0.05 ). CONCLUSION: The qualities of Flos lonicerae from the four different areas were almost the same as that of the control. This method can be used to judge the appraisal of the Flos lonicerae and to distinguish between genuine and counterfeit Flos lonicerae.

Objective To discuss the relationship between the injury patterns of medial patellofemoral ligament(MPFL) and injury degrees of vastus medialis obliquus(VMO) after acute patellar dislocation(PD). Methods Knee joint MRI was performed in 79 patients with acute PD. Images were acquired and evaluated using standardised protocols. Injury patterns of MPFL were grouped by severity (partial tear and complete tear)and location (isolated patellar-side tear (PAT), isolated femoral-side tear (FEM) and combined tear (COM) ) for analysis of the prevalence of VMO injury. The VMO elevation was calculated on sagittal and coronal planes. Results The prevalence rates of MPFL tear and VMO lesion were 96.2%(76/79)and 54.4%(43/79)after acute PD.The prevalence rate of VMO lesion was 40.6%(13/32)and 68.2%(30/44)in the partial and complete MPFL tear subgroups,respectively.Complete MPFL tear subgroup showed higher prevalence rate of VMO lesion when compared with partial tear subgroup(χ2=5.727, P=0.017). The prevalence rates of VMO lesion in the PAT, FEM and COM subgroups were 31.8% (7/22), 67.7% (21/31) and 70% (14/20), respectively. There were statistically significant differences among them(χ2=8.549,P=0.014).About the mean VMO elevation,there were statistically significant differences between the complete and partial MPFL tear subgroups, the FEM and PAT subgroups, and the COM and PAT subgroups (P=0.00). Conclusions Compared with partial MPFL tear, complete tear predisposes to VMO lesion and has a higher elevation of the torn VMO after acute PD.The femoral-sided and combined MPFL tears predispose to VMO lesion and have higher elevations of the torn VMO.

BACKGROUND: Angiogenesis is described as a complex process in which new microvessels sprout from endothelial cells of existing vasculature. This study aimed to determine whether long non-coding RNA (lncRNA) H19 induced the angiogenesis of gastric cancer (GC) and its possible mechanism. METHODS: Gene expression level was determined by quantitative real-time polymerase chain reaction and western blotting. Cell counting kit-8, transwell, 5-Ethynyl-2'-deoxyuridine (EdU), colony formation assay, and human umbilical vein endothelial cells (HUVECs) angiogenesis assay as well as Matrigel plug assay were conducted to study the proliferation, migration, and angiogenesis of GC in vitro and in vivo . The binding protein of H19 was found by RNA pull-down and RNA Immunoprecipitation (RIP). High-throughput sequencing was performed and next Gene Ontology (GO) as well as Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis was conducted to analyze the genes that are under H19 regulation. Methylated RIP (me-RIP) assay was used to investigate the sites and abundance among target mRNA. The transcription factor acted as upstream of H19 was determined through chromatin immunoprecipitation (ChIP) and luciferase assay. RESULTS: In this study, we found that hypoxia-induced factor (HIF)-1α could bind to the promoter region of H19, leading to H19 overexpression. High expression of H19 was correlated with angiogenesis in GC, and H19 knocking down could inhibit cell proliferation, migration and angiogenesis. Mechanistically, the oncogenic role of H19 was achieved by binding with the N 6 -methyladenosine (m 6 A) reader YTH domain-containing family protein 1 (YTHDF1), which could recognize the m 6 A site on the 3'-untransated regions (3'-UTR) of scavenger receptor class B member 1 (SCARB1) mRNA, resulting in over-translation of SCARB1 and thus promoting the proliferation, migration, and angiogenesis of GC cells. CONCLUSION HIF-1α induced overexpression of H19 via binding with the promoter of H19, and H19 promoted GC cells proliferation, migration and angiogenesis through YTHDF1/SCARB1, which might be a beneficial target for antiangiogenic therapy for GC.
Humans ; Cell Line, Tumor ; Cell Proliferation/genetics* ; Endothelial Cells/metabolism* ; Gene Expression Regulation ; Gene Expression Regulation, Neoplastic/genetics* ; Hypoxia ; MicroRNAs/genetics* ; RNA ; RNA, Long Noncoding/metabolism* ; RNA-Binding Proteins/metabolism* ; Scavenger Receptors, Class B/metabolism* ; Stomach Neoplasms/genetics*