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Biomedical subjects

R C Baker

Publications and source records attributed to R C Baker.

At least 19 recordsLinked to original sources
PubMed1992

Selective breeding of rats differing in sensitivity to the effects of acute ethanol administration.

Selective breeding of rats for sensitivity to the anesthetic effects of ethanol is being carried out with rats derived from the genetically heterogeneous N/Nih stock. Thirteen generations of within family selection have been achieved with replicate high (HAS), low (LAS) and control alcohol sensitive (CAS) lines. Significant separation between lines on sleep time and blood ethanol concentration (BEC) at awakening following ethanol administration has been achieved. In general, the results obtained so far replicate the findings with short (SS) and long (LS) sleep mice. One exception is that the high alcohol sensitivity rats (HAS) also appear more sensitive to pentobarbital relative to LAS rats. This finding is opposite to that which occurs with SS and LS mice where the low ethanol sensitive SS mice appear more sensitive to pentobarbital than the LS mice.

Alcoholic Intoxication↗
PubMed1992

Surface exposure of synaptosomal gangliosides from long-sleep and short-sleep mice.

A galactose oxidase/NaB[3H]4 technique was used to examine the relative surface exposure of gangliosides from whole brain synaptosomes of long-sleep (LS) and short-sleep (SS) mice. The surface exposure of the monosialoganglioside, GM1, did not differ between the two lines. Surface exposure of the polysialogangliosides GD1a, GD1b, and GT1b, however, was significantly greater in LS synaptosomes than in SS. Hydrolysis of the polysialogangliosides by neuraminidase to the end-product, GM1, at early time periods occurred more rapidly in LS than in SS synaptosomes. Upon exposure to either 250 mM or 50 mM ethanol, LS synaptosomal ganglioside surface exposure was decreased, but that of SS was increased. Pairwise comparisons of the individual ganglioside classes indicated that the decrease in LS synaptosomal ganglioside surface exposure was attributable to decreases in the polysialogangliosides, compared with controls. The ethanol-induced increase in SS synaptosomal ganglioside surface exposure, however, was mainly due to an increased surface exposure of only GD1a. These results suggest that intrinsic differences in the surface exposure of gangliosides and/or the magnitude and direction of ethanol-induced changes in ganglioside surface distribution may reflect biophysical or modulatory mechanisms by which this class of compounds modifies membrane sensitivity to ethanol. These results suggest that further studies should be performed to determine whether gangliosides are factors in genetically determined sensitivity to ethanol.

Alcoholic Intoxication↗
PubMed1992

Occult hemophilia: prolonged bleeding follows extraction.

A 51-year-old man had delayed and recurrent bleeding after tooth extractions. Occult hemophilia B was discovered. This case emphasizes the importance of evaluating patients for an underlying coagulopathy when bleeding greater than expected occurs. In this case, the patient had no personal or family history of bleeding.

Blood Loss, Surgical↗
PubMed1992

Carbamazepine overdose--the effects of multiple dose activated charcoal.

We studied five children with carbamazepine overdose. Two patients had acute overdose without previous exposure to carbamazepine while three presented with acute-on-chronic overdose. Multiple doses of activated charcoal were administered to four patients. One acute-on-chronic patient did not receive any activated charcoal. The mean half-life of carbamazepine was as follows: a) Acute vs. Acute-On-Chronic overdose: 8.63 h vs. 12.01 h (p less than 0.05); b) No Activated Charcoal vs. 30-50 g Activated Charcoal vs. 60-90 g Activated Charcoal: 23.3 h vs. 10.17 h vs. 7.21 h (p less than 0.05); c) No Activated Charcoal vs. 2-3 doses vs. 7-12 doses: 23.3 h vs. 8.96 h vs 7.55 h (ns). Although the half-life of carbamazepine decreased in a linear relationship with the total amount of activated charcoal administered (r = -0.86), there was no relationship between the time to complete recovery and administration of multiple doses of activated charcoal. Although multiple doses of activated charcoal increased the clearance of carbamazepine in our patients with overdose, it was not associated with clinical benefits.

Acute Disease↗
PubMed1991

Pitfalls in diagnosing acute otitis media.

The diagnosis of AOM in the infant and child requires an accurate history with special reference to fever, pain, and respiratory symptoms and a careful examination with particular attention to the appearance and movement of the TM. The practitioner must be wary of relying too heavily on any single physical finding, but instead consider all the variables that influence and alter the history and physical examination as summarized in Table 4. These variables include the reliability of the history, the history of previous infections, the age of the child, the appearance of the EAC, and the appearance and mobility of the TM. The importance of a correct diagnosis is crucial because of the immediate treatment and follow-up dictated by the diagnosis and because of the potential long-term effects on the child's health and development, which are described in the remaining articles in this issue of Pediatric Annals.

Child↗
PubMed1990

Incorporation, distribution, and turnover of arachidonic acid within membrane phospholipids of B220+ T cells from autoimmune-prone MRL-lpr/lpr mice.

