List all articles in the database by earliest discovery_date

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{
    "count": 24383,
    "next": "http://api.gregory-ms.com/articles/?format=api&page=1428",
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    "results": [
        {
            "article_id": 381986,
            "title": "Piet Mondrian’s trees and the evolution in understanding multiple sclerosis, Charcot Prize Lecture 2011",
            "summary": "<jats:p> Four questions were posed about multiple sclerosis (MS) at the 2011 Charcot Lecture, Oct. 22, 2011. 1. The Male/Female Disparity: Why are women developing MS so much more frequently than men? 2. Neuronal and Glial Protection: Are there guardian molecules that protect the nervous system in MS? 3. Predictive Medicine: With all the approved drugs, how can we rationally decide which one to use? 4. The Precise Scalpel vs. the Big Hammer for Therapy: Is antigen-specific therapy for demyelinating disease possible? To emphasize how our views on the pathogenesis and treatment of MS are evolving, and given the location of the talk in Amsterdam, Piet Mondrian’s progressive interpretations of trees serve as a heuristic. </jats:p>",
            "link": "https://journals.sagepub.com/doi/full/10.1177/1352458512461391",
            "published_date": "2013-01-01T00:00:00Z",
            "source": "SAGE Publications",
            "publisher": "SAGE Publications",
            "container_title": "Multiple Sclerosis Journal",
            "authors": [
                {
                    "author_id": 165992,
                    "given_name": "Lawrence",
                    "family_name": "Steinman",
                    "ORCID": "http://orcid.org/0000-0002-2437-2250",
                    "country": null
                },
                {
                    "author_id": 300624,
                    "given_name": "Robert C",
                    "family_name": "Axtell",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 300625,
                    "given_name": "Donald",
                    "family_name": "Barbieri",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 300626,
                    "given_name": "Roopa",
                    "family_name": "Bhat",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 300627,
                    "given_name": "Sara E",
                    "family_name": "Brownell",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 268453,
                    "given_name": "Brigit A",
                    "family_name": "de Jong",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 296616,
                    "given_name": "Shannon E",
                    "family_name": "Dunn",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 300628,
                    "given_name": "Jacqueline L",
                    "family_name": "Grant",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 300629,
                    "given_name": "May H",
                    "family_name": "Han",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 300630,
                    "given_name": "Peggy P",
                    "family_name": "Ho",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 300631,
                    "given_name": "Hedwich F",
                    "family_name": "Kuipers",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 300632,
                    "given_name": "Michael P",
                    "family_name": "Kurnellas",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 277199,
                    "given_name": "Shalina S",
                    "family_name": "Ousman",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 277197,
                    "given_name": "Jonathan B",
                    "family_name": "Rothbard",
                    "ORCID": null,
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2022-05-31T16:16:47.188873Z",
            "noun_phrases": [
                "Piet Mondrian’s trees",
                "the evolution",
                "multiple sclerosis",
                "Charcot Prize Lecture"
            ],
            "doi": "10.1177/1352458512470730",
            "access": "restricted",
            "takeaways": " Four questions were posed about multiple sclerosis (MS) at the 2011 Charcot Lecture, Oct. 22, 2011 . The Male/Female Disparity: Why are women developing MS so much more frequently than men? Neuronal and Glial Protection: Are there",
            "categories": []
        },
        {
            "article_id": 381195,
            "title": "The most frequently asked question to a statistician: The sample size",
            "summary": "<jats:p> The calculation of the sample size needed for a clinical study is the challenge most frequently put to statisticians, and it is one of the most relevant issues in the study design. The correct size of the study sample optimizes the number of patients needed to get the result, that is, to detect the minimum treatment effect that is clinically relevant. Minimizing the sample size of a study has the advantage of reducing costs, enhancing feasibility, and also has ethical implications. In this brief report, I will explore the main concepts on which the sample size calculation is based. </jats:p>",
