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Biomedical subjects

T Patrick

Publications and source records attributed to T Patrick.

At least 19 recordsLinked to original sources
PubMed2001

Assessing dental hygiene clinical competence for initial licensure: a Delphi study of dental hygiene program directors.

PURPOSE: The purpose of this study was to describe the best way to determine clinical competence prior to issuing the dental hygiene license. METHODS: Directors of dental hygiene programs in the United States, Puerto Rico, and the Virgin Islands were asked to describe the best way to determine clinical competence prior to issuing the dental hygiene license. Three rounds of the Delphi process were used to seek a level of consensus among panel members. A total of 44 directors (19% of the population) from dental hygiene schools participated in at least one round of the study. Sixteen directors participated in all three rounds. Likert scale and ranking questionnaires followed the initial open-ended question. RESULTS: A level of consensus was achieved on 47% of the initial statements describing the determination of clinical competence. A list of the top 10 most agreed upon responses to the initial question was generated. Ongoing process evaluations within the accredited dental hygiene program, was suggested as the best determination of clinical competence for dental hygiene licensure. CONCLUSION: The findings suggest that dental hygiene clinical competence is best determined throughout a continuum of process and product examinations, rather than in a one-time product evaluation. Accreditation was acknowledged as an important element in standardizing the assessment of clinical competence. Organized dental hygiene should develop a protocol for licensing new dental hygienists and work with state boards of dentistry on its implementation.

Administrative Personnel↗
PubMed2000

Developing a controlled vocabulary for use in a hospital information system.

In bringing a controlled vocabulary to a health information system, it is important to include those terms commonly used by those who must routinely input data to the system. We have developed a methodology whereby we can obtain "free text" descriptions of diagnoses entered by system users. We then sort those terms/concepts by system and find the appropriate "atomic" term(s). The terms are also being submitted to domain experts for appropriateness and fidelity. These concepts are then coded in an international coding system (SNOMED International) to eventually be entered into the controlled "pick list" of terms available for users to enter.

Animals↗
PubMed1997

Post-translational activation of non-homologous DNA end-joining in Xenopus oocyte extracts.

We have analysed the recircularisation of plasmid DNA, cut with two different endonucleases to generate non-homologous DNA ends, in extracts of unfertilised eggs and oocytes of Xenopus. We found that the capacity to join non-homologous DNA ends, generating diagnostic covalently closed monomer circles, appeared during oocyte maturation at the time of germinal vesicle breakdown. This enzyme function was post-translationally activated in oocyte extracts incubated with unfertilised egg extract containing active cdc2/cyclin B, or by incubation with purified cdc2/cyclin B. Dephosphorylation of egg proteins by alkaline phosphatase inhibited the ability to join non-homologous DNA ends. We show that most linear non-homologous DNA ends repaired to form closed-circular supercoiled monomers, are joined without loss of nucleotides. Following partial purification, the activity was inhibited by inhibitors of poly(ADP-Rib) polymerase, an enzyme that is inactive in oocytes, but phosphorylated and activated during maturation. Competitive inhibition of poly(ADP-Rib) polymerase by > 50 microM 3-aminobenzamide prevented the joining of both matched and non-homologous DNA ends. We conclude that post-translational phosphorylation provides one route by which end-joining of non-homologous DNA can be regulated.

Animals↗
PubMed1997

Effects of a novel inotropic agent, BAY y 5959, in conscious dogs: comparison with dobutamine and milrinone.

Traditional inotropic agents, e.g., those that increase myocardial contraction through enhanced cyclic AMP or those that increase contractility at a relatively high O2 cost are frequently not useful in the clinical setting. Accordingly, newer agents that operate through different mechanisms have been synthesized. The goal of the present study was to compare the effects of a new Ca2+ promotor, BAY y 5959, with more traditional inotropic agents, dobutamine and milrinone, in 11 conscious dogs chronically instrumented for measurement of left ventricular (LV) and arterial pressures, LV internal diameter, wall thickness, coronary blood flow, and arterial and coronary sinus O2 content. Equi-inotropic doses of BAY y 5959 (20 microg x kg(-1) x min(-1)), dobutamine (10 microg x kg(-1) x min(-1)), and milrinone (10 microg x kg(-1) x min(-1)) were selected, which increased the LV rate of pressure development in sinus rhythm by 71-78% from similar baselines. Heart rate rose with dobutamine (+24 +/- 4%) and milrinone (+23 +/- 2%) but fell with BAY y 5959 (-35 +/- 3%). Dobutamine increased myocardial O2 consumption (MV(O2)) by 88 +/- 10%. In contrast, MV(O2) increased less with BAY y 5959 (+9 +/- 3%) and milrinone (+16 +/- 5%; P < 0.05). Furthermore, mechanical efficiency was also calculated either with direct measurement of cardiac output or by pressure-volume loops. Dobutamine and milrinone did not change efficiency; however, BAY y 5959 increased efficiency by 19 +/- 5%. With the heart rate held constant, BAY y 5959 increased MV(O2) by 32 +/- 4% but still increased efficiency by 28 +/- 7%. Thus the Ca2+ promotor BAY y 5959 has unique features that might be desirable for clinical applications where inotropic support is indicated, but increased MV(O2) without enhanced mechanical efficiency is deleterious.

