Trade analysis of timber forest products between China and the United States

Forest products have become a significant part of internationally traded products. United States forestry has achieved sustainable development, with the improvement of forest management and logging systems more and more forest resources are able to be harvested. In addition to meeting their own domestic demands, the wood production of The United States also has a large surplus for export. This paper discusses the factors that influence the trade of timber forest products in China with the United States from two aspects of trade development pattern and trade friction. To look into this information sources such as forest products import and export trade between China and the United States in recent years, data for quantitative analysis, import and export commodity structure, the international market distribution, woody forest products of China import and export trade, and trade development and prospects were acquired. The results show that: The trade scale of China's wood forest products shows a dynamic growth trend, the import and export commodity structure is relatively concentrated, and the international market is mainly distributed in the United States, Japan and other developed economies. With the increasing diversification of timber forest product export markets, forestry enterprises should strengthen international production capacity and co-operation to deal with trade barriers, accelerate the transformation of the forestry industry, and implement fiscal and taxation policies to promote the sustainable development of the forest products trade

Inhibition of NMDARs in the Nucleus Reticularis of the Thalamus Produces Delta Frequency Bursting

Injection of NMDAR antagonist into the thalamus can produce delta frequency EEG oscillations in the thalamocortical system. It is surprising that an antagonist of an excitatory neurotransmitter should trigger such activity, and the mechanism is unknown. One hypothesis is that the antagonist blocks excitation of GABAergic cells, thus producing disinhibition. To test this hypothesis, we investigated the effect of NMDAR antagonist (APV) on cells of the nucleus reticularis (nRT) in rat brain slices, a thalamic nucleus that can serve as a pacemaker for thalamocortical delta oscillations and that is composed entirely of GABAergic neurons. We found, unexpectedly, that nRT cells are hyperpolarized by APV. This occurs because these cells have an unusual form of NMDAR (probably NR2C) that contributes inward current at resting potential in response to ambient glutamate. The hyperpolarization produced by APV is sufficient to deinactivate T-type calcium channels, and these trigger rhythmic bursting at delta frequency. The APV-induced delta frequency bursting is abolished by dopamine D2 receptor antagonist, indicating that dopamine and NMDAR antagonist work synergistically to stimulate delta frequency bursting. Our results have significant implications concerning the electrophysiological basis of schizophrenia and bring together the NMDAR hypofunction, dopamine, and GABA theories of the disease. Our results suggest that NMDAR hypofunction and dopamine work synergistically on the GABAergic cells of the nRT to generate the delta frequency EEG oscillations, a thalamocortical dysrhythmia (TCD) in the awake state that is an established abnormality in schizophrenia

Nifedipine promotes the proliferation and migration of breast cancer cells

Nifedipine is widely used as a calcium channel blocker (CCB) to treat angina and hypertension,but it is controversial with respect the risk of stimulation of cancers. In this study, we demonstrated that nifedipine promoted the proliferation and migration of breast cancer cells both invivo and invitro. However, verapamil, another calcium channel blocker, didn’t exert the similar effects. Nifedipine and high concentration KCl failed to alter the [Ca2+]i in MDA-MB-231 cells, suggesting that such nifedipine effect was not related with calcium channel. Moreover, nifedipine decreased miRNA-524-5p, resulting in the up-regulation of brain protein I3 (BRI3). Erk pathway was consequently activated and led to the proliferation and migration of breast cancer cells. Silencing BRI3 reversed the promoting effect of nifedipine on the breast cancer. In a summary, nifedipine stimulated the proliferation and migration of breast cancer cells via the axis of miRNA-524-5p-BRI3–Erk pathway independently of its calcium channel-blocking activity. Our findings highlight that nifedipine but not verapamil is conducive for breast cancer growth and metastasis, urging that the caution should be taken in clinic to prescribe nifedipine to women who suffering both hypertension and breast cancer, and hypertension with a tendency in breast cancers

