Some achievements have been made in the research on liver diseases in children in China, with the help of several generations of physicians for 60 years. At present, liver biopsy, examination of duodenal fluid and bile, screening for inherited metabolic diseases, and new techniques of genetic diagnosis have been conducted in China. Planned immunization with hepatitis A and B vaccines significantly reduces the incidence rates of hepatitis A and B. Remarkable achievements have been obtained in the research on cytomegalovirus infection, cytomegalovirus hepatitis, nonalcoholic fatty liver disease, autoimmune liver diseases, and drug-induced liver disease. Intensive research on liver diseases in children in China may gradually narrow the gap between China and developed countries in future.

Chronic liver diseases in children greatly affect their growth and development and quality of life in future. There are many causes of chronic liver diseases in children, and such causes, diet, and treatment guidance are closely associated with prognosis. This article discusses the guidance and follow-up of common chronic liver diseases in children, such as infantile cholestatic liver disease, chronic hepatitis B, hepatolenticular degeneration, and nonalcoholic fatter liver disease, in order to deepen the understanding of these diseases among patients, raise the awareness of follow-up in medical staff, and improve the cure rate of liver diseases with different causes and children's quality of life.

ObjectiveTo investigate the expression of sperm-associated antigen 6 (Spag6) in liver cancer tissue and its association with the clinicopathological features and prognosis of liver cancer patients, as well as the effect of Spag6 on the proliferation and migration of HCCLM3 hepatoma cells. MethodsClinical samples were collected from 102 liver cancer patients who were treated in Xiangya Hospital of Central South University from August 2006 to November 2009, and Western blot was used to measure the expression of Spag6 in hepatoma cells, normal liver tissue, tumor tissue, and corresponding adjacent tissue. Immunohistochemistry was used to measure the expression of Spag6 in 102 liver cancer tissue samples, and according to the immunohistochemical scoring criteria, the patients were divided into high Spag6 expression group and low Spag6 expression group.  Lentivirus-mediated RNA interference technique was used to silence Spag6 expression in HCCLM3 cells; Western blot was used to analyze silencing effect, wound-healing assay was used to investigate the effect of Spag6 gene silencing on the migration of HCCLM3 cells, and colony formation assay was performed to observe the effect of Spag6 gene silencing on the proliferation of HCCLM3 cells. The chi-square test was used to investigate the association between Spag6 expression and clinicopathological features of liver cancer patients, and the Kaplan-Meier survival analysis and log-rank test were used to analyze the association between Spag6 expression and the prognosis of liver cancer patients. ResultsHepatoma cells and liver cancer tissue had significantly higher expression of Spag6 than the normal LO2 cells and normal liver tissue. Immunohistochemistry showed that the expression rate of Spag6 was 58.8% (60/102) in liver cancer tissue samples and 12.7% (13/102) in adjacent tissue samples (χ2=47123,P＜0.001). According to the results of the chi-square test, Spag6 expression was associated with the number of tumor nodules, presence or absence of capsule, vascular invasion, and Edmondson-Steiner classification (χ2=8.360, 6.761, 4.344, and 7.172, P=0.004, 0.009, 0.037, and 0.007). Further analysis showed that the high Spag6 expression group had significantly lower 1-, 3-, and 5-year survival rates than the low Spag6 expression group (71.5% vs 905%,437% vs 688%, 197% vs 487%, χ2=11.228, P=0.001). Cell assays showed significant reductions in the proliferation and migration of HCCLM3 cells after Spag6 gene silencing (both P＜0.01). ConclusionSpag6 is highly expressed in hepatoma cells and liver cancer tissue, and its high expression is associated with poor clinicopathological features and postoperative survival of liver cancer. Spag6 can promote the proliferation and migration of hepatoma cells, suggesting that Spag6 may be involved in the development and progression of liver cancer. Therefore, it can be used as a reference index for predicting the prognosis of liver cancer patients and a potential target for liver cancer treatment. 

Objective To investigate the association between cerebral hemodynamic changes and neonatal hyperbilirubinemia. Methods A total of 67 neonates with hyperbilirubinemia who were admitted to our hospital from January 2014 to November 2015 were enrolled as study group, and another 36 normal healthy neonates were enrolled as control group. The two groups were compared in terms of end-diastolic velocity ( Vd) , systolic peak velocity ( Vs) , mean blood flow velocity ( Vm) , resistance index ( RI) , and pulsatility index ( PI) , and the serum level of bilirubin and systemic symptoms were observed after treatment. The t-test was used for comparison of continuous data between groups, and a Pearson correlation analysis was also performed. Results At the time of enrolment and on day 3 of treatment, the control group had significantly lower Vd, Vs, and Vm than the study group ( before treatment: t = 75. 873, 81. 589, 64. 600, 19. 834, 30. 453; day 3 of treatment: t = 39. 476, 55. 729, 35. 274, 6. 069, 9. 382, all P < 0. 001) . The study group had improvements in Vd, Vs, Vm, RI, and PI on day 3 of treatment. On day 5 of treatment, there were no significant differences in hemodynamic parameters between the two groups ( all P > 0. 05) . Serum level of bilirubin was positively correlated with Vd ( r = 0. 387, P < 0. 001) , Vs ( r = 0. 483, P < 0. 001) , and Vm ( r =0. 412, P < 0. 001) and negatively correlated with RI ( r =-0. 492, P < 0. 001) and PI ( r =-0. 497, P < 0. 001) . Conclusion Serum level of bilirubin interacts with cerebral hemodynamics, and cerebral hemodynamic parameters can provide objective evidence for evaluating disease progression and prognosis of neonatal hyperbilirubinemia.

