Knowledge, attitudes, and practice towards allergic rhinitis in patients with allergic rhinitis: a cross-sectional study.

BACKGROUND: The knowledge, attitude, and practice (KAP) of Chinese patients with allergic rhinitis (AR) on AR is poorly known. This study investigated the KAP towards AR in patients with this disease and explored the factors associated with KAP. METHODS: This cross-sectional study enrolled patients with AR in Zhangjiagang Hospital of Traditional Chinese Medicine between October 2022 and March 2023. RESULTS: This study included 656 valid questionnaires. Most participants were 26-35 years old (36.13%) and were female (55.18%). The knowledge, attitude, and practice scores were 5.70 ± 2.88 (possible range: 0-12), 29.51 ± 3.52 (possible range: 9-45), and 34.13 ± 7.55 (possible range: 9-45), indicating poor knowledge, unfavorable attitudes, and proactive practice. AR history of 3-5 years (adjusted odds ratio (adjOR) = 1.62, 95% confidence interval (CI): 1.03-2.54, P = 0.037), AR history of > 6 years (adjOR = 1.64, 95%CI: 1.06-2.54, P = 0.027), and know their own allergens (adjOR = 2.34, 95%CI: 1.28-4.25, P = 0.005) were independently associated with the sufficient knowledge. AR history of ≥ 6 years (adjOR = 0.60, 95%CI: 0.37-0.96, P = 0.035), and liking sports (adjOR = 1.58, 95%CI = 1.07-2.33, P = 0.020) were independently associated with the positive attitude. The knowledge scores (adjOR = 1.14, 95%CI: 1.05-1.22, P = 0.001), attitude scores (adjOR = 1.24, 95%CI: 1.17-1.32, P < 0.001), age 36-45 (adjOR = 2.13, 95%CI: 1.19-3.82, P = 0.011), employed (adjOR = 0.59, 95%CI: 0.37-0.94, P = 0.026), and liking sports (adjOR = 2.11, 95%CI: 1.43-3.14, P < 0.001) were independently associated with the proactive practice. CONCLUSIONS: Patients with AR have poor knowledge and unfavorable attitudes but good practice toward AR. Continuous quality teaching interventions and education on patients for AR were recommended.

Double-path parallel convolutional neural network for removing speckle noise in different types of OCT images.

Speckle noises widely exist in optical coherence tomography (OCT) images. We propose an improved double-path parallel convolutional neural network (called DPNet) to reduce speckles. We increase the network width to replace the network depth to extract deeper information from the original OCT images. In addition, we use dilated convolution and residual learning to increase the learning ability of our DPNet. We use 100 pairs of human retinal OCT images as the training dataset. Then we test the DPNet model for denoising speckles on four different types of OCT images, mainly including human retinal OCT images, skin OCT images, colon crypt OCT images, and quail embryo OCT images. We compare the DPNet model with the adaptive complex diffusion method, the curvelet shrinkage method, the shearlet-based total variation method, and the OCTNet method. We qualitatively and quantitatively evaluate these methods in terms of image smoothness, structural information protection, and edge clarity. Our experimental results prove the performance of the DPNet model, and it allows us to batch and quickly process different types of poor-quality OCT images without any parameter fine-tuning under a time-constrained situation.

Bioinformatics analysis to identify action targets in NCI-N87 gastric cancer cells exposed to quercetin.

CONTEXT: Quercetin exerts antiproliferative effects on gastric cancer. However, its mechanisms of action on gastric cancer have not been comprehensively revealed. OBJECTIVE: We investigated the mechanisms of action of quercetin against gastric cancer cells. MATERIALS AND METHODS: Human NCI-N87 gastric cancer cells were treated with 15 µM quercetin or dimethyl sulfoxide (as a control) for 48 h. DNA isolated from cells was sequenced on a HiSeq 2500, and the data were used to identify differentially expressed genes (DEGs) between groups. Then, enrichment analyses were performed for DEGs and a protein-protein interaction (PPI) network was constructed. Finally, the transcription factors (TFs)-DEGs regulatory network was visualized by Cytoscape software. RESULTS: A total of 121 DEGs were identified in the quercetin group. In the PPI network, Fos proto-oncogene (FOS, degree = 12), aryl hydrocarbon receptor (AHR, degree = 12), Jun proto-oncogene (JUN, degree = 11), and cytochrome P450 family 1 subfamily A member 1 (CYP1A1, degree = 11) with higher degrees highly interconnected with other proteins. Of the 5 TF-DEGs, early growth response 1 (EGR1), FOS like 1 (FOSL1), FOS, and JUN were upregulated, while AHR was downregulated. Moreover, FOSL1, JUN, and Wnt family member 7B (WNT7B) were enriched in the Wnt signaling pathway. DISCUSSION AND CONCLUSIONS: CYP1A1 highly interconnected with AHR in the PPI network. Therefore, FOS, AHR, JUN, CYP1A1, EGR1, FOSL1, and WNT7B might be targets of quercetin in gastric cancer.

