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SFSV have infrequently been implicated in central nervous system infections.
In addition, EETs recently have been implicated in central nociceptive and hyperalgesic responses, with different EETs potentially moderating different effects on pain perception [ 22, 30- 34].
A number of assembly factors, including RimM and RbfA, have previously been implicated in central PK formation (Clatterbuck Soper et al., 2013).
The translocator protein (TSPO), formerly known as the peripheral benzodiazepine receptor (PBR), has been implicated in central nervous system (CNS) injury and disease.
Androgens have been implicated in central events governing the regulation of distinct and diverse physiological processes in normal and neoplastic prostate cells.
DOI: http://dx.doi.org/10.7554/eLife.04491.010 Previously, several 30S assembly factors have been implicated in central PK formation providing a motivation for comparing the PK accessibility for both WT E. coli and deletion strains using the RNase H assay.
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Recently, the essential ribosomal biogenesis factor Mrd1 was implicated in central PK formation in Saccharomyces cerevisiae (Segerstolpe et al., 2013).
Additionally, abnormal H2S levels are implicated in central nervous system diseases such as Down syndrome and Alzheimer's disease.
Moreover, CaMKII is thought to be important in central sensitization [ 29– 31] and is implicated in central neuropathic pain [ 31] and long term potentiation (LTP) [ 32].
More recently, Micrococcus spp. is implicated in central venous catheter infection in patients with pulmonary hypertension receiving continuous epoprostenol infusion [ 15, 16].
However, central Ang II has also been implicated in several central nervous system disorders.
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