[Analysis on the trend of liver cancer morbidity and mortality in certain district, Suzhou City, Jiangsu Province, 2017 to 2019].

Objective: To analyze the trend of liver cancer morbidity and mortality among residents with household registration in certain District, 2017 to 2019. Methods: The crude morbidity and mortality rate of males and females in the whole population were calculated by using the relevant data from the certain District Cancer Registry and Report System and the Cause of Death Surveillance System. The standardized morbidity and mortality rate were calculated according to the age structure of 2000 National Demographic Census and Segi's world population, respectively. Trend in liver cancer morbidity and mortality were evaluated using percent change (PC), annual percentage change, and case-number-weighted annual percent change. Age-specific rates were used to analyze the epidemic trend of liver cancer with age. Results: The crude morbidity rate of liver cancer in the whole population (male and female) of the certain district from 2017 to 2019 were 18.86/100 000, 26.05/100 000 and 11.90/100 000 respectively, and the crude mortality rates were 21.20/100 000, 29.29/100 000 and 13.38/100 000 respectively. The crude morbidity and mortality rate of liver cancer among male showed a downward trend (PC=-16.77% and -20.15% respectively). The crude morbidity and mortality rate of liver cancer among female showed inconsistent changes; however, the crude morbidity rate showed a downward trend, and the crude mortality rate first increased and then decreased (PC=-19.42% and -0.30% respectively). Liver cancer morbidity and mortality rate in male after the age of 30 were increased with age. The two key points of accelerated growth were around the age of 65 and 75, and the peak of morbidity (130.78/100 000) and mortality (201.96/100 000) were after the age of 80. The morbidity and mortality rate were significantly lower in female than those of male aged 60; however, after the age of 65, the morbidity rate was increased rapidly and gradually approached as that of male. After the age of 80 (the peak morbidity and mortality were 104.40/100,000 and 132.87/100,000, respectively), male were about twice as high as those female aged between 75 and 79. Conclusion: Morbidity and mortality rate of liver cancer in the certain District showed an overall downward trend from 2017 to 2019, but it increased with age, and the disease burden was relatively high among the elderly population. Liver cancer mostly occurred in male, so the prevention and control of liver cancer epidemics in middle-aged and elderly should be actively monitored.

[Phosphonate inhibits steatosis and lobular inflammation of non-alcoholic steatohepatitis through depleting macrophages].

Objective: To explore the role of macrophages in non-alcoholic steatohepatitis (NASH) in order to provide directions for the therapeutic target of metabolic liver disease. Methods: Twenty C57BL/6 wild-type male mice at 6-8 weeks were randomly divided into two groups: 5 in the control group, methionine-and choline-deficient diet (MCD); 15 in the experimental group, MCD diet + intraperitoneal injection of disodium chlorophosphonate liposomes (to clear macrophages). Mice were fed for 4 weeks to establish NASH model. Blood, liver and spleen were collected to analyze the body mass index, liver index, spleen index, and serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Non-alcoholic steatosis (NAS) activity score was evaluated by HE and Oil Red O staining. The relative expression level of F4/80 mRNA was compared by RT-PCR. Data comparison between groups was analyzed by t-test. Results: NASH model was successfully established by feeding the mice with MCD for four week. The expression of F4/80 mRNA (t = 4.167, P < 0.01), hepatic steatosis (t = 10.70, P < 0.05), interlobular inflammatory infiltration (t = 3.08, P < 0.05), and NAS score were decreased (t = 8.06, P < 0.05) in the experimental group. At the same time, ALT level [(817.00 ± 128.90) U/L vs. (231.20 ± 36.28) U/L, t = 5.71, P < 0.01], AST level [(1 211.00 ± 248.90) U/L vs. (505.30 ± 88.20) U/L, t = 3.32, P < 0.01] was decreased significantly. However, the spleen volume and spleen index of the experimental group were larger (0.24 ± 0.01 and 0.32 ± 0.02, t = 2.41, P < 0.05), and there was no significant effect on liver ballooning, body mass index and liver index. Conclusion: In NASH, phosphonate can consume macrophages to inhibit liver inflammation and protect the damaged liver.

[Study of tumor necrosis factor receptor superfamily 1B gene polymorphism in relation to the outcomes of HCV infection].

Objective: To investigate the tumor necrosis factor receptor superfamily 1B gene (TNFRSF1B) polymorphism in relation to the outcomes of hepatitis C virus (HCV) infection. Methods: One thousand six hundred and forty-five cases without HCV infection, 545 cases with HCV clearance, and 783 cases with chronic HCV infection were enrolled. TaqMan probe method was used to investigate genotype rs1061622 (T > G) and rs1061624 (G > A). Two single nucleotide polymorphisms (SNPs) sites were genotyped and haplotypes were constructed to evaluate their relation with the outcome of HCV infection. Results: Logistic regression analysis showed that there was no relation to the two SNPs with HCV infection susceptibility and chronicity (P > 0.05). Haplotype analysis showed that carrier TA had an increased susceptibility to HCV infection [adjusted odds ratio (OR) = 1.15, 95% confidence interval (CI): 1.01 to 1.30, P = 0.038)]. Carrier TA and GG haplotypes were conducive to chronic HCV infection (adjusted OR = 1.28, 95% CI: 1.08 to 1.53, P = 0.006; OR = 1.31, 95% CI: 1.03 to 1.66, P = 0.026). Conclusion: The combinational effects of rs1061622 and rs1061624 in TNFRSF1B gene may increase the risk of HCV chronicity and infection.

