Synthesis Design and Properties of Ca5(BO3)3F: Bi3+/Eu3+: Insight into Luminescence, Temperature, and Pressure Sensing.

Nowadays, the utilization of noncontact temperature and pressure sensing is experiencing growing popularity. In this work, Bi3+, Eu3+-doped Ca5(BO3)3F (CBOF) phosphors were synthesized via an ionic liquid-assisted electrospinning approach. The effect of molecular weight of polyvinylpyrrolidone on the morphology of CBOF was investigated, and a comprehensive analysis of its formation mechanism was presented. The luminescence properties of CBOF: Bi3+, Eu3+ were studied systematically. The temperature-dependent emission of CBOF: Bi3+, Eu3+ phosphor was discussed, and it displayed thermal sensitivity, which can be attributed to the distinct thermal response emission behaviors of Bi3+ and Eu3+. The investigation of the pressure-dependent emission behavior of the CBOF: Bi3+ phosphor revealed an anomalous phenomenon: with the increase of pressure, the emission peak showed a trend of first a blue shift and then a red shift. This anomaly was discussed in detail. The phosphor exhibits visual color change (blue to cyan), remarkable pressure sensitivity (4.76 nm/GPa), and a high upper pressure limit (24.2 GPa), indicating its potential use as an optical pressure sensor. Consequently, this study presents an innovative synthetic approach for fabricating CBOF, presenting a bifunctional material with promising prospects in the fields of temperature and pressure sensing.

Pressure-Triggered Fluorescence Intensity Ratio Variations of YNbO4:Bi3+/Ln3+ (Ln = Eu or Sm) for High-Sensitivity Optical Pressure Sensing.

Optical pressure sensing by phosphors is a growing area of research. However, the main pressure measurement methods rely on the movement of the central peak position, which has significant drawbacks for practical applications. This paper demonstrates the feasibility of using the fluorescence intensity ratio (FIR) of different emission peaks for pressure sensing. The FIR (IBi3+/ILn3+) values of the synthesized YNbO4:Bi3+/Ln3+ (Ln = Eu or Sm) phosphors are all first-order exponentially related to pressure, and YNbO4:Bi3+/Ln3+ (Ln = Eu or Sm) phosphors have high pressure-sensing sensitivities (Sp and Spr), which are 6 times higher than those from our previously reported work. In addition, the changes in FIR values during the decompression process were also calculated, and the trend was similar to that during the compression process. The YNbO4:Bi3+,Eu3+ phosphor has better pressure recovery performance. In summary, the YNbO4:Bi3+/Ln3+ (Ln = Eu or Sm) phosphors reported in this paper are expected to be applied in the field of optical pressure sensing, and this study provides a new approach and perspective for designing new phosphors for pressure measurement.

A single administration of FGF2 after renal ischemia-reperfusion injury alleviates post-injury interstitial fibrosis.

BACKGROUND: Despite lack of clinical therapy in acute kidney injury (AKI) or its progression to chronic kidney disease (CKD), administration of growth factors shows great potential in the treatment of renal repair and further fibrosis. At an early phase of AKI, administration of exogenous fibroblast growth factor 2 (FGF2) protects against renal injury by inhibition of mitochondrial damage and inflammatory response. Here, we investigated whether this treatment attenuates the long-term renal interstitial fibrosis induced by ischemia-reperfusion (I/R) injury. METHODS: Unilateral renal I/R with contralateral nephrectomy was utilized as an in vivo model for AKI and subsequent CKD. Rats were randomly divided into four groups: Sham-operation group, I/R group, I/R-FGF2 group and FGF2-3D group. These groups were monitored for up to 2 months. Serum creatinine, inflammatory response and renal histopathology changes were detected to evaluate the role of FGF2 in AKI and followed renal interstitial fibrosis. Moreover, the expression of vimentin, α-SMA, CD31 and CD34 were examined. RESULTS: Two months after I/R injury, the severity of renal interstitial fibrosis was significantly attenuated in both of I/R-FGF2 group and FGF2-3D group, compared with the I/R group. The protective effects of FGF2 administration were associated with the reduction of high-mobility group box 1 (HMGB1)-mediated inflammatory response, the inhibition of transforming growth factor beta (TGF-ß1)/Smads signaling-induced epithelial-mesenchymal transition and the maintenance of peritubular capillary structure. CONCLUSIONS: A single dose of exogenous FGF2 administration 1 h or 3 days after reperfusion inhibited renal fibrogenesis and thus blocked the transition of AKI to CKD. Our findings provided novel insight into the role of FGF signaling in AKI-to-CKD progression and underscored the potential of FGF-based therapy for this devastating disease.

