New Technologies for Weed Eradication—Invasive Plants Have No Place to Hide When DNA Is Involved

Building on the advances in molecular technology, two genetic based tools are being developed by Biosecurity Queensland to improve conventional invasive plant detection, monitoring and control. Sporobolus is a genus of almost 200 grass species from tropical and subtropical parts of the world. In Australia, 19 Sporobolus species are endemic and 8 species are introduced. Of these, 10 (5 natives and 5 introduced) are closely allied species and overlapping morphological traits makes accurate identification very difficult. Five of the introduced weedy Sporobolus grasses including Giant Rat’s Tail Grass (GRT), threaten to cost the grazing industry of eastern Australia $60 million per annum, having the potential to infest 60% of Queensland and 30% of Australia. The success of four GRT biological control programs in Australia, hinge on the accurate identification of the host plant. The GRT project relies on a molecular approach to delimit and accurately identify these Sporobolus species, allowing for a more accurate and targeted control strategy to be used in the paddock. The second molecular project focuses on the dioecious Mexican bean tree (Cecropia spp.), a restricted pioneer tree that has invaded rainforests in tropical and subtropical Queensland. Molecular markers are being used to genotype an eradicated population to identify if there are any undetected parent trees within surveyed areas that may be residing in inaccessible rainforest patches, thereby preventing extirpation to occur. Dust monitoring devices to capture pollen are being trialed as an eDNA surveillance method for detecting unknown Mexican bean tree populations in remote rainforest locations

Predicting the cost of eradication for 41 Class 1 declared weeds in Queensland

The feasibility of state-wide eradication of 41 invasive plant taxa currently listed as ‘Class 1 declared pests’ under the Queensland Land Protection (Pest and Stock Route Management) Act 2002 was assessed using the predictive model ‘WeedSearch’. Results indicated that all but one species (Alternanthera philoxeroides) could be eradicated, provided sufficient funding and labour were available. Slightly less than one quarter (24.4%) (n = 10) of Class 1 weed taxa could be eradicated for less than $100 000 per taxon. An additional 43.9$100 000 and $1M per taxon. Hence, 68.3$1M per taxon. Eradication of 29.3% (n = 12) is predicted to cost more than $1M per taxon. Comparison of these WeedSearch outputs with either empirical analysis or results from a previous application of the model suggests that these costs may, in fact, be underestimates. Considering the likelihood that each weed will cost the state many millions of dollars in long-term losses (e.g. losses to primary production, environmental impacts and control costs), eradication seems a wise investment. Even where predicted costs are over$1M, eradication can still offer highly favourable benefit:cost ratios. The total (cumulative) cost of eradication of all 41 weed taxa is substantial; for all taxa, the estimated cost of eradication in the first year alone is $8 618 000. This study provides important information for policy makers, who must decide where to invest public funding

Decreased T cell reactivity to Epstein–Barr virus infected lymphoblastoid cell lines in multiple sclerosis

Objective: To investigate T cell and antibody immunity to Epstein-Barr virus (EBV) in multiple sclerosis (MS)

Increased Immunoreactivity to Two Overlapping Peptides of Myelin Proteolipid Protein in Multiple Sclerosis

We tested the proliferative responses of peripheral blood mononuclear cells from 61 patients with multiple sclerosis, 56 healthy control subjects and 52 patients with other neurological diseases to seven synthetic peptides of myelin proteolipid protein (PLP) and 19 synthetic peptides of myelin basic protein (MBP). Increased proliferative responses to two overlapping PLP peptides, PLP184-199 and PLP190-209, were found significantly more frequently in blood from patients with relapsing-remitting or secondary progressive multiple sclerosis (52.3%), but not from those with primary progressive multiple sclerosis (18.2%), than in that from healthy control subjects (8.9%) and patients with other neurological diseases (20.8%). Reactivity to these PLP peptides was most frequently seen in blood from patients with multiple sclerosis of 6-15 years duration and with moderate to severe disability (Kurtzke's Expanded Disability Status Scale > 4.0); the blood from 15 of 19 patients in this group reacted to one or both of the peptides. Both peptides could be recognized by short-term T-cell lines specific for whole PLP, and lines specific for one or other of the two overlapping peptides were able to recognize whole PLP, indicating that these peptides can be processed naturally from the intact molecule. This region of PLP is encephalitogenic in a number of strains of mice. Samples from multiple sclerosis patients did not react more frequently to any of the MBP peptides than those from healthy control subjects. The proportions of patients with other neurological diseases whose blood responded to the MBP peptides that most frequently elicited responses in blood from multiple sclerosis patients were significantly lower than the proportions of multiple sclerosis patients and healthy control subjects whose blood responded to these peptides

Circulating brain derived neurotrophic factor (BDNF) and frequency of BDNF positive T cells in peripheral blood in human ischemic stroke: effect on outcome

