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Mast cells (MCs) are ubiquitous immune cells that participate in allergic reactions through the ac- tivation of the FCeRI receptor, but also in inflammatory processes induced by various biological and non-biological compounds, neurotransmitters, and cytokines. Activation of MCs can lead to the immediate release of chemical mediators of inflammation, but it can also result in the secretion of pro-inflammatory cytokines without degranulation. In the inflammatory network, macrophages cross-talk with MCs by producing IL-1, which stimulates MCs to secrete pro-inflammatory cytokines including IL-6, TNF, IL-33 and other cytokines and chemokines. IL-37 and IL-38 are anti-inflammatory cytokines implicated in the suppression of the immune and inflammatory system. Therefore, it is pertinent to think that these cytokines can open new pathways in the field of inflammatory and immune diseases. Here we report the relationships between macrophage cytokines, MCs, and inflammation.
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Background: Psoriasis (PsO), Psoriatic arthritis (PsA), and Atopic dermatitis (AD) patients havean increased risk of sleep disorders. Although sleep disturbances are well-known among patients,caregivers’ oneiric evaluation remains poorly assessed. The objective was to quantify the sleep burdenof parents with affected children.Methods: In this multicenter cross-sectional study, we enrolled sex-age matched parents with childrenaffected by PsO, PsA, and AD. Both parents underwent the Pittsburgh Sleep Quality Index to determinetheir sleep quality.Results: We enrolled a total of 90 children (age 12.36±1.83 years, 45 male and 45 female) withpsoriasis (n=30, PASI 7.00±2.49), atopic dermatitis (n=30, SCORAD 33.13±10.03), and psoriaticarthritis (n=30, DAPSA 26.40±10.94). Patients’ Parents (age 49.83±6.69 years, 45 male and 45 female)had a PSQI of 6.17±1.91; hence 70.0%, 73.3%, and 96.7% had a bad quality of sleep, respectively,with children suffering from atopic dermatitis, psoriasis, and psoriatic arthritis. Parents with childrenaffected by psoriasis (6.23±2.46) or by psoriatic arthritis (6.73±1.42) had lower PSQI than the ones with atopic dermatitis (5.53±1.55). Interestingly, children with PsA had parents with higher risk of sleepdisturbances (OR 52.25 [95%CI 1.92-1,422.66], p=0.0189), and male gender was protective (OR 0.14[95%CI 0.02-0.86], p=0.0337).Conclusions: The sleep quality of parents is deeply influenced by the dermatological/rheumatologicaldisease in children but not by its duration. Thus, sleep evaluation in caregivers should be part of routinepatient check-ups with PsO, PsA, and AD
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Ovarian cancer (OC) has been regarded as the most malignant gynecological neoplasm and leading mor-tality-causing cancer in females worldwide. It has a high fatality rate and is difficult to be detected early. Theclassification of OC has drawn the attention of numerous researchers, while the difference between layerclassification is still unclear. This study explored the common genes between proteomics and transcriptomicsand the potential mechanism related to layer classification. Our results provide several potential biomarkersin the early diagnosis of ovarian cancer. We identified 962 differentially expressed mRNA (DEGs) and 544differentially expressed proteins (DEPs). The comprehensive analysis of the two omics found that the proteinsin the MAPK pathway showed corresponding changes in ovarian cancer progression. Furthermore, CD14and MECOM were up regulated in OC and higher in the advanced OC than in the early stage. In conclusion,our research provided 2 potential early prognostic biomarkers for OC
