Factors associated with timing of early neurological improvement after thrombolysis for ischaemic stroke.

BACKGROUND: Early neurological improvement (ENI) after fibrinolysis for ischaemic stroke is strongly associated with recanalization and favourable outcome. However, it remains unknown why some patients recover within the first hour after treatment (very ENI, VENI) whereas others recover later within 24 h. AIM: The factors associated with the timing of ENI were assessed. METHODS: Consecutive stroke patients treated with intravenous recombinant tissue plasminogen activator (rt-PA) within 4.5 h after onset in four stroke centres of our geographical area were retrospectively studied. VENI assessed at 1 h and ENI assessed at 24 h post-treatment were defined by National Institutes of Health Stroke Scale (NIHSS) improvement by 40% from baseline. RESULTS: Of 421 patients, 65 (15%) had VENI and 110 (26%) had ENI. Patients with VENI had significantly lower serum creatinine level than patients with ENI (79 ± 19 vs. 91 ± 35 µmol/l; P = 0.01). After adjustment for age, sex, baseline NIHSS, hypertension and blood glucose level, patients with low serum creatinine level were more likely to have VENI (lowest tertile, odds ratio 3.8, 95% confidence interval 1.5-9.7; intermediate tertile, odds ratio 1.8, 95% confidence interval 0.8-4.3; P for trend <0.01). VENI patients were as likely as ENI patients to have a modified Rankin scale score ≤2 at 3 months. CONCLUSIONS: Low serum creatinine levels are associated with VENI, suggesting that swiftness of the efficacy of rt-PA or of neurological recovery may depend on renal function.

Outbreak of haemolytic uraemic syndrome due to Shiga toxin-producing Escherichia coli O104:H4 among French tourists returning from Turkey, September 2011.

Eight cases of diarrhoea, including two cases of haemolytic uraemic syndrome (HUS), were identified among 22 French tourists who travelled to Turkey in September 2011. A strain of Escherichia coli O104:H4 stx2-positive, eae-negative, hlyA-negative, aggR-positive, ESBL-negative was isolated from one HUS case. Molecular analyses show this strain to be genetically similar but not indistinguishable from the E. coli O104:H4 2011 outbreak strain of France and Germany. Although the source of infection was not identified, we conclude that the HUS cases had probably been infected in Turkey.

Prevention of mutant SOD1 motoneuron degeneration by copper chelators in vitro.

An animal model of familial amyotrophic lateral sclerosis (FALS) has been generated by overexpression of human CuZn superoxide dismutase (SOD1) containing a substitution of glycine to alanine at position 93 in transgenic G93A mice. The loss of motoneurons shown in this model has been attributed to a dominant gain of function of this mutated enzyme, which might be due to copper toxicity. This hypothesis was tested in purified spinal motoneurons cultures originating from G93A transgenic embryos. Spinal motoneurons were isolated from E13 embryos by several steps including density gradient centrifugation. The effect of copper chelators on survival and neurite growth of motoneurons was investigated. Survival of G93A motoneurons was decreased by 46% as compared to wild-type motoneurons. Moreover, G93A motoneurons showed reduced neurite outgrowth. Copper chelators strikingly increased viability of G93A motoneurons (by over 200%) but had no effect on wild-type cells. Presence of DDC in the medium increases the length of neurites from G93A motoneurons. The present results suggest the capacity of copper chelators to reduce the effect of reverse function of mutated SOD1 on motoneurons.