Abstract Background Limited data exists on the link between dietary iron intake and mortality in diabetes. Our investigation aimed to explore how dietary iron intake correlates with overall and cause-specific mortality in diabetic individuals. Methods This analysis encompassed 5970 participants with diabetes from the National Health and Nutrition Examination Survey spanning 1999 to 2014. Baseline data were collected through surveys and examinations, with mortality status tracked via National Death Index records until December 31, 2015. Cox proportional hazard models were utilized to calculate hazard ratios (HR) and 95% confidence intervals (CI) for mortality from various causes, including cardiovascular disease (CVD) and cancer. Results The average iron intake among the cohort was 14.1 ± 7.4 mg daily, with an average participant age of 61.3 and 3059 (51.3%) male adults. Over 41,425 person-years of follow-up, 1497 deaths were recorded. Following adjustments for multiple variables, an iron intake between 11.1 and 14.4 mg was associated with the lowest risk of all-cause mortality (HR 0.83 [0.70, 0.99], P < 0.05) compared to the reference group (<8.3 mg). Analysis of dose-response curves revealed an L-shaped pattern in men and a J-shaped pattern in women concerning the relationship between iron intake and all-cause mortality. Conclusions Our findings suggest a nonlinear association between dietary iron intake and all-cause mortality in individuals with diabetes. Specifically, higher iron intake may increase all-cause mortality risk in men, while potentially exert a protective effect in women.

Background This meta-analysis aimed to evaluate the effectiveness of lymphadenectomy on survival and recurrence in patients with early-stage epithelial ovarian cancer (eEOC). Methods Relevant studies were searched from four online databases. Hazard ratios (HRs) with 95% confidence intervals (CIs) or risk ratios (RRs) with 95% CIs were used to evaluate the effects of lymphadenectomy on overall survival (OS), progression-free survival (PFS), and recurrence rates. A subgroup analysis was performed to explore the sources of heterogeneity, followed by sensitivity and publication bias assessments. Results Fourteen articles involving 22,178 subjects were included. Meta-analysis revealed that lymphadenectomy was significantly associated with improved OS (HR = 0.72; 95% CI:0.61, 0.84; P < 0.001), improved PFS (HR = 0.74; 95% CI: 0.67, 0.80; P < 0.001), and reduced recurrence rates (RR = 0.72; 95% CI: 0.60, 0.85; P < 0.001). Subgroup analysis showed that factors including area, histology, and source of the control group were significantly related to improved OS and PFS in patients with eEOC. Sensitivity analysis showed that the combined results were stable and reliable, and no significant publication bias was observed. Conclusions Patients with eEOC can benefit from lymphadenectomy, with improved survival outcomes (OS and PFS) and a lower recurrence rate.

Objective: This meta-analysis aimed to study the correlation between four polymorphisms in the matrix metalloproteinase (MMP) gene and risk of cervical cancer. Methods: Eligible studies were retrieved from PubMed, Cochrane Library, and Embase. Case-control studies that focused on polymorphic loci rs1799750 in MMP-1, rs243865 in MMP-2, rs3025058 in MMP-3, and rs11568818 in MMP-7 were included in the meta-analysis. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to measure the effects of interest. Quality assessment, heterogeneity analysis, publication bias evaluation, and sensitivity analyses were performed to confirm the reliability of this meta-analysis.Results: Nine studies with 3790 subjects were included. There was significant heterogeneity for rs11568818 GA vs. AA, rs3025058 5A6A vs. 6A6A, and all genetic models of rs243865. There were significant differences in rs11568818 G vs. A (OR [95% CI]: 1.3059 [1.1484; 1.4851], p value < 0.0001), GG vs. AA (OR [95% CI]: 1.6884 [1.2912; 2.2078], p value: 0.0001), GG vs. AA+GA (OR [95% CI]: 1.6884 [1.2912; 2.2078], p value: 0.0001), and GG+GA vs. AA genotype (OR [95% CI]: 1.3805 [1.1459; 1.6632], p value: 0.0007); And rs3025058 5A vs. 6A (OR [95% CI]: 1.2078 [1.0379; 1.4056], p value: 0.0147), 5A5A vs. 6A6A (OR [95% CI]: 1.4787 [1.0876; 2.0103], p value: 0.0126), and 5A5A+5A6A vs. 6A6A (OR [95% CI]: 1.2747 [1.0104; 1.6081], p value: 0.0406). There was no significant difference in any of the genetic models for rs1799750 and rs243865. No publication bias was observed in any of the genetic models.Conclusions: MMP-7 rs11568818 G/A and MMP-3 rs3025058 5A/6A were significantly associated with cervical cancer susceptibility.

