A Learning Aided Flexible Gradient Descent Approach to MISO Beamforming

This paper proposes a learning aided gradient descent (LAGD) algorithm to solve the weighted sum rate (WSR) maximization problem for multiple-input single-output (MISO) beamforming. The proposed LAGD algorithm directly optimizes the transmit precoder through implicit gradient descent based iterations, at each of which the optimization strategy is determined by a neural network, and thus, is dynamic and adaptive. At each instance of the problem, this network is initialized randomly, and updated throughout the iterative solution process. Therefore, the LAGD algorithm can be implemented at any signal-to-noise ratio (SNR) and for arbitrary antenna/user numbers, does not require labelled data or training prior to deployment. Numerical results show that the LAGD algorithm can outperform of the well-known WMMSE algorithm as well as other learning-based solutions with a modest computational complexity. Our code is available at https://github.com/XiaGroup/LAGD

OpenPARF: An Open-Source Placement and Routing Framework for Large-Scale Heterogeneous FPGAs with Deep Learning Toolkit

This paper proposes OpenPARF, an open-source placement and routing framework for large-scale FPGA designs. OpenPARF is implemented with the deep learning toolkit PyTorch and supports massive parallelization on GPU. The framework proposes a novel asymmetric multi-electrostatic field system to solve FPGA placement. It considers fine-grained routing resources inside configurable logic blocks (CLBs) for FPGA routing and supports large-scale irregular routing resource graphs. Experimental results on ISPD 2016 and ISPD 2017 FPGA contest benchmarks and industrial benchmarks demonstrate that OpenPARF can achieve 0.4-12.7% improvement in routed wirelength and more than $2\times$ speedup in placement. We believe that OpenPARF can pave the road for developing FPGA physical design engines and stimulate further research on related topics

Digital financial inclusion and the urban–rural income gap in China: empirical research based on the Theil index

This study examined the effect of digital financial inclusion in reducing the urban–rural income inequality in China. Based on citylevel panel data, the results showed that digital financial inclusion narrowed the urban–rural income gap significantly by boosting economic growth. The results were robust when the core explained variables were replaced. Heterogeneity analysis showed that digital financial inclusion indicates regional differences in narrowing the urban–rural income gap. This study puts forward corresponding countermeasures for the development of digital financial inclusion and adds to the research on this very topical subjec

Increased expression of MMP9 is correlated with poor prognosis of nasopharyngeal carcinoma

<p>Abstract</p> <p>Introduction</p> <p>The aim of the present study was to analyze the expression of matrix metalloproteinase 9 (<it>MMP9</it>) in nasopharyngeal carcinoma (NPC) and its correlation with clinicopathologic features, including the survival of patients with NPC.</p> <p>Methods</p> <p>Using real-time PCR, we detected the mRNA expression of <it>MMP9 </it>in normal nasopharyngeal tissues and nasopharyngeal carcinoma (NPC) tissues. Using immunohistochemistry analysis, we analyzed <it>MMP9 </it>protein expression in clinicopathologically characterized 164 NPC cases (116 male and 48 female) with age ranging from 17 to 80 years (median = 48.4 years) and 32 normal nasopharyngeal tissues. Cases with greater than or equal to 6 and less than 6 of the score value of cytoplasmic <it>MMP9 </it>immunostaining were regarded as high expression and low expression, respectively. The relationship between the expression levels of <it>MMP9 </it>and clinical features was analyzed.</p> <p>Results</p> <p>The expression level of <it>MMP9 </it>mRNA was markedly greater in NPC tissues than that in the nasopharyngeal tissues. Immunohistochemical analysis revealed that the protein expression of <it>MMP9 </it>detected in NPC tissues was higher than that in the nasopharyngeal tissues (<it>P </it>= 0.004). In addition, high levels of <it>MMP9 </it>protein were positively correlated with the status of lymph node metastasis (N classification) (<it>P </it>= 0.002) and clinical stage (<it>P </it>< 0.001) of NPC patients. Patients with higher <it>MMP9 </it>expression had a significantly shorter overall survival time than did patients with low <it>MMP9 </it>expression. Multivariate analysis suggested that the level of <it>MMP9 </it>expression was an independent prognostic indicator (<it>P </it>= 0.008) for the survival of patients with NPC.</p> <p>Conclusion</p> <p>High level of <it>MMP9 </it>expression is a potential unfavorable prognostic factor for patients with NPC.</p

