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Preparation and properties of the green-emitting phosphors NaCa0.98-xMgxPO4:
Bo Yue,Juan Gu,Guangfu Yin,Zhongbing Huang,Xiaoming Liao,Yadong Yao,Yunqing Kang,Panli You 한국물리학회 2010 Current Applied Physics Vol.10 No.4
In this study, a series of the green-emitting phosphors NaCa0.98-xMgxPO4:Eu2þ 0:02 was prepared through high temperature solid-state reaction. The structure and spectroscopic properties of these samples were characterized by XRD, FT-IR, reflectance spectra and photoluminescence (PL) spectra, respectively. The effect of Mg2+ co-doping concentration on the PL intensity of as-prepared samples was also investigated. The enhanced intensities of excitation and emission band of Eu2+ and a slight red-shift of the emission peak were observed due to Mg2+ co-doping. When the x value is 0.08, the phosphors possessed the maximum emission intensity monitored at 360 nm and the emission spectrum shows a single band centered at about 500 nm. The obtained phosphors had strong absorption in near-UV zone (350–400 nm), which can match the emission of near-UV light-emitting diodes. The prepared material is potential green phosphors for white LEDs.
Xiao-hui Liao,Rui-ting Long,Jun-bo Peng,Li-li Huang,Gui-ping Jiang,Yue-juan Liao,Hang Sun,Yu-dong Hu 한국분자세포생물학회 2019 Molecules and cells Vol.42 No.12
Mitochondria are highly dynamic organelles that constantly undergo fission and fusion processes that closely related to their function. Disruption of mitochondrial dynamics has been demonstrated in acute kidney injury (AKI), which could eventually result in cell injury and death. Previously, we reported that augmenter of liver regeneration (ALR) alleviates renal tubular epithelial cell injury. Here, we gained further insights into whether the renoprotective roles of ALR are associated with mitochondrial dynamics. Changes in mitochondrial dynamics were examined in experimental models of renal ischemia-reperfusion (IR). In a model of hypoxia-reoxygenation (HR) injury in vitro, dynamin-related protein 1 (Drp1) and mitochondrial fission process protein 1 (MTFP1), two key proteins of mitochondrial fission, were downregulated in the Lv-ALR + HR group. ALR overexpression additionally had an impact on phosphorylation of Drp1 Ser637 during AKI. The inner membrane fusion protein, Optic Atrophy 1 (OPA1), was significantly increased whereas levels of outer membrane fusion proteins Mitofusin-1 and -2 (Mfn1, Mfn2) were not affected in the Lv-ALR + HR group, compared with the control group. Furthermore, the mTOR/4E-BP1 signaling pathway was highly activated in the Lv-ALR + HR group. ALR overexpression led to suppression of HR-induced apoptosis. Our collective findings indicate that ALR gene transfection alleviates mitochondrial injury, possibly through inhibiting fission and promoting fusion of the mitochondrial inner membrane, both of which contribute to reduction of HK-2 cell apoptosis. Additionally, fission processes are potentially mediated by promoting tubular cell survival through activating the mTOR/4E-BP1 signaling pathway.
Han Deng,Zhaoxia Wang,Limin Liao,Juan Wu,Yue Wang 대한배뇨장애요실금학회 2022 International Neurourology Journal Vol.26 No.S1
Purpose: To determine the risk factors predicting upper urinary tract (UUT) damage using a grading system for upper urinary tract dilation (UUTD) and a descriptive system for all urinary tract dysfunction (AUTD) in patients with myelodysplasia. Methods: Six hundred thirty-seven patients with myelodysplasia were evaluated at our center from January 2008 to November 2019. Clinical data, ultrasonography, magnetic resonance urography, and video-urodynamics (VUDS) parameters were collected. Univariate and multivariate analyses were used to determine the risk factors predicting UUT damage. Results: Three hundred eighty-three males and 254 females were included. The average course of lower urinary tract symptoms (LUTS) was 14.08±7.07 years (range, 3–31 years). The urodynamic diagnoses of all patients were as follows: detrusor overactivity, 26.8%; detrusor underactivity, 6.44%; and acontractile detrusor, 66.72%. UUT damage was determined in 66.56% of the patients. Of the patients, 28.73 % had vesicoureteral reflux (VUR) during filling (bilateral, n=50; unilateral, n=133) on fluoroscopy during VUDS testing. Two hundred thirty-four patients had UUTD (bilateral, n=203; unilateral, n=31). The occurrence of hydronephrosis based on ultrasonography was closely related to ipsilateral VUR (P<0.05). Absent of bladder sensation, long-term course of LUTS, decreased maximum cystometric capacity (MCC) and bladder compliance (BC), and increased postvoid residual urine (PVR) were shown to be independent risk factors in logistic regression analysis. Conclusions: This retrospective study using UUTD and AUTD systems indicated that patients with myelodysplasia have a high incidence of UUT damage. Absence of bladder sensation, long-term course of LUTS, decreased MCC and BC, and increased PVR were independent risk factors predicting UUT damage.
Long, Rui-ting,Peng, Jun-bo,Huang, Li-li,Jiang, Gui-ping,Liao, Yue-juan,Sun, Hang,Hu, Yu-dong,Liao, Xiao-hui Korean Society for Molecular and Cellular Biology 2019 Molecules and cells Vol.42 No.12
Mitochondria are highly dynamic organelles that constantly undergo fission and fusion processes that closely related to their function. Disruption of mitochondrial dynamics has been demonstrated in acute kidney injury (AKI), which could eventually result in cell injury and death. Previously, we reported that augmenter of liver regeneration (ALR) alleviates renal tubular epithelial cell injury. Here, we gained further insights into whether the renoprotective roles of ALR are associated with mitochondrial dynamics. Changes in mitochondrial dynamics were examined in experimental models of renal ischemia-reperfusion (IR). In a model of hypoxia-reoxygenation (HR) injury in vitro, dynamin-related protein 1 (Drp1) and mitochondrial fission process protein 1 (MTFP1), two key proteins of mitochondrial fission, were downregulated in the Lv-ALR + HR group. ALR overexpression additionally had an impact on phosphorylation of Drp1 Ser637 during AKI. The inner membrane fusion protein, Optic Atrophy 1 (OPA1), was significantly increased whereas levels of outer membrane fusion proteins Mitofusin-1 and -2 (Mfn1, Mfn2) were not affected in the Lv-ALR + HR group, compared with the control group. Furthermore, the mTOR/4E-BP1 signaling pathway was highly activated in the Lv-ALR + HR group. ALR overexpression led to suppression of HR-induced apoptosis. Our collective findings indicate that ALR gene transfection alleviates mitochondrial injury, possibly through inhibiting fission and promoting fusion of the mitochondrial inner membrane, both of which contribute to reduction of HK-2 cell apoptosis. Additionally, fission processes are potentially mediated by promoting tubular cell survival through activating the mTOR/4E-BP1 signaling pathway.