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ENTPD1 antisense RNA 1 (ENTPD1-AS1), a long non-coding RNA, has been comprehensively studiedin glioblastoma multiforme. This study aimed to measure ENTPD1-AS1 expression in patients withcolorectal cancer (CRC) and identify its function in the behavior of CRC cells. The expression of ENTPD1-AS1 was measured in a panel of tissue specimens obtained from CRC patients via quantitative real-timepolymerase chain reaction. Proliferation, migration, and invasion of CRC cells were evaluated using CellCounting Kit-8, Transwell cell migration, and invasion assays. Moreover, tumor xenografts were establishedto evaluate the growth of CRC cells in vivo, and bioinformatics analysis was performed to identify putativecomplementary miRNAs that interact with ENTPD1-AS1, which was further corroborated in a seriesof mechanistic studies. We found that ENTPD1-AS1 was overexpressed in CRC based on our samplecohort’s Cancer Genome Atlas database. Interference of ENTPD1-AS1 impeded CRC cell proliferation.In addition, in vitro migration and invasion as well as in vivo tumor growth were inhibited after ENTPD1-AS1 knockdown. Mechanistically, ENTPD1-AS1 predominantly functioned as a competing endogenousRNA to sponge microRNA-432-5p (miR-432-5p), resulting in the upregulation of hepatoma-derivedgrowth factor (HDGF) expression in CRC cells. Finally, rescue function tests revealed that miR-432-5pinhibition or HDGF restoration could counteract the inhibitory effects of ENTPD1-AS1 knockdown inCRC cells. Overall, ENTPD1-AS1 may increase HDGF expression in CRC cells by sequestering miR-432-5p, thereby boosting oncogenicity. Thus, the ENTPD1-AS1/miR-432-5p/HDGF regulatory pathway mayprovide a theoretical basis for the identification of novel treatment strategies for CRC
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The growing popularity of paralympic sports and the improvement of infrastructure accessibility hasled to an increase of disabled people regularly practicing sports. However, besides the beneficial effects ofphysical activity, these athletes have a higher risk of upper limb musculoskeletal overuse disorders. Despitethis, the literature is still inconclusive about shoulder overuse injury etiology and prevention strategies.Therefore, this study aimed to evaluate the effect of a training protocol to prevent shoulder overuse syn-drome in wheelchair rugby (WR) athletes. A total of 12 athletes, affected by tetraplegia (50%), paraplegia(26%), paraparesis due to cerebral palsy (8%), transfemoral amputation (8%), and osteogenesis imper-fecta (8%) were evaluated at baseline (T0) and after 4 weeks (T1) of a self-administrated exercise program.In addition, each subject underwent a dynamometric test of the biceps brachii, deltoid and pectoralis mu-scles. A significant increase of dynamometric values was evident at T1 in all tested muscles
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Lung adenocarcinoma (LUAD) is one of the most fatal cancers, and more studies are needed fora better understanding of this disease. Studies have reported that alternative splicing (AS) in cancershas important prognostic value. Therefore, this study aimed to determine the correlation between theAS events of immune-related genes and LUAD prognosis. The gene expression matrix and clinicalinformation of patients with LUAD were downloaded from The Cancer Genome Atlas database.Univariate and multivariate Cox regression analyses were used to screen the differentially expressedAS (DEAS) events of immune-related genes related to prognosis. A protein-protein interactionnetwork was constructed using the abovementioned genes, and enrichment analysis was performed.Finally, we analyzed the regulatory relationship between DEAS events and AS factors and analyzedthe prognostic subtypes via cluster analysis. A total of 188 out of 2,227 immune-related AS events(111 of 373 immune-related genes) were significantly (p > 0.05) associated with the overall survival(OS) of patients with LUAD. Three AS types, namely alternate promoter, retained intron, and exonskip, significantly distinguished high-risk patients from low-risk patients. Further analysis revealedthat the alternatively spliced immune genes were involved in the activation of the immune responseas well as in cytokine production and signaling and that the AS events were highly correlated withsplicing factors. Finally, the immune-related genes were subgrouped into four clusters, with eachcluster differently predicting the OS of patients with LUAD. In summary, AS events in immunegenes are novel prognostic factors for LUAD and imply dysregulated AS in the immune system andabnormal antitumoral immune responses
