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Biomedical subjects

K Coy

Publications and source records attributed to K Coy.

13 recordsLinked to original sources
PubMed2001

Social-cognitive processes in preschool boys with and without oppositional defiant disorder.

The social-cognitive characteristics of 88 preschool boys with Oppositional Defiant Disorder (ODD) and 80 nondisruptive boys were assessed 3 times over a 2-year period. Three questions were addressed: (1) Do social-cognitive processes (encoding, attribution, problem solving, and response evaluation) distinguish clinic-referred preschool boys from peers without behavior problems? (2) What is the relation between preschoolers' social-cognitive processes and observed problem behavior? (3) Are the social-cognitive processes of clinic boys with ODD influenced by comorbidity with Attention Deficit Hyperactivity Disorder (ADHD)? Boys were presented hypothetical, peer-oriented social dilemmas to resolve. At all 3 assessments, clinic boys were twice as likely as were comparison group boys to generate aggressive solutions. Relative to comparison boys, clinic boys' encoding of social information was less accurate. The groups did not differ in their attributions or response evaluations. Verbal IQ and language skills were modestly correlated with problem solving and encoding. Within the clinic group, social-cognitive processes were not affected by ADHD comorbidity and they showed little relation to later diagnostic status or severity of behavior problems.

Aggression↗
PubMed2001

Intracoronary stent implantation in Jamaica. The initial experience.

Intracoronary stent implantation resulted in the complete or near complete dilatation of high grade occlusions of the left anterior descending coronary arteries in the four patients in whom it was undertaken. Intracoronary stent implantation is a useful adjunct to Percutaneous Transluminal Angioplasty (PTCA) and is applicable in selected patients with symptomatic ischaemic heart disease in a developing country with limited health resources like Jamaica. This is so since financial data presented here document the significant savings this technique (when appropriately utilised) could realise compared to the use of balloon angioplasty alone.

Aged↗
PubMed2000

Do psychosocial variables predict the physical growth of infants with orofacial clefts?

This study sought to determine whether psychosocial variables (parent-infant feeding interactions, infant temperament, maternal social support, family socioeconomic status) are important in predicting the physical growth of infants with orofacial clefts, after controlling for selected medical variables (infant health status, cleft diagnosis, and previous weight). Infant growth (weight-to-height zscores) was tracked for 2 years, and models were developed to predict growth at 3, 12, and 24 months. The authors also examined the growth trajectories of infants with different cleft types: cleft lip and palate (CLP) and cleft palate only (CPO). CPO infants showed some increase in their growth relative to the population mean over time, whereas the growth of CLP infants remained lower than the population mean at all time points. After controlling for medical variables, psychosocial variables collectively accounted for an additional 42% of the variance in infants' growth at 3 months of age, but they did not account for growth at 12 months and 24 months, largely due to the strong effect of previous growth. The authors tentatively conclude that psychosocial variables influence the early growth trajectory of infants with clefts, but subsequent growth becomes increasingly regulated by biological factors.

Child Development↗
PubMed1998

Early-Onset Oppositional Defiant Disorder: What Factors Predict Its Course?

Although the early onset of Oppositional Defiant Disorder (ODD) is associated with an elevated risk of later psychopathology (including but not limited to conduct disorder and antisocial personality disorder), little is known about the factors influencing the course of this disorder in early life. In this article we first review data and theory from four conceptually-distinct domains of risk factors for disruptive disorders (child characteristics reflecting biologic vulnerabilities, parent-child attachment, parenting practices, and family adversity). Then we describe an empirical study that examined the power of these four domains (representing 10 specific risk factors) to predict the prognosis of clinic-referred, preschool boys with ODD; risk factors were assessed when these youngsters were first evaluated in the clinic and outcomes were measured 2 years later. The primary goal was to determine the unique importance of risk factors in the context of others examined simultaneously, a strategy that few previous studies have used. We found that the four-factor risk model predicted significant variance in mother's reports of externalizing (disruptive) behavior problems at the 2-year follow-up; however, the model did not predict teacher externalizing scores or clinicians' assessments of Diagnostic and Statistical Manual (DSM) disorders, as hypothesized. Analyses of specific factors within domains suggested that three were most consistently related to the negative outcomes of ODD boys: greater use of physical discipline by parents, greater life stress for families, and a greater number of pre- and perinatal complications. Nearly a third of the variance in mothers' reports of internalizing (inhibited) problems was attributable to two of these risk factors (life events stress and birth history) and to a third factor, delayed child development.

Journal Article↗
PubMed1990

Heparin-induced hyperkalemia.

Heparin-induced hypoaldosteronism leading to hyperkalemia is an uncommon adverse effect. It appears as though heparin blocks an enzymatic step in the synthesis of aldosterone, and reduced aldosterone levels may be evident as early as four days after initiation of therapy. Although all patients who receive heparin may have reduced aldosterone levels, most are able to compensate through increased renin production and therefore remain asymptomatic. However, patients on prolonged heparin therapy or those unable to adequately increase renin production (e.g., patients with diabetes or renal insufficiency) may exhibit signs of hypoaldosteronism, such as hyperkalemia.

Adult↗
PubMed1989

Influence of beta-adrenergic blockade defined by time series analysis on circadian variation of heart rate and ambulatory myocardial ischemia.

Extended (72-hour) ambulatory electrocardiographic monitoring was used to enable time series analysis of heart rate and asymptomatic ST-segment depression in 9 patients with severe coronary artery disease. The effects of beta 1-adrenergic blockade with optimal dose metoprolol were then assessed. Data were analyzed using Fourier transformation, autocorrelation and cross-correlation to examine possible coupling between heart rate and ischemic electrocardiographic changes. A marked circadian pattern was observed for both heart rate and ambulatory myocardial ischemia, with a period of approximately 24 hours by both Fourier and autocorrelation methods. Cross-correlation revealed heart rate and ischemia to be tightly coupled with a lag of 0 hours during placebo. During beta 1 adrenergic blockade the marked circadian variation in heart rate was diminished, although some periodicity in the 24-hour region remained. Ambulatory ischemia was also markedly diminished during beta 1-adrenergic blockade; however, some residual ischemia remained that was characterized by a peak spectral activity shifted to a period of 5 to 7 hours. Heart rate and ischemia were not coupled during beta 1-adrenergic blockade, as evidenced by lack of significant cross-correlation. Thus, time series analysis suggests close coupling between the variation in heart rate and ambulatory ischemia in patients with severe coronary artery disease. Beta 1-adrenergic blockade can markedly alter the periodic characteristics of and coupling between heart rate and ischemia. Ischemia remaining during beta 1-adrenergic blockade may have different spectral characteristics than that predominating during placebo administration. These differences may be manifestations of the heterogenous pathophysiologic mechanisms responsible for ambulatory ischemia and may have therapeutic implications.

Circadian Rhythm↗
PubMed1988

Silent myocardial ischemia. Rationale for management.

Recent studies show that in many coronary artery disease patients with any form of angina, myocardial infarction, or positive exercise tests but no symptoms, most of the ischemic episodes are silent. Furthermore, evidence is building to suggest that in many patient groups, silent ischemia relates to prognosis. Numerous therapies, including nitroglycerin or isosorbide dinitrate, have been shown to modify silent ischemia and its associated risks. Studies indicate that frequency and perhaps duration of silent ischemic episodes can be modified by treatment with beta-adrenergic blockers or calcium antagonists alone or, even more effectively, with a combination of both types of agent. Many ischemic episodes persist, however, when therapy is directed only at reduction of angina. Evidence suggests that some characteristics of silent ischemia predict prognosis, whereas angina characteristics do not. Until additional data about prognosis and the influence of treatment on prognosis are available, the appropriate focus seems to be improvement of outcome in those patients who are at highest risk, rather than only reduction of chest pain.

