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The formation of rodingites has been a continually controversial topic, largely due to the absence of minerals that can be unambiguously dated. Here, we present a case study that utilized LA‐ICPMS garnet U–Pb dating, in conjunction with field investigations, petrology and Raman spectroscopy, to reveal the age and petrogenesis of rodingite in the northern North China Craton. The rodingites are spatially associated with mafic and alkaline rocks. Our findings indicate that rodingitization occurred at ca. 388 Ma, making it about 5–10 Myr younger than its mafic protoliths, but contemporaneous with the adjoining alkaline plutons. These observations suggest that the rodingitization may be attributed to hydrothermal fluids from the alkaline magmas. Our study emphasizes the importance of utilizing garnet U–Pb dating to determine the timing of rodingitization and introduces a novel perspective on the relationship between rodingitization and alkaline magmas in extensional continental settings. [ABSTRACT FROM AUTHOR]

Ancient orogens within the supercontinent like Columbia can remain stable evolution as long as the cratons. What kind of lithospheric mantle was beneath those orogens and how it evolved into a stable state are still enigmatic. The Trans‐North China orogen (TNCO) is one of the typical collisional orogens within the Columbia supercontinent and was formed at ca. 1.85 Ga. Our work reveals that a cluster of kimberlites intruded the orogenic belt at ca. 1.54 Ga. These rocks were originally generated under a thick lithosphere (>200 km). Their entrained olivine cores show a composition of overlapping olivines from refractory mantle peridotites. The results suggest a thick and refractory lithospheric mantle beneath the TNCO at ca. 1.54 Ga. Such craton‐like property may result from large volume melt extraction from the lithospheric mantle, possibly caused by the ca. 1.78 Ga large igneous event, which eventually induces the long‐term stability of the TNCO during the subsequent supercontinent cycle. [ABSTRACT FROM AUTHOR]

Aim: To explore the effect of epidermal growth factor receptor (EGFR) inhibition by erlotinib and EGFR siRNA on epidermal growth factor (EGF)-induced activation of retinal pigment epithelium (RPE) cells., Methods: Human RPE cell line (ARPE-19 cells) was activated by 100 ng/mL EGF. Erlotinib and EGFR siRNA were used to intervene EGF treatment. Cellular viability, proliferation, and migration were detected by methyl thiazolyl tetrazolium (MTT) assay, bromodeoxyuridine (BrdU) staining assay and wound healing assay, respectively. EGFR/protein kinase B (AKT) pathway proteins and N-cadherin, α-smooth muscle actin (α-SMA), and vimentin were tested by Western blot assay. EGFR was also determined by immunofluorescence staining., Results: EGF treatment for 24h induced a significant increase of ARPE-19 cells' viability, proliferation and migration, phosphorylation of EGFR/AKT proteins, and decreased total EGFR expression. Erlotinib suppressed ARPE-19 cells' viability, proliferation and migration through down regulating total EGFR and AKT protein expressions. Erlotinib also inhibited EGF-induced an increase of proliferative and migrative ability in ARPE-19 cells and clearly suppressed EGF-induced EGFR/AKT proteins phosphorylation and decreased expression of N-cadherin, α-SMA, and vimentin proteins. Similarly, EGFR inhibition by EGFR siRNA significantly affected EGF-induced an increase of cell proliferation, viability, and migration, phosphorylation of EGFR/AKT proteins, and up-regulation of N-cadherin, α-SMA, and vimentin proteins., Conclusion: Erlotinib and EGFR-knockdown suppress EGF-induced cell viability, proliferation, and migration via EGFR/AKT pathway in RPE cells. EGFR inhibition may be a possible therapeutic approach for proliferative vitreoretinopathy (PVR)., Competing Interests: Conflicts of Interest: Zhu YS, None; Zhou SR, None; Zhang HH, None; Wang T, None; Chen XD, None., (International Journal of Ophthalmology Press.)

Aim: To explore the effects of hepatocyte growth factor (HGF) on retinal pigment epithelium (RPE) cell behaviors., Methods: The human adult retinal pigment epithelial cell line-19 (ARPE-19) were treated by HGF or mesenchymal-epithelial transition factor (MET) inhibitor SU11274 in vitro . Cell viability was detected by a Cell Counting Kit-8 assay. Cell proliferation and motility was detected by a bromodeoxyuridine incorporation assay and a wound healing assay, respectively. The expression levels of MET, phosphorylated MET, protein kinase B (AKT), and phosphorylated AKT proteins were determined by Western blot assay. The MET and phosphorylated MET proteins were also determined by immunofluorescence assay., Results: HGF increased ARPE-19 cells' viability, proliferation and migration, and induced an increase of phosphorylated MET and phosphorylated AKT proteins. SU11274 significantly reduced cell viability, proliferation, and migration and decreased the expression of MET and AKT proteins. SU11274 suppressed HGF-induced increase of viability, proliferation, and migration in ARPE-19 cells. Additionally, SU11274 also blocked HGF-induced phosphorylation of MET and AKT proteins., Conclusion: HGF enhances cellular viability, proliferation, and migration in RPE cells through the MET/AKT signaling pathway, whereas this enhancement is suppressed by the MET inhibitor SU11274. HGF-induced MET/AKT signaling might be a vital contributor of RPE cells survival., Competing Interests: Conflicts of Interest: Zhou SR, None; Zhu YS, None; Yuan WT, None; Pan XY, None; Wang T, None; Chen XD, None., (International Journal of Ophthalmology Press.)

Aim: To evaluate the clinical efficacy and systemic safety profile of conbercept in clinical practice on vascular endothelial growth factor (VEGF)-A, VEGF-B, and placental growth factor (PLGF) levels after intravitreal injections for the neovascular age-related macular degeneration (AMD)., Methods: Thirty-five patients (35 eyes) with neovascular AMD received intravitreal injections of conbercept treatment with pro re nata protocol. Best-corrected visual acuity (BCVA) and central retinal thickness (CRT) were detected before the intravitreal injection and at 1, 3, and 12mo after conbercept treatment. The levels of serum VEGF-A, VEGF-B, and PLGF were measured by enzyme-linked immunosorbent assay before the injection and 1 and 12mo after conbercept treatments., Results: At baseline, the mean BCVA score was 39.89±14.64 letters. The mean BCVA scores were 51.03±15.78, 56.71±14.38, and 52.49±10.16 letters at 1, 3, and 12mo after conbercept treatment, and the BCVA improvements were all significant, respectively ( P <0.05). At baseline, the mean CRT was 436.7±141.9 µm. At 1, 3, and 12mo after conbercept treatment, the mean CRT values were 335.1±147.8, 301.1±116.5, and 312.2±98.22 µm, and the CRT improvements were all significant, respectively ( P <0.05). At baseline, 1 and 12mo after conbercept treatment, the mean levels of serum VEGF-A were 1013.8±454.3, 953.1±426.4, and 981.5±471.7 pg/mL, the mean levels of serum VEGF-B were 46.93±24.76, 42.99±19.16, and 45.32±18.76 pg/mL, the mean levels of serum PLGF at these points were 251.7±154.9, 241.3±166.7, and 245.6±147.2 pg/mL, respectively. Compared with the baseline, the levels of serum VEGF-A, VEGF-B, and PLGF did not significantly change at 1 and 12mo after conbercept treatment, respectively ( P >0.05)., Conclusion: Conbercept intravitreal injection leads to BCVA and CRT improvement, however, it does not significantly affect systemic serum VEGF-A, VEGF-B, and PLGF levels at 1 and 12mo after intravitreal injection treating neovascular AMD., (International Journal of Ophthalmology Press.)