Animals↗
PubMed1994

Effects of anaesthesia and recent surgery on diastolic function.

OBJECTIVE: The aims were to determine the effects and the extent to which halothane anaesthesia affects diastolic function both immediately after and remote from surgery and to investigate whether the effect is due to alterations in loading conditions. METHODS: Eight mongrel dogs were studied under halothane anaesthesia (0.5-1.5 end tidal vol%) with the chest closed, after acute instrumentation with left ventricular pressure transducers, left atrial and aortic catheters, and left ventricular diameter and wall thickness crystals. The same dogs were then studied in the fully conscious state, 2-3 weeks later. An additional four dogs were studied in the conscious state and then again under halothane anaesthesia remote from acute instrumentation. The left ventricular isovolumetric relaxation time constant, tau, as well as myocardial and chamber stiffness constants were used as indices of diastolic function. RESULTS: Following halothane anaesthesia and recent surgery, tau was prolonged significantly compared to the conscious state, at 30(SEM 1) v 22(1) ms (p < 0.01), but there were no changes in either myocardial or chamber stiffness. While tau remained sensitive to increased heart rate and enhanced contractility and was prolonged by increasing afterload in both the anaesthetised and conscious states, it was consistently prolonged following halothane anaesthesia and recent surgery even at matched levels of contractile states, heart rates and loading conditions, compared to the conscious state, at 26(1) v 19(1) ms (p < 0.01). When the effects of halothane anaesthesia were examined after full recovery from surgery, tau was still prolonged under halothane anaesthesia, at 29(2) v 20(1) ms (p < 0.01), compared to the conscious state, but in contrast to the findings following halothane anaesthesia and recent surgery, it was fully normalised [19(1) v 19(1) ms] when contractile state and loading conditions were matched. CONCLUSIONS: Left ventricular diastolic function is influenced markedly by halothane anaesthesia and recent surgery, and to a degree comparable to many pathological states. The effects of halothane anaesthesia and recent surgery appear to prolong the isovolumetric relaxation time constant independently of heart rate, contractility, and loading conditions and are most likely to be due to the combined direct effects of anaesthetics and acute instrumentation.

Anesthesia, Inhalation↗
PubMed1994

Smoking among low-income, pregnant women: prevalence rates, cessation interventions, and clinical implications.

Smoking has a significant effect on the major causes of death and disability among women, including coronary heart disease, stroke, cancer, and osteoporosis. When pregnant women smoke, it adversely affects not only them but also the health, development, and functioning of their unborn and young children. Of the general population of pregnant women, between 20 and 45 percent smoke. Furthermore, among low-income and less educated pregnant women, the increase in prevalence of postpartum smoking relapse rates, continued smoking, and initiation of smoking underlies the need for developing effective interventions for prevention and cessation. Although self-help, stop-smoking materials demonstrated success in several trials, interventions used in conjunction with these materials were brief with little follow-up, and did not address the need for continued intervention to help maintain abstinence or cessation after birth. This article reviews the smoking cessation trials that have assessed the effects of various interventions on cessation rates among low-income pregnant women, and describes future research needs for clinic-based smoking interventions for those women and the clinical implications for health professionals.

Adolescent↗
PubMed1994

Exercise induces cardiac dysfunction in both moderate, compensated and severe hypertrophy.

