43 research outputs found
Validation of the DECAF score to predict hospital mortality in acute exacerbations of COPD
Background
Hospitalisation due to acute
exacerbations of COPD (AECOPD) is common, and
subsequent mortality high. The DECAF score was derived
for accurate prediction of mortality and risk strati
fi
cation
to inform patient care. We aimed to validate the DECAF
score, internally and externally, and to compare its
performance to other predictive tools.
Methods
The study took place in the two hospitals
within the derivation study (internal validation) and in
four additional hospitals (external validation) between
January 2012 and May 2014. Consecutive admissions
were identi
fi
ed by screening admissions and searching
coding records. Admission clinical data, including DECAF
indices, and mortality were recorded. The prognostic
value of DECAF and other scores were assessed by the
area under the receiver operator characteristic (AUROC)
curve.
Results
In the internal and external validation cohorts,
880 and 845 patients were recruited. Mean age was
73.1 (SD 10.3) years, 54.3% were female, and mean
(SD) FEV
1
45.5 (18.3) per cent predicted. Overall
mortality was 7.7%. The DECAF AUROC curve for
inhospital mortality was 0.83 (95% CI 0.78 to 0.87) in
the internal cohort and 0.82 (95% CI 0.77 to 0.87) in
the external cohort, and was superior to other
prognostic scores for inhospital or 30-day mortality.
Conclusions
DECAF is a robust predictor of mortality,
using indices routinely available on admission. Its
generalisability is supported by consistent strong
performance; it can identify low-risk patients (DECAF
0
–
1) potentially suitable for Hospital at Home or early
supported discharge services, and high-risk patients
(DECAF 3
–
6) for escalation planning or appropriate early
palliation.
Trial registration number
UKCRN ID 14214
Larval rearing of barramundi (Lates calcarifer) in saline groundwater
Barramundi (Lates calcarifer) larvae were reared from 2 to 25 days post hatch in 14‰ saline groundwater with either no potassium supplementation (38% K-equivalence) or full potassium supplementation (100% K-equivalence). Growth, survival and swimbladder inflation of these larvae were compared against those grown in control treatments of seawater (32‰) and seawater diluted to 14‰. Those reared in saline groundwater with 38% K-equivalence exhibited complete mortality within 2 days, while those held in groundwater with full supplementation survived at a rate equal to both control treatments (pooled average 51.1 ± 0.5%). At 25 days post hatch, there was no significant difference in larval length or dry weight between those grown in the 14‰ control treatment and those in the saline groundwater with full potassium supplementation. There were no significant differences in swim bladder inflation between any of the surviving treatments (average 93.3 ± 2.5%). This is the first description of rearing barramundi larvae both in low salinity seawater and in saline groundwater and demonstrates that the requirement for potassium by larval barramundi is higher than for juveniles of the same species
Ionic mechanisms regulating thyroidal secretion: Effects of ouabain and medium sodium concentration on radioiodine release from cultured porcine thyroid cells
Role of sodium influx in thyrotrophin action: Effects of the sodium channel agonist veratridine and thyrotrophin on radioiodine turnover and membrane potential in cultured porcine thyroid cells
Cyclic AMP-stimulated fluid transport in the thyroid: Influence of thyroid stimulators, amiloride and acetazolamide on the dynamics of domes in monolayer cultures of porcine thyroid cells
Confluent monolayer cultures of porcine thyroid cells form dome-shaped elevations by local separation from the plastic culture dish. Formation of domes by epithelial cells in culture is generally considered to be evidence of fluid transport. A computer-controlled data acquisition system was developed to quantitate fluid transport in thyroid cultures by serial measurements of dome elevation. Thyrotrophin (10 mU/ml), prostaglandin E2 (PGE2; 0.01-1 mumol/l), forskolin (1 mumol/l), 8-(4-chlorophenylthio)adenosine 3':5'-cyclic monophosphate (0.5 mmol/l) and 3-isobutyl-1-methyl-xanthine (0.5 mmol/l) promoted increases in dome height over 5-120 min. Dome growth in the presence of PGE2 (1 mumol/l) was inhibited by amiloride (0.1-100 mumol/l), ouabain (200 mumol/l), or by removal of bicarbonate and glucose from the medium. In media of reduced bicarbonate concentration (1 mmol/l compared with the control concentration of 10 mmol/l), dome growth was inhibited by acetazolamide (0.01-1 mmol/l). These data are consistent with cyclic AMP-stimulated transport of fluid from apical to basal pole of the cells, dependent on sodium entry through the apical pole by an Na+/H+ exchanger
Sodium dependence of the thyrotrophin-induced depolarization in cultured porcine thyroid cells
Electrical responses of cultured porcine thyroid cells to adrenergic agents
The membrane potential of cultured porcine thyroid follicular cells depolarized by up to 20 mV from the resting value of about -73 mV on exposure to β-adrenoceptor agonists. A similar response was induced by TSH or dibutyryl cyclic AMP. α-Adrenoceptor agonists were without effect. The receptor subtype was shown to be (at least predominantly) β by the order of potency for β-agonists (isoprenaline ≃ fenoterol >> adrenaline > noradrenaline) and by the relative potency of selective β-antagonists (ICI 118,551 >> atenolol). The α-agonist phenylephrine had no effect on the TSH response but weakly inhibited the β-agonist response. Rather than a physiological antagonism between α- and β-adrenoceptor-mediated responses, this effect was shown to be due to the weak β-antagonist effect of phenylephrine since the α-antagonist phentolamine failed to potentiate the depolarizing response to the mixed agonist noradrenaline, and also failed to block the inhibitory action of phenylephrine on the β-agonist effect. Sensitivity to β-agonist was enhanced by omission of serum from the culture medium and reduced by exposure to β-agonists or a high concentration of TSH or dibutyryl cyclic AMP