Learning Segmentation Masks with the Independence Prior

An instance with a bad mask might make a composite image that uses it look fake. This encourages us to learn segmentation by generating realistic composite images. To achieve this, we propose a novel framework that exploits a new proposed prior called the independence prior based on Generative Adversarial Networks (GANs). The generator produces an image with multiple category-specific instance providers, a layout module and a composition module. Firstly, each provider independently outputs a category-specific instance image with a soft mask. Then the provided instances' poses are corrected by the layout module. Lastly, the composition module combines these instances into a final image. Training with adversarial loss and penalty for mask area, each provider learns a mask that is as small as possible but enough to cover a complete category-specific instance. Weakly supervised semantic segmentation methods widely use grouping cues modeling the association between image parts, which are either artificially designed or learned with costly segmentation labels or only modeled on local pairs. Unlike them, our method automatically models the dependence between any parts and learns instance segmentation. We apply our framework in two cases: (1) Foreground segmentation on category-specific images with box-level annotation. (2) Unsupervised learning of instance appearances and masks with only one image of homogeneous object cluster (HOC). We get appealing results in both tasks, which shows the independence prior is useful for instance segmentation and it is possible to unsupervisedly learn instance masks with only one image.Comment: 7+5 pages, 13 figures, Accepted to AAAI 201

Pathological Roles of Neutrophil-Mediated Inflammation in Asthma and Its Potential for Therapy as a Target

Asthma is a chronic inflammatory disease that undermines the airways. It is caused by dysfunction of various types of cells, as well as cellular components, and is characterized by recruitment of inflammatory cells, bronchial hyperreactivity, mucus production, and airway remodelling and narrowing. It has commonly been considered that airway inflammation is caused by the Th2 immune response, or eosinophilia, which is a hallmark of bronchial asthma pathogenesis. Some patients display a neutrophil-dominant presentation and are characterized with low (or even absent) Th2 cytokines. In recent years, increasing evidence has also suggested that neutrophils play a key role in the development of certain subtypes of asthma. This review discusses neutrophils in asthma and potentially related targeted therapies

Scale specified single shot multibox detector

Detecting objects at vastly different scales is a fundamental challenge in computer vision. To solve this, some approaches (e.g. TridentNet) investigate the effect of receptive fields, whereas other approaches (e.g. SNIP, SNIPER) are based on the image pyramid strategy. In this study, a novel single‐shot based detector, called scale specified single‐shot multibox detector (4SD) is proposed. It aims to predict objects of a specific scale range separately by using feature maps of different sizes. First, a parallel multi‐branch architecture with feature maps of different sizes is generated by scale specific inference module. Then, the authors propose a scale specific training scheme to specialise each branch by sampling object instances of proper scales for training. Results are shown on both PASCAL VOC and COCO detection. The proposed method can achieve a mean average precision of 83.1% on PASCAL VOC 2007, and 36.9% on MS‐COCO at a speed of 28 frames per second, which is superior to most single‐stage detectors

Tooth-Marked Tongue Recognition Using Gradient-Weighted Class Activation Maps

The tooth-marked tongue is an important indicator in traditional Chinese medicinal diagnosis. However, the clinical competence of tongue diagnosis is determined by the experience and knowledge of the practitioners. Due to the characteristics of different tongues, having many variations such as different colors and shapes, tooth-marked tongue recognition is challenging. Most existing methods focus on partial concave features and use specific threshold values to classify the tooth-marked tongue. They lose the overall tongue information and lack the ability to be generalized and interpretable. In this paper, we try to solve these problems by proposing a visual explanation method which takes the entire tongue image as an input and uses a convolutional neural network to extract features (instead of setting a fixed threshold artificially) then classifies the tongue and produces a coarse localization map highlighting tooth-marked regions using Gradient-weighted Class Activation Mapping. Experimental results demonstrate the effectiveness of the proposed method

Intra-bronchial epithelial Shp2 depletion exert little effects on OVA-induced inflammation and TH2 and TH17 polarization.

<p>Twenty-four hours after the last challenge, the cellular profiles (A) were analyzed, and total cell numbers (B) were counted in BALF of mice. (C) IL-4, IL-17 and foxp3 mRNA were measured in the lung tissues of the mice. (D) Ratios of TH2 (stained by FITC-CD4 and APC-IL-4) and TH17 (stained by FITC-CD4 and PE-IL-17A) in the lung homogenates. (n = 5 mice/group, in two separate experiments). Results were expressed as mean ± SEM. ^n.s.<i>p</i> >0.05. PBS_ave: average value of three PBS subgroups, including <i>CC10-rtTA /Shp2</i>^<i>f/f</i>:DOX (toxicity control, TC), <i>CC10-rtTA/(tetO)7-Cre/Shp2</i>^<i>f/f</i>:H₂O (Shp2^F/F), and <i>CC10-rtTA/(tetO)7-Cre/Shp2</i>^<i>f/f</i>:DOX (Shp2^△/△). ^n.s.<i>p>0</i>.<i>05</i>. Eos: Eosinophil, Neu: Neutrophil, Lym: Lymphocyte, Macro: Macrophage.</p

Knockout of <i>Shp2</i> in bronchial epithelial cells have a mild effect on epithelium-derived cytokine production <i>in vivo</i>.

