Organisms isolated from adults with Cystic Fibrosis

Abstract Background Patients with cystic fibrosis [CF] have frequent pulmonary exacerbations associated with the isolation of bacterial organisms from sputum samples. It is not clear however, if there are differences in the types of additional organisms isolated from patients who are infected with Burkholderia cepacia complex [BCC] or Pseudomonas aerugionsa [PA] in comparison to those who are not infected with either of these organisms [NI]. Methods Adult patients attending the regional CF unit were followed over a two year period and patients were assigned to three groups depending on whether they were known to be chronically infected with BCC, PA or NI. We compared the numbers and types of organisms which were isolated in each of these groups. Results Information was available on a total of 79 patients; BCC 23, PA 30 and NI 26. Total numbers of organisms isolated, expressed as median and IQR for each group, [P = 0.045] and numbers of co-infecting organisms [P = 0.003] were significantly higher in the BCC group compared to PA, and in the PA group [P Conclusions Total numbers of organisms isolated and numbers of co-infecting organisms were significantly higher in the BCC group compared to PA, and in the PA group compared to NI patients. Types of co-infecting organisms are similar in all groups of patients.</p

Intraischaemic hypothermia reduces free radical production and protects against ischaemic insults in cultured hippocampal slices

Hypothermia has been demonstrated to be an effective neuroprotective strategy in a number of models of ischaemic and excitotoxic neurodegeneration in vitro and in vivo. Reduced glutamate release and free radical production have been postulated as potential mechanisms underlying this effect but no definitive mechanism has yet been reported. In the current study, we have used oxygen–glucose deprivation in organotypic hippocampal slice cultures as an in vitro model of cerebral ischaemia. When assessed by propidium iodide fluorescence, reducing the temperature during oxygen–glucose deprivation to 31–33C was significantly neuroprotective but this effect was lost if the initiation of hypothermia was delayed until the post-insult recovery period. The neuroprotective effects of hypothermia were associated with a significant decrease in both nitric oxide production, as assessed by 3-amino-4-aminomethyl-2¢,7¢-difluorofluorescein fluorescence, and superoxide formation. Further, hypothermia significantly attenuated NMDA-induced nitric oxide formation in the absence of hypoxia/hypoglycaemia. We conclude that the neuroprotective effects of hypothermia are mediated through a reduction in nitric oxide and superoxide formation and that this effect is likely to be downstream of NMDA receptor activation