signal complexity
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Ionotropní glutamátové receptory NMDA typu hrají podstatnou roli v procesu synaptické plasticity, která je základem učení a paměti. Změna spojení mezi neurony je důsledkem působení jednak lokálních faktorů v synapsi a jednak celkových faktorů, které zahrnují aktivaci proteinkináz a přenos signálu do buněčného jádra, kde proteinkinázy fosforylují konstitutivně exprimované transkripční faktory, které řídí expresi tzv. genů časné odpovědi, z nichž některé jsou samy transkripční faktory a kontrolují expresi dalších cílových genů. Článek prezentuje dosud známé poznatky o mechanizmu přenosu signálu od NMDA receptoru k indukci modelového genu časné odpovědi c-fos, jehož exprese je pod kontrolou několika konstitutivních faktorů, mezi jinými CREB (cAMP-response element binding protein), který musí být fosforylován na kritickém Ser133, aby aktivoval transkripci. Rychlým důsledkem aktivace NMDA receptoru je translokace komplexu Ca2+-kalmodulin do jádra a aktivace Ca2+/kalmodulin dependentní kinázy IV. S pomalejší kinetikou dochází k aktivaci Ras-MAPK (mitogen-activated protein kinase) kinázové kaskády, která je zřejmě v signalizaci do jádra neuronu nejdůležitější a přes jiné specifické signální molekuly integruje i signalizaci využívající Ca2+ nebo cyklický AMP jako druhého posla.
Ionotropic NMDA glutamate receptors play a central role in the process of synaptic plasticity underlying learning and memory. Alteration of neuronal connections results from local effects in the target synapse as well as from the whole-cell factors that encompass activation of protein kinases and signal transduction to the cell nucleus, where the kinases phosphorylate constitutively expressed transcription factors controlling expression of a set of immediate-early genes; some of them, in turn, are themselves transcription factors and regulate expression of further target genes. The article presents some of knowledge accumulated to date, on the mechanism of signal transduction from NMDA receptor to induction of the model immediate-early gene c-fos, whose expression is controlled by several constitutive factors, among them by the CREB (cAMP-response element binding protein), that must be phosphorylated at a critical Ser133, in order to activate transcription. One fast event in response to NMDA receptor activation is translocation of the Ca2+-calmodulin complex to the cell nucleus and activation of Ca2+/calmodulin-dependent protein kinase IV. With slower kinetics, the Ras-MAPK (mitogen-activated protein kinase) kinase cascade is activated, emerging in the signalling to the neuronal nucleus as the most significant pathway, through other specific signalling molecules integrating also signals originally using Ca2+ or cyclic AMP as the second messengers.
The neural network is computational model based on the features abstraction of biological neural systems. Th e neural networks have many ways of usage in technical fi eld. Th ey have been applied successfully to speech recognition, image analysis and adaptive control, in order to construct soft ware agents or autonomous robots. In this paper is described usage of neural networks for ECG signal prediction. Th e ECG signal prediction can be used for automated detection of irregular heartbeat – extrasystole. Th e automated detection system of unexpected abnormalities is also described in this paper.
Demystifying technology series
650 s.
Following stimulation, pancreatic β-cells must orchestrate a plethora of signalling events to ensure the appropriate release of insulin and maintenance of normal glucose homeostasis. Failure at any point in this cascade leads to impaired insulin secretion, elevated blood levels of glucose and eventually type 2 diabetes mellitus. Likewise, β-cell replacement or regeneration strategies for the treatment of both type 1 and type 2 diabetes mellitus might fail if the correct cell signalling phenotype cannot be faithfully recreated. However, current understanding of β-cell function is complicated because of the highly dynamic nature of their intracellular and intercellular signalling as well as insulin release itself. β-Cells must precisely integrate multiple signals stemming from multiple cues, often with differing intensities, frequencies and cellular and subcellular localizations, before converging these signals onto insulin exocytosis. In this respect, optical approaches with high resolution in space and time are extremely useful for properly deciphering the complexity of β-cell signalling. An increased understanding of β-cell signalling might identify new mechanisms underlying insulin release, with relevance for future drug therapy and de novo stem cell engineering of functional islets.
- MeSH
- beta-buňky metabolismus MeSH
- diabetes mellitus 2. typu genetika metabolismus MeSH
- genetická predispozice k nemoci epidemiologie MeSH
- glukosa metabolismus MeSH
- hodnocení rizik MeSH
- homeostáza genetika MeSH
- incidence MeSH
- lidé MeSH
- sekrece inzulinu fyziologie MeSH
- senzitivita a specificita MeSH
- signální transdukce MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
Expression takes place for most of the jasmonic acid (JA)-induced genes in a COI1-dependent manner via perception of its conjugate JA-Ile in the SCFCOI1-JAZ co-receptor complex. There are, however, numerous genes and processes, which are preferentially induced COI1-independently by the precursor of JA, 12-oxo-phytodienoic acid (OPDA). After recent identification of the Ile-conjugate of OPDA, OPDA-Ile, biological activity of this compound could be unequivocally proven in terms of gene expression. Any interference of OPDA, JA, or JA-Ile in OPDA-Ile-induced gene expression could be excluded by using different genetic background. The data suggest individual signaling properties of OPDA-Ile. Future studies for analysis of an SCFCOI1-JAZ co-receptor-independent route of signaling are proposed.