            "link": "http://journals.sagepub.com/doi/pdf/10.1177/1352458517695471",
            "published_date": "2017-02-01T00:00:00Z",
            "source": "SAGE Publications",
            "publisher": "SAGE Publications",
            "container_title": "Multiple Sclerosis Journal",
            "authors": [
                {
                    "author_id": 149329,
                    "given_name": "Maria Pia",
                    "family_name": "Sormani",
                    "ORCID": "http://orcid.org/0000-0001-6892-104X",
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2022-05-31T16:16:47.188873Z",
            "noun_phrases": [
                "The",
                "question",
                "a statistician"
            ],
            "doi": "10.1177/1352458517695471",
            "access": "restricted",
            "takeaways": " The correct size of the study sample optimizes the number of patients needed to get the result . Minimizing the sample size of a study has the advantage of reducing costs, enhancing feasibility, and also has ethical implications .",
            "categories": []
        },
        {
            "article_id": 382027,
            "title": "Corticospinal output during muscular fatigue differs in multiple sclerosis patients compared to healthy controls",
            "summary": "<jats:sec><jats:title>Background:</jats:title><jats:p> In multiple sclerosis (MS), fatigue is a common and often disabling symptom. It has multiple causes with central motor fatigue playing an important role. </jats:p></jats:sec><jats:sec><jats:title>Objective:</jats:title><jats:p> The objective of this study was to analyse the central motor conduction changes in relation to muscle contraction force during muscle fatigue and recovery in MS patients compared to healthy controls. </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> A total of 23 MS patients with fatigue and 13 healthy subjects were assessed during 2 minutes of fatiguing exercise of the abductor digiti minimi muscle of the hand and the subsequent 7 minutes of recovery. Central motor conduction was quantified by transcranial magnetic stimulation using the triple stimulation protocol and calculating a central conduction index (CCI). </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> Force declined to 36% of the pre-exercise level (SD 16%; p &lt; 0.01) in MS patients and to 44% (SD 9%, p &lt; 0.01) in healthy subjects (group differences, not statistically significant). The decline of the CCI was significantly less marked in patients (–20%, SD 26%, p &lt; 0.05) than in healthy subjects (–57%, SD 15%, p &lt; 0.05; group differences, p &lt; 0.05). The decline of force and CCI were not correlated in either group. </jats:p></jats:sec><jats:sec><jats:title>Conclusions:</jats:title><jats:p> During a fatiguing exercise, the decline in central motor conduction is significantly less pronounced in MS patients than healthy subjects, although the reduction of force is similar. </jats:p></jats:sec>",
            "link": "https://journals.sagepub.com/doi/full/10.1177/1352458512461391",
            "published_date": "2012-02-21T00:00:00Z",
            "source": "SAGE Publications",
            "publisher": "SAGE Publications",
            "container_title": "Multiple Sclerosis Journal",
            "authors": [
                {
                    "author_id": 295770,
                    "given_name": "O",
                    "family_name": "Scheidegger",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 295771,
                    "given_name": "CP",
                    "family_name": "Kamm",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 295772,
                    "given_name": "SJ",
                    "family_name": "Humpert",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 295773,
                    "given_name": "KM",
                    "family_name": "Rösler",
                    "ORCID": null,
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2022-05-31T16:16:47.188873Z",
            "noun_phrases": [
                "Corticospinal output",
                "muscular fatigue",
                "multiple sclerosis patients",
                "healthy controls"
            ],
            "doi": "10.1177/1352458512438722",
            "access": "restricted",
            "takeaways": " Multiple sclerosis (MS) has multiple causes with central motor fatigue playing an important role . During a fatiguing exercise, the decline in central motor conduction is significantly less pronounced in MS patients than healthy subjects, although the reduction of force is similar .",
            "categories": []
        },
        {
            "article_id": 381418,
            "title": "Corticospinal tract integrity is related to primary motor cortex thinning in relapsing–remitting multiple sclerosis",
