scholarly journals Evaluation of mir-377-3p Expression in Patients with Multiple Sclerosis

2019 ◽  
Vol 1 (2) ◽  
pp. 48-54 ◽  
Author(s):  
Majid Amini Khorasgani ◽  
Parisa Mohammady Nejad ◽  
Mohammad Mehdi Moghani Bashi ◽  
Mohammad Hedayati

One of the most recent studies in the field of genetics is to investigate the role of microRNAs as biomarkers for the diagnosis of multiple sclerosis. It is an inflammatory and degenerative disease of the central nervous myelin, which is manifested in numerous small and large plaques in the white matter of the brain and spinal cord. Formerly called has-miR-377-3p, miR-377-3p is located within the chromosomal region 32q14, and is located in the SOD gene. SOD (Superoxide Dismutase) is a gene located on chromosomal region 22q21 and the protein encoded by this gene is the superoxide dismutase enzyme. The aim of this study was to evaluate the expression of miR-377 in people with RRMS (Relapsing-Remitting Multiple Sclerosis) and healthy individuals in the Isfahan population. The study included 49 patients with RRMS and 52 healthy individuals who had no history of autoimmune and inflammatory disease. Total RNA was extracted from the blood lymphocytes of the study subjects using Ficol and Trizol and then made using miRNA cDNA, cDNA specific kit, and expression was measured by real-time RT PCR in healthy subjects and patients. Was. According to the results, miR-377-3p expression was higher in patients than in healthy subjects (P = 0.036) and the sensitivity and diagnostic value of miRNA was AUC = 0.80 (Area under the Curve). ) is.  The results were consistent with previous studies and miR-377-3p could be used as a biomarker for the diagnosis of Multiple Sclerosis.

2012 ◽  
Vol 19 (3) ◽  
pp. 369-371 ◽  
Author(s):  
Deepti Anbarasan ◽  
Jonathan Howard

We discuss the case of a patient with a known history of relapsing–remitting multiple sclerosis (MS) who presented with the isolated complaint of altered visual perception in the absence of abnormalities on ophthalmological examination. To the best of the authors’ knowledge, this is the first documented case of both facial metamorphopsia and palinopsia occurring as the symptoms of demyelinating brain lesions consistent with an acute MS exacerbation. These symptoms appear to be related to active demyelination that either involved the optic radiations in the visual pathway or the visual association area in the temporo-occipital region of the left hemisphere.


2017 ◽  
Vol 3 (4) ◽  
pp. 205521731774534
Author(s):  
A Traboulsee ◽  
DKB Li ◽  
R Tam ◽  
G Zhao ◽  
A Riddehough ◽  
...  

Background Evolution of gadolinium-enhancing lesions into chronic black holes (CBH) may be reduced by interferon (IFN) therapy. Objective The objective of this paper is to assess the effect of IFN β-1a and placebo on CBH evolution and disability in patients with relapsing–remitting multiple sclerosis (RRMS), as well as CBH evolution in patients with secondary progressive multiple sclerosis (SPMS). Methods A post hoc, exploratory analysis of patients with RRMS and SPMS with monthly MRI scans (months –1 to 9) from two separate placebo-controlled clinical trials of IFN β-1a was conducted. Results In RRMS patients, the risk of ≥1 evolved CBH was lower for IFN β-1a versus placebo (odds ratio 0.42; p = 0.024); volume of newly evolved CBH was numerically reduced. A numerically higher proportion of patients with ≥1 evolving CBH vs no evolving CBH had confirmed three-month disability progression (four-year rate 55.8% vs 43.1%, respectively). Proportion of lesions evolving into CBH (patient level: 34.7% vs 12.6%, p < 0.0001; lesion level: 28.8% vs 11.0%, p < 0.0001) and evolved CBH volume (median 33.5 mm3 (Quartile 1, 0.0; Quartile 3, 173.4) vs 0.0 mm3 (0.0; 52.4); p = 0.0008) was higher for SPMS than RRMS patients treated with IFN β-1a. Conclusion In RRMS, IFN β-1a significantly decreased the proportion of new T1 Gd+ lesions evolving into CBH and the risk of developing a CBH. In patients with SPMS, more lesions develop to CBH, indicating reduced repair capacity, and the natural history of lesion development appears to be unaffected by IFN β-1a treatment.


