Model simulation of inflow water to the Baltic Sea based on ¹²9I.

The semi-enclosed Baltic Sea represents a vital economic and recreational resource for more than 90 million people inhabiting its coasts. Extensive contamination of this sea by a variety of anthropogenic pollutants has raised the concern of the people in the region. Quantifying seawater inflow is crucial for estimating potential environmental risks as well as to find the best remedial strategy. We present here a model to estimate water inflow from the North Sea to the Baltic Sea by utilizing ¹²9I as a tracer. The results predicted inflow range of 230-450 km³/y with best fit value around 330 km³/y from the North Sea to the Baltic Sea during 1980-1999. Despite limited time series data on ¹²9I, the model presented here demonstrates a new management tool for the Baltic Sea to calculate inflow water compared to conventional methods (such as salinity, temperature and hydrographic models).

MicroRNA-320 expression in myocardial microvascular endothelial cells and its relationship with insulin-like growth factor-1 in type 2 diabetic rats.

1. The aim of the present study was to determine the role of myocardial microvascular endothelial cells (MMVEC) in impaired angiogenesis of type 2 diabetic Goto-Kakizaki (GK) rats. 2. A microRNA (miRNA) microarray was used to assess miRNA expression in MMVEC from GK and Wistar rats. Upregulation of miRNA-320 was observed in MMVEC from GK rats using real-time reverse transcription-polymerase chain reaction (RT-PCR). 3. So far, nine miRNAs have been reported to target angiogenic factors and/or receptors, including kinase insert domain containing receptor (Flk-1), insulin-like growth factor 1 (IGF-1) and insulin-like growth factor 1 receptor (IGF-1R). The predicted genes targeted by miR-320 include Flk-1, IGF-1 and IGF-1R. Western blot analysis and RT-PCR were used to analyse the protein and mRNA expression, respectively, of the putative genes IGF-1 and IGF-1R. The expression of IGF-1 and IGF-1R proteins decreased significantly in diabetic MMVEC. However, the expression of IGF-1 mRNA increased rather than decreased. The mRNA expression of IGF-1R did not differ significantly between diabetic and control MMVEC. 4. Transfection of an miR-320 inhibitor into MMVEC from GK rats confirmed that miR-320 impaired angiogenesis. The proliferation and migration of diabetic MMVEC improved after transfection of the miR-320 inhibitor. In addition, the miR-320 inhibitor significantly increased the expression of IGF-1 protein, but had no effect on the expression of IGF-1R. 5. Eleven miRNAs were upregulated in MMVEC from GK rats compared with those in Wistar rats: let-7e, miR-129, miR-291-5p, miR-320, miR-327, mir-333, miR-363-5p, miR-370, miR-494, miR-503 and miR-664. 6. The results indicate that upregulation of miR-320 in MMVEC from GK rats may be responsible for the inconsistency between the expression of IGF-1 protein and mRNA and therefore related to impaired angiogenesis in diabetes. Transfection of an miR-320 inhibitor may be a therapeutic approach for the treatment of impaired angiogenesis in diabetes.