The Signal Peptidase FoSpc2 Is Required for Normal Growth, Conidiation, Virulence, Stress Response, and Regulation of Light Sensitivity in Fusarium odoratissimum.

Signal peptidase (SPase) is responsible for cleavage of N-terminal signal peptides in most secretory precursor proteins and many membrane proteins during maturation. In this study, we identified four components of the SPase complex (FoSec11, FoSpc1, FoSpc2, and FoSpc3) in the banana wilt fungal pathogen Fusarium odoratissimum. We proved that interactions exist among the four SPase subunits by bimolecular fluorescence complementation (BiFC) and affinity purification and mass spectrometry (AP-MS) assays. Among the four SPase genes, FoSPC2 was successfully deleted. FoSPC2 deletion caused defects in vegetative growth, conidiation, and virulence. Loss of FoSPC2 also affected the secretion of some pathogenicity-related extracellular enzymes, suggesting that SPase without FoSpc2 may have a lower efficiency in managing the maturation of the extracellular enzymes in F. odoratissimum. In addition, we found that the ΔFoSPC2 mutant had increased sensitivity to light, and the colonies of the mutant grew faster under all-dark conditions than under all-light conditions. We further observed that deletion of FoSPC2 affected expression of the blue light photoreceptor gene FoWC2, leading to cytoplasmic accumulation of FoWc2 under all-light conditions. Since FoWc2 has signal peptides, FoSpc2 may regulate the expression and subcellular localization of FoWc2 indirectly. Contrary to its response to light, the ΔFoSPC2 mutant displayed a significant decreased sensitivity to osmotic stress, and culturing the mutant under osmotic stress conditions restored both the localization of FoWc2 and light sensitivity of the ΔFoSPC2, suggesting that a cross talk between osmotic stress and light response pathways in F. odoratissimum and FoSpc2 takes part in these processes. IMPORTANCE In this study, we identified four components of SPase in the banana wilt pathogen Fusarium odoratissimum and characterized the SPase FoSpc2. Loss of FoSPC2 affected the secretion of extracellular enzymes, suggesting that SPase without FoSpc2 may have a lower efficiency in managing the maturation of the extracellular enzymes in F. odoratissimum. In addition, this is the first time that we have found a relationship between the SPase and fungal light response. Deletion of FoSPC2 resulted in decreased sensitivity to the osmotic stresses but with increased sensitivity to light. Continuous light inhibited the growth rate of the ΔFoSPC2 mutant and affected the cellular localization of the blue light photoreceptor FoWc2 in this mutant, but culturing the mutant under osmotic stress both restored the localization of FoWc2 and eliminated the light sensitivity of the ΔFoSPC2 mutant, suggesting that loss of FoSPC2 may affect a cross talk between the osmotic stress and light response pathways in F. odoratissimum.

Segregation of the stemness program from the proliferation program in intestinal stem cells.

Stem cells can undergo continuous self-renewal and meanwhile retain the stemness capability to differentiate to mature functional cells. However, it is unclear whether the proliferation property can be segregated from the stemness in stem cells. The intestinal epithelium undergoes fast renewal, and the Lgr5+ intestinal stem cells (ISCs) are essential to maintain homeostasis. Here, we report that methyltransferase-like 3 (Mettl3), a critical enzyme for N6-methyladenosine (m6A) methylation, is required for ISCs maintenance as its deletion results in fast loss of stemness markers but has no effect on cell proliferation. We further identify four m6A-modified transcriptional factors, whose ectopic expression can restore stemness gene expression in Mettl3-/- organoids, while their silencing leads to stemness loss. In addition, transcriptomic profiling analysis discerns 23 genes that can be segregated from the genes responsible for cell proliferation. Together, these data reveal that m6A modification sustains ISC stemness, which can be uncoupled from cell proliferation.

A Network of Sporogenesis-Responsive Genes Regulates the Growth, Asexual Sporogenesis, Pathogenesis and Fusaric Acid Production of Fusarium oxysporum f. sp. cubense.

