The second complete mitochondrial genome of Capillidium rhysosporum within the family Capillidiaceae, Entomophthorales.

The complete mitochondrial genome of the entomophthoroid fungus Capillidium rhysosporum (strain no.: ATCC 12588) was sequenced using next-generation sequencing technology. The assembled circular genome has a length of 46,756 base pairs with a GC content of 27.06%. Gene prediction identified 15 core protein-coding genes (PCGs), two rRNA genes, and 27 tRNA genes. Phylogenetic analysis confirmed that C. rhysosporum belongs to the Zoopagomycota clade and is closely related to C. heterosporum. This study presents the second complete mitochondrial genome within the family Capillidiaceae, contributing to the mitochondrial DNA database of entomophthoroid fungi.

Co-infection of Aspergillus ochraceopetaliformis strain RCEF7483 by a novel chrysovirus and a known partitivirus.

An airborne microflora isolate, Aspergillus ochraceopetaliformis RCEF7483, was found to harbor seven dsRNA elements, indicating co-infection with a novel chrysovirus and a known partitivirus. Sequence analysis and RT-PCR confirmed dsRNA5-7 as components of Aspergillus ochraceous virus (AOV), a member of the Partitiviridae family. In light of its distinct host, we have designated it Aspergillus ochraceopetaliformis partitivirus 1 (AoPV1). The dsRNA segments, named dsRNA1-4, with lengths of 3706 bp, 3410 bp, 3190 bp, and 3158 bp, respectively, constitute the genome of a novel chrysovirus designated Aspergillus ochraceopetaliformis chrysovirus 1 (AoCV1). The dsRNA1-4 segments contain five open-reading frames (ORF1-5). Specifically, ORF1 encodes a putative RNA-dependent RNA polymerase (RdRp) with a length of 1112 amino acids, and ORF2 encodes a putative coat protein (CP) spanning 976 amino acids. Additionally, ORF3-5 encode hypothetical proteins (HP1, HP2, and HP3) with lengths of 108, 843, and 914 amino acids, respectively. Comparative analysis revealed the highest similarity of dsRNA1-4 with corresponding proteins in Aspergillus terreus chrysovirus 1 (AtCV1) (RdRp, 66.58%; CP, 51.02%; HP2, 61.80%; and HP3, 41.30%). Due to falling below the threshold for a new species in the Chrysoviridae, we propose that dsRNA1-4 in A. ochraceopetaliformis strain RCEF7483 constitute the novel chrysovirus AoCV1. Moreover, phylogenetic analysis using RdRp amino acid sequences placed AoCV1 within the Alphachrysovirus genus of the Chrysoviridae family, clustering with AtCV1 and other alphachrysoviruses. Our study contributes to the understanding of mycoviruses in A. ochraceopetaliformis and expands our knowledge of the diversity and evolution of chrysoviruses in fungal hosts.

Complete genome sequence of a novel gammapartitivirus from Penicillium oxalicum RCEF7482.

Penicillium oxalicum, an important biocontrol fungus in China, has been a subject of extensive study due to its role in combating various pathogenic fungi. Despite the prevalence of mycoviruses with double-stranded (ds) RNA genomes in filamentous fungi, there has been no screening of mycoviruses in P. oxalicum. In this report, we describe the identification and characterization of a novel dsRNA virus isolated from P. oxalicum, designated as "Penicillium oxalicum partitivirus 1" (PoPV1). The genome of PoPV1 consists of two dsRNA segments, dsRNA1 (1,770 bp) and dsRNA2 (1,584 bp), each containing a single open reading frame (ORF): ORF1 and ORF2. Comparative analysis revealed that the RdRp and CP amino acid sequences of PoPV1 share the highest identity (89.18% and 73.97%, respectively) with those of Penicillium aurantiogriseum partitivirus 1 (PaPV1). Motif analysis based on RdRp amino acid sequences places PoPV1 in the genus Gammapartitivirus within the family Partitiviridae, with a distinctive motif VI (R/KV/ILGDD). Phylogenetic analysis further established a close relationship of PoPV1 to PaPV1, forming a unique clade among the gammapartitiviruses. Consequently, we propose that Penicillium oxalicum partitivirus 1 represents a new species in the genus Gammapartitivirus. This is the first report of a dsRNA virus in P. oxalicum.

