Gastric cancer (GC) is one of the most common cancers in the world. The cathepsin F (CTSF) gene has recently been found to participate in the progression of several types of cancer. However, the clinical characteristics and function of CTSF in GC as well as its molecular mechanisms are not clear. Six GC cell lines and 44 paired adjacent noncancerous and GC tissue samples were used to assess CTSF expression by quantitative polymerase chain reaction (qPCR). We used lentivirus-mediated small hairpin RNA (Lenti-shRNA) against CTSF to knock down the expression of CTSF in GC cells. Western blot and qPCR were used to analyze the mRNA and related protein expression. The biological phenotypes of gastric cells were examined by cell proliferation and apoptosis assays. Microarray-based mRNA expression profile screening was also performed to evaluate the potential molecular pathways in which CTSF may be involved. The CTSF mRNA level was associated with tumor differentiation, depth of tumor invasion, and lymph node metastasis. Downregulation of CTSF expression efficiently inhibited apoptosis and promoted the proliferation of GC cells. Moreover, a total of 1,117 upregulated mRNAs and 1,143 downregulated mRNAs were identified as differentially expressed genes (DEGs). Further analysis identified the involvement of these mRNAs in cancer-related pathways and various other biological processes. Nine DEGs in cancer-related pathways and three downstream genes in the apoptosis pathway were validated by Western blot, which was mainly in agreement with the microarray data. To our knowledge, this is the first report investigating the effect of CTSF on the growth and apoptosis in GC cells and its clinical significance. The CTSF gene may function as a tumor suppressor in GC and may be a potential therapeutic target in the treatment of GC.

HtrA serine peptidase 3 (HTRA3) participates in multiple signal pathways and plays an important regulatory role in various malignancies; however, its role on prognosis and immune infiltrates in gastric cancer (GC) remains unclear. The study investigated HTRA3 expression in tumor tissues and its association with immune infiltrates, and determined its prognostic roles in GC patients. Patients with GC were collected from the cancer genome atlas (TCGA). We compared the expression of HTRA3 in GC and normal gastric mucosa tissues with Wilcoxon rank sum test. And logistic regression was used to evaluate the relationship between HTRA3 and clinicopathological characters. Gene ontology (GO) term analysis, Gene set enrichment analysis (GSEA), and single-sample Gene Set Enrichment Analysis (ssGSEA) was conducted to explain the enrichmental pathways and functions and quantify the extent of immune cells infiltration for HTRA3. Kaplan-Meier analysis and Cox regression were performed to evaluate the correlation between HTRA3 and survival rates. A nomogram, based on Cox multivariate analysis, was used to predict the impact of HTRA3 on prognosis. High HTRA3 expression was significantly correlated with tumor histological type, histological grade, clinical stage, T stage, and TP53 status (P < 0.05). HTRA3-high GC patients had a lower 10-year progression-free interval [PFI; hazard ratio (HR): 1.46; 95% confidence interval (CI): 1.02–2.08; P = 0.038], disease-specific survival (DSS; HR: 1.65; CI: 1.08–2.52; P = 0.021) and overall survival (OS; HR: 1.59; CI: 1.14–2.22; P = 0.006). Multivariate survival analysis showed that HTRA3 was an independent prognostic marker for PFI (HR: 1.456; CI: 1.021–2.078; P = 0.038), DSS (HR: 1.650; CI: 1.079–2.522; P = 0.021) and OS [hazard ratio (HR): 1.590; 95% confidence interval (CI):1.140–2.219; P = 0.006]. The C-indexes and calibration plots of the nomogram based on multivariate analysis indicated an effective predictive performance for GC patients. GSEA showed that High HTRA3 expression may activate NF-κB pathway, YAP1/WWTR1/TAZ pathway, and TGFβ pathway. There was a negative correlation between the HTRA3 expression and the abundances of adaptive immunocytes (T helper cell 17 cells) and a positive correlation with abundances of innate immunocytes (natural killer cells, macrophages etc.). HTRA3 plays a vital role in GC progression and prognosis and could be a moderate biomarker for prediction for survival after gastrectomy.