The development of efficient and recyclable heterogeneous catalysts is an important topic. Herein, a rhodium(III) complex Cp*Rh@HATN-CTF was synthesized by the coordinative immobilization of [Cp*RhCl2]2 on a hexaazatrinaphthalene-based covalent triazine framework. In the presence of Cp*Rh@HATN-CTF (1 mo l% Rh), a series of primary amines could be obtained via the reductive amination of ketones in high yields. Moreover, catalytic activity of Cp*Rh@HATN-CTF is well maintained during six runs. The present catalytic system was also applied for the large scale preparation of a biologically active compound. It would facilitate the development of CTF-supported transition metal catalysts for sustainable chemistry.

A new-type of covalent triazine framework derived from 2,5-pyrazinedicarbonitrile as a monomer with a high N/C ratio was designed and synthesized by trimerization at 400 °C with ZnCl 2 as a catalyst and salt melt via the ionothermal technique.

A linear-organic-polymer-supported iridium complex Cp*Ir@P4VP, which is designed and synthesized by the coordinative immobilization of [Cp*IrCl2]2 on poly(4-vinylpyridine), was proven to be an efficient heterogeneous autotandem catalyst for synthesizing quinazolinones via selective hydration/acceptorless dehydrogenative coupling from o-aminobenzonitriles. Furthermore, the synthesized catalyst was recycled five times without an obvious decrease in the catalytic activity.

A Cp*Ir complex bearing a flexible bridging and functional 2,2'-methylenebibenzimidazole ligand was designed, synthesized, and found to be a general and efficient auto-tandem catalyst for the synthesis of N-methyl tertiary amines from imines via transfer hydrogenation/N-methylation with methanol as both hydrogen source and methylating reagent. In the presence of [Cp*Ir(2,2'-CH(2)BiBzImH(2))Cl][Cl], a range of desirable products were obtained in high yields with nearly complete selectivities. The reaction is highly attractive due to the highly atom economy, and minimal consumption of chemicals and energy. Notably, this research exhibits new potential of metal-ligand bifunctional catalysts for the activation of methanol as C1 source for organic synthesis. (C) 2021 Elsevier Inc. All rights reserved.

A strategy for the synthesis of alkenyl ketones via the alpha-alkylation of ketones with alkenyl ketones has proposed and accomplished. In the presence of a metal-ligand bifunctional catalyst [Cp*Ir(2,2'-bpyO) (H2O)], a series of desirable products were obtained in high yields. Mechanistic investigation revealed that functional groups in the ligand are crucial for the activity of catalyst and selective transfer hydrogenation is the determining step of the formation of alkenyl ketones as products. Notably, the present research exhibited also the unique potential of metal-ligand bifunctional catalysts for the activation of unsaturated alcohols as electrophiles for hydrogen auto-transfer process. (C) 2021 Elsevier Inc. All rights reserved.

Background: Gastric cancer (GC) has a high mortality rate in cancer-related deaths worldwide. Currently, the pathogenesis of gastric cancer progression remains unclear. Here, we identified several vital candidate genes related to gastric cancer development and revealed the potential pathogenic mechanisms using integrated bioinformatics analysis. Methods: Two microarray datasets from Gene Expression Omnibus (GEO) database integrated. Limma package was used to analyze differentially expressed genes (DEGs) between GC and matched normal specimens. DAVID was utilized to conduct Gene ontology (GO) and KEGG enrichment analysis. The relative expression of OLFM4, IGF2BP3, CLDN1 and MMP1were analyzed based on TCGA database provided by UALCAN. Western blot and quantitative real time PCR assay were performed to determine the protein and mRNA levels of OLFM4, IGF2BP3, CLDN1 and MMP1 in GC tissues and cell lines, respectively. Results: We downloaded the expression profiles of GSE103236 and GSE118897 from the Gene Expression Omnibus (GEO) database. Two integrated microarray datasets were used to obtain differentially expressed genes (DEGs), and bioinformatics methods were used for in-depth analysis. After gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichments analysis, we identified 61 DEGs in common, of which the expression of 34 genes were elevated and 27 genes were decreased. GO analysis displayed that the biological functions of DEGs mainly focused on negative regulation of growth, fatty acid binding, cellular response to zinc ion and calcium-independent cell-cell adhesion. KEGG pathway analysis demonstrated that these DEGs mainly related to the Wnt and tumor signaling pathway. Interestingly, we found 4 genes were most significantly upregulated in the DEGs, which were OLFM4, IGF2BP3, CLDN1 and MMP1. Then, we confirmed the upregulation of these genes in STAD based on sample types. In the final, western blot and qRT-PCR assay were performed to determine the protein and mRNA levels of OLFM4, IGF2BP3, CLDN1 and MMP1 in GC tissues and cell lines. Conclusion: In our study, using integrated bioinformatics to screen DEGs in gastric cancer could benefit us for understanding the pathogenic mechanism underlying gastric cancer progression. Meanwhile, we also identified four significantly upregulated genes in DEGs from both two datasets, which might be used as the biomarkers for early diagnosis and prevention of gastric cancer.