Dynamic changes and clinical significance of serum S100B protein and glial fibrillary acidic protein in patients with delayed encephalopathy after acute carbon monoxide poisoning.

OBJECTIVE: To study the dynamic changes and clinical significance of serum S100B protein and glial fibrillary acidic protein (GFAP) in patients with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). METHODS: This study was conducted among DEACMP patients who were hospitalized from November 2014 to February 2016. Serum levels of S100B and GFAP in 66 DEACMP patients were measured by ELISA. Changes in patient states were examined dynamically using activities of daily living (ADL) scale, information-memory-concentration test (IMCT) and Hasegawa's dementia scale (HDS), and compared with those of 64 patients without DE after ACMP. RESULTS: Serum S100B [(0.59 ± 0.11) ng/ml] and GFAP [(227.67 ± 12.43) ng/ml] levels of DEACMP group in acute phase were significantly higher than those of ACMP group [(0.48 ± 0.10) ng/ml and (178.91 ± 11.47) ng/ml] and DEACMP group in recovery phase [(0.49 ± 0.12) ng/ml and (179.54 ± 12.32) ng/ml] (all P<0.05). Serum S100B and GFAP levels of DEACMP group were significantly correlated in both acute and recovery phases (r=0.432 in acute phase, P=0.007; r=0.378 in recovery phase, P=0.034). ADL, HDS and IMCT scores of DEACMP group in acute phase were (45.12 ± 3.12), (7.98 ± 1.02) and (9.61 ± 1.41) points respectively, which were significantly different from those of recovery phase [(33.25 ± 3.09), (16.13 ± 1.17) and (19.54 ± 1.43) points respectively] (P<0.05). CONCLUSIONS: DEACMP was accompanied by secondary brain injury, for which glial activation may be important. Serum S100B and GFAP levels may be related to prognosis.

Effects of the Notch1 signaling pathway on human lung cancer A549 cells.

PURPOSE: To evaluate the effects of the Notch1 signaling pathway on human lung cancer A549 cells. MATERIALS AND METHODS: A549 cells were transfected with recombinant plasmids. Cell proliferation was detected by MTT assay. A tumor-bearing mouse model was established for intratumoral gene injection. Apoptosis-related factors were detected by immunohistochemical assay. Caspase-8, caspase-3, caspase-9, PI3K, pAkt and pSTAT3 expressions were detected by Western blotting. RESULTS: Compared with A549-GFP and A549 cells, A549-ICN cell growth in mice decelerated, tumor volume significantly reduced (p < 0.01), and survival time significantly increased (p < 0.05). Cyclin E and phosphorylated Rb protein expressions were significantly down-regulated. Compared with control, apoptosis-related protein Bcl-2 expression in tumors injected with Notch1 gene was significantly inhibited. After Deltex1 transfection, A549 cell proliferation decelerated, growth was significantly inhibited (p < 0.05), and survival time was significantly extended (p < 0.05). Cyclin E and mutant p53 protein expressions in tumors were down-regulated, phosphorylated Rb expression was almost completely inhibited, and Bcl-2 expression was significantly inhibited. TNF-α-related apoptosis-inducing ligand (TRAIL) inhibited A549-ICN cell growth time- and dose-dependently. After treatment for 24 h or longer, TRAIL induced apoptosis of more A549-ICN cells. Cleaved caspase-3 and cleaved caspase-9 were detected only in A549-ICN cells after 6 h of 40 ng/mL TRAIL treatment, but cleaved caspase-8 was not detected. Combining Notch1 signal with TRAIL inhibited PI3K, phosphorylated Akt and phosphorylated STAT3 expressions. CONCLUSION: The Notch1 signaling pathway may inhibit A549 cell growth in vitro and in vivo by regulating cell cycle-related and anti-apoptotic protein expressions. Notch1 activation also suppressed A549 cell apoptosis by inhibiting the PI3K/pAkt pathway and activating the caspase-3 pathway in cooperation with TRAIL.

DNAH7 mutations benefit colorectal cancer patients receiving immune checkpoint inhibitors.

Background: Colorectal cancer (CRC) is a malignant tumor associated with a high mortality rate. While the advent of immune checkpoint inhibitors (ICIs) has been a gamechanger, only a small percentage of CRC patients benefit from ICIs. The pathological mechanism of CRC is not well understood, but somatic mutations, especially missense mutations, are believed to play an important role. This study examined the relationship between ICIs in colorectal cancer and missense mutations in the axonemal dynein heavy chain gene 7 (DNAH7). Methods: A clinical cohort (n=690) and the CRC data from the publicly available Cancer Genome Atlas (TCGA) were examined. Gene Set Enrichment Analysis, ESTIMATE analysis, and clinical correlation analysis were performed to explore the effects and mechanisms of DNAH7 mutation on immunotherapy in colorectal cancer. Results: The results showed that CRC patients with DNAH7 mutations can benefit more from ICIs (P<0.05). Patients with DNAH7 mutation had higher ESTIMATE scores, immune scores, and matrix scores, compared to patients without the DNAH7 mutation (P<0.001). The transport of small molecules, keratinization, asthma, autoimmune thyroid disease, allograft rejection, and other pathways were significantly enriched in DNAH7 mutated tissues (P<0.05). The top key genes associated with the DNAH7 mutation included AQP8, MS4A12, GUCA2B, and ZG16 (P<0.01). Conclusions: The current study not only demonstrated the significance of DNAH7 as a risk factor and prognostic feature in CRC, but also revealed that DNAH7 mutations might affect the clinical efficacy of ICIs by impacting the tumor immune microenvironment.

Antitumor Effect of Demethylzeylasteral (T-96) on Triple-Negative Breast Cancer via LSD1-Mediate Epigenetic Mechanisms.

Background and Purpose. Breast cancer ranks first in the incidence of female tumors. Triple-negative breast cancer (TNBC), one type of breast cancer, is more aggressive and has a worse prognosis. Demethylzeylasteral (T-96) is isolated from Tripterygium wilfordii Hook F. Our previous study found that T96 could inhibit TNBC invasion via suppressing the canonical and noncanonical TGF-ß signaling pathways. However, the antitumor effects and mechanisms of T-96 on TNBC have not been studied. This study is aimed at investigating the antitumor effect and mechanism of T-96 on breast cancer. Experimental approach. MTT assay, Live and Dead cell assay, and TUNEL were used to observe the antitumor effect of breast cancer cells treated with T-96. siRNA of LSD1, Co-IP, and molecular docking were used to explore the direct target and mechanism of T-96. Subcutaneous murine xenograft models were used to detect the efficacy of T-96 antitumor activity in vivo. Key Results. T-96 was more susceptible to inducing the apoptosis of highly metastatic TNBC cell lines (SUM-1315). An abnormal level of histone methylation is a crucial characteristic of metastatic cancer cells. LSD1 is a histone demethylase. We found that T-96 could significantly decrease the protein expression of LSD1, increase its target protein PTEN expression and enhance histone methylation. T-96 could also down-regulate the PI3K/AKT signaling pathway, which could be blocked by PTEN. Knockdown of LSD1 by siRNA blocked the pharmacological activity of T-96. And the molecular docking predicted T-96 processed affinity toward LSD1 through hydrogen bonding. Finally, T-96 was evaluated in a murine xenograft model of SUM-1315 cells. And T-96 could significantly inhibit tumor growth without showing marked toxicity. Conclusions & Implications. The results illustrated that T-96 exerted antitumor activity in highly metastatic TNBC by inactivating the LSD1 function.

Identification of Significant Modules and Targets of Xian-Lian-Jie-Du Decoction Based on the Analysis of Transcriptomics, Proteomics and Single-Cell Transcriptomics in Colorectal Tumor.

Purpose: Colorectal cancer (CRC) remains the third most common tumor worldwide. Ulcerative colitis (UC) could cause chronic inflammation and ulcers in the colon and rectum. UC is a risk factor for a high incidence of CRC, and the incidence of UC-associated CRC (UC-CRC) is still increasing. Chinese medicine prescription, Xian-Lian-Jie-Du decoction (XLJDD), has been proven its efficacy in some UC-CRC patients. However, the mechanism of XLJDD in treating UC-CRC remains unknown. This study aimed to investigate the mechanism of XLJDD in treating UC-CRC. Methods: We constructed an AOM/DSS mouse model that could simulate the various stages of UC-CRC in humans. XLJDD and its 5 main components are used to treat the AOM/DSS model, respectively. With the power of high-throughput sequencing technology, we described the mechanism of XLJDD from transcriptomics, proteomics, and single-cell transcriptomics. Results: Our results showed that XLJDD could effectively suppress the occurrence and development of colorectal tumors. Using the weighted correlation network analysis (WGCNA), several mRNA and protein modules that respond to XLJDD have been identified. Moreover, two essential genes, Mfsd2a and Ccdc85c, were caught our attention. They were prognostic markers in CRC patients, and their expression could be significantly modulated by XLJDD, showing their potential as effective targets of XLJDD. In addition, we also discovered that XLJDD could affect the cell composition of the colorectal tumor environment, especially in the infiltration of B cells. Conclusion: We demonstrated that XLJDD could prevent the initiation and development of colorectal tumors by modulating the expression of Mfsd2a and Ccdc85c and reducing the infiltration of B cells in the tumor microenvironment of colorectal tumor.

Retraction: Cyclooxygenase-2 mediates puerarin to inhibit the invasion and metastasis of lung cancer A549 cells.

[This retracts the article DOI: 10.21037/tcr.2017.06.18.].

Inhibition of hepatocellular carcinoma tumorigenesis by curcumin may be associated with CDKN1A and CTGF.

This study aimed to explore crucial genes, transcription factors (TFs), and microRNAs (miRNAs) associated with the effects of curcumin against hepatocellular carcinoma (HCC). We downloaded data (GSE59713) from Gene Expression Omnibus to analyze differentially expressed genes (DEGs) between curcumin-treated and untreated HCC cell lines. Then, we identified the disease ontology (DO) and functional enrichment analysis of these DEGs and analyzed their protein-protein interactions (PPIs). Additionally, we constructed TF-target gene and miRNA-target gene regulatory networks and explored the potential functions of these DEGs. Finally, we detected the expression of CDKN1A, CTGF, LEF1 TF and MIR-19A regulated by curcumin in PLC/PRF/5 cells using RT-PCR. In total, 345 upregulated and 212 downregulated genes were identified. The main enriched pathway of upregulated genes was the TNF signaling pathway. The downregulated genes were significantly enriched in TGF-beta signaling pathway. In addition, most DEGs were significantly enriched in DO terms such as liver cirrhosis, hepatitis, hepatitis C and cholestasis (eg., CTGF). In the constructed PPI network, CDKN1A and CTGF were the key proteins. Moreover, LEF1, CDKN1A, and miR-19A that regulated CTGF were highlighted in the regulatory networks. Furthermore, the expression of CDKN1A, CTGF, LEF1 TF and miR-19A regulated by curcumin in PLC/PRF/5 cells was consistent with the aforementioned bioinformatics analysis results. To conclude, curcumin might exert its protective effects against HCC tumorigenesis by downregulating LEF1 and downregulating CTGF regulated by MIR-19A and upregulating CDKN1A expression.

Role of the stromal cell derived factor-1/CXC chemokine receptor 4 axis in the invasion and metastasis of lung cancer and mechanism.

BACKGROUND: Lung cancer is the most common tumor, and has the highest incidence and mortality rates among all malignant tumors. Since stromal cell derived factor-1 (SDF-1) and CXC chemokine receptor 4 (CXCR4) are specific to binding sites, they are more important than other members of the families for tumor invasion and metastasis. We herein aimed to investigate the role of the axis of chemokine SDF-1 and its receptor CXCR4 in the invasion and metastasis of lung cancer. METHODS: Sixty clinical non-small cell lung cancer (NSCLC) tissue samples were collected. The CXCR4 expressions in cancer, paracancerous and normal lung tissues were detected by immunocytochemical assay and PCR. Cells with CXCR4 overexpression (CXCR4-A549) were constructed. After induction with SDF-1, CXCR4-A549 and A549 cells were subjected to in vitro chemotaxis and invasion assays. Their proliferation and apoptosis were detected by flow cytometry. The activities of phosphoinositide 3-kinase/protein kinase B (AKT) and mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK)-related signaling pathways were detected by Western blot. The downstream signaling molecules that may be activated by SDF-1/CXCR4 were analyzed. The expressions of vascular endothelial growth factor-C and matrix metalloproteinase-2 were detected by Western blot and PCR. A mouse model was established by subcutaneous inoculation of lung cancer cells. The effects of up-regulated CXCR4 expression on the migration of lung cancer cells in vitro and their tumorigenesis and metastasis in vivo were assessed. RESULTS: There was no expression in normal or paracancerous tissues. The expression of CXCR4 mRNA in lung cancer tissues was 83.3% (50/60). The expressions of CXCR4 in lung squamous cell carcinoma and adenocarcinoma were similar (P>0.05). The expression of CXCR4 was 76.9% (10/13) in highly differentiated carcinoma, 82.1% (23/28) in moderately differentiated carcinoma and 84.2% (16/19) in lowly differentiated carcinoma (P>0.05). The expression of CXCR4 was 72.7% (8/11) in TNM stage I patients, 83.9% (26/31) in stage II patients, and 88.9% (16/18) in stage III patients, with significant correlations. After up-regulation of CXCR4, the invasion ability of CXCR4-A549 cells was increased 1.62-fold (P<0.05). ERK and AKT were significantly phosphorylated 30 min after SDF-1 treatment. The tumorigenic rates of six mice inoculated with CXCR4-A549 and A549 cells were both 100%, with the average tumor weights of (4.37±0.96 g) and (3.24±1.16 g) respectively (P<0.05). In the CXCR4-A549 group, metastatic tumors clearly formed in the lungs of 6 mice, but only 2 mice in the A549 group had tumor cell invasion. CONCLUSIONS: SDF-1/CXCR4 played a key role in the invasion and metastasis of lung cancer. The interaction between SDF-1α and CXCR4 activated a series of downstream molecules by activating ERK and AKT.

Effect of Aidi injection plus transarterial chemoembolization on primary hepatic carcinoma: a systematic review and Meta-analysis.

