Effect of extract of Rhazya stricta, a traditional medicinal plant, on rat brain tribulin.

Rhazya stricta leaves, which have both antidepressant and sedative properties in animal models, are widely used in folk medicine in the Arabian peninsula. In this study, the effects of oral administration of leaf extracts on rat brain tribulin levels [endogenous monoamine oxidase (MAO) A and B inhibitory activity], were determined. In an acute study, low doses brought about an increase in MAO A inhibitory activity, while intermediate doses caused a significant reduction. The highest doses had no significant effects on activity. There were no significant effects on MAO B inhibitory activity at any dose. Subchronic administration (21 days) caused a significant decrease in MAO A inhibitory activity, most prominent at low dosage, and an increase in MAO B inhibitory activity. Acute intramuscular administration also resulted in a similar pattern. Such paradoxical effects were at least partially explained when different extracts of the leaves were used; a weakly basic chloroform fraction caused an increase in MAO A inhibitory activity, whereas butanol extracts brought about a decrease. These fractions had no significant effects on MAO B inhibitory activity. The findings show that Rhazya stricta leaves contain at least two different components that affect MAO inhibitory activity in opposite directions. It may be that the antidepressant and sedative actions of the plant are explicable in terms of these different components.

A simplified intravenous glucose loading protocol for fluorine-18 fluorodeoxyglucose cardiac single-photon emission tomography.

The myocardial uptake of fluorine-18 fluorodeoxyglucose (FDG) has emerged as the most sensitive and specific technique for the assessment of myocardial viability. With the development of FDG single-photon emission tomography (SPET) and dual head coincidence imaging, a hindrance to the widespread clinical use of FDG cardiac imaging is the complexity of the preinjection glucose loading necessary for obtaining interpretable myocardial FDG scans. In a population of 209 patients undergoing dual-isotope single acquisition (DISA) FDG/sestamibi (MIBI) SPET, we describe the improvements in both image quality and time efficiency using a new short, simple glucose/insulin/potassium (GIK) infusion protocol prior to FDG injection as compared to a conventional oral glucose loading protocol. DISA FDG/MIBI SPET scans were performed in 111 nondiabetic patients after oral loading with 50 g of glucose (group 1). Ninety-eight consecutive nondiabetic patients were subsequently scanned following preparation with a fixed-concentration GIK infusion administered at a standardized rate (group 2). A three-point grading scale was used to assess image quality. The time to FDG injection following glucose administration was significantly shorter for the group 2 patients (39.9+/-15.6 min; range 20-105 min) than for the group 1 patients (99.5+/-30.3 min; range 56-270 min) (P<0.0001), representing a 1-h decrease in patient preparation time. More of the group 1 patients (n=30; 27%) required supplemental intravenous boluses of regular insulin than did the group 2 patients (n=13; 13%) (P<0.02). There were more excellent and good quality graded images using the GIK method (group 2) than the more traditional oral loading protocol (group 1) (P<0.02). Nine of 111 scans (8%) in group 1 were uninterpretable, whereas only one of 98 scans (1%) in group 2 was uninterpretable. Standardized infusion of a fixed concentration of GIK prior to FDG administration and continued during myocardial FDG uptake is an effective yet simple method of obtaining consistently good to excellent quality FDG SPET cardiac scans. It is preferable to conventional oral glucose loading due to decreased patient preparation time and improved image quality. The technique is safe and should improve both the clinical use and the cost-effectiveness of FDG SPET imaging for the identification of injured but viable myocardium.

Brain quinolinic acid in Alzheimer's dementia.

Quinolinic acid (QA) content was measured in postmortem frontal and temporal cortex, putamen and cerebellum obtained from patients with senile dementia of Alzheimer type (SDAT), Huntington's disease (HD) and controls, using a gas chromatography/mass spectrometry method. There were no significant group differences in QA content of any of the regions examined. The data do not support the hypothesis that an accumulation of QA plays a role in neuronal degeneration occurring in the frontal and temporal cortex, putamen and cerebellum of patients with SDAT.

Brain quinolinic acid in Huntington's disease.

Concentrations of the endogenous neurotoxic tryptophan metabolite, quinolinic acid (QA), were measured in postmortem brain tissue obtained from patients with Huntington's disease (HD) and matched controls, using a gas chromatography/mass spectrometry method. There was no significant difference in either the putamen or the frontal cortex between the HD and control groups. These results do not support the hypothesis that increased QA is responsible for neuronal degeneration in HD.

Ultrasonic and computed tomographic features of mucocele of the appendix.

The ultrasonic features in three cases and computed tomographic (CT) findings in one case of mucocele of the appendix are presented. This entity appeared cystic on sonography and may have high-intensity echoes within it. The wall was not thickened and did not contain calcification, unlike previous descriptions. On CT, the mass was of soft tissue density, while previously, it had been described as cystic. Although mucocele of the appendix has a more variable appearance on sonography and CT than previously reported, a correct preoperative diagnosis can be made in most cases. Barium enema examination or calcification in the wall or in the mass itself may be necessary to distinguish this entity from lymphoma if the lesion is of soft tissue density on CT.

In vivo assessment of decarboxylase inhibition or potentiation: urinary dopamine and L-dopa output after L-dopa administration.

In the L-Dopa treated rat, a decreased urinary output of free and conjugated dopamine and an increase in free and conjugated L-Dopa excretion after administration of decarboxylase-inhibiting drugs provide a good in vivo index of Dopa decarboxylase inhibition. With the exception of free dopamine output, which showed an equivocal change, these measurements appear to provide a good yardstick of decarboxylase status in man also. Using this approach, it was not possible to find any evidence of facilitation of decarboxylase action, in L-Dopa-treated parkinsonians given pyridoxine supplements, to account for the ability of this compound to neutralize the beneficial effect of L-Dopa.