“Resistance to beta-lactam/beta-lactamase inhibitors in en

“Resistance to beta-lactam/beta-lactamase inhibitors in enterobacteria is a growing problem that has not been intensively studied in Argentina. In the present work, 54/843 enterobacteria collected in a teaching hospital of Buenos Aires city were ampicillin-sulbactam-resistant isolates remaining susceptible to second- and third-generation cephalosporins. The enzymatic mechanisms present in the isolates, which were also amoxicillin-clavulanic acid (AMC)-resistant (18/54) were herein analyzed. Sequencing revealed two different variants of bla(TEM-1), being bla(TEM-1B)

the most frequently detected allelle (10 Escherichia colt, 3 Klebsiella pneumoniae, 2 Proteus mirabilis and 1 Raoultella terrigena) followed

by bla(TEm-1a) PR-171 solubility dmso (1 K. pneumoniae). Amoxicillin-clavulanate resistance seems to be mainly associated with TEM-1 overproduction (mostly in E. colt) or co-expressed with OXA-2-like and/or SHY beta-lactamases (K. pneumoniae and P mirabilis). A new bla(TEM) variant (TEM-163) was described in an E. coli strain having an AMC MIC value of 16/8 mu g/ml. TEM-163 contains Arg(275)Gln and His(289)Leu amino acid substitutions. On the basis of the high specific activity and low IC50 for clavulanic acid observed, the resistance pattern seems to be due to overproduction of the new variant selleck chemicals of broad spectrum beta-lactamase

rather than to an inhibitor-resistant TEM (IRT)-like behavior. (C) 2014 Asociacion Argentina de Microbiologia. Published by Elsevier Espana, S.L. All rights reserved.”
“Spontaneous and/or treatment-evoked re-modeling of the CNS following spinal Cl-amidine cord injury is a prerequisite for functional recovery. While there has been considerable interest in the role of endogenous neurotrophins in spontaneous plasticity of several populations of spinal axons, the same cannot be said for morphological changes to dendrites. Here, we examined the responses of dendrites in the mouse lateral spinal nucleus (LSN, a site of sensory integration in the dorsolateral white matter) to exogenous and endogenous neurotrophins. We performed a septuple dorsal rhizotomy, which permanently eliminates sensory input to the spinal cord, and stimulates sprouting of spinal axons. While dendrites showed no change in density following injury alone, they sprouted vigorously (a two-fold increase in density) upon addition of exogenous brain-derived neurotrophic factor (BDNF). On the other hand, endogenous nerve growth factor (NGF) severely restricted dendritic sprouting, as TrkA-Fc treatment also roughly doubled the density of dendritic processes in the LSN. Spontaneous, BDNF- and TrkA-Fc mediated sprouting was unaffected by the absence of p75(NTR).

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