<p>(A) Schematic map of the generation of triple-transgenic mice <i>CC10-rtTA/(tetO)7-Cre/Shp2</i>^<i>f/f</i>. The human <i>CC10</i> promoter was used to express the reverse tetracycline transactivator (<i>rtTA</i>) in clara cells. In the presence of DOX, <i>rtTA</i> binds to the <i>tetO-CMV</i> promoter, activating the transcription of Cre-recombinase, removing the floxed exon 4 of the <i>Shp2</i> gene, resulting in specific deletion of <i>shp2</i> in Clara cells. (B) Genotyping was performed by PCR assays using mouse tail genomic DNA. (C) Inactivation of shp2 allele was confirmed by PCR of genomic DNA isolated from lung tissues of <i>CC10-rtTA/(tetO)7-Cre/Shp2</i>^<i>f/f</i> mice after 7-day treatment with DOX (through drinking, 2 mg/ml in H₂O) or H₂O (as control). (D) OVA-induced allergic asthmatic mouse model. Five-to-seven-week animals were given drinking water with or without DOX (2mg/ml) from Day 0, then they were sensitized with intra-peritoneal injection of OVA (80ug/mice) or PBS on Day 7 and Day 21. Three consecutive challenges of OVA aerosol (1%) once a day for 3 continual days from Day 32 to Day 34 were performed; the mice were then sacrificed. (E) The levels of IL-25 and IL-33 mRNA in lung tissues were detected by RT-PCR. Results were expressed as mean ± SEM of three independent experiments. ^n.s.<i>p</i>>0.05. CF: <i>CC10-rtTA/(tetO)</i>_<i>7</i><i>-Cre/Shp2</i>^<i>f/f</i>, CTF: <i>CC10-rtTA/Shp2</i>^<i>f/f</i>. PBS_ave: average value of three PBS subgroups, including <i>CC10-rtTA /Shp2</i>^<i>f/f</i>:DOX (toxicity control, TC), <i>CC10-rtTA/(tetO)7-Cre/Shp2</i>^<i>f/f</i>:H₂O (Shp2^F/F) and <i>CC10-rtTA/(tetO)7-Cre/Shp2</i>^<i>f/f</i>:DOX (Shp2^△/△).</p

OVA- or LPS-elicited production of IL-25.

<p>(A) C57BL/6 mice were sensitized and challenged with OVA, and IL-25 mRNA in lung tissue was measured by q-PCR. (B) MTECs were treated with 20 mg/ml OVA for different periods of time (0, 8, 24 and 48 hours), followed by detection of IL-25 mRNA level. Beas-2b cells were treated with OVA of different concentrations (2 and 20 mg/ml) for 8 hours (C) or 20 mg/ml OVA for different periods of time (0, 2, 8 hours) (D), followed by detection of IL-25 mRNA. Serum-free Beas-2bs were stimulated by LPS of different concentrations (0 ng/ml, 10 ng/ml, 100 ng/ml). IL-25 mRNA (E) were detected by q-PCR, IL-25 protein released into the supernatant (F) were measured by ELISA. MTECs were treated with 100 ng/ml LPS for different periods of time (0, 8, 24 and 48 hours), IL-25 mRNA (G) were detected by q-PCR, IL-25 protein released into the supernatant (H) were measured by ELISA. Results were expressed as mean ± SEM of three independent experiments. B2Bs: Beas-2b cells. *<i>p</i> <0.05, **<i>p</i><0.01 ***<i>p</i><0.001. B2Bs: Beas-2b cells.</p

Deletion of Shp2 in bronchial epithelial cells impairs IL-25 production <i>in vitro</i>, but has minor influence on asthmatic inflammation <i>in vivo</i>

<div><p>Shp2 played an important role in cigarette-smoke-mediated inflammation, surfactant homeostasis and asthmatic airway remodeling. However, whether shp2 plays a key role in epithelium-associated allergic reaction is still unknown. In this study, LPS and OVA were observed to induce the production of IL-25 in bronchial epithelial cells <i>in vitro</i> via the activation of MAPK p38 and JNK. Furthermore, blockage of Shp2 by its specific inhibitor PHPS1 or by siRNA-mediated depletion was found to reduce the production of IL-25 in epithelial cells as well as the up-regulated LPS-triggered activation of JNK but not p38. To confirm the role of intra-bronchial epithelial Shp2 in OVA-induced allergic reaction, we generated <i>CC10-rtTA/(tetO)7-Cre/Shp2</i>^<i>f/f</i> mice, where <i>Shp2</i> was conditionally knocked out in bronchial epithelial cells. Surprisingly, specific deletion of <i>Shp2</i> in bronchial epithelial cells showed a mild but insignificant effect on the expressions of epithelium-derived cytokines as well as TH2 and TH17 polarization following allergen-induced murine airway inflammation. Collectively, our data suggested that deletion of Shp2 impaired IL-25 production in bronchial epithelial cells <i>in vitro</i>, but might yet have minor influence on OVA-induced allergic reaction <i>in vivo</i>.</p></div