2018 ◽  
Vol 20 (2) ◽  
pp. 62-66 ◽  
Author(s):  
Mihail Guranda ◽  
Marco Essig ◽  
Ariane Poulin ◽  
Reza Vosoughi

Background: Magnetic resonance imaging (MRI) is used to diagnose and monitor disease activity in relapsing-remitting multiple sclerosis (RRMS). The objective of this study was to explore the association of “ultrabright” axial fluid-attenuated inversion recovery (FLAIR) lesions with gadolinium enhancement in patients with RRMS using qualitative and quantitative approaches. Methods: MRIs from patients with RRMS from 2010 to 2015 were reviewed. Two radiologists independently identified ultrabright lesions on axial FLAIR sequences. The contrast-to-noise ratio (CNR) was measured for ultrabright and control lesions. Results: Of 301 lesions included in the study, 77 (26%) were identified by both radiologists as ultrabright. Interrater agreement was moderate (κ = 0.77, P &lt; .001). Lesions identified by both radiologists as ultrabright demonstrated an association with gadolinium enhancement (χ21 = 30.8, P &lt; .001) but were not associated with MRI magnet strength (χ21 = 0.24, P = .65). Higher CNR values were associated with gadolinium enhancement for 1.5-T studies (OR, 1.05; 95% CI, 1.02–1.07; P = .001) and 3-T studies (OR, 1.02; 95% CI, 1.02–1.03; P &lt; .001). Diagnostic accuracy of the quantitative model was good for 1.5-T studies (area under the curve, 0.79; 95% CI, 0.68–0.9; P &lt; .001) and 3-T studies (area under the curve, 0.78; 95% CI, 0.73–0.84; P &lt; .001). Positive predictive value of 100% was obtained for CNR values of 92 for 1.5-T and 184 for 3-T studies. Conclusions: Qualitatively and quantitatively identified ultrabright axial FLAIR lesions are significantly associated with gadolinium enhancement.


2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Liudmila P. Smirnova ◽  
Irina A. Mednova ◽  
Nina M. Krotenko ◽  
Valentina M. Alifirova ◽  
Svetlana A. Ivanova

This work is the first to demonstrate that class G immunoglobulins (IgGs) in patients with multiple sclerosis and healthy individuals have the ability to catalyze the dismutation reaction of the superoxide anion radical. Thus, superoxide dismutase (SOD) activity is an intrinsic property of antibodies, which is confirmed by a number of stringent criteria. SOD activity of IgGs in patients with multiple sclerosis statistically significantly exceeds such activity in healthy individuals by 2-4 times. Moreover, the maximum activity has been registered in patients with relapsing remitting multiple sclerosis. The kinetic characteristics of the SOD reaction of IgGs are several orders of magnitude lower than those for the SOD enzyme but do not differ between patients with multiple sclerosis and healthy individuals. Consequently, abzymes with SOD activity have a lower catalysis rate than that of the enzymes and form a stronger complex with the substrates. Inhibitory analysis showed that this activity is inhibited by classical metal-dependent SOD inhibitors. The activity of IgGs was inhibited by classical metal-dependent inhibitors EDTA and TETA (triethylenetetramine). Also, high catalase activity of IgGs was detected in these patients. We suggest that these abzymes help protect the body from oxidative stress.


2019 ◽  
Vol 12 (4) ◽  
pp. e227951 ◽  
Author(s):  
Yves Michiels ◽  
Olivier Bugnon ◽  
Jean-François Michiels ◽  
Sophie Mazellier

In addition to the TRANSFORMS, FREEDOMS, INFORMS studies, very few publications have identified new cases of skin cancer in patients treated with fingolimod. Here, we present the case of a 52-year-old Caucasian patient with relapsing remitting multiple sclerosis for 19 years, with a phototype II with blue eyes, light brown hair, no personal or family history of melanoma and a low number of naevi (<10). She did not experience intense sun exposure in childhood as well as severe sunburn and did not practise sessions in ultraviolet cabins. This case is distinguished from other published cases, usually superficial spreading malignant melanoma by its unclassifiable histological character. The occurrence of skin cancers in patients with multiple sclerosis remains exceptional, but new cases have recently emerged requiring the strengthening of dermatological follow-up of such patients.


Brain ◽  
2020 ◽  
Vol 143 (9) ◽  
pp. 2637-2652 ◽  
Author(s):  
Per Soelberg Sorensen ◽  
Finn Sellebjerg ◽  
Hans-Peter Hartung ◽  
Xavier Montalban ◽  
Giancarlo Comi ◽  
...  

