Some poorly reported studies may in fact be well-designed and well-conducted, but analysis suggests that inadequate reporting correlates with overstated findings10 (link)–14 . Problems related to inadequate study design surfaced early in the stroke research community, as investigators tried to understand why multiple clinical trials based on positive results in animal studies ultimately failed. Part of the problem is, of course, that no animal model can fully reproduce all the features of human stroke. It also became clear, however, that many of the difficulties stemmed from a lack of methodological rigor in the preclinical studies that were not adequately reported15 (link). For instance, a systematic review and meta-analysis of studies testing the efficacy of the free-radical scavenger NXY-059 in models of ischaemic stroke revealed that publications that included information on randomization, concealment of group allocation, or blinded assessment of outcomes reported significantly smaller effect sizes of NXY-059 in comparison to studies lacking this information10 (link). In certain cases, a series of poorly designed studies, obscured by deficient reporting, may, in aggregate, serve erroneously as the scientific rationale for large, expensive and ultimately unsuccessful clinical trials. Such trials may unnecessarily expose patients to potentially harmful agents, prevent these patients from participating in other trials of possibly effective agents, and drain valuable resources and energy that might otherwise be more productively spent.
Multiple Sclerosis
Common symptoms include visual disturbances, muscle weakness, coordination and balance difficulties, sensory abnormalities, cognitive impairments, and mood changes.
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Most cited protocols related to «Multiple Sclerosis»
We define experience as “Patients’ reports of how care was organised and delivered to meet their needs p.301” [15 (link)]. Patients’ reports could refer to either experience of health care services delivery and organisation overall or their experiences of care by specific health care personnel. We included studies that investigated adults (aged 18 years old and older) with a diagnosis of Multiple Sclerosis, who had experience of utilising health care services at any time point. There were no restrictions on subtype of Multiple Sclerosis, gender, ethnicity or frequency of use of health care. Health care in this sense referred to routine clinical care (either state funded or privately funded) not trial protocols or interventions. Excluded studies included studies that focussed on self-management and studies that investigated quality of life.
Because of the focus on Multiple Sclerosis, studies were excluded if they used a mixed sample of various conditions (e.g. studies reported a mixed sample of people with neurological conditions) or if they used a sample of mixed respondents (i.e. people with Multiple Sclerosis and their carers) where results of patients with Multiple Sclerosis could not be clearly separated. If an article had a section or subtheme on health care services but this was not the main research area of the article, then that article was included; however only data from the relevant subtheme were extracted and included in the findings. Additional exclusion criteria were articles that only described carer or health care professional experiences not patient experiences. Conference abstracts, editorials and commentaries were not included.
The study population consisted of the first ∼6000 European–Americans accrued into BioVU. The only selection criteria were that they met the general conditions for eligibility for BioVU; no clinical inclusion or exclusion criteria were applied. In the current analysis, we selected five SNPs with previously known disease associations: rs1333049 [coronary artery disease (CAD) and carotid artery stenosis (CAS)], rs2200733 [atrial fibrillation (AF)], rs3135388 [multiple sclerosis (MS) and systemic lupus erythematosus (SLE)], rs6457620 [rheumatoid arthritis (RA)], and rs17234657 [Crohn's disease (CD)]. (Some other potential associations exist for some SNPs, such as progression of carotid atherosclerosis and rs1333049, but are not represented well through ICD9 codes.) The primary outcome of this study was identification of the prior statistical associations with MS, CD, AF, CAD, SLE, CAS and RA.
Genotyping was conducted by the Vanderbilt DNA Resources Core using the mid-throughput Sequenom® genotyping platform (rs1333049, rs3135388 and rs17234657; genotyping efficiency 98.4–100%), which is based on a single base primer extension reaction coupled with mass spectrometry, or using a TaqMan assay (rs6457620 and rs2200733; genotyping efficiency 99.4% and 99.0%, respectively). Quality control procedures included examination of marker and sample genotyping efficiency, allele frequency calculations and tests of Hardy–Weinberg equilibrium.
Most recents protocols related to «Multiple Sclerosis»
Example 6
This example provides a showing of an effect of disclosed anti-PD-L1 antibodies on the progression of disease in a murine model of multiple sclerosis (MS). Anti-PD-L1 antibodies were assayed for their ability to modulate the course of disease in mice induced to develop experimental autoimmune encephalitis (EAE) as a model of MS. Disease was induced in C57Bl/6 mice following injection of myelin oligodendrocyte glycoprotein (MOG) peptide and pertussis toxin. Once symptoms of disease developed, the mice were treated every second day with an intraperitoneal injection of anti-PD-L1 antibody (0.1 mg). The results shown in
Example 3
Alternatively or in addition to all of the foregoing as it relates to gray matter, the invention further contemplates that white matter fA (fractional anisotropy) can be employed in a manner analogous to the gray matter atrophy as discussed herein in various embodiments.
Diffusion Tensor Imaging (DTI) assesses white matter, specifically white matter tract integrity. A decrease in fA can occur with either demyelination or with axonal damage or both. One can assess white matter substructures including optic nerve and cervical spinal cord.
MRIs of brain including high cervical spinal cord to be done at month 6, 1 year, and 2 years. If a decrease in fA of 10% is observed in fA of 2 tracts, treat with estriol to halt this decrease. Alternatively if fA is decreased by 10% in only one tract but that tract is associated with clinical deterioration of the disability served by that tract, treat with estriol. Poorer scores in low contrast visual acuity would correlate with decreased fA of optic nerve, while poorer motor function would correlate with decreased fA in motor tracts in cervical spinal cord.
