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Background@#and Purpose: Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe central nervous system disorder mediated by NMDAR antibodies that damages neurons. We investigated the correlation between cytoskeletal autoantibodies and the clinical severity in patients with anti-NMDAR encephalitis. @*Methods@#Non-NMDAR autoantibodies were identified by screening matched cerebrospinal fluid (CSF) and the serum samples of 45 consecutive patients with anti-NMDAR encephalitis and 60 healthy individuals against N-methyl-D-aspartate receptor 1-transfected and nontransfected human embryonic kidney 293T cells. Immunocytochemistry was performed to assess antibody binding in rat brain sections and primary cortical neurons. Cell-based assays and Western blotting were applied to identify autoantibodies targeting medium neurofilaments (NFMs). We compared clinical characteristics between patients with NMDAR encephalitis who were positive and negative for anti-NFM-autoantibodies. @*Results@#Anti-NFM autoantibodies were detected in both the serum and CSF in one patient (2%) and in the serum only in six patients (13%). No antibodies were detected in the serum of healthy controls (7/45 vs. 0/60, p=0.0016). Four of the seven patients with anti-NFM autoantibodies in serum were children (57%), and three (43%) had abnormalities in brain magnetic resonance imaging. These patients responded well to immunotherapy, and either no significant or only mild disability was observed at the last follow-up. Anti-NMDAR encephalitis did not differ with the presence of anti-NFM autoantibodies. @*Conclusions@#Anti-NFM autoantibodies may be present in patients with anti-NMDAR encephalitis, indicating underlying neuronal damage. A large cohort study is warranted to investigate the clinical differences between patients with NMDAR encephalitis according to their antiNFM antibody status.
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Immunoglobulin G against myelin oligodendrocyte glycoprotein (MOG-IgG) is detectable in neuromyelitis optica spectrum disorder (NMOSD) without aquaporin-4 IgG (AQP4-IgG), but its pathogenicity remains unclear. In this study, we explored the pathogenic mechanisms of MOG-IgG in vitro and in vivo and compared them with those of AQP4-IgG. MOG-IgG-positive serum induced complement activation and cell death in human embryonic kidney (HEK)-293T cells transfected with human MOG. In C57BL/6 mice and Sprague-Dawley rats, MOG-IgG only caused lesions in the presence of complement. Interestingly, AQP4-IgG induced astroglial damage, while MOG-IgG mainly caused myelin loss. MOG-IgG also induced astrocyte damage in mouse brains in the presence of complement. Importantly, we also observed ultrastructural changes induced by MOG-IgG and AQP4-IgG. These findings suggest that MOG-IgG directly mediates cell death by activating complement in vitro and producing NMOSD-like lesions in vivo. AQP4-IgG directly targets astrocytes, while MOG-IgG mainly damages oligodendrocytes.
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Objective To evaluate the therapeutic effect and safety of Kangai injection combined with Chemotherapy in treating Colorectal cancer. Methods The CNKI, Wanfang, CBM, VIP, Medline and Cochrane Library from inception to the August 17th 2017 were searched, and all the relevant journals, and the literature of RCTs were enrolled. The quality of RCTs was assessed by Jadad scores, meta-analyses were performed by Review Manager 5.3 software. Results 21 Chinese articles were enrolled, including three high quality article, and the Jadad average score is 2.7. 1 879 patients were included. The result of Meta-analyses showed that intervention could improve the quality of life [OR=3.29, 95% CI (2.53-4.27), P＜0.01]; improve the short-term effects [OR=1.79, 95% CI (1.36-2.37),P＜0.001]; reduce the gastrointestinal reactions [OR=0.36,95% CI (0.29-0.45), P＜0.01], reduce bone marrow suppression reaction [OR=0.35, 95% CI (0.27-0.44),P＜0.01]. reduce the peripheral neurotoxicity [OR=0.57, 95% CI (0.41-0.78), P＜0.01], improve the abnormal liver function [OR=0.0.41,95% CI (0.26-0.65), P＜0.01], and improve the abnormal renal function [OR=0.55,95% CI (0.31-0.98), P=0.04]. Conclusions The combination of Kangai injection and Chemotherapy in treating Colorectal cancer is better than only using chemotherapy. However, we need more high-quality RCTs to improve the research.