Vitamin D Signaling through Induction of Paneth Cell Defensins Maintains Gut Microbiota and Improves Metabolic Disorders and Hepatic Steatosis in Animal Models.

Metabolic syndrome (MetS), characterized as obesity, insulin resistance, and non-alcoholic fatty liver diseases (NAFLD), is associated with vitamin D insufficiency/deficiency in epidemiological studies, while the underlying mechanism is poorly addressed. On the other hand, disorder of gut microbiota, namely dysbiosis, is known to cause MetS and NAFLD. It is also known that systemic inflammation blocks insulin signaling pathways, leading to insulin resistance and glucose intolerance, which are the driving force for hepatic steatosis. Vitamin D receptor (VDR) is highly expressed in the ileum of the small intestine, which prompted us to test a hypothesis that vitamin D signaling may determine the enterotype of gut microbiota through regulating the intestinal interface. Here, we demonstrate that high-fat-diet feeding (HFD) is necessary but not sufficient, while additional vitamin D deficiency (VDD) as a second hit is needed, to induce robust insulin resistance and fatty liver. Under the two hits (HFD+VDD), the Paneth cell-specific alpha-defensins including α-defensin 5 (DEFA5), MMP7 which activates the pro-defensins, as well as tight junction genes, and MUC2 are all suppressed in the ileum, resulting in mucosal collapse, increased gut permeability, dysbiosis, endotoxemia, systemic inflammation which underlie insulin resistance and hepatic steatosis. Moreover, under the vitamin D deficient high fat feeding (HFD+VDD), Helicobacter hepaticus, a known murine hepatic-pathogen, is substantially amplified in the ileum, while Akkermansia muciniphila, a beneficial symbiotic, is diminished. Likewise, the VD receptor (VDR) knockout mice exhibit similar phenotypes, showing down regulation of alpha-defensins and MMP7 in the ileum, increased Helicobacter hepaticus and suppressed Akkermansia muciniphila. Remarkably, oral administration of DEFA5 restored eubiosys, showing suppression of Helicobacter hepaticus and increase of Akkermansia muciniphila in association with resolving metabolic disorders and fatty liver in the HFD+VDD mice. An in vitro analysis showed that DEFA5 peptide could directly suppress Helicobacter hepaticus. Thus, the results of this study reveal critical roles of a vitamin D/VDR axis in optimal expression of defensins and tight junction genes in support of intestinal integrity and eubiosis to suppress NAFLD and metabolic disorders

Cationic Polystyrene Resolves Nonalcoholic Steatohepatitis, Obesity, and Metabolic Disorders by Promoting Eubiosis of Gut Microbiota and Decreasing Endotoxemia.

A pandemic of metabolic diseases, consisting of type 2 diabetes, nonalcoholic fatty liver disease, and obesity, has imposed critical challenges for societies worldwide, prompting investigation of underlying mechanisms and exploration of low-cost and effective treatment. In this report, we demonstrate that metabolic disorders in mice generated by feeding with a high-fat diet without dietary vitamin D can be prevented by oral administration of polycationic amine resin. Oral administration of cholestyramine, but not the control uncharged polystyrene, was able to sequester negatively charged bacterial endotoxin in the gut, leading to 1) reduced plasma endotoxin levels, 2) resolved systemic inflammation and hepatic steatohepatitis, and 3) improved insulin sensitivity. Gut dysbiosis, characterized as an increase of the phylum Firmicutes and a decrease of Bacteroidetes and Akkermansia muciniphila, was fully corrected by cholestyramine, indicating that the negatively charged components in the gut are critical for the dysbiosis. Furthermore, fecal bacteria transplant, derived from cholestyramine-treated animals, was sufficient to antagonize the metabolic disorders of the recipient mice. These results indicate that the negatively charged components produced by dysbiosis are critical for biogenesis of metabolic disorders and also show a potential application of cationic polystyrene to treat metabolic disorders through promoting gut eubiosis

