Training Stronger Spiking Neural Networks with Biomimetic Adaptive Internal Association Neurons

As the third generation of neural networks, spiking neural networks (SNNs) are dedicated to exploring more insightful neural mechanisms to achieve near-biological intelligence. Intuitively, biomimetic mechanisms are crucial to understanding and improving SNNs. For example, the associative long-term potentiation (ALTP) phenomenon suggests that in addition to learning mechanisms between neurons, there are associative effects within neurons. However, most existing methods only focus on the former and lack exploration of the internal association effects. In this paper, we propose a novel Adaptive Internal Association~(AIA) neuron model to establish previously ignored influences within neurons. Consistent with the ALTP phenomenon, the AIA neuron model is adaptive to input stimuli, and internal associative learning occurs only when both dendrites are stimulated at the same time. In addition, we employ weighted weights to measure internal associations and introduce intermediate caches to reduce the volatility of associations. Extensive experiments on prevailing neuromorphic datasets show that the proposed method can potentiate or depress the firing of spikes more specifically, resulting in better performance with fewer spikes. It is worth noting that without adding any parameters at inference, the AIA model achieves state-of-the-art performance on DVS-CIFAR10~(83.9\%) and N-CARS~(95.64\%) datasets.Comment: Accepted by ICASSP 202

Training Robust Spiking Neural Networks on Neuromorphic Data with Spatiotemporal Fragments

Neuromorphic vision sensors (event cameras) are inherently suitable for spiking neural networks (SNNs) and provide novel neuromorphic vision data for this biomimetic model. Due to the spatiotemporal characteristics, novel data augmentations are required to process the unconventional visual signals of these cameras. In this paper, we propose a novel Event SpatioTemporal Fragments (ESTF) augmentation method. It preserves the continuity of neuromorphic data by drifting or inverting fragments of the spatiotemporal event stream to simulate the disturbance of brightness variations, leading to more robust spiking neural networks. Extensive experiments are performed on prevailing neuromorphic datasets. It turns out that ESTF provides substantial improvements over pure geometric transformations and outperforms other event data augmentation methods. It is worth noting that the SNNs with ESTF achieve the state-of-the-art accuracy of 83.9\% on the CIFAR10-DVS dataset.Comment: Accepted by ICASSP 202

Identification of resection plane for anatomical liver resection using ultrasonography-guided needle insertion

PurposesTo set up an easy-handled and precise delineation of resection plane for hepatic anatomical resection (AR).MethodsCases of AR using ultrasonography-guided needle insertion to trace the target hepatic vein for delineation of resection planes [new technique (NT) group, n = 22] were retrospectively compared with those without implementation of this surgical technique [traditional technique (TT) group, n = 29] in terms of perioperative courses and surgical outcomes.ResultsThe target hepatic vein was successfully exposed in all patients of the NT group, compared with a success rate of 79.3% in the TT group (P < 0.05). The average operation time and intraoperative blood loss were 280 ± 32 min and 550 ± 65 ml, respectively, in the NT group. No blood transfusion was required in either group. The postoperative morbidities (bile leakage and peritoneal effusion) were similar between groups. No mortality within 90 days was observed.ConclusionsUltrasonography-guided needle insertion is a convenient, safe and efficient surgical approach to define a resection plane for conducting AR

High Expression of Ten Eleven Translocation 1 Is Associated with Poor Prognosis in Hepatocellular Carcinoma