The conidia produced by Fusarium oxysporum f. sp. cubense (Foc), the causative agent of Fusarium Wilt of Banana (FWB), play central roles in the disease cycle, as the pathogen lacks a sexual reproduction process. Until now, the molecular regulation network of asexual sporogenesis has not been clearly understood in Foc. Herein, we identified and functionally characterized thirteen (13) putative sporulation-responsive genes in Foc, namely FocmedA(a), FocmedA(b), abaA-L, FocflbA, FocflbB, FocflbC, FocflbD, FocstuA, FocveA, FocvelB, wetA-L, FocfluG and Foclae1. We demonstrated that FocmedA(a), abaA-L, wetA-L, FocflbA, FocflbD, FocstuA, FocveA and Foclae1 mediate conidiophore formation, whereas FocmedA(a) and abaA-L are important for phialide formation and conidiophore formation. The expression level of abaA-L was significantly decreased in the ΔFocmedA(a) mutant, and yeast one-hybrid and ChIP-qPCR analyses further confirmed that FocMedA(a) could bind to the promoter of abaA-L during micro- and macroconidiation. Moreover, the transcript abundance of the wetA-L gene was significantly reduced in the ΔabaA-L mutant, and it not only was found to function as an activator of micro- and macroconidium formation but also served as a repressor of chlamydospore production. In addition, the deletions of FocflbB, FocflbC, FocstuA and Foclae1 resulted in increased chlamydosporulation, whereas FocflbD and FocvelB gene deletions reduced chlamydosporulation. Furthermore, FocflbC, FocflbD, Foclae1 and FocmedA(a) were found to be important regulators for pathogenicity and fusaric acid synthesis in Foc. The present study therefore advances our understanding of the regulation pathways of the asexual development and functional interdependence of sporulation-responsive genes in Foc.

One-Step Synthesis of Peptide-Gold Nanoclusters with Tunable Fluorescence and Enhanced Gene Delivery Efficiency.

In this study, peptide-gold nanoclusters with tunable fluorescence were prepared by a simple "one-pot" method, which were used for gene localization and delivery in vivo to achieve efficient intracellular colocalization, uptake, and transfection. The efficiency of pDNA transfection was up to 70.6%, and there was no obvious cytotoxicity. This study proves that the simple-composition and bio-friendly peptide-gold nanoclusters are promising gene delivery carriers and can provide a powerful theoretical and experimental basis for the application of peptide-metal nanocomplexes in gene delivery and other biomedicine fields.

ERRγ, a Novel Biomarker, Associates with Pathoglycemia of Endometrial Cancer to Predict Myometrial Invasion.

We aim to investigate the correlation between the expression of estrogen-related receptor γ (ERRγ) and endometrial cancer (EC) progression and to evaluate the potential of ERRγ as a new biomarker for EC diagnosis. We analyzed the ERRγ expression profile and the correlation with the corresponding clinical characteristics of EC samples from The Cancer Genome Atlas (TCGA), the Clinical Proteomic Tumor Analysis Consortium (CPTAC) databases, and the International Cancer Genome Consortium (ICGC) databases. Immunohistochemical (IHC) analysis was conducted on tissue samples, and enzyme linked immunosorbent assay (ELISA) was used in serum samples to detect the levels of ERRγ. The diagnostic performance of ERRγ proteins was assessed using the receiver operating characteristic (ROC). ERRγ showed notably higher expression in EC tissues than in normal endometrium tissues (P < 0.001), which was consistent with the result of TCGA. Overexpression of ERRγ was significantly associated with deep myometrial invasion of EC (P=0.004), and fasting blood glucose (FBG) was higher in EC patients with deep myometrial invasion than in those with superficial myometrial invasion (P=0.040). Further analysis using ELISA showed that the serum ERRγ level was positively correlated with FBG (R = 0.355, P < 0.001). ERRγ is overexpressed in EC and may be involved in regulating glucose metabolism and promoting myometrial invasion of EC. In addition, the area under the ROC curve (AUC) for ERRγ was 0.834, in distinguishing EC patients from healthy individuals, presented 84.0% and 80.0% sensitivity and specificity, respectively, and serum ERRγ has a good diagnostic performance in distinguishing EC patients from healthy people and may be a promising noninvasive biomarker in EC.

Self-assembly of peptide nanofibers with chirality-encoded antimicrobial activity.

