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Biomedical subjects

R L Hopkins

Publications and source records attributed to R L Hopkins.

At least 19 recordsLinked to original sources

Spontaneous subcutaneous emphysema.

Subcutaneous emphysema is an unusual complication of bronchiolitis. The investigators describe a patient with bronchiolitis who developed extensive subcutaneous emphysema. Despite an alarming appearance, the patient recovered with symptomatic care and observation. Review of the literature shows a multitude of causes of subcutaneous emphysema. The vast majority of cases resolve without intervention.

Bronchiolitis

Pediatric intraosseous infusion.

Venous access in the infant and child is always challenging. The hypotensive child who is deteriorating needs rapid volume expansion and medications. Vascular collapse and previous venous cut-downs can preclude easy cannulation of vessels. Intraosseous infusion of fluids and drugs can be readily performed. The technique is easily mastered and there are few complications.

Catheterization, Peripheral

Haziness of the right hemithorax in a newborn.

We describe a neonate with an accessory diaphragm, a rare congenital anomaly. It almost always occurs in the right hemithorax, which appears diffusely hazy on the anterior chest roentgenogram. The lateral chest roentgenogram is essential in the diagnosis of this condition.

Diaphragm

Ribonucleoside and deoxyribonucleoside triphosphate pools during 2-aminopurine mutagenesis in T4 mutator-, wild type-, and antimutator-infected Escherichia coli.

Ribonucleoside and deoxyribonucleoside triphosphate pools have been measured in Escherichia coli infected with bacteriophage T4 DNA polymerase mutator, wild type, and antimutator alleles during mutagenesis by the base analogue 2-aminopurine. ATP and GTP pools expand significantly during mutagenesis, while CTP and UTP pools contract slightly. The DNA polymerase (gene 43) alleles and an rII lesion perturb normal dNTP pools more than does the presence of 2-aminopurine. We find no evidence that 2-aminopurine induces mutations indirectly by causing an imbalance in normal dNTP pools. Rather, it seems likely that, by forming base mispairs with thymine and with cytosine, 2-aminopurine is involved directly in causing bidirectional A.T in equilibrium G.C transitions. The ratios for 2-aminopurine deoxyribonucleoside triphosphate/dATP pools are 5-8% for tsL56 mutator and 1-5% for tsL141 antimutator and 43+ alleles. We conclude that the significant differences observed in the frequencies of induced transition mutations in the three alleles can be attributed primarily to the properties of the DNA polymerases with their associated 3'-exonuclease activities in controlling the frequency of 2-aminopurine.cystosine base mispairs.

2-Aminopurine

The biochemical basis of 5-bromouracil- and 2-aminopurine-induced mutagenesis.

We describe in vitro measurements of heteroduplex base mispaired intermediates involving 5-bromouracil and 2-aminopurine in A X T----G X C and G X C----A X T transition mutation pathways. For the case of 2-aminopurine, 2-aminopurine X cytosine mispairs are formed at a much higher frequency than adenine X cytosine mispairs in either transition pathway. For the case of 5-bromouracil, at least a 40-fold increase in 5-bromouracil X guanine mispairs are observed over thymine X guanine mispairs but only in the G X C----A X T pathway. In the A X T----G X C pathway, mispairs involving 5-bromouracil are formed 2.5-fold more frequently to those involving thymine suggesting perhaps that 5-bromouracil may exhibit substantially different base-pairing behavior depending on whether it is present as a template base or as a deoxyribonucleosides triphosphate substrate. The effect of the base analogs on dNTP pool size perturbations is discussed. A measurement of dNTP pools in 2-aminopurine mutagenized bacteriophage T4-infected cells is presented. An approximate eight-fold expansion in common dNTP pools is observed in a ts L141 antimutator genetic background compared to wild type T4 43+ and ts L56 mutator backgrounds. The effects of distorted dNTP pools on mutagenesis will be considered.

2-Aminopurine

Differential auscultation of the acutely ill patient.

The differential stethoscope is a unique instrument that assists in rapid evaluation of pulmonary problems in the acutely ill patient. Simultaneous auscultation of homologous lung segments eliminates the problem of variability of breathing rate and pattern that must be confronted in conventional auscultation.

Auscultation

Calculation of infusion rates of vasoactive substances.

We present a framework for understanding calculations of continuous infusions of vasoactive substances. Several simplified methods for establishing initial concentrations and infusion rates of drug are derived, their applicability is discussed, and examples are given.

Blood Vessels

Steam vaporizer injuries.

There were an estimated 656 cases of vaporizer-related injuries seen in hospital emergency departments in 1979. Two cases of burns with respiratory involvement are described. Both children were directly exposed to steam from commercial vaporizers and suffered cutaneous and respiratory burns. These cases emphasize the hazards of steam vaporizers, devices that have no proven therapeutic benefits.

Aminophylline

Deoxyribonucleotide pools, base pairing, and sequence configuration affecting bromodeoxyuridine- and 2-aminopurine-induced mutagenesis.

Despite recent experiments showing that BrdUrd-induced mutagenesis can be independent of the level of bromouracil (BrUra) substitution [Kaufman, E.R. & Davidson, R.L. (1978) Proc. Natl. Acad. Sci. USA 75, 4982-4986; Aebersold, P.M. (1976) Mutat. Res. 36, 357-362], BrUra.G base mispairs are a major determinant of mutagenesis. We propose that the experiments cited above are sensitive predominantly to G . C leads to A . T transitions driven by the immeasurably small but highly mutagenic substitution of BrUra for cytosine and not by the gross substitution of BrUra for thymine in DNA. More generally, we show how accumulated evidence suggests that both BrdUrd and 2-aminopurine have two mutagenic effects intracellularly: perturbation of normal deoxyribonucleoside triphosphate pools and analogue mispairs in DNA. We propose a molecular basis for various observations of normal exogenous deoxyribonucleosides as synergists and counteragents to base analogue mutagenesis. A model is proposed to explain the antipolarity of BrdUrd and 2-aminopurine mutagenesis--i.e., why mutants at hot spots for induction by one base analogue are usually hot spots for reversion by the other. It is concluded that the configuration of the neighboring nucleotides surrounding the base analogue mispair, and not the base analogue's preference for inducing A . T leads to G . C or G . C leads to A . T errors, is responsible for the antipolarity of BrdUrd and 2-aminopurine mutagenesis.

2-Aminopurine