The metabolism of AA-containing phosphoglycerides within T cell membranes leads to the generation of second messengers that appear to play a crucial role in transmembrane signal transduction. To test the hypothesis that aberrations in the movement of arachidonoyl-phospholipids are associated with and may potentially contribute to abnormal T cell function, the incorporation, distribution, and turnover of AA within the membrane glycerolipids of cells that are known to exhibit immunoregulatory disturbances was examined. Thy-1+, Ly-1+, L3T4-, Lyt-2-, B220+ T cells from autoimmune MRL-lpr/lpr mice were used as the cellular model. In contrast to control lymph node T cells, which preferentially incorporate labeled AA into phosphatidylcholine (PC), B220+ T cells displayed a predilection for distributing [3H]arachidonate into phosphatidylinositol (PI). The arachidonoyl-phospholipid pools were normal in B220+ T cells. The constitutive turnover of [3H]arachidonoyl-PI was significantly enhanced and that of [3H]arachidonate-PC substantially reduced in B220+ T cell compared with control cells. Using membrane homogenates B220+ T cells demonstrated a functional increase in the levels of lyso-PI. Intact B220+ T cells prelabeled with [3H]myoinositol and cultured in the absence of stimulation with exogenous antigens or mitogens, exhibited increased production of lyso-PI. The data indicate that the preferential formation of [3H]arachidonoyl-PI in B220+ T cells is the result of greatly increased, constitutive PI turnover that appears to be due to a membrane phospholipase A2 activity. It remains possible that disturbances in the movement of arachidonate within phospholipids of B220+ T cells play a role in the expression of aberrant immunological activity.

Animals↗
PubMed1990

The effect of drugs on lung hyperreactivity in Sephadex treated rats.

The injection of Sephadex G200 intravenously into rats induced a blood eosinophilia and an hyper-reactivity of lung parenchymal strips to 5-hydroxytryptamine (5HT) and carbachol. The blood eosinophilia and the hyper-reactivity to 5HT reached a maximum at the same time and before that to carbachol. It was shown previously that the reduction of the blood eosinophilia by treatment with dexamethasone, dapsone, phenidone, isoprenaline and aminophylline also reduced the hyper-reactivity to 5HT. In this study we found that only dexamethasone reduced the hyper-reactivity to carbachol.

Animals↗
PubMed1990

The effects of drugs on Sephadex-induced eosinophilia and lung hyper-responsiveness in the rat.

1. Rats given an intravenous injection of Sephadex particles (0.5 mg of G200 in 1 ml of saline) on days 0, 2 and 5 had a blood eosinophilia which was maximal on day 7. 2. On day 7, broncho-alveolar lavage (BAL) fluids taken from the rats contained an increased number of eosinophils and fewer mononuclear cells but there was no change in the small number of neutrophils. In addition the rats were hyper-sensitive to the increase in resistance to artificial respiration produced by 5-hydroxytryptamine (5-HT), given intravenously, with a shift to the left of the log dose-response curve. Lung parenchymal strips, taken from the rats on days 6, 7 and 8, were hyper-reactive to 5-HT with an increase in slope of the log dose-response curve. 3. Compounds with a wide variety of activities were evaluated for their effects on the blood eosinophilia on day 7 when given before each injection of Sephadex. The eosinophilia was reduced by glucocorticosteroids, beta-adrenoceptor agonists, aminophylline, dapsone and phenidone. 4. Dexamethasone, isoprenaline, dapsone and phenidone at doses that reduced the blood eosinophilia also reduced the changes in number of leucocytes in the BAL fluids and the hyper-responsiveness to 5-HT in vivo and in vitro, except that the effects of dapsone on the hyper-sensitivity to 5-HT in vivo did not reach significance. Aminophylline was the least effective of the drugs at reducing the blood eosinophilia and its effects on the other changes did not reach significance. Sodium cromoglycate reduced the BAL eosinophilia but had no effect on the other changes produced by Sephadex. 5. The correlation coefficients between blood eosinophil numbers and reactivity to 5-HT in vitro and sensitivity in vivo were r = 0.76, (n = 88; P < 0.001) and r = 0.53, (n = 61; P < 0.001) respectively. 6. Doses of dexamethasone, isoprenaline, dapsone and phenidone that reduced the blood eosinophilia when given before each injection of Sephadex were inactive when given up to 8 h after the Sephadex. 7. These data show an association between blood eosinophilia and hyper-responsiveness of the lung. The blood eosinophilia in the rats was triggered within the first few hours of injecting the Sephadex and drugs have been identified which inhibit this trigger.

Animals↗
PubMed1990

Differential effects of norepinephrine on phosphatidylinositol 4,5-bisphosphate stimulated hydrolysis in brains of mice genetically selected for differences in ethanol sensitivity.

