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In order to examine the intensity of surficial sediment resuspension in Lake Taihu, a large shallow lake in eastern China, suspended sediment concentrations (SSCs) were measured on the basis of analysis of water samples collected using an innovative multi-level water sampler. The results show that under calm weather conditions, the SSC is relatively homogenous through the entire water column. However, when strong winds occur, the SSC in the bottom layer is 1-2 orders of magnitude greater than in the surface layer; thus, in this case, the amount of total suspended matter in the water column cannot be estimated using the SSC values of the surface layer alone. Furthermore, the depth of disturbance, or the thickness of the sediment layer that is set in motion by wind-wave induced currents, is of the order of 10 0 mm.

ObjectiveThis paper investigated the effects of STAT3 through promoting FOXP1 transcription on proliferation, apoptosis and invasion in glioma cells.MethodsQuantitative real‐time PCR (qRT‐PCR) and Western blot assay were administered to assess the mRNA and protein expression levels of STAT3 and FOXP1 in glioma tissues and cells, respectively. Luciferase reporter and Chromatin Immunoprecipitation (ChIP) assays were implemented to determine the correlation between STAT3 and FOXP1. MTT and colony formation assays were conducted to identify cell growth. Flow cytometry was run to detect the cell apoptosis rate of glioma cells. Transwell assays were conducted to reveal cell invasion ability.ResultsThe mRNA and protein expression levels of STAT3 were highly expressed in glioma tissues and cells. After cells transfected with siRNA of STAT3, both STAT3 and FOXP1 were simultaneously downregulated. STAT3 directly regulated FOXP1 transcription. STAT3 promoted cell proliferation, inhibited cell apoptosis and enhanced cell invasion through promoting FOXP1 transcription in glioma cells.ConclusionIn summary, STAT3 gene was a transcriptional regulator of FOXP1. Depleted STAT3 restrained cell proliferation and invasion, promoted cell apoptosis in glioma cells. This molecular mechanism between STAT3 and FOXP1 can serve as a therapeutic target for glioma treatment.