Early detection and appropriate medical treatment are of great use for ear disease. However, a new diagnostic strategy is necessary for the absence of experts and relatively low diagnostic accuracy, ...in which deep learning plays an important role. This paper puts forward a mechanic learning model which uses abundant otoscope image data gained in clinical cases to achieve an automatic diagnosis of ear diseases in real time. A total of 20,542 endoscopic images were employed to train nine common deep convolution neural networks. According to the characteristics of the eardrum and external auditory canal, eight kinds of ear diseases were classified, involving the majority of ear diseases, such as normal, Cholestestoma of the middle ear, Chronic suppurative otitis media, External auditory cana bleeding, Impacted cerumen, Otomycosis external, Secretory otitis media, Tympanic membrane calcification. After we evaluate these optimization schemes, two best performance models are selected to combine the ensemble classifiers with real-time automatic classification. Based on accuracy and training time, we choose a transferring learning model based on DensNet-BC169 and DensNet-BC1615, getting a result that each model has obvious improvement by using these two ensemble classifiers, and has an average accuracy of 95.59%. Considering the dependence of classifier performance on data size in transfer learning, we evaluate the high accuracy of the current model that can be attributed to large databases. Current studies are unparalleled regarding disease diversity and diagnostic precision. The real-time classifier trains the data under different acquisition conditions, which is suitable for real cases. According to this study, in the clinical case, the deep learning model is of great use in the early detection and remedy of ear diseases.
This paper proposes a deep learning priors-based data reconstruction method of 1D isometric feature mapping (ISOMAP) representations. ISOMAP is a classical algorithm of nonlinear dimensionality ...reduction (NLDR) or manifold leaning (ML), which is devoted to questing for the low dimensional structure of high dimensional data. The reconstruction of ISOMAP representations, or the inverse problem of ISOMAP, reestablishes the high dimensional data from its low dimensional ISOMAP representations, and owns a bright future in data representation, generation, compression and visualization. Due to the fact that the dimension of ISOMAP representations is far less than that of the original high dimensional data, the reconstruction of ISOMAP representations is ill-posed or undetermined. Hence, the residual learning of deep convolutional neural network (CNN) is employed to boost reconstruction performance, via achieving the priors between the low-quality result of general ISOMAP reconstruction method and its residual relative to the original data. In the situation of 1D representations, it is evaluated by the experimental results that the proposed method outbalances the state-of-the-art methods, such as nearest neighbor (NN), discrete cosine transformation (DCT) and sparse representation (SR), in reconstruction performance of video data. In summary, the proposed method is suitable for low-bitrate and high-performance applications of data reconstruction.
Macrophage activation plays a crucial role in regulating adipose tissue inflammation and is a major contributor to the pathogenesis of obesity-associated cardiovascular diseases. On various types of ...stimuli, macrophages respond with either classic (M1) or alternative (M2) activation. M1- and M2-mediated signaling pathways and corresponding cytokine production profiles are not completely understood. The discovery of microRNAs provides a new opportunity to understand this complicated but crucial network for macrophage activation and adipose tissue function.
We have examined the activity of microRNA-223 (miR-223) and its role in controlling macrophage functions in adipose tissue inflammation and systemic insulin resistance. miR-223(-/-) mice on a high-fat diet exhibited an increased severity of systemic insulin resistance compared with wild-type mice that was accompanied by a marked increase in adipose tissue inflammation. The specific regulatory effects of miR-223 in myeloid cell-mediated regulation of adipose tissue inflammation and insulin resistance were then confirmed by transplantation analysis. Moreover, using bone marrow-derived macrophages, we demonstrated that miR-223 is a novel regulator of macrophage polarization, which suppresses classic proinflammatory pathways and enhances the alternative antiinflammatory responses. In addition, we identified Pknox1 as a genuine miR-223 target gene and an essential regulator for macrophage polarization.
For the first time, this study demonstrates that miR-223 acts to inhibit Pknox1, suppressing proinflammatory activation of macrophages; thus, it is a crucial regulator of macrophage polarization and protects against diet-induced adipose tissue inflammatory response and systemic insulin resistance.