Activation of autophagy contributes to the renoprotective effect of postconditioning on acute kidney injury and renal fibrosis.

Ischemia/Reperfusion injury contributes to acute kidney injury (AKI) and subsequent chronic kidney disease (CKD) including renal fibrosis. Autophagy is a cytoplasmic components degradation pathway that has complex function in the development of various diseases such as fibrosis in kidney. Our previous work demonstrated that postconditioning (POC) showed excellent therapeutic effect on renal fibrosis via inhibiting the overproduction of reactive oxygen species (ROS) after reperfusion. But the connection of autophagy and POC in the renoprotective effect remains unclear. Here, we defined the relevance of autophagy and POC in the protective effect on AKI and subsequent renal fibrosis. We found that at two days after I/R injury, POC largely reduced renal tubular epithelial cell apoptosis and improved renal function; autophagy was significantly activated in kidneys of the POC rats. At two months after reperfusion, the I/R injury rats displayed severe renal fibrosis and epithelial-mesenchymal transition (EMT), whereas these were remarkably attenuated in the POC treated rats. Overall, our results demonstrated that POC could reduce renal damage and attenuate the degree of EMT after I/R injury via enhanced activation of autophagy.

Effect of interaction between Pd and Fe in modified red mud on catalytic decomposition of toluene.

As an industrial solid waste produced by alumina industry, red mud was modified as support of Pd catalysts for toluene catalytic oxidation in this paper. The xPd/MRM catalysts had high activity for toluene catalytic oxidation, and the 0.3Pd/MRM catalyst showed the best catalytic performance (T50 = 175 °C and T100 = 200 °C). The results indicated that the prepared 0.3Pd/MRM catalyst had more ratio of surface-adsorbed oxygen and Fe3+, rather than MRM and RM, which benefitted to the toluene oxidation. The excessive Pd species and the growth of the PdO nanoparticles negatively affected the catalytic efficiency of toluene. 0.4Pd/MRM activity decreased because of PdO aggregation in the catalyst, which could be confirmed by TEM analysis. The results of XPS, H2-TPR, FT-IR, O2-TPD, and Raman examination revealed that the formation of Pd-O-Fe under the interaction between Fe in MRM and Pd (Pd2+ + Fe 2+ → Pd0 + Fe3+) increased the electron transfer and raised the mobility of surface-adsorbed oxygen. Furthermore, in situ DRIFTS and GC-MS were used to detect intermediate products of catalytic reactions, and the reaction mechanism of catalysts was also studied. The catalytic oxidation of toluene on 0.3Pd/MRM catalyst might have two reaction paths simultaneously. The first reaction path would be toluene → species benzyl → benzaldehyde → benzoic acid → long-chain aldehydes or carboxylic acids → CO2 and H2O. The second reaction path would be toluene → benzene → phenol → long-chain aldehydes or carboxylic acids → CO2 and H2O.

Corrigendum: FGF10 Protects Against Renal Ischemia/Reperfusion Injury by Regulating Autophagy and Inflammatory Signaling.

[This corrects the article DOI: 10.3389/fgene.2018.00556.].

Fibroblast Growth Factor 10 Attenuates Renal Damage by Regulating Endoplasmic Reticulum Stress After Ischemia-Reperfusion Injury.