1Department of Emergency Surgery, The Affiliated Huaian No.1 People’s Hospital of Nanjing Medical University, Huai’an, Jiangsu, People’s Republic of China; 2Department of Emergency, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, People’s Republic of China; 3Department of Cardio-Thoracic Surgery, The Affiliated Huaian No.1 People’s Hospital of Nanjing Medical University, Huai’an, Jiangsu, People’s Republic of China; 4Department of General Surgery, The Affiliated Huaian No.1 People’s Hospital of Nanjing Medical University, Huai’an, Jiangsu, People’s Republic of China Background and Objectives: RING finger protein 38 (RNF38) has been reported to be

目的 探讨乙肝肝硬化患者全血红细胞体积分布宽度(RDW)的特点及临床意义.方法 回顾性分析2018年1月至12月上海市第六人民医院感染科76例住院患者,其中包括31例乙肝肝硬化患者及45例慢性乙型肝炎(CHB)患者,观察患者RDW、血小板(PLT)、血清丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、总胆红素(TBIL)、白蛋白、前白蛋白水平、活化部分凝血活酶时间(APTT)和凝血酶原时间(PT)、HBeAg水平及HBV-DNA载量.结果 乙肝肝硬化组RDW水平显著高于CHB组(t=4.46,P<0.01)及健康对照组(t=8.01,P<0.01),CHB组RDW水平显著高于健康对照组(t=4.97,P<0.01);Child-Pugh评分为C的肝硬化组患者全血RDW水平显著高于评分为A和B的患者(t=7.28,P<0.01;t=2.29,P<0.05),Child-Pugh评分为B的患者血RDW水平显著高于评分为A的患者(t=3.10,P<0.01).CHB组及乙肝肝硬化组RDW水平均与总胆红素水平呈正相关(r=0.45,P<0.01;r=0.41,P<0.02),与白蛋白呈负相关(r=-0.43,P<0.01;r=-0.57,P<0.01),与前白蛋白亦呈负相关(r=-0.47,P<0.01;r=-0.48,P<0.01);乙肝肝硬化组RDW水平与Child-Pugh评分呈正相关(r=0.67,P<0.01).各组RDW水平与血小板、ALT、AST、HBeAg水平、HBV-DNA载量无显著相关性.结论 RDW在乙肝肝硬化患者中显著升高,能反映肝硬化患者病情的严重程度,是肝硬化病情进展的一个参考指标.

BACKGROUND AND OBJECTIVES:RING finger protein 38 (RNF38) has been reported to be involved in the tumorigenesis of several tumors, but its role in colorectal cancer (CRC) is still not investigated. In the present study, we aimed to investigate the effect of RNF38 in CRC cells.MATERIALS AND METHODS:The public tumor databases GEPIA and Kaplan-Meier Plotter were used to analyze RNF38 expression and patients' overall survival in CRC. The qRT-PCR was carried out to assess the mRNA levels of RNF38 and LDB1. Western blot and co-immunoprecipitation were used to detect protein expression and ubiquitination. CCK-8 assay was performed to analyze CRC cell growth and viability.RESULTS:RNF38 was found downregulated in CRC tumor tissues and cell lines, and CRC patients with high RNF38 expression had a longer overall survival than patients with low RNF38 expression. Our further investigations showed that RNF38 interacted with LDB1, and downregulated LDB1 expression by inducing its polyubiquitination. Moreover, overexpression of RNF38 inhibited CRC cell growth but enforced LDB1 could significantly antagonize RNF38-induced cell growth inhibition in CRC cells. Additionally, RNF38/LDB1 axis was involved in the drug sensitivity of 5-FU to CRC cells.CONCLUSION:Our studies suggested that RNF38 was functional in CRC cells, and downregulated CRC cell growth by inducing LDB1 polyubiquitination, which indicated that RNF38 could be as a novel target for CRC therapy.

