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Pirfenidone (esbiret) is an established anti-fibrotic and anti-inflammatory drug used to treat idiopathic pulmonary fibrosis. In the present study, the dose-dependent effects of pirfenidone on the cell cycle, proliferation and expression of heat shock protein (HSP)-47 and collagen type I in a cultured rat hepatic stellate cell line (HSC-T6) were investigated. Following pirfenidone treatment, cell proliferation was determined using the cell counting kit-8 assay and the cell cycle was measured using flow cytometry. HSP-47 expression was estimated using western blot analysis and collagen type I mRNA was assessed using reverse transcription quantitative polymerase chain reaction. Pirfenidone induced significant dose-dependent inhibition of proliferation in HSC-T6 cells. Cell viability was unaffected by treatment with pirfenidone (0, 10 or 100 µM) for 24 and 72 h. However, after 24 h, HSC-T6 cells exhibited dose-dependent decreases in HSP-47 protein and collagen I mRNA levels. In conclusion, pirfenidone inhibited HSC-T6 cell proliferation, arrested the cell cycle and reduced the expression of HSP-47 and collagen type I, indicating that pirfenidone may be a promising drug in the treatment of liver fibrosis. [ABSTRACT FROM AUTHOR]

We study a crowdsourcing-based diagnosis algorithm, which is against the fact that currently we do not lack medical staff, but high level experts. Our approach is to make use of the general practitioners' efforts: For every patient whose illness cannot be judged definitely, we arrange for them to be diagnosed multiple times by different doctors, and we collect the all diagnosis results to derive the final judgement. Our inference model is based on the statistical consistency of the diagnosis data. To evaluate the proposed model, we conduct experiments on both the synthetic and real data; the results show that it outperforms the benchmarks. [ABSTRACT FROM AUTHOR]

Doxorubicin (DOX) has been widely used to treat cancers as a first-line antitumor drug. However, it causes severe, irreversible, dose-dependent cardiotoxicity. To evaluate the protective effects of naringin (NRG) on cardiotoxicity, the authors investigated the molecular mechanism of the p38MAPK signaling pathway. H9c2 cells were treated for 24 h by using 5 µmol/l DOX without or with being pretreated by 1 µM NRG for 150 min or by 3 µM SB203580 for 60 min. Cell viability was detected by cell counting kit-8 assay. Intracellular reactive oxygen species (ROS) levels were detected based on the oxidative conversion of 2',7'-dichlorfluorescein-diacetate (cell-permeable) to dichlorofluorescein (fluorescent). The expression of p38MAPK was determined by western blotting. The expression level of p-p38MAPK in H9c2 cells, which was significantly increased by exposure to 5 µM DOX for 60 min (P<0.01), was significantly decreased by pretreatment with 1 µM NRG for 150 min beforehand (P<0.01). The viability of H9c2 cells pretreated for 150 min with 1 µM NRG was significantly enhanced compared with that using DOX directly (P<0.01). Intracellular ROS levels were significantly reduced by being pretreated with 1 µM NRG for 150 min or with 3 µM SB203580 for 60 min before the cells were exposed to 5 µM DOX. Collectively, NRG protected H9c2 cells against the cardiotoxicity induced by DOX through suppressing the expression and activity of the p38MAPK pathway. The findings provided valuable evidence for the possible use of NRG to relieve DOX-induced cardiotoxicity. [ABSTRACT FROM AUTHOR]

We formulate a multi-matrices factorization model (MMF) for the missing sensor data estimation problem. The estimation problem is adequately transformed into a matrix completion one. With MMF, an n-by-t real matrix, R, is adopted to represent the data collected by mobile sensors from n areas at the time, T1, T2, . . ., Tt, where the entry, Ri,j, is the aggregate value of the data collected in the ith area at Tj. We propose to approximate R by seeking a family of d-by-n probabilistic spatial feature matrices, U(1), U(2), . . ., U(t), and a probabilistic temporal feature matrix, V ∈ ℝdxt, where Rj ≈ U(j)TTj. We also present a solution algorithm to the proposed model. We evaluate MMF with synthetic data and a real-world sensor dataset extensively. Experimental results demonstrate that our approach outperforms the state-of-the-art comparison algorithms. [ABSTRACT FROM AUTHOR]