FoxO gene family evolution in vertebrates

<p>Abstract</p> <p>Background</p> <p>Forkhead box, class O (FoxO) belongs to the large family of forkhead transcription factors that are characterized by a conserved forkhead box DNA-binding domain. To date, the FoxO group has four mammalian members: FoxO1, FoxO3a, FoxO4 and FoxO6, which are orthologs of DAF16, an insulin-responsive transcription factor involved in regulating longevity of worms and flies. The degree of homology between these four members is high, especially in the forkhead domain, which contains the DNA-binding interface. Yet, mouse FoxO knockouts have revealed that each FoxO gene has its unique role in the physiological process. Whether the functional divergences are primarily due to adaptive selection pressure or relaxed selective constraint remains an open question. As such, this study aims to address the evolutionary mode of FoxO, which may lead to the functional divergence.</p> <p>Results</p> <p>Sequence similarity searches have performed in genome and scaffold data to identify homologues of FoxO in vertebrates. Phylogenetic analysis was used to characterize the family evolutionary history by identifying two duplications early in vertebrate evolution. To determine the mode of evolution in vertebrates, we performed a rigorous statistical analysis with FoxO gene sequences, including relative rate ratio tests, branch-specific <it>d</it>_<it>N</it>/<it>d</it>_{<it>S </it>}ratio tests, site-specific <it>d</it>_<it>N</it>/<it>d</it>_{<it>S </it>}ratio tests, branch-site <it>d</it>_<it>N</it>/<it>d</it>_{<it>S </it>}ratio tests and clade level amino acid conservation/variation patterns analysis. Our results suggest that FoxO is constrained by strong purifying selection except four sites in FoxO6, which have undergone positive Darwinian selection. The functional divergence in this family is best explained by either relaxed purifying selection or positive selection.</p> <p>Conclusion</p> <p>We present a phylogeny describing the evolutionary history of the FoxO gene family and show that the genes have evolved through duplications followed by purifying selection except for four sites in FoxO6 fixed by positive selection lie mostly within the non-conserved optimal PKB motif in the C-terminal part. Relaxed selection may play important roles in the process of functional differentiation evolved through gene duplications as well.</p

Modulation of Actin Filament Dynamics by Inward Rectifying of Potassium Channel Kir2.1

Apart from its ion channel properties, the Kir2.1 channel has been found in tumors and cancer cells to facilitate cancer cell motility. It is assumed that Kir2.1 might be associated with cell actin filament dynamics. With the help of structured illumination microscopy (SIM), we show that Kir2.1 overexpression promotes actin filament dynamics, cell invasion, and adhesion. Mutated Kir2.1 channels, with impaired membrane expression, present much weaker actin regulatory effects, which indicates that precise Kir2.1 membrane localization is key to its actin filament remolding effect. It is found that Kir2.1 membrane expression and anchoring are associated with PIP2 affinity, and PIP2 depletion inhibits actin filament dynamics. We also report that membrane-expressed Kir2.1 regulates redistribution and phosphorylation of FLNA (filamin A), which may be the mechanism underlying Kir2.1 and actin filament dynamics. In conclusion, Kir2.1 membrane localization regulates cell actin filaments, and not the ion channel properties. These data indicate that Kir2.1 may have additional cellular functions distinct from the regulation of excitability, which provides new insight into the study of channel proteins

Clinical Efficacy and Meta-Analysis of Stem Cell Therapies for Patients with Brain Ischemia

Objective. Systematic review and meta-analysis to observe the efficacy and safety of stem cell transplantation therapy in patients with brain ischemia. Methods. We searched Cochrane Library, PubMed, Ovid, CBM, CNKI, WanFang, and VIP Data from its inception to December 2015, to collect randomized controlled trials (RCT) of stem cell transplantation for the ischemic stroke. Two authors independently screened the literature according to the inclusion and exclusion criteria, extracted data, and assessed the risk of bias. Thereafter, meta-analysis was performed. Results. Sixteen studies and eighteen independent treatments were included in the current meta-analysis. The results based upon the pooled mean difference from baseline to follow-up points showed that the stem cell transplantation group was superior to the control group with statistical significance in the neurologic deficits score (NIHSS, MD = 1.57; 95% CI, 0.64-2.51; I2 = 57 %; p = 0.001), motor function (FMA, MD = 4.23; 95% CI, 3.08-5.38; I2 = 0 %; p <0.00001), daily life ability (Barthel, MD = 8.37; 95% CI, 4.83-11.91; I2 = 63 %; p <0.00001), and functional independence (FIM, MD = 8.89; 95% CI, 4.70-13.08; I2 = 79 %; p <0.0001). Conclusions. It is suggested that the stem cell transplantation therapy for patients with brain ischemic stroke can significantly improve the neurological deficits and daily life quality, with no serious adverse events. However, higher quality and larger data studies are required for further investigation to support clinical application of stem cell transplantation