Abstract MicroRNA‐26a‐5p (miR‐26a‐5p) has been reported to be involved in the tumorigenesis of several tumors, but its function in breast cancer is still unknown. In this study, miR‐26a‐5p was found significantly downregulated in both of the breast cancer tissues and cell lines, and low expression of miR‐26a‐5p predicted a poor prognosis for breast cancer patients. Overexpression of miR‐26a‐5p could significantly inhibit breast cancer cell growth. Further studies revealed that overexpression of miR‐26a‐5p downregulated the protein levels of Cyclin D1, CDK4, and CDK6, but upregulated the expression levels of p21, p27, and p53. In mechanism, miR‐26a‐5p targeted the 3′UTR of ring finger protein 6 (RNF6) mRNA and inhibited RNF6 expression in breast cancer cells. Moreover, overexpression of miR‐26a‐5p inhibited RNF6/ERα/Bcl‐xL axis in breast cancer cells. In contrast, inhibiting miR‐26a‐5p upregulated RNF6/ERα/Bcl‐xL axis. Further studies indicated that miR‐26a‐5p mediated RNF6/ERα/Bcl‐xL axis through regulating the stability of ERα protein. Collectively, downregulation of miR‐26a‐5p plays essential roles in breast cancer by mediating RNF6/ERα/Bcl‐xL axis, which might provide important implications for the therapeutics of breast cancer.

Purpose: To elucidate the potential role of long non-coding RNA (lncRNA) DUXAP8 in the malignant progression of colorectal cancer (CRC) and its possible molecular mechanism. Methods: The expression level of lncRNA DUXAP8 in CRC tissues and matched paracancerous tissues was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Meanwhile, its level in CRC patients with different tumor sizes and tumor grades was determined. The regulatory effects of DUXAP8 on the behaviors of CRC cells were evaluated by cell counting kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) and Transwell assay. The interaction between LSD1, EZH2 and DUXAP8 was evaluated by RNA-protein interactions and RIP assay. Linear regression analyses were conducted to examine the correlation between DUXAP8 and LSD1, EZH2. Results: LncRNA DUXAP8 was upregulated in CRC tissues and cell lines. Its level remained higher in CRC with larger tumor size or higher tumor grade. Knockdown of DUXAP8 suppressed the proliferative, migratory and invasive abilities of DLD-1 and SW480 cells. Both RF classifier and SVM classifier predicted the pronounced accuracies of LSD1 and EZH2. RIP assay further demonstrated the interaction between DUXAP8 and LSD1, EZH2. Knockdown of LSD1 or EZH2 could attenuate the proliferative rate of CRC cells. Moreover, the mRNA levels of LSD1 and EZH2 were positively correlated with DUXAP8 in CRC. Conclusions: LncRNA DUXAP8 accelerates the malignant progression of CRC via positively regulating EZH2 and LSD1.

Background and objective RNF6, an E3 ligase, has been reported to play an important role in the tumorigenesis in several tissues, but its role in gastric cancer is still unknown. In this study, we aimed to investigate the biological function and molecular mechanisms of RNF6 in gastric cancer. Materials and methods The expression levels of RNF6 were detected by quantitative real-time PCR (qRT-PCR) and immunoblotting in gastric cancer tissues and cell lines. Cell Counting Kit-8 assay was performed to evaluate cell proliferation. Cell apoptosis was analyzed by flow cytometer and immunoblotting. Luciferase assay, immunoblotting and qRT-PCR were performed to explore the activation of STAT3. Immunoprecipitation was performed to evaluate the ubiquitination of SHP-1. Results In this study, RNF6 was found to be upregulated in both primary tissues and cell lines of gastric cancer. Knockdown or overexpression of RNF6 inhibited or promoted cell growth of gastric cancer cells. Knockdown of RNF6 also induced the cleavage of PARP and promoted cell apoptosis in gastric cancer cells. In addition, knockdown of RNF6 also increased the cytotoxicity of doxorubicin against gastric cancer. Moreover, knockdown of RNF6 inhibited STAT3-derived luciferase activity and downregulated the phosphorylation of STAT3, but upregulated the protein level of SHP-1. Knockdown of RNF6 downregulated the expression of MCL1 and XIAP, which are target genes of STAT3. Further studies showed that RNF6 regulated the stability of SHP-1 by inducing its polyubiquitination. Conclusion These results demonstrated that RNF6 was highly expressed in gastric cancer and regulated the growth of gastric cancer cells by affecting SHP-1/STAT3 signaling, which suggested that RNF6 could be a novel target for gastric cancer therapy.

