Stroke is an acute cerebral vascular disease, which is likely to cause long-term disabilities and death. Acute ischemic lesions occur in most stroke patients. These lesions are treatable under accurate diagnosis and treatments. Although diffusion-weighted MR imaging (DWI) is sensitive to these lesions, localizing and quantifying them manually is costly and challenging for clinicians. In this paper, we propose a novel framework to automatically segment stroke lesions in DWI. Our framework consists of two convolutional neural networks (CNNs): one is an ensemble of two DeconvNets (Noh et al., 2015), which is the EDD Net; the second CNN is the multi-scale convolutional label evaluation net (MUSCLE Net), which aims to evaluate the lesions detected by the EDD Net in order to remove potential false positives. To the best of our knowledge, it is the first attempt to solve this problem and using both CNNs achieves very good results. Furthermore, we study the network architectures and key configurations in detail to ensure the best performance. It is validated on a large dataset comprising clinical acquired DW images from 741 subjects. A mean accuracy of Dice coefficient obtained is 0.67 in total. The mean Dice scores based on subjects with only small and large lesions are 0.61 and 0.83, respectively. The lesion detection rate achieved is 0.94.
Yak is one of the largest native mammalian species at the Himalayas, the highest plateau area in the world with an average elevation of >4,000 m above the sea level. Yak is well adapted to high altitude environment with a set of physiological features for a more efficient blood flow for oxygen delivery under hypobaric hypoxia. Yet, the genetic mechanism underlying its adaptation remains elusive. We conducted a cross-tissue, cross-altitude, and cross-species study to characterize the transcriptomic landscape of domestic yaks. The generated multi-tissue transcriptomic data greatly improved the current yak genome annotation by identifying tens of thousands novel transcripts. We found that among the eight tested tissues (lung, heart, kidney, liver, spleen, muscle, testis, and brain), lung and heart are two key organs showing adaptive transcriptional changes and >90% of the cross-altitude differentially expressed genes in lung display a nonlinear regulation. Pathways related to cell survival and proliferation are enriched, including PI3K-Akt, HIF-1, focal adhesion, and ECM–receptor interaction. These findings, in combination with the comprehensive transcriptome data set, are valuable to understanding the genetic mechanism of hypoxic adaptation in yak.
In this study, we investigated the in vivo role of adiponectin, an adipocytokine, on the development of atherosclerosis in rabbits mainly using adenovirus expressing adiponectin gene (Ad-APN) and intravascular ultrasonography. Serum adiponectin concentrations in rabbits after Ad-APN local transfer to abdominal aortas increased about nine times as much as those before transfer (P!0 . 01), about ten times as much as the levels of endogenous adiponectin in adenovirus expressing b-galactosidase gene (Ad-bgal) treated rabbits (P!0 . 01), and about four times as much as those in the aorta of non-injured rabbits on a normal cholesterol diet (P!0 . 01). Ultrasonography revealed a significantly reduced atherosclerotic plaque area in abdominal aortas of rabbits infected through intima with Ad-APN, by 35 . 2% compared with the area before treatment (P!0 . 01), and by 35 . 8% compared with that in Ad-bgal-treated rabbits (P!0 . 01). In rabbits infected through adventitia, Ad-APN treatment reduced plaque area by 28 . 9% as compared with the area before treatment (P!0 . 01) and 25 . 6% compared with that in Ad-bgal-treated rabbits (P!0 . 01). Adiponectin significantly suppressed the mRNA expression of vascular cell adhesion molecule-1 (VCAM-1) by 18 . 5% through intima transfer (P!0 . 05) and 26 . 9% through adventitia transfer (P!0 . 01), and intercellular adhesion molecule-1 (ICAM-1) by 40 . 7% through intima transfer (P!0 . 01), and 30 . 7% through adventitia transfer (P!0 . 01). However, adiponectin had no effect on the expression of types I and III collagen. These results suggest that local adiponectin treatment suppresses the development of atherosclerosis in vivo in part by attenuating the expression of VCAM-1 and ICAM-1 in vascular walls.
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