Infection with a novel polymycovirus enhances growth, conidiation and sensitivity to UV-B irradiation of the entomopathogenic fungus Metarhizium anisopliae.

Metarhizium anisopliae is a well-studied entomopathogenic fungus that is widely used in biological control programs. The presence of polymycoviruses in this fungus is common, but their effects on fungal development and stress tolerance are not well understood. In this study, we report the discovery of a novel double-stranded RNA virus, named Metarhizium anisopliae polymycovirus 1 (MaPmV1), which comprises four dsRNAs ranging from 2.4 to 1.4 kbp in length. Phylogenetic analysis revealed that MaPmV1 belongs to the Polymycoviridae family. Biological comparison between MaPmV1-infected (Vi) and -free (Vf) isogenic lines showed that MaPmV1 remarkably enhances the growth rate and conidiation of the host fungus. The upregulation of growth- and conidiation-related genes in Vi strains supports this finding. In addition, MaPmV1 increases the sensitivity of the host to UV-B irradiation, which is evidenced by the downregulation of DNA damage repair genes in Vi strains. However, MaPmV1 does not appear to have any significant impact on the virulence of M. anisopliae. Furthermore, overexpression of individual viral proteins in M. anisopliae did not result in any significant phenotypic alterations, indicating that MaPmV1-mediated changes are not related to a single viral protein. Overall, our findings suggest that mycoviruses can be exploited to enhance fungal development in entomopathogenic fungi, which may lead to improved conidium production on a large scale.

Corrigendum: Cuproptosis key gene FDX1 is a prognostic biomarker and associated with immune infiltration in glioma.

[This corrects the article DOI: 10.3389/fmed.2022.939776.].

Sitravatinib is a potential EGFR inhibitor and induce a new death phenotype in Glioblastoma.

Glioblastoma (GBM) is a highly lethal neurological tumor that presents significant challenge for clinicians due to its heterogeneity and high mortality rate. Despite extensive research, there is currently no effective drug treatment available for GBM. Research evidence has consistently demonstrated that the epidermal growth factor receptor (EGFR) promotes tumor progression and is associated with poor prognosis in several types of cancer. In glioma, EGFR abnormal amplification is reported in approximately 40% of GBM patients, with overexpression observed in 60% of cases, and deletion or mutation in 24% to 67% of patients. In our study, Sitravatinib, a potential EGFR inhibitor, was identified through molecular docking screening based on protein structure. The targeting of EGFR and the tumor inhibitory effect of Sitravatinib on glioma were verified through cellular and in vivo experiments, respectively. Our study also revealed that Sitravatinib effectively inhibited GBM invasive and induced DNA damage and cellular senescence. Furthermore, we observed a novel cell death phenotype induced by Sitravatinib, which differed from previously reported programmed death patterns such as apoptosis, pyroptosis, ferroptosis, and necrosis.

The CDK inhibitor AT7519 inhibits human glioblastoma cell growth by inducing apoptosis, pyroptosis and cell cycle arrest.

Glioblastoma multiforme (GBM) is the most lethal primary brain tumor with a poor median survival of less than 15 months. However, clinical strategies and effective therapies are limited. Here, we found that the second-generation small molecule multi-CDK inhibitor AT7519 is a potential drug for GBM treatment according to high-throughput screening via the Approved Drug Library and Clinical Compound Library (2718 compounds). We found that AT7519 significantly inhibited the cell viability and proliferation of U87MG, U251, and patient-derived primary GBM cells in a dose-dependent manner. Furthermore, AT7519 also inhibited the phosphorylation of CDK1/2 and arrested the cell cycle at the G1-S and G2-M phases. More importantly, AT7519 induced intrinsic apoptosis and pyroptosis via caspase-3-mediated cleavage of gasdermin E (GSDME). In the glioblastoma intracranial and subcutaneous xenograft assays, tumor volume was significantly reduced after treatment with AT7519. In summary, AT7519 induces cell death through multiple pathways and inhibits glioblastoma growth, indicating that AT7519 is a potential chemical available for GBM treatment.

Cuproptosis key gene FDX1 is a prognostic biomarker and associated with immune infiltration in glioma.

