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Biomedical subjects

M K Ellis

Publications and source records attributed to M K Ellis.

22 records · Page 2Linked to original sources
PubMed1982

Development of sucking in term infants from birth to four hours postbirth.

The development of sucking response was investigated in 30 clinically normal infants from 1 or 5 minutes postbirth until their first feeding 4 hours later. Maximum sucking pressures were measured with a research nipple attached to a portable electronic suckometer. Mean suction (negative pressure) began at 5 Torr at birth, peaked at 103 Torr at 90 minutes, and decreased thereafter to 65 Torr at 4 hours. Expression (positive pressure) began at 12 Torr, rose to 29, and decreased to 25. Mean expression pressures correlated with feeding scale scores, r = +.44(24); p less than .025, but suction pressures did not, r = +.26(24); p less than .1. Normative data were gathered on 10 additional stabilized newborns who had been fed twice successfully. Suction pressures were 96 Torr on Day 1, and 103 Torr on Day 2; expression pressures were 25 and 24 Torr, respectively. These pressures approximate those recorded in newborns between 1 and 2 hours postbirth.

Biomechanical Phenomena↗
PubMedDate not supplied

Characterization of the interaction of 2-[2-nitro-4-(trifluoromethyl)benzoyl]-4,4,6,6,-tetramethyl- cyclohexane-1,3,5-trione with rat hepatic 4-hydroxyphenylpyruvate dioxygenase.

The synthetic beta-triketones are a novel family of chemicals, developed as herbicides that have activity on grass and broadleaf weeds and are selective in corn. Toxicological evaluation of a number of these chemicals has established that they interfere with rat hepatic tyrosine catabolism in vivo by inhibiting the enzyme 4-hydroxyphenylpyruvate dioxygenase (HPPD). This paper describes the kinetics of inhibition of rat hepatic HPPD in vitro by the representative beta-triketone 2-[2-nitro-4-(trifluoromethyl)benzoyl]-4,4,6,6- tetramethylcyclohexane-1,3,5-trione (1). A marked inhibition of rat hepatic HPPD was observed when 1 was incubated with the enzyme for 3 min at 37 degrees C prior to the initiation of the enzyme reaction by the addition of substrate. In this system, a concentration of 200 nM 1 resulted in a > 90% loss of HPPD activity, and an apparent IC50 was established at approximately 50 nM. The rate constant for the inactivation of HPPD by 1 was (1.5 +/- 0.2) x 10(-5) s-1 nM-1 as determined by progress curve data of oxygen consumed by HPPD with time. This inhibition is reversible in that the enzyme-inhibitor complex slowly dissociates, with approximately 5.5 +/- 0.6% of the enzyme activity being recovered by 6 h at 25 degrees C (t1/2, 25 degrees C, estimated at 101 +/- 14 h). In short, our studies establish 1 to be a tight-binding inhibitor of rat hepatic HPPD in vitro. This inhibition is characterized by the rapid inactivation of HPPD by the formation of an enzyme-inhibitor complex that dissociates extremely slowly with recovery of enzyme activity.

4-Hydroxyphenylpyruvate Dioxygenase↗
PubMedDate not supplied

Bilateral retinal embolization associated with intralesional corticosteroid injection for capillary hemangioma of infancy.

A 2-month-old female infant underwent intralesional corticosteroid injection for a capillary hemangioma that was causing amblyopia of the right eye from ptosis, globe displacement, and astigmatism. Forty-eight hours after the injection, the infant's parents noted that she was visually inattentive. On examination, she could not fixate or follow with either eye, and an afferent pupillary defect was present in the left eye. Ophthalmoscopy showed scattered areas of intraretinal hemorrhage in the right eye and extensive preretinal and intraretinal hemorrhages in the left eye. Ten months after injection, the hemangioma had greatly regressed, and visual acuity in the right eye was felt to be normal. The left eye had unsteady fixation with a persistent afferent pupillary defect and macular scarring. Retrograde flow of the corticosteroid suspension through the hemangioma's feeder vessels, probably originating from both ophthalmic arteries, is the most likely explanation for this complication.

Betamethasone↗