The nanostructured antimicrobial agents, self-assembled by the antimicrobial peptides (AMPs), represent an intriguing platform for the treatment of pathogens. Although the structural characteristics significantly influence antimicrobial functionality, the role of chirality is usually ignored and still unclear. Herein, two homochiral AMPs (all L- or all D-amino acids), including C16-LV4LR4 (LL) and C16-DV4DR4 (DD), and a heterochiral AMP with alternating D-/L-amino acids, C16-DV4LR4 (DL), were self-assembled into left-handed, right-handed, and right-handed helical nanofibers, respectively. The valine configuration determined the supramolecular chirality of the nanofibers. However, the DL molecules exhibited a highly aggregated propensity to form more stable helical nanofibers with a lower degree of twist and a larger helical pitch. This characteristic resulted in the optimal antimicrobial activity of the DL nanofibers against both Gram-negative and Gram-positive bacteria. Furthermore, the membrane permeability assay confirmed the higher activity for damaging the cell membrane by the DL nanofibers. These results demonstrated the significance of molecular chirality in directing the self-assembly of the amphiphilic peptides, eventually affecting their antimicrobial activity. This study opens up the possibility to fabricate promising nanostructured antimicrobial materials by controlling the chirality and structure of the materials.

ERRα inhibitor acts as a potential agonist of PPARγ to induce cell apoptosis and inhibit cell proliferation in endometrial cancer.

Two transcriptional factors, peroxisome proliferator-activated receptor-γ (PPARγ) and estrogen-related receptor-α (ERRα), have been reported to be key regulators of cellular energy metabolism. However, the relationship between ERRα and PPARγ in the development of endometrial cancer (EC) is still unclear. The expression levels of PPARγ and ERRα in EC were evaluated by quantitative real-time PCR, western blot, tissue array and immunohistochemistry. A significant negative correlation was identified between PPARγ and ERRα expression in women with EC (ρ=-0.509, P<0.001). Bioinformatics analyses showed that PPARγ and ERRα can activate or inhibit the same genes involved in cell proliferation and apoptosis through a similar ModFit. ERRα activation or PPARγ inhibition could promote proliferation and inhibit apoptosis through the Bcl-2/Caspase3 pathways. Both PPARγ and ERRα can serve as serum tumor markers. Surprisingly, as evaluated by receiver operating characteristic (ROC) curves and a logistic model, a PPARγ/ERRα ratio≤1.86 (area under the ROC curve (AUC)=0.915, Youden index=0.6633, P<0.001) was an independent risk factor for endometrial carcinogenesis (OR=14.847, 95% CI= 1.6-137.748, P=0.018). EC patients with PPARγ(-)/ERRα(+) had the worst overall survival and disease-free survival rates (both P<0.001). Thus, a dynamic imbalance between PPARγ and ERRα leads to endometrial carcinogenesis and predicts the EC prognosis.

Green fluorescent protein inspired fluorophores.

Green fluorescence proteins (GFP) are appealing to a variety of biomedical and biotechnology applications, such as protein fusion, subcellular localizations, cell visualization, protein-protein interaction, and genetically encoded sensors. To mimic the fluorescence of GFP, various compounds, such as GFP chromophores analogs, hydrogen bond-rich proteins, and aromatic peptidyl nanostructures that preclude free rotation of the aryl-alkene bond, have been developed to adapt them for a fantastic range of applications. Herein, we firstly summarize the structure and luminescent mechanism of GFP. Based on this, the design strategy, fluorescent properties, and the advanced applications of GFP-inspired fluorophores are then carefully discussed. The diverse advantages of bioinspired fluorophores, such as biocompatibility, structural simplicity, and capacity to form a variety of functional nanostructures, endow them potential candidates as the next-generation bio-organic optical materials.

PGC-1α and ERRα in patients with endometrial cancer: a translational study for predicting myometrial invasion.

BACKGROUND: PGC-1α and ERRα are closely related to tumor formation and progression. However, the mechanism underlying the involvement of PGC-1α/ERRα in regulating invasion and migration in endometrial cancer remains to be explored. RESULTS: Elevated levels of PGC-1α and ERRα were associated with advanced myometrial invasion, and PGC-1α and Vimentin expression was related to the depth of myometrial invasion in premenopausal endometrial cancer. Silencing of PGC-1α reduced ERRα activation and inhibited epithelial-mesenchymal-transition phenotypes, resulting in significant inhibition of invasion and migration. Overexpression of ERRα led to enhanced PGC-1α expression and increased activity of TFEB, promoting epithelial-mesenchymal-transition in endometrial cancer cells. CONCLUSIONS: PGC-1α and ERRα induce the epithelial-mesenchymal-transition therefore invasion and migration in endometrial cancer, and may be novel biomarkers to predict the risk of advanced myometrial invasion. METHODS: PGC-1α, ERRα, and vimentin expression was analyzed in tissue microarrays using immunohistochemistry. PGC-1α and ERRα expression in endometrial cancer cell lines was investigated using quantitative PCR and western blotting analyses after infection with lentivirus-mediated small interfering RNA (siRNA) targeting PGC-1α (siRNA-PGC-1α) or overexpressing ERRα. E-cadherin and vimentin levels were determined using western blotting and cell immunouorescence analyses. Cell migration and invasiveness were evaluated using scratch and trans-well chamber assays.