Objective To investigate the clinical effect of liver transplantation in the treatment of hepatolenticular degeneration ( HLD) and the prognosis of HLD patients. Methods A retrospective analysis was performed for the clinical data of 15 HLD patients who underwent liver transplantation in Changzheng Hospital of Second Military Medical University from June 2003 to January 2017. Friedman test of K related samples test was used for comparison of data between groups, and Wilcoxon one-sample test of 2 related samples test was used for comparison of data between two groups. Results Of all patients, 13 underwent standard orthotopic liver transplantation, and 2 underwent modified piggyback liver transplantation. One patient died of multiple organ failure during the perioperative period and 2 were lost to follow-up at half a year after surgery. Of all patients, one lived for 14 months, one lived for 5 years and 8 months, and the other ten patients were still alive up to now. Six patients suffered from acute rejection reaction ( AR) , among whom four were improved after conventional hormone pulse therapy, one was improved and discharged after antiviral therapy with ganciclovir for cytomegalovirus infection, and the other one patient was improved and discharged after the second liver transplantation at 5 months after surgery due to poor response to hormone pulse therapy and chronic rejection reaction. Ten patients had varying degrees of improvement in positive Kayser-Fleischer ring, and three patients achieved varying degrees of improvement in severe neuropsychiatric symptoms and had a basically normal neuropsychiatric state at half a year to one year after surgery.One patient died in the perioperative period, and the other 14 patients had a significant improvement in liver function at 1 month after surgery, and the level of ceruloplasmin gradually increased to a normal level. Conclusion Orthotopic liver transplantation can effectively improve copper metabolism, liver function, and neuropsychiatric symptoms in HLD patients and increase their quality of life and long-term survival rates.

Objective To investigate the interaction between autophagy and lipid metabolism in nonalcoholic fatty liver disease ( NAFLD) .Methods Human hepatocytes ( steatosis) were cultured in vitro to establish a cell model of NAFLD. Rapamycin was used to induce autophagy and 3-methyladenine was used to inhibit autophagy. MTT colorimetry was used to measure cell viability. ELISA was used to measure the levels of triglyceride ( TG) , alanine aminotransferase ( ALT) , aspartate aminotransferase ( AST) , lactate dehydrogenase ( LDH) , gamma-glutamyl transpeptidase ( GGT) , and albumin ( Alb) . IF method was used to determine the location and distribution of LC3-II. Western blot was used to measure LC3-II/LC3-I ratio. An analysis of variance was used for comparison of continuous data between groups, and the SNK-q test was used for further comparison between two groups. Results Compared with the steatosis group, the induced autophagy group had significant reductions in absorbance and cell viability ( HL-7702 cells: q = 4. 160 and 4. 110, P < 0. 05; SK-HEP-1 cells: q = 4. 407 and 4. 032, P < 0. 05) . Compared with the control group, the steatosis group had significant increases in the levels of TG, ALT, AST, LDH, GGT, and Alb ( HL-7702 cells: q = 5. 316, 3. 730, 4. 013, 6. 967, 6. 192, and 5. 531, P < 0. 05; SK-HEP-1 cells: q = 4. 963, 3. 603, 4. 774, 7. 479, 6. 319, and 5. 193, P < 0. 05) . Compared with the steatosis group, the induced autophagy group had significant reductions in the levels of TG, ALT, AST, LDH, GGT, and Alb ( HL-7702 cells: q = 4. 978, 3. 695, 3. 960, 5. 130, 4. 695, and 3. 192, P < 0. 05; SK-HEP-1 cells: q = 3. 846, 5. 575, 4. 184, 5. 019, 4. 203, 3. 049, P < 0. 05) . The induced autophagy group had the highest percentage of LC3-II-positive HL-7702 cells ( 90. 1%) and LC3-II-positive SK-HEP-1 cells ( 80. 0%) , followed by the steatosis group ( 47. 2% LC3-II-positive HL-7702 cells and 48. 4% LC3-II-positive SK-HEP-1 cells) and the autophagy inhibition group ( 30. 2% LC3-II-positive HL-7702 cells and 45. 5% LC3-II-positive SK-HEP-1 cells) . The induced autophagy group had a significant increase in LC3-II/IC3-I ratio compared with the steatosis group ( HL-7702 cells: q = 6. 786, P < 0. 05;SK-HEP-1 cells: q = 5. 926, P < 0. 05) . Conclusion Upregulation of autophagy can promote the elimination of liver fat, while downregulation of autophagy can promote lipid accumulation.