A decision support tool for the management of freshwater pest fish incursions in Australia

There are no national emergency response arrangements for freshwater pest fish incursions in Australia. Individual States and Territories vary widely in their current response arrangements to freshwater pest fish incursions, with many being dealt with on an ad‐hoc basis and with varying degrees of efficacy. In recognition of this, the Invasive Animals Cooperative Research Centre funded a project to ‘Advance the development of national emergency response arrangements for freshwater fish incursions in Australia’. One of the recommendations of this project was creating a web‐based support tool (DST) to provide direction and assistance in managing freshwater pest fish incursions. This article describes the DST created. The DST leads the user through a series of questions relating to the species sighting, details of the fish and its capture, and site information at a particular location. These questions address issues that managers must consider when choosing appropriate control techniques. Information entered in two sections (site details and fish details) influence the suggested control techniques. The final product of the DST is a standard online report that contains a summary of all information entered and a ranking of the most common control techniques used in Australia. The report is then submitted to and assessed by the relevant State Government authority responsible for the management of freshwater pest fish incursions. Managers are then able to consider their options, taking into consideration current permits, resources and capability. The DST is anticipated to maximize the speed and quality of freshwater pest fish incursion reporting and to help the responsible government agency decide on the most appropriate management action. The DST will also provide government agency staff access to other relevant information and facilitate consistency in the decision‐making approach by government agencies throughout Australia.     

Determination of Gangliosides in Six Human Primary Medulloblastomas

The ganglioside composition of six human medulloblastomas was analyzed. The characterization was performed by thin-layer chromatography, sialidase hydrolysis, and immunological staining with a panel of characterized antiganglioside monoclonal antibodies. The total ganglioside content ranged from 60 to 1,130 nmol of ganglioside sialic acid/g wet weight. Neuronal gangliosides (gangliotetraose series) were found in varying amounts in all medulloblastomas. Gangliosides of the neolactotetraose series (3'-LM1 and LD1) were present in all specimens, and the lactotetraose series ganglioside 3'-isoLM1 was found in all cases showing astrocytic differentiation. This supports our previous findings that 3'-isoLM1 is a marker for proliferating astroglial cells.     

In vivo growth conditions suppress the expression of ganglioside GM2 and favour that of lacto series gangliosides in the human glioma D-54MG cell line

The human glioma D-54MG cell line grownin vitro primarily expresses ganglio series gangliosides, particularly GM2. Subcutaneous injection of these cells into nude mice produced xenografts with an increased content of the human glioma-associated lacto series gangliosides, primarily 3-isoLM1, an alteration that was dose dependent, with the highest dose (1×10⁸) resulting in a phenotype that was most like that of the inoculum. After one passagein vivo, the lacto series dominated and reached a proportional level that was kept throughout the 10 passages. The mRNA levels of the GM2-synthase clearly coincided with GM2 expression and was 20 times higher in cells grownin vitro than in those grownin vivo. These results support the view that ganglioside expression in human gliomas is strongly influenced by environmental factors. Abbreviations: The gangliosides have been designated according to Svennerholm (Eur J Biochem (1977)79: 11–21) GM3, II³NeuAc-LacCer; GM2, II³NeuAc-GgOse₃Cer; GM1, II³NeuAc-GgOse₄Cer; GD3, II³(NeuAc)₂-LacCer; GD2, II³(NeuAc)₂-GgOse₃Cer; GD1a, IV³NeuAc, II³NeuAc-GgOse₄Cer; GD1b, II³(NeuAc)₂-GgOse₄Cer; GT1b, IV³NeuAc, II³(NeuAc)₂-GgOse₄Cer; 3-LM1, IV³NeuAc-nLcOse₄Cer; 3-isoLM1, IV³NeuAc-LcOse₄Cer; 3,6-isoLD1, IV³NeuAc, III⁶NeuAc-LcOse₄Cer; 38-LM1, IV³(NeuAc)₂-nLcOse₄Cer. MAb(s), monoclonal antibody (ies); the designation LM1 is used when both 3-isoLM1 and 3-LM1 and LD1, when both 36-isoLD1 and 38-LD1 are included.     

17 β-Estradiol Enhances the Outgrowth and Survival of Neocortical Neurons in Culture

Results of this investigation demonstrate that exposure to 17 -estradiol differentially and significantly regulates cortical nerve cell outgrowth depending on the cortical region. Parietal and occipital neurons treated with 1 nM 17 -estradiol showed a greater magnitude of neuronal outgrowth whereas outgrowth of temporal cortex neurons was decreased in the presence of 1 nM 17 -estradiol. Frontal cortex neurons showed a consistent enhancement of neuronal outgrowth that did not reach statistical significance. The dose response profile for 17 -estradiol regulation of the macromorphological features exhibited a bimodal dose response relationship whereas the dose response profile for 17 -estradiol regulation of the micromorphological features exhibited a dose response more characteristic of an inverted V-shaped function. An antagonist to the NMDA receptor antagonist, AP5, abolished the growth promoting effect of 17 -estradiol whereas the nuclear estrogen receptor antagonist ICI 182,780 did not. Lastly, neocortical neurons exposed to 17 -estradiol exhibited greater viability and survival than control neurons over a two week period. These data indicate that 17 -estradiol can enhance the growth and viability of select populations of neocortical neurons and that the growth promoting effects of 17 -estradiol can be blocked by an antagonist to the NMDA glutamate receptor and not by an antagonist to the estrogen nuclear receptor.     

