Bacteraemia caused by beta-haemolytic streptococci in North Queensland: changing trends over a 14-year period.

Group A streptococci (GAS) are usually the predominant species in cases of bacteraemia caused by ß haemolytic streptococci (BHS). An increasing worldwide incidence of invasive disease from non-group A BHS has been reported. Little is known about the changing trends in invasive disease caused by BHS in Australia. North Queensland has a relatively large indigenous population, who experience significantly higher rates of group A-related disease than the non-indigenous population. This prospective study examined changing trends of disease from large colony BHS that group with A, B, C and G antisera over a 14-year period at the single large tertiary referral hospital in the area. We identified 392 bacteraemic episodes caused by BHS. GAS were most commonly isolated (49%), with adjusted rates remaining stable over the period. There was a significant increase in the incidence of non-neonatal bacteraemia caused by group B streptococci (GBS) over the study period (r = 0.58; p 0.030), largely driven by infection in older, non-indigenous women. Rates of bacteraemia caused by group C streptococci also experienced a modest, but significant, increase over time (r = 0.67; p 0.009). GAS, which had no predominant emm type, were seen most commonly in indigenous subjects (52%). Mortality rates ranged from 3.2% (group G) to 10.3% (group C), with a rate of 7.9% associated with group A disease. The marked rise in GBS disease has been noted worldwide, but the relatively low incidence in indigenous Australian patients has not been described before, despite the burden of well-recognized risk factors for GBS disease within this group.

Identifying the carotid 'high risk' plaque: is it still a riddle wrapped up in an enigma?

The selection of patients for many vascular interventions has largely been based on the severity of luminal narrowing. However, histological data from the coronary and carotid circulations suggest that other plaque features such as inflammation and fibrous cap thickness may be more important in predicting future thrombo-embolic events. This paper reviews the available evidence for identifying carotid atheroma at high risk of being associated with clinical events. Despite a large number of imaging and biomarker studies, 'presenting symptoms' remains the most clearly identified risk predictor for ischaemic stroke in patients with carotid stenosis. At present, no imaging modality or plasma biomarker has clearly identified a high risk sub-group of asymptomatic carotid stenoses for which the benefit of carotid intervention is comparable to that of symptomatic atherosclerosis. Emerging developments in MRI, transcranial Doppler and scintigraphic imaging hold some promise for the future. However, the multiple mechanisms and sites determining ischaemic stroke occurrence in association with atherosclerosis suggests that systemic therapies are likely to be the most powerful modality in the management of asymptomatic disease.

Solution and film properties of sodium caseinate/glycerol and sodium caseinate/polyethylene glycol edible coating systems.

The aim of this study is to determine the effects of plasticizer hydrogen bonding capability and chain length on the molecular structure of sodium caseinate (NaCAS), in NaCAS/glycerol and NaCAS/polyethylene glycol 400 (PEG) systems. Both solution and film phases were investigated. Glycerol and PEG reduced the viscosity of aqueous NaCAS, with the latter having a greater effect. This was explained in terms of protein/plasticizer aggregate size and changes to the conformation of the caseinate chain. In the film phase, glycerol caused more pronounced changes to the film tensile strength compared with PEG. However, the effect of glycerol on film water vapor permeability was smaller. These observations are attributed to the differences in plasticizer size and hydrogen bonding strength that controls the protein-plasticizer and protein-protein interactions in the films. Glass transition calculations from the tensile strength data indicate that the distribution of bonding interactions is more homogeneous in NaCAS/PEG films than in NaCAS/glycerol films.

Identification of adenosine functional groups involved in substrate binding by the ribonuclease P ribozyme.

The RNA component of bacterial ribonuclease P (RNase P) binds to substrate pre-tRNAs with high affinity and catalyzes site-specific phosphodiester bond hydrolysis to generate the mature tRNA 5' end. Herein we describe the use of biotinylated pre-tRNA substrates to isolate RNase P ribozyme-substrate complexes for nucleotide analogue interference mapping of ribozyme base functional groups involved in substrate recognition. By using a series of adenosine base analogues tagged with phosphorothioate substitutions, we identify specific chemical groups involved in substrate binding. Only 10 adenosines in the Escherichia coli ribozyme show significant sensitivity to interference: A65, A66, A136, A232-234, A248, A249, A334, and A347. Most of these adenosine positions are universally conserved among all bacterial RNase P RNAs; however, not all conserved adenosines are sensitive to analogue substitution. Importantly, all but one of the sensitive nucleotides are located at positions of intermolecular cross-linking between the ribozyme and the substrate. One site of interference that did not correlate with available structural data involved A136 in J11/12. To confirm the generality of the results, we repeated the interference analysis of J11/12 in the Bacillus subtilis RNase P ribozyme, which differs significantly in overall secondary structure. Notably, the B. subtilis ribozyme shows an identical interference pattern at the position (A191) that is homologous to A136. Furthermore, mutation of A136 in the E. coli ribozyme gives rise to a measurable increase in the equilibrium binding constant for the ribozyme-substrate interaction, while mutation of a nearby conserved nucleotide (A132) that is not sensitive to analogue incorporation does not. These results strongly support direct participation of nucleotides in the P4, P11, J5/15, and J18/2 regions of ribozyme structure in pre-tRNA binding and implicate an additional region, J11/12, as involved in substrate recognition. In aggregate, the interference results provide a detailed chemical picture of how the conserved nucleotides adjacent to the pre-tRNA substrate contribute to substrate binding and provide a framework for subsequent identification of the specific roles of these chemical groups in substrate recognition.