Contaminants in Foods of Animal Origin in Cameroon: A One Health Vision for Risk Management "".

Foods of animal origin represent an important share in the diet of Cameroonian populations. Cameroon is known to be a food basket in the west and central Africa sub-region, and an important supplier of foods on the international markets. In the meantime, food importation is continuously increasing to meet the high demand of a more westernized segment of the population.

Effects of isoflurane on the expressed Cav2.2 currents in Xenopus oocytes depend on the activation of protein kinase Cδ and its phosphorylation sites in the Cav2.2α1 subunits.

The effects of isoflurane on the modulation of two neuronal voltage-gated calcium channels (Ca(v); Ca(v)2.1 and 2.2) by protein kinase C (PKC) isozymes βII, ε or δ and their combination were examined.

Inhibition of isoflurane-induced increase of cell-surface redistribution and activity of glutamate transporter type 3 by serine 465 sequence-specific peptides.

Excitatory amino acid transporters (EAAT) transport glutamate into cells to regulate glutamate neurotransmission and to maintain nontoxic extracellular glutamate levels for neurons. We showed previously that the commonly used volatile anesthetic isoflurane increases the transporting activity of EAAT3, the major neuronal EAAT. This effect requires a protein kinase C (PKC) α-mediated and S465-dependent EAAT3 redistribution to the plasma membrane.

'To swim or not to swim': the impact of jellyfish stings causing Irukandji Syndrome in Tropical Queensland.

Aim: This manuscript presents both demographic and descriptive data related to a distressing clinical condition known as Irukandji syndrome. Chart audit and observation data were collected to explore trends in patient characteristics and to review the current practices surrounding the management of the syndrome by advanced practice ED nurses.

Background: Irukandji syndrome, a known health emergency in northern Australia, causes severe symptoms such as muscle pains, nausea and vomiting, headache and chest pain causing clinical challenges for emergency nurses.

The importance of serine 161 in the sodium channel beta3 subunit for modulation of Na(V)1.2 gating.

Voltage-gated sodium (Na) channels contribute to the regulation of cellular excitability due to their role in the generation and propagation of action potentials. They are composed of a pore-forming alpha subunit and are modulated by at least two of four distinct beta subunits (beta1-4). Recent studies have implicated a role for the intracellular domain of beta subunits in modulating Na channel gating and trafficking.

Site-specific regulation of CA(V)2.2 channels by protein kinase C isozymes betaII and epsilon.

Ca(v)2.2 high voltage-gated calcium channels are regulated by phorbol-12-myristae, 13-acetate (PMA) via Ser/Thr protein kinase C (PKC) phosphorylation sites in the I-II linker and C-terminus of the alpha(1) 2.2 subunit.

Protein kinase C isozyme-specific potentiation of expressed Ca v 2.3 currents by acetyl-beta-methylcholine and phorbol-12-myristate, 13-acetate.

Protein kinase C (PKC) is implicated in the potentiation of Ca v 2.3 currents by acetyl-beta-methylcholine (MCh), a muscarinic M1 receptor agonist or phorbol-12-myristate, 13-acetate (PMA). The PKC isozymes responsible for the action of MCh and PMA were investigated using translocation as a measure of activation and with isozyme-selective antagonists and siRNA.

Regulation of ghrelin structure and membrane binding by phosphorylation.

The peptide hormone ghrelin requires Ser-3 acylation for receptor binding, orexigenic and anti-inflammatory effects. Functions of desacylghrelin are less well understood. In vitro kinase assays reveal that the evolutionarily conserved Ser-18 in the basic C-terminus is an excellent substrate for protein kinase C.

Examining the knowledge, attitude and use of research by nurses.

Aim: This study sought to determine the knowledge, attitudes and use of research by nurses.

Background: There is little evidence about whether nurses are aware of using research and how much research they use in their clinical practice.

Method: Using a descriptive design, 347 registered and Enrolled Nurses completed the Edmonton Research Orientation Survey.

Initial three-dimensional reconstructions of protein kinase C delta from two-dimensional crystals on lipid monolayers.

Two-dimensional crystals of protein kinase C delta (PKCdelta) and of its regulatory domain (RDdelta) were grown on lipid monolayers and analyzed by electron microscopy at tilt angles varying from -50 degrees to +55 degrees. Although the crystals exhibit pseudo-3-fold symmetry, analysis of difference phase residuals indicates that there is only one way to align the crystals for merging so the data were processed in plane group P1. Three-dimensional reconstructions generated for several two-dimensional crystals each of PKCdelta and RDdelta show good agreement and are consistent with membrane attachment via a single C1 subdomain, a small surface contact by one or two loops from the C2 domain, and, in intact PKCdelta, a small appendage from the catalytic domain, probably V5.

Critical role of serine 465 in isoflurane-induced increase of cell-surface redistribution and activity of glutamate transporter type 3.