BACKGROUND: Ventricular hypertrophy begins as a physiological adaptation to cardiac overload but progresses to a pathological state. We examined whether the extent of hypertrophy influenced the response to exercise in terms of its effects on regional and global ventricular function and transmural myocardial blood flow distribution. METHODS AND RESULTS: Left ventricular (LV) hypertrophy was induced by aortic banding in puppies. The effects of treadmill exercise were compared in sham-operated control dogs (n = 7) and in dogs with moderate LV hypertrophy (47% increase in LV wt/body wt, n = 7) with normal baseline levels of LV systolic and diastolic wall stress and dogs with severe LV hypertrophy (85% increase in LV wt/body wt, n = 18), which exhibited elevated levels of LV systolic wall stress at baseline. The dogs with severe LV hypertrophy were further subdivided into those with either elevated or normal baseline levels of LV end-diastolic pressure and wall stress. The response to exercise in dogs with moderate LV hypertrophy was directionally similar to that of sham-operated control dogs for systemic hemodynamics and global and regional LV function, ie, full and subendocardial wall thickening rose, as did mean and diastolic arterial pressures, shortening fraction, and Vcf. The endocardial/epicardial blood flow ratio did not fall during exercise in these two groups. However, relations comparing either LV shortening, Vcf, or wall thickening with LV systolic wall stress during exercise demonstrated depressed myocardial function in the dogs with moderate LV hypertrophy. In contrast, in dogs with severe LV hypertrophy, exercise reduced LV shortening fraction, Vcf, mean and diastolic arterial pressures, and full and subendocardial wall thickening, and the endocardial/epicardial blood flow ratio fell to 0.73 +/- 0.07. There were no differences observed between the two subgroups with severe LV hypertrophy, but the global and regional wall function responses to exercise were more severely impaired than those in dogs with moderate LV hypertrophy. CONCLUSIONS: Responses of global and regional LV function and transmural myocardial blood flow distribution to exercise were clearly abnormal in dogs with severe LV hypertrophy with elevated baseline levels of LV systolic wall stress whether or not baseline levels of LV end-diastolic wall stress were elevated. Thus, it required more severe LV hypertrophy as well as elevated levels of LV wall stress to elicit qualitatively abnormal regional and global hemodynamic responses to exercise. However, even with moderate LV hypertrophy, which was well compensated under baseline conditions, qualitatively impaired contraction-afterload relations were observed during the stress of exercise.

Animals↗
PubMed1993

Childbearing.

Explore the source record for details and available documents.

Female↗
PubMed1978

Measurement of multiple simultaneous small dimensions and study of arterial pressure-dimension relations in conscious animals.

This paper describes the development of several important modifications that were incorporated into the ultrasonic, transit-time dimension system in order to obtain multiple simultaneous, instantaneous, and continuous measurements of the external dimensions of the aorta and its major branches in conscious, unrestrained animals. At operation a pair of small piezoelectric crystals was sutured to arterial adventitia, and a miniature pressure gauge was implanted in the vessel at the same cross-sectional plane. After recovery from surgery, wall motion was not altered appreciably and scarring was minimal. This technique allows long-term monitoring of aortic pressure-dimension relations and is applicable for small (fetal and neonatal) as well as large (adult dogs and sheep) animals. When vessel wall thickness is measured, stress-radius analysis can be performed so as to compute vascular elastic stiffness as a function of stress. Moreover, the suitability for radiotelemetry of the pressure and dimension signals measured with this technique enables the study of these parameters in unrestrained animals, e.g., during spontaneous severe exercise.

Angiotensins↗
PubMed1972

Left ventricular response to severe exertion in untethered dogs.

The left ventricular response to severe exercise was studied by telemetering direct measurements of left ventricular diameter (D) and pressure (P) and aortic blood flow from healthy dogs running at speeds up to 30 mph in the field. Severe exercise increased cardiac output from 101 to 478 ml/kg per min, heart rate from 95 to 297 beats/min, stroke volume from 31 to 44 ml, left ventricular isolength (iso) systolic pressure from 120 to 186 mm Hg, left ventricular end diastolic pressure from 6 to 18 mm Hg, and left ventricular end diastolic diameter from 58.9 to 60.1 mm, while end systolic diameter decreased from 53.0 to 52.2 mm. Two indices of myocardial contractility, (dP/dt)/P increased from 37 to 92 sec(-1), while dD/dt, the velocity of myocardial fiber shortening at isolength, rose from 54 to 119 mm/sec. All of these changes were statistically significant. When, in resting dogs, heart rate was first raised to exercise levels by electrical stimulation, severe exercise subsequently increased left ventricular end diastolic diameter more profoundly, from 55.7 to 59.7 mm, while end systolic diameter remained constant and the increases in left ventricular pressure, (dP/dt)/P and velocity(iso) were roughly comparable to those occurring during exercise in spontaneous rhythm. After propranolol, 1.0 mg/kg, severe exercise resulted in significantly smaller increases in cardiac output (from 82 to 240 ml/kg), in heart rate (from 87 to 186 beats/min), in left ventricular pressure(iso) (from 122 to 150 mm Hg), in (dP/dt)/P (from 32 to 44 sec(-1)), in velocity(iso) (from 47 to 59 mm/sec), and in slightly greater increases in end diastolic diameter, from 59.8 to 62.0 mm and pressure from 8 to 22 mm Hg, while end systolic diameter did not change significantly.Thus, the left ventricle responds to severe exercise with near maximal increases in heart rate and contractility, while significant increases in end diastolic diameter (Frank-Starling mechanism) and stroke volume occur as well. When heart rate was held constant severe exercise produced similar increases in contractility but end systolic size failed to diminish and the increases in end diastolic size were greater. Beta adrenergic receptor blockade interfered with the chronotropic and particularly the inotropic response to severe exercise and while the participation of the Frank-Starling mechanism was somewhat greater, the latter was not sufficient to increase cardiac output normally.