            "summary": "<jats:sec><jats:title>Background:</jats:title><jats:p> The relationship between white matter injury and cortical atrophy development in relapsing–remitting multiple sclerosis (RRMS) remains unclear. </jats:p></jats:sec><jats:sec><jats:title>Objectives:</jats:title><jats:p> To investigate the associations between corticospinal tract integrity and cortical morphology measures of the primary motor cortex in RRMS patients and healthy controls. </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> 51 RRMS patients and 30 healthy controls underwent MRI examination for cortical reconstruction and assessment of corticospinal tract integrity. Partial correlation and multiple linear regression analyses were used to investigate the associations of focal and normal appearing white matter (NAWM) injury of the corticospinal tract with thickness and surface area measures of the primary motor cortex. Relationships between MRI measures and clinical disability as assessed by the Expanded Disability Status Scale and disease duration were also investigated. </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> In patients only, decreased cortical thickness was related to increased corticospinal tract NAWM mean, axial and radial diffusivities in addition to corticospinal tract lesion volume. The final multiple linear regression model for PMC thickness retained only NAWM axial diffusivity as a significant predictor (adjusted R<jats:sup>2</jats:sup>= 0.270, p= 0.001). Clinical measures were associated with NAWM corticospinal tract integrity measures. </jats:p></jats:sec><jats:sec><jats:title>Conclusions:</jats:title><jats:p> Primary motor cortex thinning in RRMS is related to alterations in connected white matter and is best explained by decreased NAWM integrity. </jats:p></jats:sec>",
            "link": "http://journals.sagepub.com/doi/pdf/10.1177/1352458515576985",
            "published_date": "2015-03-19T00:00:00Z",
            "source": "SAGE Publications",
            "publisher": "SAGE Publications",
            "container_title": "Multiple Sclerosis Journal",
            "authors": [
                {
                    "author_id": 143256,
                    "given_name": "Niels",
                    "family_name": "Bergsland",
                    "ORCID": "http://orcid.org/0000-0002-7792-0433",
                    "country": null
                },
                {
                    "author_id": 215351,
                    "given_name": "Maria Marcella",
                    "family_name": "Laganà",
                    "ORCID": "http://orcid.org/0000-0001-7848-1711",
                    "country": "IT"
                },
                {
                    "author_id": 222744,
                    "given_name": "Eleonora",
                    "family_name": "Tavazzi",
                    "ORCID": "http://orcid.org/0000-0003-2580-3646",
                    "country": null
                },
                {
                    "author_id": 302429,
                    "given_name": "Matteo",
                    "family_name": "Caffini",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 256762,
                    "given_name": "Paola",
                    "family_name": "Tortorella",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 167196,
                    "given_name": "Francesca",
                    "family_name": "Baglio",
                    "ORCID": "http://orcid.org/0000-0002-6145-5274",
                    "country": null
                },
                {
                    "author_id": 302430,
                    "given_name": "Giuseppe",
                    "family_name": "Baselli",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 152733,
                    "given_name": "Marco",
                    "family_name": "Rovaris",
                    "ORCID": "http://orcid.org/0000-0001-9691-1957",
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2022-05-31T16:16:47.188873Z",
            "noun_phrases": [
                "Corticospinal tract integrity",
                "primary motor cortex thinning",
                "multiple sclerosis"
            ],
            "doi": "10.1177/1352458515576985",
            "access": "restricted",
            "takeaways": " The relationship between white matter injury and cortical atrophy development in relapsing–remitting multiple sclerosis remains unclear . 51 RRMS patients and 30 healthy controls underwent MRI examination for cortical reconstruction and assessment of corticospinal tract integrity .",
            "categories": []
        },
        {
            "article_id": 381728,
            "title": "Daclizumab reduces CD25 levels on T cells through monocyte-mediated trogocytosis",
