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E B Martin

Publications and source records attributed to E B Martin.

6 recordsLinked to original sources
PubMed2002

Enhanced bio-manufacturing through advanced multivariate statistical technologies.

The paper describes the interrogation of data, from a reaction vessel producing an active pharmaceutical ingredient (API), using advanced multivariate statistical techniques. Due to the limited number of batches available, data augmentation was used to increase the number of batches thereby enabling the extraction of more subtle process behaviour from the data. A second methodology investigated was that of multi-group modelling. This allowed between cluster variability to be removed, thus allowing attention to focus on within process variability. The paper describes how the different approaches enabled the realisation of a better understanding of the factors causing the onset of an impurity formation to be obtained as well demonstrating the power of multivariate statistical data analysis techniques to provide an enhanced understanding of the process.

Artifacts↗
PubMed1999

Aerosol delivery of diethylenetriamine/nitric oxide, a nitric oxide adduct, causes selective pulmonary vasodilation in perinatal lambs.

Postnatal adaptation of the pulmonary circulation is mediated partly by endothelium-derived nitric oxide (NO). Recent studies have demonstrated that inhaled NO causes selective and sustained vasodilation in infants with persistent pulmonary hypertension of the newborn. Because the short half-life of NO limits its clinical application, we hypothesized that aerosol delivery of an NO-adduct, diethylenetriamine (DETANO), can cause sustained and selective pulmonary vasodilation. To test the acute effects of DETANO, we studied the pulmonary vascular response of late-gestation fetal lambs (n = 8; age = 138 days; term = 147) to aerosolized DETANO in the presence of an endothelium-derived NO inhibitor, nitro-L-arginine. To determine whether DETANO has a sustained effect, fetal lambs were ventilated with FiO2 0.10 before and 15 minutes after they were treated with aerosolized DETANO. Fetal lambs were acutely prepared. Nitro-L-arginine (1 mg/min x 30 minutes) was infused into the left pulmonary artery before ventilation with FiO2 1.00 for 30 minutes, followed by continued ventilation with FiO2 0.10 for 10 minutes. This represented the control period. Ventilation was continued with FiO2 1.00, and aerosolized DETANO was given in doses of 0.1, 0.4, and 1.0 mg. Fifteen minutes after the last dose of DETANO was administered, animals were ventilated with FiO2 0.10. In the control period, during ventilation with FiO2 0.10, left pulmonary artery flow was 122+/-33 mL/min and decreased to 104+/-22 mL/min. Aerosol delivery of DETANO increased left pulmonary artery flow to 176+/-26 mL/min (P<.05) and had no effect on aortic pressure or heart rate. After DETANO was administered, ventilation with FiO2 0.10 did not cause any change in left pulmonary artery flow. We conclude that DETANO can cause selective fetal pulmonary vasodilation. Aerosol delivery of DETANO may increase the clinical applications of NO.

Aerosols↗
PubMed1996

Ventilation-induced pulmonary vasodilation at birth is modulated by potassium channel activity.

At birth, pulmonary blood flow rapidly increases 8- to 10-fold, and pulmonary arterial pressure falls by 50% within 24 h. The postnatal adaptation of the pulmonary circulation is mediated, in part, by endothelium-derived nitric oxide (EDNO). Recent studies suggest that EDNO may reduce vascular resistance, in part, by activating K+ channels. We hypothesized that K+ channels modulate the changes in pulmonary hemodynamics associated with birth. To test this hypothesis, we studied the effect of K+ channel inhibition on two separate, but interdependent stimuli: 1) mechanical ventilation with low inspired O2 concentrations (designed to maintain normal fetal blood gas tensions) and 2) mechanical ventilation with high inspired O2 concentrations. Tetraethyl-ammonium (TEA, 1 mg/min for 100 min; n = 5), a nonspecific K+ channel blocker, glibenclamide (Gli, 1 mg/min for 30 min; n = 6), an ATP-sensitive K+ channel blocker, or saline (n = 7) was infused into the left pulmonary artery (LPA) of acutely instrumented fetal lambs. The umbilical-placental circulation remained intact, and lambs were ventilated with 0.10 inspired O2 concentration (FIO2) for 60 min, followed by 1.0 FIO2 for 20 min. Neither TEA nor Gli had an effect on basal pulmonary tone. TEA attenuated the increase in LPA flow and decrease in pulmonary vascular resistance in response to mechanical ventilation with 0.10 and 1.0 FIO2; Gli had no effect. These results support the hypothesis that non-ATP-sensitive K+ channels modulate the transition from fetal to neonatal pulmonary circulation.

Adenosine Triphosphate↗
PubMedDate not supplied

Inhibition of light emission from the bioluminescent bacterium Vibrio fischeri after exposure to triclosan and related hygiene care products.

The affect of the anti-microbial agent triclosan (alternative names Microban and Irgasan DP300) on the light emission by the bioluminescent bacterium Vibrio fischeri was determined. Triclosan at concentrations greater than 0.2% (w/v) caused cell lysis and immediate (< 5 s) loss of light emission. Exposure to triclosan at lower concentrations caused a decrease in light output over time. The rate of the decrease in light output followed a cuboid relationship, of which the initial rate (first 60 s) of light loss was proportional to the concentration of triclosan. The effect on light output by two commercially available hygiene products containing triclosan also caused a similar response in light loss.

Anti-Infective Agents, Local↗