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Biomedical subjects

L Taylor

Publications and source records attributed to L Taylor.

At least 235 records · Page 13Linked to original sources

The Landau-Kleffner syndrome of acquired epileptic aphasia: unusual clinical outcome, surgical experience, and absence of encephalitis.

The syndrome of acquired verbal auditory agnosia in childhood with mutism and epileptic discharges has been described in over 100 cases. An encephalitic etiology has often been postulated but never proved. We report two patients with this syndrome who were treated surgically. Despite careful search, no pathologic evidence of encephalitis was found. One patient, with the typical course, had no seizures but striking positive correlation between epileptic discharge and language disorder; the second, after classic onset, developed intractable temporal lobe epilepsy, a previously unreported outcome of this syndrome. EEG discharges are generalized, bilateral, multifocal, or with shifting predominance but mainly temporal in 85% of reported cases, and unilateral, also predominantly temporal, in 15%. Language areas are preferentially involved. This syndrome has certain biologic features that resemble the benign epilepsies of childhood and may be the result of the unusual localization of the epileptic abnormality.

Adult↗

Effect of confinement method on physiology and production of gestating gilts.

Four replicates of 12 Dekalb crossbred gilts were blocked by breeding dates and randomly allotted to four treatments: tethers, crates, loose stalls and dirtlot. Ear vein cannulas were established and blood samples obtained from each gilt on d 2, 9 and 65 of treatment Blood cell counts, blood chemistry profile (12 items), triiodothyronine (T3), thyroxine (T4), basal cortisol and cortisol in response to administration of adrenocorticotrophic hormone (CR-ACTH) were determined. Tethered gilts had depressed CR-ACTH at d 2, probably related to their active struggles against the tethers during the initial period following restraint. Triiodothyronine was greatest in gilts housed loose with access to stalls, probably reflecting the fighting that often occurred among those gilts, and was lowest in gilts on dirtlot on d 2. Glutamic pyruvate transaminase was elevated in gilts on dirtlot at d 9 and 65, probably a result of their increased exercise. Behaviors indicative of "restlessness" were negatively correlated with CR-ACTH at d 9 and 65. Gilts were initially stressed when restrained in tethers, but their CR-ACTH became equivalent to that of gilts in other housing by 9 d. Housing had no effect on production.

Animals↗

Phenytoin reduces excitatory synaptic transmission and post-tetanic potentiation in the in vitro hippocampus.

Phenytoin (10-100 microM) was studied on excitatory synaptic transmission and post-tetanic potentiation (PTP) in the in vitro rat hippocampus. Synaptic potentials were studied using extracellular, intracellular and single-electrode voltage clamp techniques. Field excitatory postsynaptic potentials were recorded from the apical dendrites of CA1 pyramidal cells after Schaffer collateral stimulation. Intracellularly recorded excitatory postsynaptic potentials and excitatory postsynaptic currents were recorded in CA3 pyramidal cells after mossy fiber stimulation and in the presence of 10 microM picrotoxinin. In the CA1 region, phenytoin elicited a reversible depression of field excitatory postsynaptic potentials as well as reduced the time constant of decay of PTP from 79 sec to 47 sec with no change in the magnitude of potentiation. Higher concentrations of phenytoin (100 microM) had a general depressant effect on both the amplitude and time course of PTP. In CA3 cells, phenytoin (10 microM) reduced the mossy fiber synaptic conductance but did not change its reversal potential. Phenytoin (10 microM) also reduced the time constant of decay of PTP of the mossy fiber to CA3 synapse, while having no effect on the magnitude of potentiation. These results show that therapeutically relevant concentrations of phenytoin depress both low-frequency synaptic transmission and the time course of short-term potentiation. Both actions may be involved in the anticonvulsant properties of phenytoin.

Animals↗

The effect of bovine serum albumin on the synthesis of prostaglandin and incorporation of [3H]acetate into platelet-activating factor.

