59 research outputs found
Collaborative e-Purchasing for Hospitals: IT for Addressing Collaborative Purchasing Impediments
The benefits of collaborative purchasing are many, yet in the healthcare sector, in particular at hospitals, it is still uncommon. In this paper we identify major impediments for collaborative purchasing, resulting in a first component of our proposed collaborative e-purchasing model for hospitals; as a second component it contains a collaborative purchasing typology. After analysis of a first validation round with hospital purchasing professionals, the results show four applicable purchasing types and fourteen collaborative purchasing impediments that are perceived as important for hospitals. The model is further extended by possible IT solutions, identified by experts, addressing the specific fourteen impediments. We conclude that the collaborative e-purchasing model can be used by healthcare consortia, branche organizations, partnering healthcare institutes and multi-site healthcare institutes as a means to help identifying strategies to initiate, manage and evaluate collaborative purchasing practices
Role of the Helicobacter pylori outer-membrane proteins AlpA and AlpB in colonization of the guinea pig stomach
The human gastric pathogen Helicobacter pylori expresses several putative
outer-membrane proteins (OMPs), but the role of individual OMPs in
colonization of the stomach by H. pylori is still poorly understood. The
role of four such OMPs (AlpA, AlpB, OipA and HopZ) in a guinea pig model
of H. pylori infection has been investigated. Single alpA, alpB, hopZ and
oipA isogenic mutants were constructed in the guinea pig-adapted,
wild-type H. pylori strain GP15. Guinea pigs were inoculated
intragastrically with the wild-type strain, single mutants or a mixture of
the wild-type and a single mutant in a 1: 1 ratio. Three weeks after
infection, H. pylori could be isolated from stomach sections of all
animals that were infected with the wild-type, the hopZ mutant or the oipA
mutant, but from only five of nine (P = 0.18) and one of seven (P = 0.02)
animals that were infected with the alpA or alpB mutants, respectively.
The hopZ and oipA mutants colonized the majority of animals that were
inoculated with the strain mixture, whereas alpA and alpB mutants could
not be isolated from anim
Raman spectroscopy-based identification of nosocomial outbreaks of the clonal bacterium Escherichia coli
DNA-based techniques are frequently used to confirm the relatedness of putative outbreak isolates. These techniques often lack the discriminatory power when analyzing closely related microbes such as E. coli. Here the value of Raman spectroscopy as a typing tool for E. coli in a clinical setting was retrospectively evaluated
NikR mediates nickel-responsive transcriptional induction of urease expression in Helicobacter pylori
The important human pathogen Helicobacter pylori requires the abundant
expression and activity of its urease enzyme for colonization of the
gastric mucosa. The transcription, expression, and activity of H. pylori
urease were previously demonstrated to be induced by nickel
supplementation of growth media. Here it is demonstrated that the HP1338
protein, an ortholog of the Escherichia coli nickel regulatory protein
NikR, mediates nickel-responsive induction of urease expression in H.
pylori. Mutation of the HP1338 gene (nikR) of H. pylori strain 26695
resulted in significant growth inhibition of the nikR mutant in the
presence of supplementation with NiCl(2) at > or =100 microM, whereas the
wild-type strain tolerated more than 10-fold-higher levels of NiCl(2).
Mutation of nikR did not affect urease subunit expression or urease enzyme
activity in unsupplemented growth media. However, the nickel-induced
increase in urease subunit expression and urease enzyme activity observed
in wild-type H. pylori was absent in the H. pylori nikR mutant. A similar
lack of nickel responsiveness was observed upon removal of a 19-bp
palindromic sequence in the ureA promoter, as demonstrated by using a
genomic ureA::lacZ reporter gene fusion. In conclusion, the H. pylori NikR
protein and a 19-bp operator sequence in the ureA promoter are both
essential for nickel-responsive induction of urease expression in H.
pylori
Does CDX2 expression predict Barrett's metaplasia in oesophageal columnar epithelium without goblet cells?
