• MeSH
• Evoked Potentials MeSH
• Adaptation, Physiological MeSH
• Visual Perception MeSH

• MeSH
• Evoked Potentials MeSH
• Physical Stimulation MeSH
• Adaptation, Physiological MeSH
• Visual Perception MeSH

• MeSH
• Adaptation, Ocular MeSH
• Darkness MeSH

• MeSH
• Data Interpretation, Statistical MeSH
• Computer Simulation MeSH
• Surveys and Questionnaires MeSH
• Psychometrics MeSH
• Publication type
• Monograph MeSH

• Conspectus
• Fyziologie člověka a srovnávací fyziologie
• NML Fields
• statistika, zdravotnická statistika

The innate immunity is frequently accepted as a first line of relatively primitive defense interfering with the pathogen invasion until the mechanisms of 'privileged' adaptive immunity with the production of antibodies and activation of cytotoxic lymphocytes 'steal the show'. Recent advancements on the molecular and cellular levels have shaken the traditional view of adaptive and innate immunity. The innate immune memory or 'trained immunity' based on metabolic changes and epigenetic reprogramming is a complementary process insuring adaptation of host defense to previous infections.Innate immune cells are able to recognize large number of pathogen- or danger- associated molecular patterns (PAMPs and DAMPs) to behave in a highly specific manner and regulate adaptive immune responses. Innate lymphoid cells (ILC1, ILC2, ILC3) and NK cells express transcription factors and cytokines related to subsets of T helper cells (Th1, Th2, Th17). On the other hand, T and B lymphocytes exhibit functional properties traditionally attributed to innate immunity such as phagocytosis or production of tissue remodeling growth factors. They are also able to benefit from the information provided by pattern recognition receptors (PRRs), e.g. γδT lymphocytes use T-cell receptor (TCR) in a manner close to PRR recognition. Innate B cells represent another example of limited combinational diversity usage participating in various innate responses. In the view of current knowledge, the traditional black and white classification of immune mechanisms as either innate or an adaptive needs to be adjusted and many shades of gray need to be included.

• MeSH
• Adaptive Immunity * MeSH
• B-Lymphocytes immunology   MeSH
• Killer Cells, Natural immunology   MeSH
• Cytokines genetics   immunology   MeSH
• Humans MeSH
• Immunity, Innate * MeSH
• T-Lymphocytes immunology   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH

Although physiological responses to chronic hypoxia, including pulmonary hypertension and right ventricular hypertrophy, have been well described, the molecular mechanisms involved in cardiopulmonary adaptations are still not fully understood. We hypothesize that adaptive responses to chronic hypoxia are the result of altered transcriptional regulations in the right and left ventricles. Here we report results from the gene expression profiling of adaptive responses in a chronically hypoxic heart. Of 11 analyzed candidate genes, the expression of seven and four genes, respectively, was significantly altered in the right ventricle of hypoxic male and female mice. In the transcriptional profile of the left ventricle, we identified a single expression change in hypoxic males (Vegfa gene). To directly test the role of HIF1, we analyzed the expression profile in Hif1a partially deficient mice exposed to moderate hypoxia. Our data showed that Hif1a partial deficiency significantly altered transcriptional profiles of analyzed genes in hypoxic hearts. The expression changes were only detected in two genes in the right ventricle of Hif1a(+/-) males and in one gene in the right ventricle of Hif1a(+/-) females. First, our results suggest that hypoxia mainly affects adaptive expression profiles in the right ventricle and that each ventricle can respond independently. Second, our findings indicate that HIF1a plays an important role in adaptive cardiopulmonary responses and the dysfunction of HIF1 pathways considerably affects transcriptional regulation in the heart. Third, our data reveal significant differences between males and females in cardiac adaptive responses to hypoxia and indicate the necessity of optimizing diagnostic and therapeutic procedures in clinical practice, with respect to sex.

• MeSH
• Time Factors MeSH
• Chronic Disease MeSH
• Hypoxia-Inducible Factor 1, alpha Subunit deficiency   genetics   metabolism   MeSH
• Adaptation, Physiological MeSH
• Transcription, Genetic MeSH
• Hematocrit MeSH
• Hypoxia genetics   metabolism   physiopathology   MeSH
• Cardiomegaly genetics   metabolism   physiopathology   MeSH
• Blood Pressure MeSH
• RNA, Messenger metabolism   MeSH
• Disease Models, Animal MeSH
• Mice, Inbred C57BL MeSH
• Mice, Knockout MeSH
• Mice MeSH
• Hypertension, Pulmonary genetics   metabolism   physiopathology   MeSH
• Reverse Transcriptase Polymerase Chain Reaction MeSH
• Gene Expression Regulation MeSH
• Sex Factors MeSH
• Ventricular Function genetics   MeSH
• Heart Ventricles metabolism   physiopathology   MeSH
• Gene Expression Profiling methods   MeSH
• Body Weight MeSH
• Vascular Endothelial Growth Factor A genetics   MeSH
• Animals MeSH
• Check Tag
• Male MeSH
• Mice MeSH
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Comparative Study MeSH