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Background: Aside from the clinical benefits of trastuzumab in treating HER2- positive breast cancer,cardiotoxicity is identified as a major side effect. Cardiac function should be closely monitored before,during, and after trastuzumab therapy.Aim: To assess cardiac function during trastuzumab therapy and the effect of risk factors (RF) forcardiotoxicity and cardiovascular (CV) diseases in HER2-positive breast cancer patients.Materials and Methods: Ninety-six HER2-positive female breast cancer patients (mean age, 59.57±9.6years) were enrolled in the study. At the time, they were on sequential therapy with anthracyclines (IVto VI cycles) within the FAC regimen (fluorouracil 500 mg/m 2 , doxorubicin 50 mg/m 2 , cyclophosphamide500 mg/m 2 ) applied per 21 days, and after that, trastuzumab therapy (6 mg/kg of body weight, per21 days for one year). In all patients, blood pressure (BP), heart rate (HR), electrocardiographic andechocardiographic parameters (left ventricular ejection fraction – LVEF (%), fractional shortening –FS (%), end-diastolic diameter – EDD (mm), and left ventricular mass – LVM (g)) were assessed at thebeginning and after the therapy with trastuzumab.Results: There were no significant changes in arterial BP before and after trastuzumab in the examinedpatients. Ectopic beats (EB) were registered during the therapy in 11 patients, supraventricular in 7, andventricular extrasystoles in 4 patients on the electrocardiogram (ECG). In most of the patients with EB inthe middle of the treatment period with trastuzumab, sinus tachycardia was also recorded. At the end oftrastuzumab therapy in the examined group, LVEF decreased by 1.73 %, FS by 0.86 %, EDD increasedby 1.26 mm, and LVM increased by 9.6 g. Cardiotoxicity was registered in 4 (4.17%) patients. Greaterleft ventricular dysfunction was observed in older patients, patients with prior radiation therapy, andthose with three or more cardiovascular risk factors (CVRF).Conclusion: This study shows that the treatment with trastuzumab does not significantly affect BPand ECG changes. The rate of cardiotoxicity after trastuzumab therapy was low and was expressedthrough reduction of LVEF, an increase in EDD, and LVM. In patients with three or more CVRFs, therewas a higher decrease of LVEF than in patients without any cardiovascular risk factors
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The authors investigated the function of the apoptotic antagonistic transcription factor (AATF) inlipopolysaccharide (LPS)-induced H9C2 cell apoptosis and proliferation. After transfecting H9C2 cellswith short hairpin RNA (shRNA), a shAATF-162 gene interference model was established. Cells weredivided into mock, shRNA, and shNC groups and were treated with LPS. The cell counting kit-8 (CCK-8) assay and annexin V PE/7-AAD staining were used to assess cell viability and apoptosis, respectively.The protein levels of p53 upregulated modulator of apoptosis (PUMA) and phorbol-12-myristate-13-ac-etate-induced protein 1 (NOXA) were determined using western blotting. Interleukin 6 and tumor ne-crosis factor α (TNF-α) secretion was determined using enzyme-linked immunosorbent assay (ELISA)and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Results of the CCK-8assay showed that AATF knockdown decreased proliferation and potentiated apoptosis in LPS-inducedH9C2 cells compared with that in the shRNA and mock groups. The western blotting results indicatedthat AATF knockdown increased PUMA and NOXA protein levels in LPS-induced H9C2 cells comparedto that in the shNC and mock groups. ELISA and RT-qPCR results showed that AATF knockdown sig-nificantly decreased the LPS-induced secretion of IL-6 and TNF-α in H9C2 cells compared to that in theshNC and mock groups. This study showed that AATF inhibition attenuated cell viability, potentiatedapoptosis, and decreased the LPS-induced secretion of IL-6 and TNF-α in H9C2 cells
