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COVID-19, which first appeared in China, has so far caused an unexpected number of deaths, as our immune system has not been able to annihilate the SARS-CoV-2 virus. SARS-CoV-2 reacts to both innate and acquired immunity. In the first instance, when the virus enters our organism, it is attacked by innate immune cells, including macrophages and mast cells (MCs), which produce defensive cytokines such as IL-1, IL-6, IL-33 and TNF; but the overproduction of these cytokines is very harmful to the patient. Here, in this editorial, we report that the inflammatory cytokine network established in COVID-19, in the most serious cases, can lead to the death of the patient. Therefore, it is pertinent to think that by blocking the pro-inflammatory cytokines that cause the “cytokine storm”, a great therapeutical benefit can be achieved for COVID-19 disease.
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This study aimed to analyze the acute effect of n-3 PUFA on TNF-a and MDA levels after anaerobic exercise. This experimental study involved 16 healthy adult men randomly selected with a BMI range of 19.00-24.00, and age ranged from 20-30 years. Subjects were selected randomly and then divided into 2 groups: group K1 using placebo and group K2 using n-3 PUFAs at a dose of 540 mg EPA and 360 DHA. The intervention was carried out 24 hours after the research subjects completed the anaerobic exercise. The data in this study were TNF-a levels measured using a human ELISA kit, and MDA was measured using a spectrophotometer taken before and after the intervention. The test of different levels of TNF-a in K2 (p<0.05) p=0.027, K1 (p>0.05) p=0.327, so that n-3 PUFAs significantly reduced TNF-a levels and the test of different levels of MDA in the group K2 (p> 0.05) p = 0.511, K2 (p> 0.05) p = 0.541 so that n-3 PUFAs did not significantly reduce MDA levels. Thus, it can be concluded that the administration of n-3 PUFAs has been shown to reduce TNF-a levels without a decrease in Malondialdehyde (MDA) levels after anaerobic exercise.
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Background: Angiogenesis is a crucial factor for the pathogenesis and growth of fibroids. Among various growth factors, transforming growth factor (TGFβ1) and vascular endothelial growth factor (VEGF) are up-regulated in leiomyomas and have angiogenic as well as pro-atherogenic properties. Subsequently, their elevated values may be involved in developing cardiovascular disorders.Objective: The current study was planned to evaluate the role of growth factors in females with uterine fibroids and investigate the future risks of developing cardiovascular disorders (CVD) in these patients.Method: Eighty-two subjects of uterine fibroids and eighty-two healthy controls were selected from tertiary care hospitals. Enzyme-linked immunosorbent assay (ELISA) was utilized to assess growth factors. Results: The levels of TGFβ1 and VEGF were significantly higher (P < 0.001) in patients with uterine fibroids compared to healthy females without uterine fibroids.Conclusion: High level of circulating growth factors in patients with uterine fibroids prognosticate (CVD) events in these patients.
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BACKGROUND: Circular RNAs (circRNAs) have been demonstrated to function in tumorigenesis and cancer progression. Nonetheless, the molecular mechanisms of circRNAs in colorectal cancer (CRC) have not been fully clarified.METHODS: The circRNA expression profile dataset GSE138589 was analyzed to find the differentially expressed circRNA in CRC. Circ_0000419, microRNA (miR)-580, and DNA methyltransferase 3 beta (DNMT3B) expressions in CRC were detected by qRT-PCR. The biological function of circ_0000419 on the growth, migration and invasion of CRC cells were analyzed by the CCK-8 method and Transwell experiment. Dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay, and RNA pull-down experiment were performed to validate the interrelationship among circ_0000419, miR-580, and DNMT3B. Then the regulatory function of circ_0000419 and miR-580 on DNMT3B expression was then measured by Western blot.RESULTS: Circ_0000419 expression was up-regulated, and miR-580 expression was down-regulated in CRC tissues and cell lines. Circ_0000419 was positively linked to CRC patients’ T stage and lymph node metastasis. Circ_0000419 knockdown or miR-580 overexpression impeded CRC cells’ growth, migration, and invasion. Circ_0000419 expression was negatively correlated with miR-580 expression in CRC tissues. Circ_0000419 was identified as a molecular sponge for miR-580, and DNMT3B was identified as a targetgene of miR-580. Furthermore, miR-580 inhibition or DNMT3B overexpression reversed the biological effects of circ_0000419 knockdown on CRC cells’ proliferation, migration, and invasion.CONCLUSION: Circ_0000419 exerts a pro-cancer effect in modulating CRC cell proliferation, migration, and invasion by regulating the miR-580/DNMT3B axis.