Recent studies have found that the protein encoded by the FDX1 gene is involved in mediating Cuproptosis as a regulator of protein lipoylation and related to immune response process of tumors. However, the specific biological function of FDX1 in glioma is currently unclear. To explore the potential function of FDX1, this study explored the correlation between the expression of FDX1 in cancers and survival prognosis by analyzing the public databases of GEPIA and Cbioportal. Immune infiltration was analyzed by the TIMER2.0 database in tumors. The possible biological processes and functions of FDX1-related in glioma were annotated through gene enrichment. Relationship between Cuproptosis and autophagy was explored through gene co-expression studies. Summary and conclusions of this study: (1) FDX1 is highly expressed in gliomas and associated with poor prognosis in low-grade gliomas (LGG). (2) Gene annotation indicates that FDX1 is mainly involved in the tumor protein lipoylation and cell death. (3) FDX1 expression is positively correlated with the infiltration of immune cells. (4) LIPT2 and NNAT, two other genes involved in lipoylation, may be unidentified marker gene for Cuproptosis. And the Cuproptosis genes related to FDX1 were positively correlated with the expression of autophagy marker genes Atg5, Atg12, and BECN-1. This evidence suggests that there may be some interaction between FDX1 mediated Cuproptosis and autophagy. In summary, FDX1 may serve as a potential immunotherapy target and prognostic marker for Glioma.

A gold nanoparticle doped flexible substrate for microplastics SERS detection.

Due to overuse of plastic products, decomposed microplastics (MPs) are widely spread in aquatic ecosystems, and will cause irreparable harm to the human body through the food chain. Traditional MP detection methods require cumbersome sample pre-processing procedures and complex instruments, so there is an urgent demand to develop methods to achieve simple on-site detection. Herein, a simple, sensitive, accurate, and stable MP detection method based on surface-enhanced Raman scattering (SERS) is investigated. Considering the hydrophobic problems of MPs, gold nanoparticle (AuNP) doped filter paper as a flexible SERS substrate is applied to capture MPs in the fiber pores. Benefitting from the electromagnetic (EM) hot spots generated by AuNPs, the Raman signal of MPs can be effectively enhanced. Meanwhile, the flexible SERS substrate has good sensitivity to a minimum detectable concentration of 0.1 g L-1 for polyethylene terephthalate (PET) in water, and the maximum enhancement factor (EF) can reach 360.5. Furthermore, the practicability of the developed method has been proved by the successful detection of MPs in tap water and pond water. This research provides an easy process, high sensitivity, and good reproducibility method for MP detection.

New Autophagy-Ferroptosis Gene Signature Predicts Survival in Glioma.

Background: Ferroptosis plays an important role in glioma and significantly affects the prognosis, but the specific mechanism has not yet been elucidated. Recent studies suggest that autophagy regulates the process of ferroptosis. This study aimed to find potential autophagy-ferroptosis genes and explore the prognostic significance in glioma. Methods: Ferroptosis and autophagy genes were obtained from two online databases (zhounan.org/ferrdb and autophagy.lu/). The RNAseq data and clinical information were obtained from the Chinese Glioma Genome Atlas (CGGA) database (http://www.cgga.org.cn/). Univariate, multivariate, lasso and Cox regression analysis screened out prognosis-related genes, and a risk model was constructed. Receiver operating characteristic (ROC) curve analysis evaluated the predictive efficiency of the model. Finally, a nomogram was constructed to more accurately predict the prognosis of glioma. Results: We developed a Venn diagram showing 23 autophagy-ferroptosis genes. A total of 660 cases (including RNA sequences and complete clinical information) from two different cohorts (training group n = 413, verification group n = 247) of the CGGA database was acquired. Cohorts were screened to include five prognosis-related genes (MTOR, BID, HSPA5, CDKN2A, GABARAPLA2). Kaplan-Meier curves showed that the risk model was a good prognostic indicator (p < 0.001). ROC analysis showed good efficacy of the risk model. Multivariate Cox analysis also revealed that the risk model was suitable for clinical factors related to prognosis, including type of disease (primary, recurrence), grade (III-IV), age, temozolomide treatment, and 1p19q state. Using the five prognosis-related genes and the risk score, we constructed a nomogram assessed by C-index (0.7205) and a calibration plot that could more accurately predict glioma prognosis. Conclusion: Using a current database of autophagy and ferroptosis genes, we confirmed the prognostic significance of autophagy-ferroptosis genes in glioma, and we constructed a prognostic model to help guide treatment for high grade glioma in the future.