The binding of fatty acids by bovine serum albumin (BSA) is well documented. However, the interaction between the synthesis of prostaglandins (PGs) and the trapping of arachidonate released from cellular lipid stores is not as well understood. In this communication, we relate the trapping of fatty acids to the synthesis of PGs and the incorporation of [3H]acetate into platelet-activating factor (PAF). Our results show that, as determined by radioimmunoassay, BSA inhibits bradykinin (BK) (5 ng/ml) and ionophore A23187 (10 microM)-stimulated synthesis of PGs in human embryo lung fibroblasts (IMR-90) in a concentration-dependent manner. Experiments using prelabel with [3H]arachidonate followed by extraction and thin-layer chromatography show that, in the presence of 2 mg/ml BSA, IMR-90 release essentially only fatty acid following stimulation with bradykinin. Little if any prostaglandin and no endoperoxide are detected. In the same experiment, in absence of BSA, about 70% of the released label is detected as prostaglandin. alpha-Cyclodextrin, another trapper of fatty acid, inhibits PG synthesis in much the same way. BSA and alpha-cyclodextrin also inhibit prostacyclin synthesis in endothelial cells derived from the calf pulmonary artery. However, the inhibition of PG synthesis in these cells is not as complete as that in the IMR-90. In contrast to the effect of the trappers on PG synthesis, BSA and alpha-cyclodextrin are observed to potentiate BK- and ionophore-stimulated incorporation of [3H]acetate into PAF in the endothelial cells. The labeled PAF is not released from the cells in either the presence or absence of the trappers, leading us to conclude that BSA causes an increase in acetate-labeled cellular PAF by trapping released fatty acid.

Acetates↗

Comparison of prostaglandin synthesis by endothelial cells from blood vessels originating in the rat, baboon, calf and human.

The synthesis of prostaglandins (PGs) was determined in endothelial cells obtained from various vessels from baboon, human and rat both by radioimmunoassay and prelabel of the cells with [3H] arachidonate. Cells were stimulated with bradykinin, ionophore A23187 or 10 microM arachidonate. Although prostacyclin (PGI2) has proven to be the major prostaglandin product of human umbilical vein and calf pulmonary artery endothelial cells, our results show that PGI2 is frequently not the major prostaglandin product of endothelial cells from other vessels. For example baboon endothelial cells lining the large vessels, aorta and cephalic vein produce mainly PGF2a with only small amounts of PGE2 and PGI2. Human endothelial cells from saphenous vein also produce mainly PGF2a. Baboon, human and rat adipose capillary endothelial cells make predominantly PGE2 and PGI2 with rat making significant amounts of PGF2a in addition. Endothelial cells from the rat aorta produced predominantly prostacyclin.

6-Ketoprostaglandin F1 alpha↗

Varicella-zoster virus specifies a thymidylate synthetase.

A homology search of proteins predicted from the recently reported complete DNA sequence of varicella-zoster virus (VZV) revealed that the product of gene 13 was highly homologous to eukaryotic and prokaryotic thymidylate synthetases (TSs). The VZV protein was shown to be a TS by three functional tests. Firstly, a plasmid designed to express the native protein was able to complement a strain of Escherichia coli in which the natural TS gene is deleted. Secondly, in an enzyme assay for TS, extracts of the complemented strain were capable of releasing tritiated water from 2'-deoxy[5-3H]uridylate. Thirdly, these extracts contained a protein that bound isotopically labelled 5-fluoro-2'-deoxyuridylate, a ligand specific for the active site of TS. In addition, a novel ligand-binding protein was detected in human cells infected with VZV.

Base Sequence↗

Aspirin and dipyridamole in the prevention of acute coronary thrombosis complicating coronary angioplasty.