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Background and objective: Renal interstitial fibrosis (RIF) is a common pathological feature ofvarious chronic kidney diseases that progress to end-stage renal failure. The LMX1B gene plays animportant role in embryonic development, an important factor in regulating kidney development andmaintaining podocyte function. In the present study, we aimed to explore whether LMX1B regulatesPHB levels in the progression of RIF.Methods: A hypoxic/reoxygenation model in renal tubular epithelial cells (RTECs) was used tosimulate chronic injury in obstructive renal disease. Subcellular localization of LMX1B and prohibitin(PHB) 1 was observed using confocal laser microscopy. ROS and MDA levels were measured accordingto the reagent test kit protocols. The expression of LMX1B, PHB1, PHB2, TGF-β1, Col-IV, and FN wastested by western blotting, and the gray value of the band was analyzed using Image J.Results: LMX1B and PHB1 were both located in the nucleus of RTECs. The levels of PHB1 andPHB2 were closely associated with LMX1B levels. Overexpression of LMX1B in RTECs significantlyincreased the expression of PHB1 after H/R treatment. Moreover, the expression of TGF-β1, Col-IV,and FN was significantly decreased in RTECs infected with LMX1B lentiviral activation particles thanin control lentiviral activation-particle-infected RTECs. PHB1 levels were significantly decreased inLMX1B shRNA-transfected RTECs compared to control shRNA-transfected cells. Additionally, LMX1Boverexpression effectively inhibited hypoxia/reoxygenation (H/R)-induced ROS and MDA levels.Conclusion: The results demonstrated that LMX1B and PHB1 colocalized in the nucleus of RTECs,and LMX1B positively regulated PHB1 in an RTEC model system under H/R conditions. It plays aprotective role in hypoxic RTECs and inhibits RIF caused by RTEC injury
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Background: There is an increase in the number of premature births due to the premature rupture of thefetal membrane (PROM). Premature infants are more susceptible to infection, but early signs of infectioncan be difficult to detect in neonates. Soluble trigger receptor -1 (sTREM-1) was expressed by myeloid cell,mid-regional pro-adrenomedullin (MR-proADM), and IL-6 may be useful markers for detecting earlyneonatal infection. Methods: A retrospective analysis was conducted in 689 premature infants with andwithout PROM to determine the risk factors for infection in PROM. The correlations between neonatalinfection after PROM and sTREM-1, MR-proADM, and IL-6 levels of the umbilical cord blood wereassessed in a cohort of 50 singleton infants. Results: Premature infants with PROM were divided intoinfected (n=151) and non-infected (n=234) groups and compared to 304 premature infants without PROM.No correlation was observed between PROM and ethnicity, gestational age, gender, or twin gestation. Asignificant correlation was observed between infection and PROM. In the PROM infants, there was anoteworthy correlation between gestational age and infection. Umbilical cord blood levels of sTREM-1,MR-proADM, and IL-6 were remarkably higher in the infected group than in the uninfected group.Conclusion: Infection during pregnancy is the main risk factor for PROM. In PROM neonates, gestationalage could be a major risk factor for infection. Umbilical cord blood sTREM-1 and MR-proADM levels,and to a lesser degree IL-6 levels, may be useful to predict early PROM and neonatal infection