This paper discusses low-cost 3D indoor positioning with Bluetooth smart device and least square methods. 3D indoor location has become more and more attractive and it hasn’t been well resolved. ...Almost each smart phone has a Bluetooth component and it can be used for indoor positioning and navigation in the nature of things. Least square algorithms are the powerful tools for linear and nonlinear parameters estimation. Various linear and nonlinear least square methods and their theoretical basics and application performance for indoor positioning have been studied. Simulation and hardware experiments results prove that nonlinear least square method is suitable for parameters estimation of Bluetooth signal propagation, and generalized least square method has better performance than total least square methods. Simulation and hardware experiments results also show that proposed method has the advantages of low cost, lost power consumption, perfect availability and high location accuracy.
OBJECTIVE—Vascular cells, particularly endothelial cells, adopt aerobic glycolysis to generate energy to support cellular functions. The effect of endothelial glycolysis on angiogenesis remains ...unclear. 6-Phosphofructo-2-kinase/fructose-2, 6-bisphosphatase, isoform 3 (PFKFB3) is a critical enzyme for endothelial glycolysis. By blocking or deleting PFKFB3 in endothelial cells, we investigated the influence of endothelial glycolysis on angiogenesis both in vitro and in vivo.
APPROACH AND RESULTS—Under hypoxic conditions or after treatment with angiogenic factors, endothelial PFKFB3 was upregulated both in vitro and in vivo. The knockdown or overexpression of PFKFB3 suppressed or accelerated endothelial proliferation and migration in vitro, respectively. Neonatal mice from a model of oxygen-induced retinopathy showed suppressed neovascular growth in the retina when endothelial PFKFB3 was genetically deleted or when the mice were treated with a PFKFB3 inhibitor. In addition, tumors implanted in mice deficient in endothelial PFKFB3 grew more slowly and were provided with less blood flow. A lower level of phosphorylated protein kinase B was observed in PFKFB3-knockdown endothelial cells, which was accompanied by a decrease in intracellular lactate. The addition of lactate to PFKFB3-knockdown cells rescued the suppression of endothelial proliferation and migration.
CONCLUSIONS—The blockade or deletion of endothelial PFKFB3 decreases angiogenesis both in vitro and in vivo. Thus, PFKFB3 is a promising target for the reduction of endothelial glycolysis and its related pathological angiogenesis.
Closed-loop architecture is widely utilized in automatic control systems and attains distinguished dynamic and static performance. However, classical compressive sensing systems employ an open-loop ...architecture with separated sampling and reconstruction units. Therefore, a method of iterative compensation recovery for image compressive sensing is proposed by introducing a closed-loop framework into traditional compressive sensing systems. The proposed method depends on any existing approaches and upgrades their reconstruction performance by adding a negative feedback structure. Theoretical analysis of the negative feedback of compressive sensing systems is performed. An approximate mathematical proof of the effectiveness of the proposed method is also provided. Simulation experiments on more than 3 image datasets show that the proposed method is superior to 10 competing approaches in reconstruction performance. The maximum increment of the average peak signal-to-noise ratio is 4.36 dB, and the maximum increment of the average structural similarity is 0.034 based on one dataset. The proposed method based on a negative feedback mechanism can efficiently correct the recovery error in the existing image compressive sensing systems.