Bioinspired Fluorescent Peptidyl Nanoparticles with Rainbow Colors.

The growing enthusiasm to mimic the luminous properties of fluorescent proteins (FPs) has expanded to include the potential biomedical applications of FP analogues. We developed a series of non-fluorescent oligopeptides (Fc-(X)n; where X = F, Y, W, and H; n = 1-3) that can aggregate into fluorescent nanoparticles with rainbow colors, termed the peptidyl rainbow kit (PRK). The PRK encompasses the full visible color spectrum, and its photoluminescent properties may have originated from aggregation-induced emission (AIE). Intermolecular forces restricted the intramolecular motions of the oligopeptide residues, providing a barrier to non-radiative conformational relaxation pathways and leading to AIE fluorescence. The PRK oligopeptides are pH sensitive, biocompatible, and photostable under physiological conditions, making the PRK a promising fluorescence candidate for biomedical applications.

Genome-wide DNA copy number profiling and bioinformatics analysis of ovarian cancer reveals key genes and pathways associated with distinct invasive/migratory capabilities.

Ovarian cancer (OC) metastasis presents major hurdles that must be overcome to improve patient outcomes. Recent studies have demonstrated copy number variations (CNVs) frequently contribute to alterations in oncogenic drivers. The present study used a CytoScan HD Array to analyse CNVs and loss of heterozygosity (LOH) in the entire genomes of 6 OC patients and human OC cell lines to determine the genetic target events leading to the distinct invasive/migratory capacities of OC. The results showed that LOH at Xq11.1 and Xp21.1 and gains at 8q21.13 were novel, specific CNVs. Ovarian cancer-related CNVs were then screened by bioinformatics analysis. In addition, transcription factors-target gene interactions were predicted with information from PASTAA analysis. As a result, six genes (i.e., GAB2, AKT1, EGFR, COL6A3, UGT1A1 and UGT1A8) were identified as strong candidates by integrating the above data with gene expression and clinical outcome data. In the transcriptional regulatory network, 4 known cancer-related transcription factors (TFs) interacted with 6 CNV-driven genes. The protein/DNA arrays revealed 3 of these 4 TFs as potential candidate gene-related transcription factors in OC. We then demonstrated that these six genes can serve as potential biomarkers for OC. Further studies are required to elucidate the pathogenesis of OC.

Epidemiology of electrical burns: a 10-year retrospective analysis of 376 cases at a burn centre in South China.

OBJECTIVE: To investigate the epidemiological profile and associated outcomes of electrical injuries at a major burn centre in southern China. METHODS: This retrospective study enrolled consecutive electrical burn patients admitted to the burn centre of the First Affiliated Hospital of Guangxi Medical University between 2008 and 2017. Demographic and clinical data and outcomes were recorded. Mann-Whitney U tests/Pearson's chi-squared tests were used to examine the differences between low-voltage and high-voltage injuries. RESULTS: There were 217 high-voltage injuries and 159 low-voltage injuries. High-voltage burns were frequently observed between March and August, and low-voltage burns peaked between June and September. Burn patients were mainly men. Most burns occurred in participants aged 21 to 50 years and in industrial workers and electricians at work or householders at home. Only one person with high-voltage burns died (a mortality rate of 0.46%). Amputation rates were 37.33% for high-voltage burns and 22.01% for low-voltage burns. High-voltage injuries were associated with more extensive burns, longer hospital stays, and more complications and amputations. CONCLUSIONS: More attention should be paid to prevention of electrical burns in male adults. Particular focus is needed on industrial workers, incidents in the spring and summer, and high-voltage injuries.

Dual targeting of estrogen receptor α and estrogen-related receptor α: a novel endocrine therapy for endometrial cancer.

