A specific, highly active malate dehydrogenase by redesign of a lactate dehydrogenase framework

Three variations to the structure of the nicotinamide adenine dinucleotide (NAD)-dependent L-lactate dehydrogenase from Bacillus stearothermophilus were made to try to change the substrate specificity from lactate to malate: Asp197----Asn, Thr246----Gly, and Gln102----Arg). Each modification shifts the specificity from lactate to malate, although only the last (Gln102----Arg) provides an effective and highly specific catalyst for the new substrate. This synthetic enzyme has a ratio of catalytic rate (kcat) to Michaelis constant (Km) for oxaloacetate of 4.2 x 10(6)M-1 s-1, equal to that of native lactate dehydrogenase for its natural substrate, pyruvate, and a maximum velocity (250 s-1), which is double that reported for a natural malate dehydrogenase from B. stearothermophilus.     

The life cycle of Chloromyxum auratum (Myxozoa) from goldfish, Carassius auratus (L.), involves an antonactinomyxon actinospore

The myxozoan parasite Chloromyxum auratum Hallett, Atkinson, Holt, Banner & Bartholomew, 2006 , was shown experimentally to have a two‐host life cycle which involved a previously undescribed antonactinomyxon actinospore stage. Myxospores obtained from gall bladders of naturally infected feral goldfish, Carassius auratus (L.), were used to infect samples of mixed species of oligochaete worms obtained from the same locality as the fish: Fern Ridge Dam, Oregon, USA. After some 110 days post‐exposure, actinospores were detected from the water above the oligochaetes. The 18S rDNA sequence of these actinospores was identical to the original myxospores. Spore release was sporadic, of low intensity and short duration, which confounded efforts to identify the host oligochaete species and infect naïve fish. This is the first life cycle that incorporates an actinospore of the collective group Antonactinomyxon, and the first life cycle demonstrated in the laboratory for a species of Chloromyxum.     

Idiopathic muscle necrosis in the Norway lobster, Nephrops norvegicus (L.): aetiology, pathology and progression to bacteraemia

The pathology and progression of idiopathic muscle necrosis (IMN) in Nephrops norvegicus and possible aetiologies have been investigated. Trawl capture, aerial exposure and handling initiate IMN, and the condition can be induced through periods of aerial exposure alone, in the absence of trawling. Within 24-48 h after trawl capture IMN progresses to a multi-species bacterial septicaemia, with moribund animals exhibiting clinical signs. The aetiology of this condition has been examined using molecular (16S rRNA gene sequencing) and biochemical (standard taxonomic assays, Biolog) criteria to characterize bacterial isolates from moribund and healthy animals. Histopathology of the IMN phase reveals a loss of sarcomeric structure with necrotic lesions containing pyknotic nuclei, fragments of myofibrils and connective tissue elements. In the bacterial phase there is extensive loss of abdominal muscle structure, and the presence of rod-shaped Gram-negative bacteria in the degrading tissues. The results demonstrate that the IMN condition is connected to stressful conditions imposed on N. norvegicus, but involves no pathogenic agents. This is followed by an opportunistic bacterial infection that causes further tissue spoilage. It is believed that the primary cause of both IMN and bacteraemia is imposed stress, but they are expressed in different time courses.     

Do Environmental Worldviews and Distrust Influence Action for Adaptation to Environmental Change Among Small-Scale Woodland Managers?

Small-scale Forestry - Forest and woodland owners and managers are generally perceived to be acting slowly in addressing environmental change by adapting their forestry practice. Diversification of...