Search PubMed⌕ Search

Biomedical subjects

R M Nelson

Publications and source records attributed to R M Nelson.

At least 73 records · Page 4Linked to original sources
PubMed1991

Clinical tests applicable to the study of chronic low-back disability.

This symposium has evaluated the possible directions to be taken in designing reliable and valid questionnaires, screening examinations, and paraclinical tests applicable to studies in LBP. The detailed design of such test instruments, field testing, measures of reliability, and validity represent the next step if the current barriers to collaborative clinical research in LBP are to be overcome.

Back Pain↗
PubMed1991

Plasma beta-endorphin in neonates: effect of prematurity, gender, and respiratory status.

A consecutive cohort of 87 infants (46 infants less than 37 weeks gestational age and 41 term infants greater than or equal to 37 weeks gestation) admitted to the Neonatal Intensive Care Unit (NICU) and a convenience cohort of 27 term well babies at the University of Nebraska Medical Center (Omaha, NE) were evaluated for plasma beta-endorphin (beta E) levels during the first 4 h after birth. Demographic data, maternal history, and respiratory status at the time of sampling as well as development of documented apneic episodes during the initial hospitalization were analyzed for all infants. All NICU infants had higher plasma beta E levels than the control infants. Premature infants had significantly higher neonatal plasma beta E levels than term infants in either the control or NICU groups, but the response was gender specific; premature males had higher plasma beta E than premature females (P = 0.008). Perinatal stress, including respiratory problems, was associated with the increase in plasma beta E, but prematurity and being male were significantly predictors of an elevated plasma beta E level. Immaturity in respiratory control, as evaluated by the development of documented apneic episodes during the infant's initial hospitalization, did not correlate with an elevated perinatal plasma beta E level.

Apgar Score↗
PubMed1991

An electrodynographic study of foot function in shoes of varying heel heights.

Forty-three female test subjects had electrodynographic gait analysis performed in barefoot, low-heel shoe, and high-heel shoe conditions. Comparisons of segmental foot function, actual pressures, and pressure durations were determined. The findings suggest that an increased duration of forefoot loading, rather than an increased actual pressure, is responsible for pedal pathology secondary to wearing high-heel shoes. Contrary to previous reports in the literature, evidence of abnormal pronation in high heels was not found in this study.

Biomechanical Phenomena↗
PubMed1991

Prostaglandin F1 alpha levels during and after neonatal extracorporeal membrane oxygenation.

Infants receiving extracorporeal membrane oxygenation therapy undergo long-term cardiopulmonary bypass, are systemically heparinized, and frequently receive platelet transfusions. Prostacyclin is a powerful inhibitor of platelet aggregation as well as a potent vasodilator. The levels of its stable metabolite prostaglandin F1 alpha increase significantly in children undergoing cardiopulmonary bypass during heart operations but decrease to preoperative levels after bypass. To determine the effect of long-term bypass on prostacyclin levels, multiple plasma samples were analyzed in 10 human neonates both during extracorporeal membrane oxygenation therapy and within 24 hours after extracorporeal membrane oxygenation. Prostaglandin F1 alpha, the stable metabolite of prostacyclin, was quantitated by radioimmunoassay in picograms per milliliter. Prostaglandin F1 alpha levels were elevated while the patients received extracorporeal membrane oxygenation therapy but decreased with duration of extracorporeal membrane oxygenation. In most infants, prostaglandin F1 alpha levels rose again during weaning from extracorporeal membrane oxygenation and remained elevated for 24 hours after extracorporeal membrane oxygenation. Extracorporeal membrane oxygenation course influenced circulating prostaglandin F1 alpha levels. Fluctuating prostaglandin F1 alpha levels are of clinical significance in the management of vasomotor tone and platelet function, common problems in the care and the prevention of hemorrhage in these critically ill infants.

Blood Platelets↗
PubMed1989

Antithrombin inactivation by neutrophil elastase requires heparin.

In certain thrombotic states, large declines in the levels of functional circulating antithrombin occur, which may reflect the highly active nature of the endothelial surface in suppressing excessive amounts of activated coagulation enzymes. Alternatively, we have recently observed an unexpected and paradoxical in vitro functioning of heparin that could result in the inactivation of antithrombin in pathologic conditions. Specifically, antithrombin was rendered nonfunctional as an inhibitor of clotting enzymes as a result of a limited, heparin-dependent cleavage by neutrophil elastase. This inactivation occurred only in the presence of the active anticoagulant heparin fraction, which suggested that the heparin-antithrombin complex was the substrate for elastase attack. Interestingly, neutrophil elastase was found to bind tightly to heparin and heparin-like materials. Neutrophil elastase has been previously linked to nonspecific proteinolysis occurring in inflammatory thrombotic reactions. This affinity of both antithrombin and elastase for heparin suggests a novel mechanism of potential specificity. An important component of this hypothesis is the localization of the elastase/antithrombin reaction away from the high circulating levels of elastase inhibitors. The proposed inactivation of antithrombin on the vascular surface would likely occur only in pathologic states associated with neutrophil sequestration and activation. Nevertheless, this mechanism could lead to a localized reversal of the nonthrombogenic nature of the endothelium and potentially lead to significant reductions of functional antithrombin in certain disease states.