Background: Intestinal metaplasia (Barrett's oesophagus), but not cardiac-type mucosa in columnar-lined oesophagus, is regarded as premalignant. As intestinal metaplasia and cardiac-type mucosa are endoscopically indiscernible, it is difficult to take targeted samples from columnar-lined oesophagus with consequently a risk of having undetected intestinal metaplasia. Aim: To investigate whether the intestinal markers CDX2, MUC2 and villin can predict the presence of undetected intestinal metaplasia in columnar-lined oesophagus. Methods: Presence of intestinal metaplasia or cardiac-type mucosa was identified in 122 biopsy sets of columnar-lined oesophagus from 61 patients, collected at two subsequent follow-up upper endoscopies. CDX2, MUC2 and villin expression were determined by immunohistochemistry. Results: All intestinal metaplasia samples (55) were positive for CDX2 and MUC2 and 32 of 55 for vil
Role of the rdxA and frxA genes in oxygen-dependent metronidazole resistance of Helicobacter pylori
Almost 50 % of all Helicobacter pylori isolates are resistant to
metronidazole, which reduces the efficacy of metronidazole-containing
regimens, but does not make them completely ineffective. This discrepancy
between in vitro metronidazole resistance and treatment outcome may
partially be explained by changes in oxygen pressure in the gastric
environment, as metronidazole-resistant (MtzR) H. pylori isolates become
metronidazole-susceptible (MtzS) under low oxygen conditions in vitro. In
H. pylori the rdxA and frxA genes encode reductases which are required for
the activation of metronidazole, and inactivation of these genes results
in metronidazole resistance. Here the role of inactivating mutations in
these genes on the reversibility of metronidazole resistance under low
oxygen conditions is established. Clinical H. pylori isolates containing
mutations resulting in a truncated RdxA and/or FrxA protein were selected
and incubated under anaerobic conditions, and the effect of these
conditions on the MICs of metronidazole, amoxycillin, clarithromycin and
tetracycline, and cell viability were determined. While anaerobiosis had
no effect on amoxycillin, clarithromycin and tetracycline resistance, all
isolates lost their metronidazole resistance when cultured under anaerobic
conditions. This loss of metronidazole resistance also occurred in the
presence of the protein synthesis inhibitor chloramphenicol. Thus,
factor(s) that activate metronidazole under low oxygen tension are not
specifically induced by low oxygen conditions, but are already present
under microaerophilic conditions. As there were no significant differences
in cell viability between the clinical isolates, it is likely that neither
the rdxA nor the frxA gene participates in the reversibility of
metronidazole resistance
Transcriptional profiling of Helicobacter pylori Fur- and iron-regulated gene expression
Intracellular iron homeostasis is a necessity for almost all living
organisms, since both iron restriction and iron overload can result in
cell death. The ferric uptake regulator protein, Fur, controls iron
homeostasis in most Gram-negative bacteria. In the human gastric pathogen
Helicobacter pylori, Fur is thought to have acquired extra functions to
compensate for the relative paucity of regulatory genes. To identify H.
pylori genes regulated by iron and Fur, we used DNA array-based
transcriptional profiling with RNA isolated from H. pylori 26695 wild-type
and fur mutant cells grown in iron-restricted and iron-replete conditions.
Sixteen genes encoding proteins involved in metal metabolism, nitrogen
metabolism, motility, cell wall synthesis and cofactor synthesis displayed
iron-dependent Fur-repressed expression. Conversely, 16 genes encoding
proteins involved in iron storage, respiration, energy metabolism,
chemotaxis, and oxygen scavenging displayed iron-induced Fur-dependent
expression. Several Fur-regulated genes have been previously shown to be
essential for acid resistance or gastric colonization in animal models,
such as those encoding the hydrogenase and superoxide dismutase enzymes.
Overall, there was a partial overlap between the sets of genes regulated
by Fur and those previously identified as growth-phase, iron or acid
regulated. Regulatory patterns were confirmed for five selected genes
using Northern hybridization. In conclusion, H. pylori Fur is a versatile
regulator involved in many pathways essential for gastric colonization.
These findings further delineate the central role of Fur in regulating the
unique capacity of H. pylori to colonize the human stomach
Detection of Helicobacter pylori in bile of cats
Lymphocytic cholangitis (LC) in cats is a biliary disease of unknown etiology. Helicobacter spp. were recently implicated in human primary sclerosing cholangitis (PSC) and primary biliary cirrhosis (PBC). Because of the similarities between PSC/PBC with LC, we hypothesized that Helicobacter spp. are involved in feline LC. A PCR with Helicobacter genus-specific 16S rRNA primers was performed on DNA isolated from feline bile samples. Four of the 15 (26%) LC samples were positive, whereas only 8/51 (16%) of non-LC samples were PCR positive (p=0.44). Sequence analysis of the amplicons revealed a 100% identity with the Helicobacter pylori specific DNA fragments. Our data suggest an etiological role of H. pylori in feline LC and that cats are a potential zoonotic reservoir
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