BACKGROUND: Endometrial cancer (EC) is a hormone dependent carcinoma that may involve complex molecular mechanisms. Endocrine therapy by blocking the estrogen and estrogen receptor α (ERα) has been effective in breast cancer, while it is still controversial in EC. Recently, estrogen-related receptor α (ERRα) was proven to be another endocrine therapy target. METHODS: The anti-tumor effect of selective estrogen receptor modulators (SERMs) and XCT790 (XCT) used alone or in combination were evaluated in both of ERα-positive (ERα+) and ERα-negative (ERα-) EC cells. ERα and ERRα mRNA were tested by qPCR, while the protein was detected by Western blot. The proliferation was tested by MTS and cell cycle, apoptosis rate were analyzed by flow cytometry. RESULTS: A relatively high dose (10 µM) of tamoxifen (TAM) suppressed the expression of ERα and ERRα in two types of EC cells. However, 10 µM raloxifene (RAL) exhibited no effect on ERα and ERRα, while 10 µM XCT down regulated ERRα specifically, but not ERα in all EC cells. When dual targeting on ERα and ERRα by combining TAM with XCT, the proliferation inhibitory effect and apoptosis reached the strongest in all EC cells (P<0.05). Moreover, the inhibitory effect of proliferation was attributed significantly to the G0/G1 arrest (P<0.05). Interestingly, the apoptosis induced by combining TAM with XCT were obviously higher in ERα+ EC cells than ERα- EC cells (P<0.05). CONCLUSION: Taken together, the results indicate that dual targeting on ERα and ERRα represents a better anti-tumor effect, which provides a novel endocrine based therapy strategy for EC.

Clinical analysis of neoadjuvant chemotherapy in patients with advanced vulvar cancer: A STROBE-compliant article.

To investigate the effect of neoadjuvant chemotherapy in patients with advanced vulvar cancer and to provide references for clinical treatment.Clinical and pathological data of 12 patients with advanced vulvar carcinoma were collected. The response and operability rates, adverse effects, and prognosis of neoadjuvant chemotherapy were retrospectively analyzed.The mean patient age was 45.8 (range 26-69) years. Among 12 patients, 9 underwent treatment with bleomycin and cisplatin with or without vincristine. The overall response rate was 67%. Five patients (56%) experienced grade 1 or 2 bone marrow suppression or gastrointestinal reactions. Seven patients (78%) underwent radical surgery. The mean overall survival time was 34.1 (range 3-69) months, the mean progression free survival time was 26 (range 3-69) months, and the 1-year survival rate was 83%. The other 3 patients received combined paclitaxel and cisplatin treatment. The overall response rate was 67%. All 3 patients (100%) experienced grade 2 hair loss or anemia and 2 of them (67%) underwent radical vulvectomy. The mean overall survival time was 11.7 (range 5-15) months, the mean progression free survival time was 7.7 (range 3-15) months and the 1-year survival rate was 100%. Time to overall survival and progression free survival were not significantly different between the 2 groups (P = .46 and P = .39).Owing to their high overall response rate and tolerable adverse effects, either bleomycin-cisplatin-based or paclitaxel-based neoadjuvant chemotherapy regimen can be considered a therapeutic option for advanced vulvar cancer.

Novel endocrine therapeutic strategy in endometrial carcinoma targeting estrogen-related receptor α by XCT790 and siRNA.

PURPOSE: To explore the targeted therapy of estrogen-related receptor α (ERRα) in endometrial cancer (EC) cells and its potential mechanisms. METHODS: The mRNA and protein expression levels of ERRα and estrogen receptor α (ERα) were detected by qPCR and Western blotting in RL-952, AN3-CA, HEC-1A, and HEC-1B EC cell lines. After treatment with the ERRα-specific antagonist XCT790 or infection with lentivirus-mediated small interfering RNA (siRNA) targeting the ERRα (siRNA-ERRα), cell proliferation and apoptosis were evaluated by MTS assay and flow cytometry. After treatment with siRNA-ERRα, the expression profiles of transcription factors (TFs) were analyzed by protein/DNA arrays in EC cells. RESULTS: The relative mRNA levels of ERRa in RL-952 (1±0.0831) and AN3-CA (1.162±0.0325) were significantly higher than those in HEC-1A (0.3081±0.0339) and HEC-1B (0.1119±0.0091) (P<0.05), and similar results were observed for ERRα protein levels. A higher ratio of ERa/ERRa was observed in ERα-positive RL-952 (10-fold) and ANC-3A (8.5-fold) cells, whereas a lower ratio was observed in ERα-negative HEC-1A (3.75-fold) and HEC-1B cells (0-fold). Both - exogenous XCT790 and endogenous siRNA-ERRα - can decrease the expression of ERRα, thereby inhibiting proliferation but promoting apoptosis in both ERα-positive and -negative EC cells. The XCT790 presented higher proliferation-inhibition and apoptosis rates in the ERα-positive than ERα-negative cells, whereas the siRNA-ERRα exhibited higher proliferation-inhibition and apoptosis rates in the ERα-negative than in ERα-positive cells. In total, 3 upregulated and 17 downregulated TFs were screened out by knocked-down expression of ERRα in all EC cells. Among them, the upregulated TFs organic cation transporter 3/4(Oct3/4), hepatic nuclear factor 4 (HNF4), HNF4 and chicken ovalbumin upstream TF (COUP-TF) as well as downregulated transcription factor EB (TFEB) were found to be statistically significant (P<0.05). CONCLUSION: Targeting ERRα provides a promising novel endocrine therapeutic strategy.