Animals↗
PubMed1971

The peripheral vascular response to severe exercise in untethered dogs before and after complete heart block.

The peripheral vascular response to severe exercise was studied in 11 healthy conscious dogs instrumented with Doppler ultrasonic flow probes on the mesenteric, renal, and iliac arteries, and miniature pressure gauges in the aorta. The response to severe exercise was restudied in six of these dogs after recovery from a second operation producing complete heart block by the injection of formalin into the atrioventricular (AV) node. Three of these dogs also exercised while their ventricles were paced at rates of 100/min and 200/min. The untethered normal dogs ran at speeds of 15-25 miles/hr behind a mobile recording unit for a distance averaging 1.5 miles, while continuous measurements of arterial blood pressure and blood flow were telemetered and recorded on magnetic tape. Severe exercise in normal dogs increased heart rate from 84 to 259/min, arterial pressure from 89 to 140 mm Hg, flow resistance in the mesenteric and renal beds by 59 and 52% respectively, and iliac blood flow 479% above control, while mesenteric and renal blood flows remained constant and iliac resistance decreased by 73%. In dogs with complete AV block, severe exercise at speeds of 10-18 miles/hr increased heart rate from 47 to 78/min, mean arterial pressure from 81 to 89 mm Hg, iliac flow 224%, resistance in the renal bed by 273%, and mesenteric bed by 222% while it decreased blood flow in mesenteric and renal beds by 61 and 65% respectively, and iliac resistance by 62%. A similar response occurred during exercise with pacing at 100/min, but when paced at 200/min a more normal exercise response reappeared. Thus, in normal dogs the peripheral vascular response to severe exercise involved increases in heart rate, arterial pressure and visceral resistance but visceral blood flow did not decrease. In dogs with heart block, where the ability to increase heart rate is severely compromised, compensatory reduction of mesenteric and renal blood flows occurred.

Abdomen↗
PubMed1971

Effects of cardiac depression and of anesthesia on the myocardial action of a cardiac glycoside.

The effects of ouabain (G-strophanthin) 20 mug/kg, on left ventricular (LV) pressure (P), diameter (D), velocity of contraction (dD/dt), and dP/dt were studied in conscious dogs instrumented with ultrasonic diameter gauges and miniature pressure gauges. The effects of ouabain were compared on separate occasions in the same dogs after cardiac depression with propranolol, 3.0 mg/kg, and also after general anesthesia with Na pentobarbital, 30 mg/kg. Maximal pressor effects were observed in the first 10 min, but maximal effects on the contractile state occurred at 30 min after ouabain. At this time, in conscious dogs, ouabain had increased LV isolength systolic pressure by 5%, LV isolength velocity by only 9%, and LV (dP/dt)/P by 21%, while end systolic diameter (ESD) decreased slightly and end diastolic diameter (EDD) and heart rate (HR) were unchanged. After anesthesia, ouabain increased LV systolic pressure by 8%, velocity 32%, (dP/dt)/P by 47%, and ESD decreased by 1.2 mm while EDD rose slightly and HR fell by 26 beats/min. Returning HR to control with atrial pacing decreased EDD 0.9 mm below control. After cardiac depression with propranolol, ouabain caused responses similar to those observed in the anesthetized dogs. Thus, the cardiac glycoside was found to exert only minor inotropic effects on the nonfailing heart of conscious dogs but far more striking inotropic responses in the anesthetized state.

Acetylcholine↗