23 research outputs found
Prognostic model to predict postoperative acute kidney injury in patients undergoing major gastrointestinal surgery based on a national prospective observational cohort study.
Background: Acute illness, existing co-morbidities and surgical stress response can all contribute to postoperative acute kidney injury (AKI) in patients undergoing major gastrointestinal surgery. The aim of this study was prospectively to develop a pragmatic prognostic model to stratify patients according to risk of developing AKI after major gastrointestinal surgery. Methods: This prospective multicentre cohort study included consecutive adults undergoing elective or emergency gastrointestinal resection, liver resection or stoma reversal in 2-week blocks over a continuous 3-month period. The primary outcome was the rate of AKI within 7 days of surgery. Bootstrap stability was used to select clinically plausible risk factors into the model. Internal model validation was carried out by bootstrap validation. Results: A total of 4544 patients were included across 173 centres in the UK and Ireland. The overall rate of AKI was 14·2 per cent (646 of 4544) and the 30-day mortality rate was 1·8 per cent (84 of 4544). Stage 1 AKI was significantly associated with 30-day mortality (unadjusted odds ratio 7·61, 95 per cent c.i. 4·49 to 12·90; P < 0·001), with increasing odds of death with each AKI stage. Six variables were selected for inclusion in the prognostic model: age, sex, ASA grade, preoperative estimated glomerular filtration rate, planned open surgery and preoperative use of either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. Internal validation demonstrated good model discrimination (c-statistic 0·65). Discussion: Following major gastrointestinal surgery, AKI occurred in one in seven patients. This preoperative prognostic model identified patients at high risk of postoperative AKI. Validation in an independent data set is required to ensure generalizability
COBALT AND BACTERIAL GROWTH, WITH SPECIAL REFERENCE TO PROTEUS VULGARIS
For the past five years we have been engaged in an investigation of the effect of cobalt on the growth and metabolism of bacteria, especially of Proteus vul-garis. The emphasis on Proteus followed requests for aid in the control of growth of this penicillin- and sulfa-resistant organism in cases of peritonitis, cystitis, and eye infections. Interest in cobalt as a growth inhibitor of microorganisms has been extremely limited. Such studies as have been made deal primarily with the concentrations of the metal necessary to kill the cells of bacteria, yeast, or paramecia after a given period of exposure (Bokorny, 1905, 1913; Krauss and Collier, 1931; John-son, Carver, and Harryman, 1942). Apart from observations on the therapeutic use of cobalt in the treatment of tuberculosis (Renon, 1915; Rondoni, 1920; Mascherpa, 1929), no attempt, so far as we are aware, has been made to study in detail the nature of the action of cobalt on bacteria. In this paper we shall consider only those aspects of the growth-inhibitory effect of cobalt on bacteria, particularly P. vulgaris, which are of a cultura
Validation of Serum Neurofilament Light Chain as a Biomarker of Parkinson's Disease Progression
Background: The objective of this study
was to assess neurofilament light chain as a Parkinson’s
disease biomarker.
Methods: We quantified neurofilament light chain in
2 independent cohorts: (1) longitudinal cerebrospinal fluid
samples from the longitudinal de novo Parkinson’s disease cohort and (2) a large longitudinal cohort with serum
samples from Parkinson’s disease, other cognate/neurodegenerative disorders, healthy controls, prodromal conditions, and mutation carriers.
Results: In the Parkinson’s Progression Marker Initiative
cohort, mean baseline serum neurofilament light chain
was higher in Parkinson’s disease patients (13 � 7.2
pg/mL) than in controls (12 � 6.7 pg/mL), P = 0.0336.
Serum neurofilament light chain increased longitudinally in
Parkinson’s disease patients versus controls (P < 0.01).
Motor scores were positively associated with neurofilament light chain, whereas some cognitive scores
showed a negative association.
Conclusions: Neurofilament light chain in serum samples is increased in Parkinson’s disease patients versus healthy controls, increases over time and with age,
and correlates with clinical measures of Parkinson’s
disease severity. Although the specificity of neurofilament light chain for Parkinson’s disease is low, it
is the first blood-based biomarker candidate that could
support disease stratification of Parkinson’s disease
versus other cognate/neurodegenerative disorders,
track clinical progression, and possibly assess responsiveness to neuroprotective treatments. However, use of
neurofilament light chain as a biomarker of response
to neuroprotective interventions remains to be assessed