Biomedical subjects

K A Bowen

Publications and source records attributed to K A Bowen.

3 recordsLinked to original sources

PubMed1998

Pediatric death certification.

OBJECTIVE: To determine location, manner, and physician certifier of pediatric deaths. DESIGN: A descriptive study of death certificate information for all child deaths (aged birth through 17 years) for the years 1995 and 1996. SETTING: Urban county of more than 780,000 population. MAIN OUTCOME MEASURES: Field of specialty of physician certifiers, location of death, and category of deaths certified by the medical examiner. RESULTS: Of 361 child deaths, 42.6% were certified by the medical examiner, 24.1% by neonatologists, 10.0% by obstetricians, 8.0% by pediatric critical care specialists, and 5.3% by general pediatricians. The remaining deaths were certified by pediatric subspecialists, surgeons, family practitioners, emergency medicine specialists, hospital pathologists, and law enforcement officials. The medical examiner certified deaths due to trauma (64.5%), sudden infant death syndrome (13.5%), unexplained or suspicious causes (9.7%), medical or surgical complications (3.9%), or because no other physician certifier was available (5.8%). Most children were pronounced dead at hospitals, but 10.0% died at home, 4.4% on roads, and 2.5% on public or private lands. CONCLUSIONS: General pediatricians are unlikely to be directly involved in the care of most children who die and are therefore unlikely to sign the death certificate. Education about death and dying issues should be available for all pediatricians but should be directed at those specialists most likely to provide care during critical events. Support services for families need to be community based and accessible to survivors.

Adolescent↗

PubMed1988

Attenuation of endothelium-mediated vasodilation by halothane.

To determine whether halothane alters endothelium-mediated vasodilation of vascular smooth muscle, isolated ring preparations of rabbit aorta and canine femoral and carotid arteries were suspended for isometric tension recordings in Krebs-Ringer bicarbonate solution at 37 degrees C. Acetylcholine and bradykinin have been shown to relax these norepinephrine contracted arteries via an endothelium-dependent process. In this study, these relaxations were reversibly and significantly attenuated by 2% halothane. However, halothane did not affect relaxations caused by nitroglycerin, which, in these vessels, acts by an endothelium independent mechanism. These results suggest that halothane is not interfering with cyclic guanylate-monophosphate mediated relaxation of vascular smooth muscle, but may interfere with the synthesis, release, or transport of the endothelium-derived relaxing factor. In addition, during contractions evoked by norepinephrine, halothane caused significant decreases in tension in both the canine carotid and rabbit aortic preparations, but increased tension in the femoral artery rings. These effects were not altered by mechanical removal of the endothelium. These results suggest a direct action of halothane on the vascular smooth muscle, which can result in either an increase or decrease in tension, depending on the specific vessel. In addition to its direct vascular effect, this study suggests a new action of halothane; it interferes with endothelium-derived relaxing factor-mediated relaxation of vascular smooth muscle. This action may contribute in part to the vascular alterations seen clinically during administration of halothane.

Animals↗

PubMed1985

Evidence for titratable gating charges controlling the voltage dependence of the outer mitochondrial membrane channel, VDAC.

A voltage-dependent anion-selective channel, VDAC, is found in outer mitochondrial membranes. VDAC's conductance is known to decrease as the transmembrane voltage is increased in either the positive or negative direction. Charged groups on the channel may be responsible for this voltage dependence by allowing the channel to respond to an applied electric field. If so, then neutralization of these charges would eliminate the voltage dependence. Channels in planar lipid bilayers which behaved normally at pH 6 lost much of their voltage dependence at high pH. Raising the pH reduced the steepness of the voltage dependence and raised the voltage needed to close half the channels. In contrast, the energy difference between the open and closed state in the absence of a field was changed very little by the elevated pH. The groups being titrated had an apparent pK of 10.6. From the pK and chemical modification, lysine epsilon amino groups are the most likely candidates responsible for VDAC's ability to respond to an applied electric field.

Animals↗