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Background: Sleep disturbances are rather common in psoriasis (PsO) and psoriatic arthritis (PsA) patients; however, it is still unclear if they depend intrinsically on PsO/PsA or the predisposing comorbidities such as metabolic syndrome. Methods: This is a multicenter cross-sectional assessing the sleep quality in partners of PsO/PsA patients. Patients and patients’ partners were recruited consecutively. After a dermatological visit to the patient, the partner was interviewed to score his/her quality of sleep with Pittsburgh Sleep Quality Index (PSQI). Results: A sample of 84 subjects (aged 45.38±8.55 years, 42 males and 42 females, with an average BMI of 25.24±1.75 kg/m2) were included. Fifty-two (61.9%) of them developed PsO or PsA before starting the relationship. Although the average PSQI was 4.79±1.47, the prevalence rate of poor sleep raters (PSQI ≥5) was 42 (50.0%). At the multivariate regression, the best independent predictors of sleep quality were “having a PsO/PsA child” and “having a partner affected by PsO since before relationship”. More in detail, the former predicted a worse sleep quality [OR 6.98 (95%CI 1.39-35.06)] and the latter a better sleep quality [OR 0.07 (95%CI 0.02-0.23)]. Specifically, performing a subgroup analysis among those who had a child and stratifying according to the presence of an affected child, no differences could be found for each parameter under study, except for PSQI, which was significantly higher in spouses with affected children (6.68±1.11 versus 4.35±1.11, p<0.001). Conclusions: The present study showed that having a child significantly negatively impacted on sleep quality of the parent, whereas having a partner being affected by PsO since before the beginning of the relationship protected against poor sleep quality. Having a child affected by PsO was, instead, a risk factor.
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Objective: We aimed to investigate the key mechanism of the DNA damage response (DDR) mutation in hepatocellular carcinoma (HCC) and construct a prognostic signature for HCC.Methods: Gene expression RNA-Seq data, somatic mutations, and clinical information were downloaded from The Cancer Genome Atlas-Liver Hepatocellular Carcinoma (TCGA-LIHC) dataset. Using survival analysis, stromal score correlation analysis, and DDR mutation-related differential analysis, the stromal prognostic differentially expressed mRNAs in the mutation vs no-mutation group were identified. Then immune infiltration analysis, functional enrichment analysis, and prognostic risk score model construction and evaluation were carried out. Moreover, a novel prognostic nomogram was established using the risk score and independent clinical prognostic factors.Results: The proportions of resting dendritic cells and naïve CD4 T cells differed significantly between the DDR mutation and no-mutation groups. Moreover, the stromal differentially expressed genes (DEGs) in the mutation vs no-mutation group were significantly enriched in DNA replication, with a significant association with DDR. Furthermore, two stromal prognostic DEGs (SCML2 and CCDC134) were identified to construct a prognostic risk model, and the risk score was confirmed as an independent prognostic biomarker in patients with HCC. The established nomogram could predict survival probability at 1, 2, and 3 years.Conclusion: Our data reveal that the DDR mutation-related stromal prognostic gene signature is associated with survival outcomes and the immune microenvironment in patients with HCC. The prognostic nomogram may help improve the clinical outcomes of patients with HCC undergoing personalized treatment.
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Smoking has been found to contribute to the development of chronic obstructive pulmonary disease (COPD), with incompletely reversible airflow limitation. TTN-AS1 has been confirmed to modulate cell proliferation and apoptosis, but its expression in COPD patients and its function in lung bronchial epithelial cell injury remain elusive. The profiles of TTN-AS1 and miR-15b-5p in COPD patients and cigarette smoke extract (CSE)-induced 16HBE cells (in vitro COPD model) were examined by real-time quantitative PCR (RT-qPCR). We applied TTN-AS1 overexpression plasmids and miR-15b-5p mimics for gain-of-function assay. Cell proliferation was tested by the cell counting kit-8 (CCK-8) assay, while cell apoptosis was evaluated by flow cytometry (FCM), TdT-mediated dUTP nick end labeling (TUNEL) staining, and Western blot (WB), respectively. Meanwhile, the profiles of inflammatory cytokines were testified by enzyme-linked immunosorbent assay (ELISA), and the levels of COX2, iNOS and NF-κB were monitored by WB. Besides, the targeting correlation between TTN-AS1 and miR-15b-5p was predicted by the Starbase database. Moreover, the binding association between the two was further measured by the dual-luciferase reporter assay and RNA immunoprecipitation (RIP) method. Our findings showed that TTN-AS1 expression was dramatically strengthened, while miR-15b-5p profiles were curbed in CSE-treated 16HBE cells and serum of COPD patients (compared with healthy donors). Functionally, overexpressing TTN-AS1 aggravated CSE-induced cell viability inhibition and apoptosis and intensified inflammations in 16HBE. Furthermore, miR-15b-5p up-regulation eased CSE-mediated cell damage and inflammation and reversed the effects of TTN-AS1. Mechanically, TTN-AS1 targeted and repressed miR-15b-5p. In conclusion, TTN-AS1 and miR-15b-5p are promising diagnostic molecules for COPD, and TTN-AS1 aggravates CSE-induced human bronchial epithelial cell apoptosis by regulating miR-15b-5p.
