Prediction of traffic flow based on deep learning

Deep neural networks (DNNs) have recently demonstrated the capability to predict traffic flow with big data. Although existing DNN models can provide better performance than shallow models, it is still an open question to make full use of the spatio-temporal characteristics of traffic flows to improve performance. We propose a novel deep architecture combining CNN and LSTM for traffic flow (RCF) predictio. The model uses CNN to explore temporal correlation and LSTM to explore spatial correlation . Factors such as weather and historical period data are also added to the feature. Its advantage lies in making full use of the spatial-temporal correlation of traffic data and more comprehensively considered the impact of multiple related factors. Aiming at the difficult problem of obtaining spatial features, a feature selection method based on Random Forests is proposed. We use the gini score to represent the spatial connection between intersections to form a network graph constructed based on data.  The experimental results show that based on the random forest feature selection and RCF model, the accuracy of traffic prediction reaches 90%

A Small Ku-Band Polarization Tracking Active Phased Array for Mobile Satellite Communications

A compact polarization tracking active phased array for Ku-band mobile satellite signal reception is presented. In contrast with conventional mechanically tracking antennas, the approach presented here meets the requirements of beam tracking and polarization tracking simultaneously without any servo components. The two-layer stacked square patch fed by two probes is used as antenna element. The impedance bandwidth of 16% for the element covers the operating frequency range from 12.25 GHz to 12.75 GHz. In the presence of mutual coupling, the dimensional parameters for each element of the small 7 × 7 array are optimized during beam scanning and polarization tracking. The compact polarization tracking modules based on the low-temperature cofired ceramic (LTCC) system-in-package (SiP) technology are proposed. A small active phased array prototype with the size of 120 mm (length) × 120 mm (width) × 55 mm (height) is developed. The measured polarization tracking patterns of the prototype are given. The polarization tracking beam can be steered in the elevation up to 50°. The gain of no less than 16.0 dBi and the aperture efficiency of more than 50% are obtained. The measured and simulated polarization tracking patterns agreed well

Nr1d1 Mediated Cell Senescence in Mouse Heart-Derived Sca-1+CD31− Cells

Aim: Sca-1+CD31− cells are resident cardiac progenitor cells, found in many mammalian tissues including the heart, and able to differentiate into cardiomyocytes in vitro and in vivo. Our previous work indicated that heart-derived Sca-1+CD31− cells increased the Nr1d1 mRNA level of Nr1d1 with aging. However, how Nr1d1 affects the senescence of Sca-1+CD31− cells. Methods: Overexpression and knockdown of Nr1d1 in Sca-1+CD31− cells and mouse cardiac myocyte (MCM) cell lines were performed by lentiviral transduction. The effects of Nr1d1 abundance on cell differentiation, proliferation, apoptosis, cell cycle, and transcriptomics were evaluated. Moreover, binding of Nr1d1 to the promoter region of Nr4a3 and Serpina3 was examined by a luciferase reporter assay. Results and Conclusions: Upregulation Nr1d1 in young Sca-1+CD31− cells inhibited cell proliferation and promoted apoptosis. However, depletion of Nr1d1 in aged Sca-1+CD31− cells promoted cell proliferation and inhibited apoptosis. Furthermore, Nr1d1 was negatively associated with cell proliferation, promoting apoptosis and senescence-associated beta-galactosidase production in MCMs. Our findings show that Nr1d1 stimulates Serpina3 expression through its interaction with Nr4a3. Nr1d1 may therefore act as a potent anti-aging receptor that can be a therapeutic target for aging-related diseases

Mitochondrial Membrane Remodeling

Mitochondria are key regulators of many important cellular processes and their dysfunction has been implicated in a large number of human disorders. Importantly, mitochondrial function is tightly linked to their ultrastructure, which possesses an intricate membrane architecture defining specific submitochondrial compartments. In particular, the mitochondrial inner membrane is highly folded into membrane invaginations that are essential for oxidative phosphorylation. Furthermore, mitochondrial membranes are highly dynamic and undergo constant membrane remodeling during mitochondrial fusion and fission. It has remained enigmatic how these membrane curvatures are generated and maintained, and specific factors involved in these processes are largely unknown. This review focuses on the current understanding of the molecular mechanism of mitochondrial membrane architectural organization and factors critical for mitochondrial morphogenesis, as well as their functional link to human diseases.Peer reviewe