To test the hypothesis that pretreatment with adequate antiplatelet therapy reduces the likelihood of acute coronary thrombosis during routine percutaneous transluminal coronary angioplasty (PTCA), we reviewed, blinded to treatment group, the films and records of 300 consecutive initially successful PTCAs. Films before PTCA, immediately after, and at least 30 min after the last balloon inflation were assessed for the presence of any thrombus at the PTCA site. We excluded 37 patients who received streptokinase before PTCA or who had 100% occlusion or thrombus on pre-PTCA films. New thrombi were classified as clinically significant (defined as causing 100% occlusion or requiring emergency surgery or streptokinase therapy) or as not significant (not causing an acute problem or requiring intervention). Patients were classified into three groups, based on the type and extent of antiplatelet therapy received. Group 1 (no aspirin, n = 121) consisted of patients who did not receive aspirin either before admission or in hospital before PTCA (with or without dipyridamole). Group 2 (standard treatment, n = 110) received aspirin with or without dipyridamole but did not receive both drugs before admission and in hospital before PTCA. Group 3 (maximal treatment, n = 32) received both aspirin and dipyridamole before admission and in hospital before PTCA. New thrombi were detected at 39 (14.8%) PTCA sites, of which 15 (5.7% of all PTCA sites) were considered clinically significant. Group 1 had the highest incidence of both thrombus (21.5%) and clinically significant thrombus (10.7%). A reduction was seen in group 2 in thrombus (11.8%; p = .07) and in clinically significant thrombus (1.8%; p = .005). Group 3 had no thrombus (p = .001) and no clinically significant thrombus (p = .04). In addition to inadequate pretreatment with antiplatelet therapy, univariate analyses demonstrated several other risk factors for thrombus: higher percent diameter stenosis before PTCA (p less than .008), higher platelet count (p = .013), and current smoking (p = .03). Only higher platelet count (p less than .001) and inadequate pretreatment (p = .001) were associated with clinically significant thrombus. Stepwise logistic regression analysis demonstrated that for thrombus, the lack of effective antiplatelet therapy was the most discriminatory variable, followed by current smoking, higher percent diameter stenosis, and dissection. For clinically significant thrombus, once the lack of pretreatment with effective antiplatelet therapy was considered, no other factors added significant discriminatory information.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Disease↗

Synthetic human parathyroid hormone fragment stimulates prostaglandin E2 synthesis by chick calvariae.

Synthetic human PTH N-terminal 1-34 peptide [hPTH-(1-34)] stimulates prostaglandin (PG) production by chick calvariae in culture. PGE2 was the predominant PG found by both RIA and HPLC. Stimulation of PGE2 synthesis was significant at 50 ng/ml (1.2 X 10(-8) M) hPTH-(1-34) and was dose dependent at concentrations up to 0.6 microgram/ml (1.4 X 10(-7) M). Continuous exposure of calvariae to hPTH-(1-34) showed that PGE2 production increased significantly by 1 h, reached a maximum at 24 h, and then persisted over 96 h. Indomethacin at concentrations above 5 X 10(-7) M inhibited PGE2 synthesis by both control and hPTH-(1-34)-treated bones. PTH-(1-34) stimulated bone cells to convert arachidonic acid to PGE2, but did not activate the bone to release stored arachidonate. In summary, our results show that hPTH-(1-34) stimulates PGE2 synthesis by chick calvariae. This endogenous PGE2 may be involved in bone remodeling.

6-Ketoprostaglandin F1 alpha↗

Hemodynamic and metabolic effects of cerebral revascularization.

Pre- and postoperative positron emission tomography (PET) was performed in six patients undergoing extracranial to intracranial bypass procedures for the treatment of symptomatic extracranial carotid occlusion. The six patients were all men, aged 52 to 68 years. Their symptoms included transient ischemic attacks (five cases), amaurosis fugax (two cases), and completed stroke with good recovery (one case). Positron emission tomography was performed within 4 weeks prior to surgery and between 3 to 6 months postoperatively, using oxygen-15-labeled CO, O2, and CO2 and fluorine-18-labeled fluorodeoxyglucose. Cerebral blood flow (CBF), cerebral blood volume (CBV), cerebral metabolic rates for oxygen and glucose (CMRO2 and CMRGlu), and the oxygen extraction fraction (OEF) were measured in both hemispheres. Preoperatively, compared to five elderly control subjects, patients had increased CBV, a decreased CBF/CBV ratio, and decreased CMRO2, indicating reduced cerebral perfusion pressure and depressed oxygen metabolism. The CBF was decreased in only one patient who had bilateral carotid occlusions; the OEF, CMRGlu, and CMRO2/CMRGlu and CMRGlu/CBF ratios were not significantly different from control measurements. All bypasses were patent and all patients were asymptomatic following surgery. Postoperative PET revealed decreased CBV and an increased CBF/CBV ratio, indicating improved hemodynamic function and oxygen hypometabolism. This was associated with increased CMRO2 in two patients in whom the postoperative OEF was also increased. The CMRGlu and CMRGlu/CBF ratio were increased in five patients. Changes in CBF and the CMRO2/CMRGlu ratio were variable. One patient with preoperative progressive mental deterioration, documented by serial neuropsychological testing and decreasing CBF and CMRO2, had improved postoperative CBF and CMRO2 concomitant with improved neuropsychological functioning. It is concluded that symptomatic carotid occlusion is associated with altered hemodynamic function and oxygen hypometabolism. Cerebral revascularization results in decreased CBV, indicating improved hemodynamic reserve, but does not consistently improve oxygen metabolism.