Background: Many studies have identified trimethylamine N-oxide (TMAO) as a new risk factor of cardiovascular diseases. It has been suggested that TMAO promotes atherosclerosis development. However, the underlying mechanism is still unclear. Methods: Apoe-/- mice were fed a high-fat diet and given water with or without TMAO for 8-week. Histological and immunohistological analyses were used to evaluate the atherogenic effect of TMAO in vivo. We also employed peritoneal elicited macrophages and RAW264.7 to assess the role of MAPK/JNK pathway in TMAO-induced formation of foam cells. Results: TMAO significantly promoted plaque progression in apoe-/- mice fed with high-fat diet for 8 weeks. Besides, macrophage recruitment, CD36 and proinflammatory cytokine expressions were enhanced by TMAO in plaque lesions. In vitro, TMAO increased the macrophage migration and the expression of TNF-alpha, IL-6 and ICAM1. In addition, CD36 expression and foam cell formation induced by ox-LDL were also enhanced by TMAO, which could be attenuated by siRNA-mediated knockdown of CD36. We additionally used MAPK inhibitor (SB230580) and JNK inhibitor (SP600125) to assess the MAPK/JNK pathway in TMAO-induced CD36 expression. Western blotting showed that both SB230580 and SP600125 could reduce the expression of CD36 induced by ox-LDL and TMAO. Moreover, SB230580 and SP600125 could also reduce the formation of foam cells. Conclusions: TMAO promotes the atherosclerosis in vivo and in vitro. CD36/MAPK/JNK pathway may play a crucial role in TMAO-induced formation of foam cells.

Infiltrating monocytes have been demonstrated to contribute to tissue damage in experimental models of liver injury and fibrosis. However, less is known about monocyte infiltration in the livers of patients with chronic liver diseases (CLD). In the present study, we demonstrated that CD68+ hepatic macrophages and MAC387+ infiltrating monocytes were significantly increased in the livers of CLD patients with different etiologies as compared with normal liver tissue. In addition, CLD patients with higher inflammatory grading scores had more CD68+ macrophages and MAC387+ monocytes infiltration in their livers compared to those with lower scores. Significantly more MAC387+ infiltrating monocytes were found in the liver tissue of CLD patients with higher fibrotic staging scores compared to those with lower scores. Monocyte chemoattractant protein-1 (MCP-1) expression was significantly increased in the livers of CLD patients with different etiologies. MCP-1 staining scores were significantly positively associated with the numbers of MAC387+ infiltrating monocytes in CLD patients. Taken together, our results demonstrate that infiltrating monocytes may play a pathological role in exacerbating chronic liver inflammation and fibrosis in CLD. MCP-1 may be involved in the monocyte infiltration and progression of liver inflammation and fibrosis in CLD.

