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J J Franks

Publications and source records attributed to J J Franks.

At least 37 records · Page 2Linked to original sources
PubMed1994

Incongruous item generation effects: a multiple-cue perspective.

In a series of studies, generation effects were obtained under encoding conditions designed to induce incongruous, unrelated item generation. Experiments 1 and 2, using free- and cued-recall measures, respectively, provided evidence that this unrelated generation effect was due to response-specific processing. Experiment 3 demonstrated a lack of relation between free recall and indices of clustering. A preliminary protocol study suggested that Ss generate multiple items in their search for appropriate unrelated responses. In Experiments 4 and 5, conditions designed to produce more extensive multiple generations demonstrated enhanced free recall. These results supported a multiple-cue account of facilitated recall for incongruous item generation. The multiple-cue perspective is consistent with traditional conceptualizations of memory, such as the principle of congruity, and contemporary distinctions between cue-target relational and item-specific processing.

Adult↗
PubMed1994

Nature of cholinesterase in the rat retina.

The occurrence of cholinesterases has been demonstrated in retinas of several mammalian species. Histochemical staining techniques indicate that the acetylcholinesterases (AChE) are present in amacrine cells and their neighboring bipolar cells. However, the nature of retinal cholinesterases and their interactions with specific cholinesterase inhibitors are not known. Therefore, we have studied the inhibition of the rat retinal cholinesterase activity by BW284C51, a selective inhibitor of AChE, and iso-OMPA, a selective inhibitor of butyrylcholinesterase (BChE). Retinas from Zivic-Miller rats were solubilized by sonication in phosphate buffer (0.134 M, pH 7.2) at 4 degrees C for 20 min. The cholinesterase activity in the sonicate was determined by a radiometric method using 14C-acetylcholine (ACh) as substrate (10(-2) M). Excess 14C-ACh was adsorbed by Amberlite CG-120 cation exchange resin. 14C-acetate formed and retained in the aqueous medium was determined by liquid scintillation counting. This study gave the following results: (a) Rat retinal sonicate gave total cholinesterase activity of 3.76 mumol of ACh hydrolyzed/mg protein/15 min; (b) This activity was inhibited by BW284C51 (IC50, 0.115 microM). Iso-OMPA (IC50, 500 microM) did not cause significant inhibition at 0.115 microM. These observations suggest that the rat retinal cholinesterase is predominantly AChE.

Animals↗
PubMed1994

S-adenosyl-L-methionine-mediated enzymatic methylations in the rat retinal membranes.

Enzymatic step-wise methylation of membrane phosphatidylethanolamine (PE) to phosphatidyl-N-methylethanolamine (PME) and then phosphatidyl-choline (PC) has been known to alter membrane properties and responsiveness of cells for activation of receptors by chemical transmitters. Conversion of PE to PME and PME to PC in the presence of S-adenosyl-L-methionine (SAM) are catalyzed by two phospholipid N-methyltransferases, PMT I and PMT II, of which PMT I is the rate limiting enzyme. Retina is a good neuronal model for chemical transmission. However, retina was not studied for PMT activity. Therefore, we studied the rat retina for PMT I activity. Methylation of PE in the rat retinal sonicates was assayed using 3H-SAM (2 microM) at 37 degrees C in Tris-glycylglycine buffer (50 mM, pH 8.0) and methylated phospholipids were extracted with chloroform/methanol/HCl (2/1/0.02, v/v) and separated by thin layer chromatography on Silica Gel G plates. Chromatograms were developed in a solvent system of propionic acid/n-propyl alcohol/chloroform/water (2/2/1/1, v/v). This study gave the following results: (a) the total methylated phospholipids were (M +/- SE, N = 5) 19.90 +/- 4.03 fmol/mg protein/min; (b) the major methylated phospholipid was PME (4.21 +/- 0.68 fmol/mg protein/min; (c) the fatty acid methylesters formed by fatty acid carboxymethylase (FACM) which accumulated in the solvent front amounted to 18.82 +/- 2.84 fmol/mg protein/min. Both PMT I and FACM were inhibited by S-adenosyl-L-homocysteine (I50, 1.2-5 microM). These observations indicate that rat retina contains both PMTs and FACM.