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Background: Allergic rhinitis (AR) is a commonly diagnosed disease worldwide, which seriously compromises people’s quality of life and health. The imbalance of T helper (Th) cell differentiation and dysregulation of related cytokine expression underlay the immunological basis of AR. 5-azacytidine (5-aza) is a pyrimidine nucleoside analogue that can inhibit the secretion of pro-inflammatory factors and improve the transcription ofanti-inflammatory factors. This study explored the effects of 5-aza on the differentiation of Th1/Th2 and Th17/ regulatory T cells (Treg) cell subsets and the expressions of related cytokines in AR. Objective: To investigate the effects of 5-aza on CD4+ T lymphocyte Th1/Th2 and Th17/Treg cell subsets and cytokines IFN-γ, IL-4, GATA3, ROR-γ, and Foxp3 in AR patients and rats.Materials and methods: 98 normal controls and 88 AR patients were recruited for the isolation of CD4+ T lymphocytes. The mRNA expressions of IFN-γ, IL-4, GATA3, ROR-γ, and Foxp3 were detected by using RT-qPCR. A rat model of AR was established. The mRNA and protein expressions of cytokines IFN-γ, IL-4, GATA3, ROR-γ, and Foxp3 in AR rats were detected using RT-qPCR and Western blotting. ELISA was used to detect the levels of IFN-γ, IL-4, GATA3, ROR-γ, and Foxp3 cytokines in the serum of rats. Flow cytometry was performed to detect the differentiation ratio of Th1, Th2, Th17, and Treg cell subsets.Results: The mRNA expressions of IFN-γ, IL-4, GATA3, and ROR-γ were increased and Foxp3 was decreased in AR patients and AR rats. The protein expressions of IFN-γ, IL-4, GATA3, and ROR-γ were increased and Foxp3 was decreased in AR rats. 5-aza intervention decreased the mRNA and protein expressions of IFN-γ, IL-4, GATA3, and ROR-γ and increased the mRNA and protein expression of Foxp3 in AR rats. The number of Th1, Th2, and Th17 cell subsets was increased and Treg was decreased in AR rats, while the number of Th1, Th2, and Th17 cell subsets was decreased and Treg was increased significantly after 5-aza intervention.Conclusion: The number and relative expressions of Th1, Th2, and Th17 cell subsets were increased in AR, while the Treg cell subset was decreased. Methyltransferase inhibitor 5-aza downregulated the number of Th1, Th2, and Th17 cell subsets and upregulated the Treg cell subset. The expressions of cytokines IFN-γ, IL-4, GATA3, ROR-γ, and Foxp3 were regulated by methyltransferase inhibitor 5-aza.
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This study investigated key ubiquitination-related genes associated with cervical cancer. We downloaded standardized gene expression profiles (GSE39001, GSE63514, GSE52903, GSE9750, GSE6791, and GSE7803) to analyze differentially expressed genes (DEGs) between the tumor and normal samples. By comparing with ubiquitination-related genes downloaded from hUbiquitome, key ubiquitination-related DEGs (BRCA1, CCNE2, HLTF, ICAM1, KIF15, PCNA, and PTTG1) were identified, followed by mutation and copy number alteration (CNA), immune infiltration, methylation, and protein expression analyses. Based on The Cancer Genome Atlas (TCGA) data of cervical cancer, prognosis and gene set enrichment analysis were conducted. BRCA1 was mainly subjected to somatic mutation. ICAM1 expression was positively correlated with the abundance of neutrophils and dendritic cells. In different CNA groups of HLTF and PTTG1, the abundance of more immune cells exhibited a significant difference. HLTF and ICAM1 were negatively correlated with more methylation sites. High BRCA1, PCNA, and ICAM1 expression were associated with favorable survival. BRCA1 was significantly enriched in mismatch repair and homologous recombination; ICAM1 was enriched in chemokine signaling pathway and cell adhesion molecules, and PCNA was involved in DNA replication and cell cycle. Our findings reveal that these key ubiquitination-related genes may affect cervical cancer development and prognosis.