Antithrombins↗
PubMed1989

Inactivation of human antithrombin by neutrophil elastase. Kinetics of the heparin-dependent reaction.

Human neutrophil elastase catalyzes the inactivation of antithrombin by a specific and limited proteinolytic cleavage. This inactivation reaction is greatly accelerated by an active anticoagulant heparin subfraction with high binding affinity for antithrombin. A potentially complex reaction mechanism is suggested by the binding of both neutrophil elastase and antithrombin to heparin. The in vitro kinetic behavior of this system was examined under two different conditions: 1) at a constant antithrombin concentration in which the active anticoagulant heparin was varied from catalytic to saturating levels; and 2) at a fixed, saturating heparin concentration and variable antithrombin levels. Under conditions of excess heparin, the inactivation could be continuously monitored by a decrease in the ultraviolet fluorescence emission of the inhibitor. A Km of approximately 1 microM for the heparin-antithrombin complex and a turnover number of approximately 200/min was estimated from these analyses. Maximum acceleratory effects of heparin on the inactivation of antithrombin occur at heparin concentrations significantly lower than those required to saturate antithrombin. The divergence in acceleratory effect and antithrombin binding contrasts with the anticoagulant functioning of heparin in promoting the formation of covalent antithrombin-enzyme complexes and is likely to derive from the fact that neutrophil elastase is not consumed in the inactivation reaction. A size dependence was observed for the heparin effect since an anticoagulantly active octasaccharide fragment of heparin, with avid antithrombin binding activity, was without effect on the inactivation of antithrombin by neutrophil elastase. Despite the completely nonfunctional nature of elastase-cleaved antithrombin and the altered physical properties of the inhibitor as indicated by fluorescence and sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the inactivated inhibitor exhibited a circulating half-life in rabbits that was indistinguishable from native antithrombin. These results point to an unexpected and apparently contradictory function for heparin which may relate to the properties of the vascular endothelium in pathological situations.

Antithrombins↗
PubMed1989

Vasoconstriction in telencephalic microvessels: a response to one model for intraventricular hemorrhage in beagle pups.

Telencephalic microvessels were morphologically and morphometrically evaluated in beagle pups at 24, 48, and 72 hours of age following an experimental insult consisting of exposure to acute hypovolemic hypotension followed by rapid corrective blood reinfusion. Animals were anesthetized throughout the procedure and maintained for 75 minutes prior to sacrifice. Microvessels from the germinal matrix, where intraventricular hemorrhage (IVH) most commonly occurs, were compared to those of the adjacent cerebral cortex and choroid plexus. Perfusion, fixation and processing of the tissue followed our previously published protocol (Leuschen et al.: Anatomical Record 208:435-443, 1984). Both germinal matrix and cortical microvessels had collapsed lumens and normal endothelial cell morphology; mitochondria contained distinct cristae, junctional complexes were present and a basement lamina completely surrounded most vessels. Morphometric data on matrical and cortical microvessels supported vasoconstriction. Microvessels from choroid plexus were not vasoconstricted; tight junctions were infrequently seen and microvesicular elements were present. An increased cerebral blood flow to the germinal matrix and the adjacent cerebral cortex has been reported during and immediately following hypovolemic hypotensive insult. By 75 minutes following insult, our ultrastructural studies support a rebound phenomena including vasoconstriction of microvessels. The resulting vasoconstriction and associated cerebral ischemia may play an important role in subsequent tissue damage to the matrical area and ultimately to the etiology of IVH.

Animals↗
PubMed1989

A general method of site-specific mutagenesis using a modification of the Thermus aquaticus polymerase chain reaction.

