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Grant support (GS) in the MEDLINE database refers to funding agencies and contract numbers. It is important for funding organizations to track their funding outcomes from the GS information. As such, how to accurately and automatically extract funding information from biomedical literature is challenging. In this paper, we present a pipeline system called GrantExtractor that is able to accurately extract GS information from fulltext biomedical literature. GrantExtractor effectively integrates several advanced machine learning techniques. In particular, we use a sentence classifier to identify funding sentences from articles first. A bi-directional LSTM and the CRF layer (BiLSTM-CRF), and pattern matching are then used to extract entities of grant numbers and agencies from these identified funding sentences. After removing noisy numbers by a multi-class model, we finally match each grant number with its corresponding agency. Experimental results on benchmark datasets have demonstrated that GrantExtractor clearly outperforms all baseline methods. It is further evident that GrantExtractor won the first place in Task 5C of 2017 BioASQ challenge, with achieving the Micro-recall of 0.9526 for 22,610 articles. Moreover, GrantExtractor has achieved the Micro F-measure score as high as 0.90 in extracting grant pairs. [ABSTRACT FROM AUTHOR]

Myocardial infarction and following reperfusion therapy-induced myocardial ischemia/reperfusion (I/R) injury have been recognized as an important subject of cardiovascular disease with high mortality. As the antiarrhythmic agent, Wenxin Granule (WXG) is widely used to arrhythmia and heart failure. In our pilot study, we found the antioxidative potential of WXG in the treatment of myocardial I/R. This study is aimed at investigating whether WXG could treat cardiomyocyte hypoxia/reoxygenation (H/R) injury by inhibiting oxidative stress in mitochondria. The H9c2 cardiomyocyte cell line was subject to H/R stimuli to mimic I/R injury in vitro . WXG was added to the culture medium 24 h before H/R exposing as pretreatment. Protein kinase C- δ (PKC- δ ) inhibitor rottlerin or PKC- δ lentivirus vectors were conducted on H9c2 cells to downregulate or overexpress PKC- δ protein. Then, the cell viability, oxidative stress levels, intracellular and mitochondrial ROS levels, mitochondrial function, and apoptosis index were analyzed. In addition, PKC- δ protein expression in each group was verified by western blot analysis. Compared with the control group, the PKC- δ protein level was significantly increased in the H/R group, which was remarkably improved by WXG or rottlerin. PKC- δ lentivirus vector-mediated PKC- δ overexpression was not reduced by WXG. WXG significantly improved H/R-induced cell injury, lower levels of SOD and GSH/GSSG ratio, higher levels of MDA, intracellular and mitochondrial ROS content, mitochondrial membrane potential and ATP loss, mitochondrial permeability transition pore opening, NOX2 activation, cytochrome C release, Bax/Bcl-2 ratio and cleaved caspase-3 increasing, and cell apoptosis. Similar findings were obtained from rottlerin treatment. However, the protective effects of WXG were abolished by PKC- δ overexpression, indicating that PKC- δ was a potential target of WXG treatment. Our findings demonstrated a novel mechanism by which WXG attenuated oxidative stress and mitochondrial dysfunction of H9c2 cells induced by H/R stimulation via inhibitory regulation of PKC- δ /NOX2/ROS signaling., Competing Interests: There is no conflict of interest in this article., (Copyright © 2020 Qihui Jin et al.)

Objective To investigate the vasodilative and endothelial-protective effects and the underlying mechanisms of total flavonoids from Astragalus (TFA). Methods The vasodilative activities of TFA were measured with a myograph ex vivo using rat superior mesenteric arterial rings. The primary human umbilical vein endothelial cell (HUVEC) viabilities were assayed using the cell counting kit-8 after hypoxia or normoxia treatment with or without TFA. Akt, P-Akt, eNOS, P-eNOS, Erk, P-Erk, Bcl-2 and Bax expression were analyzed using western blotting. Results TFA showed concentration-dependent vasodilative effects on rat superior mesenteric arterial rings, but had no effects on normal or potassium chloride precontracted arterial rings. TFA did not affect HUVEC viabilities in normoxia, but dramatically promoted cell proliferation in the concentration range of 1 to 30 µg/mL under hypoxia. Moreover, TFA significantly increased the ratios of P-Akt/Akt and P-eNOS/eNOS in vascular endothelial cells under hypoxic conditions, but did not change the P-Erk/Erk or Bcl-2/Bax ratios. Conclusions TFA might exhibit vasorelaxant and endothelial-protective effects via the Akt/eNOS signaling pathway.