BackgroundReports indicate that those most vulnerable to developing severe coronavirus disease 2019 (COVID-19) are older adults and those with underlying illnesses, such as diabetes mellitus, hypertension, or cardiovascular disease, which are common comorbidities among patients undergoing maintenance hemodialysis. However, there is limited information about the clinical characteristics of hemodialysis patients with COVID-19 or about interventions to control COVID-19 in hemodialysis centers.MethodsWe collected data retrospectively through an online registration system that includes all patients receiving maintenance hemodialysis at 65 centers in Wuhan, China. We reviewed epidemiologic and clinical data of patients with laboratory-confirmed COVID-19 between January 1, 2020 and March 10, 2020.ResultsOf 7154 patients undergoing hemodialysis, 154 had laboratory-confirmed COVID-19. The mean age of the 131 patients in our analysis was 63.2 years; 57.3% were men. Many had underlying comorbidities, with cardiovascular disease (including hypertension) being the most common (68.7%). Only 51.9% of patients manifested fever; 21.4% of infected patients were asymptomatic. The most common finding on chest computed tomography (CT) was ground-grass or patchy opacity (82.1%). After initiating comprehensive interventions—including entrance screening of body temperature and symptoms, universal chest CT and blood tests, and other measures—new patients presenting with COVID-19 peaked at 10 per day on January 30, decreasing to 4 per day on February 11. No new cases occurred between February 26 and March 10, 2020.ConclusionsWe found that patients receiving maintenance hemodialysis were susceptible to COVID-19 and that hemodialysis centers were high-risk settings during the epidemic. Increasing prevention efforts, instituting universal screening, and isolating patients with COVID-19 and directing them to designated hemodialysis centers were effective in preventing the spread of COVID-19 in hemodialysis centers.

Purpose Early-stage hepatocellular carcinoma (E-HCC) is being diagnosed increasingly, and in one half of diagnosed patients, recurrence will develop. Thus, it is urgent to identify recurrence-related markers. We investigated the effectiveness of CpG methylation in predicting recurrence for patients with E-HCCs. Patients and Methods In total, 576 patients with E-HCC from four independent centers were sorted by three phases. In the discovery phase, 66 tumor samples were analyzed using the Illumina Methylation 450k Beadchip. Two algorithms, Least Absolute Shrinkage and Selector Operation and Support Vector Machine-Recursive Feature Elimination, were used to select significant CpGs. In the training phase, penalized Cox regression was used to further narrow CpGs into 140 samples. In the validation phase, candidate CpGs were validated using an internal cohort (n = 141) and two external cohorts (n = 191 and n =104). Results After combining the 46 CpGs selected by the Least Absolute Shrinkage and Selector Operation and the Support Vector Machine-Recursive Feature Elimination algorithms, three CpGs corresponding to SCAN domain containing 3, Src homology 3-domain growth factor receptor-bound 2-like interacting protein 1, and peptidase inhibitor 3 were highlighted as candidate predictors in the training phase. On the basis of the three CpGs, a methylation signature for E-HCC (MSEH) was developed to classify patients into high- and low-risk recurrence groups in the training cohort ( P < .001). The performance of MSEH was validated in the internal cohort ( P < .001) and in the two external cohorts ( P < .001; P = .002). Furthermore, a nomogram comprising MSEH, tumor differentiation, cirrhosis, hepatitis B virus surface antigen, and antivirus therapy was generated to predict the 5-year recurrence-free survival in the training cohort, and it performed well in the three validation cohorts (concordance index: 0.725, 0.697, and 0.693, respectively). Conclusion MSEH, a three-CpG-based signature, is useful in predicting recurrence for patients with E-HCC.

The pandemic of novel coronavirus disease 2019 (COVID-19) is posing a threat to all populations, especially those with underlying diseases like cardiovascular diseases, diabetes, or kidney diseases (1,2). Patients with kidney failure who require hemodialysis (HD) or peritoneal dialysis (PD) to sustain their lives often have accompanying damaged immune systems and multiple coexisting disorders; hence, there is a need for special care for these patients under the COVID-19 outbreak. Our recent study demonstrated a high prevalence and poor prognosis of COVID-19 in patients on HD (3), but its effect on patients on PD is still unknown. In this multicentered study, all 818 patients on maintenance PD from four large medical institutions in Wuhan, China, from January 1, 2020 to April 12, 2020 were included. To minimize contact with potential infectious environments of patients on PD, routine visits to PD centers were stopped and substituted by regular online follow-up by health care workers, and medicines and dialysates were provided through a home delivery service by volunteers. Medical staff members were trained to triage patients so that they attended the outpatient PD department or the fever clinic, or they stayed at home, depending on different conditions. Initial nucleic acid testing (3) and antibody testing (4) against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) were performed in symptomatic patients on PD, and screening of the entire Wuhan population at the end of May 2020 identified no new patients among the PD population. Diagnosis of COVID-19 and disease severity were determined according to the COVID-19 guidelines of the National Health Commission of China (seventh edition). The sensitivity and specificity of the antibody assay were 87.3% and 100%, respectively. Clinical outcomes were monitored up to when the patient died or the date of April 22, 2020. Spent dialysates of infected patients were collected in designated containers, then disinfected with twice the volume of2.0 g/L hypochlorite solution for 2 hours, and drained into the sluice of the ward. Of 818 patients on PD, eight patients were diagnosed with COVID-19 during the studied period; the incidence rate of symptomatic SARS-CoV-2 infection was 2.44 per 1000 person-months. As shown in Table 1, the median age of patients with COVID-19 was similar to that of patients without COVID-19 on PD. Although no significant differences were detected, the median total Kt/V urea , ultrafiltration, and residual urine production H.