Renal ischemia-reperfusion (I/R) injury is a predominant cause of acute kidney injury (AKI), the pathologic mechanism of which is highly complex involving reactive oxygen species (ROS) accumulation, inflammatory response, autophagy, apoptosis as well as endoplasmic reticulum (ER) stress. Fibroblast growth factor 10 (FGF10), as a multifunctional growth factor, plays crucial roles in embryonic development, adult homeostasis, and regenerative medicine. Herein, we investigated the molecular pathways underlying the protective effect of FGF10 on renal I/R injury using Sprague-Dawley rats. Results showed that administration of FGF10 not only effectively inhibited I/R-induced activation of Caspase-3 and expression of Bax, but also alleviated I/R evoked expression of ER stress-related proteins in the kidney including CHOP, GRP78, XBP-1, and ATF-4 and ATF-6. The protective effect of FGF10 against apoptosis and ER stress was recapitulated by in vitro experiments using oxidative damaged NRK-52E cells induced by tert-Butyl hydroperoxide (TBHP). Significantly, U0126, a selective noncompetitive inhibitor of MAP kinase kinases (MKK), largely abolished the protective role of FGF10. Taken together, both in vivo and in vitro experiments indicated that FGF10 attenuates I/R-induced renal epithelial apoptosis by suppressing excessive ER stress, which is, at least partially, mediated by the activation of the MEK-ERK1/2 signaling pathway. Therefore, our present study revealed the therapeutic potential of FGF10 on renal I/R injury.

Fibroblast Growth Factor 2 Attenuates Renal Ischemia-Reperfusion Injury via Inhibition of Endoplasmic Reticulum Stress.

Acute kidney injury (AKI) is a serious clinical disease that is mainly caused by renal ischemia-reperfusion (I/R) injury, sepsis, and nephrotoxic drugs. The pathologic mechanism of AKI is very complex and may involve oxidative stress, inflammatory response, autophagy, apoptosis, and endoplasmic reticulum (ER) stress. The basic fibroblast growth factor (FGF2) is a canonic member of the FGF family that plays a crucial role in various cellular processes, including organ development, wound healing, and tissue regeneration. However, few studies have reported the potential therapeutic effect of FGF2 in the repair of renal ischemic injury in the past two decades. In the present study, we investigated the protective effect of FGF2 on renal I/R injury using Sprague-Dawley and NRK-52E cells. Our results showed that FGF2 significantly attenuates the apoptosis of kidney tissues after I/R injury through the inhibition of excessive ER stress. Moreover, FGF2 also alleviated the excessive ER stress and apoptosis in cultured NRK-52E cells injured by tert-Butyl hydroperoxide (TBHP). Significantly, phosphatidylinositol 3-kinase (PI3K)-selective inhibitor LY294002 and mitogen-activated protein kinase kinase (MEK)-selective inhibitor U0126 were utilized in the present study to examine the protective mechanism of FGF2. Our in vitro experimental results confirmed that both LY294002 and U0126 largely abolished the protective effect of FGF2. Taken together, the findings of the present study indicated that FGF2 attenuates I/R-induced renal epithelial apoptosis by suppressing excessive ER stress via the activation of the PI3K/AKT and MEK-ERK1/2 signaling pathways.

FGF10 Protects Against Renal Ischemia/Reperfusion Injury by Regulating Autophagy and Inflammatory Signaling.

Ischemia-reperfusion (I/R) is a common cause of acute kidney injury (AKI), which is associated with high mortality and poor outcomes. Autophagy plays important roles in the homeostasis of renal tubular cells (RTCs) and is implicated in the pathogenesis of AKI, although its role in the process is complex and controversial. Fibroblast growth factor 10 (FGF10), a multifunctional FGF family member, was reported to exert protective effect against cerebral ischemia injury and myocardial damage. Whether FGF10 has similar beneficial effect, and if so whether autophagy is associated with the potential protective activity against AKI has not been investigated. Herein, we report that FGF10 treatment improved renal function and histological integrity in a rat model of renal I/R injury. We observed that FGF10 efficiently reduced I/R-induced elevation in blood urea nitrogen, serum creatinine as well as apoptosis induction of RTCs. Interestingly, autophagy activation following I/R was suppressed by FGF10 treatment based on the immunohistochemistry staining and immunoblot analyses of LC3, Beclin-1 and SQSTM1/p62. Moreover, combined treatment of FGF10 with Rapamycin partially reversed the renoprotective effect of FGF10 suggesting the involvement of mTOR pathway in the process. Interestingly, FGF10 also inhibited the release of HMGB1 from the nucleus to the extracellular domain and regulated the expression of inflammatory cytokines such as TNF-α, IL-1ß and IL-6. Together, these results indicate that FGF10 could alleviate kidney I/R injury by suppressing excessive autophagy and inhibiting inflammatory response and may therefore have the potential to be used for the prevention and perhaps treatment of I/R-associated AKI.