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Cases of newly developed advanced schistosomiasis (NDAS) have occurred in areas where schistosomiasis transmission has been blocked for more than 25 years. The causes and pathogenesis of NDAS are still unknown. Diagnosis of NDAS relies on historical investigation and clinical symptoms, such as liver fibrosis, hepatic ascites and abnormal biochemical indexes in serum. It is important but difficult at this stage to develop a new tool for early screening and rapid diagnosis. In this study, serum peptides from thirty patients with NDAS and thirty healthy controls were captured with weak cation exchange magnetic beads, and subjected to MALDI-TOF mass spectrometry and ClinProTools analysis. Eleven peaks with m/z 924, 2661, 2953, 2991, 3241, 3884, 5337, 5905, 5943, 7766 and 9289 were decreased and three peaks with m/z 1945, 2082 and 4282 were increased in the NDAS group. The proteomic detection pattern (PDP) was established with 14 different peptide peaks, and its sensitivity and specificity were investigated with a blind test. The peptide mass fingerprints of sera from 50 NDAS patients and 100 healthy controls were double-blind subjected to the PDP method, and 50 patients and 92 healthy controls were classified as NDAS and healthy separately, which showed 100% sensitivity and 92% specificity. Our results showed that the PDP could be a new and useful method to detect NDAS.

Background: It has been documented that Helicobacter hepaticus (H hepaticus) infection is linked to chronic hepatitis and liver cancer. However, our understanding of the molecular mechanisms underlying progression of the H hepaticus‐induced hepatic inflammation to cellular hepatocarcinoma is still limited. Materials and methods: In our study, male BALB/c mice were infected by H hepaticus for 8, 12, 16, 20, and 24 weeks. Histopathology, H hepaticus colonization dynamics, select signaling pathways, and expression of key inflammatory cytokines in the liver were examined. Results: We found that H hepaticus was detectible in feces of mice at 7 days postinfection (DPI) by PCR, but it was not detected in the livers by PCR until 8 weeks postinfection (WPI). In addition, abundance of colonic and hepatic H hepaticus was progressively increased over the infection duration. H hepaticus‐induced hepatic inflammation and fibrosis were aggravated over the infection duration, and necrosis or cirrhosis developed in the infected liver at 24 WPI H hepaticus infection increased levels of alanine aminotransferase and aspartate aminotransferase. Moreover, mRNA levels of Il‐6 and Tnf‐α were significantly elevated in the livers of H hepaticus‐infected mice compared to uninfected control from 8 WPI to 24 WPI. Furthermore, Stat3, nuclear factor‐κB (p65), and MAPK (Erk1/2 and p38) were activated by H hepaticus infection. Conclusions: These data demonstrated that male BALB/c mice can be used as a new mouse model of H hepaticus‐induced liver diseases and that the H hepaticus‐induced liver injury is triggered by NF‐κB, Jak‐Stat, and MAPK signaling pathways. [ABSTRACT FROM AUTHOR]