Non-alcoholic fatty liver disease (NAFLD) is closely associated with obesity and insulin resistance. To better understand the pathophysiology of obesity-associated NAFLD, the present study examined ...the involvement of liver and adipose tissues in metformin actions on reducing hepatic steatosis and inflammation during obesity. C57BL/6J mice were fed a high-fat diet (HFD) for 12 weeks to induce obesity-associated NAFLD and treated with metformin (150 mg/kg/d) orally for the last four weeks of HFD feeding. Compared with HFD-fed control mice, metformin-treated mice showed improvement in both glucose tolerance and insulin sensitivity. Also, metformin treatment caused a significant decrease in liver weight, but not adiposity. As indicated by histological changes, metformin treatment decreased hepatic steatosis, but not the size of adipocytes. In addition, metformin treatment caused an increase in the phosphorylation of liver AMP-activated protein kinase (AMPK), which was accompanied by an increase in the phosphorylation of liver acetyl-CoA carboxylase and decreases in the phosphorylation of liver c-Jun N-terminal kinase 1 (JNK1) and in the mRNA levels of lipogenic enzymes and proinflammatory cytokines. However, metformin treatment did not significantly alter adipose tissue AMPK phosphorylation and inflammatory responses. In cultured hepatocytes, metformin treatment increased AMPK phosphorylation and decreased fat deposition and inflammatory responses. Additionally, in bone marrow-derived macrophages, metformin treatment partially blunted the effects of lipopolysaccharide on inducing the phosphorylation of JNK1 and nuclear factor kappa B (NF-κB) p65 and on increasing the mRNA levels of proinflammatory cytokines. Taken together, these results suggest that metformin protects against obesity-associated NAFLD largely through direct effects on decreasing hepatocyte fat deposition and on inhibiting inflammatory responses in both hepatocytes and macrophages.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Adenosine 2A receptor (A2AR) exerts protective roles in endotoxin‐ and/or ischemia‐induced tissue damage. However, the role for A2AR in nonalcoholic fatty liver disease (NAFLD) remains largely ...unknown. We sought to examine the effects of global and/or myeloid cell‐specific A2AR disruption on the aspects of obesity‐associated NAFLD and to elucidate the underlying mechanisms. Global and/or myeloid cell–specific A2AR‐disrupted mice and control mice were fed a high‐fat diet (HFD) to induce NAFLD. In addition, bone marrow–derived macrophages and primary mouse hepatocytes were examined for inflammatory and metabolic responses. Upon feeding an HFD, both global A2AR‐disrupted mice and myeloid cell–specific A2AR‐defcient mice revealed increased severity of HFD‐induced hepatic steatosis and inflammation compared with their respective control mice. In in vitro experiments, A2AR‐deficient macrophages exhibited increased proinflammatory responses, and enhanced fat deposition of wild‐type primary hepatocytes in macrophage–hepatocyte cocultures. In primary hepatocytes, A2AR deficiency increased the proinflammatory responses and enhanced the effect of palmitate on stimulating fat deposition. Moreover, A2AR deficiency significantly increased the abundance of sterol regulatory element‐binding protein 1c (SREBP1c) in livers of fasted mice and in hepatocytes upon nutrient deprivation. In the absence of A2AR, SREBP1c transcription activity was significantly increased in mouse hepatocytes. Conclusion: Taken together, our results demonstrate that disruption of A2AR in both macrophage and hepatocytes accounts for increased severity of NAFLD, likely through increasing inflammation and through elevating lipogenic events due to stimulation of SREBP1c expression and transcription activity. (Hepatology 2018;68:48‐61).
Obesity is an ongoing pandemic and serves as a causal factor of a wide spectrum of metabolic diseases including diabetes, fatty liver disease, and cardiovascular disease. Much evidence has ...demonstrated that nutrient overload/overnutrition initiates or exacerbates inflammatory responses in tissues/organs involved in the regulation of systemic metabolic homeostasis. This obesity-associated inflammation is usually at a low-grade and viewed as metabolic inflammation. When it exists continuously, inflammation inappropriately alters metabolic pathways and impairs insulin signaling cascades in peripheral tissues/organs such as adipose tissue, the liver and skeletal muscles, resulting in local fat deposition and insulin resistance and systemic metabolic dysregulation. In addition, inflammatory mediators, e.g., proinflammatory cytokines, and excessive nutrients, e.g., glucose and fatty acids, act together to aggravate local insulin resistance and form a vicious cycle to further disturb the local metabolic pathways and exacerbate systemic metabolic dysregulation. Owing to the critical role of nutrient metabolism in controlling the initiation and progression of inflammation and insulin resistance, nutritional approaches have been implicated as effective tools for managing obesity and obesity-associated metabolic diseases. Based on the mounting evidence generated from both basic and clinical research, nutritional approaches are commonly used for suppressing inflammation, improving insulin sensitivity, and/or decreasing fat deposition. Consequently, the combined effects are responsible for improvement of systemic insulin sensitivity and metabolic homeostasis.
PDF
