https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49080 Wed 03 May 2023 16:15:11 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45670 Wed 02 Nov 2022 16:06:29 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46722 Tue 29 Nov 2022 11:20:34 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:43350 Tue 28 Nov 2023 15:50:13 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36181 in silico and in vitro studies have identified factor Xa as an appropriate activating agent, and the phospholipid Actin FS as a cofactor for a Xa clotting time (TenaCT) test. A proof-of-concept study was designed to (1) explore the reproducibility of the TenaCT test and (2) explore factors that could affect the performance of the test. In vitro clotting time tests were carried out using plasma from 20 healthy volunteers. The effect of enoxaparin was determined at concentrations of 0.25, 0.50, and 1.0 IU/mL. Clotting times for the volunteers were significantly prolonged with increasing enoxaparin concentrations. Clotting times were significantly shortened for frozen plasma samples. No significant differences in prolongation of clotting times were observed between male and female volunteers or between the 2 evaluated age groups. The clotting times were consistent between 2 separate occasions. The TenaCT test was able to distinguish between the subtherapeutic and therapeutic concentrations of enoxaparin. Plasma should not be frozen prior to performing the test, without defining a frozen plasma reference range. This stu dy provided proof-of-concept for a Xa-based test that can detect enoxaparin dose effects, but additional studies are needed to further develop the test.]]> Tue 25 Feb 2020 10:13:34 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33780 Tue 03 Sep 2019 18:01:49 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:50513 Thu 27 Jul 2023 14:20:52 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:31207 E_max model linked to a turnover model for coagulation proteins. In the joint model, an unexpected pharmacodynamic lag was identified and the estimated degradation half-life of VK-dependent coagulation proteins were in agreement with previously published values. The model provided an adequate fit to the observed data. Conclusion: The joint model represents the first work to quantify the influence of warfarin on all six VK-dependent coagulation proteins simultaneously. Future work will expand the model to predict the influence of exogenously administered VK on the time course of clotting factor concentrations after warfarin overdose and during perioperative warfarin reversal procedures.]]> Sat 24 Mar 2018 08:44:46 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14411 Sat 24 Mar 2018 08:24:54 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14372 Sat 24 Mar 2018 08:23:10 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14374 Sat 24 Mar 2018 08:23:09 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14377 Sat 24 Mar 2018 08:23:08 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14863 90) of seizure, respectively. Results: A linear logistic regression model described the data. Simulation from the model showed that the probability of seizure was 0.05 (0.03–0.08), 0.19 (0.09–0.35) and 0.75 (0.30–0.96) at 1000, 5000 and 10 000 mg, respectively (median and 95% credible interval). At the mean dose of 2100 mg the odds ratios (OR) in the presence of SDAC, WBI and SDAC/WBI were 0.48 (0.25–0.89), 0.71 (0.35–1.22) and 0.25 (0.08–0.62), respectively. A modified Gompertz model described the time to seizure events. Simulations from the Gompertz model showed that the t₉₀ values for first seizure was 26 h and was not affected by dose or decontamination procedure. Conclusion: SDAC/WBI provided greater benefits than the sum of the independent effects of SDAC and WBI. Patients should be observed for at least 24 h for seizures based on the dose and risk of seizure occurring.]]