Long non-coding RNAs (lncRNAs) have been known to partake in the development and the immune escape of hepatocellular carcinoma (HCC). The initial microarray analysis of GSE115018 expression profile revealed differentially expressed lncRNA fetal-lethal non-coding developmental regulatory RNA (FENDRR) in HCC. Therefore, this study’s main purpose was to explore the mechanism of tumor suppressor lncRNA FENDRR in regulating the immune escape of HCC cells. Notably, it was further validated through this study that lncRNA FENDRR competitively bound to microRNA-423-5p (miR-423-5p), and miR-423-5p specifically targeted growth arrest and DNA-damage-inducible beta protein (GADD45B). The effects that lncRNA FENDRR and miR-423-5p have on the cell proliferation and apoptosis, the immune capacity of regulatory T cells (Tregs), and the tumorigenicity of HCC cells were examined through overexpressing or the knocking down of lncRNA FENDRR and miR-423-5p both in vitro and in vivo . Subsequently, lncRNA FENDRR and GADD45B were revealed to have poor expressions in HCC. Meanwhile, miR-423-5p was highly expressed in HCC. Importantly, overexpressed lncRNA FENDRR and downregulated miR-423-5p diminished cell proliferation and tumorigenicity, and promoted apoptosis in HCC cells, thus regulating the immune escape of HCC mediated by Tregs. Taken conjointly, lncRNA FENDRR inhibited the Treg-mediated immune escape of HCC cells by upregulating GADD45B by sponging miR-423-5p.

Patients receiving maintenance hemodialysis (MHD) are highly vulnerable to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The current study was designed to evaluate the prevalence of SARS-CoV-2 infection based on both nucleic acid testing (NAT) and antibody testing in Chinese patients receiving MHD.

Hepatocellular carcinoma (HCC) is a prevalent malignancy characterized by aggressiveness and poor prognosis; however, the molecular mechanism remains to be fully identified. Based on the analysis of The Cancer Genome Atlas (TCGA) database, melanoma-associated antigen A3 (MAGEA3) and long non-coding RNA (lncRNA) LINC01234 were upregulated in HCC and associated with poor prognosis of HCC. We investigated the mechanism of how MAGEA3 and LINC01234 influenced HCC cellular functions and cisplatin resistance. MAGEA3 depletion inhibited proliferation, invasion, and cisplatin resistance of HepG2 cells and Huh7 cells in vitro, reduced resistance-associated protein 2 (MRP2), MRP3, and multidrug resistance protein 1 (MDR-1) expression, and elevated ALB expression. RNA pull-down and RIP assays identified the binding of LINC01234 and MAGEA3 to microRNA-31-5p (miR-31-5p). LINC01234 could restore MAGEA3 expression by binding to miR-31-5p. Furthermore, we delivered plasmids into HepG2 cells and Huh7 cells to alter the expression of LINC01234 and miR-31-5p. When miR-31-5p was downregulated, the proliferation and invasion of HepG2 cells and Huh7 cells were enhanced and the cisplatin-induced apoptosis was inhibited, while LINC01234 knockdown could diminish the effects caused by miR-31-5p depletion. In summary, these data highlight the vital role of MAGEA3/LINC01234/miR-31-5p axis in the HCC progression and chemoresistance of HCC cells.

The adsorption behaviors of tea polyphenols (TP) on wool, silk, and nylon at pH 4.0 were investigated. The Langmuir-Nernst model had the best fitting to the adsorption isotherms. The analysis of adsorption mechanism suggested that the hydrogen bonding and electrostatic interactions operating between TP and fibers contribute to Langmuir adsorption, whereas other interactions (hydrophobic interaction and van der Waals forces) contribute to Nernst partition adsorption. Langmuir adsorption had greater contribution to total adsorption of TP on nylon, whereas partition adsorption imparted greater influence to TP adsorption on silk. In terms of the mordant dyeing of TP, silk and wool displayed much deeper color than nylon due to their higher content of the functional groups having the complex-forming ability, although they had lower adsorption capability for TP than nylon. The colors of the dyed fabrics mordanted with different metallic salts as well as their depth, were greatly dependent on the chemical nature of mordants and fibers, the metal ion-TP-fiber complexforming ability, and the related complex structure.

Purpose:We proposed to investigate the effects of miR-452-3p on the proliferation and mobility of hepatocellular carcinoma (HCC) cells by targeting cytoplasmic polyadenylation element binding protein 3/estimated glomerular filtration rate (CPEB3/EGFR) axis.Methods:Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect miR-452-3p expression in 84 pairs of HCC tissues and adjacent tissues. Luciferase reporter assay was employed to examine the relationship between miR-452-3p and CPEB3. Microculture tetrazolium (MTT) assay, colony formation assay, flow cytometry detection, wound healing assay, and transwell assay were used to detect cell proliferation, cycle arrest, apoptosis, and mobility, respectively, in HCC, HepG2, and Huh-7. Western blot was used to detect protein expression levels in EGFR signaling pathway. Kaplan-Meier survival analysis was conducted to analyze the correlation between the miR-452-3p and CPEB3 expression levels and the survival of patients with HCC.Results:MiRNA-452-3p was found significantly upregulated in 84 human HCC sample tissues and cells in comparison with adjacent tissues and normal liver epithelial cells (P < .01). Luciferase reporter assay demonstrated that CPEB3 was a direct target of miR-452-3p. Overexpression of miR-452-3p promoted cell proliferation and mobility and suppressed apoptosis. MiR-452-3p enhanced EGFR and phosphorylated AKT (pAKT) expression but inhibited p21 expression level.Conclusion:MiR-452-3p promoted HCC cell proliferation and mobility by directly targeting the CPEB3/EGFR axis.