A Spatial-Channel-Temporal-Fused Attention for Spiking Neural Networks.

Spiking neural networks (SNNs) mimic brain computational strategies, and exhibit substantial capabilities in spatiotemporal information processing. As an essential factor for human perception, visual attention refers to the dynamic process for selecting salient regions in biological vision systems. Although visual attention mechanisms have achieved great success in computer vision applications, they are rarely introduced into SNNs. Inspired by experimental observations on predictive attentional remapping, we propose a new spatial-channel-temporal-fused attention (SCTFA) module that can guide SNNs to efficiently capture underlying target regions by utilizing accumulated historical spatial-channel information in the present study. Through a systematic evaluation on three event stream datasets (DVS Gesture, SL-Animals-DVS, and MNIST-DVS), we demonstrate that the SNN with the SCTFA module (SCTFA-SNN) not only significantly outperforms the baseline SNN (BL-SNN) and two other SNN models with degenerated attention modules, but also achieves competitive accuracy with the existing state-of-the-art (SOTA) methods. Additionally, our detailed analysis shows that the proposed SCTFA-SNN model has strong robustness to noise and outstanding stability when faced with incomplete data, while maintaining acceptable complexity and efficiency. Overall, these findings indicate that incorporating appropriate cognitive mechanisms of the brain may provide a promising approach to elevate the capabilities of SNNs.

Endovascular Treatment for Isolated Infected Iliac Artery Aneurysms.

PURPOSE: Isolated infected iliac artery aneurysms (IIIAAs) are extremely rare, life-threatening, and intractable. This study aimed to evaluate the outcomes of endovascular treatment in patients with IIIAAs. METHODS: A retrospective study was conducted for all patients who underwent endovascular treatment for IIIAAs between June 2012 and June 2022 in 3 hospitals. The clinical data and follow-up outcomes were reviewed and assessed. RESULTS: Fifteen patients were included in this study. The median age was 69 years, 12 patients (80%) were men, and 8 (53%) had hypertension. Most of the patients presented with abdominal or lumbar pain (87%) and fever (60%). The offending pathogen was identified in 11 patients (73%). Fifteen patients had a total of 16 IIIAAs, with 12 (75%) involving the common iliac artery. The immediate technical success rate was 100%, and the 30-day mortality was 7%. Infection-related complications occurred in 2 patients (13%) during hospitalization who were treated by open surgery at a later stage. The median follow-up was 23 months (range: 6-80 months, mean: 32 ± 25 months). Aneurysm recurrence was identified in one patient (7%) 5 months after endovascular repair. It was managed by endovascular stent-graft repair with percutaneous catheter drainage. No patients died during the follow-up period. CONCLUSION: Endovascular treatment is feasible, safe, and effective for patients with IIIAAs, achieving acceptable clinical outcomes. Infection surveillance with essential reintervention should be considered for potential infection-related complications. CLINICAL IMPACT: This study first reported that 15 patients underwent endovascular treatment for primary isolated infected iliac artery aneurysms (IIIAAs). It showed a good early and midterm outcomes. This is the first and largest multi-center study and the first literature review of IIIAAs. It provides an evidence that endovascular treatment is feasible, safe, and effective to treat IIIAAs. It suggests endovascular treatment is a promising alternative or a bridge to conventional open surgery for IIIAAs. This may promote endovascular therapy in the management of IIIAAs. It would help clinicians to make an appropriate treatment choice for IIIAAs.

Platelet/Lymphocyte Ratio Predicted Long-Term Prognosis for Acute Upper Extremity Deep Vein Thrombosis from a Retrospective Study.

Background: In this study, we aimed to determine the mortality risk factors and whether placement of a vena cava filter improves the prognosis of acute upper extremity deep vein thrombosis (UEDVT). Methods: Clinical data and follow-up results were retrospectively analyzed. Cox regression analysis was conducted to identify the risk factors associated with all-cause mortality in all patients and subgroups of patients. Results are expressed as hazard ratio (HR) with 95% confidence intervals (95% CI). Receiver operating characteristic curves (ROC) were used to determine the optimal cut-off value. Kaplan-Meier survival curves were constructed and compared by the Log rank test. Results: The study cohort comprised 109 patients of median age 56 years (47.5, 64.5). The median follow-up time was 25 months (8, 47): 39 patients (35.8%) had died by 12 months, 55 (50.5%) by 36 months, and 60 (55%) by the end of follow-up. Presence of malignancy (HR: 5.882, 95% CI: 2.128-16.667), D-dimer (HR: 1.56, 95% CI: 1.09-1.94), platelet/lymphocyte ratio (PLR; HR: 2.02, 95% CI: 1.15-3.54), and the systemic immune/inflammatory index (SII; HR: 1.471, 95% CI: 1.062-1.991) were identified as independent risk factors for mortality. Subgroup analysis of patients with malignancy determined gender (HR: 2.936, 95% CI: 1.599-5.393) and PLR (HR: 1.427,95% CI: 1.023-1.989) as independent risk factors. Kaplan-Meier analysis showed that the mortality rate was much higher in patients with malignancy, high D-dimer (≥ 0.92ug/mL), high PLR (≥ 291) and high SII (≥ 1487). However, there was no significant difference between patients with and without vena cava filters. Conclusion: In this study, we identified PLR as an new independent predictor of mortality in patients with acute UEDVT. Emergency placement of a vena cava filter did not improve long-term prognosis.