            "summary": "<jats:p> Daclizumab is a humanized monoclonal antibody that prevents interleukin-2 (IL-2) binding to CD25, blocking IL-2 signaling by cells that require high-affinity IL-2 receptors to mediate IL-2 signaling. The phase 2a CHOICE study evaluating daclizumab as a treatment for multiple sclerosis (MS) included longitudinal analysis of activated T cell counts. Whereas an exposure-dependent relationship was observed between daclizumab and reductions in HLA-DR<jats:sup>+</jats:sup>-activated T cells, a similar relationship was not observed for reductions in CD25 levels. The objective of this report is to determine the mechanism by which daclizumab reduces CD25 levels on peripheral blood mononuclear cells (PBMCs) using cytometric techniques. Daclizumab reduced T cell CD25 levels through a mechanism that required the daclizumab-Fc domain interaction with Fc receptors (FcR) on monocytes, but not on natural killer (NK) cells, and was unrelated to internalization or cell killing. Activated CD4<jats:sup>+</jats:sup> T cells and FoxP3<jats:sup>+</jats:sup> Treg cells showed evidence of trogocytosis of the CD25 antigen in the presence of monocytes. A daclizumab variant that retained affinity for CD25 but lacked FcR binding did not induce trogocytosis and was significantly less potent as an inhibitor of IL-2-induced proliferation of PBMCs. In conclusion, Daclizumab-induced monocyte-mediated trogocytosis of CD25 from T cells appears to be an additional mechanism contributing to daclizumab inhibition of IL-2 signaling. </jats:p>",
            "link": "https://journals.sagepub.com/doi/full/10.1177/1352458513519180",
            "published_date": "2013-07-11T00:00:00Z",
            "source": "SAGE Publications",
            "publisher": "SAGE Publications",
            "container_title": "Multiple Sclerosis Journal",
            "authors": [
                {
                    "author_id": 285623,
                    "given_name": "Y",
                    "family_name": "Zhang",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 285624,
                    "given_name": "M",
                    "family_name": "McClellan",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 285625,
                    "given_name": "L",
                    "family_name": "Efros",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 285626,
                    "given_name": "D",
                    "family_name": "Shi",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 285628,
                    "given_name": "B",
                    "family_name": "Bielekova",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 285630,
                    "given_name": "MT",
                    "family_name": "Tang",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 285632,
                    "given_name": "V",
                    "family_name": "Vexler",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 285633,
                    "given_name": "JP",
                    "family_name": "Sheridan",
                    "ORCID": null,
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2022-05-31T16:16:47.188873Z",
            "noun_phrases": [
                "Daclizumab",
                "CD25 levels",
                "T cells",
                "monocyte-mediated trogocytosis"
            ],
            "doi": "10.1177/1352458513494488",
            "access": "open",
            "takeaways": " Daclizumab is a humanized monoclonal antibody that prevents interleukin-2 (IL-2) binding to CD25, blocking IL-2 signaling . The objective of this report is to determine the mechanism by which daclizmab reduces CD25 levels on peripheral blood mononuclear cells (PBMCs) using cytometric techniques .",
            "categories": []
        },
        {
            "article_id": 382081,
            "title": "The role of mitochondria in axonal degeneration and tissue repair in MS",
            "summary": "<jats:p> Axonal injury is a key feature of multiple sclerosis (MS) pathology and is currently seen as the main correlate for permanent clinical disability. Although little is known about the pathogenetic mechanisms that drive axonal damage and loss, there is accumulating evidence highlighting the central role of mitochondrial dysfunction in axonal degeneration and associated neurodegeneration. The aim of this topical review is to provide a concise overview on the involvement of mitochondrial dysfunction in axonal damage and destruction in MS. Hereto, we will discuss putative pathological mechanisms leading to mitochondrial dysfunction and recent imaging studies performed in vivo in patients with MS. Moreover, we will focus on molecular mechanisms and novel imaging studies that address the role of mitochondrial metabolism in tissue repair. Finally, we will briefly review therapeutic strategies aimed at improving mitochondrial metabolism and function under neuroinflammatory conditions. </jats:p>",
            "link": "https://journals.sagepub.com/doi/full/10.1177/1352458512440349",
            "published_date": "2012-06-21T00:00:00Z",
            "source": "SAGE Publications",
            "publisher": "SAGE Publications",
            "container_title": "Multiple Sclerosis Journal",
            "authors": [
                {