Aged↗

Cost savings through community access to the NSW Poisons Information Centre.

In addition to handling urgent emergency calls for advice about major poisonings, the NSW Poisons Information Centre handles calls from the general community about poisonings of a much more minor nature. Although these poisonings may be perceived by the callers to be significant, the only action required is either reassurance that there is, in fact, no problem or simple treatment that does not require further intervention. The study demonstrates that callers in this category would have sought professional advice elsewhere had the Centre not existed and the subsequent cost effectiveness of the Centre's role in taking these calls.

Community Health Services↗

Plasma and synovial fluid kinetics of flurbiprofen in rheumatoid arthritis.

Clinical assessment, plasma and synovial fluid kinetics were studied in 29 rheumatoid patients receiving 100 mg flurbiprofen twice daily. Clinical assessment and pharmacokinetic measurements varied widely within the group of patients. The average values for plasma clearance, volume of distribution and elimination halflife of flurbiprofen were 0.65 +/- 0.24 ml min-1 kg-1, 0.160 +/- 0.093 l kg-1 and 3.1 +/- 1.7 h, respectively. Synovial fluid drug concentrations peaked later and were lower than corresponding plasma concentrations: 5.2 h and 4.4 mg l-1 as against 1.49 h and 12.5 mg l-1, respectively. At 48 h after an oral dose of flurbiprofen, all the drug had been cleared from the synovial fluid. Synovial fluid drug concentrations were not related to synovial fluid albumin concentration or pH. There was a weak relationship between synovial fluid drug concentration and the thermographic measurements of disease activity. The fractions of flurbiprofen not bound to protein in synovial fluid and plasma were not significantly different. A simple model is proposed to account for the plasma and synovial fluid pharmacokinetics.

Adolescent↗

Anomalous binding of DPDPE as a result of batch variability.

The binding of the delta selective agonist [3H]DPDPE to diencephalic rat brain tissue was examined. Although most material examined gave rise to a single receptor model, one commercial preparation (Amersham, batch 8) suggested a two receptor model. Purification by HPLC removed a minor component and restored a single receptor model to the major component.

Animals↗

Diagnostic considerations in virilization: iodomethyl-norcholesterol scanning in the localization of androgen secreting tumors.

Accurate localization of the source of androgen hypersecretion is critical to the appropriate surgical or medical management of women with virilization. Seven patients with virilization and hyperandrogenism of various causes were evaluated with the use of sequential studies: testosterone stimulation and suppression tests; computerized tomography (CT); selective venous catheterization; and 131I-iodomethyl-norcholesterol (NP-59) scintigraphy. Comparison of the diagnostic accuracies of these localization studies with the ultimate diagnoses in this group of virilized women showed that: endocrinologic suppression/stimulation studies are of limited value in tumor localization and helpful only in patients with steroidogenic enzyme deficiencies; both selective catheterization and CT scanning may provide spurious localization data; and NP-59 scintigraphy, by depicting both the anatomic localization and functional androgen hypersecretion, may provide the most significant localization data in the evaluation of patients with virilizing syndromes.

Adenoma↗