Similarly, to analyse differences between sleep groups and concurrent amyloid burden, we examined data from the subset that had completed at least one PiB PET study [n(%) = 108 (17.4%)]. Kruskal–Wallis tests were used to assess the difference between sleep groups in estimated concurrent global PiB DVR and amyloid chronicity, and Fisher’s exact test was used to analyse the concurrent amyloid PET status difference between sleep groups. In sensitivity analyses, we tested whether there was significant difference of amyloid burden at the most recent PET scan across the alternative sleep group assignments. In the imputed data set, 285 (23.0%) had at least one PiB PET scan, and we tested the difference in estimated concurrent and most recent global PiB DVR and amyloid chronicity among sleep groups.
We compared corrected Akaike information criteria (AICc) model fit statistics across otherwise identical models and considered |ΔAICc| values <2 to represent comparable models. Linear regression was performed for the association between sleep groups and concurrent cognitive composite scores after we removed stroke (n = 10), epilepsy/seizures (n = 13), multiple sclerosis (n = 5) and Parkinson’s disease (n = 2). Since APOE genotype associates with cognition, additional linear regression was performed including APOE e4 carriers in the model, and we compared model fits with the fits of the model in Aim 2 with the participants who have APOE data (n = 538). ΔAICc values were reported.
The timing of vaccinations followed the guidelines set by the EMA and the protocol set by the Ministry of Health in Cyprus, where the second dose was administered 3 weeks after the initial dose of BNT162b2 and the booster dose administered 3 months after the second dose. Blood samples were collected from all volunteers 3 months after the second vaccination dose. Reviewing preliminary results warranted additional analysis from a select MS group, as such MS volunteers receiving fingolimod were asked to return for another blood sample at least 2 weeks after receiving the booster dose. Note that due to the volunteering nature of the study, some volunteers were not willing to further donate blood. Additionally, due to volunteers getting infected with SARS-CoV-2 during the time between vaccination doses, a follow-up sample was not suitable for the purpose of the study.
Blood samples were collected in tubes containing clotting activators at the COVID-19 sampling unit of The Cyprus Institute of Neurology and Genetics. Following blood collection, samples were centrifuged for 10 min at 500 × g at 20°C to obtain cell-free serum. Serum was stored at −20°C until analysis.
We recruited 50 healthy older adults (14 male, 36 female) aged 50–80 years with stable health as the control group. People with any comorbid neurological, cardiovascular, or musculoskeletal disease that might affect the assessment were excluded.
The 15-item UEFI has demonstrated excellent test–retest reliability (ICC2, 1 = 0.95) in people with upper extremity musculoskeletal disorders (19 (link)). However, its reliability in people with stroke has not been evaluated. Assuming that an ICC value for assessing test–retest reliability of the 15-item UEFI in people with stroke was 0.9, a sample size of ≥46 subjects was required to achieve 80% power to detect an ICC of 0.9 with a null hypothesis ICC of 0.8 and a significance level of 0.05. To evaluate the ability of the C-UEFI to discern differences between different groups, ≥50 people with chronic stroke and ≥50 healthy controls were required with a CA0 value of 0.3 and CA1 value of 0.7 (28 (link)). A sample of >100 people with chronic stroke were regarded as reasonable based on the exploratory factor analysis (EFA) estimation (29 (link)). Thus, 101 people with stroke were recruited for this study.
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More about "Multiple Sclerosis"
This condition is associated with a variety of symptoms, including visual disturbances, muscle weakness, coordination and balance difficulties, sensory abnormalities, cognitive impairments, and mood changes.
The pathogenesis of MS involves an aberrant immune response that targets the myelin sheath, the protective layer surrounding nerve fibers.
This results in the formation of scarred or hardened (sclerotic) areas, which disrupt the efficient transmission of electrical signals within the CNS, leading to the characteristic symptoms.
Advances in research and diagnostic tools have significantly improved our understanding of MS.
Techniques like GraphPad Prism 7, a powerful data analysis and graphing software, have enabled researchers to visualize and interpret complex datasets related to MS pathology and disease progression.
Additionally, the use of specialized columns, such as the Superdex 200 HR 10/30, has facilitated the purification and analysis of proteins involved in the disease process.
Genetic and molecular profiling have also played a crucial role in MS research.
The SAS version 9.4 software has been utilized to conduct statistical analyses of genetic and genomic data, while the Mouse Multiple Sclerosis RT2 Profiler PCR Array has enabled the investigation of gene expression patterns associated with the disease.
The HumanRef-8 v3.0 expression beadchip, a microarray platform, has also been employed to study the transcriptional changes in human MS samples.
Immunological aspects of MS have been extensively explored, with tools like Protein G Sepharose, a resin for purifying immunoglobulins, and Incomplete Freund's adjuvant, an immunostimulant, playing key roles in experimental models and therapeutic development.
The ISelect HD, a custom genotyping array, has been utilized to identify genetic variants associated with MS susceptibility.
To streamline and optimize MS research, innovative platforms like PubCompare.ai have emerged.
This AI-driven tool leverages the power of machine learning to help researchers locate the best protocols, products, and experimental approaches from the vast body of scientific literature, preprints, and patents.
By utilizing the QuickCalcs software, researchers can quickly perform statistical analyses and compare the performance of different protocols, ultimately enhancing the efficiency and impact of their MS studies.
In summary, the field of Multiple Sclerosis research has seen significant advancements, with the integration of cutting-edge tools and technologies.
By harnessing the power of these resources, researchers can gain deeper insights into the pathogenesis, diagnosis, and treatment of this complex neurological disorder, ultimately improving the quality of life for individuals living with MS.