Lovastatin corrects ERK pathway hyperactivation in fragile X syndrome: potential of platelet’s signaling cascades as new outcome measures in clinical trials

Aim: To establish whether platelets from fragile X syndrome (FXS) individuals recapitulate FXS mouse neurons’ defects in ERK and Akt pathways, and to evaluate the effect of lovastatin on these pathways.

Methods: ERK and Akt phosphorylation (pERK, pAkt) statuses were assessed with quantitative Western blotting before and after a 12-week lovastatin trial.

Results: Levels of pERK and pAkt were increased in FXS platelets, and lovastatin specifically normalized ERK activity. Changes in ERK phosphorylation were correlated with clinical response to lovastatin.

Conclusions: Platelets’ signaling pathways provide biomarkers that can be used as treatment outcome measures in FXS clinical trials.     

Human brain gangliosides: developmental changes from early fetal stage to advanced age

The developmental profiles of the four major brain gangliosides, GM1, GD1a, GD1b, and GT1b, were examined in human frontal lobe covering the period from 10 fetal weeks to 80 years of age. The ganglioside concentration increased approx. 3-fold from the 10th gestational week to the age of about 5 years. Gangliosides GM1 and GD1a increased 12-15-fold during the same period. The most rapid increase of GM1 and GD1a occurred around term, during the period for dendrite arborization, outgrowth of axons and synaptogenesis. GT1b showed a quite different developmental curve. It was the major ganglioside during the 3rd to 5th gestational month, whereafter its concentration dropped rapidly to term, from which time the concentration then increased up to 50 years of age. Similar curves were found for the other gangliosides of the b-series, GD3, GD2, GD1b and GQ1b. Ganglioside 3'-isoLM1 was a characteristic early fetal ganglioside which dropped rapidly to the 5th gestational month, reached a small peak around term and then disappeared during adulthood. The concentration of gangliosides of the neolacto series was larger than that of the lacto series during the whole developmental period. In the beginning of the second trimester, 3'-LM1 constituted 2% and LD1 10% of total ganglioside sialic acid. The new findings demonstrate more dynamic changes of the ganglioside patterns during development than noted in previous studies.     

Mechanism of inhibitory action by salts in the feeding behaviour of the blowfly, Phormia regina

Blowfly proboscis extension during stimulation of labellar sugar receptors can be inhibited by the presence of salt. The possibility that the salt receptor might initiate a central nervous inhibitory state is investigated behaviourally and electrophysiologically using simultaneous recordings from labellar chemoreceptors and the extensor muscle of the haustellum. While a mixture of 100 mM sucrose and 4 M NaCl applied to a single sensillum does cause inhibition, the same compounds applied separately simultaneously on separate sensilla do not. A mixture of 100 mM sucrose and 4 M NaCl does not produce central nervous effects such as motor response decrement to repeated stimulation; nor does it produce an enhanced motor response resulting from cross-channel summation when applied simultaneously with 100 mM sucrose on another sensillum. These results argue that the inhibitory effect of mixtures containing sugar and salt can be explained by inhibition of the sugar receptor without having to invoke a central inhibitory mechanism.     

Sialosyllactotetraosylceramide, 3''-isoLM1, a Ganglioside of the Lactotetraose Series Isolated from Normal Human Infant Brain

A ganglioside antigen was detected in infant human brains by the monoclonal antibody C-50. Structural analysis of the isolated ganglioside antigen showed it to be 3'-isoLM1, sialosyllactotetraosylceramide. The concentration of this ganglioside in human infant brain was 0.5 nmol/g.     

Membrane lipids of human peripheral nerve and spinal cord.

Major membrane lipids were determined in specimens of human peripheral nerve (cauda equina) and spinal cord of 10 subjects aged 20-70 years. The same lipids were also assayed in myelin from the same tissues isolated with two different procedures and in myelin of cauda equina from 3 subjects aged 17-91 years isolated with a third method. The concentrations (mean and standard deviation) of phospholipids were 90 +/- 11 and 96 +/- 9 nmol/g fresh weight; of cholesterol 70 +/- 15 and 101 +/- 16; of cerebroside 19 +/- 3 and 41 +/- 7; of sulfatide 10 +/- 1 and 11 +/- l; and of gangliosides 0.80 +/- 0.08 and 0.40 +/- 0.05 N in cauda equina and spinal cord, respectively. The proportion of ethanolamine phosphoglyceride was lower and that of sphingomyelin higher in cauda equina than in spinal cord. The myelin of peripheral nerve and spinal cord contained almost the same proportions of lipids as the whole tissue. The protein-bound sialic acid content was 3-fold higher than the lipid-bound sialic acid content in cauda myelin. The fatty acid patterns of choline, ethanolamine, inositol and serine phosphoglycerides of spinal cord and its myelin, were very similar to those of cerebral white matter, while the phosphoglycerides of cauda equina had higher proportions of monoenoic acids and lower proportions of polyunsaturated fatty acids. The fatty acid patterns of sphingomyelin, cerebroside and sulfatide of spinal cord were similar to those of cerebral white matter, while those of cauda equina contained significantly more saturated fatty acids. This suggests that the lipid and fatty acid compositions of peripheral nerve are particularly suitable for the formation of a tightly packed myelin membrane which can be a powerful shield against infections and other injuries.