Objective: To analyze the changing trend of liver cancer disease burden and its age, period and cohort effects in China from 1990 to 2023, so as to provide a basis for improving liver cancer prevention and treatment strategies. Methods: Data on incidence, mortality, disability-adjusted life years (DALY), standardized incidence, standardized mortality, and standardized DALY rate of liver cancer in China from 1990 to 2023 were collected from the Global Burden of Disease (GBD) 2023 database. The trends in standardized incidence, standardized mortality, and standardized DALY rate of liver cancer were analyzed using the average annual percent change (AAPC). The effects of age, period, and birth cohort on the incidence, mortality, and DALY rate were evaluated using the age-period-cohort model. Results: Standardized incidence, standardized mortality, and standardized DALY rate of liver cancer in China from 1990 to 2023 showed downward trends (AAPC=-1.009%, -1.275%, and -1.399%, all P<0.05). The age-period-cohort model showed that liver cancer incidence, mortality, and DALY rates increased and then decreased with age, and peaked in the groups aged 75-<80 years, 90-<95 years, and 65-<70 years, at 44.86/105, 50.88/105, and 908.28/105, respectively. Using the period 2000-2004 as the reference group, the risks of liver cancer incidence and mortality increased over time. Incidence risk was highest in 2020-2023 (RR=1.089, 95%CI: 1.078-1.099), and mortality risk was highest in 2015-2019 (RR=1.082, 95%CI: 1.075-1.089). Disability risk decreased over time, with the highest risk in 1995-1999 (RR=1.046, 95%CI: 1.044-1.049). Using the 1960-1964 birth cohort as the reference, incidence, mortality, and disability risks decreased with later birth cohorts. The 1920-1924 birth cohort had the highest incidence risk (RR=2.059, 95%CI: 1.988-2.132), mortality risk (RR=2.252, 95%CI: 2.191-2.315), and disability risk (RR=1.646, 95%CI: 1.625-1.668). Conclusions The overall burden of liver cancer in China showed a downward trend from 1990 to 2023, but the burden remained high among the elderly. The risks of incidence and mortality increased over time, while the risk of disability decreased. The risks of incidence, mortality, and disability all decreased with later birth years.

【Objective】 To analyze the polymorphism of erythrocyte membrane blood group glycoprotein A (GPA) related gene GYPA in high and low endemic population for clonidia sinensis infection, aimed at investigating the correlation between erythrocyte transmembrane glycoproteins and clonorchis sinensis infection. 【Methods】 From Dec 2019 to Jun 2020, anticoagulant blood samples were randomly collected in WuMing district (n=700) and GuiGang district (n=500 ) of Nanning city, and the IgG antibody to clonorchis sinensis in plasma was detected, and the DNA of leukocyte was extracted. The full-length exon and partial intron of GYPA gene were sequenced, mutations were characterized by gene cloning, and the risk of infection was calculated by chi-square test. 【Results】 The yield rate of IgG antibody was 62.7% (439/700) in WuMing district and 3.4% (17/500) in GuiGang district(P<0.05). The insertion of base C at the 54th position of intron-2 in GYPA gene caused the reading frame shift. The mutation was presented in 23.9% (105/439) and 17.6% (3/17) of the population with clonorchis sinensis exposure in WuMing and GuiGang area, respectively, while 49.4% (129/261) and 54.7% (264/483) in the negative population, respectively (P<0.05). 【Conclusion】 The infection rate of clonorchis sinensis in WuMing district was higher than that in GuiGang district. The mutation rate of reading frame shift caused by the insertion of base C at the 54th position of GYPA intron-2 was much lower in the positive population of clonorchis sinensis infection than the negative population, suggesting that the mutation is a protective gene in the negative population of clonorchis sinensis infection. It is necessary to study the mechanism of clonorchis sinensis infection and the mutation point of this gene in order to facilitate the early diagnosis of disease, blood transfusion management, treatment and prevention.

Objective To study the molecular genetic background of Bel subtype at ABO blood group.Methods Three samples and fifteen samples were diagnosed as Bel subgroup and normal control samples by serological test,respectively.The extracted DNA was genotyped by sequence specific primer- polymerase chain reaction foilowed by sequencing for Exon6 and exon7 at ABO locus and clones were sequenced.Results A novel Bel variant allele(GenBank EF117687) was identified in a Bel individual.The Bel allele was different from the regular B101 allele by single 952G>A missense mutation in exon7.resulting in an amino acid subsfitution of Val for Met at 318 locus.No mutations were detected in the fifteen control samples and the other two Bel allele samples.Conclusions The mutation position was fimt found to lie on coding region of ABO gene behind nucleotide 930.The mutation of G952A in the al,3 galactosyhransferase gene may be one of the molecular genetic basis of Bel ohenotype.

Objective To identify novel ABO allele in Chinese population. Methods The ABO blood group was tested by serological method, and then genotyped by sequence-specific primer (PCR-SSP) , gene cloning and sequence analysis. Results A healthy blood dornor who was diagnosed as having A2 subgroup and A2O1genotype was subjected to ABO gene cloning and sequence analysis. The haplotype-specific sequence analysis indicate that two single-base deletions, where G-deletion at nucleotide position 261 and A-deletion at nucleotide position 496 were determined in the O1 allele. The nucleotide sequence of the novelO1 allele were identical to ABO 0101 allele except for A-deletion at nucleotide position 496 in exon7 of ABO locus. Conclusion We defined this 0 allele as a novel O1 variant allele, and its registered number by GenBank is AY374123.

Objective To study the mutation of FUT1 and FUT2 genes in para-Bombay individual.Methods Direct DNA sequencing of FUT1 and FUT2 gene coding region were analyzed in two individuals with para-Bombay phenotype.Results One individual lost one of the three AG repeats located at nucleotides 547~552 of the FUT1 gene, whereas two of the three T repeats located at nucleotides 880~882 were deleted in the other.Conclusion Two frame-shift mutations of FUT1 gene are responsible for the H antigen deficiency