Farnesoid X receptor via Notch1 directs asymmetric cell division of Sox9+ cells to prevent the development of liver cancer in a mouse model.

BACKGROUND: Asymmetrical cell division (ACD) maintains the proper number of stem cells to ensure self-renewal. The rate of symmetric division increases as more cancer stem cells (CSCs) become malignant; however, the signaling pathway network involved in CSC division remains elusive. FXR (Farnesoid X receptor), a ligand-activated transcription factor, has several anti-tumor effects and has been shown to target CSCs. Here, we aimed at evaluating the role of FXR in the regulation of the cell division of CSCs. METHODS: The FXR target gene and downstream molecular mechanisms were confirmed by qRT-PCR, Western blot, luciferase reporter assay, EMAS, Chip, and IF analyses. Pulse-chase BrdU labeling and paired-cell experiments were used to detect the cell division of liver CSCs. Gain- and loss-of-function experiments in Huh7 cells and mouse models were performed to support findings and elucidate the function and underlying mechanisms of FXR-Notch1 in liver CSC division. RESULTS: We demonstrated that activation of Notch1 was significantly elevated in the livers of hepatocellular carcinoma (HCC) in Farnesoid X receptor-knockout (FXR-KO) mice and that FXR expression negatively correlated with Notch1 level during chronic liver injury. Activation of FXR induced the asymmetric divisions of Sox9+ liver CSCs and ameliorated liver injury. Mechanistically, FXR directs Sox9+ liver CSCs from symmetry to asymmetry via inhibition of Notch1 expression and activity. Deletion of FXR signaling or over-expression of Notch1 greatly increased Notch1 expression and activity along with ACD reduction. FXR inhibited Notch1 expression by directly binding to its promoter FXRE. FXR also positively regulated Numb expression, contributing to a feedback circuit, which decreased Notch1 activity and directed ACD. CONCLUSION: Our findings suggest that FXR represses Notch1 expression and directs ACD of Sox9+ cells to prevent the development of liver cancer.

Toehold-Mediated Strand Displacement Reaction for Dual-Signal Electrochemical Assay of Apolipoprotein E Genotyping.

Apolipoprotein E (apoE) polymorphic genes are one of the main genetic determinants of Alzheimer's disease (AD) risk. Relying on the toehold-mediated strand displacement reaction (SDR), the dual-signal electrochemical assay of apoE genotyping with potential applications in the early diagnosis of AD has been achieved. The displacement of the surface-confined methylene blue- and ferrocene-capped detection probe-modified gold nanoparticles (AuNPs) by the complementary sequences (Tc 1 and Tc 2, fragment of allele ε4 at codon 112 and that of allele ε3 or ε4 at codon 158, respectively), triggered by the highly specific SDR, results in decreased voltammetric signals. In contrast, partial strand displacement caused by the single mismatched sequences (Tsm 1 and Tsm 2, fragment of allele ε2 or ε3 at codon 112 and that of allele ε2 at codon 158, respectively) produces larger voltammetric signals. The proposed method serves as a versatile platform for the discrimination of six apoE genotypes, including three homozygotes (ε2/2, ε3/3, and ε4/4) and three heterozygotes (ε2/3, ε2/4, and ε3/4), and for the quantification of apoE ε3/3 from genomic DNA extracts of AD patients.

Three-Dimensional DNA Nanomachine Combined with Toehold-Mediated Strand Displacement Reaction for Sensitive Electrochemical Detection of MiRNA.

MicroRNA (miRNA) serves as an ideal biomarker for diagnosis, prognosis, and therapy of various human cancers. The rationally designed three-dimensional (3D) DNA nanomachine was constructed on the matrixes of magnetic beads, and the high density of gold nanoparticles (AuNPs) on each magnetic bead and further enlargement of the AuNPs lead to the anchoring of numerous DNA walkers and signal probes on the AuNPs. With the combination of toehold-mediated strand displacement reaction (SDR), amplified electrochemical detection of miRNA is performed. The existence of miRNA triggers the toehold-mediated SDR and the released DNA walker probe is hybridized with the ferrocene (Fc)-tagged signal probe. The cleavage of the duplex by the nicking endonuclease detaches the signal probe from the magnetic nanocomposites. The oxidation current of Fc moieties was found to be inversely proportional to the concentrations of miRNA-182 between 1.0 fM and 2 pM. The assay is highly selective for discrimination of miRNAs with similar sequences. The feasibility of the method for sensitive detection of the expression levels of miRNA-182 from serum samples of glioma patients at different stages was demonstrated. The sensing protocol holds great promise for early diagnosis and prognosis of the cancer cases with abnormal miRNA expression.

