Intrauterine Exposure to Long-Chain Perfluorocarboxylic Acids (PFCAs) Were Associated with Reduced Primary Bile Acids in Three-Year-Old Children: Findings from a Prospective Birth Cohort Study.

Bile acids (BAs) play a crucial role in lipid metabolism of children. However, the association between per- and polyfluoroalkyl substance (PFAS) exposure and BAs profiles in children is scarce. To address this need, we selected 252 children from the Maoming Birth Cohort and measured 32 PFAS, encompassing short- and long-chain perfluorocarboxylic acids (PFCAs) and perfluorosulfonic acids (PFSAs) in the cord blood. Additionally, we analyzed nine primary and eight secondary BAs in the serum of three-year-old children. Generalized linear models with FDR-adjusted and Bayesian kernel machine regression (BKMR) were used to explore the associations of individual and mixture effects of PFAS and BAs. We found negative associations between cord blood long-chain PFCAs and serum primary BAs in three-year-old children. For example, one ln-unit (ng/mL) increase of perfluoro-n-tridecanoic acid (PFTrDA), perfluoro-n-undecanoic acid (PFUnDA) and perfluoro-n-decanoic acid (PFDA) were associated with decreased taurochenodeoxycholic acid, with estimated percentage change of -24.28% [95% confidence interval (CI): -36.75%, -9.35%], -25.84% (95% CI: -39.67%, -8.83%), and -22.97% (95% CI: -34.45%, -9.47%) respectively. Notably, the observed association was more pronounced in children with lower vegetable intake. Additionally, the BKMR model also demonstrated a monotonical decline in primary BAs as the PFAS mixture increased. We provided the first evidence between intrauterine PFAS and its mixture exposure with BAs in children. Further large-sample-size studies are needed to verify this finding.

Primary hepatic lymphoma presenting as pyogenic liver abscess: A case report.

BACKGROUND: Primary hepatic lymphoma (PHL) is a lymphoproliferative disorder confined to the liver without peripheral lymph node involvement and bone marrow invasion. PHL is extremely rare in clinical practice. The etiology and pathogenesis of PHL are largely unknown. There are no common standard protocols or guidelines for the treatment of PHL. CASE SUMMARY: We report the case of a 66-year-old man who presented with fever and abdominal pain for three weeks. Computed tomography and magnetic resonance imaging scans showed a pyogenic liver abscess. The patient underwent a right posterior hepatectomy. The surgical pathology revealed aggressive B-cell lymphoma, with a primary consideration of diffuse large B-cell lymphoma of non-germinal center origin. CONCLUSION: This article reviews the characteristics, mechanism and treatment of PHL and provides insight into the diagnosis of PHL.

Treatment of experimental non-alcoholic steatohepatitis by targeting α7 nicotinic acetylcholine receptor-mediated inflammatory responses in mice.

Non­alcoholic fatty liver disease (NAFLD) is one of the most common types of liver disease, affecting up to 30% of the general population worldwide. Non­alcoholic steatohepatitis (NASH) is a severe form of NAFLD without any effective therapies available. The present study showed that activation of α7­nicotinic acetylcholine receptor (α7 nAChR) may be a novel potential strategy for NASH therapy. Treatment with the α7 nAChR agonist nicotine for three weeks obviously attenuated hepatic steatosis in a high-fat diet­induced mouse model of NASH. Investigation of the underlying mechanism showed that nicotine reduced the secretion of the pro­inflammatory cytokines tumor necrosis factor α and interleukin 6 in vitro and in vivo. Inflammation is an integral part of NASH and is the most prevalent form of hepatic pathology found in the general population; therefore, the effect of α7 nAChR activation against NASH may be ascribed to its anti­inflammatory effects. In addition, the present study showed that nicotine­stimulated α7 nAChR activation led to a significant downregulation of nuclear factor kappa B (NK­κB) and extracellular signal-regulated kinase (ERK). It therefore appeared that activation of α7 nAChR suppressed the production of pro­inflammatory cytokines through NK­κB and ERK pathways. In conclusion, the present study indicated that targeting α7 nAChR may represent a novel treatment strategy for NASH.

