117 research outputs found
Auctioning Bulk Mobile Messages
The search for enablers of continued growth of SMS traffic, as well as
the take-off of the more diversified MMS message contents, open up for
enterprises the potential of bulk use of mobile messaging , instead of
essentially one-by-one use. In parallel, such enterprises or value
added services needing mobile messaging in bulk - for spot use or for
use over a prescribed period of time - want to minimize total
acquisition costs, from a set of technically approved providers of
messaging capacity.
This leads naturally to the evaluation of auctioning for bulk SMS or
MMS messaging capacity, with the intrinsic advantages therein such as
reduction in acquisition costs, allocation efficiency, and optimality.
The paper shows, with extensive results as evidence from simulations
carried out in the Rotterdam School of Management e-Auction room, how
multi-attribute reverse auctions perform for the enterprise-buyer, as
well as for the messaging capacity-sellers. We compare 1- and 5-round
auctions, to show the learning effect and the benefits thereof to the
various parties. The sensitivity will be reported to changes in the
enterprise's and the capacity providers utilities and priorities
between message attributes (such as price, size, security, and
delivery delay). At the organizational level, the paper also considers
alternate organizational deployment schemes and properties for an
off-line or spot bulk messaging capacity market, subject to technical
and regulatory constraints
Reduction of recurrent ischemia with abciximab during continuous ECG-ischemia monitoring in patients with unstable angina refractory to standard treatment (CAPTURE)
BACKGROUND: In the CAPTURE (c7E3 Fab Anti Platelet Therapy in Unstable
REfractory angina) trial, 1265 patients with refractory unstable angina
were treated with abciximab or placebo, in addition to standard treatment
from 16 to 24 hours preceding coronary intervention through 1 hour after
intervention. To investigate the incidence of recurrent ischemia and the
ischemic burden, a subset of 332 patients (26%) underwent continuous
vector-derived 12-lead ECG-ischemia monitoring. METHODS and RESULTS:
Patients were monitored from start of treatment through 6 hours after
coronary intervention. Ischemic episodes were detected in 31 (18%) of the
169 abciximab and in 37 (23%) of the 163 placebo patients (NS). Only 9
(5%) of abciximab versus 22 (14%) of placebo patients had >/=2 ST episodes
(P<0.01). In patients with ischemia, abciximab significantly reduced total
ischemic burden (P<0.02), which was calculated alternatively as the total
duration of ST episodes per patient, the area under the curve of the ST
vector magnitude during episodes, or the sum of the areas under the curves
of 12 leads during episodes. Twenty-one patients (6%) suffered a
myocardi
Comparison of usefulness of computer assisted continuous 48-h 3-lead with 12-lead ECG ischaemia monitoring for detection and quantitation of ischaemia in patients with unstable angina
AIMS: The selection of ECG leads used for ST monitoring may influence detection and quantitation of ischaemia. METHODS: We compared on-line continuous 48-h 12-lead against 3-lead ST monitoring in 130 unstable angina patients (Mortara. ELI-100). Onset and offset of ST episodes were defined by the lead with the first > or = 100 microV ST change relative to baseline and the lead with the latest return to baseline ST level, respectively. ST episodes were calculated for 12 leads and 3 leads (V2, V5, III) separately. RESULTS: ST episodes were detected in 88 patients (77%) by 12-lead and in 71 patients (62%) by 3-lead ST monitoring (P < 0.02). The median number (25.75%) of episodes/patient was 1 (0.3) for 3-lead and 2 (1.6) for 12-lead (P < 0.0001). The total duration of ischaemia detected during 12-lead far exceeded 3-lead monitoring: 12.3 (1, 58.2) and 1.7 (0, 23.3) min respectively (P < 0.0001). The probability of recurrent ischaemia declined most during the first 24 h of monitoring. After a period without ST changes of 1, 12, 24 and 36 h, the probabilities of recurrent ischaemia were 63, 31, 14 and 9%, respectively. CONCLUSIONS: Continuous 12-lead ST monitoring increases detection rate and duration of ST episodes compared to 3-lead ST monitoring. The use of continuous 12-lead ECG monitoring devices on emergency wards and coronary care units is recommended
Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC): Compound heterozygous mutation in the claudin 16 (CLDN16) gene
<p>Abstract</p> <p>Background</p> <p>Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC) is an autosomal recessive disorder of renal calcium and magnesium wasting frequently complicated by progressive chronic renal failure in childhood or adolescence.</p> <p>Methods</p> <p>A 7 year old boy was investigated following the findings of marked renal insufficiency and nephrocalcinosis in his 18-month old sister. He too was found to have extensive nephrocalcinosis with increased fractional excretion of magnesium: 12.4% (<4%) and hypercalciuria: 5.7 mmol (< 2.5/24 hours). He had renal impairment, partial distal renal tubular acidosis and defective urinary concentrating ability. Therapy with thiazide diuretics and magnesium supplements failed to halt the progression of the disorder. Both children subsequently underwent renal transplantation. Both children's parents are unaffected and there is one unaffected sibling.</p> <p>Results</p> <p>Mutation analysis revealed 2 heterozygous mutations in the claudin 16 gene <it>(CLDN16</it>) in both affected siblings; one missense mutation in exon 4: C646T which results in an amino acid change Arg216Cys in the second extracellular loop of <it>CLDN16 </it>and loss of function of the protein and a donor splice site mutation which changes intron 4 consensus splice site from 'GT' to 'TT' resulting in decreased splice efficiency and the formation of a truncated protein with loss of 64 amino acids in the second extracellular loop.</p> <p>Conclusion</p> <p>The mutations in <it>CLDN16 </it>in this kindred affect the second extra-cellular loop of claudin 16. The clinical course and molecular findings suggest complete loss of function of the protein in the 2 affected cases and highlight the case for molecular diagnosis in individuals with FHHNC.</p
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