Real-time surface plasmon resonance monitoring of site-specific phosphorylation of p53 protein and its interaction with MDM2 protein.

Phosphorylation serves as an important post-translational modification implicated in cellular signaling and regulation. In this work, real-time monitoring of site-specific phosphorylation of p53 protein by several protein kinases, followed by its interaction with MDM2 protein was conducted using surface plasmon resonance (SPR). The binding of phosphorylated p53 to MDM2 yields a smaller SPR signal in comparison with that in the case of unphosphorylated p53 protein. Three specific protein kinases were involved in the in situ phosphorylation of the surface-confined p53 protein, and the binding kinetics between the phosphorylated p53 and MDM2 protein was monitored. The results indicate that phosphorylation of Ser15 and Ser37 at the p53 transactivation domain 1 (TAD1) by DNA-dependent protein kinase (DNA-PK) is critical for inhibiting the p53-MDM2 interaction, and the weaker binding affinity is most likely caused by the hydrophobicity change in the vicinity of the MDM2-binding motif or phosphorylation-induced p53 conformational change. In contrast, phosphorylation of Ser46 at the p53 TAD2 domain by c-Jun NH2-terminal kinase 2α2 (JNK2α2) exerts a weaker influence on the binding affinity, whereas phosphorylation of Ser376 and Ser378 at the C-terminus of p53 by protein kinase C (PKC) appears to have little effect. The feasibility of the method for the screening of the DNA-PK inhibitor and the inhibitor of p53-MDM2 interaction has been demonstrated and the half-maximal inhibitory concentration (IC50) values of wortmannin and Nutlin-3 (21 nM and 83 nM, respectively) were highly comparable with those obtained by other methods. The proposed method holds great promise for monitoring protein phosphorylation and unraveling the post-translational modification mechanism.

Dual-channel surface plasmon resonance monitoring of intracellular levels of the p53-MDM2 complex and caspase-3 induced by MDM2 antagonist Nutlin-3.

MDM2 can mediate the degradation of tumor suppressor p53 through an autoregulatory feedback loop, in which MDM2 abolishes wild-type p53 function and accelerates malignant transformation. However, the incorporation of MDM2 antagonist Nutlin-3 could reactivate the transcriptional activity of p53, up-regulate caspase-3, and induce apoptosis. In this work, the simultaneous and label-free monitoring of p53-MDM2 complex and caspase-3 levels in cancer cells before and after Nutlin-3 treatment was conducted using dual-channel surface plasmon resonance (SPR). The p53-MDM2 complex was captured in one fluidic channel covered with consensus double-stranded (ds)-DNA, while the other channel was pre-immobilized with caspase-3-specific biotinylated DEVD-containing peptides. To amplify the SPR signals, the attachment of streptavidin (SA)-conjugated anti-MDM2 antibody in both channels was achieved. The signal diversity before and after Nutlin-3 treatment is indicative of the difference in the levels of the intracellular p53-MDM2 complex and caspase-3. The limit of detection for p53-MDM2 and caspase-3 down to 4.54 pM and 0.03 ng mL-1, respectively, was attained. Upon treatment with Nutlin-3, MCF-7 cancer cells with wild-type p53 showed decreased expression of the p53-MDM2 complex and an increased caspase-3 level, while MDA-MB-231 cancer cells with mutant p53 exhibited an elevated caspase-3 level and unchanged p53-MDM2 complex expression. The apoptosis of MCF-7 and MDA-MB-231 cancer cells upon Nutlin-3 treatment follows a p53-dependent and a p53-independent pathway, respectively. The proposed method is sensitive, selective and label-free, holding great promise for assaying intracellular p53-MDM2 complex and caspase-3 levels and differentiating Nutlin-3-mediated p53-dependent or p53-independent apoptotic pathways.

Voltammetric determination of the Alzheimer's disease-related ApoE 4 gene from unamplified genomic DNA extracts by ferrocene-capped gold nanoparticles.