- MeSH
- Arabidopsis metabolismus MeSH
- cyklopentany metabolismus MeSH
- isoleucin analogy a deriváty metabolismus MeSH
- nenasycené mastné kyseliny metabolismus MeSH
- oxylipiny metabolismus MeSH
- proteiny huseníčku metabolismus MeSH
- regulátory růstu rostlin metabolismus MeSH
- signální transdukce fyziologie MeSH
- Publikační typ
- časopisecké články MeSH
BACKGROUND: The presence of parasite interference signals could cause serious problems in the registration of ECG signals and many works have been done to suppress electromyogram (EMG) artifacts noises and disturbances from electrocardiogram (ECG). Recently, new developed techniques based on global and local transforms have become popular such as wavelet shrinkage approaches (1995) and time-frequency dependent threshold (1998). Moreover, other techniques such as artificial neural networks (2003), energy thresholding and Gaussian kernels (2006) are used to improve previous works. This review summarizes windowed techniques of the concerned issue. METHODS AND RESULTS: We conducted a mathematical method based on two sets of information, which are dominant scale of QRS complexes and their domain. The task is proposed by using a varying-length window that is moving over the whole signals. Both the high frequency (noise) and low frequency (base-line wandering) removal tasks are evaluated for manually corrupted ECG signals and are validated for actual recorded ECG signals. CONCLUSIONS: Although, the simplicity of the method, fast implementation, and preservation of characteristics of ECG waves represent it as a suitable algorithm, there may be some difficulties due to pre-stage detection of QRS complexes and specification of algorithm's parameters for varying morphology cases.
- MeSH
- algoritmy MeSH
- elektrokardiografie MeSH
- lidé MeSH
- počítačové zpracování signálu MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
Over the recent years, our understanding of the cell death machinery of mature erythrocytes has been greatly expanded. It resulted in the discovery of several regulated cell death (RCD) pathways in red blood cells. Apoptosis (eryptosis) and necroptosis of erythrocytes share certain features with their counterparts in nucleated cells, but they are also critically different in particular details. In this review article, we summarize the cell death subroutines in the erythroid precursors (apoptosis, necroptosis, and ferroptosis) in comparison to mature erythrocytes (eryptosis and erythronecroptosis) to highlight the consequences of organelle clearance and associated loss of multiple components of the cell death machinery upon erythrocyte maturation. Recent advances in understanding the role of erythrocyte RCDs in health and disease have expanded potential clinical applications of these lethal subroutines, emphasizing their contribution to the development of anemia, microthrombosis, and endothelial dysfunction, as well as their role as diagnostic biomarkers and markers of erythrocyte storage-induced lesions. Fas signaling and the functional caspase-8/caspase-3 system are not indispensable for eryptosis, but might be retained in mature erythrocytes to mediate the crosstalk between both erythrocyte-associated RCDs. The ability of erythrocytes to switch between eryptosis and necroptosis suggests that their cell death is not a simple unregulated mechanical disintegration, but a tightly controlled process. This allows investigation of eventual pharmacological interventions aimed at individual cell death subroutines of erythrocytes.
- MeSH
- apoptóza MeSH
- buněčná smrt MeSH
- eryptóza * MeSH
- erytrocyty * metabolismus cytologie MeSH
- ferroptóza MeSH
- lidé MeSH
- nekroptóza MeSH
- regulovaná buněčná smrt MeSH
- signální transdukce * MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- MeSH
- branched DNA signal amplification assay metody využití MeSH
- dipeptidylpeptidasa 4 agonisté dějiny MeSH
- dipeptidylpeptidasy a tripeptidylpeptidasy analýza MeSH
- finanční podpora výzkumu jako téma MeSH
- lidé MeSH
- nádory štítné žlázy diagnóza MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- abstrakt z konference MeSH
Ethanol is linked to several pathologies like alcohol liver injury, neurotoxicity, cardiomyopathy, fetal alcoholic syndrome or cancer. It is generally accepted that oxidative stress plays a central role in their pathogenesis. After chronic and excessive consumption, alcohol may accelerate oxidative mechanisms both directly via increased production of reactive oxygen species and indirectly by impairing protective mechanisms against them. Ethanol, its metabolites arising during its metabolic degradation as well as novel compounds formed via ethanol induced oxidative stress, especially during the action of the ethanol inducible microsomal cytochrome CYP2E1, may apart from direct damage to biological structures affect signal transduction pathways thus modulating and potentiating damage. Alteration of the redox status of cells following chronic ethanol misuse may have profound effects on cellular function and viability and lead to cell death and tissue damage. These changes linked to pathologic processes in the organism, are related to alteration of intracellular signaling pathways associated with protein kinases and transcription factor activation. Mainly mitogen activated protein kinase (MAPK) family, transcription factors-nuclear factor kappaB (NF-kappaB) and activating protein 1 (AP-1) are involved in the deterioration of cells and organs. The response is cell-type specific and depends on the dose of ethanol. Oxido-reduction balance, regulatory disturbances and signal transduction cascades responsible for alcoholic damage have been partially described, nevertheless, further studies are required to allow future novel diagnostic and therapeutical strategies. We are only at the beginning ...
- MeSH
- alkoholické nemoci jater metabolismus MeSH
- ethanol metabolismus MeSH
- financování organizované MeSH
- játra metabolismus MeSH
- Kupfferovy buňky enzymologie MeSH
- lidé MeSH
- mitogenem aktivované proteinkinasy metabolismus MeSH
- NF-kappa B metabolismus MeSH
- oxidační stres genetika MeSH
- signální transdukce fyziologie MeSH
- TNF-alfa metabolismus MeSH
- transkripční faktor ATF1 metabolismus MeSH
- Check Tag
- lidé MeSH