Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.12.2 (MEK)
 18,161 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study reports on the findings from the investigation into small-scale (6.25 mL) MFCs, connected together as a network of multiple units. The MFCs contained unmodified (no catalyst) carbon fibre electrodes and for initial and later experiments, a standard ion-exchange membrane for the proton transfer from the anode to the cathode. The anode microbial culture was of the type commonly found in domestic wastewater fed with 5 mM acetate as the carbon-energy (C/E) source. The cultures were mature and acclimatised in the MFC environment for approximately 2 months before being re-inoculated in the experimental MFC units. The cathode was of the O(2) diffusion open-to-air type, but for the purposes of the polarization experiments, the cathodic electrodes were moistened with ferricyanide. The main aim of this study was to investigate the effects of connecting multiples of MFC units together as a method of scale up by using stacks and comparison of the effects of different PEM and MFC structural materials on the performance. Impedance matching (maximum-power-transfer) was achieved through calculation of total internal impedance. Three different PEM materials were compared in otherwise identical MFCs in sets of three. For individual isolated MFCs, Hyflon E87-03 was shown to produce twice, whilst E87-10 produced approximately 1.5 times the power output of the control (standard) PEM. However, when MFCs containing the E87-03 and E87-10 membranes were connected in a stack, the system suffered from severe instability and cell reversal. To study the effects of the various polymeric MFC structural materials, four small-scale units were manufactured from three different types of RP material; acrylo-butadiene-styrene coated (ABS), ABS coated (ABS-MEK) and polycarbonate (polyC). The stack of four (4) units prototyped out of polyC produced the highest power density values in polarisation experiments (80 mW/m(2)).
 ...
PMID:Improved energy output levels from small-scale Microbial Fuel Cells. 1954 Jan 72

In ascidians the cell cycle machinery has been studied mainly in oocytes while ascidian embryos have been used to dissect the mechanism that controls asymmetric cell division (ACD). Here we overview the most specific and often exceptional points and events in cell cycle control in ascidian oocytes and early embryos. Mature stage IV eggs are arrested at metaphase I due to cytostatic factor (CSF). In vertebrates, unfertilized eggs are arrested at metaphase II by CSF. Meta II-CSF is mediated by the Mos/MEK/MAPK/Erp1 pathway, which inhibits the ubiquitin ligase APC/C(cdc20) preventing cyclin B destruction thus stabilizing MPF activity. CSF is inactivated by the fertilization Ca(2+) transient that stimulates the destruction of Erp1 thus releasing APC/C(cdc20) from inhibition. Although many of the components of CSF are conserved between the ascidian and the vertebrates, the lack of Erp1 in the ascidians (and indeed other invertebrates) is notable since the Mos/MAPK pathway nonetheless mediates Meta I-CSF. Moreover, since the fertilization Ca(2+) transient targets Erp1, it is not clear how the sperm-triggered Ca(2+) transient in ascidians (and again other invertebrates) stimulates cyclin B destruction in the absence of Erp1. Nonetheless, like mammalian eggs, sperm trigger a series of Ca(2+) oscillations that increases the rate of cyclin B destruction and the subsequent loss of MAPK activity leading to meiotic exit in ascidians. Positive feedback from MPF maintains the Ca(2+) oscillations in fertilized ascidian eggs ensuring the eventual loss of MPF stimulating the egg-to-embryo transition. Embryonic cell cycles in the ascidian are highly stereotyped where both the rate of cell division and the orientation of cell division planes are precisely controlled. Three successive rounds of ACD generate two small posterior germ cell precursors at the 64 cell stage. The centrosome-attracting body (CAB) is a macroscopic cortical structure visible by light microscopy that causes these three rounds of ACD. Entry into mitosis activates the CAB causing the whole mitotic spindle to rotate and migrate toward the cortical CAB leading to a highly ACD whereby one small cell is formed that inherits the CAB and approximately 40 maternal postplasmic/PEM RNAs including the germ cell marker vasa.
 ...
PMID:Cell cycle in ascidian eggs and embryos. 2163 Jan 45