Safety, pharmacokinetics, and antiviral activity of the cyclophilin inhibitor NIM811 alone or in combination with pegylated interferon in HCV-infected patients receiving 14 days of therapy.

BACKGROUND: Cyclophilin inhibitors have shown activity against a variety of viruses, including HCV. NIM811, a novel, non-immunosuppressive cyclophilin inhibitor was studied in ascending doses in a randomized, double-blind, placebo-controlled 14-day trial in genotype 1 HCV patients. Doses of 10 up to 600 mg were given orally once or twice daily as monotherapy (9:3 randomization of NIM811:placebo). 600 mg or placebo bid for 14 days was then co-administered with pegylated interferon alpha (PEG-IFN-α) administered on days 1 and 8 to genotype 1 relapsers. RESULTS: NIM811 was well tolerated at all doses. Although lack of antiviral effect was noted in the monotherapy arms, liver transaminase normalization occurred at doses over 75 mg. Mild, clinically non-significant elevations of bilirubin, and significant declines in platelet numbers were observed in the 400 and 600 mg bid groups. In the combination group, the mean HCV RNA decline was 2.85 log, compared to a 0.56 log in the PEG-IFN alone arm. The mean ALT (alanine transaminase) declined significantly by day 14 in the combination, but was unchanged in the PEG-IFN alone group. In the combination therapy group, the mean platelets were 203×10(9)/L at baseline and fell to 105×10(9)/L by day 14; for patients treated with PEG-IFN the values were 177×10(9)/L and 139×10(9)/L. There was a significant increase in bilirubin, although this did not reach clinically concerning levels. There were no severe or serious adverse events. The pharmacokinetics in both monotherapy and combination arms were dose linear and not affected by PEG-INF. CONCLUSION: NIM811 monotherapy resulted in a normalization of liver transaminases in the absence of significant virological response. The combination of NIM811 and pegylated interferon alpha showed significant antiviral activity compared to interferon alone in genotype 1 HCV relapsers. The use of oral cyclophilin inhibitors as part of a combination regime for treatment of hepatitis C, especially to deter resistance, holds promise.

Prevalence of antibody to hepatitis E virus among haemodialysis patients in Taiwan: possible infection by blood transfusion.

BACKGROUND/AIMS: A higher prevalence of anti-hepatitis E virus (HEV) in non-endemic viral hepatitis such as in Germany has been reported in our previous study. The aim of this study was to assess the seroepidemiology of HEV among haemodialysis (HD) patients in Shin-Kong Hospital, Taiwan, and to evaluate whether there was an increased risk of infection and exposure to HEV even in an area of endemic viral hepatitis. METHODS: Serum samples obtained from 400 Taiwanese patients on chronic HD (group 1), 400 sex- and age-matched healthy subjects (group 2) and hospital patients (group 3) were tested for the IgG anti-HEV. RESULTS: The prevalence of anti-HEV among the HD patients and the healthy controls were 31 and 8.9%, respectively. The difference (22%) was statistically significant (p < 0.01). In comparison, the anti-HEV in hospital patients was 16%. CONCLUSION: The study indicated a significantly higher risk of HEV infection among patients on chronic HD in endemic regions of viral hepatitis such as Taiwan. Mostly because of anaemia, HD patients usually received packed transfusion (red blood cells) if their haemoglobin was low. It is possible that HEV infection may be transmitted through blood transfusions in an endemic area. In such areas, appropriate strategies should be adopted to prevent the risk of HEV among HD patients.