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Circular RNAs (circRNAs) serve as important regulators in cancer biology. The goal of the presentresearch is to investigate the biological functions and mechanism of circ_0005075 in colorectalcancer (CRC). The expressions of circ_0005075, miR-431, and DDX5 mRNA were quantified in CRCtissues and cell lines by quantitative real-time polymerase chain reaction (qRT-PCR). Cell countingkit-8 (CCK-8) assay, Transwell assay, and flow cytometry were conducted for assessing CRC cellproliferation, migration, invasion, cell cycle distribution, and apoptosis. Bioinformatics analysis andluciferase reporter assay were used for identifying the binding site between circ_0005075 and miR-431.Western blotting was employed for the quantification of DDX5, E-cadherin, N-cadherin, and Vimentinprotein expressions. The upregulation of circ_0005075 expression and the down-regulation of miR-431 expression were observed in CRC tissues and cell lines. Knockdown of circ_0005075 triggered theinhibition of proliferation, migration, and invasion of CRC cells, induced cell cycle arrest in G0/G1phase, and promoted cell apoptosis. Circ_0005075 could function as a molecular sponge for miR-431. Inaddition, circ_0005075 could repress miR-431 expression to up-regulate DDX5 expression in CRC cells.Circ_0005075, regulating miR-431/DDX5 pathway, promotes CRC progression
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Prostate cancer is a commonly seen male cancer in the world. In the present study, we explored therole of Notch1 and how it is regulated in the progression of prostate cancers. Firstly, Notch1 was highlyexpressed in prostate cancer cell lines PC3 and Du145, compared with normal human prostate cellcontrol cell RWPE-1. Knockdown Notch1 by specific shRNA significantly suppressed cell proliferationof PC3 cells. Has-miR-449a is found to negatively regulate the expression of Notch1 in human prostatecancer cells. Moreover, MiR-449a mimics suppresses cell viability of PC3 cells, and miR-449a inhibitorpromotes cell proliferation of PC3 cells. Furthermore, transfection with miR-449a decreased the levelof Notch1 and increased the autophagy activity of human prostate cancer cells. In conclusion, miR-449a negatively regulates the expression of Notch1 and inhibits the cell proliferation of human prostatecancer cells partly due to increasing the cell autophagy of PC3 cells
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This study aimed to analyze the factors related to acute kidney injury (AKI) in patients with heatstroke (HS). Patients with HS who visited the hospital from January 2013 to December 2019 were retrospectively analyzed. These patients were divided into an AKI and a non-AKI group based on the presence of AKI. Patients in the AKI group were further divided into the transient and persistent AKI groups. The differences in clinical characteristics between the AKI and the non-AKI group and the persistent AKI group and transient AKI group were analyzed to study the related factors of the occurrence of AKI. Male patients were more prone to AKI (P = 0.01). Compared with the non-AKI group, HS patients with AKI had a higher core body temperature (CBT) (P < 0.001) and lower mean arterial pressure (MAP) (P = 0.004). In addition, the incidence of mechanical ventilation, renal replacement therapy (RRT), and blood transfusion were higher in the AKI group (P < 0.001). However, the proportion of patients among whom cooling the CBT to 38.9°C within 30 min had taken place was lower (P = 0.007), and the risk of Disseminated Intravascular Coagulation (DIC) and death was higher (P < 0.001). There was no statistical difference in age, basic disease, heat index, and other indexes (P > 0.05). Compared with the transient AKI group, patients with persistent AKI had higher serum creatinine (Scr) levels, WBC counts, a higher rate of transfusion, DIC and death (P < 0.05), and a lower rate of cooling the CBT to 38.9°C within 30 min from the discovery of unconsciousness (P = 0.006). There were no significant differences between the two groups in terms of gender, age, highest CBT and MAP at admission, RRT, mechanical ventilation, or other factors (P > 0.05). Multivariate logistic regression analysis showed that the highest CBT (OR2.54; 1.007–6.42) and the Scr level on admission (OR 1.13; 1.07–1.18) were risk factors for AKI in HS patients (P < 0.05). The highest CBT and Scr levels on admission are independent risk factors for AKI, while the duration and progression of AKI may be associated with delayed CBT cooling.
