PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “brain proteomics”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

850 records · Page 48Linked to original sources

Strengths and weaknesses of EST-based prediction of tissue-specific alternative splicing.

BACKGROUND: Alternative splicing contributes significantly to the complexity of the human transcriptome and proteome. Computational prediction of alternative splice isoforms are usually based on EST sequences that also allow to approximate the expression pattern of the related transcripts. However, the limited number of tissues represented in the EST data as well as the different cDNA construction protocols may influence the predictive capacity of ESTs to unravel tissue-specifically expressed transcripts. METHODS: We predict tissue and tumor specific splice isoforms based on the genomic mapping (SpliceNest) of the EST consensus sequences and library annotation provided in the GeneNest database. We further ascertain the potentially rare tissue specific transcripts as the ones represented only by ESTs derived from normalized libraries. A subset of the predicted tissue and tumor specific isoforms are then validated via RT-PCR experiments over a spectrum of 40 tissue types. RESULTS: Our strategy revealed 427 genes with at least one tissue specific transcript as well as 1120 genes showing tumor specific isoforms. While our experimental evaluation of computationally predicted tissue-specific isoforms revealed a high success rate in confirming the expression of these isoforms in the respective tissue, the strategy frequently failed to detect the expected restricted expression pattern. The analysis of putative lowly expressed transcripts using normalized cDNA libraries suggests that our ability to detect tissue-specific isoforms strongly depends on the expression level of the respective transcript as well as on the sensitivity of the experimental methods. Especially splice isoforms predicted to be disease-specific tend to represent transcripts that are expressed in a set of healthy tissues rather than novel isoforms. CONCLUSIONS: We propose to combine the computational prediction of alternative splice isoforms with experimental validation for efficient delineation of an accurate set of tissue-specific transcripts.

Alternative Splicing↗

On the molecular basis of the receptor mosaic hypothesis of the engram.

1. This paper revisits the so-called "receptor mosaic hypothesis" for memory trace formation in the light of recent findings in "functional (or interaction) proteomics." The receptor mosaic hypothesis maintains that receptors may form molecular aggregates at the plasma membrane level representing part of the computational molecular networks. 2. Specific interactions between receptors occur as a consequence of the pattern of transmitter release from the source neurons, which release the chemical code impinging on the receptor mosaics of the target neuron. Thus, the decoding of the chemical message depends on the receptors forming the receptor mosaics and on the type of interactions among receptors and other proteins in the molecular network with novel long-term mosaics formed by their stabilization via adapter proteins formed in target neurons through the incoming neurotransmitter code. The internalized receptor heteromeric complexes or parts of them may act as transcription factors for the formation of such adapter proteins. 3. Receptor mosaics are formed both at the pre- and postsynaptic level of the plasma membranes and this phenomenon can play a role in the Hebbian behavior of some synaptic contacts. The appropriate "matching" of the pre- with the postsynaptic receptor mosaic can be thought of as the "clamping of the synapse to the external teaching signal." According to our hypothesis the behavior of the molecular networks at plasma membrane level to which the receptor mosaics belong can be set in a "frozen" conformation (i.e. in a frozen functional state) and this may represent a mechanism to maintain constant the input to a neuron. 4. Thus, we are suggesting that molecular networks at plasma membrane level may display multiple "attractors" each of which stores the memory of a specific neurotransmitter code due to a unique firing pattern. Hence, this mechanism may play a role in learning processes where the input to a neuron is likely to remain constant for a while.

Animals↗

Planktonic or biofilm growth affects survival, hydrophobicity and protein expression patterns of a pathogenic Campylobacter jejuni strain.

The effect of planktonic or biofilm modes of growth on survival, hydrophobicity and cellular protein expression patterns of a pathogenic Campylobacter jejuni strain were determined. This was achieved by growing the strain in brain heart infusion broth (with 1% yeast extract), or attached to glass beads in the same medium, at 37 degrees C for 48 h under microaerophilic conditions. Cells from the broth or the bead surfaces were stored at different temperatures (4, 10, 25 and 37 degrees C) for 28 days in phosphate buffered saline (PBS) and monitored at appropriate time intervals for culturable numbers and hydrophobicity by standard methods. In addition, cells were inoculated onto the surface of two processed meat products (a bologna and a summer sausage) vacuum packaged and stored at 4 degrees C for 28 days. Numbers of culturable cells were monitored at appropriate time intervals by standard methods. Cells from the broth or the bead surfaces were also examined for protein expression using two-dimensional protein electrophoresis. Results indicated that numbers of culturable cells in phosphate buffered saline decreased from approximately 6 log colony forming units (cfu) g(-1) to undetectable levels within 14-day storage in a temperature dependent manner. Hydrophobicity of broth grown cells decreased from 15% to 0% adherence to xylene over the same time in a temperature independent manner. Cells grown in a biofilm mode initially displayed a <0.3% adherence to xylene which was maintained during storage. Furthermore, cells grown in the biofilm mode decreased in number more rapidly on storage in buffer than their counterparts grown in broth. Numbers of culturable cells on meat decreased from approximately 5 log cfu g(-1) to undetectable levels within 14-day storage in a product dependent manner, with the most rapid decrease observed for the more acidic summer sausage. Cells grown in a biofilm mode decreased in number more rapidly on storage than broth grown cells. The protein expression patterns differed between planktonic and biofilm cells with seven unique and 12 up-regulated protein spots expressed in a growth mode specific manner. A number of the differentially expressed spots were tentatively identified, by comparison to existing literature, as surface- and stress-associated proteins. Despite the elicitation of some putative stress proteins, this study importantly indicates that biofilm cells of C. jejuni are less resistant to stress than their planktonic counterparts and may lack a sophisticated adaptive stress-resistance response. These findings have implication in determining the risks of infection associated with C. jejuni contamination on food.

Bacterial Adhesion↗

Modern diagnostics in chronic myeloproliferative diseases (CMPDs).

According to the new WHO classification a group of chronic myeloproliferative diseases (CMPDs) were defined: chronic myeloid leukemia (CML), chronic neutrophilic leukemia (CNL), chronic eosinophilic leukemia and hypereosinophilic syndrome (CEL/HES), polycythemia vera (PV), chronic idiopathic myelofibrosis (with extramedullary hematopoiesis, CIMF), essential thrombocythemia (ET), and so called CMPD/unclassifiable. As clinical features and laboratory findings differ widely between these diseases several diagnostic approaches are mandatory at diagnosis for classification and are needed also for follow up studies, especially for the measurement of minimal residual disease (MRD). We here outline the laboratory set up at diagnosis and during follow up in CMPDs with specific focus on the respective therapeutical consequences. Only by using a comprehensive diagnostic panel including cytomorphology, cytogenetics, and molecular genetic methods establishing the correct diagnosis, optimizing treatment as well as evaluating treatment response is possible in CMPDs today.

Blood Cell Count↗