Gaze-Informed egocentric action recognition for memory aid systems

Egocentric action recognition has been intensively studied in the fields of computer vision and clinical science with applications in pervasive health-care. The majority of the existing egocentric action recognition techniques utilize the features extracted from either the entire contents or the regions of interest in video frames as the inputs of action classifiers. The former might suffer from moving backgrounds or irrelevant foregrounds usually associated with egocentric action videos, while the latter may be impaired by the mismatch between the calculated and the ground truth regions of interest. This paper proposes a new gaze-informed feature extraction approach, by which the features are extracted from the regions around the gaze points and thus representing the genuine regions of interest from a first person of view. The activity of daily life can then be classified based only on the identified regions using the extracted gaze-informed features. The proposed approach has been further applied to a memory support system for people with poor memory, such as those with Amnesia or dementia, and their carers. The experimental results demonstrate the efficacy of the proposed approach in egocentric action recognition and thus the potential of the memory support tool in health care

Enhanced Gradient-Based Local Feature Descriptors by Saliency Map for Egocentric Action Recognition

Egocentric video analysis is an important tool in healthcare that serves a variety of purposes, such as memory aid systems and physical rehabilitation, and feature extraction is an indispensable process for such analysis. Local feature descriptors have been widely applied due to their simple implementation and reasonable efficiency and performance in applications. This paper proposes an enhanced spatial and temporal local feature descriptor extraction method to boost the performance of action classification. The approach allows local feature descriptors to take advantage of saliency maps, which provide insights into visual attention. The effectiveness of the proposed method was validated and evaluated by a comparative study, whose results demonstrated an improved accuracy of around 2%

4-Hydr­oxy-2,2,6,6-tetra­methyl­piperidinium chloride–hydroxonium chloride (3/1)

The crystal structure of the title compound, C9H20NO+·Cl−·0.33(H3O+·Cl−), is composed of 4-hydr­oxy-2,2,6,6-tetra­methyl­piperidinium cations, hydroxonium cations and chloride anions, which are connected via O—H⋯O, O—H⋯Cl and N—H⋯Cl hydrogen bonding. The 4-hydr­oxy-2,2,6,6-tetra­methyl­piperidinium cation and one of the two crystallographically independent chloride anions are located on a mirror plane. The hydroxonium cation is located on a threefold axis and the second crystallographically independent chloride anion is located on a sixfold rotoinversion axis. Due to symmetry, the hydroxonium cation is disordered over two positions

Notch1 is required for hypoxia-induced proliferation, invasion and chemoresistance of T-cell acute lymphoblastic leukemia cells

Background Notch1 is a potent regulator known to play an oncogenic role in many malignancies including T-cell acute lymphoblastic leukemia (T-ALL). Tumor hypoxia and increased hypoxia-inducible factor-1α (HIF-1α) activity can act as major stimuli for tumor aggressiveness and progression. Although hypoxia-mediated activation of the Notch1 pathway plays an important role in tumor cell survival and invasiveness, the interaction between HIF-1α and Notch1 has not yet been identified in T-ALL. This study was designed to investigate whether hypoxia activates Notch1 signalling through HIF-1α stabilization and to determine the contribution of hypoxia and HIF-1α to proliferation, invasion and chemoresistance in T-ALL. Methods T-ALL cell lines (Jurkat, Sup-T1) transfected with HIF-1α or Notch1 small interference RNA (siRNA) were incubated in normoxic or hypoxic conditions. Their potential for proliferation and invasion was measured by WST-8 and transwell assays. Flow cytometry was used to detect apoptosis and assess cell cycle regulation. Expression and regulation of components of the HIF-1α and Notch1 pathways and of genes related to proliferation, invasion and apoptosis were assessed by quantitative real-time PCR or Western blot. Results Hypoxia potentiated Notch1 signalling via stabilization and activation of the transcription factor HIF-1α. Hypoxia/HIF-1α-activated Notch1 signalling altered expression of cell cycle regulatory proteins and accelerated cell proliferation. Hypoxia-induced Notch1 activation increased the expression of matrix metalloproteinase-2 (MMP2) and MMP9, which increased invasiveness. Of greater clinical significance, knockdown of Notch1 prevented the protective effect of hypoxia/HIF-1α against dexamethasone-induced apoptosis. This sensitization correlated with losing the effect of hypoxia/HIF-1α on Bcl-2 and Bcl-xL expression. Conclusions Notch1 signalling is required for hypoxia/HIF-1α-induced proliferation, invasion and chemoresistance in T-ALL. Pharmacological inhibitors of HIF-1α or Notch1 signalling may be attractive interventions for T-ALL treatment

Correlation of caveolin-1 expression with microlymphatic vessel density in colorectal adenocarcinoma tissues and its correlation with prognosis

