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Detecting and locating surface defects in textured materials is a crucial but challenging problem due to factors such as texture variations and lack of adequate defective samples prior to testing. In this paper we present a novel unsupervised method for automatically detecting defects in fabrics based on a deep convolutional generative adversarial network (DCGAN). The proposed method extends the standard DCGAN, which consists of a discriminator and a generator, by introducing a new encoder component. With the assistance of this encoder, our model can reconstruct a given query image such that no defects but only normal textures will be preserved in the reconstruction. Therefore, when subtracting the reconstruction from the original image, a residual map can be created to highlight potential defective regions. Besides, our model generates a likelihood map for the image under inspection where each pixel value indicates the probability of occurrence of defects at that location. The residual map and the likelihood map are then synthesized together to form an enhanced fusion map. Typically, the fusion map exhibits uniform gray levels over defect-free regions but distinct deviations over defective areas, which can be further thresholded to produce a binarized segmentation result. Our model can be unsupervisedly trained by feeding with a set of small-sized image patches picked from a few defect-free examples. The training is divided into several successively performed stages, each under an individual training strategy. The performance of the proposed method has been extensively evaluated by a variety of real fabric samples. The experimental results in comparison with other methods demonstrate its effectiveness in fabric defect detection.

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BIRC5 encodes the protein survivin, a member of the inhibitor of apoptosis family. Survivin is highly expressed in a variety of cancers but has very low expression in the corresponding normal tissues, and its expression is often associated with tumor metastasis and chemoresistance. We report that survivin was highly expressed in ovarian cancer and strongly correlated with patient overall poor survival. For the first time, we provide experimental evidence that survivin is involved in epithelial to mesenchymal transition (EMT) in ovarian cancer cells. Lentiviral CRISPR/Cas9 nickase vector mediated BIRC5 gene editing led to the inhibition of EMT by upregulating epithelial cell marker, cytokeratin 7 and downregulating mesenchymal markers: snail2, β-catenin, and vimentin in both ovarian cancer SKOV3 and OVCAR3 cells. Consistent with this molecular approach, pharmacological treatment of ovarian cancer cells using a small molecule survivin inhibitor, YM155 also inhibited EMT in these ovarian cancer cell lines. Overexpression of BIRC5 promoted EMT in SKOV3 cells. Using molecular or pharmacological approaches, we found that cell proliferation, migration, and invasion were significantly inhibited following BIRC5 disruption in both cell lines. Inhibition of BIRC5 expression also sensitized cell responses to paclitaxel treatment. Moreover, loss of BIRC5 expression attenuated TGFβ signaling in both SKOV3 and OVCAR3 cells. Collectively, our studies demonstrated that disruption of BIRC5 expression inhibited EMT by attenuating the TGFβ pathway in ovarian cancer cells.

Background Intensive malaria transmission along international borders is a significant impediment to malaria elimination in the Greater Mekong Subregion (GMS) of Southeast Asia. Passive case detection (PCD) was used to study the dynamics and trends of malaria transmission at the China–Myanmar border to provide epidemiologic information for improved malaria control. Methods PCD was conducted in one hospital and 12 clinics near the Laiza town in northeast Myanmar from 2011 to 2016. Clinical malaria was diagnosed by microscopy and demographic information was captured using a structured questionnaire at the time of the patient’s presentation for care. Results Over the study period, 6175 (19.7%) malaria cases were confirmed by microscopy from 31,326 suspected cases. The four human malaria parasite species were all identified, with Plasmodium vivax and Plasmodium falciparum accounting for 5607 (90.8%) and 481 (7.8%) of the confirmed cases, respectively. In contrast to the steady decline of malaria in the general GMS, the study site had an upward trend of malaria incidence with vivax malaria outbreaks in 2013 and 2016. Adult males, children under the age of 15, and those with occupations such as farming, being a soldier or student, had significantly higher risks of clinical malaria compared to having fevers from other aetiologies. A self-reported history of clinical malaria was also associated with a higher risk of confirmed malaria. Conclusions The China–Myanmar border area has experienced an overall upward trend of malaria incidence in recent years with P. vivax becoming the predominant species. Evidence-based control strategies need to focus on high-risk populations.

In animal models of experimental cerebral malaria (ECM), neuropathology is associated with an overwhelming inflammatory response and sequestration of leucocytes and parasite-infected red blood cells in the brain. Here we explored the effect of vitamin D (VD, cholecalciferol) treatment on host immunity and outcome of ECM in C57BL/6 mice during Plasmodium berghei ANKA (PbA) infection. We observed that oral administration of VD both before and after PbA infection completely protected mice from ECM. VD administration significantly dampened the inducible systemic inflammatory responses with reduced circulating cytokines IFN-γ and TNF and decreased expression of these cytokines by the spleen cells. Meanwhile, VD also resulted in decreased expression of the chemokines CXCL9 and CXCL10 and cytoadhesion molecules (ICAM-1, VCAM-1 and CD36) in the brain, leading to reduced accumulation of pathogenic T cells in the brain and ultimately substantial improvement of the blood-brain barriers of PbA-infected mice. In addition, VD inhibited the differentiation, activation and maturation of splenic dendritic cells. Meanwhile, regulatory T cells and IL-10 expression levels were upregulated upon VD treatment. These data collectively demonstrated the suppressive function of VD on host inflammatory responses, which provides significant survival benefits in the murine ECM model.

ABI-231 is a potent, orally bioavailable tubulin inhibitor that interacts with the colchicine binding site and is currently undergoing clinical trials for prostate cancer. Guided by the crystal structure of ABI-231 in complex with tubulin, we performed structure–activity relationship studies around the 3-indole moiety that led to the discovery of several potent ABI-231 analogues, most notably 10ab and 10bb. The crystal structures of 10ab and 10bb in complex with tubulin confirmed their improved molecular interactions to the colchicine site. In vitro, biological studies showed that new ABI-231 analogues disrupt tubulin polymerization, promote microtubule fragmentation, and inhibit cancer cell migration. In vivo, analogue 10bb not only significantly inhibits primary tumor growth and decreases tumor metastasis in melanoma xenograft models but also shows a significant ability to overcome paclitaxel resistance in a taxane-resistant PC-3/TxR model. In addition, pharmacological screening suggested that 10bb has a low risk of potential off-target function.

Microtubules are involved in many critical cellular processes including cell division, cell shape maintenance, vesicle transportation and motility regulation. Disruption of tubulin dynamics is a well-validated cancer drug target with several FDA approved, highly efficacious tubulin inhibitors targeting the taxane or the vinca binding sites. Despite the tremendous successes for these clinical tubulin inhibitors, their limitations are also apparent, particularly in the development of transporter mediated drug resistance. While currently there are no FDA approved inhibitors targeting the colchicine binding site in tubulin, extensive preclinical studies have suggested that colchicine binding site inhibitors (CBSIs) have significantly less susceptibility to transporter medicated drug resistance. The presence of one or more heterocyclic moieties is often critical for the antiproliferative activities for most of these CBSIs. This article aims to review the structures and antiproliferative activities of most recently developed heterocyclic CBSIs from 2013 to present. We focus this review on compounds that are designed based on the CA-4, chalcone and PTOX scaffolds which are well established to interact with the colchicine binding site in tubulin.