A novel semisupervised support vector machine classifier based on active learning and context information

This paper proposes a novel semisupervised support vector machine classifier (Formula presented.) based on active learning (AL) and context information to solve the problem where the number of labeled samples is insufficient. Firstly, a new semisupervised learning method is designed using AL to select unlabeled samples as the semilabled samples, then the context information is exploited to further expand the selected samples and relabel them, along with the labeled samples train (Formula presented.) classifier. Next, a new query function is designed to enhance the reliability of the classification results by using the Euclidean distance between the samples. Finally, in order to enhance the robustness of the proposed algorithm, a fusion method is designed. Several experiments on change detection are performed by considering some real remote sensing images. The results show that the proposed algorithm in comparison with other algorithms can significantly improve the detection accuracy and achieve a fast convergence in addition to verify the effectiveness of the fusion method developed in this paper

Resibufogenin Targets the ATP1A1 Signaling Cascade to Induce G2/M Phase Arrest and Inhibit Invasion in Glioma

Resibufogenin (RB) is a major active ingredient in the traditional Chinese medicine Chansu and has garnered considerable attention for its efficacy in the treatment of cancer. However, the anticancer effects and underlying mechanisms of RB on glioblastoma (GBM) remain unknown. Here, we found that RB induced G2/M phase arrest and inhibited invasion in a primary GBM cell line, P3#GBM, and two GBM cell lines, U251 and A172. Subsequently, we demonstrated that RB-induced G2/M phase arrest occurred through downregulation of CDC25C and upregulation of p21, which was caused by activation of the MAPK/ERK pathway, and that RB inhibited GBM invasion by elevating intercellular Ca2+ to suppress the Src/FAK/Paxillin focal adhesion pathway. Intriguingly, we confirmed that upon RB binding to ATP1A1, Na+-K+-ATPase was activated as a receptor and then triggered the intracellular MAPK/ERK pathway and Ca2+-mediated Src/FAK/Paxillin focal adhesion pathway, which led to G2/M phase arrest and inhibited the invasion of GBM cells. Taken together, our findings reveal the antitumor mechanism of RB by targeting the ATP1A1 signaling cascade and two key signaling pathways and highlight the potential of RB as a new class of promising anticancer agents.publishedVersio

Miniaturized Computational Photonic Molecule Spectrometer

Miniaturized spectrometry system is playing an essential role for materials analysis in the development of in-situ or portable sensing platforms across research and industry. However, there unavoidably exists trade-offs between the resolution and operation bandwidth as the device scale down. Here, we report an extreme miniaturized computational photonic molecule (PM) spectrometer utilizing the diverse spectral characteristics and mode-hybridization effect of split eigenfrequencies and super-modes, which effectively eliminates the inherent periodicity and expands operation bandwidth with ultra-high spectral resolution. These results of dynamic control of the frequency, amplitude, and phase of photons in the photonic multi-atomic systems, pave the way to the development of benchtop sensing platforms for applications previously unfeasible due to resolution-bandwidth-footprint limitations, such as in gas sensing or nanoscale biomedical sensing

Thiabendazole Inhibits Glioblastoma Cell Proliferation and Invasion Targeting Mini-chromosome Maintenance Protein 2

Thiabendazole (TBZ), approved by the US Food and Drug Administration (FDA) for human oral use, elicits a potential anticancer activity on cancer cells in vitro and in animal models. Here, we evaluated the efficacy of TBZ in the treatment of human glioblastoma multiforme (GBM). TBZ reduced the viability of GBM cells (P3, U251, LN229, A172, and U118MG) relative to controls in a dose- and time-dependent manner. However, normal human astrocytes (NHA) exhibited a greater IC50 than tumor cell lines and were thus more resistant to its cytotoxic effects. 5-Ethynyl-2′-deoxyuridine (EdU)-positive cells and the number of colonies formed were decreased in TBZ-treated cells (at 150 μM, P < 0.05 and at 150 μM, P < 0.001, respectively). This decrease in proliferation was associated with a G2/M arrest as assessed with flow cytometry, and the downregulation of G2/M check point proteins. In addition, TBZ suppressed GBM cell invasion. Analysis of RNA sequencing data comparing TBZ-treated cells with controls yielded a group of differentially expressed genes, the functions of which were associated with the cell cycle and DNA replication. The most significantly downregulated gene in TBZ-treated cells was mini-chromosome maintenance protein 2 (MCM2). SiRNA knockdown of MCM2 inhibited proliferation, causing a G2/M arrest in GBM cell lines and suppressed invasion. Taken together, our results demonstrated that TBZ inhibited proliferation and invasion in GBM cells through targeting of MCM2.publishedVersio

A Trimodel SAR Semisupervised Recognition Method Based on Attention-Augmented Convolutional Networks

Semisupervised learning in synthetic aperture radars (SARs) is one of the research hotspots in the field of radar image automatic target recognition. It can efficiently deal with challenging environments where there are insufficient labeled samples and large unlabeled samples in the SAR dataset. In recent years, consistency regularization methods in semisupervised learning have shown considerable improvement in recognition accuracy and efficiency. Current consistency regularization approaches suffer from two main shortcomings: first, extracting all of the relevant information in the image target is difficult owing to the inability of conventional convolutional neural networks to capture global relational information; second, the standard teacher–student regularization methodology causes confirmation biases due to the high coupling between teacher and student models. This article adopts an innovative trimodel semisupervised method based on attention-augmented convolutional networks to address the aforementioned obstacles. Specifically, we develop an attention mechanism incorporating a novel positional embedding method based on recurrent neural networks and integrate this with a standard convolutional network as a feature extractor, to improve the network's ability to extract global feature information from images. Furthermore, we address the confirmation bias problem by introducing a classmate model to the standard teacher–student structure and utilize the model to impose a weak consistency constraint designed on the student to weaken the strong coupling between the teacher and the student. Comparative experiments on the Moving and Stationary Target Acquisition and Recognition dataset show that our method outperforms state-of-the-art semisupervised methods in terms of recognition accuracy, demonstrating its potential as a new benchmark approach for the deep learning and SAR research community