> Sat 24 Mar 2018 08:21:09 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14471 Sat 24 Mar 2018 08:18:50 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:10455 Sat 24 Mar 2018 08:09:17 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:10751 1 g) were recruited from 2 state poison centers and a tertiary toxicology unit over 5 years. A 1-page clinical research form was used to collect clinical information. Copies of all electrocardiograms were obtained. Electrocardiogram parameters (QRS and QT intervals) were manually measured as previously described, and plots of QT-heart rate (HR) pairs were compared with the QT nomogram. There were 83 patients with amisulpride overdoses with a median age of 29 years (interquartile range [IQR], 23-40 years), and 42 (51%) were female. The median dose ingested was 6 g (IQR, 3-13 g, range, 1.2-120 g). The median HR was 66 beats/min (IQR, 60-81 beats/min). Bradycardia occurred in 20 cases (24%), and hypotension in 19 (23%). From 440 electrocardiograms (average of 5 per case; range, 1-15), an abnormal QT-HR pair occurred in 61 cases (73%). Torsades de pointes developed in 6 cases (7%), with doses of 4, 4.6, 18, 24, 32, and 80 g. The patient taking 32 g died after a cardiac arrest. Widened QRS did not occur except transient rate-dependent bundle-branch block in 3 cases. There were significant associations of bradycardia, hypokalemia, and hypocalcaemia, with QT prolongation and torsades de pointes. Central nervous system effects were uncommon with coma in 7 cases, seizures in 2, and dystonic reactions in 2. Amisulpride overdose commonly causes QT prolongation, bradycardia, and hypotension. Torsades de pointes occurred commonly enough to suggest that amisulpride is highly cardiotoxic in overdose.]]> Sat 24 Mar 2018 08:08:22 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21477 Sat 24 Mar 2018 08:03:42 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:5173 Sat 24 Mar 2018 07:47:42 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:29671 –1 provided a stable model and lowest objective function. This represents extremely rapid absorption with a half-life of 5 min. The final model had a clearance of 41.9 l h^–1 and volume of distribution of the central compartment of, 73.6 l. Median and interquartile range of initial (alpha) half-life was 0.32 h (0.26–0.37 h) and second (beta) half-life was 3.0 h (2.5–3.6 h). Simulations indicate that 10 mg alone provides an 80% probability of being above the lower limit of quantification (5 μg l^–1) for 7 h, 2 h longer than for 5 mg. Giving two 10 mg doses increased this duration to 10 h. Conclusions: Intramuscular droperidol is rapidly absorbed with high therapeutic concentrations after 5 and 10 mg doses, and supports clinical data in which droperidol sedates rapidly for up to 6 h.]]> Sat 24 Mar 2018 07:32:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:27040 Sat 24 Mar 2018 07:25:25 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26190 Sat 24 Mar 2018 07:24:09 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26752 -1, 5340 l and 130 l h^-1, respectively. The calculated half-life of sertraline following overdose was 28 h (IQR 19.4-30.6h). When given up to 4 h post-overdose, SDAC significantly increased the clearance of sertraline by a factor of 1.9, decreased the area under the curve and decreased the maximum plasma concentration (C_max). Conclusions: Sertraline had linear kinetics in overdose with parameter values similar to those in therapeutic use. SDAC is effective in increasing clearance when given 1.5 to 4 h post-overdose.]]> Mon 23 Sep 2019 11:21:00 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:44173 Mon 10 Oct 2022 10:13:31 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:39807 Fri 24 Jun 2022 08:46:01 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49785 10,000 U/L)]. The odds of (mild or severe) myotoxicity was lower in patients that received early antivenom (within 6 hours post-bite) compared to those that received late or no antivenom (odd ratio was 0.186; 95% confidence interval, 0.052–0.664). A population pharmacokinetic-pharmacodynamic (PKPD) model was developed to describe the relationship between the time course of venom (a mixture of toxins) and effect (elevated CK). In addition, a kinetic-pharmacodynamic (KPD) model was developed to describe the relationship between time course of a theoretical toxin and effect. Model development and parameter estimation was performed using NONMEM v7.3. No single set of parameter values from either the PKPD or KPD models were found that could accurately describe the time course of different levels of severity of myotoxicity. The predicted theoretical toxin half-life from the KPD model was 11 ± 3.9 hours compared to the half-life of venom of 5.3 ± 0.36 hours. This indicates that the putative causative toxin’s concentration-time profile does not parallel that of venom. Conclusion: Early antivenom administration reduces the incidence of myotoxicity. The venom concentration profile does not appear to be the driver for myotoxicity following envenomation. Additional factors that affect the sensitivity of the patient to snake venom/toxins must be explored to understand the relationship with myotoxicity.]]> Fri 02 Jun 2023 17:21:37 AEST ]]>