Animals↗
PubMed1994

The effect of hepatectomy and plasma cholinesterase inhibition on cocaine metabolism and cardiovascular responses in pigs.

To determine the effects of total hepatectomy and inhibition of plasma cholinesterase activity on cocaine metabolism, we measured plasma concentrations of cocaine and its three major metabolites, benzoylecgonine, ecgonine methyl ester, and norcocaine, by high-performance liquid chromatography in three groups of male pigs. Pigs were anesthetized with sodium thiopental and lungs were ventilated with nitrous oxide in oxygen. A right carotid arterial cannula and an internal jugular venous catheter were then inserted for the administration of cocaine and for blood sampling. A Swan-Ganz catheter was inserted through the right internal jugular vein. Group 1 pigs underwent sham operation; group 2 and 3 pigs underwent hepatectomy and portocaval shunt. In addition, group 3 pigs were treated with tetraisopropyl pyrophosphoramide, a specific plasma cholinesterase inhibitor. After this preparation, pigs were given 4 mg/kg cocaine intravenously over 2 minutes. After cocaine injection, 4 ml blood was collected into heparinized test tubes containing 2.5% sodium fluoride for determination of cocaine and its metabolites at 2, 5, 10, 15, 30, 45, 60, 90, 120, 180, 240, and 300 minutes. We also measured hemodynamic responses after cocaine administration, including heart rate and rhythm, cardiac output, and arterial blood pressure. Data were analyzed by analysis of variance. Blood levels of cocaine and its metabolites were significantly different among the three groups (p < 0.05 by analysis of variance). Our results show that total hepatectomy was associated with a marked slowing of cocaine metabolism, absence of norcocaine, and increased benzoylecgonine levels when compared with the baseline values in the control pigs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Elevated fibrin-related and fibrinogen-related antigens in patients with liver disease.

Patients with liver disease have a variety of coagulation abnormalities. These derangements are of uncertain origin and do not always correlate with disease severity or activity. We have measured the levels and proportions of the total fibrin-related and fibrinogen-related antigens, the principal fibrin (D-dimer) and fibrinogen (D-monomer) degradation fragments and intermediates of fibrin formation (fibrin monomers) in patients with a variety of acute and chronic liver diseases in whom all known other precipitating causes of disseminated intravascular coagulation had been excluded. Fibrin-related and fibrinogen-related antigens were extracted from serum using antihuman fibrinogen-IgG covalently bound to activated amino-phenylthioether paper disks and were subjected to 4% to 11% sodium dodecyl sulfate-polyacrylamide gel electrophoresis under nonreducing conditions. Fibrin-related and fibrinogen-related antigen proportions were determined by densitometry, and their levels were measured by radioimmunoassay. Levels of total fibrin-related and fibrinogen-related antigens (and D-dimer) were significantly elevated (p less than 0.01) in patients with cirrhosis (121 to 641 ng/ml) and hepatocellular carcinoma (416 to 8,786 ng/ml) when compared with patients with acute viral hepatitis (84 to 322 ng/ml) and control subjects (38 to 186 ng/ml). In addition, D-monomer levels were elevated. These findings strongly suggest that disseminated intravascular coagulation is a component of the coagulopathy of certain liver diseases. Because fibrin-related and fibrinogen-related antigens have anticoagulant, vasoactive and immunosuppressive properties, their elevated presence may be biologically significant in these patients.

Adult↗
PubMed1991

Fibrin and fibrinogen-related antigens in systemic sclerosis (scleroderma)

Abnormalities in fibrin deposition are implicated in the pathogenesis of vascular occlusion in systemic sclerosis. We have used a technique that involves electrophoresis and densitometric analysis of captured fibrin- and fibrinogen-related antigens to measure the concentration of the individual fibrin and fibrinogen degradation products in 13 patients with systemic sclerosis and in 15 healthy control subjects. As a group, patients with systemic sclerosis had markedly elevated levels of total fibrin-related antigen (p = 0.0007) and D-dimer (p = 0.0004), the terminal degradation product of cross-linked fibrin. The levels of fibrin monomer, an intermediate product in the conversion of fibrinogen to cross-linked fibrin, and of D-monomer, a terminal breakdown fragment of fibrinogen and fibrin monomer, were also elevated (p less than 0.005). We conclude that patients with systemic sclerosis have evidence of enhanced fibrin formation and degradation.