[Effects of Fuzheng Huayu Capsule on the ratio of TGF-beta1/BMP-7 of chronic viral hepatitis B fibrosis patients of Gan-Shen insufficiency blood-stasis obstruction syndrome].

OBJECTIVE: To observe the effects of Fuzheng Huayu Capsule (FHC) on the liver function, HBV DNA quantization, the ratio of transforming growth factor-beta1/bone morphogenetic protein-7 (TGF-beta1/ BMP-7) of peripheral blood mononuclear cells (PBMCs), HBV DNA YMDD variation, and the liver tissue pathology of chronic viral hepatitis B fibrosis patients of Gan-Shen insufficiency blood-stasis obstruction syndrome (GSIBSOS) on the basis of antiviral treatment by lamivudine. METHODS: Eighty chronic viral hepatitis B fibrosis patients of GSBSOS were randomly assigned to two groups. Patients in the control group (43 cases) were treated with lamivudine alone, while those in the treatment group (37 cases) were treated with lamivudine + FHC. The treatment period lasted for 6 months. By the end of treatment lamivudine was continually given to all patients, and patients were followed up for 6 months. Before and after treatment, liver tissue pathology was examined by liver biopsy. The serum HBV DNA quantization, the ratio of TGF-beta1/BMP-7 were determined by fluorescence quantitative polymerase chain reaction (PCR). HBV DNA YMDD variation was tested by the end of follow-ups. RESULTS: Better effects were obtained in decreasing the levels of ALT, AST, and HBV DNA after 6 months of treatment in the two groups, with statistical difference when compared with before treatment in the same group, but with no statistical difference between the two groups. At the end of the 6th month follow-up, YMDD variation occurred in 9 cases of the control group and in 5 cases of the treatment group, with statistical difference between the two groups (P < 0.05). FHC could significantly reduce the ratio of TGF-beta1/BMP-7, significantly lower in the treatment group (0.09 vs 0.25, P < 0.05). In the aspect of liver tissue pathological changes, the rates of inflammatory activity over G3 and fibrosis degree S3 in the treatment group were significantly lower than those in the control group (P < 0.05). CONCLUSIONS: On the basis antiviral treatment of lamivudine for chronic viral hepatitis B fibrosis patients of BSOS, additional application of FHC could lower the HBV DNA YMDD variation, improve the hepatic inflammation and fibrosis, and exert anti-fibrosis by decreasing the ratio of TGF-beta1/BMP-7.

Differential gene expression between asymptomatic HBV carriers and normal adults.

BACKGROUND: There are more than 100 million asymptomatic HBV carriers (ASCs) in China and they are at a high risk of developing liver disease, which creates a serious health problem. But more than 90% of normal adults clear virus from primary HBV infection, so the difference of gene expression between ASCs and normal adults determines the differential outcomes. To identify differentially expressed genes in ASCs compared to normal adults, we used suppression subtractive hybridization to compare gene expression. METHODS: cDNA subtracted libraries were constructed by suppression subtracted hybridization from peripheral blood monocytes of ASCs and normal adults, the subtracted clones were prescreened by dot blot hybridization, and the levels of genes of interest were confirmed by real-time reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: One hundred and two and 96 positive clones were acquired from the A-N and N-A libraries, respectively, and 14 and 11 clones were identified by dot blot hybridization in the A-N and N-A libraries. Two genes were confirmed as differentially expressed between a set of ASC and normal adult samples by real-time RT-PCR. CONCLUSIONS: Differentially expressed genes in peripheral blood mononuclear cells between ASCs and normal adults were isolated by suppression subtractive hybridization, and included some new genes. Of the upregulated genes in ASCs, checkpoint suppressor 1 is associated with DNA damage-induced cell cycle arrest. Perforin 1 is associated with inflammation. The information about such alterations in gene expression could be useful for elucidating the mechanisms of ASC pathogenesis.