                    "author_id": 245519,
                    "given_name": "J",
                    "family_name": "van Horssen",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 245521,
                    "given_name": "ME",
                    "family_name": "Witte",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 245523,
                    "given_name": "O",
                    "family_name": "Ciccarelli",
                    "ORCID": null,
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2022-05-31T16:16:47.188873Z",
            "noun_phrases": [
                "The role",
                "mitochondria",
                "axonal degeneration",
                "tissue repair",
                "MS"
            ],
            "doi": "10.1177/1352458512452924",
            "access": "restricted",
            "takeaways": " Axonal injury is a key feature of multiple sclerosis (MS) pathology . Little is known about the pathogenetic mechanisms that drive axonal damage and loss . There is accumulating evidence highlighting the central role of mitochondrial dysfunction in axonal degeneration and associated neurodegeneration .",
            "categories": []
        },
        {
            "article_id": 380969,
            "title": "A contemporary profile of primary progressive multiple sclerosis participants from the NARCOMS Registry",
            "summary": "<jats:sec><jats:title>Background:</jats:title><jats:p> Primary progressive multiple sclerosis (PPMS) represents 10%–15% of all multiple sclerosis (MS) diagnoses. Information regarding socio-demographic and clinical characteristics of persons with PPMS is limited. </jats:p></jats:sec><jats:sec><jats:title>Objective:</jats:title><jats:p> To characterize persons with PPMS in the North American Research Committee on Multiple Sclerosis (NARCOMS) Registry. </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> We compared demographic and health-related characteristics of NARCOMS Registry participants reporting PPMS in the spring 2015 update survey with those reporting relapsing-remitting multiple sclerosis (RRMS) and secondary progressive multiple sclerosis (SPMS), with characteristics of published PPMS cohorts. </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> Of 8004 responders, 6774 self-reported a clinical course of PPMS, SPMS, or RRMS. The PPMS cohort ( n = 632, 9.3%) reported a mean (standard deviation (SD)) age of 64.3 (8.9) years; 62.7% were female; the SPMS and RRMS cohorts were younger and had a higher proportion of females. The NARCOMS PPMS cohort differed in age, time from onset and diagnosis, and proportion of females compared to population-based and clinical trial cohorts. Median (25%, 75%) number of comorbidities was 2 (1, 2) for each cohort with vascular comorbidities being most frequently reported. </jats:p></jats:sec><jats:sec><jats:title>Conclusion:</jats:title><jats:p> The NARCOMS population provides a different perspective on persons with PPMS than clinical trials. A better understanding of the characteristics of persons with PPMS may help address unmet needs in this population. </jats:p></jats:sec>",
            "link": "http://journals.sagepub.com/doi/pdf/10.1177/1352458517711274",
            "published_date": "2017-05-19T00:00:00Z",
            "source": "SAGE Publications",
            "publisher": "SAGE Publications",
            "container_title": "Multiple Sclerosis Journal",
            "authors": [
                {
                    "author_id": 147498,
                    "given_name": "Amber",
                    "family_name": "Salter",
                    "ORCID": "http://orcid.org/0000-0002-1088-110X",
                    "country": "US"
                },
                {
                    "author_id": 308994,
                    "given_name": "Nina P",
                    "family_name": "Thomas",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 205363,
                    "given_name": "Tuula",
                    "family_name": "Tyry",
                    "ORCID": "http://orcid.org/0000-0002-9282-3455",
                    "country": null
                },
                {
                    "author_id": 246840,
                    "given_name": "Gary R",
                    "family_name": "Cutter",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 159118,
                    "given_name": "Ruth Ann",
                    "family_name": "Marrie",
                    "ORCID": "http://orcid.org/0000-0002-1855-5595",
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2022-05-31T16:16:47.188873Z",
            "noun_phrases": [
                "A contemporary profile",
                "primary progressive multiple sclerosis participants",
                "the NARCOMS Registry"
            ],
            "doi": "10.1177/1352458517711274",
            "access": "restricted",
            "takeaways": " Primary progressive multiple sclerosis (PPMS) represents 10%–15% of all multiple sclerosis diagnoses . A better understanding of the characteristics of persons with PPMS may help address unmet needs in this population .",