Adult↗
PubMed1991

Halothane-induced alteration in the fluidity of rat brain synaptosomal membranes and its relationship to anesthesia.

Concentrations of halothane 1.43% or higher abolished the pain response and induced anesthesia. Halothane increased membrane fluidity of synaptosomes and microsomes both at non-anesthetic and anesthetic concentrations. Changes in fluidity in synaptosomes did not return to control levels even after the animals recovered from anesthesia. Alteration in membrane fluidity by halothane is a non-selective effect and may not play a definitive role in anesthesia.

Anesthesia↗
PubMed1991

Amino acids fail to prevent halothane depression of albumin synthesis: studies in the isolated perfused rat liver.

Halothane (1.3 MAC) and ethanol (0.4%) depress albumin synthesis in isolated perfused rat livers (IPRLs). Addition of amino acids prevents depression by ethanol. We have examined the effects of amino acids on albumin synthesis by IPRLs exposed to halothane. Seventeen livers were perfused with a mixture of rat erythrocytes and rabbit plasma. Five were exposed to oxygen/carbon dioxide alone and 12 to oxygen/carbon dioxide with 1.5% halothane. A mixture of 10 essential amino acids was added to the perfusate of six of the halothane-exposed livers to a concentration approximately 10 times the normal rat plasma level. Perfusate concentrations of newly synthesized albumin were measured by radial immunodiffusion, and the rate of synthesis for the 4.25-h study period was calculated. The mean +/- SEM albumin synthetic rate (mg/h per 300-g rat) in the control group (12.13 +/- 1.36) was significantly greater than in the group receiving halothane alone (6.98 +/- 0.92). Amino acid treatment failed to prevent halothane depression of albumin synthesis (8.68 +/- 0.84). Thus, although amino acids block ethanol depression of albumin synthesis, we could show no such effect in rat livers exposed to halothane.

Amino Acids, Essential↗
PubMed1991

Fibrin- and fibrinogen-related antigens in patients with venous disease and venous ulceration.

Abnormalities in systemic fibrinolysis have been implicated in the pathogenesis of venous ulceration. Patients with venous disease have a prolonged euglobulin lysis time and elevated plasma fibrinogen levels, yet little is known about the metabolism of fibrinogen and fibrin in such patients. In this study, we have used a technique that involves electrophoresis and densitometric analysis of captured fibrin-related antigens to measure the concentration and proportions of the individual fibrin and fibrinogen degradation products in patients with venous disease of the lower extremity. As a group, patients with venous disease had markedly elevated levels of total fibrin-related antigen and D-dimer, the terminal degradation product of cross-linked fibrin. Levels of D-monomer, the breakdown product of fibrinogen and non-cross-linked fibrin monomer, and a measure of fibrinogenolysis were normal in all patients. In patients with ulcers, the levels of D-dimer were disproportionately higher than expected from fibrin monomer levels. On an individual basis, significant elevations of D-dimer were present in six (55%) of the 11 patients with venous disease with ulcers and in three (43%) of the seven patients with venous disease without ulcers. We conclude that patients with venous disease have uniform evidence for enhanced fibrin formation, as evidenced by elevated levels of total fibrin-related antigen and D-dimer. This is regardless of whether the venous disease is accompanied by ulceration.

Antigens↗
PubMed1990

In vitro effects of fluoride and bromide on pseudocholinesterase and acetylcholinesterase activities.

The in vitro effects of two metabolites of inhalational anaesthetics, fluoride and bromide, on pseudocholinesterase (PCHE) and acetylcholinesterase (ACHE) activities in the blood samples of seven healthy patients were studied. The PCHE and ACHE activities were determined by kinetic spectrophotometric methods. Fluoride at the levels achieved with clinical concentrations of enflurane and sevoflurane (25-75 microM.L-1) inhibited PCHE activity by 28-65 per cent (P less than 0.01) and ACHE activity by less than five per cent (P greater than 0.05). Bromide at the levels achieved with clinical concentrations of inhalational anaesthetics had no significant effect on either PCHE or ACHE activity. We recommend caution when succinylcholine and/or ester type local anaesthetics are used in the immediate postoperative period following enflurane or sevoflurane anaesthesia. We also recommend that blood drawing for PCHE activity be delayed at least until 24 hr following enflurane or sevoflurane anaesthesia.

