Kirkebynoer5767

Omega-3 fatty acids reduced SLE activity [SMD -0.33 (95CI -0.57, -0.09), low certainty evidence, moderate effect size]. Transforming the SMD to the SLE Disease Activity Index (SLEDAI) scale, omega-3 fatty acids reduced disease activity by 0.9 (95CI -1.6, -0.3, I

 = 0%) SLEDAI points compared to placebo.

This meta-analysis suggests that omega-3 fatty acids could provide therapeutic benefit in addition to immunosuppressive regimens used for SLE.

This meta-analysis suggests that omega-3 fatty acids could provide therapeutic benefit in addition to immunosuppressive regimens used for SLE.

Polymyalgia rheumatica (PMR) is a common musculoskeletal inflammatory disease that may occur with giant-cell arteritis (GCA) or in an isolated form. While the incidence is highest in the elderly, there is a paucity of data on its presentation, clinical course and response to treatment in younger individuals.

We conducted a retrospective review of 40 patients who were diagnosed with isolated PMR under the age of 60 and 178 patients diagnosed above this age, taking into account clinical and laboratory data and treatment history.

Patients who were diagnosed at a younger age had lower acute-phase reactant levels at diagnosis but not after initiation of treatment or at the time of relapse. The risk of relapse was lower in the group diagnosed under age 60 (35% vs 55%). GSK923295 Kinesin inhibitor and maximal glucocorticoid doses, use of glucocorticoid-sparing agents and duration of glucocorticoid treatment, did not differ between the groups. In multivariate analysis, younger age at diagnosis was associated with cervical pain and male gender.

Compared to patients diagnosed above age 60, patients diagnosed with PMR at a younger age have a lower risk of relapse, but similar long-term outcomes with regards to continued need for treatment.

Compared to patients diagnosed above age 60, patients diagnosed with PMR at a younger age have a lower risk of relapse, but similar long-term outcomes with regards to continued need for treatment.The Fingolimod (FTY720, Gilenya) is clinically approved for the treatment of multiple sclerosis (MS). Its therapeutic effect on MS is based on the ability to bind sphingosine 1-phosphate (S1P) receptors and block the exit of immune cells from the lymphoid organs, thus preventing immune cell-dependent injury to the central nervous system (CNS). We showed recently that, besides the S1P-related activity, the FTY720 also down-regulates RhoA, which is a master regulator of the actin cytoskeleton. Our previous studies showed that FTY720 also down-regulates Rictor, which is a signature molecule of mTORC2 complex, which regulates RhoA and dictates actin cytoskeleton specificity. Because, our previous studies showed that chronic rejection correlates with the upregulation of RhoA and mTORC2 components and that the inhibition of RhoA pathway prevents chronic rejection, here we studied the effect of FTY720 on the chronic rejection of rat and mouse cardiac allografts. We show that FTY720 in conjunction with the inhibitors of early T cell response, (CTA4-Ig in mice and Everolimus in rats) blocks macrophage infiltration into the grafts and prevents chronic rejection of rat and mouse cardiac transplants. This indicates that FTY720 may be repurposed from the MS application to the clinical transplantation as an anti-chronic rejection drug.The chemotherapy toward glioblastoma (GBM) is severely challenged by blood-brain barrier and dose-limiting toxicity. Herein, we adopt brain delivery of Plk1 inhibitor volasertib (Vol), which is highly specific and presents low off-target toxicity, as a new means to treat GBM, for which angiopep-2-docked chimaeric polypeptide polymersome (ANG-CPP) was designed and prepared from poly(ethylene glycol)-b-poly(L-tyrosine)-b-poly(L-aspartic acid) for loading Vol to its watery interior via electrostatic interactions. ANG-CPP loaded with 13.9 wt% Vol (ANG-CPP-Vol) exhibited a small size of about 76 nm, superb colloidal stability (against dilution, serum and long-term storage), and enzyme-triggered drug release behavior (about 73% of Vol released within 8 h with proteinase K). In sharp contrast to free Vol, ANG-CPP-Vol induced complete G2/M cell cycle arrest in U-87 MG GBM cells giving 7.8-times better anti-tumor activity, prolonged circulation time and largely increased GBM enrichment. ANG-CPP-Vol effectively suppressed the growth of orthotopic U-87 MG GBM and significantly boosted mice survival rate. Importantly, ANG-CPP-Vol showed further reduced toxicity over free Vol. This great safety and remarkable efficacy of ANG-CPP-Vol renders it a high potential for treating GBM.Alzheimer (AD) is a degenerative disease that can lead memory loss and behavioral dysfunction. Aβ protein and phosphorylation of Tau protein are related to the onset of AD. However, at present, its treatment and drugs are limited. The purpose of our study is to evaluate whether phosphocreatine (PCr) could protect neuronal injury induced by Aβ protein in vivo and in vitro through AKT/GSK-3β/Tau/APP/CDK5 pathways. Differentiated PC-12 cells were cultured with Aβ25-35 for 24 h, while the mice were injected with D-Galactose for eight weeks, both of them were pretreated with PCr for 2 h. #link# The results showed PCr could obviously induce cells and hippocampus apoptosis using DAPI and TUNEL. PCr decreased the levels of intercellular reactive oxygen species (ROS) and malondialdehyde (MDA), and increased the activities of superoxide dismutase (SOD). Besides, the apoptosis pathway was detected using Western blot, showing that PCr could significantly reduce caspase-3, caspase-9, Bcl-2/Bax expression in vivo and in vitro. At the same time, PCr could decreased Ca2+ and apoptosis by Flow Cytometry in PC-12 cells. We observed that the morphological alteration of hippocampus injury was mitigated with the pretreatment of PCr. Furthermore, PCr pretreatment could decrease Aβ25-35-induced PC-12 cells apoptosis with APP cDNA transfection, which up-regulated AKT/GSK-3β/CDK5 pathways and induced Tau phosphorylation. In summary, PCr could reduce Aβ25-35 toxicity to protect neuronal cells via AKT/GSK-3β/CDK5 pathways.