A specific mutagenic change in the cDNA of human protein S was introduced by a modification of the polymerase chain reaction that permits the introduction of a mutation at any position in a double-stranded DNA molecule. The method employed four synthetic oligonucleotide primers. One oligonucleotide contained a single-base mismatch to direct the mutagenesis; the other three oligonucleotides were designed to allow selective amplification of the mutated sequence with Thermus aquaticus polymerase. The mutagenized cDNA was cloned into a plasmid vector and transformed into Escherichia coli RR1 cells for characterization. The desired cytosine to guanine change in the target cDNA was confirmed by the predicted appearance of an AluI restriction site and by dideoxynucleotide sequencing. No other sequence changes were detected within the amplified region. This method of site-specific mutagenesis can be applied to any linear double-stranded DNA large enough for primer annealing and obviates specialized cloning vectors, DNA constructs, and selection techniques. It has the advantage over a recently published PCR technique (R. Higuchi, B. Krummel, and R. Saki (1988) Nucleic Acids Res. 16, 7351-7367) in requiring no diafiltration to remove primers between steps and in requiring only a single mutagenic oligonucleotide to be synthesized for each mutant construct made after the initial one.

Base Sequence↗
PubMed1989

Ventilatory changes in convalescent infants positioned in car seats.

Because premature infants have been shown to be at risk for hypoxia and bradycardia when positioned in standard car seats, this study was done to confirm this finding in a larger sample, to investigate convalescent term infants in the neonatal intensive care unit for respiratory compromise in car seats, and to determine the physiologic mechanism or mechanisms responsible. Extensive multichannel polygraph recordings were obtained and pulmonary function tests were performed on 50 convalescent infants from the neonatal intensive care unit before, during, and after placement in a Cosco-Peterson First Ride car seat. Mean total dynamic compliance, total pulmonary resistance, and work of breathing improved in the car seat. Thirty percent of premature infants experienced hypoxia, bradycardia, or both in a car seat; in this group, tidal volume was lower (p = 0.02). In 11 of 16 infants with abnormal findings, oxygen desaturation was temporally related to episodes of short and mixed apnea. No term convalescent infant experienced respiratory difficulty in a car seat regardless of primary diagnosis. We conclude that premature infants may have respiratory compromise of a multifactorial nature when in car seats. Further development of car seats is necessary if such respiratory problems are to be avoided.

Airway Resistance↗
PubMed1988

PhDs in pediatric departments.

A survey on PhDs in academic pediatric departments was sent to members of the Association of Medical School Pediatric Department Chairmen (70% responded). Significant numbers (14.5%) of pediatric faculty members hold PhDs. Another 3.6% hold PhDs/MDs. Research is their major responsibility in every subspecialty except psychology. The majority of PhDs (51%) are assistant professors (8% tenured) in contrast to 37% of MD faculty (14% tenured). The majority of PhDs at full professor (56%) are tenured compared with only 44% of MDs. Separate criteria exist for promotion for PhDs in 42% of departments. For promotion to associate professor, the mean number of refereed publications is 18 (median, 15); for full professor, the number ranges from ten to 50 (median, 40). Extramural research funding carries the highest weight in evaluating research efforts. PhDs could impact significantly on long-range planning in academic pediatric departments.

Faculty, Medical↗
PubMed1987

Heparin promotes the inactivation of antithrombin by neutrophil elastase.

Heparin is an acceleratory cofactor for antithrombin, a circulating inhibitor of blood coagulation enzymes. The presence of heparin on blood vessel walls is believed to contribute to the nonthrombogenic properties of those surfaces. In apparent opposition to this function, heparin was found to greatly accelerate the in vitro inactivation of antithrombin by neutrophil elastase. Inactivation rates in solution were potentiated several hundredfold by specific heparin fractions with anticoagulant activity. Although the data suggest that a heparin-antithrombin complex is essential for the inactivation by elastase to occur, the enzyme itself interacts tightly with heparin. These results suggest a mechanism which, if operating in vivo, could lead to a localized neutralization of the anticoagulant function of heparin at the endothelial surface.

Antithrombin III↗
PubMed1987

Intrapartum fetal heart rate patterns and neonatal intraventricular hemorrhage.

A goal for the obstetrician and neonatologist is to screen for risk factors associated with intraventricular hemorrhage (IVH) in the low-birthweight infant. Perinatal events that lead to neonatal metabolic and cardiovascular derangements seem to provoke IVH, and conflicting reports have implicated labor as being contributory. A fetal heart rate (FHR) abnormality during premature labor may be a predictor of subsequent neonatal IVH. For this reason, 5 years of FHR tracings at two university medical centers were reviewed for inborn infants who were delivered after premature labor and weighed less than or equal to 2000 gm. Sixty-four infants developed IVH, but pre-existing labor with a discernible FHR pattern was recorded in only 38 (59%) cases. Interpretations were reassuring in 17 (45%) cases, suspicious in 7 (18%) cases, and ominous in 14 (37%) cases. This proportion of FHR patterns was not significantly different from a matched group of premature infants without IVH during the same period. Interpretations of intrapartum FHR patterns of low-birthweight infants are limited, especially before 30 weeks gestation, and not useful in predicting neonatal IVH.

Adult↗