Search

[Objective] Electric technology innovation is the key to promote energy technology revolution. This study aimed to clarify the strategic orientation of the electric technology innovation in China and examine its spatiotemporal pattern and sources, to provide a scientific evidence for accelerating China’s electric technology innovation. [Methods] Based on the statistical data of H02 patents, this study evaluated the spatial and temporal distribution characteristics of China’s electric technology innovation by constructing an absolute index, a relative index, and structural specialization coefficient. It analyzed the sources of the spatial differentiation of electric technology innovation from two dimensions of space and patent structure by using the Dagum Gini index and variance decomposition. [Results] The results show that: (1) The level of electric technology innovation showed an upward trend, and it decreased from the east to the west. The innovation capacity was mainly concentrated in the shape, structure, and application of electric products. (2) The spatial differentiation degree of the invention patent specialization coefficient was larger than that of the utility model patent, and the number of regions belonging to the utility model patent specialization category was more than that of the invention patent specialization category. (3) Compared with intraregional variation and superimposed over density, the interregional variation had a greater driving effect on the spatial differentiation of electric technology innovation. The utility model patents had a stronger driving effect on the spatial differentiation of electric technology innovation, while invention patents had the opposite effect. [Conclusion] This study contributes to coordinate the balanced development of regional electric technology innovation and explore the effective ways to improve the level of electric technology innovation.

Background Diabetic kidney disease (DKD) poses a significant challenge globally as a complication of diabetes. Hyaluronan (HA), a critical non-sulfated glycosaminoglycan in the extracellular matrix, plays a pivotal role in the progression of DKD. This study assesses the predictive significance of HA's corresponding receptor, RHAMM (receptor for HA-mediated motility), in DKD pathogenesis in type 2 diabetes (T2DM) patients. Methods Enzyme-linked immunosorbent assays were utilized to measure plasma and urine levels of HA, CD44 and RHAMM in 99 diabetic patients. Immunohistochemistry staining was employed to examine HA deposition, CD44 and RHAMM expressions from 18 biopsy-proven DKD patients. Spearman correlation analysis, linear regression and receiver operating characteristic (ROC) analysis were conducted to establish associations between plasma HA, CD44 and RHAMM levels, and clinical parameters in DKD patients with T2DM. Results Elevated plasma and urine HA, CD44 and RHAMM levels were notably observed in the severe renal dysfunction group. Plasma RHAMM exhibited positive correlations with HA (r = 0.616, P  < .001) and CD44 (r = 0.220, P  < .001), and a negative correlation with estimated glomerular filtration rate (eGFR) (r = –0.618, P  < .001). After adjusting for other potential predictors, plasma RHAMM emerged as an independent predictor of declining eGFR (β = –0.160, P  < .05). Increased HA, CD44 and RHAMM levels in kidney biopsies of DKD patients were closely associated with heightened kidney injury. The ROC curve analysis highlighted an area under the curve (AUC) of 0.876 for plasma RHAMM, indicating superior diagnostic efficacy compared to CD44 in predicting DKD pathogenesis. The combined AUC of 0.968 for plasma RHAMM, HA and CD44 also suggested even greater diagnostic potential for DKD pathogenesis. Conclusion These findings provide initial evidence that elevated RHAMM levels predict DKD pathogenesis in T2DM patients. The formation of a triple complex involving HA, CD44 and RHAMM on the cell surface shows promise as a targetable biomarker for early intervention to mitigate severe renal dysfunctions. [ABSTRACT FROM AUTHOR]

Circular RNA is a non-coding RNA that acts as a sponge for RNA, regulates cleavage and transcription, translates proteins and interacts with RNA-binding proteins. In recent years, studies have found that the abnormal expression of circular RNA in tumor tissues is closely related to the occurrence, development and prognosis of lung cancer and it is expected to be a biomarker for the diagnosis, treatment and prognosis of lung cancer. Therefore, this paper reviews the research progress of circular RNA as a biomarker of lung cancer.

