BACKGROUND: Experimental autoimmune encephalomyelitis has become the most classical animal model for multiple sclerosis. However, the experimental autoimmune encephalomyelitis model of China presented one-way course of disease. By using proteolipid protein 139-151 and proteolipid protein 178-191, relapse remitting experimental autoimmune encephalomyelitis models may be induced in SJL/J mice which were susceptible to immune, which have similar clinical situation, course and histologicallterations to multiple sclerosis.OBJECTIVE: To establish the relapse remitting experimental autoimmune encephalomyelitis mouse model induced by proteolipid protein, which has similar clinical situation, course and histological alterations to multiple sclerosis.DESIGN: Completely randomized controlled study.SETTING: The centre of Neuro-information, and Neurological Institute,General Hospital of Chinese PLA.MATERIALS: The study was carried out at the Laboratory of Neuro-pathology, General Hospital of Chinese PLA, from February to June 2004.Sixty female SJL/J mice with 8-12 weeks old were selected and randomly divided into proteolipid protein 139-151 group and proteolipid protein-178-191 group with 30 in each.INTERVENTIONS: After injected with proteolipid protein-139-151 or proteolipid protein-178-191, the models of relapse remitting experimental autoimmune encephalomyelitis were induced, and the body weight and neurological signs of each female SJL/J mouse were viewed. The tissue morphological changes of models were observed with hematoxylin and eosin and uxol fast blue stain.MAIN OUTCOME MEASURES: The neurological symptoms and signs,features of relapse and remitting and the perivascular inflammatory cell infiltration, demyelinated lesion of the model of experimental autoimmune encephalomyelitis mouse induced by two proteolipid protein peptides.RESULTS: All 60 mice entered the final analysis. ① Significant neurological symptoms, signs and features of relapse and remitting was manifested in the model of experimental autoimmune encephalomyelitis mouse induced by two proteolipid protein peptides. Obvious phenomena of perivascular inflammatory cuffing, satellitism, predominant perivascular inflammatory cell infiltration and demyelinated lesion were found in spinal and cerebral tissue. ②Changes of body mass: Before immunity, the body mass of mice in two groups was( 17. 84 ± 2.59) g and (17. 88 ± 0.52) g respectively. Onset of relapse of the mice in proteolipid protein-178-191 group was earlier and faster, their body mass had no distinctive change after immunization and the mean body mass was(23.52 ± 2.37) g till the 60th day. Meanwhile, Onset of relapse of the mice in proteolipid protein-139-151 group was later and slower. After the immunity, the body mass of mice was little decrease, and the body mass was (16. 70 ±0.46) g on the 60th day. ③ Neural functional scores: The highest functional scores in the two groups were not different(3.86 ± 1.10vs 3.71 ±1.05, t=0.49, P=0.628).CONCLUSION: The two different antigenic peptides of proteolipid protein can all cause the autoimmune response of central nervous system. Both models have the same characters of relapse and remitting and the severity has no significant difference. But compared with proteolipid protein 139- 151 group,onset and recover of the experimental autoimmune encephalomyelitis of the mice in proteolipid protein 178-191 group were earlier, as well as weight variance was larger, which maybe due to the different structure of two peptides.

Circular RNA (circRNA) is involved in tumor progression. CircPVT1 is an oncogene that is abnormally expressed and correlated with a variety of tumors. It can regulate tumors' malignant behavior and affect the survival and prognosis of patients. This article reviews research on the regulatory roles of circPVT1 in tumors to provide references for accurate treatment.

The Wnt signaling pathway plays key roles in various developmental processes. Wnt5a, which activates the non-canonical pathway, has been shown to be particularly important for axon guidance and outgrowth as well as dendrite morphogenesis. However, the mechanism underlying the regulation of Wnt5a remains unclear. Here, through conditional disruption of Foxg1 in hippocampal progenitors and postmitotic neurons achieved by crossing Foxg1