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sp. hordei. In a barley transgenic line with a lower Lr34 expression level, a quantitative resistance against Puccinia hordei was still observed, but without a significant redistribution of abscisic acid or apparent leaf tip necrosis. Thus, our results imply that fine-tuning the Lr34 expression level is essential to balance disease resistance versus leaf tip necrosis to deploy transgenic Lr34 in breeding programs.The root phenotype is an important aspect of plant architecture and plays a critical role in plant facilitation of the extraction of water and nutrition from the soil. MicroRNAs (miRNAs) are classes of small RNAs with important roles in regulating endogenous gene expression at the post-transcriptional level that function in a range of plant development processes and in the response to abiotic stresses. However, little is known concerning the molecular mechanism of miRNAs in regulating the generation and development of plant root architecture. Herein, we demonstrated that potato miR160a/b acted as a critical regulator and affected plant root architecture by targeting the mRNA of StARF10 and StARF16 for cleavage. The miR160a/b precursor was cloned from potato. Quantitative PCR assays showed that the expression levels of miR160 and its targets were down- or up-regulated with the development of potato roots, respectively. Moreover, transgenic lines with suppressed stu-miR160 expression were established with the short tandem targets mimic (STTM), and the results showed that the ectopic expression of miR160a/b altered the levels of auxin and the expression of auxin signaling-related genes and caused drastic change in root architecture compared with that in control plants. Suppressing the expression of miR160 led to a severe reduction in root length, an increase in the number of lateral roots, and a decrease in fresh root weight in potato. Collectively, our data established a key role of miR160 in modulating plant root architecture in potato.Ocrelizumab and siponimod have a scientifically proven effect in progressive MS and decrease the risk of disability in the short-term. The primary endpoints in the pivotal trials of ocrelizumab and siponimod were reported as a hazard ratio of 3-month confirmed disability progression, which was reported to be 0.76-0.79. Based on this, both drugs were subsequently licensed for use in patients with progressive multiple sclerosis. Hazard ratios are not easily communicated to patients and therefore the alternative endpoint average postponement of disability was calculated with data from the pivotal trials. After two years of treatment, the average postponement of disability was 16 days per year with ocrelizumab and 19 days with siponimod. Over time, the average postponement of disability reached a plateau, when further treatment added little value. Taken together, these data suggest that these interventions have a short-lived and limited clinical effect in patients with progressive MS.Fatigue is the most common symptom and a leading cause of disability multiple sclerosis (MS). Despite the lack of evidence, several medications are frequently prescribed by physicians to ameliorate fatigue in patients with MS. However, a recent study demonstrated that improvement in fatigue severity with these medications appears to be due to placebo effect and is also is associated with more frequent adverse events than the placebo. These findings raise ethical concerns surrounding the initiation and discontinuation of these treatments for fatigue in MS. Starting these medications for the treatment of MS fatigue for their placebo effect may not be justified. However, stopping the medications in patients who report symptomatic benefits and have no side effects may also not be ethical. In MS care non-pharmacological approaches for fatigue treatment, such as exercise and cognitive behavioral therapy, should now be prioritized. Novel study designs may be necessary to address placebo response in future clinical trials evaluating interventions for fatigue in MS.

The present study aims to identify and analyze the characteristics of highly cited publications on Multiple sclerosis in the Science Citation Index Expanded.

Documents that had 100 citations or more were considered as the highly cited documents. Highly cited publications were analyzed in the distribution of document types, languages, publication years, Web of Science categories, and journals as well as publication performance of countries, institutions, and authors. The six and five publication indicators were applied to compare publications of the countries and the institutes respectively. selleck inhibitor Highly cited authors were analyzed by Y-index.

In general, articles spent about 12 years to be highly cited articles. The USA dominated the production by the six publication indicators. Harvard University was the most active in research on multiple sclerosis while the University of California, Los Angeles in the USA shows the most independent research. M. Filippi was recognized as the most productive author who had the most articles as the corresponding author.

The findings may be of interest to multiple sclerosis researchers and policymakers all around the world.

The findings may be of interest to multiple sclerosis researchers and policymakers all around the world.

Tight junction proteins contribute to maintenance of epithelial and endothelial barriers such as the intestinal barrier and the blood brain barrier (BBB). Increased permeability of these barriers has been linked to disease activity in MS and there is currently a lack of easily accessible biomarkers predicting disease activity in MS.

To investigate whether levels of circulating tight junction proteins occludin and zonula occludens-1 (ZO-1) are associated with biomarkers of inflammation and disease activity; and to determine whether they could serve as clinical biomarkers.

We prospectively included 72 newly diagnosed patients with relapsing remitting MS or clinically isolated syndrome with no prior disease modifying therapy (DMT) use and 50 healthy controls (HCs). Patients were followed with blood samples, 3tesla MRI, and clinical evaluation for 12 months. Occludin, ZO-1, calprotectin and soluble urokinase-type plasminogen activator receptor (suPAR) were measured by ELISA; serum neurofilament light (NfL) and IL-6 by single-molecule array (SIMOA).