Abstract In the past decade, changes have occurred in the spectrum of multiple sclerosis courses. The natural history of multiple sclerosis appears milder from the first sign of demyelinating disease to the progressive course, probably as a result of an interplay between several factors including changes in the diagnostic criteria, changes in the epidemiology of multiple sclerosis, impact of early and appropriate disease-modifying treatment and improvement of the general state of health in the population. It has been suggested to regard incidental findings of demyelinating lesions in MRI in individuals without any history of clinical symptoms consistent with neurological dysfunction, so-called radiological isolated syndrome, as the initial course of multiple sclerosis. New diagnostic criteria have enabled the multiple sclerosis diagnosis in many patients at the first clinical demyelinating event, clinically isolated syndrome. The remaining patients with clinically isolated syndrome have a more benign prognosis, and for relapsing-remitting multiple sclerosis, the prognosis has become more favourable. Reduced disease activity in patients with relapsing-remitting multiple sclerosis can partly be ascribed to more efficacious new disease-modifying therapies but decrease in disease activity has also be seen in placebo-treated patients in clinical trials. This may be explained by several factors: change in the diagnostic criteria, more explicit inclusion criteria, exclusion of high-risk patients e.g. patients with co-morbidities, and more rigorous definitions of relapses and disease worsening. However, these factors also make the disease course in patients treated with disease-modifying therapies seem more favourable. In addition, change in the therapeutic target to stable disease (no evidence of disease activity = no relapses, no disease worsening and no MRI activity) could by itself change the course in relapsing-remitting multiple sclerosis. The effectiveness of disease-modifying drugs has reduced the transition from relapsing-remitting to secondary progressive multiple sclerosis. The concept of progressive multiple sclerosis has also evolved from two very distinct categories (primary progressive and secondary progressive multiple sclerosis) to a unified category of progressive multiple sclerosis, which can then be split into the categories of active or inactive. Also, an increasing tendency to treat progressive multiple sclerosis with disease-modifying therapies may have contributed to change the course in progressive multiple sclerosis. In conclusion, during the past decade the entire course of multiple sclerosis from the first sign of a demyelinating disorder through the progressive course appears to be milder due to a complex interplay of several factors.


2015 ◽  
Vol 7 (2) ◽  
Author(s):  
Nafiseh Mohebi ◽  
Mehdi Moghaddasi ◽  
Maryam Zaribafian

Neurofibromatosis type 1 (NF-1) is a common hereditary neuro-cutaneous disease, with known gene mutations, that mainly involves the skin and nervous system. Multiple sclerosis (MS) is an acquired inflammatory disease in which the myelin of nerve cells in the brain and spinal cord is damaged. These two disease do not share any apparent pathological similarities. We herein present a 32-year-old woman with definite NF-1, who has recently been diagnosed with MS, which to the best of our knowledge is a rare co-occurrence. Though there are often neurologic sign and symptoms in patients with NF-1, they should not always be considered as the natural history of the disease, and other overlapped pathologies should be kept in mind, in order to not miss or postpone the efficient treatment.


2012 ◽  
Vol 19 (7) ◽  
pp. 885-890 ◽  
Author(s):  
Rodica Bălaşa ◽  
Zoltan Bajko ◽  
Adina Huţanu

Background: Interleukin-17 (IL-17), which is secreted by Th17 cells, is a proinflammatory cytokine that is implicated in the pathogenesis of multiple sclerosis (MS) and plays a role in nonresponse of MS patients to interferon-β (IFN-β) therapy. Objectives: The purpose of this study was to establish a correlation between nonresponders (NR) and IL-17A serum titers and binding antibodies (BAbs) to IFN-β, as well as to find a correlation between IL-17A serum levels and other features of MS patients. Methods: Our prospective study included 72 inactive relapsing–remitting multiple sclerosis (RRMS) patients that had been treated for at least 18 months with IFN-β and 15 healthy subjects. We determined the serum levels of IL-17A and of BAbs. IL-17A levels were considered elevated (IL-17A+) if the recorded value was greater than 1.6 pg/ml. Results: Twenty-seven patients (37.5%) were NR and had a significantly higher serum IL-17A level compared to the responders group. Nineteen patients (26.4%) were IL-17A+ and had had a significantly higher number of relapses in the previous year and a higher Expanded Disability Status Score. The majority of IL-17A+ patients were NR and had a shorter MS duration. Conclusions: RRMS patients with high serum IL-17A levels do not respond well to IFN-β therapy and have shorter MS duration compared to patients with low IL-17A levels. This response is not influenced by the presence of BAbs.


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