[Association between TNFRSF11A and TNFRSF11B gene polymorphisms and the outcome of hepatitis C virus infection].

Objective: To explore the relationship between the tumor necrosis factor receptor superfamily members 11A (TNFRSF11A) and 11B (TNFRSF11B) gene polymorphisms and the outcome of hepatitis C virus (HCV) infection. Methods: In this case-control study, 749 cases of persistent HCV infection, 494 cases of spontaneous clearance and 1 486 control subjects were included from 2008 to 2016. TaqMan-MGB probe method was used to detect the genotype of TNFRSF11A rs1805034 and TNFRSF11B rs2073617. The genotypes distribution of the two single nucleotide polymorphisms (SNP) were analyzed in different populations. Results: Co-dominant model showed that individuals carrying the rs2073617 CC genotype were prone to have chronic HCV infection, compared with individuals carrying the rs2073617 TT genotype (OR=1.517, 95%CI: 1.055-2.181, P=0.024). Recessive model results showed that individuals carrying rs2073617 CC genotype were more likely to develop chronic HCV infection compared with individuals carrying rs2073617 TT or TC genotype (OR=1.435, 95%CI: 1.033-1.996, P=0.032). Additive model showed that the risk for chronic HCV infection increased with the increase of the number of rs2073617 C alleles (OR=1.204, 95%CI: 1.013-1.431, P=0.035). Conclusion: The genetic polymorphism of TNFRSF11B rs2073617 might be related with the chronicity of HCV infection.

[Association between nuclear factor kappa-light-chain-enhancer of activated B cells genetic polymorphisms and HCV susceptibility among the Chinese population under high-risk].

Objective: To explore the association between nuclear factor kappa-light-chain-enhancer of activated genetic polymorphisms in B cells (NF-κB) and the HCV susceptibility, among the Chinese population. Methods: A total of 1 679 participants were enrolled; including 503 drug users and 1 176 other participants at risk under the exposure for blood. By using the logistic regression analysis, related risk factors for HCV infection among subjects were analyzed. Two NF-κB pathway variants, NF-κB1 rs72696119 and REL rs13031237 were then genotyped by TaqMan assay method. Logistic regression analysis was performed to analyze the association between gene polymorphisms and the susceptibility on HCV. Results: Among the drug users, women (OR=0.408, 95%CI: 0.308-0.767) appeared to be associated with the decreased risk for HCV infection, while factors as drug injection (OR=8.817, 95%CI: 5.577-13.937) and the duration of drug-intake >5.5 years (OR=2.891, 95%CI: 1.824-4.583) were associated with the increased risk for HCV infection. Among the participants who had been exposed to blood, women (OR=3.431, 95%CI: 2.360-4.988) were associated with the increased risk for HCV infection, while the levels of education beyond elementary school (OR=0.613, 95%CI: 0.429-0.876) were associated with the decreased risk for HCV infection. Compared to the reference NF-κB1 rs72696119 CC genotype, the carriage of GG genotype was associated with an increased risk of susceptibility on HCV (OR=1.412, 95%CI: 1.035-1.927) among the total study population. Results from the interaction analysis showed that there was no interactive effects appeared between rs72696119 and route of infection, or between rs72696119 and gender among the total population under study (all P>0.05). Conclusion: NF-κB1 polymorphism rs72696119 and related factors seemed associated with the susceptibility to HCV infection among high-risk Chinese populations.

[A study on the development of the nitrergic neurons in the large intestine of human fetus].

By using histochemical methed of NADPH-diaphorse, the development of the nitrergic neurons in the large intestine of human fetus were studied. The results showed: At the fifth month of gestation, weak positive reaction of nitric oxide synthase (NOS) appeared in part of the round cells of intermuscular ganglia. The round cells differentiated into the nitrergic nerve cells. At the sixth month, the bodies of nitrergic neurons were obviously enlarged, the processes of which were lengthened. The nitrergic nerve fibers were seen in the muscle layer, the submucosa and the base of the intestinal gland. The growth and development of nitrergic neurons reached its peak at the seventh month. The number of intermuscular ganglionic cells was increased. The density of nitrergic nerve fibers was increased in the inner circular muscle layer, and have bead-like structures. At the eighth to tenth month, the staining intensity of nitrergic neurons was increased. The myenteric plexus was densely distributed with nitrergic nerve cell bodies, whereas the submucosa and the inner circular muscle layers contained only a few neurons. The nitrergic nerve fibers were observed in all layer of large intestine, the density of the distribution of nitrergic nerve fibers was by far the highest in the inner circular muscle layer, less in the submucosa and outer longitudinal muscle layer, and only a few were found in the mucous layer. To our knowledge, it is the first time that the development of nitrergic neurons in the large intestine of human fetus was demonstrated.