TRIM56 promotes malignant progression of glioblastoma by stabilizing cIAP1 protein

Background The tripartite motif (TRIM) family of proteins plays a key role in the developmental growth and therapeutic resistance of many tumors. However, the regulatory mechanisms and biological functions of TRIM proteins in human glioblastoma (GBM) are not yet fully understood. In this study, we focused on TRIM56, which emerged as the most differentially expressed TRIM family member with increased expression in GBM. Methods Western blot, real-time quantitative PCR (qRT-PCR), immunofluorescence (IF) and immunohistochemistry (IHC) were used to study the expression levels of TRIM56 and cIAP1 in GBM cell lines. Co-immunoprecipitation (co-IP) was used to explore the specific binding between target proteins and TRIM56. A xenograft animal model was used to verify the tumor promoting effect of TRIM56 on glioma in vivo. Results We observed elevated expression of TRIM56 in malignant gliomas and revealed that TRIM56 promoted glioma progression in vitro and in a GBM xenograft model in nude mice. Analysis of the Human Ubiquitin Array and co-IPs showed that cIAP1 is a protein downstream of TRIM56. TRIM56 deubiquitinated cIAP1, mainly through the zinc finger domain (amino acids 21–205) of TRIM56, thereby reducing the degradation of cIAP1 and thus increasing its expression. TRIM56 also showed prognostic significance in overall survival of glioma patients. Conclusions TRIM56-regulated post-translational modifications may contribute to glioma development through stabilization of cIAP1. Furthermore, TRIM56 may serve as a novel prognostic indicator and therapeutic molecular target for GBM.publishedVersio

Loss of COPZ1 induces NCOA4 mediated autophagy and ferroptosis in glioblastoma cell lines

Dysregulated iron metabolism is a hallmark of many cancers, including glioblastoma (GBM). However, its role in tumor progression remains unclear. Herein, we identified coatomer protein complex subunit zeta 1 (COPZ1) as a therapeutic target candidate which significantly dysregulated iron metabolism in GBM cells. Overexpression of COPZ1 was associated with increasing tumor grade and poor prognosis in glioma patients based on analysis of expression data from the publicly available database The Cancer Genome Atlas (P < 0.001). Protein levels of COPZ1 were significantly increased in GBM compared to non-neoplastic brain tissue samples in immunohistochemistry and western blot analysis. SiRNA knockdown of COPZ1 suppressed proliferation of U87MG, U251 and P3#GBM in vitro. Stable expression of a COPZ1 shRNA construct in U87MG inhibited tumor growth in vivo by ~60% relative to controls at day 21 after implantation (P < 0.001). Kaplan–Meier analysis of the survival data demonstrated that the overall survival of tumor bearing animals increased from 20.8 days (control) to 27.8 days (knockdown, P < 0.05). COPZ1 knockdown also led to the increase in nuclear receptor coactivator 4 (NCOA4), resulting in the degradation of ferritin, and a subsequent increase in the intracellular levels of ferrous iron and ultimately ferroptosis. These data demonstrate that COPZ1 is a critical mediator in iron metabolism. The COPZ1/NCOA4/FTH1 axis is therefore a novel therapeutic target for the treatment of human GBM.publishedVersio

An application of nonsmooth critical point theory

We consider a class of elliptic equation with natural growth. We obtain a region of the natural growth term with precise lower boundary less than zero

Dietary Supplementation of L-Arginine and N-Carbamylglutamate Attenuated the Hepatic Inflammatory Response and Apoptosis in Suckling Lambs with Intrauterine Growth Retardation

L-arginine (Arg) is a semiessential amino acid with several physiological functions. N-Carbamylglutamate (NCG) can promote the synthesis of endogenous Arg in mammals. However, the roles of Arg or NCG on hepatic inflammation and apoptosis in suckling lambs suffering from intrauterine growth restriction (IUGR) are still unclear. The current work is aimed at examining the effects of dietary Arg and NCG on inflammatory and hepatocyte apoptosis in IUGR suckling lambs. On day 7 after birth, 48 newborn Hu lambs were selected from a cohort of 432 twin lambs. Normal-birthweight and IUGR Hu lambs were allocated randomly (n=12/group) to control (CON), IUGR, IUGR+1% Arg, or IUGR+0.1% NCG groups. Lambs were fed for 21 days from 7 to 28 days old. Compared with CON lambs, relative protein 53 (P53), apoptosis antigen 1 (Fas), Bcl-2-associated X protein (Bax), caspase-3, cytochrome C, tumor necrosis factor alpha (TNF-α), nuclear factor kappa-B (NF-κB) p65, and NF-κB pp65 protein levels were higher (P<0.05) in liver from IUGR lambs, whereas those in liver from IUGR lambs under Arg or NCG treatment were lower than those in IUGR lambs. These findings indicated that supplementing Arg or NCG reduced the contents of proinflammatory cytokines at the same time when the apoptosis-related pathway was being suppressed, thus suppressing the IUGR-induced apoptosis of hepatic cells