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Cervical cancer (CC) is one of the most common female malignancies, and cisplatin-based chemotherapy is routinely utilized in patients with locally advanced stage. Exploration of the pathogenesis and molecular mechanism of CC is pivotal for the development of effective treatments for this disease. N6-Methyladenosine (m6A) modification, the most prevalent modification of eukaryotic messenger RNA (mRNA), is involved in the progression of various tumours, however, as the key component of m6A methylation, Wilms’ tumor 1-associated protein (WTAP) has not been well studied in CC. WTAP is a nuclear protein that is ubiquitously expressed in many tissues, therefore this study investigated the biological role and underlying mechanism of WTAP in CC. Western blot, RT-qPCR, and immunofluorescence techniques were used to detect the expression of WTAP in CC tumour tissues, adjacent tissues, and CC cell lines. We clarified the effects of WTAP on CC cells using cell proliferation assays and colony formation experiments. We then applied RNA sequencing combined with Gene Expression Omnibus data to screen for candidate targets of WTAP. The results demonstrated that in CC cell lines and tissues, WTAP was significantly overexpressed and exerted a pro-oncogenic influence. We determined that WTAP regulated breast Cancer Susceptibility Protein-1 (BRCA1) expression, thereby affecting the proliferation of CC cells.
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Background: We aimed to explore the potential protective effect of angiotensin (Ang) 1-7 in rat vascular smooth muscle cells (VSMCs) following exposure to high glucose and the mechanism of its effect on nitric oxide (NO) synthesis.Methods: Rat VSMCs were cultured with/without high glucose, Ang 1-7, and methyl-β-cyclodextrin (MβCD). The expression levels of caveolin-1 (Cav-1), inducible nitric oxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS)/phosphorylated eNOS (Ser1177) were evaluated by western blotting and immunofluorescence staining. NO, superoxide dismutase (SOD), malondialdehyde (MDA) and peroxynitrite (ONOO-) levels in cell culture supernatants were measured by enzyme-linked immunosorbent assay. Intracellular calcium content was determined by flow cytometry.Results: VSMCs cultured with high glucose exhibited striking increases in Cav-1, MDA, iNOS, ONOO-, and intracellular Ca2+, as well as reductions in eNOS phosphorylation, SOD, and NO production. Ang 1-7 treatment reversed the effects of high glucose in these cells.Conclusion: Ang 1-7 increases NO synthesis by regulating Cav-1 expression, Cav-1–eNOS interaction, oxidative stress, and intracellular Ca2+ levels in rat VSMCs cultured in high glucose.
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Background: Coronary artery aneurysm (CAA) is a rare condition in 0.3-4.9% of patients undergoing coronary angiography (CAG). Effort angina is the most common clinical manifestation in patients with CAA, along with dyspnea, arrhythmias, acute myocardial infarction (MI), congestive heart failure, cardiac arrest, or unstable angina. Its treatment options mainly include medical therapy, surgical resection, coronary artery bypass grafting (CABG), and percutaneous coronary intervention (PCI).Case report: This case report summarizes our experience of treating MI caused by a thrombotic CAA. A 54-year-old woman presented with an acute ST-elevation myocardial infarction (STEMI) caused by thrombotic occlusion of a CAA in the left anterior descending (LAD) artery. She was treated withpercutaneous transluminal coronary angioplasty (PTCA) and was subsequently referred to our institution due to recurrence of chest pain and persistence of ST-wave changes. The patient’s clinical symptoms resolved after 10 days of anticoagulation (enoxaparin) and dual antiplatelet therapy (aspirin, clopidogrel). However, repeat CAG revealed recanalization and a fusiform aneurysm with thrombosis in the LAD. The patient was discharged in good physical condition with an indication for continuous anticoagulation (enoxaparin) and dual antiplatelet therapy (aspirin and clopidogrel).Conclusion: In the setting of acute MI, PTCA of an aneurysmal vessel followed by long-term anticoagulation may be associated with good clinical outcomes and could be considered a reasonable treatment choice. Additionally, intravascular ultrasound (IVUS) assessment remains extremely useful as a diagnostic tool and guide for treatment.
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To evaluate the diagnostic value of magnetic resonance high-resolution black blood imaging in intracranial arterial stenosis, forty-six patients who underwent intracranial artery examination were selected for MRA, DSA and magnetic resonance high-resolution black blood imaging. The black blood and MRA technology results were compared with the DSA results. The sensitivity, specificity, accuracy, positive predictive value and negative predictive value of MRA were 67.85%, 66.67%, 48.27%, 65.51%, 68.96%, respectively. The high-resolution black blood imaging results were 94.11%, 95.83%, 58.62%, 96.96% and 92%, respectively, and except for accuracy, the difference between MRA and high-resolution black blood imaging was statistically significant (P<0.05). In conclusion, the magnetic resonance high-resolution blackblood technique is highly valued in diagnosing intracranial arterial stenosis.
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