Soluble epoxide hydrolase (sEH) catalyzes the conversion of epoxyeicosatrienoic acids into less active eicosanoids, and inhibitors of sEH have anti-inflammatory and antiapoptotic properties. Based on previous observations that sEH inhibition attenuates cisplatin-induced nephrotoxicity by modulating nuclear factor-κB signaling, we hypothesized that this strategy would also attenuate cisplatin-induced renal apoptosis. Inhibition of sEH with AR9273 [1-adamantan-1-yl-3-(1-methylsulfonyl-piperidin-4-yl-urea)] reduced cisplatin-induced apoptosis through mechanisms involving mitochondrial apoptotic pathways and by reducing reactive oxygen species. Renal mitochondrial Bax induction following cisplatin treatment was significantly decreased by treatment of mice with AR9273 and these antiapoptotic effects involved p38 mitogen-activated protein kinase signaling. Similar mechanisms contributed to reduced apoptosis in Ephx2(-/-) mice treated with cisplatin. Moreover, in pig kidney proximal tubule cells, cisplatin-induced mitochondrial trafficking of Bax and cytochrome c, caspase-3 activation, and oxidative stress are significantly attenuated in the presence of epoxyeicosatrienoic acids (EETs). Collectively, these in vivo and in vitro studies demonstrate a role for EETs in limiting cisplatin-induced renal apoptosis. Inhibition of sEH represents a novel therapeutic strategy for protection against cisplatin-induced renal damage.

Uncoupling protein 1 (UCP1) plays a central role in nonshivering thermogenesis in brown fat; however, its role in beige fat remains unclear. Here we report a robust UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca[sup.2+] cycling by sarco/endoplasmic reticulum Ca[sup.2+]-ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2). Inhibition of SERCA2b impairs UCP1-independent beige fat thermogenesis in humans and mice as well as in pigs, a species that lacks a functional UCP1 protein. Conversely, enhanced Ca[sup.2+] cycling by activation of [alpha]1- and/or [beta]3-adrenergic receptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes. In the absence of UCP1, beige fat dynamically expends glucose through enhanced glycolysis, tricarboxylic acid metabolism and pyruvate dehydrogenase activity for ATP-dependent thermogenesis through the SERCA2b pathway; beige fat thereby functions as a 'glucose sink' and improves glucose tolerance independently of body weight loss. Our study uncovers a noncanonical thermogenic mechanism through which beige fat controls whole-body energy homeostasis via Ca[sup.2+] cycling., Author(s): Kenji Ikeda [1, 2, 3]; Qianqian Kang [1, 2, 3]; Takeshi Yoneshiro [1, 2, 3]; Joao Paulo Camporez [4]; Hiroko Maki [5]; Mayu Homma [5]; Kosaku Shinoda [1, 2, [...]

Fatigue is related to a variety of chronic diseases and has become a hot research topic in recent years. Various bioactive components have been extracted from hairtail fish (Trichiurus lepturus); however, none of these studies involved the anti-fatigue activity of hairtail fish glycoprotein (HGP). Thus, antioxidant experiments were conducted in vitro, and the anti-fatigue activity of HGP was further evaluated in BALB/c mice. The effects of HGP on the behavior of BALB/c mice were verified by classical behavioral experiments, and the indicators related to anti-fatigue activity were detected. The results showed that the antioxidant capacity in vitro of HGP increased gradually in the concentration range of 10 to 100 mg/mL. HGP improved the exercise ability of the mice. HGP was also found to significantly (p < 0.05) reduce the serum levels of lactate dehydrogenase (LDH), blood lactic acid (BLA), blood urea nitrogen (BUN), and creatine kinase (CK). The contents of liver glycogen (LG) and muscle glycogen (MG) were also significantly (p < 0.05) increased by HGP. Malondialdehyde (MDA) content in the serum and brains of the mice was significantly (p < 0.05) reduced and catalase (CAT), glutathione peroxidase (GPX), and superoxide dismutase (SOD) were significantly (p < 0.05) increased by HGP, especially in the middle- and high-dose groups. These results enhance our understanding of the anti-fatigue function of HGP and lay an important foundation for the further development and utilization of hairtail fish resources. [ABSTRACT FROM AUTHOR]