Characterization of the complete plastid genome of Abies forrestii (Pinaceae) from southwest China.

Abies forrestii is endemic to southwest China and ecologically important as a major component of the cold temperate forests. This study was the first report complete chloroplast (cp) genome of A. forrestii. The complete chloroplast genome was 120,022 bp in size. In total, 114 genes were identified, including 68 peptide-encoding genes, 35 tRNA genes, four rRNA genes, six open reading frames and one pseudogene. Thirteen genes contain introns. In phylogenetic analysis, A. forrestii was found to be closely related with A. nukiangensis, A. fanjingshanensis and A. delavayi subsp. fansipanensis. Our study will provide potential genetic resources for further evolutionary studies of this ecologically important species.

Impaired AGO2/miR-185-3p/NRP1 axis promotes colorectal cancer metastasis.

Increasing evidence suggests that global downregulation of miRNA expression is a hallmark of human cancer, potentially due to defects in the miRNA processing machinery. In this study, we found that the protein expression of Argonaute 2 (AGO2), a key regulator of miRNA processing, was downregulated in colorectal cancer (CRC) tissues, which was also consistent with the findings of the Clinical Proteomic Tumor Analysis Consortium (CPTAC). Furthermore, the correlation between the levels of AGO2 and epithelial-mesenchymal transition (EMT) markers (E-cadherin and vimentin) indicated that reduced levels of AGO2 promoted EMT in CRC. Low expression of AGO2 was an indicator of a poor prognosis among CRC patients. Knockdown of AGO2 in CRC cells promoted migration, invasion and metastasis formation in vitro and in vivo but had no influence on proliferation. To provide detailed insight into the regulatory roles of AGO2, we performed integrated transcriptomic, quantitative proteomic and microRNA sequencing (miRNA-seq) analyses of AGO2 knockdown cells and the corresponding wild-type cells and identified neuropilin 1 (NRP1) as a new substrate of AGO2 via miR-185-3p. Our data provided evidence that knockdown of AGO2 resulted in a reduction of miR-185-3p expression, leading to the upregulation of the expression of NRP1, which is a direct target of miR-185-3p, and elevated CRC cell metastatic capacity. Inhibition of NRP1 or treatment with a miR-185-3p mimic successfully rescued the phenotypes of impaired AGO2, which suggested that therapeutically targeting the AGO2/miR-185-3p/NRP1 axis may be a potential treatment approach for CRC.

Identifying Refractory Epilepsy Without Structural Abnormalities by Fusing the Common Spatial Patterns of Functional and Effective EEG Networks.

Drug refractory epilepsy (RE) is believed to be associated with structural lesions, but some RE patients show no significant structural abnormalities (RE-no-SA) on conventional magnetic resonance imaging scans. Since most of the medically controlled epilepsy (MCE) patients also do not exhibit structural abnormalities, a reliable assessment needs to be developed to differentiate RE-no-SA patients and MCE patients to avoid misdiagnosis and inappropriate treatment. Using resting-state scalp electroencephalogram (EEG) datasets, we extracted the spatial pattern of network (SPN) features from the functional and effective EEG networks of both RE-no-SA patients and MCE patients. Compared to the performance of traditional resting-state EEG network properties, the SPN features exhibited remarkable superiority in classifying these two groups of epilepsy patients, and accuracy values of 90.00% and 80.00% were obtained for the SPN features of the functional and effective EEG networks, respectively. By further fusing the SPN features of functional and effective networks, we demonstrated that the highest accuracy value of 96.67% could be reached, with a sensitivity of 100% and specificity of 92.86%. Overall, these findings not only indicate that the fused functional and effective SPN features are promising as reliable measurements for distinguishing RE-no-SA patients and MCE patients but also may provide a new perspective to explore the complex neurophysiology of refractory epilepsy.

USP11 induce resistance to 5-Fluorouracil in Colorectal Cancer through activating autophagy by stabilizing VCP.

