جستجوی مقالات مرتبط با کلیدواژه « Myelin-Oligodendrocyte Glycoprotein » در نشریات گروه « پزشکی »

 The N-terminal domain of the myelin oligodendrocyte glycoprotein (MOG) has been shown to generate experimental autoimmune encephalomyelitis (EAE), an animal model of MS. A considerable amount of MOG must be accessible for EAE induction. Here, for the first time, Response Surface Methodology-Box-Behnken (RSM-BBD) was employed to identify the ideal culture conditions for causing Escherichia coli (E. coli) BL21 to overproduce the Thioredoxin-MOG (Trx-MOG) fusion protein. The RSM method is a powerful, efficient, and reliable alternative to the One-Factor-At-A-Time (OFAT) method in optimizing process variables, allowing for a smaller number of experimental runs, investigating variable interaction, and being cheaper and less time-consuming.

 Here, using the 29 experimental assays, the direct and indirect effects of factors including post-induction time, IPTGinducer concentration, pre-induction optical density, and post-induction temperature on the protein expression level content were evaluated.

 The proposed quadratic model demonstrated a significant effect of the two variables A (time) and C (temperature) on protein synthesis. An inducer concentration of 0.491 mM, the pre-induction optical density (OD600) of 0.8, and a temperature of 23 °C for 23.878 hours were found to be the best growth conditions for high yield Trx-MOG synthesis. The optimum protein concentration was attained (163.96 µg/mL) and was within the range of (200.04 µg/mL), which was the value predicted.

 The study concluded that RSM optimization effectively increased the production of Trx-MOG in E. coli, which could have the potential for large-scale fermentation.

This study was aimed to test simultaneous detection of antibodies to myelin oligodendrocyte glycoprotein (MOG)/aquaporin‑4 (AQP4) in serum samples of patients with clinically-diagnosed optic neuritis (ON), by fixed cell-based immunofluorescence assay (CBIFA). The study involved 237 serum samples of patients with ON which were tested for MOG and AQP4 antibodies using fixed CBIFA kit which utilizes AQP4 or MOG protein transfected cells as a substrate. Of 237 serum samples, 22 (9%) were positive for AQP4, 66 (28%) were positive for MOG, and 138 (58%) were negative for both AQP4 and MOG antibodies. 11 (5%) patients with clinically-diagnosed multiple sclerosis (MS) were negative for both antibodies. None of the samples were positive for both AQP4 and MOG. Among 237, 132 women [18 (13.6%) and 37 (28%)] and 105 men [4 (3.8%) and 29 (27.6%)] were positive for AQP4/MOG antibodies and remaining percentage belonged to double negative and MS. Seropositivity rate was higher in women than men. Antibodies to MOG were significantly higher than AQP4 antibodies and evenly found in all age groups. There was no ambiguous result encountered in the study. In this study, the seropositivity for antibodies to MOG is more than AQP4 antibody in patients with ON. Fixed CBIFA is a useful tool for laboratory diagnosis of ON in the clinical setting of neuro-ophthalmology to plan the next line of treatment management effectively.

The aim of this study was to evaluate the status of anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in patients with transverse myelitis (TM) and compare the clinical and imaging characteristics of MOG immunoglobulin G (IgG)-positive with negative cases.

This cohort study enrolled 71 patients diagnosed with new-onset of TM who were being followed at a referral university clinic in Isfahan, Iran, from November 2016 to January 2019. Magnetic resonance imaging (MRI) images and blood samples for anti-MOG, anti-aquaporin 4 (anti-AQP4) (using the cell-based technique), and vasculitis-related antibodies were collected from patients. Outcomes were assessed by the evolution of the Expanded Disability Status Scale (EDSS) score and brain and spinal cord imaging findings  within three months. All patients underwent imaging and clinical assessment during a mean period of one year as a follow-up. We compared the characteristics of clinical and radiological outcomes in MOG-IgG-positive and negative cases.

Of the total population studied, there were 26.8% men and 73.2% women, with a mean age of 33 ± 10 years. 12 (16.9%) patients were seropositive for MOG antibody and 17 (89.5%) were positive for anti-AQP4 antibodies. There was no significant association between anti-MOG antibody seropositivity and age, gender distribution, the presence of other autoimmune diseases, and number and interval of relapses. However, the involvement site of the spine at first imaging was significantly different between seronegative and seropositive patients.

In patients with MOG antibody disease (MOG-AD) TM, the MRI findings suggest a preferential involvement of the cervical-thoracic section in seropositive cases which may help differentiate from non-MOG demyelination TM.

The absence of Aquaporin-4 Antibody (AQP4-Ab) in a fraction of the Neuromyelitis Optica Spectrum Disorder (NMOSD) patients has led to a search for other serologic markers. Myelin Oligodendrocyte Glycoprotein (MOG) is a protein component of the myelin sheets encapsulating the neural fibers.

We aimed to compare the presence and levels of anti-MOG (Ig-G) in a group of seronegative NMOSD patients with a healthy control group. Materials &

In this cross-sectional study, 30 NMOSD patients with negative AQP-Ab status, who were referred to the Neurology Clinic of Kashani University Hospital in Isfahan City, Iran, from March 2015 to March 2016, and 26 healthy controls were consecutively recruited. Their baseline demographic and clinical data were recorded. Serum anti-MOG levels were measured in both groups. The obtained data were analyzed using the Student t-test, Mann-Whitney U, and Chisquare test in SPSS V. 18.

The anti-MOG test results were statistically higher in patients (n=12, 37.5%) compared to controls (n=0, 0%) (P<0.0001). The level of anti-MOG in Healthy Control (HC) was higher compared to patients with negative anti-MOG (P<0.0001) and was lower than patients with positive anti-MOG (P<0.0001).

Our study showed that nearly one-third of seronegative NMOSD patients were positive for MOG-Ab. Further studies are needed to assess the characteristics and outcome of these patients.

Myelin-Oligodendrocyte Glycoprotein (MOG) is an adhesive molecule responsible for myelin sheath structural integrity and maintenance. Patients with spectrum of inflammatory demyelinating disease particularly in central nervous system are reported to have antibodies against this protein. Diseases such as multiple sclerosis, clinically isolated syndrome, neuro-myelitis optica (NMO) spectrum disorders, acute disseminated encephalomyelitis, transverse myelitis and Optic neuritis seemed to have a correlation with anti-MOG antibodies. MRI findings of seropositive cases revealed spinal lesions, particularly in lower segments. For treatment of these patients methotrexate and azathioprine are suggested. Plasmaphresis and intravenous immunoglobulin may be useful too. However fingolimod and interferons can deteriorate the conditions. Finally it is concluded that anti-MOG antibodies can be a biomarker for CNS demyelinating disorders.