Current evidence strongly supports the idea that the predominant effect of TCF7L2 dysfunction on type 2 diabetes development is mediated through impairment of insulin secretion [ 11, 15– 17, 20], a finding that would be consistent, for example, with the known effects of other (non-homologous) TCF genes (TCF1 [also known as HNF1A] and TCF2 [also known as HNF1B]) that are causal for MODY [ 4].
These activities could range, for example, from associating with known terrorists in an Al Qaeda hujra (guest house) to sneaking across the border into Afghanistan from Pakistan's Taliban-controlled tribal zones with a group of Taliban insurgents.
For example, cell proteins with known RNA helicase and DNA repair activities were identified, and these activities might conceivably be related to assisting DNA synthesis during reverse transcription [2].
For example, among those with known DM, anxiety and other psychological factors may influence their response to the questions about MSCs.
For example, among those with known diabetes, the presence of complications is associated with a reduced HRF and the greater the number or severity of complications, the greater the decrease in HRF.
In other words, the network constructs a model based on examples of data with known output.
Black circles show positive examples of structures with known reacting atoms in case of a C-hydroxylation and b N-dealkylation reactions catalysed by CYP2D6.
There were no examples of genes with known, significant physiological functions in this category.
Examples are individuals with known or frequent exposure, such as contacts of infectious pulmonary TB patients or drug users.
There were no conserved examples of genes with known functions being found in the coastal isolates, but not the Sargasso Sea metagenomic data, or vice versa, suggesting that core regions of these diverse SAR11 genomes are relatively conserved in gene content.