• MeSH
• Adaptation, Physiological MeSH
• Adolescent MeSH
• Cold Temperature MeSH
• Posture MeSH
• Proteinuria etiology   MeSH
• Check Tag
• Adolescent MeSH

• MeSH
• Eye Movements MeSH
• Psychomotor Disorders MeSH
• Saccades MeSH

• Conspectus
• Psychologie
• NML Fields
• oftalmologie
• psychologie, klinická psychologie
• NML Publication type
• kolektivní monografie

The miRNA-206 and miRNA-23a play an important role in muscle tissue hypertrophy, regeneration and atrophy. Both of these miRNAs have been highlighted as promising adaptation predictors; however, the available evidence on associations is inconclusive. Therefore, our aim was to assess the expression levels of these two miRNAs as predictors of change in muscle function during strength training and physical inactivity among dialysed patients. For this purpose, 46 haemodialysis patients were monitored for 12-weeks of either intradialytic strength training (EXG, n = 20) or physical inactivity during dialysis (CON, n = 26). In both groups of patients, we assessed the baseline expression levels of miRNA-23a and miRNA-206 and the isometric force generated during hip flexion (HF) contraction before and after the 12-week period. Among the EXG group, the expression of miRNA-206 predicted the change in HF (R2 = 0.63, p = 0.0005) much more strongly than the expression of miRNA-23a (R2 = 0.21, p = 0.027). Interestingly, baseline miRNA-23a (R2 = 0.30, p = 0.006) predicted the change in HF much more than miRNA-206 (p = ns) among the CON group. Our study indicates that the baseline expression of miRNA-206 could predict the response to strength training, while miRNA-23a could serve as a potential predictive marker of functional changes during physical inactivity in dialysis patients.

• MeSH
• Biomarkers analysis   MeSH
• Renal Dialysis methods   MeSH
• Adaptation, Physiological MeSH
• Physical Conditioning, Animal * MeSH
• Muscle, Skeletal metabolism   physiopathology   MeSH
• Middle Aged MeSH
• Humans MeSH
• MicroRNAs analysis   genetics   MeSH
• Resistance Training * MeSH
• Sedentary Behavior * MeSH
• Aged MeSH
• Case-Control Studies MeSH
• Check Tag
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH

Mycobacterium tuberculosis (Mtb) remains a major threat worldwide, although only a fraction of infected individuals develops tuberculosis (TB). TB susceptibility is shaped by multiple genetic factors, and we performed comparative immunological analysis of two mouse strains to uncover relevant mechanisms underlying susceptibility and resistance. C57BL/6 mice are relatively TB-resistant, whereas I/St mice are prone to develop severe TB, partly due to the MHC-II allelic variant that shapes suboptimal CD4+ T cell receptor repertoire. We investigated the repertoires of lung-infiltrating helper T cells and B cells at the progressed stage in both strains. We found that lung CD4+ T cell repertoires of infected C57BL/6 but not I/St mice contained convergent TCR clusters with functionally confirmed Mtb specificity. Transcriptomic analysis revealed a more prominent Th1 signature in C57BL/6, and expression of pro-inflammatory IL-16 in I/St lung-infiltrating helper T cells. The two strains also showed distinct Th2 signatures. Furthermore, the humoral response of I/St mice was delayed, less focused, and dominated by IgG/IgM isotypes, whereas C57BL/6 mice generated more Mtb antigen-focused IgA response. We conclude that the inability of I/St mice to produce a timely and efficient anti-Mtb adaptive immune responses arises from a suboptimal helper T cell landscape that also impacts the humoral response, leading to diffuse inflammation and severe disease.

• MeSH
• Adaptive Immunity * genetics   MeSH
• B-Lymphocytes immunology   MeSH
• Genetic Predisposition to Disease * MeSH
• Disease Models, Animal MeSH
• Mycobacterium tuberculosis * immunology   MeSH
• Mice, Inbred C57BL * MeSH
• Mice MeSH
• Lung immunology   pathology   MeSH
• Receptors, Antigen, T-Cell genetics   immunology   MeSH
• Tuberculosis * immunology   genetics   MeSH
• Animals MeSH
• Check Tag
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH