PubMed Health⌕ Search

Biomedical subjects

D Coulter

Publications and source records attributed to D Coulter.

At least 19 recordsLinked to original sources
PubMed2001

Developmental outcomes of children with hearing loss born in Colorado hospitals with and without universal newborn hearing screening programs.

The developmental outcomes of children born in hospitals with universal newborn hearing screening programs were compared with children born in hospitals without universal newborn hearing screening programs. Eight-four percent of children born in screening hospitals were early-identified with hearing loss prior to 6 months of age as compared to 8% of the children in the non-screen group. The participants in the screen group had an average language quotient of 82 while the participants in the non-screen group had an average language quotient of 62. Children in the screen group had better receptive and expressive language quotients, more different consonants in the spontaneous phonetic repertoire, better speech intelligibility, and larger expressive vocabulary inventories. Odds risk ratio estimates indicate that 80% of the children with cognitive quotients 80 or greater or four out of five children had language quotients within the normal range, 80 or greater, when they were in the screen group.

Age Factors↗
PubMed2000

Lemons into lemonade.

A booming economy can make layoffs in the biotechnology industry a blessing in disguise.

Biotechnology↗
PubMed2000

The Colorado Newborn Hearing Screening Project: effects on speech and language development for children with hearing loss.

OBJECTIVE: To compare the speech and language development of children with bilateral hearing loss and normal cognition who were born in hospitals with universal newborn hearing screening to that of their peers who were born in hospitals without this screening program. STUDY DESIGN: Subjects for the major analyses are 50 Colorado children (25 matched pairs) from 9 to 61 months old who are participants in a study of the development of children birth to six with bilateral hearing loss. Analyses included parametric dependent t-tests and analysis of covariance, nonparametric chi-squared and Wilcoxon signed rank tests, descriptive statistics and odds ratios. RESULTS: Newborn screening programs for hearing loss are positively related to scores in expressive and receptive language (p < 0.001) and vocabulary production (p < 0.001) on standardized inventories; speech intelligibility (p = 0.015) from independent ratings; number of different simple consonants (p < 0.01) and consonant blends (p = 0.026) from phonological transcripts; and total number of intelligible words (p < 0.01) and number of different words produced (p < 0.01) from computer analysis of videotaped language samples. CONCLUSION: Hospital-based newborn hearing screening programs are positively related to language and speech performance for children in early intervention programs who are deaf and hard of hearing.

Child Development↗
PubMed1987

Transformation of NIH 3T3 cells by cotransfection with c-src and nuclear oncogenes.

pp60c-src, the cellular homolog of the Rous sarcoma virus transforming protein, does not completely transform cells even when present at high levels, but has been shown to be involved in polyomavirus-induced transformation when activated by polyomavirus middle T (pmt)-antigen binding. Here we show that cotransfection, but not solo transfection, of expression plasmids for c-src and either adenovirus E1A, v-myc, c-myc, or the 5' half of polyomavirus large T (pltN) antigen into NIH 3T3 cells induces anchorage-independent growth, enhanced focus formation, and, for pltN cotransfection, tumorigenicity in adult NFS mice. Enhancement of transformation was not observed with polyomavirus small t (pst) antigen. Cotransfection of c-src with pltN induced modification of pp60c-src that altered its electrophoretic mobility and in vivo phosphorylation state and stimulated its in vitro kinase activity. Similar alterations were not seen after c-src-E1A cotransfection, suggesting that at least two different mechanisms of enhancement are involved.

Adenovirus Early Proteins↗
PubMed1986

C-kinase activation prolongs Ca2+-dependent inactivation of K+ currents.

Voltage-dependent K+ currents, IA and ICa2+-K+, across the soma membrane of the Hermissenda Type B photoreceptor, have been shown to remain reduced during retention of classically conditioned behavior. IA and ICa2+-K+ undergo prolonged reduction due to [Ca2+]i elevation produced by a single pairing of a light step with a command depolarization or by iontophoretic injection of Ca2+. One pathway which could contribute to the conversion of transient Ca2+-mediated reduction of K+ currents to the persistent reduction observed with conditioning is that involving C-kinase. To examine the role of C-kinase in the long-term regulation of K+ currents, isolated Type B somata were exposed to at least 25-30 minutes' incubation in artificial sea water (ASW) containing the C-kinase activators 1-oleoyl-2-acetyl-glycerol (OAG) or 12-deoxyphorbol 13-isobutyrate 20-acetate (DPBA) or control substances [e.g., distearyolglycerol (DiSG)]. After exposure to activator (but not to control solutions) and voltage-clamp conditions which caused elevation of cytosolic Ca2+, reductions of IA and ICa2+-K+ were observed which did not reverse (up to 3 hr), even after the activator was removed. Without conditions which induced elevation of cytosolic calcium prolonged incubation with the C-kinase activators had no effect on the membrane currents. Similar exposure of homogenates of the Hermissenda nervous system to OAG and Ca2+ caused enhanced phosphorylation of specific proteins, indicating the presence of C-kinase in the Hermissenda nervous system.

Animals↗
PubMed1985

Alexander's disease.

This is the first pathologic report of an infant at 37 weeks' gestation with Alexander's disease. The findings demonstrate that the disease can arise in utero and be extensive at birth before myelination begins.

Adult↗
PubMed1981

Growth characteristics of MOPC-315 plasmacytoma and response to anticancer agents.

We examined the growth characteristics and response to anticancer agents of the murine plasmacytoma MOPC-315, a rapidly growing and widely disseminating tumor syngeneic in BALB/c mice. The doubling time for the tumor was approximately 24 hours, and about 1 in 100 cells was tumorigenic. We developed a spleen colony assay for the clonogenic component of the tumor and used it to define the dose-response relationships for various anticancer agents, including melphalan, cyclophosphamide, 1,3-bis(chloroethyl)-1-nitrosourea, 5-fluouracil, gamma-radiation, methotrexate, methylprednisolone, cytosine arabinoside, and vincristine.

Animals↗
PubMed1981

Contrasting cytotoxicity kinetics of 5-azacytidine and dihydro-5-azacytidine hydrochloride in L1210 leukemia in mice.

For a comparison of the kinetics of the cytotoxicity of dihydro-5-azacytidine hydrochloride (DHAzaCR) and 5-azacytidine (AzaCR) in L1210 leukemia, the spleen colony assay was used to determine the surviving fraction of normal hematopoietic colony-forming units (NCFU) and leukemia colony-forming units (LCFU). Increasing doses of DHAzaCR above 1 mg per mouse enhanced cytotoxicity to LCFU but not to NCFU. The NCFU dose-survival curve showed a plateau with DHAzaCR, such that increasing the dose from 1 to 80 mg per mouse produced no further decrease in NCFU survival. In contrast, AzaCR produced a biphasic dose-NCFU survival curve without a plateau. Although DHAzaCR produced less cytotoxicity on a milligram basis than did AzaCR, both DHAzaCR and AzaCR elicited a biphasic dose-survival curve for LCFU. An infusion of DHAzaCR was less cytotoxic than was a similar dose of DHAzaCR administered as an iv bolus. Although high doses of AzaCR administered as an iv bolus. Although high doses of AzaCR delayed LCFU repopulation, both low and high doses of DHAzaCR were associated with prompt LCFU repopulation. Confirming this prompt repopulation of LCFU, there was a good correlation between the increase in life-span of mice with leukemia predicted by LCFU data following DHAzaCR treatment, compared to the discrepancy between predicted survival and observed survival following AzaCR. Therefore, the kinetics of cytotoxicity of DHAzaCR differ from those of AzaCR.

Animals↗
PubMed1981

Comparison of cytotoxic action of iphosphamide and cyclophosphamide.

We compared the cytotoxic effects of cyclophosphamide and iphosphamide on normal hematopoietic colony-forming units (NCFU) and L1210 leukemia colony-forming units (LCFU), using the quantitative spleen colony assay. Cyclophosphamide was more cytotoxic for NCFU than iphosphamide, but both agents had a similar cytotoxic effect on LCFU survival, whether given as a single injection or a 24-hour infusion. Although both agents were less cytotoxic for LCFU when administered in 24-hour infusions, host toxicity indicated that correspondingly larger doses of each agent could be given by infusion. The two agents also exhibited very similar cell-killing kinetics.

Animals↗
PubMed1980

Cytotoxicity of adriamycin combined with methotrexate against L1210 leukemia in mice.