AbstractObjectiveTo study the expression of caveolin-1 in colorectal adenocarcinoma tissues and its correlation with microlymphatic vessel density (LMVD), and to investigate the clinical pathological prognostic significance of caveolin-1 and LMVD in patients with colorectal cancer.MethodsThe expression of caveolin-1 and LMVD in 45 specimens of normal colorectal tissues, and 90 specimens of colorectal adenocarcinoma tissues were detected by immunohistochemistry technique. The correlation between their expression and the clinicopathologic features was analyzed. Multivariable Cox regression was used to analyze the association between the laboratory indices and overall survival time.ResultsThe positive rates of caveolin-1 in colorectal adenocarcinoma tissues were significantly higher than those in normal colorectal tissues (P < 0.01). LMVD in colorectal adenocarcinoma tissues were significantly higher than those in normal colorectal tissues (P < 0.01). Mean LMVD in group with caveolin-1 positive was significantly higher than in that with caveolin-1 negative. The median survival time was 26.7 months. Cox regression analysis showed that the caveolin-1 expression, invation depth, lymph node metastasis, TNM stage, liver metastasis and LMVD were independent risk factors of overall survival time of patients with colorectal carcinoma.ConclusionsCaveolin-1 may contribute to the lymphangiogenesis in the tumor. During the occurrence and development of colorectal adenocarcinoma, there is a close relationship between the expression of caveolin-1 and lymphatic microvessel of tumor. Caveolin-1 expression and microlymphatic vessel density are significant prognostic value of colorectal carcinoma

Growth factor for therapeutic angiogenesis in ischemic heart disease: A meta-analysis of randomized controlled trials

Aim: This study was designed to systematically evaluate the effects of growth factor (GF) for therapeutic angiogenesis on ischemic heart disease (IHD) by pooling the results of randomized controlled trials (RCTs).Methods and Results: PubMed, EMBASE, and CENTRAL databases were searched from inception to October 2022. RCTs, investigating the effects of GF therapy on IHD, were included. The risk bias of included study was assessed according to Cochrane tool. Weighted mean difference (WMD), calculated with fixed effect model or random effect model, was used to evaluate the effects of GF therapy on left ventricular ejection fraction (LVEF) and Canadian Cardiovascular Society (CCS) angina class. Relative risk (RR) was used to evaluate the effects of GF therapy on all-cause mortality, major adverse cardiovascular events (MACE) and revascularization. Meta-analysis, meta-regression analysis and publication bias analysis were performed by RevMan 5.3 or Stata 15.1 software. Twenty-nine studies involving 2899 IHD patients (1,577 patients in GF group and 1,322 patients in control group) were included. Compared with the control group, GF therapy did not reduce all-cause mortality (RR: 0.82; 95% CI: 0.54–1.24; p = 0.341), MACE [(RR: 0.83; 95% CI: 0.61–1.12; p = 0.227), revascularization (RR: 1.27, 95% CI: 0.82–1.96, p = 0.290) and CCS angina class (WMD: −0.08, 95% CI: −0.36 to 0.20, p = 0.560). However, GF therapy could increase LVEF during short-term follow-up (&lt;1 year).Conclusion: GF for therapeutic angiogenesis was beneficial for increasing LVEF during short-term follow-up (&lt;1 year), however, the therapy was not efficacious in decreasing all-cause mortality, MACE and revascularization

Analysis of EGFR signaling pathway in nasopharyngeal carcinoma cells by quantitative phosphoproteomics

<p>Abstract</p> <p>Background</p> <p>The epidermal growth factor receptor (EGFR) is usually overexpressed in nasopharyngeal carcinoma (NPC) and is associated with pathogenesis of NPC. However, the downstream signaling proteins of EGFR in NPC have not yet been completely understood at the system level. The aim of this study was identify novel downstream proteins of EGFR signaling pathway in NPC cells.</p> <p>Results</p> <p>We analyzed EGFR-regulated phosphoproteome in NPC CNE2 cells using 2D-DIGE and mass spectrometry analysis after phosphoprotein enrichment. As a result, 33 nonredundant phosphoproteins including five known EGFR-regulated proteins and twenty-eight novel EGFR-regulated proteins in CNE2 were identified, three differential phosphoproteins were selectively validated, and two differential phosphoproteins (GSTP1 and GRB2) were showed interacted with phospho-EGFR. Bioinformatics analysis showed that 32 of 33 identified proteins contain phosphorylation modification sites, and 17 identified proteins are signaling proteins. GSTP1, one of the EGFR-regulated proteins, associated with chemoresistance was analyzed. The results showed that GSTP1 could contribute to paclitaxel resistance in EGF-stimulated CNE2 cells. Furthermore, an EGFR signaling network based on the identified EGFR-regulated phosphoproteins were constructed using Pathway Studio 5.0 software, which includes canonical and novel EGFR-regulated proteins and implicates the possible biological roles for those proteins.</p> <p>Conclusion</p> <p>The data not only can extend our knowledge of canonical EGFR signaling, but also will be useful to understand the molecular mechanisms of EGFR in NPC pathogenesis and search therapeutic targets for NPC.</p

Construction of a cross-species cell landscape at single-cell level.

Individual cells are basic units of life. Despite extensive efforts to characterize the cellular heterogeneity of different organisms, cross-species comparisons of landscape dynamics have not been achieved. Here, we applied single-cell RNA sequencing (scRNA-seq) to map organism-level cell landscapes at multiple life stages for mice, zebrafish and Drosophila. By integrating the comprehensive dataset of > 2.6 million single cells, we constructed a cross-species cell landscape and identified signatures and common pathways that changed throughout the life span. We identified structural inflammation and mitochondrial dysfunction as the most common hallmarks of organism aging, and found that pharmacological activation of mitochondrial metabolism alleviated aging phenotypes in mice. The cross-species cell landscape with other published datasets were stored in an integrated online portal-Cell Landscape. Our work provides a valuable resource for studying lineage development, maturation and aging