A sensitive method is described for detection of the apoE 4 gene detection which is important for early diagnosis of Alzheimer's disease. It is based on signal amplification by using ferrocene (Fc) capped gold nanoparticles modified with streptavidin. The immobilized oligonucleotide probe captures complementary apoE 4 gene. This is followed by the specific recognition of the GCGC sequences which are hydrolyzed by the restriction enzyme HhaI. Cleavage only occurs at the complementary apoE 4 duplex, while mismatches prevent enzymatic cleavage. Thus, the apoE 4 sequence can be discriminated against other apoE sequences. Benefitting from amplified signal by Fc-capped nanoparticle/streptavidin and the recognition of HhaI, the detection limit is as low as 0.1 pM of the ApoE 4 gene. Four genomic DNA samples extracted from blood were analyzed for the presence of the apoE 4 gene. The approach presented here will provide viable proof-of-principle for an enzyme-assisted electrochemical assay for the apoE 4 gene in genomic DNAs. Graphical abstract Schematic presentation of amplified voltammetric detection of Alzheimer's Disease-related apoE 4 gene from unamplified genomic DNA extracts via ferrocene capped gold nanoparticle/streptavidin.

Triple Stimuli-Responsive Magnetic Hollow Porous Carbon-Based Nanodrug Delivery System for Magnetic Resonance Imaging-Guided Synergistic Photothermal/Chemotherapy of Cancer.

The premature leakage of anticancer drugs during blood circulation may the damage immune system, normal cells, and tissues. Constructing targeted nanocarriers with pH, glutathione, and NIR triple-responsive property can effectively avoid the leakage of anticancer drugs before they arrive at the targeted site. In this paper, magnetic hollow porous carbon nanoparticles (MHPCNs) were successfully fabricated as nanocarrier. Poly(γ-glutamic acid) was used to cap the pores of MHPCNs. The photothermal conversion property of carbon and iron oxide (Fe3O4) nanomaterials was utilized to perform photothermal therapy to overcome multidrug-resistance produced by chemotherapy. The biodistribution of nanoparticles was investigated by magnetic resonance imaging. Experiments in vivo confirm the efficient accumulations of nanoparticles at tumor sites. Meanwhile, tumor growth was effectively inhibited via synergistic photothermal/chemotherapy with minimal side effects.

Comparative proteomic analysis of rats subjected to water immersion and restraint stress as an insight into gastric ulcers.

In the present study, comparative proteomic analysis was performed in rats subjected to water immersion­restraint stress (WRS). A total of 26 proteins were differentially expressed and identified using matrix­assisted laser desorption/ionization time of flight mass spectrometry. Among the 26 differentially expressed protein spots identified, 13 proteins were significantly upregulated under WRS, including pyruvate kinase and calreticulin, which may be closely associated with energy metabolism. In addition, 12 proteins were downregulated under WRS, including hemoglobin subunit ß­2 and keratin type II cytoskeletal 8, which may be important in protein metabolism and cell death. Gene Ontology analysis revealed the cellular distribution, molecular function and biological processes of the identified proteins. The mRNA levels of certain differentially expressed proteins were analyzed using fluorescence quantitative polymerase chain reaction analysis. The results of the present study aimed to offer insights into proteins, which are differentially expressed in gastric ulcers in stress, and provide theoretical evidence of a radical cure for gastric ulcers in humans.

[Relationship between liver mass and soluble intercellular adhesion molecule-1 in patients with liver cirrhosis].

OBJECTIVE: To investigate the relation of liver mass to, liver hymodynamics and soluble intercellular adhesion molecule-1 in patients with liver cirrhosis. METHODS: The liver mass was measured by liver biopsy, hepatic hemodynamics by ultrasonography, and the contents of hyalurionic acid (HA), human procollagen III (HPC III) and collagen type IV (C IV) by radioimmunoassay in 100 patients with liver cirrhosis in compensation stage and 30 normal control subjects. RESULTS: Greater liver mass was accompanied by more severe liver fibrosis and reduced liver blood flow. The contents of HA, HPC III and C IV were obvious higher in the patients than in the normal controls (P<0.05) and increased with the liver mass. The liver mass was positively related to serum liver fibrosis indices (r=0.5612, P<0.05). CONCLUSION: Liver mass in patients with liver cirrhosis is related to hepatic hemodynamics, indices for liver fibrosis and liver pathology.