The aim of this study was to analyze the changes in complements C3 and C4 and C-reactive protein (CRP) in patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), and to evaluate the role of these indices in the differential diagnosis of SLE and RA. The first 347 patients with SLE, 382 patients with RA and 66 patients with erythema nodosum were selected for the measurement of complement and CRP levels in the serum, the erythema nodosum patients were the control group. The roles of the complements and CRP in the differential diagnosis and disease activity evaluation of SLE and RA were analyzed with SPSS 13.0. Complement C3 and C4 levels were significantly reduced in patients with SLE compared with those in the control group. However, in RA patients, the CRP level was increased. In addition, the levels of complements C3 and C4 in patients with SLE were much lower than those in patients with RA and the level of CRP in RA patients was much higher than that in patients with SLE. The reduction of complement C3 levels in SLE patients, and increase of CRP and complement C4 in patients with RA were associated with a higher risk of joint pain, butterfly rash and oral ulcer. These results show that the disease activity of SLE was negatively correlated with complement C3 and C4, and the disease activity of RA was positively correlated with CRP. With the increase in disease activity, the levels of complements C3 and C4 in patients with SLE were gradually reduced and the level of CRP in patients with RA was increased. There were distinctive differences in the levels of complements C3 and C4 and CRP between SLE and RA patients. The differences are useful in disease activity evaluation and the differential diagnosis of the two diseases that have similar symptoms.

With the advantages of environmental safety, convenience in preparation and storage, facility in morphologic discrimination, and outstanding performance in terms of sensitivity and specificity, the in vitro culture method could be applied to identify B. hominis for both clinical diagnosis and field study purposes.

Probiotics may offer an attractive alternative for standard antibiotic therapy to treat Clostridium difficile infections (CDI). In this study, the antibacterial mechanism in vitro of newly isolated B. amyloliquefaciens C-1 against C. difficile was investigated. The lipopeptides surfactin, iturin, and fengycin produced by C-1 strongly inhibited C. difficile growth and viability. Systematic research of the bacteriostatic mechanism showed that the C-1 lipopeptides damage the integrity of the C. difficile cell wall and cell membrane. In addition, the lipopeptide binds to C. difficile genomic DNA, leading to cell death. Genome resequencing revealed many important antimicrobial compound-encoding clusters, including six nonribosomal peptides (surfactins (srfABCD), iturins (ituABCD), fengycins (fenABCDE), bacillibactin (bmyABC), teichuronic, and bacilysin) and three polyketides (bacillaene (baeEDLMNJRS), difficidin (difABCDEFGHIJ), and macrolactin (mlnABCDEFGHI)). In addition, there were other beneficial genes, such as phospholipase and seven siderophore biosynthesis gene clusters, which may contribute synergistically to the antibacterial activity of B. amyloliquefaciens C-1. We suggest that proper application of antimicrobial peptides may be effective in C. difficile control.

To investigate the injury and pathogenesis of Clonorchis sinensis (C. sinensis) to hepatocytes, the liver samples from Wistar rats and patients with C. sinensis infection were examined. The typical histopathological findings of clonorchiasis were observed in rats 4 to 12 weeks postinfection, and majority hepatocytes exhibited hydropic degeneration, even some hepatocytes showed densely condensed nuclei suggesting apoptosis in liver tissue. Apoptosis was found around the central vein or portal areas of liver tissue in rat infected with C. sinensis by transferase uridyl nick end labeling (TUNEL) assay. Compared with normal control, TUNEL-positive cells in liver tissue increase from 4 to 12 weeks postinfection with the peak at 8 weeks. Furthermore, the expression of mRNA and protein of Fas, FasL, and caspase-3 was stronger in infected group than normal control using semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry. Autopsy specimens from four patients infected with C. sinensis have the same findings detected by histopathology, TUNEL, and immunohistochemistry. These findings suggest that the C. sinensis can stimulate both hepatocytic apoptosis and hydropic degeneration that may be responsible for relationship between clinical manifestations and liver lesions in patients with clonorchiasis. These data also indicate a role for Fas/FasL-mediated pathway in the apoptosis that occurs in response to C. sinensis infection.

As the most common intracranial malignant neoplasms, astrocytomas are characterized by high neovascularization and severe peritumoral brain edema (PTBE). Angiogenesis is a prerequisite for the growth of solid tumors, including astrocytoma, and brain-specific angiogenesis inhibitor 1 (BAI1) is a novel angiogenesis inhibitor. In the present study, the expression levels of BAI1, vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) were investigated using immunohistochemical methods in 90 human brain astrocytoma specimens of various pathological grades and in 11 normal human brain tissues. Vascular endothelial cells were stained for CD105 and the microvessel density (MVD) was assessed. The volume of astrocytoma and PTBE in each case was evaluated by magnetic resonance imaging (MRI). The results showed that BAI1 was highly expressed in the normal brain tissues, but that the expression decreased with the rising pathological grades of astrocytoma, MVD number and PTBE, indicating that BAI1 expression was inversely correlated with these factors. Furthermore, it was observed that the expression of VEGF and bFGF were inversely correlated with BAI1 expression in the human brain astrocytomas. These results indicate that the BAI1 gene may be used as a marker of decreased tumor progression and tumoral neovascularization, as well as PTBE.