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Objective: This study aimed to develop an amino acid metabolism-related gene signature for recur-rence prediction in colon adenocarcinoma (COAD).Methods: We downloaded RNA sequencing profiles of COAD from The Cancer Genome Atlas(TCGA) as a training set and GSE39582 from the Gene Expression Omnibus database as a validationset. Differentially expressed RNAs (DERs) were screened from recurrence tumor samples by definedthresholds. The amino acid metabolism-related gene signature was identified by LASSO cox regressionanalysis. Independent prognostic clinical factors were also assessed by using survival analysis. A riskscore (RS) signature was established and validated in two independent datasets.Results: We obtained 498 differentially expressed mRNAs and 71 differentially expressed lncRNAsbased on data mining. Compared with amino acid metabolism genes of Gene Set Enrichment Analysis da-tabase, we screened 197 overlapped DERs. A twelve genes-based RS signature was established. This modelexhibited a high accuracy for recurrence prediction with an area under the ROC curve (AUC) of 0.924and 0.843 in TCGA and GSE39582, respectively. In addition, pathological stage and RS model status wereidentified as independent clinical factors associated with recurrence. The combined model integratingthese two factors reached a higher AUC value of 0.940 in the TCGA dataset and 0.876 in the validation set.Conclusion: We established a high accuracy prognostic model for recurrence prediction. Our find-ings suggested that the combined model can identify high-risk recurrence COAD patients and might bea reliable tool for decision-making in a clinic
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Long non-coding RNA small nucleolar RNA host gene 7 (lncRNA SNHG7) and microRNA-34a (miR-34a) have been implicated in ovarian cancer (OC) development. Furthermore, the binding of SNHG7 to miR-34a is widely recognized in numerous cancers. Therefore, our research intended to explore the specific mechanism of SNHG7 and miR-34a in OC. SNHG7, miR-34a, and endothelial differentiation gene (EDG) 4 expression in harvested OC tissues and cells were measured by RT-qPCR. Dual-luciferase reporter gene assay and RIP assay were implemented to assess the binding of SNHG7 to miR-34a, and of miR-34a to EDG4. Gain- and loss-of-function assays were implemented in OC cells, followed by scratch test and Transwell assay of cell migration and invasion, respectively. The epithelial-mesenchymal transition (EMT) and the PI3K/AKT pathway-related proteins were measured by Western blot analysis. SNHG7 and EDG4 were overexpressed, but miR-34a was poorly expressed in OC tissues and cells. miR-34a bound to SNHG7 and targeted directly EDG4, and SNHG7 activated the PI3K/AKT pathway in OC cells. Furthermore, SNHG7 or EDG4 silencing, miR-34a overexpression, or PI3K/AKT pathway bluntness diminished OC cell invasion, migration, and EMT. Collectively, SNHG7 downregulation repressed EMT of OC cells via miR-34a-targeted EDG4 and the PI3K/AKT pathway.
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Different types of lung cancer, such as nonsmall-cell lung carcinoma (NSCLC), show the specificexpression of long non-coding ribonucleic acids (LncRNAs). There is evidence showing the possiblecorrelation between the expression of LncRNAs in tumor tissues and plasma exosomes. The presentstudy aimed to evaluate the expression level of LncRNAs in NSCLC patients in the cancerous tissues andadjacent non-cancerous tissue and the circulating exosomes. The tumor and adjacent non-canceroustissue samples of 142 patients with NSCLC were collected. Extracellular vesicles were isolated by theultracentrifuge method, and the nanoparticle tracking and the flow cytometry analysis were performedto identify the exosome fraction. The relative expression of the five LncRNAs, including AFAP1-AS1,BANCR, ANRIL, CCAT1, and GAS5, between tumor tissue, adjacent non-cancerous tissue, and plasmaexosomes were evaluated by quantitative real-time RT-PCR. Among 142 NSCLC samples, the expressionof lncRNA-GAS5 in tumor tissue was correlated with lncRNA-ANRIL in tumor tissue (p=0.035, C=0.177),while the rest of the lncRNAs did not show a significant correlation in tumor tissue. Expression of thefive different lncRNAs did not show any correlation in normal tissue and exosome content. Among thefive lncRNAs, only lncRNA-BANCR expression in ANCT was correlated with the exosomal expression(p=0.027, C=0.186). In conclusion, the present research demonstrated that a panel consisting of these fivelncRNAs could be helpful in the diagnosis of NSCLC
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