Pri-miR-124 rs531564 polymorphism and colorectal cancer risk.

MiR-124 functions as a tumor suppressor and plays an important role in tumorigenesis. A common polymorphism (rs531564, C>G) in the pri-miR-124 has been recently studied in connection with cancer risk. The aim of the present study was to investigate the association between pri-miR-124 rs531564 polymorphism and the risk and clinicopathological characteristics of colorectal cancer (CRC). Two case-control studies involving 900 CRC patients and 1110 cancer-free controls showed that pri-miR-124 rs531564 polymorphism was significantly associated with the decreased risk of CRC in Xuzhou population [GG vs. CC: OR = 0.25, 95%CI = 0.09-0.67, P = 0.003; (CG+GG) vs. CC: OR = 0.73, 95%CI = 0.56-0.94, P = 0.01; GG vs. (CC+CG): OR = 0.27, 95%CI = 0.10-0.70, P = 0.004; G vs. C: OR = 0.70, 95%CI = 0.56-0.89, P = 0.003], Bengbu population [GG vs. CC: OR = 0.20, 95%CI = 0.04-0.90, P = 0.02; GG vs. (CC+CG): OR = 0.21, 95%CI = 0.05-0.95, P = 0.03; G vs. C: OR = 0.72, 95%CI = 0.54-0.98, P = 0.03] and pooled population [GG vs. CC: OR = 0.26, 95%CI = 0.11-0.59, P<0.001; (CG+GG) vs. CC: OR = 0.76, 95%CI = 0.62-0.93, P = 0.008; GG vs. (CC+CG): OR = 0.27, 95%CI = 0.12-0.62, P < 0.001; G vs. C: OR = 0.71, 95%CI = 0.59-0.85, P<0.001]. Additionally, pri-miR-124 rs531564 polymorphism was significantly associated with the decreased risk of poor differentiation and lymph node metastasis of CRC. Our results suggest that pri-miR-124 rs531564 polymorphism may be a genetic modifier for developing CRC. However, further studies are needed to validate our findings.

Non-association of IL-16 rs4778889 T/C polymorphism with cancer risk in Asians: a meta-analysis.

The IL-16 rs4778889 T/C polymorphism is associated with cancer risk. However, the results are conflicting. We performed this meta-analysis to derive a more precise estimation of the relationship. A comprehensive literature search was performed using PubMed, Embase and Web of Science databases. Odds ratio (OR) and 95% confidence interval (CI) were used to assess the strength of association. A total of 6 studies including 1,603 cases and 2,342 controls were identified. With all studies involved, results showed no statistically significant association between IL-16 rs4778889 T/C polymorphism and cancer risk (CC vs. CT+TT: OR=0.74, 95%CI: 0.55-1.02, Ph=0.15; CC+CT vs. TT: OR=0.89, 95%CI: 0.72-1.10, Ph =0.03; CC vs. TT: OR=0.73, 95%CI: 0.53- 1.00, Ph =0.08; CT vs. TT: OR=0.91, 95%CI: 0.79-1.05, Ph =0.08; C vs. T: OR=0.89, 95%CI: 0.74-1.07, Ph =0.02). In addition, the results were not changed when studies were stratified by cancer type. However, to verify our findings, it is essential to perform more well-designed studies with larger sample sizes in the future.

Establishment of a cerebral schistosomiasis experimental model in rabbits.

OBJECTIVE: The present study aimed to establish a cerebral schistosomiasis model in rabbits, to provide a valuable tool for morphological analysis, clinical manifestation observation, as well as investigations into immunological reactions and pathogenesis of focal inflammatory reaction in neuroschistosomiasis (NS). METHODS: Sixty New Zealand rabbits were randomly assigned into operation, sham-operation and normal groups. Rabbits in the operation group received direct injection of dead schistosome eggs into the brain, while their counterparts in the sham-operation group received saline injection. Rabbits in the normal group received no treatment. Base on the clinical manifestations, rabbits were sacrificed on days 3, 5, 7, 10, 20, and 30 post injection, and brain samples were sectioned and stained with hematoxylin-eosin. Sections were observed under the microscope. RESULTS: The rabbits in the operation group exhibited various neurological symptoms, including anorexy, partial and general seizures, and paralysis. The morphological analysis showed several schistosome eggs in the nervous tissue on day 3 post operation, with very mild inflammation. On days 7-10 post operation, several schistosome eggs were localized in proximity to red blood cells with many neutrophilic granulocytes and eosinophilic granulocytes around them. The schistosome eggs developed into the productive granuloma stage on days 14-20 post operation. On day 30, the schistosome eggs were found to be in the healing-by-fibrosis stage, and the granuloma area was replaced by fibrillary glia through astrocytosis. The sham-operation group and the normal group showed negative results. CONCLUSION: This method might be used to establish the cerebral schistosomiasis experimental model. Several factors need to be considered in establishing this model, such as the antigenic property of eggs, the time of scarification, and the clinical manifestations.

Research development of the pathogenesis pathways for neuroschistosomiasis.

The infection of the central nervous system (CNS) by schistosome may or may not have clinical manifestations. When symptomatic, neuroschistosomiasis (NS) is one of the most severe presentations of schistosome infection. Among the NS symptoms, cerebral invasion is mostly caused by Schistosoma japonicum (S. japonicum), and the spinal cord symptoms are mainly caused by S. mansoni or S. haematobium. There are 2 main pathways by which schistosomes cause NS: egg embolism and worm migration, via either artery or vein system, especially the valveless perivertebral Batson's plexus. The adult worm migrates anomalously through the above pathways to the CNS where they lay eggs. Due to the differences in species of schistosomes and stages of infection, mechanisms vary greatly. The portal hypertension with hepatosplenic schistosomiasis also plays an important role in the pathogenesis. Here the pathways through which NS occurs in the CNS were reviewed.