Glutamate transporters (also called excitatory amino acid transporters, EAATs) bind extracellular glutamate and transport it to intracellular space to regulate glutamate neurotransmission and to maintain extracellular glutamate concentrations below neurotoxic levels. We previously showed that isoflurane, a commonly used anesthetic, enhanced the activity of EAAT3, a major neuronal EAAT. This effect required a protein kinase C (PKC) alpha-dependent EAAT3 redistribution to the plasma membrane.

Inhibitory role of Ser-425 of the alpha1 2.2 subunit in the enhancement of Cav 2.2 currents by phorbol-12-myristate, 13-acetate.

Voltage-gated calcium channels (Ca(v)) 2.2 currents are potentiated by phorbol-12-myristate, 13-acetate (PMA), whereas Ca(v) 2.3 currents are increased by both PMA and acetyl-beta-methylcholine (MCh).

Sequential phosphorylation mediates receptor- and kinase-induced inhibition of TREK-1 background potassium channels.

Background potassium channels determine membrane potential and input resistance and serve as prominent effectors for modulatory regulation of cellular excitability. TREK-1 is a two-pore domain background K+ channel (KCNK2, K2P2.1) that is sensitive to a variety of physicochemical and humoral factors.

Role of alpha1 2.3 subunit I-II linker sites in the enhancement of Ca(v) 2.3 current by phorbol 12-myristate 13-acetate and acetyl-beta-methylcholine.

Potentiation of Ca(v) 2.3 currents by phorbol 12-myristate 13-acetate (PMA) or acetyl-beta-methylcholine (MCh) may be due to protein kinase C (PKC)-mediated phosphorylation of the alpha1 2.3 subunit.

Identification of sites responsible for potentiation of type 2.3 calcium currents by acetyl-beta-methylcholine.

To address mechanisms for the differential sensitivity of voltage-gated Ca2+ channels (Cav) to agonists, channel activity was compared in Xenopus oocytes coexpressing muscarinic M(1) receptors and different Cav alpha1 subunits, all with beta1B,alpha2/delta subunits. Acetyl-beta-methylcholine (MCh) decreased Cav 1.2c currents, did not affect 2.

Two-dimensional crystal structures of protein kinase C-delta, its regulatory domain, and the enzyme complexed with myelin basic protein.

Two-dimensional crystals of protein kinase C (PKC) delta, its regulatory domain (RDdelta), and the enzyme complexed with the substrate myelin basic protein have been grown on lipid monolayers composed of phosphatidylcholine: phosphatidylserine: diolein (45:50:5, molar ratio). Images have been reconstructed to 10-A resolution. The unit cells of all three proteins have cell edges a = b and interedge angle gamma = 60 degrees.

Protein kinase C-eta regulates resistance to UV- and gamma-irradiation-induced apoptosis in glioblastoma cells by preventing caspase-9 activation.

Both increased cell proliferation and apoptosis play important roles in the malignant growth of glioblastomas. We have demonstrated recently that the differential expression of protein kinase C (PKC)-eta increases the proliferative capacity of glioblastoma cells in culture; however, specific functions for this novel PKC isozyme in the regulation of apoptosis in these tumors has not been defined. In the present study of several glioblastoma cell lines, we investigated the role of PKC-eta in preventing UV- and gamma-irradiation-induced apoptosis and in caspase-dependent signaling pathways that mediate cell death.

Activation-dependent degradation of protein kinase C eta.

Prolonged activation of protein kinase Cs (PKCs) by long-term treatment of cells with phorbol ester tumor promoters down-regulates the expression of many PKCs. To investigate the molecular mechanisms involved in the down-regulation of PKC eta, we expressed the novel PKCs eta and θ and various mutant forms in baby hamster kidney cells. Upon overexpression, constitutively active PKC eta, but not wild type or kinase-dead PKC eta, underwent rapid degradation to generate several lower molecular weight polypeptides.

Phorbol 12-myristate 13-acetate induces protein kinase ceta-specific proliferative response in astrocytic tumor cells.

Protein kinase C (PKC) activation has been implicated in cellular proliferation in neoplastic astrocytes. The roles for specific PKC isozymes in regulating this glial response, however, are not well understood. The aim of this study was to characterize the expression of PKC isozymes and the role of PKC-eta expression in regulating cellular proliferation in two well characterized astrocytic tumor cell lines (U-1242 MG and U-251 MG) with different properties of growth in cell culture.

Lipid-dependent activation of protein kinase C-alpha by normal alcohols.

Significant stimulation of protein kinase C-alpha (PKCalpha) by n-alcohols was observed in characterized lipid systems composed of phosphatidylcholine/phosphatidylserine/dioleoylglycerol (PC/PS/DO). The logarithm of the alcohol concentrations to achieve half-maximal PKC stimulation (ED(50)) and of the maximal PKC stimulation by alcohols were both linear functions of alcohol chain length, consistent with the Meyer-Overton effect. Binding of phorbol esters to PKC was not significantly affected by octanol.