Background. DNA methylation patterns have been found to be distinct between tumor and normal patients. However, the effect of DNA demethylation enzymes, ten eleven translocation (TET) proteins, has not been comprehensively characterized in liver cancer. In this research, we sought to unravel the linkage of TET proteins with prognosis, immune characteristics and biological pathways in hepatocellular carcinoma (HCC). Materials and Methods. Four independent datasets with gene expression data and clinical data of HCC samples were downloaded from public databases. CIBERSORT, single sample Gene Set Enrichment Analysis (ssGSEA), MCP-counter, and TIMER were implemented to evaluate immune cell infiltration. limma was employed to screen differentially expressed genes (DEGs) between two groups. The demethylation-related risk model was established by using univariate Cox regression analysis, the least absolute shrinkage and selection operator (LASSO), and stepwise Akaike information criterion (stepAIC). Results. TET1 was significantly higher expressed in tumor samples than that in normal samples. HCC patients with advanced stages (III+IV) and grades (G3+G4) had higher TET1 expression compared to early stages (I+II) and grades (G1+G2). HCC samples with high TET1 expression had worse prognosis than that with low expression. High and low TET1 expression groups had distinct immune cell infiltration and response to immunotherapy and chemotherapy. We identified 90 DEGs related to DNA demethylation in high vs. low TET1 expression groups. Furthermore, we established a risk model based on 90 DEGs containing seven key prognostic genes (SERPINH1, CDC20, HACD2, SPHK1, UGT2B15, SLC1A5, and CYP2C9) with effectiveness and robustness in predicting HCC prognosis. Conclusions. Our study suggested TET1 as a potential indicator in HCC progression. TET1 was closely involved in immune infiltration and activation of oncogenic pathways. The DNA demethylation-related risk model was potential to be applied for predicting HCC prognosis in clinics

Expression of glioma-associated oncogene 2 (Gli 2) is correlated with poor prognosis in patients with hepatocellular carcinoma undergoing hepatectomy

Abstract Background Our previous studies showed that glioma-associated oncogene (Gli)2 plays an important role in the proliferation and apoptosis resistance of hepatocellular carcinoma (HCC) cells. The aim of this study was to explore the clinical significance of Gli2 expression in HCC. Methods Expression of Gli2 protein was detected in samples from 68 paired HCC samples, the corresponding paraneoplastic liver tissues, and 20 normal liver tissues using immunohistochemistry. Correlation of the immunohistochemistry results with clinicopathologic parameters, prognosis, and the expression of E-cadherin, N-cadherin, and vimentin were analyzed. Results Immunohistochemical staining showed high levels of Gli2 protein expression in HCC, compared with paraneoplastic and normal liver tissues (P P r = −0.302, P r = −0.468, P P P Conclusions Expression of Gli2 is high in HCC tissue, and is associated with poor prognosis in patients with HCC after hepatectomy.</p

Role of AP-2α and MAPK7 in the regulation of autocrine TGF-β/miR-200b signals to maintain epithelial-mesenchymal transition in cholangiocarcinoma

Abstract Background Cholangiocarcinoma (CCA) is characterized by early lymphatic, metastasis, and low survival rate. Epithelial-mesenchymal transition (EMT) is able to induce tumor metastasis. Although the TGF-β/miR-200 signals promote EMT in various types of cancer, the regulatory mechanism in CCA is still unclear. Methods Expression of miR-200b, TGF-β, and EMT markers were measured in tumor samples and cell lines by qRT-PCR and western blot. CCK8 assay was performed to measure the cell viability. Transwell assay was used to evaluate migration and invasion. The target genes of miR-200b and transcription factor of TGF-β were analyzed using dual-luciferase reporter system. Results We have demonstrated that CCA exhibited remarkable EMT phenotype and miR-200b was reduced in CCA patients (n = 20) and negatively correlated to TGF-β. Moreover, two CCA cells, HCCC, and RBE, with epithelial appearances treated with TGF-β, showed fibroblastic-like cell morphology with downregulated miR-200b expression. Forced expression of miR-200b abrogated TGF-β-induced EMT initiation, with decreased cell proliferation, migration, and invasion in vitro. Also, TFAP2A (encode AP-2α) and MAPK7 were found to be targeted by miR-200b to downregulate EMT and AP-2α inhibited miR-200b by directly promoting transcription of TGFB1. Overexpression of MAPK7 significantly reversed miR-200b-induced inhibition of EMT, migration, and proliferation by increasing the expression of TGF-β, cyclin D1, and Cdk2. Further, the administration of miR-200b induced a remarkably tumor regression in vivo and reduced the effect of TGF-β-related EMT in AP-2α and MAPK7-dependent manner. Conclusions Our study highlights that miR-200b-based gene therapy is effective in the treatment of CCA

Percutaneous Microwave Coagula-tion for the Treatment of Small Solitary Focal Nodular Hyperplasia of Liver

