ObjectiveSeveral molecular markers were evaluated for their reliability in detecting Angiostrongylus cantonensis in wild rodent feces and for determining the infection status of these rodents. MethodsA total of 128 wild rodents were captured in Huashan Town， Huadu district， Guangzhou. Their fecal samples were collected and total DNA was extracted with the FastDNA SPIN Kit for Soil. PCR amplification was performed to obtain cytb， cox I and ITS2 gene fragments， followed by Sanger sequencing and phylogenetical analysis. ResultsAmong all 128 fecal samples， only 5 had clean PCR bands and unambiguous cytb sequences suitable for reliable species identification. The infection rate of A. cantonensis was 7.58% （5/66） in Rattus norvegicus， whereas no cytb fragments were detected in Rattus tanezumi， Rattus losea， Suncus murinus and Bandicota indica. These data indicate that R. norvegicus is a highly suitable host for A. cantonensis， and the cytb gene serves as an effective molecular marker for detecting A. cantonensis in wild rodent feces. ConclusionThe cytb is an effective molecular marker for detecting A. cantonensis in wild rodent feces， enabling long-term surveillance of its prevalence and potential public health threat.

Aim To investigate the effects of pyrrolidine dithiocarbamate (PDTC) on D-galactosamine/lipopolysaccharides (GalN/LPS)-induced acute apoptotic liver injury and its mechanism.Methods All mice were randomly divided into four groups.Mice in GalN/LPS group were co-injected with GalN (600 mg·kg~(-1),ip) and LPS (20 μg·kg~(-1), ip). Mice in PDTC+GalN/LPS group were injected with two doses of PDTC,one (100 mg·kg~(-1), ip) at 24 h before LPS and the other at 2 h before LPS (20 μg·kg~(-1), ip).Mice in control groups were treated with PDTC (100 mg·kg~(-1), ip) or saline. Ten mice in each group were observed for animal survival within 72 h after LPS treatment. Six mice in each group were sacrificed 1.5 h after LPS for collecting blood and isolating livers. The expression of hepatic TNF-α mRNA was determined by reverse transcription and polymerase chain reaction (RT-PCR). Hepatic nuclear factor-κB (NF-κB) binding activity was measured with electrophoretic mobility shift assay (EMSA).Twelve mice in each group were sacrificed 8 h after LPS treatment. Serum was collected for measurement of alanine aminotransferase (ALT) and hepatocellular apoptosis and histological examination.Results Co-injection of GalN and LPS markedly increased serum ALT activity. Histopathological examination of liver sections revealed that GalN/LPS induced hepatic congestion, necrosis and massive macrophages infiltration, and increased the number of TUNEL-positive cells in mouse liver.GalN/LPS treatments, led to 90% mortality within 72 h with severe congestion and necrosis in the liver of all the dead mice. PDTC pretreatment significantly inhibited GalN/LPS-induced hepatic NF-κB activation and TNF-α expression. In contrast, PDTC aggravated GalN/LPS-triggered hepatocellular apoptosis, increased serum ALT activity, exacerbated hepatic hemorrhage and necrosis, and accelerated death.Conclusion PDTC aggravates GalN/LPS-induced acute apoptotic liver injury via inhibiting NF-κB-mediated anti-apoptotic effects.