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Objective To study the seropositive ratio of the antibody to aquporin 4 (AQP4-IgG) and myelin oligodendrocytes glycoprotein antibody(MOG-IgG)in patients with autoimmune-associated central nervous system (CNS) diseases. Meanwhile, epidemiology and clinical manifestation and diagnosis,laboratory examination and magnetic resonance imaging(MRI)of AQP4-IgG seropositive and MOG-IgG seropositive patients are described. Methods 2068 patients serum samples were collected and enrolled in the multi-center research. The methodology of cell-mediated immunofluorescence staining was used to detect serum AQP4-IgG and MOG-IgG. Clinic medical records were collected and characteristics of epidemiology and manifestation were compared. Results 681 patients were AQP4-IgG seropositive and 110 patients were MOG-IgG seropositive. The female/male ratio and age of onset of patients with AQP4-IgG seropositive(616 female and 65 male,female:male=9.50:1.00;Age of onset=41.7±14.9)were significantly higher than that of patients with MOG-IgG (57 female and 53 male, female:male=1.08:1.00, P<0.0001; Age of onset=27.0 ±17.7, P<0.0001). The optic neuritis was significantly higher in patients with AQP4-IgG seropositive and patients with MOG-IgG seropositive (38.4% vs.53.5%, P<0.05).Among patients with AQP4-IgG seropositive, 42.14% conformed the diagnostic criteria of neuromyelitis optica (NMO),which was higher than that of patients with MOG-IgG seropositive (13.64%, P<0.0001). Laboratory examination showed that there was no significant difference in cerebrospinal fluid protein levels between patients with AQP4-IgG seropositive and those with MOG-IgG seropositive.MRI imaging suggested that AQP4-IgG positive patients were more common in cervical thoracic spinal cord lesions, while MOG-IgG positive patients were more involved in thoracolumbar spinal cord. The study also found that these two groups of patients could be comorbid with other autoimmune antibodies. Conclusions This multi-center research has revealed that patients with AQP4-IgG seropositive and those with MOG-IgG seropositive display differences in epidemiology,clinic manifestations and diagnosis,laboratory examination and MRI imaging. AQP4-IgG and MOG IgG auto-antibody detection are necessary for clinic diagnosis and differential diagnosis.
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In the middle of the 20th century, the United States first proposed the medical humanities theory to campus and offered a variety of medical humanities curriculum, hoping that medical students would have a better understanding of diseases, pain, show themselves more compassion, and foster their communication skills. In recent years, the medical humanities education played a positive role in developing and improving medical students’ comprehensive ability as well as their diagnosis and treatment technology. Currently, American pays more attention to establish a unified and objective standard to evaluate the effect of medical humanities curriculum. Meanwhile, many experts give some suggestions to the medical humanities education.
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Objective Vessel injury provokes the release of angiotensin II that influences the proliferation and migration of vascular smooth muscle cells (VSMCs). T lymphocytes produced, interleukin 10 is of immunoregulatory function. The purpose of this study is to determine the effects of recombinant human interleukin 10 (rhIL 10) on the proliferation of isolated rat vascular smooth muscle cell and the activity of p44/p42 mitogen activated protein kinase (MAPK) promoted by angiotensin II. Methods Rat aortic VSMCs were cultured and treated with rhIL 10 or angiotensin II, and then co treated with rhIL 10 and angiotensin II. The proliferation was quantified by colormetric assay. The p44/p42 MAPK activity was evaluated by the immunobloting technique using anti p44/p42 phospho MAPK antibody. Results Compared with control group, angiotensin II stimulated significantly VSMCs proliferation(1 311?0 201 vs 0 781?0 236, P 0 05), but significantly inhibited VSMCs proliferation induced by angiotensin II at a dose of 1,10,100 ng/ml (0 984?0 172 , 0 932?0 134 , 0 784?0 097 vs 1 311?0 201, P
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Objective:To explore the action of the second signal system in the activatied and proliferating T cells and the induction of apoptosis of the hepatoma cells.Methods:The T cells were costimulated by anti CD28 and anti CD80(B7.1)McAb and acted on the hepatoma cells(BEL 7402),then testing the concentration of cAMP?cGMP and Ca 2+ in the T cells and the apoptosis of the hepatoma cells.Results:The concentration of cAMP was increased temporarily at first,then decreased rapidly,and increased 1 2 times again when acted on the hepatoma cells.The concentration of cGMP was increased 6 8 times fast and the concentration of Ca 2+ obviously increased 2 3 times too.The peak of them was at the fourth day and positive related to apoptosis of the hepatoma cells.Conclusion:The level of the second signal system of cAMP?cGMP and Ca 2+ were significant correlated with the T cells activated and porliferating and the cytotoxic effect.
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AIM: To determine the effects of recombinant human interleukin-10(rhIL-10) on proliferation of vascular smooth muscle cells(VSMC) by TNF-? and PDGF-BB and neointimal hyperplasia after rat carotid arterial injury.METHODS: Rat aortic VSMC was cultured and treated with rhIL-10 with or without tumor necrosis factor-?(TNF-?) and platelet-derived growth factor-BB (PDGF-BB), respectively.Proliferation of VSMC was quantified by colormetric assay.Cell cycle analysis was performed by flow cytomertry.SD rats were treated with recombinant human IL-10(rhIL-10) for 3 days after carotid arteries injury.Neointima to media area ratio at the site of arterial injury was measured at 28 days after balloon injury.RESULTS: Compared to control,both TNF-? and PDGF-BB stimulated VSMC proliferation. rhIL-10 alone had no effect on VSMC growth.With TNF-? or PDGF-BB stimulation,rhIL-10,at dose as low as 10 ?g/L,inhibited VSMC growth( P