Abstract Background: Whether percutaneous microwave coagulation (PMC) is safe and effective for the treatment of symptomatic focal nodular hyperplasia (FNH) of the liver remains unknown. Methods: Between January 2006 and September 2015, sixteen patients with solitary symptomatic FNHs in the liver (the largest diameter less than 5 cm) were treated by PMC. The safty and effectiveness were analyzed. Results: There were 4 males and 12 females. All these patients suffered from upper abdominal pain. The FNHs ranged in size from 3.2 cm to 5.0 cm (3.9 cm ± 0.12 cm). All the PMC procedures were performed successfully. All 16 patients had symptomatic improvement after the treatment with no procedure-related morbidity or mortality. Among 16 patients, 15 (93.8%) patients with FNHs were assessed to be ablated completely by CT examination performed within four weeks after PMC treatment. One patient failed to follow up regularly, but showed up 2 years and 7 months later for suffering upper abdominal pain again with original FNH enlargement, and the patient received surgical resection of the FNH and achieved asymptomatic aftermath. Conclusion: PMC is safe and effectiveness for symptomatic liver FNHs. PMC should be considered to be an alternative modality for those solitary FNHs with less than 5 cm in diameter

MiR-324-5p Suppresses Hepatocellular Carcinoma Cell Invasion by Counteracting ECM Degradation through Post-Transcriptionally Downregulating ETS1 and SP1.

Hepatocellular carcinoma (HCC) is one of the common malignancies, which is highly metastatic and the third common cause of cancer deaths in the world. The invasion and metastasis of cancer cells is a multistep and complex process which is mainly initiated by extracellular matrix (ECM) degradation. Aberrant expression of microRNA has been investigated in HCC and shown to play essential roles during HCC progression. In the present study, we found that microRNA-324-5p (miR-324-5p) was downregulated in both HCC cell lines and tissues. Ectopic miR-324-5p led to the reduction of HCC cells invasive and metastatic capacity, whereas inhibition of miR-324-5p promoted the invasion of HCC cells. Matrix metalloproteinase 2 (MMP2) and MMP9, the major regulators of ECM degradation, were found to be downregulated by ectopic miR-324-5p, while upregulated by miR-324-5p inhibitor. E26 transformation-specific 1 (ETS1) and Specificity protein 1 (SP1), both of which could modulate MMP2 and MMP9 expression and activity, were presented as the direct targets of and downregulated by miR-324-5p. Downregulation of ETS1 and SP1 mediated the inhibitory function of miR-324-5p on HCC migration and invasion. Our study demonstrates that miR-324-5p suppresses hepatocellular carcinoma cell invasion and might provide new clues to invasive HCC therapy

MiR-324-5p is downregulated in both HCC cell lines and tissues.

<p><b>A.</b> Real-time PCR analysis of miR-324-5p expression in hepatocellular carcinoma cell lines (HepG2, Hep3B, MHCC97H, MHCC97L, BEL-7402, Huh7, SMMC-7721, PLC/PRF/5 and QGY-7703), compared with normal liver epithelial THLE3 cells. <b>B.</b> The expression of miR-324-5p was examined in eleven paired cancerous tissues (T) and their adjacent noncancerous hepatic tissues (ANT). The result is performed as the ratio of T and ANT. The average miR-324-5p expression was normalized using U6 expression. Each bar represents the mean ± SD of three independent experiments. * <i>P</i> <0.05.</p

Inhibition of miR-324-5p promotes invasion and migration of HCC cells.

<p><b>A.</b> Representative micrographs (left) and quantifications (right) of wound healing assay of the HCC cells, transfected with miR-324-5p inhibitor or negative control (NC). Wound closures were photographed at 0, 12 and 24 hours after wounding. <b>B.</b> Representative micrographs (left) and quantifications (right) of indicated invading cells in a Matrigel-coated Transwell assay. <b>C.</b> Representative micrographs of indicated cells grown on Matrigel for 10 days in 3-Dimensional Cell Culture. <b>D.</b> Real-time PCR analysis of MMP2 and MMP9 expression in indicated cells. <i>GAPDH</i> served as control. <b>E.</b> The activity of MMP2 and MMP9 in indicated cells determined by ELISA assay. Each bar represents the mean ± SD of three independent experiments. * <i>P</i> <0.05.</p