HBV/HCV dual infection is not uncommon, especially in highly endemic areas and among individuals at elevated risk of infection, because of the common transmission mode of hepatitis B virus (HBV) and hepatitis C virus (HCV) and may be underestimated due to the presence of occult HBV infection. HBV/HCV dual infection is associated with more rapid progression to advanced severe liver disease, severely increased fibrosis or cirrhosis, liver decompensation, and the development of hepatocellular carcinoma, thus requiring effective antiviral treatment. However, the intracellular interaction between HBV and HCV has not been fully elucidated at present. This paper summarizes the recent research on HBV/HCV dual infection and the current status of treatment and emphasizes the aspects that need further clarification in order to provide a basis for exploring treatment strategies for dual infection.

HBV/HCV dual infection is not uncommon, especially in highly endemic areas and among individuals at elevated risk of infection, because of the common transmission mode of hepatitis B virus (HBV) and hepatitis C virus (HCV) and may be underestimated due to the presence of occult HBV infection. HBV/HCV dual infection is associated with more rapid progression to advanced severe liver disease, severely increased fibrosis or cirrhosis, liver decompensation, and the development of hepatocellular carcinoma, thus requiring effective antiviral treatment. However, the intracellular interaction between HBV and HCV has not been fully elucidated at present. This paper summarizes the recent research on HBV/HCV dual infection and the current status of treatment and emphasizes the aspects that need further clarification in order to provide a basis for exploring treatment strategies for dual infection.

INTRODUCTION: Fragile X syndrome (FXS) is the most prevalent X-linked intellectual disability (ID) and a leading genetic cause of autism, characterised by cognitive and behavioural impairments. The hyperexpansion of a CGG repeat in the fragile X mental retardation 1 (FMR1) gene leads to abnormal hypermethylation, resulting in the lack or absence of its protein. Tools for establishing the diagnosis of FXS have been extensively developed, including assays based on triplet-primed polymerase chain reaction (TP-PCR) for detection and quantification of the CGG trinucleotide repeat expansion, as well as determination of the methylation status of the alleles. This study aimed to utilise a simple, quick and affordable method for high sensitivity and specificity screening and diagnosis of FXS in institutionalised individuals with ID. METHODS: A total of 109 institutionalised individuals at the Center for Social Rehabilitation of Intellectual Disability Kartini, Temanggung, Central Java, Indonesia, were screened in a three-step process using FastFrax™ Identification, Sizing and Methylation Status Kits. RESULTS: Two samples that were classified as indeterminate with respect to the 41-repeat control at the identification step were subsequently determined to be non-expanded by both sizing and methylation status analyses. Two samples classified as expanded at the identification step were determined to carry full mutation expansions > 200 repeats that were fully methylated using sizing and methylation status analyses, respectively, yielding a disease prevalence of 1.83%. CONCLUSION Repeat expansion and methylation-specific TP-PCR is practical, effective and inexpensive for the diagnosis of FXS, especially in high-risk populations of individuals with ID of undetermined aetiology.

[ ABSTRACT] AIM:To study the effects of nuclear factor kappa B ( NF-κB) on human hepcidin expression in fer-ric ammonium citrate ( FAC)-induced HH4 hepatocytes.METHODS:Non-transformed HH4 cells were exposed to FAC at concentrations of 0.1, 1, 5 and 10 mmol/L for 48 h.The expression of iron regulatory gene hepcidin was determined by semi-quantitative RT-PCR.The effects of NF-κB on hepcidin transcriptional activity were detected using chromatin immuno-precipitation (ChIP), electrophoretic mobility shift assay (EMSA) and dual-luciferase reporter assay system, combined with the inhibition experiments of intracellular NF-κB activity.RESULTS: FAC at concentrations of 5 mmol/L and 10 mmol/L significantly enhanced the expression of hepcidin.The results of ChIP and EMSA showed the binding of NF-κB to the upstream of hepcidin promoter.Treatment with NF-κB inhibitor BAY 11-7082 attenuated hepcidin expression.The lucif-erase activity in the cells transfected with recombinant luciferase reporter plasmid was obviously higher than that in control group.CONCLUSION:NF-κB is the transcription factor that contributes to hepcidin expression in iron overload-induced HH4 cells.

Objective To assess the diagnostic value of 99Tcm-ECD SPECT for hyperacute cerebral ischemia using rats models.Methods A stable and permanent acute cerebral ischemia model using unilateral middle cerebral occlusion was tested in 24 healthy SD rats.The rats were randomly divided into 6 groups according to the time duration between imaging and induced-ischemia (1,2,3,4,5 and 6 h,respectively).The rats were sacrificed immediately after 99Tcm-ECD SPECT/CT imaging and then the brain tissue was dissected for triphenyl tetrazolium chloride (TTC) and HE staining.The count ratio of affected cortex to the contralateral cortex of ＜ 50％ was defined as ischemia on micro SPECT/CT.The volume of the ischemic area was calculated on both SPECT/CT and TTC images.Paired t test was used to determine the statistical difference between the volumes on SPECT/CT and TTC staining.Results The ischemia volume evaluated by TTC staining at 1,2,3,4,5 and 6 h after occlusion was (73.98 ± 27.76),(90.75 ±29.00),(135.00±40.83),(136.25±22.51),(158.50±32.72) and (168.00±32.75) mm3,respectively.The corresponding ischemia volume evaluated by micro SPECT/CT was (98.50 ± 27.77),(110.40±26.80),(157.00±36.82),(165.50±26.54),(175.75±31.16) and (177.25 ±34.33) mm3,respectively,which was concordant with that by TTC staining at each time point (t:-1.681 to-0.390,all P ＞0.05).The ischemic area on micro SPECT/CT imaging was consistent with the pink area by TTC staining.The volume evaluated by micro SPECT/CT tended to be constant 3 h after the occlusion.The ischemia volume showed no significant difference among 3,4,5 and 6 h (all P ＞ 0.05).Conclusions Micro SPECT/CT may have an haemodynamic value for evaluating in vivo cerebral ischemia applied in a rat model.It might have clinical value for the evaluation and decision-making of ultra acute cerebral infarctions.