Isolation and partial amino acid sequencing of the small subunit of ribulose-1,5-bisphosphate carboxylase/oxygenase from three species of orchid

Small subunits of ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) have been purified from 3 species of orchid in the genus Cymbidium by gel filtration followed by preparative sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE) and electroelution. The samples were subjected to amino acid composition analysis and partial N-terminal amino acid sequencing. The sequencing data clearly confirm that one of the species examined is the hybrid offspring of a cross between the other two.     

The gene encoding the nucleocapsid protein of Gill-associated nidovirus of Penaeus monodon prawns is located upstream of the glycoprotein gene

The ORF2 gene of Gill-associated virus (GAV) of Penaeus monodon prawns resides 93 nucleotides downstream of the ORF1a-ORF1b gene and encodes a 144-amino-acid hydrophilic polypeptide (15,998 Da; pI, 9.75) containing 20 basic (14%) and 13 acidic (9%) residues and 19 prolines (13%). Antiserum to a synthetic ORF2 peptide or an Escherichia coli-expressed glutathione S-transferase-ORF2 fusion protein detected a 20-kDa protein in infected lymphoid organ and gill tissues in Western blots. The GAV ORF2 fusion protein antiserum also cross-reacted with the p20 nucleoprotein in virions of the closely related Yellow head virus. By immuno-gold electron microscopy, it was observed that the ORF2 peptide antibody localized to tubular GAV nucleocapsids, often at the ends or at lateral cross sections. As GAV appears to contain only two structural protein genes (ORF2 and ORF3), these data indicate that GAV differs from vertebrate nidoviruses in that the gene encoding the nucleocapsid protein is located upstream of the gene encoding the virion glycoproteins.     

Effects of surface texture and interrelated properties on marine biofouling: a systematic review

This systematic review examines effects of surface texture on marine biofouling and characterizes key research methodologies. Seventy-five published articles met selection criteria for qualitative analysis; experimental data from 36 underwent quantitative meta-analysis. Most studies investigated fouling mechanisms and antifouling performance only in laboratory assays with one to several test species. Textures were almost exclusively a single layer of regularly arranged geometric features rather than complex hierarchical or irregular designs. Textures in general had no effect or an inconclusive effect on fouling in 46% of cases. However, effective textures more often decreased (35%) rather than increased (19%) fouling. Complex designs were more effective against fouling (51%) than were regular geometric features (32%). Ratios of feature height, width, or pitch to organism body length were significant influences. The authors recommend further research on promising complex and hierarchical texture designs with more test species, as well as field studies to ground-truth laboratory results.     

Towards a Case Definition for Devil Facial Tumour Disease: What Is It?

In the mid 1990s an emerging disease characterised by the development of proliferative lesions around the face of Tasmanian devils (Sarcophilus harrisii) was observed. A multi-disciplinary approach was adopted to define the condition. Histopathological and transmission electron microscopic examination combined with immunohistochemistry help define Devil Facial Tumour Disease (DFTD) as a neoplastic condition of cells of neuroendocrine origin. Cytogenetic analysis of neoplastic tissue revealed it to be markedly different from normal devil tissue and having a consistent karyotype across all tumours examined. Combined with evidence for Major histocompatability (MHC) gene analysis there is significant evidence to confirm the tumour is a transmissible neoplasm.     

Evaluating the effectiveness of road mitigation measures

The last 20 years have seen a dramatic increase in efforts to mitigate the negative effects of roads and traffic on wildlife, including fencing to prevent wildlife-vehicle collisions and wildlife crossing structures to facilitate landscape connectivity. While not necessarily explicitly articulated, the fundamental drivers behind road mitigation are human safety, animal welfare, and/or wildlife conservation. Concomitant with the increased effort to mitigate has been a focus on evaluating road mitigation. So far, research has mainly focussed on assessing the use of wildlife crossing structures, demonstrating that a broad range of species use them. However, this research has done little to address the question of the effectiveness of crossing structures, because use of a wildlife crossing structure does not necessarily equate to its effectiveness. The paucity of studies directly examining the effectiveness of crossing structures is exacerbated by the fact that such studies are often poorly designed, which limits the level of inference that can be made. Without well performed evaluations of the effectiveness of road mitigation measures, we may endanger the viability of wildlife populations and inefficiently use financial resources by installing structures that are not as effective as we think they are. In this paper we outline the essential elements of a good experimental design for such assessments and prioritize the parameters to be measured. The framework we propose will facilitate collaboration between road agencies and scientists to undertake research programs that fully evaluate effectiveness of road mitigation measures. We discuss the added value of road mitigation evaluations for policy makers and transportation agencies and provide recommendations on how to incorporate such evaluations in road planning practices.     