            "categories": []
        },
        {
            "article_id": 382033,
            "title": "Cognitive impairment is associated with reduced bone mass in multiple sclerosis",
            "summary": "<jats:p>Background: Multiple sclerosis (MS) has been associated with reduced bone mineral density (BMD), yet the underlying causes are not fully known. The recent discovery that bone homeostasis is directly regulated by the brain led us to hypothesize that it may be impaired by MS pathology. As cognitive impairment (CI) is a well-documented correlate of MS-related brain pathology, we tested the hypothesis that it is associated with reduced BMD.</jats:p><jats:p>Objective: We aimed to determine if CI is associated with reduced BMD in patients with MS.</jats:p><jats:p>Methods: We retrospectively studied the medical records of 56 patients with MS, ≤50 years old, with Expanded Disability Status Scale score ≤4.5 and with dual X-ray absorptiometry (DEXA) BMD measurement within 1 year of neuropsychological testing with a standard battery (MACFIMS).</jats:p><jats:p>Results: In total, 23 (41.1%) MS patients had osteopenia or osteoporosis. Mean femur BMD was significantly lower in patients with MS with CI (0.89±0.12 g/cm<jats:sup>2</jats:sup>) compared with intact patients (0.99±0.17 g/cm<jats:sup>2</jats:sup>, p=0.009). In the cognitively impaired group, 59.3% had either osteopenia or osteoporosis, compared with 24.1% in the non-cognitively impaired group (odds ratio=4.57, p=0.008).</jats:p><jats:p>Conclusion: CI is associated with reduced BMD in patients with MS, suggesting that central mechanisms involved in bone homeostasis may be directly impaired by MS-related inflammatory and neurodegenerative processes.</jats:p>",
            "link": "https://journals.sagepub.com/doi/full/10.1177/1352458512461391",
            "published_date": "2012-03-14T00:00:00Z",
            "source": "SAGE Publications",
            "publisher": "SAGE Publications",
            "container_title": "Multiple Sclerosis Journal",
            "authors": [
                {
                    "author_id": 277318,
                    "given_name": "Sonia",
                    "family_name": "Batista",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 276968,
                    "given_name": "Barbara",
                    "family_name": "Teter",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 277319,
                    "given_name": "Karen",
                    "family_name": "Sequeira",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 277320,
                    "given_name": "Sowmya",
                    "family_name": "Josyula",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 277321,
                    "given_name": "Marietta",
                    "family_name": "Hoogs",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 237074,
                    "given_name": "Ralph HB",
                    "family_name": "Benedict",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 152480,
                    "given_name": "Bianca",
                    "family_name": "Weinstock-Guttman",
                    "ORCID": "http://orcid.org/0000-0001-6732-151X",
                    "country": null
                },
                {
                    "author_id": 332013,
                    "given_name": "Murali",
                    "family_name": "Ramanathan",
                    "ORCID": "http://orcid.org/0000-0002-9943-150X",
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2022-05-31T16:16:47.188873Z",
            "noun_phrases": [
                "Cognitive impairment",
                "reduced bone mass",
                "multiple sclerosis"
            ],
            "doi": "10.1177/1352458512440206",
            "access": "restricted",
            "takeaways": " Multiple sclerosis (MS) has been associated with reduced bone mineral density . Recent discovery that bone homeostasis is directly regulated by the brain led us to hypothesize that it may be impaired by MS pathology . Cognitive impairment (CI) is a well-documented correlate of MS-related brain pathology .",
            "categories": []
        },
        {
            "article_id": 380858,
            "title": "Commentary on Al Hussona et al. ‘New-onset seizures as a sole clinical presentation of multiple sclerosis’",
            "summary": "<jats:p> Despite the now significant contribution of magnetic resonance imaging, the accurate and timely diagnosis of multiple sclerosis (MS) is still clinically challenging. Al Hussona et al., with their case series, highlight the complexities of attributing paroxysmal, and in particular cortical, symptoms such as epileptic seizures to inflammatory demyelinating lesions, and establishing a diagnosis of MS based on them. In such circumstances an MS diagnosis is likely to be more tentative than for more typical MS presentations, and treatment choices should be weighed accordingly. </jats:p>",