The effects of norepinephrine on phosphoinositide turnover were evaluated in five brain regions of the long sleep (LS) and short sleep (SS) mice. These mice were selectively bred for differences in central nervous system sensitivity to ethanol with the LS exhibiting much greater sensitivity to a hypnotic dose of ethanol than the SS, as determined by the ability of the mice to regain their righting reflex. Norepinephrine (10(-3) M, 10(-4) M, and 10(-5) M) significantly increased phosphoinositide turnover in the hippocampus, hypothalamus, locus ceruleus, cerebellum, and cortex within each line of mice. Basal and norepinephrine-stimulated phosphoinositide turnover were significantly higher in the SS mice as compared with the LS mice in the cerebellum and cortex but not the other brain regions. Incorporation of 3H-inositol into 3H-phosphatidylinositols was not different between SS and LS mice in the cerebellum and cortex. The greater norepinephrine-stimulated phosphoinositide turnover in the cerebellum and cortex of the SS versus the LS mice may contribute to the CNS sensitivity to ethanol in these two lines of mice. However, ethanol (500 mM) had no effect on basal or norepinephrine-stimulated phosphoinositide turnover in any of the five brain areas examined in the LS and SS mice.

Animals↗
PubMed1990

A part-time Level II fieldwork program.

This paper describes an alternative to the traditional Level II fieldwork program for master's degree students in occupational therapy. In this part-time 9-month program, students complete the fieldwork requirement while simultaneously balancing academic responsibilities. One advantage of this program over the traditional 3-month program is that the extended length of time offers students the opportunity to develop clinical skills beyond the technical level.

Clinical Competence↗
PubMed1990

Ethanol inhibits zymosan-stimulated and enhances nonstimulated platelet-activating factor production in a clonal macrophage cell line.

Ethanol was examined for its effects on zymosan phagocytosis and synthesis of platelet-activating factor (PAF) using a clonal macrophage cell line. PAF, identified as 1-O-alkyl-2-acetyl-sn-glycerol-3-phosphocholine, is a biologically active ether phospholipid produced by various cells types. PAF also activates a variety of inflammatory cells including the cells which produce PAF. Ethanol at 20 to 100 mM inhibited phagocytosis of unopsonized zymosan and concomitantly decreased PAF concentration in the stimulated macrophages. In contrast, in cells not stimulated with zymosan, ethanol increased the recoverable PAF. Ethanol, at 100 mM, inhibited the uptake of exogenous PAF but did not alter the distribution of PAF metabolites in the clonal macrophage cell line. The effect ethanol has on PAF synthesis appears dependent on the activation state of the cell. Two situations were identified in this study: 1) one linked to phagocytosis or cell stimulation which is inhibited by ethanol, and 2) PAF synthesis which is not dependent on overt cell activation that is enhanced by ethanol.

Animals↗
PubMed1989

Indomethacin-induced oligohydramnios.

A case of reversible indomethacin-induced oligohydramnios is presented. This case suggests a relationship between the dose of indomethacin and the quantity of amniotic fluid.

Adult↗
PubMed1989

Investigations of the role of protein kinase C in the acute sedative effects of ethanol.

The activity of protein kinase C (PKC) in whole brain and brain areas of mice selectively bred for resistance (short sleep, SS) or sensitivity (long sleep, LS) to the acute ataxic effect of ethanol has been investigated. The cytosolic and membrane fractions of whole brain PKC activities are significantly less in LS mice than in SS mice. There are significant differences in PKC activity between brain areas in both the SS and LS lines. Ethanol given in ataxic doses results in significantly increased amounts in PKC activity in whole brain cytosolic fractions and in some brain areas but equally in both SS and LS mice. Ethanol added in vitro reduced enzyme activity slightly in SS brain membranes, suggesting that the mechanism of the increase in PKC activity seen after in vivo administration is indirect. These results indicate that PKC is not involved in the mechanism whereby LS and SS mice differ in alcohol sensitivity. Direct intracerebroventricular (ICV) injection of phorbol myristate acetate (PMA), an activator of PKC, resulted in increased sleep times in both SS and LS mice. ICV injection of PMA also caused a more marked decrease in body temperature in LS than in SS mice. The half-life of PMA in brain was determined to be 9.6 hr and no metabolites could be detected. At limiting calcium concentrations, PMA added in vitro activated PKC equally well in both lines. However, PMA given ICV did not alter the level of PKC as determined in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effects of ethanol on human platelets stimulated with platelet-activating factor, a biologically active ether phospholipid.

The interaction between ethanol and 1-0-alkyl-2-acetyl-sn-glycerol-3-phosphocholine (platelet activating factor, PAF) was addressed using platelets obtained from normal nonalcoholic volunteers. Ethanol at concentrations of 20 to 100 mM inhibited PAF activation of human platelets. Ethanol inhibited prominently the second or arachidonic acid metabolite dependent wave of platelet aggregation, which occurs with human platelets in citrated plasma. It also inhibited serotonin release and thromboxane A2 formation associated with this secondary phase of aggregation. Ethanol did not readily inhibit the primary wave of PAF-induced aggregation. The incorporation of PAF into platelets or metabolism of PAF was not influenced by up to 100 mM ethanol. Since ethanol inhibited only the secondary response, a direct interaction between PAF, ethanol, and a platelet PAF receptor is unlikely. The effect of ethanol on PAF-induced platelet aggregation shows a selectivity similar to that demonstrated by other investigators for epinephrine and adenosine diphosphate.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