Adrenergic beta-Antagonists↗
PubMed1987

Effects of titrated beta blockade (metoprolol) on silent myocardial ischemia in ambulatory patients with coronary artery disease.

This study investigates effects of beta-adrenergic blockade on total silent ischemic time assessed by ambulatory electrocardiographic monitoring and its relation to heart rate and time of day in ambulatory men with coronary artery disease. Metoprolol, when titrated to optimal dose in a controlled trial in 9 patients, reduced both total silent ischemic time (from 156 +/- 65 to 20 +/- 15 minutes, p = 0.04) and frequency of silent ischemic episodes (from 8 +/- 2 to 2 +/- 2 episodes, p = 0.03) compared with placebo. Mean daily heart rate was reduced, from 82 +/- 2 beats/min during placebo to 58 +/- 1 beats/min, as was heart rate at onset of 1 mm of ST-segment depression (106 +/- 2 to 74 +/- 4 beats/min, both p less than 0.001). Heart rate increased 10 +/- 1 beats/min during silent ischemia with placebo therapy, but increased only 4 +/- 1 beats/min during metoprolol treatment (p less than 0.03). During placebo administration the largest proportion of silent ischemic time occurred between 0600 and 1200 hours. Metoprolol attenuated this circadian variation in silent ischemia while reducing (p less than 0.05) total silent ischemic time in all periods. Thus, beta-adrenergic blockade reduces the frequency of silent myocardial ischemic episodes and total silent ischemic time, while mean daily heart rate and heart rate at onset of ischemia and maximal ischemia decrease. Metoprolol treatment also attenuates circadian variation of silent ischemia. These data may be interpreted to suggest that beta-adrenergic activation operates in the pathogenesis of silent myocardial ischemia and its circadian variation.

Aged↗
PubMed1982

Regulation of de novo purine biosynthesis in Chinese hamster cells.

Regulation of de novo purine biosynthesis was examined in two Chinese hamster cell lines, CHO and V79. De novo purine biosynthesis is inhibited at low concentrations of adenine. The mechanism of inhibition was studied using the RNA and protein synthesis inhibitors actinomycin D, cycloheximide, and azacytidine. Although all three inhibitors rapidly inhibited de novo purine biosynthesis in vivo, neither adenine nor the RNA and protein synthesis inhibitors could be found to have an effect in vitro on either phosphoribosylpyrophosphate (PRPP) synthetase or amido phosphoribosyltransferase, the first enzymes of the de novo pathway. However, in the presence of actinomycin D, cycloheximide, and azacytidine, there was a 50% or greater reduction in PRPP concentrations. This reduction in PRPP levels is correlated with a 2-fold increase in purine nucleotides in the acid-soluble pool. It is proposed that in the presence of the metabolic inhibitors there is an increase in nucleotide pools due to degradation of RNA, with a resulting feedback inhibition on de novo purine biosynthesis. In contrast to a previous report (Martin, D. W., Jr., and Owen, N. T. (1972) J. Biol. Chem. 247, 5477-5485), we could find no evidence for a repressor type mechanism in these cells.

Adenine↗
PubMed1982

Genetic instability at the adenine phosphoribosyltransferase locus in mouse L cells.

Resistance to adenine analogs such as 2,6-diaminopurine occurs at a rate of approximately 10(-3) per cell per generation in mouse L cells. This resistance is associated with a loss of detectable adenine phosphoribosyltransferase activity. Other genetic loci in L cells have the expected mutation frequency (approximately 10(-6)). Transformation of L cell mutants with Chinese hamster ovary cell DNA results in transformants with adenine phosphoribosyltransferase activity characteristic of Chinese hamster ovary cells. No activation of the mouse gene occurs on hybridization with human fibroblasts. That this high frequency event is the result of mutation rather than an epigenetic event is supported by antigenic and reversion studies of the 2,6-diaminopurine-resistant clones. These results are consistent with either a mutational hot-spot, a locus specific mutator gene, or a site of integration of an insertion sequence.

Adenine Phosphoribosyltransferase↗