Human pose estimation is the basis of many downstream tasks, such as motor intervention, behavior understanding, and human-computer interaction. The existing human pose estimation methods rely too much on the similarity of keypoints at the image feature level, which is vulnerable to three problems: object occlusion, keypoints ghost, and neighbor pose interference. We propose a dual-space-driven topology model for the human pose estimation task. Firstly, the model extracts relatively accurate keypoints features through a Transformer-based feature extraction method. Then, the correlation of keypoints in the physical space is introduced to alleviate the error localization problem caused by excessive dependence on the feature-level representation of the model. Finally, through the graph convolutional neural network, the spatial correlation of keypoints and the feature correlation are effectively fused to obtain more accurate human pose estimation results. The experimental results on real datasets also further verify the effectiveness of our proposed model.
Background: First-episode schizophrenia (FES) and anti-NMDAR encephalitis are different disorders with similar psychiatric symptoms, and both diseases are associated with the inflammatory system. In this study, we compared hematological parameters and inflammation ratios in anti-NMDAR encephalitis, FES, and healthy control. Methods: We enrolled 106 patients (53 FES patients and 53 anti-NMDAR encephalitis patients) and 59 healthy controls. The values of the neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), monocyte-lymphocyte ratio (MLR), and systemic immune-inflammation index (SII) were used to evaluate inflammation. Other parameters such as the white blood cell (WBC), platelet (PLT), uric acid (UA), total bilirubin (TBIL), total bile acid (TBA), and serum albumin counts were also used to compare inflammation ratios between these two diseases. Results: SII, NLR, PLR, MLR, and serum albumin levels were statistically significantly different between these three groups (p < 0.05). The values of SII, NLR, PLR, and MLR were significantly higher in the anti-NMDAR encephalitis group than those in the FES group (p < 0.05), and the values in both diseases were more increased than those in HC (p < 0.05). The serum albumin level was significantly lower in anti-NMDAR encephalitis than in FES (p < 0.05). WBC, neutrophil, lymphocyte, and monocyte counts showed significantly higher levels in the anti-NMDAR encephalitis group and FES group separately (p < 0.05). Other parameters like TBA, TBIL, and UA showed no difference between groups. Conclusion: In summary, this is a relatively new study that is innovative by comparing some inflammation markers of peripheral blood in two diseases with clinically psychotic symptoms. These two diseases are related to the inflammatory system, proving that NMDAR dysfunction is related to psychotic symptoms. Besides, NLR, PLR, MLR, and serum albumin can be used as biomarkers to distinguish the two diseases. The serum albumin level in patients with anti-NMDAR encephalitis was lower than that in patients with schizophrenia.
To study the antitumor activity of engineered fusion of tumor cell and dendritic cells (DC).J558 tumor cells were transfected with mouse IL-12 (mIL-12) gene and then fused with DCs to develop a hybrid-engineered tumor vaccine. BALB/c mice were challenged with wild-type J558 tumor cells 14 days after vaccinated with hybrid-engineered J558.mIL-12 was detected at (870 +/- 60) pg.(10(5) cells)(-1).ml(-1) in the culture supernatants and the cell-fusion rate was about 30% by co-focal microscopy. In addition, the lymphocytes from popliteal nodes and groin nodes of these mice vaccinated with hybrid-engineered J558 secreted higher levels of IFN-gamma than that of other control mice, and vaccination of mice with the fusion vaccine induced more efficient tumor-specific CTL cytotoxicity against wild-type tumor cells in vitro and with efficient antitumor immunity in vivo.It suggested that vaccination of mice with the fusion vaccine induced stronger Th1-dominant responses and this approach could perhaps be applied to clinical settings of DCs-based cancer vaccines.
Abstract Profound secretory dysfunction can be associated with relatively modest lymphocytic infiltration of the lacrimal and salivary glands of Sjögren's syndrome (SjS) patients. SjS patients' sera contain autoantibodies to M3 muscarinic acetylcholine receptors (MAChR) that have variously been reported to have agonistic and antagonistic effects. We sought to identify consequences of chronic agonist stimulation by maintaining acinar cells from rabbit lacrimal glands for 20 h in the presence or absence of 10 µ m carbachol (CCh). Exposure to CCh diminished the cells' ability to elevate cytosolic Ca 2+ and secrete β‐hexosaminidase in response to acute stimulation with 100 µ m CCh, but it enhanced their secretory responses to phenylephrine and ionomycin. Secretory vesicles appeared normal by electron microscopy, but confocal fluorescence microscopy revealed depletion of the secretory vesicle membrane marker, rab3D, and decreased ability to recruit secretory transport vesicles in response to acute 100 µ m CCh. Additionally, the apical cortical actin cytoskeleton was disrupted and diminished compared to the basal–lateral cortical network. Subcellular fractionation analyses revealed that total membrane phase protein content was increased. The contents of β‐hexosaminidase and MAChR relative to total protein were not significantly altered, and MAChR abundance in the plasma membrane fraction was increased as the result of redistribution from endomembrane pools. However, relative cellular contents of the heterotrimeric guanosine triphosphate (GTP)‐binding proteins, G q and G 11 , were decreased. Additional biochemical changes included decreased contents of 47 kDa G s and G i3 , protein kinase Cα and rab3D and polymeric immunoglobulin (Ig) receptors; internalization of Na,K‐ATPase from the plasma membranes to endomembrane compartments and decreased content of β‐hexosaminidase in the lysosomes. The observations demonstrate that chronic exposure to a MAChR agonist induces refractoriness to optimal stimulation, without causing receptor downregulation, by downregulating postreceptor‐signalling mediators and effectors. The cells' secretory mechanisms for IgA and electrolytes also appear to be impaired, as does their ability to properly sort proteins to the lysosomes.
Normal cells express functional tumor suppressor WW domain-containing oxidoreductase (WWOX), designated WWOXf. UV irradiation induces WWOXf cells to undergo bubbling cell death (BCD) - an event due to the accumulation of nuclear nitric oxide (NO) gas that forcefully pushes the nuclear and cell membranes to form one or two bubbles at room temperature (22 °C) and below. In contrast, when WWOX-deficient or -dysfunctional (WWOXd) cells are exposed to UV and/or cold shock, the cells undergo nuclear pop-out explosion death (POD). We aimed to determine the morphological and biochemical changes in WWOXf cells during BCD versus apoptosis.
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