Systematic balance exercises influence cortical activation and serum BDNF levels in older adults

We sought to investigate whether systematic balance training modulates brain area activity responsible for postural control and influence brain-derived neurotrophic factor (BDNF) mRNA protein expression. Seventy-four older adults were randomly divided into three groups (mean age 65.34 ± 3.79 years, 30 females): Classic balance exercises (CBT), virtual reality balance exercises (VBT), and control (CON). Neuroimaging studies were performed at inclusion and after completion of the training or 12 weeks later (CON). Blood samples were obtained to measure BDNF expression. The study revealed significant interaction of sessions and groups: In the motor imagery (MI) condition for supplementary motor area (SMA) activity (Fat peak = 5.25, p < 0.05); in the action observation (AO) condition for left and right supramarginal gyrus/posterior insula (left: Fat peak = 6.48, p < 0.05; right: Fat peak = 6.92, p < 0.05); in the action observation together with motor imagery (AOMI) condition for the middle occipital gyrus (laterally)/area V5 (left: Fat peak = 6.26, p < 0.05; right: Fat peak = 8.37, p < 0.05), and in the cerebellum–inferior semilunar lobule/tonsil (Fat peak = 5.47, p < 0.05). After the training serum BDNF level has increased in CBT (p < 0.001) and in CBT compared to CON (p < 0.05). Systematic balance training may reverse the age-related cortical over-activations and appear to be a factor mediating neuroplasticity in older adults

Systemic response to rupture of intracranial aneurysms involves expression of specific gene isoforms

Abstract Background Rupture of an intracranial aneurysm (IA) causes a systemic response that involves an immune/inflammatory reaction. Our previous study revealed a downregulation of genes related to T lymphocytes and an upregulation of genes related to monocytes and neutrophils after IA rupture. It remains unknown whether that resulted from alterations in transcription or cell count. We sought to characterize the systemic response to IA rupture through analysis of transcript expression profiles in peripheral blood cells. We also investigated effects of IA rupture on the composition of mononuclear cells in peripheral blood. Methods We included 19 patients in the acute phase of IA rupture (RAA, first 72 h), 20 patients in the chronic phase (RAC, 3–15 months), and 20 controls. Using deep transcriptome sequencing, we analyzed the expression of protein-coding and noncoding RNAs. Expression levels, transcript biotypes, alternative splicing and other features of the regulated transcripts were studied. A functional analysis was performed to determine overrepresented ontological groups among gene expression profiles. Flow cytometry was used to analyze alterations in the level of mononuclear leukocyte subpopulations. Results Comparing RAA and controls, we identified 491 differentially expressed transcripts (303 were downregulated, and 188 were upregulated in RAA). The results indicate that the molecular changes in response to IA rupture occur at the level of individual transcripts. Functional analysis revealed that the most impacted biological processes are related to regulation of lymphocyte activation and toll-like receptor signaling pathway. Differences between RAC and controls were less prominent. Analysis of leukocyte subsets revealed a significantly decreased number of CD4+ lymphocytes and increase of classical and intermediate monocytes in RAA patients compared to controls. Conclusions IA rupture in the acute phase strongly influences the transcription profiles of peripheral blood cells as well as the composition of mononuclear cells. A specific pattern of gene expression alteration was found, suggesting a depression of lymphocyte response and enhancement of monocyte activity

Infection with human coronavirus NL63 enhances streptococcal adherence to epithelial cells

Understanding the mechanisms of augmented bacterial pathogenicity in post-viral infections is the first step in the development of an effective therapy. This study assessed the effect of human coronavirus NL63 (HCoV-NL63) on the adherence of bacterial pathogens associated with respiratory tract illnesses. It was shown that HCoV-NL63 infection resulted in an increased adherence of Streptococcus pneumoniae to virus-infected cell lines and fully differentiated primary human airway epithelium cultures. The enhanced binding of bacteria correlated with an increased expression level of the platelet-activating factor receptor (PAF-R), but detailed evaluation of the bacterium–PAF-R interaction revealed a limited relevance of this process

Gene expression profiling of blood in ruptured intracranial aneurysms : in search of biomarkers

The molecular mechanisms underlying the systemic response to subarachnoid hemorrhage (SAH) from ruptured intracranial aneurysms (RAs) are not fully understood. We investigated whether the analysis of gene expression in peripheral blood could provide clinically relevant information regarding the biologic consequences of SAH. Transcriptomics were performed using Illumina HumanHT-12v4 microarrays for 43 RA patients and 18 controls (C). Differentially expressed transcripts were analyzed for overrepresented functional groups and blood cell type-specific gene expression. The set of differentially expressed transcripts was validated using quantitative polymerase chain reaction in an independent group of subjects (15 RA patients and 14 C). There were 135 differentially expressed genes (false discovery rate ⩽1%, absolute fold change ⩾1.7): the abundant levels of 78 mRNAs increased and 57 mRNAs decreased. Among RA patients, transcripts specific to T lymphocyte subpopulations were downregulated, whereas those related to monocytes and neutrophils were upregulated. Expression profiles of a set of 16 genes and lymphocyte-to-monocyte-and-neutrophil gene expression ratios distinguished RA patients from C. These results indicate that SAH from RAs strongly influences the transcription profiles of blood cells. A specific pattern of these changes suggests suppression in lymphocyte response and enhancements in monocyte and neutrophil activities. This is probably related to the immunodepression observed in SAH