Effect of serum albumin on in vitro displacement of valproic acid by ceftriaxone and nafcillin.
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Biomedical subjects
Publications and source records attributed to R Dean.
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We hypothesized that the feeding difficulties experienced by premature infants are related to immature peristaltic activity and that a bowel accelerant might promote feeding in prematures. We administered metoclopramide (Meto) to 14 infants admitted to the Intensive Care Nursery at The University of Chicago between January 1, 1984, and January 1, 1987. Each infant had failed enteral feeding on at least two separate occasions. At the time of initiation of Meto, the group of infants tolerated only 11.7 +/- (SEM) 3.6 cm3/kg/day enterally. Feeding tolerance improved steadily after Meto was initiated, and by 29 days the infants tolerated 134 +/- 12.6 cm3/kg/day enterally. The average slope of the post-Meto feeding regression lines was +4.21 +/- 0.94 cm3/kg/day/day, significantly greater than -0.67 +/- 0.59 cm3/kg/day/day pre-Meto. The percentage of feedings followed by significant gastric residual volumes was 33.1 +/- 4.6% pre-Meto, compared to 6.9 +/- 2.5% post-Meto. No child receiving Meto developed any extrapyramidal neurologic symptoms, worsening of hepatic function, or necrotizing enterocolitis. Meto may have a role in the treatment of premature infants with enteral feeding intolerance.
Lung ventilation and perfusion (V/Q) scintigraphy is usually indicated when pulmonary embolism (PE) is a suspected diagnosis. Typically, V/Q scintigraphic interpretation is reported as a "normal," "low," "intermediate," or "high probability" of PE. Although a "low probability" interpretation does not exclude the diagnosis of PE, it significantly reduces the likelihood. We retrospectively analyzed up to one year of follow-up in 90 patients who were clinically suspected of having PE, but in whom V/Q scintigraphy implied a low probability of PE. None of the 90 patients demonstrated clinical evidence of PE subsequent to the V/Q scan. Our findings suggest that significant pulmonary embolism is uncommon and that the clinical course appears to be predictable in patients with a low probability V/Q scan.
Expression of the c-ras oncogene was determined in growing early and late passage human (IMR-90) fibroblasts using northern blot analysis of total cellular RNA. It was found that late passage cells demonstrated lower levels of c-ras by about four fold when compared to levels found in early passage cells. Southern blot analysis of genomic DNA from early and late passage fibroblasts digested with either SacI or BamHI showed somewhat increased hybridization levels in early passage cells compared to late passage cells. Data is discussed in relation to a previous report of c-ras expression and gene amplification.
Expression of the c-myc oncogene was determined in pre-confluent early and late passage human (IMR-90) fibroblast by dot blot analysis of cellular mRNA. Significant decreases in c-myc levels were found in late passage when compared to levels found in early passage cells. Cells restimulated with serum after serum restriction also showed reduced levels of c-myc in late passage. Confluent cells expressed levels of c-myc similar to that of pre-confluent cells, when serum stimulation was the same in both cases. Southern blots of Eco R1 digested DNA showed 2 fragments of similar size hybridizing to c-myc sequences in both early and late passage cells.
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Prenalterol (levo-1-[4-hydroxyphenoxy]-3-isopropyl-amino-2-propanol), a new stimulant of cardiac beta-adrenergic receptors in man, induces cardiovascular malformations when topically administered to 2 1/2- through 5 1/2-day chick embryos (Hamburger-Hamilton stages 17-27). Ventricular septal defects (VSD) located in the middle portion of the conal septum and classified as the simple, punched-out type VSD without septal malalignment were the predominant malformations observed throughout the developmental period tested. Arch malformations of the aortic circulation were also observed throughout the test interval, while anomalies of the pulmonary system were observed only at Hamburger-Hamilton stages 17 and 26-27. At stage 25 prenalterol demonstrated an acute toxicity significantly less than (1/50-1/20) epinephrine (P = .035 at concentrations of 8-10 mM) but was relatively equipotent with epinephrine in producing cardiovascular malformations. The effective median concentrations of the two agents were comparable (0.5-1.0 mM). The spectra of malformations induced by prenalterol and epinephrine were qualitatively similar. Malformations included absence of the right and/or left third aortic arch (innominate arteries), persistent remnant of the left fourth aortic arch, and VSD. These results support a previously proposed theory by these investigators that hyperstimulation of cardiac beta-adrenergic receptors in the chick embryo produces cardiovascular malformations.
