether HMGB1 plays a role in the preventive mechanism of simvastatin from atherosclerosis (AS)., Methods: Sixty Wistar rats were divided randomly into three groups: control group, model group and simvastatin treatment group. Gastric gavage of vitamin D3 with high fat food was used to reproduce atherosclerotic rat model. The rats in the treatment group were treated with simvastatin of 2.5 mg x kg(-1) x d(-1) (gastric perfusion) 8 weeks after fat diet. The expression of the histopathology and protein of HMGB1 in atherosclerotic plaques of the aorta was observed by immunohistochemistry at 10 weeks and 12 weeks. The gene expression of HMGB1 at atherosclerotic plaques of aorta was observed with real time-polymerase chain reaction (RT-PCR). The morphology of the atherosclerotic plaques was observed., Results: The expression of HMGB1 increased significantly in atherosclerotic plaques in model group, and simvastatin could evidently inhibit the expression of HMGB1, and it was more obvious in 12-week group. Compared with control group, the HMGB1 mRNA expression was upregulated in all atherosclerotic model groups (10 weeks: 19.695+/- 1.418 vs. 2.981+/-0.753, 12 weeks: 20.542+/-1.132 vs. 3.219+/-0.332, both P<0.01). In the simvastatin treatment group, the gene expression of HMGB1 was lower than the age-match model group at 10 weeks (15.798+/-0.891) and 12 weeks (12.641+/-0.734), and in the 12-week treatment group it was lower than that in the 10-week treatment group (P<0.05 or P<0.01). In the model group, the ring-shape calcified atherosclerotic plaques were extensively found in the wall of the aorta. Simvastatin could obviously inhibit the formation of the atherosclerotic plaques, and the effect was more obvious in the 12-week treatment group than that of the 10-week treatment group., Conclusion: Simvastatin can alleviate the formation of the atherosclerotic plaques in the atherosclerotic rats, decrease the protein and mRNA expression of HMGB1. The results suggest that the vessels are protected from forming AS through alleviating inflammatory reaction.