The aim of this study is to analyze the application of early rehabilitation nursing in nursing intervention of neurological impairment among patients with acute ischemic stroke. 116 patients with acute ischemic stroke were selected as the research subjects in this paper. The patients were divided into 58 experimental (early rehabilitation care) and 58 control (routine rehabilitation care) groups according to the difference of care protocols, all of which were performed magnetic resonance imaging on. An image resolution reconstruction algorithm on the basis of deep convolutional neural network is proposed for MRI image processing. The results show that peak signal to noise ratio (PSNR) and structural similarity index measure (SSIM) of the included algorithm were remarkably greater than those of compressed sensing (CS) algorithm and nonlocal similarity and block low rank prior-based NSBL algorithm. Running time was shorter than that of the latter two algorithms P < 0.05 . The neurological impairment scores of patients in the experimental group 3 and 5 weeks after treatment were obviously lower than those of patients in the control group P < 0.05 . The Barthel indexes of patients in the experimental group 3 and 5 weeks after treatment were obviously higher than those of patients in the control group P < 0.05 . FugI-Meyer assessment (FMA) and Disability of Arm-Shoulder-Hand (DASH) scores of patients in the experimental group 3 and 5 weeks after treatment were obviously lower than those of patients in control group P < 0.05 . The results show that the deep learning algorithm for MRI image processing performance is better than the traditional algorithm. It not only improves the image quality but also improves the processing efficiency. Early rehabilitation nursing and routine rehabilitation nursing can effectively improve the neurological deficit symptoms, limb motor function, and daily living ability of patients with acute ischemic stroke, and the effect of early rehabilitation nursing is the best.

HtrA serine peptidase 4 (HTRA4), which belongs to the AB family of proteases/chapterones, participates in multiple signal pathways and plays an important regulatory role in some malignancies; however, its role in the prognosis and immune infiltrates of gastric cancer (GC) remains unclear. HTRA4 expression was thus investigated in tumor tissues, and its association with immune infiltrates was assessed, to determine its prognostic roles in GC patients. Data for patients with GC was collected from three GEO datasets. This study has investigated if high expression levels of HTRA4 are associated with a poor prognosis in GC patients, especially in T2,T3,N1,NI&N2&N3,M1,stage3 and HER2+ subgroups. HTRA4 was positively correlated with CD8+ T cells, CD4+ memory activated T cells, gamma delta T cells, and M2 macrophages in the GC microenvironment. Gene Ontology and Gene set Enrichment Analysis showed that HTRA4 was enriched in some immune-related pathways. High expression levels of HTRA4 were significantly correlated with tumors in the T stage, N stage, and clinical stage, as well as those of histological grade. In summary, HTRA4 was found to play a vital role in the progression of GC and may be a predictive biomarker for the survival of GC patients.

Toll‐interacting protein (Tollip) is a multifunctional regulator in cellular activities. However, whether its functions are subjected to post‐translational modifications remains elusive. Here, we identified ubiquitination as a post‐translational modification on Tollip. We found that Tollip interacted with ring finger protein 167 (RNF167) through its C‐terminal coupling of ubiquitin to ER degradation (CUE) domain, and RNF167 functioned as the potential E3 ligase to attach K33‐linked poly‐ubiquitin chains to the Lys235 (K235) site of Tollip. Furthermore, we discovered Tollip could inhibit TNF‐α‐induced nuclear factor‐kappa B (NF‐κB) and mitogen‐activated protein kinase (MAPK) activation, and substitution of Lys235 on Tollip to arginine failed to suppress TNF‐α‐NF‐κB/MAPK (JNK) cascades, revealing the role of Tollip and its ubiquitination in NF‐κB/MAPK pathways. Thus, our study reveals the novel biological function of Tollip and RNF167‐dependent ubiquitination of Tollip in TNF‐α signaling.