Mitochondrial protein dysfunction in pathogenesis of neurological diseases

Mitochondria are essential organelles for neuronal function and cell survival. Besides the well-known bioenergetics, additional mitochondrial roles in calcium signaling, lipid biogenesis, regulation of reactive oxygen species, and apoptosis are pivotal in diverse cellular processes. The mitochondrial proteome encompasses about 1,500 proteins encoded by both the nuclear DNA and the maternally inherited mitochondrial DNA. Mutations in the nuclear or mitochondrial genome, or combinations of both, can result in mitochondrial protein deficiencies and mitochondrial malfunction. Therefore, mitochondrial quality control by proteins involved in various surveillance mechanisms is critical for neuronal integrity and viability. Abnormal proteins involved in mitochondrial bioenergetics, dynamics, mitophagy, import machinery, ion channels, and mitochondrial DNA maintenance have been linked to the pathogenesis of a number of neurological diseases. The goal of this review is to give an overview of these pathways and to summarize the interconnections between mitochondrial protein dysfunction and neurological diseases.Peer reviewe

Promoter Hypermethylation-mediated Inactivation of LRRC4 in Gliomas

<p>Abstract</p> <p>Background</p> <p>Leucine-rich repeat C4 protein (<it>LRRC4</it>) is a new member of the leucine-rich repeat (LRR) superfamily. It is not only a brain-specific gene but also a novel candidate for tumor suppression. <it>LRRC4 </it>inactivation is commonly found in glioma cell lines and primary glioma biopsies. However, little is known about the mechanism controlling <it>LRRC4 </it>expression. In a previous study, we did not find any genetic alteration in <it>LRRC4 </it>in primary glioma, which led us to explore an alternative mechanism underlying this phenomenon.</p> <p>Methods</p> <p>In the present paper, we cloned the <it>LRRC4 </it>promoter with characteristics of a CpG island by luciferase reporter assay. Then, the CpG methylation status around the <it>LRRC4 </it>promoter region in glioma cell lines and primary gliomas was examined by methylation-specific PCR and bisulfite DNA sequencing. In order to demonstrate a functional association between <it>LRRC4 </it>promoter methylation and its gene inactivation, we performed DNA demethylation analysis with two human glioma cell lines using methylation-specific PCR and RT-PCR.</p> <p>Results</p> <p>The sequence spanning positions -835 to -293 relative to the translation start site was identified as the LRRC4 promoter; this sequence is a TATA- and CAAT- less, high GC content region. It was found that <it>LRRC4 </it>promoter activity is strongly suppressed after treatment with SssI methylase in vitro. Furthermore, LRRC4 promoter methylation was observed by methylation-specific PCR in two glioma cell lines and all 30 primary glioma specimens, but not in normal brain tissue. Bisulfite DNA sequencing showed that most of the CpG sites were located around the <it>LRRC4 </it>promoter methylated in glioma cells and tissues, but not in normal brain tissue. In addition, the methylase inhibitor 5-Aza-2'-deoxycytidine could induce <it>LRRC4 </it>mRNA expression and <it>LRRC4 </it>promoter partial demethylation in SF126 and SF767 glioma cells.</p> <p>Conclusion</p> <p>Methylation-mediated inactivation of <it>LRRC4 </it>is a frequent and glioma-specific event, and it may be a potential biomarker for diagnosis or prognosis, or serve as a therapeutic target.</p

The Role of Scleraxis in Fate Determination of Mesenchymal Stem Cells for Tenocyte Differentiation