            "link": "http://journals.sagepub.com/doi/pdf/10.1177/1352458518781978",
            "published_date": "2018-06-19T00:00:00Z",
            "source": "SAGE Publications",
            "publisher": "SAGE Publications",
            "container_title": "Multiple Sclerosis Journal",
            "authors": [
                {
                    "author_id": 150000,
                    "given_name": "Declan",
                    "family_name": "Chard",
                    "ORCID": "http://orcid.org/0000-0003-3076-2682",
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2022-05-31T16:16:47.188873Z",
            "noun_phrases": [
                "Commentary",
                "Al Hussona",
                "et al",
                "‘New-onset seizures",
                "a sole clinical presentation",
                "multiple sclerosis"
            ],
            "doi": "10.1177/1352458518781978",
            "access": "open",
            "takeaways": " Al Hussona et al. highlight the complexities of attributing paroxysmal, and in particular cortical, cortical, symptoms to inflammatory demyelinating lesions . In such circumstances an MS",
            "categories": []
        },
        {
            "article_id": 382075,
            "title": "Subcutaneous administration of alemtuzumab in patients with highly active multiple sclerosis",
            "summary": "<jats:p> Alemtuzumab is an anti-CD52 monoclonal antibody with remarkable efficacy in relapsing multiple sclerosis (MS). In clinical trials and off-label use in MS, alemtuzumab has been administered intravenously (IV). Alemtuzumab is approved for chronic lymphoid leukemia as IV. Oncology guidelines recommend alemtuzumab subcutaneous (SC) over IV. There is no report of alemtuzumab SC in MS. We report two patients with highly active relapsing MS who were treated with SC alemtuzumab, had significant improvement and tolerated SC alemtuzumab well without the typical infusion-associated adverse events. SC alemtuzumab in MS warrants further studies as this may enhance patient convenience and minimize infusion-associated adverse events. </jats:p>",
            "link": "https://journals.sagepub.com/doi/full/10.1177/1352458512440349",
            "published_date": "2012-01-17T00:00:00Z",
            "source": "SAGE Publications",
            "publisher": "SAGE Publications",
            "container_title": "Multiple Sclerosis Journal",
            "authors": [
                {
                    "author_id": 297831,
                    "given_name": "Jai S",
                    "family_name": "Perumal",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 297832,
                    "given_name": "Farng",
                    "family_name": "Foo",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 297833,
                    "given_name": "Perry",
                    "family_name": "Cook",
                    "ORCID": null,
                    "country": null
                },
                {
                    "author_id": 244105,
                    "given_name": "Omar",
                    "family_name": "Khan",
                    "ORCID": null,
                    "country": null
                }
            ],
            "relevant": null,
            "ml_prediction_gnb": false,
            "ml_prediction_lr": false,
            "ml_prediction_lsvc": false,
            "discovery_date": "2022-05-31T16:16:47.188873Z",
            "noun_phrases": [
                "Subcutaneous administration",
                "alemtuzumab",
                "patients",
                "highly active multiple sclerosis"
            ],
            "doi": "10.1177/1352458511435716",
            "access": "restricted",
            "takeaways": " Alemtuzumab is an anti-CD52 monoclonal antibody with remarkable efficacy in relapsing multiple sclerosis . In clinical trials and off-label use in MS has been administered intravenously (IV), alemt",
            "categories": [
                {
                    "category_id": 2,
                    "category_description": "LEMTRADA, or Alemtuzumab, is a prescription medicine used to treat relapsing forms of multiple sclerosis (MS), to include relapsing-remitting disease and active secondary progressive disease, in adults. Since treatment with LEMTRADA can increase your risk of getting certain conditions and diseases, LEMTRADA is generally prescribed for people who have tried 2 or more MS medicines that have not worked well enough. LEMTRADA is not recommended for use in patients with clinically isolated syndrome (CIS). It is not known if LEMTRADA is safe and effective for use in children under 17 years of age.\n\nhttps://www.lemtrada.com/",
                    "category_name": "Alemtuzumab",
                    "category_slug": "alemtuzumab",
                    "category_terms": [
                        "alemtuzumab",
                        "lemtrada"
                    ],
                    "article_count": 114
                }
            ]
        }
    ]
}