Hydatid disease in Western Australia: a novel approach to education and surveillance

Hydatid disease (echinococcosis) remains a public health and economic problem of global proportion. Treatment usually requires major surgery and the prognosis for some forms of the disease is poor. The variable transmission patterns exhibited by the causative agents of this complex zoonosis, and inadequate support both internationally and nationally, have resulted in the establishment of control campaigns that are usually organized and funded at a local level. Here, Andrew Thompson, Ian Robertson, Robin Gasser and Clare Constantine describe a novel, targeted campaign of education and surveillance that has recently been initiated in Western Australia, where a totally artificial cycle of transmission for Fchinococcus granulosus has been established as a result of human activity.     

Organic synthesis in algal cells separated into age groups by fractional centrifugation

Summary Synthesis of organic matter was studied in cells of the green, high-temperature alga Chlorella 7-11-05 separated from a nonsynchronized population into fractions of predominantly small or large cells by centrifugation. Rates of synthetic activity were determined as changes in optical density, dry weight, and packed volume of cells in several suspending fluids and under various light intensity conditions.It was found that synthetic activity of the smaller (younger) cell fraction was invariably higher than that of the larger (older) cell fraction, provided a reasonably good separation of cells into size fractions was achieved during centrifugation and the difference between size composition of these fractions was maintained throughout observation.An occasional lack of difference in the performance of the small- and large-cell fractions, or even a higher synthetic activity of the originally large-cell fraction, was traced to cell division taking place during observation. Under conditions favorable to cell division, the large-cell fraction was progressively enriched with smaller (younger) cells, the average age composition of the originally large-cell fraction was shifted toward younger age, and the metabolic activity of the large-cell fraction increased to the extent that, in some experiments, it surpassed that of the originally small-cell fraction.The decline in synthetic activity of cells in the course of cell development previously observed on synchronized cells was thus substantiated on nonsynchronized populations in the absence of the light: dark synchronizing agent and is, therefore, characteristic of normal cell development.     

Expression of a dominant negative mutant innexin in identified neurons and glial cells reveals selective interactions among gap junctional proteins

Neurons and glia of the medicinal leech CNS express different subsets of the 21 innexin genes encoded in its genome. We report here that the punctal distributions of fluorescently tagged innexin transgenes varies in a stereotypical pattern depending on the innexin expressed. Furthermore, whereas certain innexins colocalize extensively (INX1 and INX14), others do not (e.g., INX1 and INX2 or INX6). We then demonstrate that the mutation of a highly conserved proline residue in the second transmembrane domain of innexins creates a gap junction protein with dominant negative properties. Coexpressing the mutated INX1 gene with its wild type blocks the formation of fluorescent puncta and decouples the expressing neuron from its normal gap junction‐coupled network of cells. Similarly, expression of an INX2 mutant transgene (a glial cell innexin), blocks endogenous INX2 puncta and wild‐type transgene puncta, and decouples the glial cell from the other glial cells in the ganglion. We show in cell culture with dye‐uptake and plasma membrane labeling experiments that the mutant innexin transgene is not expressed on the cell membrane but instead appears to accumulate in the cell's perinuclear region. Lastly, we use these mutant innexin transgenes to show that the INX1 mutant transgene blocks not only INX1 puncta formation, but also puncta of INX14, with which INX1 usually colocalizes. By contrast, the formation of INX6 puncta was unaffected by the INX1 mutant. Together, these experiments suggest that leech innexins can selectively interact with one another to form gap junction plaques, which are heterogeneously located in cellular arbors. © 2013 Wiley Periodicals, Inc. Develop Neurobiol 73: 571–586, 2013     

Reginald Ernest Moreau

Ohne ZusammenfassungÜbersetzung: E. Schüz     

A tandem chromatographic column method for assaying cAMP-dependent protein kinase and protein kinase C with synthetic peptide substrates

A method was devised for assaying protein kinases that phosphorylate either Kemptide, such as cAMP-dependent protein kinase, or a glycogen synthase peptide, which is an excellent substrate for protein kinase C. Upon sequential processing of reaction mixtures through tandem columns of cation and anion exchange resins, radioactivity in background samples is nearly nil and the yield of phosphorylated peptides is high. This method reduces labor, radioactivity, enzyme requirements, and costs of assaying protein kinases.     

Expression of GTP-binding protein alpha subunits in human thymocytes

The aim of this study was to test the effect of vitamins A and E in reducing oxyradical effects and myocardial damage after ischemia — reperfusion in the rabbit heart. Oxyradical effects were indirectly assessed by hydroperoxide initiated chemiluminescence and myocardial damage was evaluated by qualitative and quantitative electron microscopy. Left anterior coronary artery was ligated in control and vitamin-treated rabbits for 30 min and then reperfused for 10 min. Rabbits were pretreated with 150 mg vitamin E and 60000 IU vitamin A 24 h before surgery. After 10 min of reperfusion full-thickness needle samples were obtained from five different myocardial areas (three ventricular and two septal areas) and used for the determination of hydroperoxide-initiated chemiluminescence and ultrastructural damage. In the control group, hydroperoxide-initiated chemiluminescence was 18400±500 cpm/mg protein for the non-ischemic and non-reperfused ventricular areas, and 40500±1800 cpm/mg protein for ischemic-reperfused ventricular areas. In the vitamin-treated group, hydroperoxide-initiated chemiluminescence was decreased by 8% in the non ischemic and non reperfused ventricular areas and by 51–75% in the ventricular ischemic and reperfused areas. The two septal areas in the control group gave chemiluminescences of 6800±1200 cpm/mg protein (non ischemic-non reperfused) and 17000±2000 cpm/mg protein (ischemia-reperfusion). In the vitamin-treated group, chemiluminescence decreased by 4 and 58%, respectively.The ischemia-reperfused areas showed extensive edema, margination of nuclear chromatin and swollen mitochondria with disrupted cristae including rupture of the inner and outer mitochondrial membranes. Assessment of mitochondrial damage in electron micrographs by stereological counting and grading indicated 77% of damaged mitochondria. These hearts displayed the early sings of irreversible damage and infarction. Rabbits pretreated with vitamins A and E showed a 18% of damaged mitochondria in the same areas (p<0.001) and relative preservation of myocyte subcellular structures.The results indicated that vitamins A and E reduce hydroperoxide-initiated chemiluminescence and myocardial cell damage during ischemia-reperfusion in the rabbit.