The present findings support the hypothesis that ACE I/D and APO E gene polymorphisms may play a role in the development of acute kidney injury after cardiac surgery. However, AGTR1 does not have a unique association with postoperative renal impairment.

Elevated levels of homocysteine is a risk factor for coronary artery disease. The C677T transition in methylenetetrahydrofolate reductase (MTHFR) is associated with increased homocysteine levels in the general population. We analysed the association between the MTHFR C677T polymorphism and serum homocysteine concentrations in patients with coronary artery disease (CAD). Allele frequencies for the 'C' (wild-type) and 'T' alleles were 0.71 and 0.29 in CAD patients and 0.70 and 0.30 in controls, respectively. There was no difference in the distribution of MTHFR genotypes between patients with CAD and control subjects (p > 0.05). In the patient group, homocysteine levels were higher than controls but not significantly (13.99 +/- 7.44 vs. 11.77 +/- 5.18 micromol l(-1); p > 0.05). Serum homocysteine concentration was significantly higher in the TT genotype with respect to CC and CT genotypes in both the control group (p < 0.01) and patient group (p < 0.01). Systolic and diastolic blood pressures in subjects with different MTHFR genotypes did not differ significantly. In conclusion, MTHFR C677T mutation was significantly related to hyperhomocysteinemia. In spite of the clear effect of the MTHFR polymorphism on elevated homocysteine levels, we did not observe any associations among the MTHFR genotypes with a the risk of CAD in the Turkish population.

The strictly anaerobic Gram-negative bacteria Butyricimonas species have recently been described in human faeces and have to our knowledge not been isolated in infectious clinical materials. We report the first case of Butyricimonas virosa bacteraemia in a 72-year-old man with colon adenocarcinoma, who underwent aortic aneurysm replacement surgery.

These results suggest that prophylactic use of FK506, azathioprine and L-carnitine protects motor neuron cells from ischemic spinal cord injury.

The study was designed to clarify whether captopril, an angiotensin-coverting enzyme inhibitor, will reduce the injury of global ischaemia and reperfusion after cardioplegic arrest in isolated guinea pig hearts, in a modified Langendorff model. The hearts were randomly allocated into four groups (n = 10 in each) and subjected to 90 min of normothermic global ischemia, followed by 30 min of reperfusion; in all groups, cardioplegic arrest was achieved by administering St. Thomas's Hospital cardioplegic solution (STHCS). The first group was utilized as the control group. In the second group, captopril (200 mumol/L) was added to STHCS. In the third group, oral pretreatment was carried out (0.3 mg/kg captopril was given twice a day for 10 days). In the fourth group, oral pretreatment was achieved and captopril-enriched solution was applied in the first 5 min of reperfusion. Although the study groups showed better recovery of contractility than the control group, in the fourth group the hearts had the best left ventricular contractile function, where contractile force (g contractility/g heart weight) was 55.4% +/- 3.8% of the preischameic values. Groups I, II, and III achieved 31.0% +/- 3.2%, 41.6% +/- 3.8%, and 48.3% +/- 3.9% of their preischaemic contractile force values. Creatine kinase leakage was significantly lower and postischaemic coronary flows, too, were significantly higher in the fourth group. Coronary flow after reperfusion increased from 48.5 +/- 6.7 to 65.2 +/- 7.1 ml/min g heart in group 4 (p < 0.05). Myocardial lipid peroxides and glutathione contents showed that there was a correlation between the depletion of myocardial glutathione content and increased lipid peroxidation. These preliminary results showed that: the addition of captopril to reperfusion solution and oral preconditioning improved post-ischameic myocardial function and decreased myocardial injury.