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Biomedical subjects

B L Bayer

Publications and source records attributed to B L Bayer.

At least 19 recordsLinked to original sources
PubMed1993

L-deprenyl in the treatment of mild dementia of the Alzheimer type: preliminary results.

OBJECTIVE: To examine the short-term cognitive and behavioral effects of L-deprenyl in persons with mild dementia of the Alzheimer type (DAT) over a 2-month period. DESIGN: A 15-month randomized, double-blind, placebo-controlled trial using a parallel-group design. This report deals with the first 2 months of the trial. PARTICIPANTS: 39 subjects with mild DAT (CDR 1) selected using NINCDS-ADRDA criteria. MEASURES: A battery of neuropsychological tests and clinical rating scales. RESULTS: The placebo and L-deprenyl subjects were similar at baseline on the clinical and neuropsychological tests. There was no evidence of a L-deprenyl effect on any clinical or neuropsychological measures after 2 months. CONCLUSION: L-deprenyl did not have a measurable impact on behavior or cognitive function over a 2-month period in this group of subjects with mild DAT.

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PubMed1993

L-deprenyl in the treatment of mild dementia of the Alzheimer type: results of a 15-month trial.

OBJECTIVE: To examine the cognitive and behavioral effects of L-deprenyl in persons with mild dementia of the Alzheimer type (DAT) over a 15-month period. DESIGN: A 15-month randomized, double-blind, placebo-controlled trial using a parallel-group design. PARTICIPANTS: 39 subjects with mild DAT (CDR 1) selected using NINCDS-ADRDA criteria. OUTCOME MEASURES: A battery of neuropsychological tests and clinical rating scales. RESULTS: The placebo and L-deprenyl subjects were similar at baseline on the clinical and neuropsychological tests. The total score on the Brief Psychiatric Rating Scale (BPRS) was significantly less after 15 months in subjects taking L-deprenyl. The only individual item of the BPRS which differed between groups was disorientation. There was no evidence of a L-deprenyl effect on any other clinical or neuropsychological measure after 2, 8, or 15 months. CONCLUSION: L-deprenyl did appear to have a slight effect on a single measure of psychopathology, the BPRS. It did not have a measurable impact on any other measure of behavior or cognitive function over a 15-month period in this group of subjects with mild DAT and did not appear to slow the progression of the disease.

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PubMed1992

Validation of a telephone version of the mini-mental state examination.

OBJECTIVE: To assess the construct validity of a telephone-administered version of the Mini-Mental State Examination (MMSE). DESIGN: Validity testing by comparing a telephone version of the MMSE administered first to a face-to-face evaluation done several days later. SETTING: Outpatient geriatric assessment center. SUBJECTS: 100 of 175 consecutive referrals. MAIN OUTCOME MEASURES: MMSE and a brief neuropsychological screening test (BNPS) face-to-face and a telephone version of the MMSE as part of the Adult Lifestyles and Function Interview (ALFI-MMSE). RESULTS: Test scores of the two MMSE versions correlated strongly for all subjects (Pearson's r = 0.85, P = 0.001) and remained significant for the cognitively intact (P = 0.02) and questionably (P = 0.002), mildly (P = 0.0001), and moderately (P = 0.003) demented. Comparison of the two versions' equivalent 22 items revealed no significant difference for scores of all subjects (P = 0.07) but with a trend toward higher scores in the original version. Diminished hearing, reported either by the subject (P = 0.003) or by the collateral source (P = 0.02) was associated with lower scores on the telephone version. Five individual test items were biased by the route of test administration. Sensitivity and specificity relative to the BNPS were 67% and 100% for the ALFI-MMSE and 68% and 100% for the MMSE, respectively. CONCLUSION: The scores on the ALFI-MMSE correlated strongly with the scores of the original version given face-to-face in subjects undergoing geriatric assessment. The results indicate that the ALFI-MMSE could be a useful and economical tool to screen for cognitive impairment.

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PubMed1981

[Stimulation of prostacyclin biosynthesis as a possible mechanism of action of dipyridamole (author's transl)].

In microsomes of pig aorta, isolated perfused hearts of guinea-pigs, rabbit vessel preparations and homogenates of rat lungs 2,6-bis-[bis-(beta-hydroxyethyl)-amino]-4,8-dipiper-idino-pyrimido-[5,4-d]pyrimidine (dipyridamole) application caused a marked stimulation of prostacyclin biosynthesis. The oxygen incorporation into arachidonic acid indicating cyclooxygenase and lipoxydase activity under the influence of lyophilised ram vesicle microsomes was increased by dipyridamole. The formation of malondialdehyde and thromboxane A2 in platelet rich plasma of rabbits remained uninfluenced. On the other side the formation of thromboxane A2 was moderately inhibited in homogenates of guinea-pig lungs. The arachidonic acid-induced thrombus formation and following death of rabbits remained uninfluenced. The results indicate that dipyridamole causes a relatively specific alteration of the prostaglandin metabolism stimulating the biosynthesis of prostacyclin but without effect or only moderate inhibition of the formation of thromboxane A2. These effects could be looked upon as an important mechanism for the cardiovascular action of the drug.

Animals↗
PubMed1979

Actions of prostaglandin precursors and other unsaturated fatty acids on conduction time and refractory period in the cat heart in situ.

1 The effect of arachidonic, dihomo-gamma-linolenic, linoleic, alpha-linolenic and oleic acid, given by intravenous infusion, on conduction time and functional refractory period have been studied in the cat heart in situ. 2 The prostaglandin precursors, arachidonic acid and dihomo-gamma-linolenic acid, prolonged the conduction time and the functional refractory period. Linoleic acid was also effective but to a lesser degree. alpha-Linolenic acid and oleic acid showed no or only a weak effect in thie respect. 3 Pretreatment was indomethacin diminished or abolished the actions of the three effective fatty acids but not those of prostaglandin E2. 4 The results suggest that the effects of prostaglandin prostaglandin precursors on conduction time and refractory period are responsible for their antiarrhythmic effectiveness and that these effects are attributable to their endogenous conversion into prostaglandins.

Action Potentials↗
PubMed1979

Anti-aggregatory effect of prostacyclin (PGI2) in vivo.

Prostacyclin (PGI2) when infused intravenously reduced the mortality of rabbits given high intravenous doses of arachidonic acid (AA). Prostaglandins E1 and D2 were ineffective. Indomethacin pretreatment abolished the toxic AA effect. Since the lethal effect of AA is partly due to the formation of platelet aggregates it is concluded that PGI2 is a most potent anti-aggregatory prostaglandin in vivo.

Animals↗
PubMed1976

[The influence on heart conduction time and refractory period of in vitro and in vivo prostaglandins].

The effects of PGE1, PGE2 and PGF2alpha on conduction time and functional refractory period in the isolated rabbit atrium and in the cat heart in vivo were investigated. In the isolated rabbit atrium the PGs (10(-8)--10(-5) g/ml) were without any effect in this respect. In contrast there was a dose-dependent decrease of conduction time and prolongation of functional refractory period in the cat heart in vivo following PG-infusions (2,0--8,0 mug/kg/min i.v. over a period of 5 min). These findings indicate the absence of a direct quinidine-like membrane action of PGs in the heart. The indirect, depressive effects of PGs on conduction time and functional refractory period in the heart in vivo, should be considered responsible for the antiarrhythmic action of PGs.

Ajmaline↗