Indomethacin decreased intracranial pressure and cerebral blood flow, and increased cerebral perfusion pressure, while maintaining tissue properties of further extracting O(2). The increase in both autoregulatory values reveals an enhancement of cerebral microvasculature reactivity under indomethacin, during hypertensive and--especially--during hypotensive situations.

ᰔThe presence of aac(6Ј)-Ib-cr is associated with decreased susceptibility to aminoglycosides (kanamycin, amikacin, and tobramycin) and to norfloxacin and ciprofloxacin (9). This allelic variant of aac(6Ј)-Ib was found to be linked to the extendedspectrum ␤-lactamase (ESBL) gene bla in isolates from many countries (4, 6, 7), while association of aac(6Ј)-Ib with the bla CTX-M-2 ESBL gene has been widely reported in Uruguay and Argentina (3,11).In this work we looked for the presence of aac(6Ј)-Ib and the aac(6Ј)-Ib-cr variant and their putative ESBL coresistance markers in fecal isolates of enterobacteria resistant to ciprofloxacin and/or ceftazidime from inpatients in an intensive care unit (ICU) in Montevideo, Uruguay.From 1 March to 31 October 2006, 106 patients were admitted to this ICU and followed daily until discharge. Rectal swabs obtained at 1, 4, 7, 10, 13, and 16 days after admission were plated on MacConkey agar plus ceftazidime (4 mg/liter) or ciprofloxacin (2 mg/liter). Enterobacterial isolates were identified by classical methods, including only the first isolate of each bacterial species per patient in this study.Antibiotic resistance profiling, screening, and confirmatory testing for ESBL detection were performed by disk diffusion assay, and results were interpreted following the CLSI guidelines (2).A total of 58/106 patients (55.2%) were colonized with ciprofloxacin-and/or ceftazidime-resistant enterobacteria, and 68 isolates were included in this study. Of these, 48 were resistant to gentamicin and 24 to amikacin (Table 1).All aminoglycoside-resistant isolates were screened for aac(6Ј)-Ib by PCR; amplicons were analyzed by restriction with BstF5I, as described by Park et al. (8). PCR products that were not digested by the enzyme [tentatively assigned to aac(6Ј)-Ibcr] were confirmed to contain aac(6Ј)-Ib-cr by double-strand sequencing. Only two Escherichia coli isolates were positive for aac(6Ј)-Ib-cr detection.Recalling the observed links between bla CTX-M-15 and aac(6Ј) 6,7) and between aac(6Ј)Ib and bla CTX-M-2 , the two aac(6Ј)-Ib-cr-positive isolates were further analyzed by PCR to detect CTX-M-1 and CTX-M-2 group ESBL genes using previously described primers (3, 5). Both isolates were positive only for CTX-M-1 group genes, identified as bla CTX-M-15 after sequencing.Both isolates were obtained at the time of patient admission into the ICU and showed identical pulsed-field gel electrophoresis patterns (10). Both patients were previously hospitalized before ICU admission, suggesting that this strain could be endemic in the hospital, where it could be horizontally transferred. All the other E. coli isolates yielded different pulsotypes (data not shown) compared with these.PCR assays for the detection of class 1 integrons and ISCR1 elements were performed according to the method of Di Conza et al. (3). Both isolates carried a class 1 integron containing the dfr17 and aadA5 gene cassettes, while ISCR1 elements were not detected.So far we have not been able to transfer these resistance genes, e...

A sharp dynamic vasodilator response could not be sustained, and a slow or absent reaction to a sudden hypotensive challenge could show an acceptable cerebral autoregulation in the steady state. We found that patients with impaired static cerebral autoregulation had a poor outcome, whereas those with preserved static cerebral autoregulation experience favorable outcomes.

Trypanosoma cruzi, the aetiological agent of Chagas disease, has a highly efficient detoxification system to deal with the oxidative burst imposed by its host. One of the antioxidant enzymes involved is the cytosolic tryparedoxin peroxidase (c-TXNPx), which catalyses the reduction to hydrogen peroxide, small-chain organic hydroperoxides and peroxynitrite. This enzyme is present in all parasite stages, and its overexpression renders parasites more resistant to the oxidative defences of macrophages, favouring parasite survival. This work addressed the study of the specific humoral and cellular immune response triggered by c-TXNPx in human natural infection. Thus, sera and peripheral blood mononuclear cells (PBMC) were collected from chronically infected asymptomatic and cardiac patients, and non-infected individuals. Results showed that levels of IgG antibodies against c-TXNPx were low in sera from individuals across all groups. B-cell epitope prediction limited immunogenicity to a few, small regions on the c-TXNPx sequence. At a cellular level, PBMC from asymptomatic and cardiac patients proliferated and secreted interferon-γ after c-TXNPx stimulation, compared with mock control. However, only proliferation was higher in asymptomatic patients compared with cardiac and non-infected individuals. Furthermore, asymptomatic patients showed an enhanced frequency of CD19 CD69 cells upon exposure to c-TXNPx. Overall, our results show that c-TXNPx fails to induce a strong immune response in natural infection, being measurable only in those patients without any clinical symptoms. The low impact of c-TXNPx in the human immune response could be strategic for parasite survival, as it keeps this crucial antioxidant enzyme activity safe from the mechanisms of adaptive immune response.