Read, Watch, and Move: Reinforcement Learning for Temporally Grounding Natural Language Descriptions in Videos

The task of video grounding, which temporally localizes a natural language description in a video, plays an important role in understanding videos. Existing studies have adopted strategies of sliding window over the entire video or exhaustively ranking all possible clip-sentence pairs in a pre-segmented video, which inevitably suffer from exhaustively enumerated candidates. To alleviate this problem, we formulate this task as a problem of sequential decision making by learning an agent which regulates the temporal grounding boundaries progressively based on its policy. Specifically, we propose a reinforcement learning based framework improved by multi-task learning and it shows steady performance gains by considering additional supervised boundary information during training. Our proposed framework achieves state-of-the-art performance on ActivityNet'18 DenseCaption dataset and Charades-STA dataset while observing only 10 or less clips per video.Comment: AAAI 201

Curcumin alleviates diabetic cardiomyopathy in experimental diabetic rats.

Diabetic cardiomyopathy (DCM), characterized by myocardial structural and functional changes, is an independent cardiomyopathy that develops in diabetic individuals. The present study was sought to investigate the effect of curcumin on modulating DCM and the mechanisms involved.An experimental diabetic rat model was induced by low dose of streptozoticin(STZ) combined with high energy intake on rats. Curcumin was orally administrated at a dose of 100 or 200 mg · kg(-1) · d(-1), respectively. Cardiac function was evaluated by serial echocardiography. Myocardial ultrastructure, fibrosis area and apoptosis were assessed by histopathologic analyses. Metabolic profiles, myocardial enzymes and oxidative stress were examined by biochemical tests. Inflammatory factors were detected by ELISA, and interrelated proteins were measured by western blot.Rats with DCM showed declined systolic myocardial performance associated with myocardial hypertrophy and fibrosis, which were accompanied with metabolism abnormalities, aberrant myocardial enzymes, increased AGEs (advanced glycation end products) accumulation and RAGE (receptor for AGEs) expression, elevated markers of oxidative stress (MDA, SOD, the ratio of NADP(+)/NADPH, Rac1 activity, NADPH oxidase subunits expression of gp91(phox) and p47(phox) ), raised inflammatory factor (TNF-α and IL-1β), enhanced apoptotic cell death (ratio of bax/bcl-2, caspase-3 activity and TUNEL), diminished Akt and GSK-3β phosphorylation. Remarkably, curcumin attenuated myocardial dysfunction, cardiac fibrosis, AGEs accumulation, oxidative stress, inflammation and apoptosis in the heart of diabetic rats. The inhibited phosphorylation of Akt and GSK-3β was also restored by curcumin treatment.Taken together, these results suggest that curcumin may have great therapeutic potential in the treatment of DCM, and perhaps other cardiovascular disorders, by attenuating fibrosis, oxidative stress, inflammation and cell death. Furthermore, Akt/GSK-3β signaling pathway may be involved in mediating these effects

Curumin inhibited AGEs accumulation and RAGE expression in the heart of experimental diabetic rats.

<p>A: Representative immunohistochemical staining and quantitative analysis of AGEs. n = 5 per group. AGEs: advanced glycation end products. B: PCR analysis of RAGE mRNA expression. n = 3 per group. C: western blots analysis of RAGE. RAGE: receptor for advanced glycation end products. n = 3 per group. Data are mean ± SEM. ^*<i>P</i><0.05 vs control group; ^#<i>P</i><0.05 vs DM group.</p

Curcumin (Cur) alleviated DM-induced left ventricular disfunction.

<p>IVSD, interventricular septal diastolic wall thickness; LVEDD, left ventricular end diastolic diameter; LVESD, left ventricular end systolic diameter; FS, fractional shortening = [(LVEDD-LVESD)/LVEDD] ×100%; EF, ejection fraction = [(LVEDD³-LVESD³)/LVEDD³] ×100%. Data are means ± SEM;</p><p><i>P</i><0.05 vs control group;</p>#<p><i>P</i><0.05 vs DM group; n = 6 per group.</p

Curcumin activated Akt and inactivated GSK-3β in the heart of experimental diabetic rats.

<p>A: western blots analysis of p-Akt and Akt. B: western blots analysis of p-GSK-3β and GSK-3β. Data are mean ± SEM. n = 3 per group. ^*<i>P</i><0.05 vs control group; ^#<i>P</i><0.05 vs DM group; <b>^†</b><i>P</i><0.05 vs DM+Cur100 mg/kg group.</p

Curcumin (Cur) prevented metabolism abnormalities.

<p>TG: triglycerides; TC: total cholesterol; Body weight and heart weight were measured on the day the rat was killed. Blood glucose, TG and TC levels were measured in the basal fasting state on the day the rat was killed. Data are means ± SEM;</p>*<p><i>P</i><0.05 vs control group;</p>#<p><i>P</i><0.05 vs DM group; n = 8–10 per group.</p

Curcumin attenuated pathological change in the heart of experimental diabetic rats.

<p>A: Representative pictures of myocardial tissue sections stained with hematoxylin and eosin (magnification = 400×). n = 6 per group. Arrow <b><i>a</i></b> indicates perinuclear vacuolization; arrow <b><i>b</i></b> indicates cardiomyocyte hypertrophy; B: Representative pictures of myocardial tissue sections stained with masson’s trichrome (magnification = 400×). n = 6 per group. Arrow <b><i>c</i></b> indicates myocardial fibrosis stained in blue; C: Representative transmission electron micrographs of left ventricular specimens. n = 3 per group. Arrow <b><i>d</i></b> indicates destruction and loss of myofibrils; arrow <b><i>e</i></b> indicates swollen mitochondria; arrow <b><i>f</i></b> indicates a number of glycogen lysis; D: Quantitative analysis of cardiomyocyte cell diameter. n = 6 per group; E: Quantitative analysis of fibrosis area. n = 6 per group. Data are mean ± SEM.^*<i>P</i><0.05 vs control group; ^#<i>P</i><0.05 vs DM group.</p

Curumin inhibited myocardial injury, inflammation and oxidative stress in experimental diabetic rats.

<p>A: Curumin inhibited serum myocardial enzyme release. CK-MB: creatine kinase-MB; LDH: Lactate dehydrogenase; AST: aspartate amino transferase; B: Curumin reduced the levels of IL-1β in serum. IL-1β: interleukin-1beta. C: Curumin reduced the levels of TNF-α in serum. TNF-α: tumor necrosis factor alpha. D: Curumin increased SOD activity in heart tissue. SOD: superoxide dismutase. E: Curumin decreased MDA content in heart tissue. MDA: malondialdehyde. Data are mean ± SEM.^*<i>P</i><0.05 vs control group; ^#<i>P</i><0.05 vs DM group; <b>^†</b><i>P</i><0.05 vs DM+Cur100 mg/kg group. n = 8–10 per group.</p