The combination of adriamycin and methotrexate was found in mice to be synergistic in cytotoxicity to L1210 leukemia cells for a range of time intervals between the two agents. Cytotoxicity for normal hematopoietic stem cells was less than additive. Spleen colony assays were used to quantitate both cell populations. Increase in life-span assays yielded similar results. Also, the extent of synergy was dependent on the dose of adriamycin only.

Animals↗
PubMed1979

Pathophysiologic studies of calves given 3-methylindole intraruminally.

Intraruminal administration of 0.25 g of 3-methylindole (3MI; skatole/kg of body weight) to seven young calves generally caused mild respiratory signs and lesions, accompanied by only slight changes in cardiopulmonary function. Moderate depression, trembling, and irregular respiratory rate were observed between postadministration hours (PAH) 6 and 12. By PAH 24 at this dosage, abnormal clinical signs were not present. Statistically significant (P less than or equal to 0.05) changes observed in blood gas data from the seven calves were a decrease in aortic oxygen tension at PAH 12, increases in free-flowing venous oxygen tension in the intervals between PAH 6 and 12 and between PAH 6 and 24, and an increase in occluded venous oxygen tension at PAH 24. All calves had increases (although generally not statistically significant) in heart rate, cardiac output, cardiac index, stroke volume, and stroke index after 3MI administration. Mean aortic and pulmonary arterial pressure changes were generally small and variable. At necropsy, the lungs of the calves did not collapse when the thorax was opened. Patchy areas of consolidation (0.5 cm in diameter) were scattered throughout the parenchyma. Pulmonary edema or emphysema was not observed grossly. Microscopically, the alveolar septae were irregularly thickened because of edema, infiltration by polymorphonuclear and mononuclear cells, and vascular congestion. Interstitial lesions were patchy in distribution and severity and corresponded to the areas of consolidation observed grossly. Alveolar epithelial hypertrophy and hyperplasia were present, and an occasional focus of alevoli contained fluid of edema. Degeneration of individual hepatocytes was observed in scattered areas of the liver, especially in the periportal areas. It was concluded that differences in 3MI dosage response may exist between young calves and adult cattle in which calves are more resistant to the pulmonary cytotoxicity of 3MI.

Animals↗
PubMed1978

Kinetics of cytotoxicity of VM-26 and VP-16-213 on L1210 leukemia and hematopoietic stem cells.

The in vivo effects of VM-26 and VP-16-213 upon hematopoietic stem cells and L1210 leukemia cells were quantitated using the spleen-colony assay technique. The effect of VM-26 on leukemia cells was further quantitated using an endpoint dilution assay. The dose-response curves for leukemic clonogenic cells for both agents when given by iv injection were exponential and biphasic, indicating the existence of two populations. The survival of leukemia cells when VM-26 was administered as a 24-hour infusion was less than that found for equivalent doses administered as single injections. The survival kinetics with respect to time for a low dose (0.02 mg/mouse) and a high dose (0.15 mg/mouse) of VM-26 were similar in that the decrease in survival was rapid, reaching a maximum effect within 4 hours after administration. With the low dose, repopulation of the femoral marrow started immediately, whereas with the high dose, there was a 20-hour delay in repopulation. The data from the increase in lifespan studies were in excellent agreement with the quantitative assays. The dose-response curves for the normal hematopoietic clonogenic cells were also exponential, but these cells were much less sensitive to the agents than were the leukemia cells.

Animals↗
PubMedDate not supplied

Effect of fluctuations in albumin on serum fructosamine assay.

Serum fructosamine, albumin and plasma glucose were studied in eight patients during recovery from diabetic ketoacidosis, and in eight patients with "decompensated" diabetes without acidosis. In the ketoacidotic group, serum fructosamine had fallen significantly by a mean of 12% by 8h, and fell further during the remainder of the study. A smaller but significant fall in fructosamine (mean 6.1%) was seen in the decompensated group after only 18 h, with again a further fall thereafter. These changes in serum fructosamine were accompanied by decreases in serum albumin. However, when fructosamine was corrected by calculating a fructosamine/albumin index (FAI) (fructosamine X 100/albumin), the FAI did not change significantly in either group until a small reduction was noted in the ketoacidotic group at 5 days, which might reasonably be expected as an index of intermediate-term glycaemia. Therefore minor fluctuations in albumin levels seen in diabetic patients can affect fructosamine, and correction may be be advisable for the test to be a valid measure of glycosylated serum proteins.

Acidosis↗