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Frequencies of sister chromatid exchanges (SCE) were analyzed in bone marrow cells of mice injected with mitomycin C (MMC) both before and during infusion with bromodeoxyuridine (BrdU). Administration of MMC at 1, 6.5, and 13 hours after the onset of BrdU infusion resulted in the induction of approximately 45 SCE/cell, independent of time of administration. When MMC was injected 26 hours prior to BrdU infusion, only baseline levels of SCE were noted. The effects of multiple doses of MMC (chronic administration) were examined in mice treated with 1--5 mg/kg on a weekly or bimonthly basis. SCE analysis was performed one week after the final injection. At all doses and with all treatment regimes, SCE frequencies did not differ from control levels. The results indicate that most or all MMC-induced DNA damage that results in SCE formation is removed in a single cell cycle after its administration.
The hepatic tumor cell line (HTC) was tested for the ability to produce sister chromatid exchanges (SCEs) in response to chemical carcinogens which require activation. Without the addition of exogenous microsomal enzyme preparations, cyclophosphamide, N-nitrosodiethylamine (DEN) and aflatoxin B1 (AFB1) induced significant levels of SCEs in these cells. Mitomycin C (MMC) and ultraviolet light, which do not require activation, also produced significant levels of SCEs. The induction of SCEs in HTC cells by AFB1 was shown to be inhibited by estradiol, a known inhibitor of microsomal activating enzymes. For the carcinogens tested, the HTC cell SCE assay was quite sensitive and comparable to other mammalian test systems. Exceptional sensitivity was found in the case of AFB1. SCE analysis of HTC cells offers a simplified system of detecting carcinogens requiring activation. This system also has the potential of investigating interactions between agents such as steroid hormones and carcinogens.
An 18-year-old man with a history of Cushing's disease was treated with a total right and a near total left adrenalectomy in 1956. Pathologic examination of the operative specimen revealed bilateral adrenal hyperplasia. After 13 years, recurrence of symptoms of cortisol excess necessitated cobalt irradiation to the pituitary, which was without clinical effect. After an initial response to the adrenolytic agent, o,p'-DDD, partial relapse occurred. At this time, the recognition of an abdominal mass prompted abdominal exploration revealing a huge adrenal myelolipoma containing adrenal cortical cells distributed diffusely throughout the tumor. Symptoms of adrenal insufficiency developed, and adrenal steroid secretion did not respond to exogenous adrenocorticotropic hormone postoperatively. The case illustrates that adrenal myelolipomas may become very large with continued stimulation by adrenocorticotropic hormone, may contain significant amounts of adrenal cortical tissue, and may be associated with clinical hypercortisolism.
Fifty bacterial strains shown resistant to ampicillin, cephalothin or tetracycline by Kirby-Bauer disk diffusion susceptibility testing were isolated from patients with urinary infections. Inhibitory activity in urine of volunteers given these antimicrobial agents and tube dilution sensitivity testing indicated that agar disk diffusion gradients do not provide sufficiently high antimicrobial concentrations to predict accurately clinical efficacy.
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Unidirectional incompatibility selection is examined as an alternate mechanism of natural selection to cytoplasmic male sterility (CMS) for generating cytonuclear disequilibria. Differences in the dynamics and equilibrium behavior of cytonuclear disequilibria between these two cytonuclear selection models may allow for statistical tests of CMS vs. unidirectional incompatibility between mating cytotypes. Unlike CMS without migration, unidirectional incompatibility causes the cytoplasmic allele frequency to change over time rather than remain constant, and the nuclear allele frequencies hitchhike on the cytoplasmic frequencies. The decay of disequilibria is also distinctive in the absence of migration. Furthermore, in comparing both models with migration it is seen that the opportunity for internal equilibrium can be two or three times higher in a unidirectional incompatibility vs. CMS model. An example is presented that shows how unidirectional incompatibility can be statistically eliminated as a possible mechanism of cytonuclear selection.