Vascular endothelial growth factor (VEGF) serves an important role in promoting angiogenesis and tissue regeneration. However, the lack of an effective delivery system that can target this growth factor to the injured site reduces its therapeutic efficacy. Therefore, in the current study, collagen‑binding VEGF was constructed by fusing a collagen‑binding domain (CBD) to the N‑terminal of native VEGF. The CBD‑VEGF can specifically bind to collagen which is the major component of the extracellular matrix in fibrotic liver. The anti‑fibrotic effects of this novel material were investigated by the carbon tetrachloride (CCl4)‑induced liver fibrotic mouse model. Mice were injected with CCl4 intraperitoneally to induce liver fibrosis. CBD‑VEGF was injected directly into the liver tissue of mice. The liver tissues were stained with hematoxylin and eosin for general observation or with Masson's trichrome staining for detection of collagen deposition. The hepatic stellate cell activation, blood vessel formation and hepatocyte proliferation were measured by immunohistochemical staining for α‑smooth muscle actin, CD31 and Ki67 in the liver tissue. The fluorescent TUNEL assay was performed to evaluate the hepatocyte apoptosis. The present study identified that the CBD‑VEGF injection could significantly promote vascularization of the liver tissue of fibrotic mice and attenuate liver fibrosis. Furthermore, hepatocyte apoptosis and hepatic stellate cell activation were attenuated by CBD‑VEGF treatment. CBD‑VEGF treatment could additionally promote hepatocyte regeneration in the liver tissue of fibrotic mice. Thus, it was suggested that CBD‑VEGF may be used as a novel therapeutic intervention for liver fibrosis.

AIM:To investigate the association of serum gamma-glutamyl transferase (GGT) levels with chronic hepatitis B infection and hepatitis B e antigen (HBeAg) seroconversion.METHODS:A retrospective study was performed on clinical data collected from patients who had been positive for hepatitis B surface antigen for > 6 mo and who were antiviral-treatment naïve (n = 215) attending the Hepatitis Clinic at Nanjing Drum Tower Hospital between August 2010 and December 2013. Healthy individuals without liver disease (n = 83) were included as controls. Patients were categorized into four groups based on disease status as recommended by the European Association for the Study of the Liver: immune tolerance (IT; n = 47), HBeAg-positive hepatitis (EPH; n = 93), HBeAg-negative hepatitis (ENH; n = 20), and inactive carrier (IC; n = 55). Prediction of complete response (CR) based on serum GGT was also examined in EPH patients (n = 33) treated for 48 wk with nucleos(t)ide analogue (NA) therapy, including lamivudine plus adefovir combination therapy (n = 20) or entecavir monotherapy (n = 13). CR was defined as a serum hepatitis B virus DNA level < 500 copies/mL and HBeAg seroconversion by 48 wk of treatment.RESULTS:Serum GGT levels were significantly increased in EPH and ENH patients relative to the IT, IC, and healthy control groups (P < 0.01 for all). However, no significant difference in serum GGT levels was found between the EPH and ENH groups. Baseline serum GGT levels were significantly higher in patients who achieved CR (7/33; 21.2%) compared to patients in the non-CR group (26/33; 78.8%; P = 0.011). In addition, the decline in serum GGT was greater in CR patients compared to non-CR patients after 24 wk and 48 wk of treatment (P = 0.012 and P = 0.008, respectively). The receiver operating characteristic curve yielded a sensitivity of 85.71% and a specificity of 61.54% at a threshold value of 0.89 times the upper limit of normal for baseline serum GGT in the prediction of CR following NA therapy.CONCLUSION:Serum GGT is significantly elevated in EPH and ENH patients and is a potential biomarker for the prediction of HBeAg seroconversion following NA therapy.

AIM:To investigate the association between red cell distribution width (RDW) and the severity of hepatitis B virus (HBV)-related liver diseases.METHODS:Sixty-nine patients with chronic hepatitis B (CHB) and 61 patients with HBV-related liver cirrhosis were enrolled in the present study. Forty-one healthy individuals were included as controls. Hematological parameters, hepatitis B e-antigen (HBeAg) status, HBV DNA levels and liver biochemistry were analyzed. Child-Pugh scores and Model for End-Stage Liver Disease (MELD) scores of the patients with HBV-related liver cirrhosis were calculated.RESULTS:The RDW was significantly higher in patients with HBV-related liver cirrhosis as compared with CHB patients and healthy controls. RDW was slightly higher in CHB patients as compared with healthy controls. An increasing correlation of RDW with Child-Pugh grades was found. RDW was positively correlated with Child-Pugh scores and MELD scores. In patients with HBV-related liver cirrhosis, RDW was also positively correlated with total bilirubin and negatively correlated with hemoglobin and serum albumin concentration. However, no significant difference was found between HBeAg positive and negative patients and no significant correlation between RDW and HBV DNA levels was found.CONCLUSION:The RDW was elevated in CHB patients and patients with HBV-related liver cirrhosis and was positively correlated with the severity of HBV-related liver cirrhosis. RDW is a potential index to assess the severity of HBV-related liver diseases.