Inhibition of pyruvate kinase M2 by reactive oxygen species contributes to the development of pulmonary arterial hypertension

Aims Pulmonary arterial hypertension [1] is a proliferative disorder associated with enhanced proliferation and suppressed apoptosis of pulmonary artery smooth muscle cells (PASMCs). Reactive oxygen species (ROS) is implicated in the development of PAH and regulates the vascular tone and functions. However, which cellular signaling mechanisms are triggered by ROS in PAH is still unknown. Hence, here we wished to characterize the signaling mechanisms triggered by ROS. Methods and Results By Western blots, we showed that increased intracellular ROS caused inhibition of the glycolytic pyruvate kinase M2 (PKM2) activity through promoting the phosphorylation of PKM2. Monocrotaline (MCT)-induced rats developed severe PAH and right ventricular hypertrophy, with a significant increase in the P-PKM2 and decrease in pyruvate kinase activity which could be attenuated with the treatments of PKM2 activators, FBP and l-serine. The antioxidant NAC, apocynin and MnTBAP had the similar protective effects in the development of PAH. In vitro assays confirmed that inhibition of PKM2 activity could modulate the flux of glycolytic intermediates in support of cell proliferation through the increased pentose phosphate pathway (PPP). Increased ROS and decreased PKM2 activity also promoted the Cav1.2 expression and intracellular calcium. Conclusion Our data provide new evidence that PKM2 makes a critical regulatory contribution to the PAHs for the first time. Decreased pyruvate kinase M2 activity confers additional advantages to rat PASMCs by allowing them to sustain anti-oxidant responses and thereby support cell survival in PAH. It may become a novel treatment strategy in PAH by using of PKM2 activators

Learning Large-scale Location Embedding From Human Mobility Trajectories with Graphs

An increasing amount of location-based service (LBS) data is being accumulated and helps to study urban dynamics and human mobility. GPS coordinates and other location indicators are normally low dimensional and only representing spatial proximity, thus difficult to be effectively utilized by machine learning models in Geo-aware applications. Existing location embedding methods are mostly tailored for specific problems that are taken place within areas of interest. When it comes to the scale of a city or even a country, existing approaches always suffer from extensive computational cost and significant data sparsity. Different from existing studies, we propose to learn representations through a GCN-aided skip-gram model named GCN-L2V by considering both spatial connection and human mobility. With a flow graph and a spatial graph, it embeds context information into vector representations. GCN-L2V is able to capture relationships among locations and provide a better notion of similarity in a spatial environment. Across quantitative experiments and case studies, we empirically demonstrate that representations learned by GCN-L2V are effective. As far as we know, this is the first study that provides a fine-grained location embedding at the city level using only LBS records. GCN-L2V is a general-purpose embedding model with high flexibility and can be applied in down-streaming Geo-aware applications

Multi-Objective Considered Process Parameter Optimization of Welding Robots Based on Small Sample Size Dataset

The welding process is characterized by its high energy density, making it imperative to optimize the energy consumption of welding robots without compromising the quality and efficiency of the welding process for their sustainable development. The above evaluation objectives in a particular welding situation are mostly influenced by the welding process parameters. Although numerical analysis and simulation methods have demonstrated their viability in optimizing process parameters, there are still limitations in terms of modeling accuracy and efficiency. This paper presented a framework for optimizing process parameters of welding robots in industry settings, where data augmentation was applied to expand sample size, auto machine learning theory was incorporated to quantify reflections from process parameters to evaluation objectives, and the enhanced non-dominated sorting algorithm was employed to identify an optimal solution by balancing these objectives. Additionally, an experiment using Q235 as welding plates was designed and conducted on a welding platform, and the findings indicated that the prediction accuracy on different objectives obtained by the enlarged dataset through ensembled models all exceeded 95%. It is proven that the proposed methods enabled the efficient and optimal determination of parameter instructions for welding scenarios and exhibited superior performance compared with other optimization methods in terms of model correctness, modeling efficiency, and method applicability