Elevated expression of CDK4 in lung cancer

<p/> <p>Background</p> <p>The aim of the present study was to analyze the expression of Cyclin-dependent kinase 4 (<it>CDK4</it>) in lung cancer and its correlation with clinicopathologic features. Furthermore, the involvement of <it>CDK4</it>-mediated cell cycle progression and its molecular basis were investigated in the pathogenesis of lung cancer.</p> <p>Methods</p> <p>Using immunohistochemistry analysis, we analyzed <it>CDK4 </it>protein expression in 89 clinicopathologically characterized lung cancer patients (59 males and 30 females) with ages ranging from 36 to 78 years and compared them to 23 normal lung tissues. Cases with cytoplasmic and nuclear <it>CDK4 </it>immunostaining score values greater than or equal to 7 were regarded as high expression while scores less than 7 were considered low expression. The correlation between the expression level of <it>CDK4 </it>and clinical features was analyzed. Furthermore, we used lentiviral-mediated shRNA to suppress the expression of CDK4 and investigate its function and molecular mechanism for mediating cell cycle progression.</p> <p>Results</p> <p>The expression level of <it>CDK4 </it>protein was significantly increased in lung cancer tissues compared to normal tissues (<it>P </it>< 0.001). In addition, high levels of <it>CDK4 </it>protein were positively correlated with the status of pathology classification (<it>P </it>= 0.047), lymph node metastasis (<it>P </it>= 0.007), and clinical stage (<it>P </it>= 0.004) of lung cancer patients. Patients with higher <it>CDK4 </it>expression had a markedly shorter overall survival time than patients with low <it>CDK4 </it>expression. Multivariate analysis suggested the level of <it>CDK4 </it>expression was an independent prognostic indicator (<it>P </it>< 0.001) for the survival of patients with lung cancer. Use of lentiviral-mediated shRNA to inhibit the expression of <it>CDK4 </it>in lung cancer cell line A549 not only inhibited cell cycle progression, but also dramatically suppressed cell proliferation, colony formation, and migration. Furthermore, suppressing <it>CDK4 </it>expression also significantly elevated the expression of cell cycle regulator <it>p21</it></p> <p>Conclusion</p> <p>Overexpressed <it>CDK4 </it>is a potential unfavorable prognostic factor and mediates cell cycle progression by regulating the expression of <it>p21 </it>in lung cancer</p

Association of the Synapse-Associated Protein 97 (SAP97) Gene Polymorphism With Neurocognitive Function in Schizophrenic Patients

The SAP97 gene is located in the schizophrenia susceptibility locus 3q29, and it encodes the synaptic scaffolding protein that interacts with the N-methyl-D-aspartate (NMDA) receptor, which is presumed to be dysregulated in schizophrenia. In this study, we genotyped a single-nucleotide polymorphism (SNP) (rs3915512) in the SAP97 gene in 1114 patients with schizophrenia and 1036 healthy-matched controls in a Han Chinese population through the improved multiplex ligation detection reaction (imLDR) technique. Then, we analyzed the association between this SNP and the patients' clinical symptoms and neurocognitive function. Our results showed that there were no significant differences in the genotype and allele frequencies between the patients and the controls for the rs3915512 polymorphism. However, patients with the rs3915512 polymorphism TT genotype had higher neurocognitive function scores (list learning scores, symbol coding scores, category instances scores and controlled oral word association test scores) than the subjects with the A allele (P = 4.72 × 10−5, 0.027, 0.027, 0.013, respectively). Our data are the first to suggest that the SAP97 rs3915512 polymorphism may affect neurocognitive function in patients with schizophrenia