OBJECTIVE: To assess the efficacy and safety of Aidi injection plus transarterial chemoembolization (TACE) in patients with primary hepatic carcinoma. METHODS: A comprehensive research of seven electronic databases was performed for comparative studies evaluating Aidi injection combined with TACE for primary hepatic carcinoma until September 2016. Two authors independently extracted data and assessed the methodological quality of the included trials using the Cochrane risk of bias tool from the Cochrane Handbook version 5.1.0. Data was synthesized by using RevMan 5.3 software. RESULTS: Forty-nine studies involving 3435 patients met the inclusion criteria, most of which were low methodological quality. Compared with TACE alone, Aidi injection plus TACE can significantly improve the efficiency rate [RR = 1.33, 95%CI (1.24, 1.43), P < 0.000 01], clinical beneficial rate [RR = 1.25, 95% CI (1.17, 1.33), P < 0.000 01], survival rate [6 months, RR = 1.19, 95% CI (1.09, 1.29), P < 0.0001], 12 months, [RR = 1.37, 95% CI (1.24, 1.52), P < 0.000 01], 18 months, [RR = 2.00, 95% CI (1.26, 3.20), P < 0.004], 24 months, [RR = 1.44, 95% CI (1.22, 1.70), P < 0.0001], 36 months, [RR = 1.50, 95% CI (1.07, 2.11), P = 0.02 < 0.05], quality of life [RR = 1.84, 95% CI (1.64, 2.05), P < 0.000 01] and immune function [CD3+, MD = 11.12, 95% CI (7.93, 14.30), P < 0.000 01], CD4+, [MD = 10.37, 95% CI (7.29, 13.45), P < 0.000 01], CD4+/CD8+, [MD = 0.30, 95% CI (0.07, 0.53), P = 0.01 < 0.05], NK, [MD = 7.49, 95% CI (6.64, 8.34), P < 0.000 01]. A significant improvement was also found in improvement of symptoms [RR = 1.64, 95%CI (1.38, 1.94), P < 0.000 01], leukopenia [RR = 0.60, 95% CI (0.54, 0.66), P < 0.000 01], thrombocytopenia [RR = 0.46, 95% CI (0.34, 0.61), P < 0.000 01], nausea and vomiting incidence [RR = 0.66, 95% CI (0.54, 0.81), P < 0.0001), liver damage rate [RR = 0.57, 95% CI (0.42, 0.77), P = 0.0003 < 0.05), and kidney damage rate [RR = 0.18, 95% CI (0.05, 0.68), P = 0.01 < 0.05]. CONCLUSION: The results suggested that Aidi injection plus TACE significantly improve the clinical effect of TACE, and reduce the incidence of adverse events. However, rigorous multicenter trials with larger size are warranted to further confirm the findings.

Chinese Herbal Medicine for Aspirin Resistance: A Systematic Review and Meta-Analysis.

OBJECTIVES: To assess the effectiveness and safety of Chinese herbal medicine (CHM) for the treatment of aspirin resistance (AR). METHODS: A comprehensive research of seven electronic databases was performed for comparative studies evaluating CHM for AR. Two authors independently extracted data and assessed the methodological quality of the included trials using the Cochrane risk of bias tool. Data wasere synthesized by using RevMan 5.3 software. (PROSPERO Registration #CRD42015020182). RESULTS: 18 randomized controlled trials (RCTs) involving 1,460 patients were included. 15 RCTs reported significant difference in the reduction of platelet aggregation rate (PAR) induced by adenosine diphosphate (ADP) (P<0.05), and 11 reported significant effect of CHM plus aspirin to reduce PAR induced by arachidonic acid (AA) (P<0.05) compared with aspirin 100mg/d treatment. The pooling data of 3 RCTs showed the thromboxane B2 (TXB2) in patients with CHM plus aspirin versus aspirin were significantly reduced (Random Effect model (RE), Standard Deviation (SD) = -95.93, 95% Confidential Interval (CI)[-118.25,-73.61], P<0.00001). Subgroup analysis showed that TXB2 (Fixed Effect model (FE), SD = -89.23, 95%CI[-121.96,-56.49], P<0.00001) had significant difference in Tongxinluo capsule plus aspirin versus aspirin. 2 RCTs reported the clinical effective rate, and the meta-analysis result showed a significant difference in intervention and control group (FE, Relative Risk (RR) = 1.67, 95%CI[1.15, 2.42], P = 0.007<0.05). In 4 trials, CHM plus aspirin had better effects of reducing the reoccurrence of cerebral infarction than aspirin (FE, RR = 0.24, 95%CI [0.11, 0.49], P<0.0001). And one trial showed that CHM plus aspirin could decrease the National Institutes of Health Stroke Scale (NHISS) score (P<0.05) and increase the Barthel Index (BI) score (P<0.05). 4 trials stated that there were no adverse effects occurred in intervention group, and analysis showed significant difference of CHM or CHM plus aspirin in reducing the occurrence of adverse events (FE, RR = 0.22, 95%CI[0.13, 0.39], P<0.00001). 5 trials claimed that the CHM monotherapy and CHM adjunctive therapy for AR did not add the risk of bleeding (FE, RR = 0.50, 95%CI[0.20, 1.22], P = 0.13>0.05). CONCLUSIONS: CHM may be effective and safe as an alternative and collaborative therapy for AR. However, the current evidence and potential promising findings should be interpreted with caution due to poor and varying methodological quality of included studies and the heterogeneity of interventions. Thus, further exploration of this strategy with adequately powered RCTs is warranted.