The aim of this study was to measure the levels of circulating BDNF and the frequency of BDNF-producing T cells after acute ischaemic stroke. Serum BDNF levels were measured by ELISA. Flow cytometry was used to enumerate peripheral blood leukocytes that were labelled with antibodies against markers of T cells, T regulatory cells (Tregs), and intracellular BDNF. There was a slight increase in serum BDNF levels after stroke. There was no overall difference between stroke patients and controls in the frequency of CD4(+) and CD8(+) BDNF+ cells, although a subgroup of stroke patients showed high frequencies of these cells. However, there was an increase in the percentage of BDNF+ Treg cells in the CD4(+) population in stroke patients compared to controls. Patients with high percentages of CD4(+) BDNF+ Treg cells had a better outcome at 6 months than those with lower levels. These groups did not differ in age, gender or initial stroke severity. Enhancement of BDNF production after stroke could be a useful means of improving neuroprotection and recovery after stroke. (C) 2015 Elsevier B.V. All rights reserved

Corrigendum to "A Study Of Human T-Cell Lines Generated From Multiple Sclerosis Patients And Controls By Stimulation With Peptides Of Myelin Basic Protein" (J. Neuroimmunol. 70, 65-74)

The amino acid sequences of the 5D and 5E synthetic peptides used in the above study inadvertently contained two lysine K residues (MYKKDSH) instead of the one K residue (MYKDSH) present in the natural sequences of the 21.5 and 20.2 kDa isoforms of human myelin basic protein. Thus, the sequences published in Table 1 correctly describe the peptides that were used, but peptides 5D and 5E differ from native myelin basic protein sequences by the insertion of an additional lysine residue. This extra lysine residue in peptides 5D and 5E should be considered when interpreting the proliferative and cytotoxic responses to these two peptides. However, it has no impact on the responses to any of the other peptides including all those representing the 18.5 kDa isoform or on the overall conclusions of the paper. The authors apologise for any confusion caused

A Study Of Human T-Cell Lines Generated From Multiple Sclerosis Patients And Controls By Stimulation With Peptides Of Myelin Basic Protein

We generated T-cell lines from the peripheral blood of controls and of patients with multiple sclerosis (MS) by stimulation with overlapping synthetic peptides representing the entire sequences of all four isoforms of human myelin basic protein (MBP). The T-cell lines reacted to a wide range of epitopes in the major isoforms of MBP and to epitopes that were present only in the minor isoforms. Many MS patients and controls had T-cells responding to one or more cryptic MBP epitopes, as indicated by the generation of a peptide-specific T-cell line(s) by stimulation with synthetic peptides but not by stimulation with whole MBP. About one-third of the peptide-generated lines were cytotoxic. Although we have shown that this technique of peptide stimulation is effective in generating human antiviral cytotoxic CD8+ T-cell lines, all the cytotoxic MBP-specific lines generated by this method were predominantly CD4+. Our study did not reveal any significant differences, between MS patients and controls, in reactivity to epitopes within any of the isoforms of MBP

No Association Between MTHFR A1298C and MTRR A66G Polymorphisms, and MS in an Australian Cohort

Multiple sclerosis (MS) is a complex neurological disease that affects the central nervous system (CNS) resulting in debilitating neuropathology. Pathogenesis is primarily defined by CNS inflammation and demyelination of nerve axons. Methionine synthase reductase (MTRR) is an enzyme that catalyzes the remethylation of homocysteine (Hcy) to methionine via cobalamin and folate dependant reactions. Cobalamin acts as an intermediate methyl carrier between methylenetetrahydrofolate reductase (MTHFR) and Hcy. MTRR plays a critical role in maintaining cobalamin in an active form and is consequently an important determinant of total plasma Hcy (pHcy) concentrations. Elevated intracellular pHcy levels have been suggested to play a role in CNS dysfunction, neurodegenerative, and cerebrovascular diseases. Our investigation entailed the genotyping of a cohort of 140 cases and matched controls for MTRR and MTHFR, by restriction length polymorphism (RFLP) techniques. Two polymorphisms: MTRR A66G and MTHFR A1298C were investigated in an Australian age and gender matched case-control study. No significant allelic frequency difference was observed between cases and controls at the α = 0.05 level (MTRR χ^2 = 0.005, P = 0.95, MTHFR χ^2 = 1.15, P = 0.28). Our preliminary findings suggest no association between the MTRR A66G and MTHFR A1298C polymorphisms and MS

Allelic Variation Investigation of the Estrogen Receptor Within an Australian Multiple Sclerosis Population

Multiple Sclerosis (MS) is a central nervous system (CNS) chronic inflammatory demyelinating disease leading to various neurological disabilities. The disorder is more prevalent for women with a ratio of 3:2 female to male. Objectives: To investigate variation within the estrogen receptor 1 (ESR1) polymorphism gene in an Australian MS case-control population using two intragenic restriction fragment length polymorphisms; the G594A located in exon 8 detected with the BtgI restriction enzyme and T938C located in intron 1, detected with PvuII. One hundred and ten Australian MS patients were studied, with patients classified clinically as Relapsing Remitting MS (RR-MS), Secondary Progressive MS (SP-MS) or Primary Progressive MS (PP-MS). Also, 110 age, sex and ethnicity matched controls were investigated as a comparative group. No significant difference in the allelic distribution frequency was found between the case and control groups for the ESR1 PvuII (P = 0.50) and Btg1 (P = 0.45) marker. Our results do not support a role for these two ESR1 markers in multiple sclerosis susceptibility, however other markers within ESR1 should not be excluded for potential involvement in the disorder