Acetylcholinesterase↗
PubMed1990

Halothane and isoflurane alter phospholipid transmethylation in rat brain synaptosomes.

The mechanism of action of inhalational anesthetics is unknown, but neuronal membrane alteration is a favored hypothesis. Since phospholipid methylation and translocation play a key role in the transmission of biologic signals across cell membranes, we examined the effect of two commonly used halogenated anesthetics, halothane and isoflurane, on phospholipid methylation in rat brain synaptosomes. Using S-adenosyl-L-[3H-methyl]methionine as a donor, we found a two-fold increase in 3H-methyl incorporation into phospholipids in synaptosomes taken from rats exposed to concentrations that just abolish pain response, but not in rats exposed to higher or lower concentrations. Methylation was not increased in rats newly recovered from anesthesia. Halothane added to synaptosomes taken from rats not previously exposed to anesthetics stimulated 3H-methyl incorporation over a wide range of concentrations. Enhancement of phospholipid methylation by halothane and isoflurane may effect an alteration of neural signal transduction that results in the anesthetic state.

Animals↗
PubMed1988

The inhibitory effect of metoclopramide on plasma cholinesterase activity.

The in vitro effect of metoclopramide on plasma cholinesterase (PCHE) activity was studied to investigate a mechanism for metoclopramide-induced prolongation of succinylcholine action. The mean PCHE of the control samples was 0.86 +/- 0.02 unit.ml-1. PCHE activity in the presence of metoclopramide, at concentrations of 0.05, 0.10, 0.50, 1.0, 2.5 and 5.0 micrograms.ml-1, was reduced to 0.78 +/- 0.02, 0.69 +/- 0.04, 0.50 +/- 0.03, 0.39 +/- 0.02, 0.24 +/- 0.01 and 0.15 +/- 0.01 unit.ml-1, respectively. Our data demonstrated that PCHE activity was significantly depressed by metoclopramide at all concentrations studied (p less than 0.001). Our data also show that the concentration of metoclopramide required to inhibit 50 per cent of PCHE activity (I50) was 0.8 micrograms.ml-1 (2.4 x 10(-6) M). We recommend caution when succinylcholine and or ester type local anaesthetics are administered to patients who are also receiving metoclopramide, especially in high doses.

Adult↗
PubMed1988

Halothane decreases albumin and transferrin synthesis: studies in the isolated, perfused rat liver and in the intact rat.

Isolated perfused rat livers exposed to 1.5% halothane (equivalent to 1.35 MAC) in O2/CO2 or to O2/CO2 alone produced urea, as well as albumin and transferrin (both measured by immunodiffusion), at constant rates during a 4.25-h perfusion. Urea production did not differ in the two treatment groups, but halothane depressed albumin and transferrin synthesis 43% and 45%, respectively. Intact rats were also exposed to halothane, after which albumin synthesis was measured by the (14C)carbonate technique. The minimum halothane concentration required to insure sufficient relaxation for ventilation was selected and ranged from 1.0 to 1.5%. Measurements were made in control rats not exposed to halothane (group I) and in halothane exposed rats immediately after 1 h of anesthesia (group II), 24 h after the start of 1 h of anesthesia (group III), and immediately after 1/2 h of anesthesia preceded by a 1-h exposure 24 h earlier (group IV). Single exposures to halothane (groups II and III) resulted in a decrease in albumin synthesis immediately or 24 h later that did not differ significantly from controls (group I). However, halothane given twice to rats at 24-h intervals (group IV) reduced their mean albumin synthesis rate to half that of controls. The early onset and constancy of halothane depression of export protein synthesis by isolated, perfused livers may reflect a response to halothane itself, rather than an effect resulting from the accumulation of halothane metabolites. Similarly, reduction of albumin synthesis in intact rats immediately after a second halothane exposure may indicate a response to halothane, rather than to halothane metabolites.

Albumins↗
PubMed1988

Cimetidine does not affect plasma cholinesterase activity.

