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Thygesen Rye posted an update a month ago
Infants rarely imitated their mothers, suggests a creative self-motivated learning mechanism that requires further investigation.Chronic lymphocytic leukaemia is one of the most common types of adult leukaemia. Cancer-related systemic inflammation response has been characterized to correlate with therapeutic outcome in patients with cancer. The C-reactive protein-to-albumin (CRP/ALB) ratio (CAR), which is an inflammatory marker, has been reported as a novel prognostic factor in several cancers. The aim of our study was to evaluate the prognostic value of the CAR in patients with chronic lymphocytic leukaemia (CLL). We retrospectively reviewed the clinical characteristics of 322 newly diagnosed CLL patients, investigated the correlations among pretreatment CAR, treatment-free survival (TFS) and overall survival (OS), assessed the prognostic effect of the CAR to compare with other inflammation-related prognostic index by the area under the curve (AUC), and combined CAR and CLL-international prognostic index (CLL-IPI) together to improve the current prognostic system. The results showed that CAR was an independent prognostic factor for OS. Furthermore, the predictive and discriminatory capacity of CLL-IPI together with CAR level was superior to that of CLL-IPI alone for OS. In conclusion, serum CRP and ALB levels are both simple and easily accessible parameters, whose ratio CAR may be good candidates for predicting prognosis in the future clinical practice of CLL.Theoretical accounts and preliminary evidence suggest that Mindfulness-Based Interventions (MBIs) improve cognitive function, but reviews of empirical studies have provided mixed results. selleck inhibitor To clarify empirical evidence, we conducted a meta-analysis of 25 studies (n = 1439) and examined the effects of MBIs on four cognitive domains attention, working memory, long-term memory, and executive function. The summary effect sizes indicate that MBIs produce non-significant effects on attention (SMD = 0.07), working memory (SMD = 0.16), and long-term memory (SMD = -0.12), while a small effect was observed for executive function (SMD = 0.29). Given significant heterogeneity across studies, we conducted meta-regression analyses with sample characteristics, age, number of treatment sessions, treatment duration, intervention type, control group type, and study design. We found moderating effects of intervention type on attention and executive function. Although the current study highlights preliminary evidence for improvements in executive function, overall results suggest non-significant findings for attention, working memory, and long-term memory. To draw a firm conclusion, further research is needed to address methodological challenges in meta-analysis and the limitations of existing studies.
To gain further insight in the immunopathology underlying multifocal motor neuropathy (MMN) by exploring the association between MMN and the human leukocyte antigen (HLA) class II DRB1, DQB1, and DQA loci in depth and by correlating associated haplotypes to detailed clinical and anti-ganglioside antibody data.
We performed high-resolution HLA-class II typing for the DRB1, DQB1, and DQA1 loci in 126 well-characterized MMN patients and assessed disease associations with haplotypes. We used a cohort of 1305 random individuals as a reference for haplotype distribution in the Dutch population.
The DRB1*1501-DQB1*0602 haplotype (OR 1.6 , p < 0.05) and the DRB1*1201-DQB1*0301 haplotype (OR 2.7 , p < 0.05) were more frequent in patients with MMN than in controls. These haplotypes were not associated with disease course, response to treatment or anti-ganglioside antibodies.
MMN is associated with the DRB1*1501-DQB1*0602 and DRB1*1201-DQB1*0301 haplotypes. These HLA molecules or gene variants in their immediate vicinity may promote the specific inflammatory processes underlying MMN.
MMN is associated with the DRB1*1501-DQB1*0602 and DRB1*1201-DQB1*0301 haplotypes. These HLA molecules or gene variants in their immediate vicinity may promote the specific inflammatory processes underlying MMN.Ghrelin has been identified as a multifunctional peptide that has a potential application for treating Parkinson’s disease (PD). The objective of this study was to assess the effects of subcutaneous administration of low-dose ghrelin via miniosmotic pumps on PD progression. The decreased levels of total and active ghrelin in plasma were rescued by ghrelin administration in PD mice. Interestingly, ghrelin did not affect weight gain in wild-type mice but improved weight loss in PD mice. We observed the attenuation of dopaminergic neuron loss in substantia nigra and a low level of dopamine content in the striatum in PD mice with ghrelin treatment. Ghrelin administration could improve the microenvironment of dopaminergic neurons by inhibiting microglial proliferation and proinflammatory cytokine expression and could enhance cell survival by upregulating Bcl-2/Bax ratio and superoxide dismutase1 protein level in the substantia nigra of PD mice. Subcutaneous administration of low-dose ghrelin could prevent the onset of the progression of PD and also provide a possible method for ghrelin application to cure PD.Understanding the cellular processes that lead to Alzheimer’s disease (AD) is critical, and one key lies in the genetics of families with histories of AD. Mutations a complex known as COPI were found in families with AD. The COPI complex is involved in protein processing and trafficking. Intriguingly, several recent publications have found components of the COPI complex can affect the metabolism of pathogenic AD proteins. We reduced levels of the COPI subunit α-COP, altering maturation and cleavage of amyloid precursor protein (APP), resulting in decreased release of Aβ-42 and decreased accumulation of the AICD. Depletion of α-COP reduced uptake of proteopathic Tau seeds and reduces intracellular Tau self-association. Expression of AD-associated mutant α-COP altered APP processing, resulting in increased release of Aβ-42 and increased intracellular Tau aggregation and release of Tau oligomers. These results show that COPI coatomer function modulates processing of both APP and Tau, and expression of AD-associated α-COP confers a toxic gain of function, resulting in potentially pathogenic changes in both APP and Tau.