The Top 10 fungal pathogens in molecular plant pathology

The aim of this review was to survey all fungal pathologists with an association with the journal Molecular Plant Pathology and ask them to nominate which fungal pathogens they would place in a 'Top 10' based on scientific/economic importance. The survey generated 495 votes from the international community, and resulted in the generation of a Top 10 fungal plant pathogen list for Molecular Plant Pathology. The Top 10 list includes, in rank order, (1) Magnaporthe oryzae; (2) Botrytis cinerea; (3) Puccinia spp.; (4) Fusarium graminearum; (5) Fusarium oxysporum; (6) Blumeria graminis; (7) Mycosphaerella graminicola; (8) Colletotrichum spp.; (9) Ustilago maydis; (10) Melampsora lini, with honourable mentions for fungi just missing out on the Top 10, including Phakopsora pachyrhizi and Rhizoctonia solani. This article presents a short resumé of each fungus in the Top 10 list and its importance, with the intent of initiating discussion and debate amongst the plant mycology community, as well as laying down a bench-mark. It will be interesting to see in future years how perceptions change and what fungi will comprise any future Top 10.     

Peroxisome proliferator-activated receptor-gamma agonist 15-deoxy-Delta(12,14)-prostaglandin J(2) ameliorates experimental autoimmune encephalomyelitis

Peroxisome proliferator-activated receptors (PPAR) are members of a nuclear hormone receptor superfamily that includes receptors for steroids, retinoids, and thyroid hormone, all of which are known to affect the immune response. Previous studies dealing with PPAR-gamma expression in the immune system have been limited. Recently, PPAR-gamma was identified in monocyte/macrophage cells. In this study we examined the role of PPAR-gamma in experimental autoimmune encephalomyelitis (EAE), an animal model for the human disease multiple sclerosis. The hypothesis we are testing is whether PPAR-gamma plays an important role in EAE pathogenesis and whether PPAR-gamma ligands can inhibit the clinical expression of EAE. Initial studies have shown that the presence of the PPAR-gamma ligand 15-deoxy-Delta(12,14)-PGJ(2) (15d-PGJ2) inhibits the proliferation of Ag-specific T cells from the spleen of myelin basic protein Ac(1-11) TCR-transgenic mice. 15d-PGJ2 suppressed IFN-gamma, IL-10, and IL-4 production by both Con A- and myelin basic protein Ac(1-11) peptide-stimulated lymphocytes as determined by ELISA and ELISPOT assay. Culture of encephalitogenic T cells with 15d-PGJ2 in the presence of Ag reduced the ability of these cells to adoptively transfer EAE. Examination of the target organ, the CNS, during the course of EAE revealed expression of PPAR-gamma in the spinal cord inflammatory infiltrate. Administration of 15d-PGJ2 before and at the onset of clinical signs of EAE significantly reduced the severity of disease. These results suggest that PPAR-gamma ligands may be a novel therapeutic agent for diseases such as multiple sclerosis.     

Enzyme‐immunoassay for the measurement of luteinizing hormone in the serum of African elephants (Loxodonta africana)

Circulating patterns of progesterone and luteinizing hormone (LH) in the elephant have been well characterized, and routine monitoring of these hormones is now viewed as a valuable tool for making informed decisions about the reproductive management of elephants in captivity. Currently, LH monitoring in elephants is done with radio‐immunoassays (RIAs); unfortunately, the use of radioactive materials in RIAs limits their application to institutions with laboratory facilities equipped for the storage and disposal of radioactive waste. Enzyme‐immunoassays (EIAs) offer an inexpensive and more zoo‐friendly alternative to RIA. This work reports on an EIA capable of quantifying circulating LH in African elephants. The EIA employs a biotin label and microtiter plates coated with goat anti‐mouse gamma globulin. LH surges in African elephants (n=3) increased fivefold over baseline concentrations (1.00±0.1 ng/ml vs. 0.2±0.1 ng/ml) and occurred 19.3±0.2 days apart. Ovulatory LH surges were associated with an increase in serum progestogens from 4.8±0.4 ng/ml to 11.7±0.4 ng/ml. The ability to quantify reproductive hormones in elephants via EIA is an important step in the process of making endocrine monitoring more accessible to zoos housing these species. Zoo Biol 21:403–408, 2002. © 2002 Wiley‐Liss, Inc.