Mesenchymal stem cells (MSCs) are pluripotent cells that primarily differentiate into osteocytes, chondrocytes, and adipocytes. Recent studies indicate that MSCs can also be induced to generate tenocyte-like cells; moreover, MSCs have been suggested to have great therapeutic potential for tendon pathologies. Yet the precise molecular cascades governing tenogenic differentiation of MSCs remain unclear. We demonstrate scleraxis, a transcription factor critically involved in embryonic tendon development and formation, plays a pivotal role in the fate determination of MSC towards tenocyte differentiation. Using murine C3H10T1/2 pluripotent stem cells as a model system, we show scleraxis is extensively expressed in the early phase of bone morphogenetic protein (BMP)-12-triggered tenocytic differentiation. Once induced, scleraxis directly transactivates tendon lineage-related genes such as tenomodulin and suppresses osteogenic, chondrogenic, and adipogenic capabilities, thus committing C3H10T1/2 cells to differentiate into the specific tenocyte-like lineage, while eliminating plasticity for other lineages. We also reveal that mechanical loading-mediated tenocytic differentiation follows a similar pathway and that BMP-12 and cyclic uniaxial strain act in an additive fashion to augment the maximal response by activating signal transducer Smad8. These results provide critical insights into the determination of multipotent stem cells to the tenocyte lineage induced by both chemical and physical signals

BMP-12 Treatment of Adult Mesenchymal Stem Cells In Vitro Augments Tendon-Like Tissue Formation and Defect Repair In Vivo

We characterized the differentiation of rat bone marrow-derived mesenchymal stem cells (BM-MSCs) into tenocyte-like cells in response to bone morphogenetic protein-12 (BMP-12). BM-MSCs were prepared from Sprague-Dawley rats and cultured as monolayers. Recombinant BMP-12 treatment (10 ng/ml) of BM-MSCs for 12 hours in vitro markedly increased expression of the tenocyte lineage markers scleraxis (Scx) and tenomodulin (Tnmd) over 14 days. Treatment with BMP-12 for a further 12-hour period had no additional effect. Colony formation assays revealed that ∼80% of treated cells and their progeny were Scx- and Tnmd-positive. BM-MSCs seeded in collagen scaffolds and similarly treated with a single dose of BMP-12 also expressed high levels of Scx and Tnmd, as well as type I collagen and tenascin-c. Furthermore, when the treated BM-MSC-seeded scaffolds were implanted into surgically created tendon defects in vivo, robust formation of tendon-like tissue was observed after 21 days as evidenced by increased cell number, elongation and alignment along the tensile axis, greater matrix deposition and the elevated expression of tendon markers. These results indicate that brief stimulation with BMP-12 in vitro is sufficient to induce BM-MSC differentiation into tenocytes, and that this phenotype is sustained in vivo. This strategy of pretreating BM-MSCs with BMP-12 prior to in vivo transplantation may be useful in MSC-based tendon reconstruction or tissue engineering

<i>Zbtb40</i> Deficiency Leads to Morphological and Phenotypic Abnormalities of Spermatocytes and Spermatozoa and Causes Male Infertility

Studies on the gene regulation of spermatogenesis are of unusual significance for maintaining male reproduction and treating male infertility. Here, we have demonstrated, for the first time, that a loss of ZBTB40 function leads to abnormalities in the morphological and phenotypic characteristics of mouse spermatocytes and spermatids as well as male infertility. We revealed that Zbtb40 was expressed in spermatocytes of mouse testes, and it was co-localized with γH2AX in mouse secondary spermatocytes. Interestingly, spermatocytes of Zbtb40 knockout mice had longer telomeres, compromised double-strand break (DSB) repair in the sex chromosome, and a higher apoptosis ratio compared to wild-type (WT) mice. The testis weight, testicular volume, and cauda epididymis body weight of the Zbtb40+/− male mice were significantly lower than in WT mice. Mating tests indicated that Zbtb40+/− male mice were able to mate normally, but they failed to produce any pups. Notably, sperm of Zbtb40+/− mice showed flagellum deformities and abnormal acrosome biogenesis. Furthermore, a ZBTB40 mutation was associated with non-obstructive azoospermia. Our results implicate that ZBTB40 deficiency leads to morphological and phenotypic abnormalities of spermatocytes and spermatids and causes male infertility. This study thus offers a new genetic mechanism regulating mammalian spermatogenesis and provides a novel target for gene therapy in male infertility