Blood samples were drawn from 10 ASA physical status 1 and 2 patients before (baseline) and after the administration of cimetidine to determine the in vivo effect of cimetidine on plasma cholinesterase (PCHE) activity. The in vitro effects of cimetidine at different plasma concentrations were also studied using the same blood samples. PCHE activity in the baseline samples was 432 +/- 4.6 (mean +/- SEM) U/ml, the dibucaine number 82. Administration of oral cimetidine (300 mg) the night before and 2 hours before surgery, failed to have any effect on PCHE activity (no in vivo effect). Plasma cholinesterase activity in the presence of cimetidine in vitro at plasma concentrations of 1.5, 15, 150, and 1500 micrograms/ml was 428, 420, 397, and 177 U/ml, respectively. Thus, in vitro data showed that cimetidine at plasma concentrations (1.5 to 15 micrograms/ml) achieved with clinical doses also has no effect on PCHE activity.

Adult↗
PubMed1987

Fibrin and fibrinogen-related antigens in patients with stable and unstable coronary artery disease.

Coronary-artery thrombosis may be important in the pathogenesis of unstable angina at rest. To study this possibility, we measured the serum concentrations of fibrin-related antigen, D dimer (the principal breakdown fragment of fibrin), and fibrin monomer (an intermediate product of fibrin formation) in the serum of five groups of subjects. These included 10 healthy controls, 10 controls with noncardiac pain, and three groups of 10 patients each with chronic stable angina, unstable angina at rest, or acute myocardial infarction. The concentration of fibrin-related antigen (normal range, 48 to 184 ng per milliliter) was normal in the control patients with noncardiac pain (63 to 202 ng per milliliter) and in patients with chronic stable angina (95 to 186), but it was increased in patients with unstable angina (401 to 2507) or acute myocardial infarction (470 to 1930) (P less than 0.001). D dimer concentrations in patients with unstable angina (178.3 to 310.6 ng per milliliter) or acute myocardial infarction (103.9 to 321.6) were higher than those in patients with chronic stable angina (28.6 to 52.1), in controls with noncardiac pain (44.7 to 53.1), and in healthy controls (40.4 to 50.3) (P less than 0.001). Concentrations of fibrin monomer were highest in patients with acute myocardial infarction (247.5 to 571.3 ng per milliliter) (P less than 0.001), intermediate in those with unstable angina (54.7 to 241.7) (P less than 0.001), and normal (normal range, 14.5 to 19.8 ng per milliliter) in controls with noncardiac pain (12.0 to 18.4). and patients with chronic stable angina (10.7 to 17.6). These findings suggest the presence of an active thrombotic process in patients with unstable angina at rest or acute myocardial infarction. The data do not prove that the coronary arteries were the site of the thrombotic process, but the observations are consistent with the hypothesis that thrombus formation may have an important role in the pathogenesis of these conditions.

Angina Pectoris↗
PubMed1987

A diazophenylthio-ether-IgG probe for analysing fibrin- and fibrinogen-related antigens.

A technique for identifying and quantitating fibrin- and fibrinogen-related antigens (FRAs) in serum is described. Panspecific antifibrinogen IgG is bound covalently to diazotized aminophenylthio-ether cellulose paper discs. Under conditions of antibody excess, a disc probe extracts 95% of all fibrinogen-related antigen from appropriately diluted serum samples. Bound antigen is then eluted from the washed probe and electrophoresed on 4-11% gradient SDS-polyacrylamide gels. Derivatives of cross-linked fibrin, non-cross-linked fibrin and fibrinogen may thus be identified by their molecular weights, and their relative concentrations determined by densitometric analysis. The total amount of FRA is estimated by a radio-immunoassay which uses labelled D-dimer as the competitive antigen. The probes can extract as little as 0.20 and 0.15 microgram/ml of D-dimer and D-monomer, respectively. Specific FRA binding was confirmed with Western blotting. Potential interfering substances do not influence antigen binding to the discs and, since complete elution of all antigens is achieved, discs may be re-used. This procedure provides estimates of the serum levels of fragments YY, DY, X, DD, Y and D. The procedure is simple to perform and, as a research tool, may help to delineate some of the features of clotting disturbances in clinical states.

Animals↗