Chemotherapy plays an important role in the treatment of patients with colorectal cancer (CRC). However, the resistance to chemotherapy severely affects the prognosis of CRC patients and the mechanisms are still poorly understood. Our study investigated the role of ubiquitin-specific protease 11 (USP11) in CRC chemotherapy and found that USP11 could induce resistance to 5-fluorouracil by activating autophagy. A series of in vitro and in vivo experiments revealed that USP11 promoted autophagy through AMPK/Akt/mTOR pathway via stabilizing valosin-containing protein (VCP). Overall, our study demonstrated that USP11 might be valuable to predict the chemotherapeutic sensitivity and improve the prognosis of CRC patients.

Estradiol is significantly associated with prognosis in non-surgical liver cancer patients: from bench to bedside.

There are rarely systematic studies to analyze the prognostic factors among non-surgical liver cancer patients. Whether there is a gender difference in the survival of non-surgical liver cancer patients and what may cause this difference is still unclear. A total of 12,312 non-surgical liver cancer patients were enrolled in this study. Age, race, sex, grade, tumor TNM stage, marital status, tumor size, and histological type were independent risk factors in liver cancer and were confirmed in the validation cohort. Before menopause, females demonstrated a better mean survival probability than males (39.4±1.4 vs. 32.7±0.8 months, respectively; p<0.001), and continued in post-menopause. The results of differentially expressed genes (DEGs) and KEGG pathway analysis showed that there were significant differences in steroid hormone biosynthesis between male and female liver cancer patients. In vitro experiments revealed that estradiol inhibited the proliferation of hepatocellular cancer cell lines and increased apoptosis, but estrone exerted no effect. In conclusion, gender differences in prognosis among non-surgical liver cancer patients were confirmed and attributable primarily to estradiol.

Polo-like kinase 3 inhibits glucose metabolism in colorectal cancer by targeting HSP90/STAT3/HK2 signaling.

BACKGROUND: Polo-like kinase 3 (PLK3) has been documented as a tumor suppressor in several types of malignancies. However, the role of PLK3 in colorectal cancer (CRC) progression and glucose metabolism remains to be known. METHODS: The expression of PLK3 in CRC tissues was determined by immunohistochemistry. Cells proliferation was examined by EdU, CCK-8 and in vivo analyses. Glucose metabolism was assessed by detecting lactate production, glucose uptake, mitochondrial respiration, extracellular acidification rate, oxygen consumption rate and ATP production. Chromatin immunoprecipitation, luciferase reporter assays and co-immunoprecipitation were performed to explore the signaling pathway. Specific targeting by miRNAs was determined by luciferase reporter assays and correlation with target protein expression. RESULTS: PLK3 was significantly downregulated in CRC tissues and its low expression was correlated with worse prognosis of patients. In vitro and in vivo experiments revealed that PLK3 contributed to growth inhibition of CRC cells. Furthermore, we demonstrated that PLK3 impeded glucose metabolism via targeting Hexokinase 2 (HK2) expression. Mechanically, PLK3 bound to Heat shock protein 90 (HSP90) and facilitated its degradation, which led to a significant decrease of phosphorylated STAT3. The downregulation of p-STAT3 further suppressed the transcriptional activation of HK2. Moreover, our investigations showed that PLK3 was directly targeted by miR-106b at post-transcriptional level in CRC cells. CONCLUSION: This study suggests that PLK3 inhibits glucose metabolism by targeting HSP90/STAT3/HK2 signaling and PLK3 may serve as a potential therapeutic target in colorectal cancer.

USP11 promotes growth and metastasis of colorectal cancer via PPP1CA-mediated activation of ERK/MAPK signaling pathway.

BACKGROUND: USP11 is an ubiquitin-specific protease that plays an important role in tumor progression via different mechanisms. However, the expression and prognostic significance of USP11 in colorectal cancer (CRC) remain unknown. METHODS: Bioinformatics analyses, qRT-PCR, western blotting, and immunohistochemistry were applied for investigating USP11 expression in CRC tissues. Kaplan-Meier analysis with log-rank test was used for survival analyses. LC-MS/MS was performed for identifying potential protein interactions with USP11. In vitro and in vivo assays were used for exploring the function of USP11 during the progression of CRC. FINDINGS: USP11 was overexpressed in CRC tissues and functioned as an oncogene. Overexpression or knockdown of USP11 promoted or inhibited, respectively, the growth and metastasis of CRC cells in vitro and in vivo. Mechanically, USP11 stabilized PPP1CA by deubiquitinating and protecting it from proteasome-mediated degradation. Moreover, the USP11/PPP1CA complex promoted CRC progression by activating the ERK/MAPK signaling pathway. INTERPRETATION: USP11 promoted tumor growth and metastasis in CRC via the ERK/MAPK pathway by stabilizing PPP1CA, suggesting USP11 is a potential prognostic marker. FUND: This work was supported by National Natural Science Foundation of China (NSFC81530044, NSFC81220108021, NSFC81802343), Technology Major Project of China Grants 2017ZX10203206, Shanghai Sailing Program (19YF1409600) and The project of Shanghai Jiaotong University (YG2017QN30).