1. The presence of xanthine was required for the inhibition of bovine milk xanthine oxidase by o-iodosobenzoate, iodoacetamide, hydrogen peroxide or p-chloromercuribenzoate. 2. Inactivation by p-chloromercuribenzoate was very rapid, was reversed by cysteine and was less in the presence of FAD. Lineweaver-Burk plots showed that the inactivation by p-chloromercuribenzoate was competitive with substrate. 3. Inactivation by o-iodosobenzoate, iodoacetamide or hydrogen peroxide could not be reversed by cysteine or xanthine. However, the presence of xanthine during the incubation with inhibitor protected the enzyme against o-iodosobenzoate but not against iodoacetamide or hydrogen peroxide. 4. p-Chloromercuribenzoate protected the enzyme against inactivation by hydrogen peroxide.

Amides↗

PubMedDate not supplied

Cortical and subcortical neuropeptides in Alzheimer's disease.

Given the clinical features of AD, the severe atrophy of cerebral cortex that accompanies the disease, and the predominant cortical location of plaques and tangles, it is not surprising to find the most consistent changes in neuropeptides in this disease occurring in the cerebral cortex. The neuropeptide changes that have been reproducibly demonstrated in AD are reduced hippocampal and neocortical SS and CRF concentrations and a reduced CSF level of SS. In cerebral cortex, SS and CRF are found in GABAergic local circuit neurons in layers II, III, and VI. The function of these neurons is not well established, although these cells may act to integrate the flow of incoming and outgoing information in cerebral cortex. If this is true, then dysfunction of this integration could produce widespread failure of cerebrocortical function, resulting in the various neurobehavioral deficits seen in AD. The interpretation of neuropeptide changes in subcortical brain regions, either those that project to cortex, or those that are the efferent targets of cortical projections, is also uncertain. The observed neuropeptide abnormalities in these brain regions in AD are less consistent than are those seen in cerebral cortex. Perhaps the most intriguing result in these regions is the increases in galanin-immunoreactive terminals seen in the nucleus basalis of AD brains. Galanin has been shown to inhibit acetylcholine release and to impair memory function in rats (46,113).(ABSTRACT TRUNCATED AT 250 WORDS)

Alzheimer Disease↗

PubMedDate not supplied

Development of a computer-based battery designed to screen adults for neuropsychological impairment.

The initial step in the development of a new computer-based neuropsychological testing system is described. A new hardware-software system and a screening battery consisting of an orientation task and five cognitive tests has been implemented. This novel screening battery is designed for use in identifying individuals among exposed groups who may require more extensive follow-up neuropsychological evaluation. Sophisticated, but currently available, and relatively inexpensive hardware and software technology are employed, introducing an improvement over existing computer-based batteries. Use of a digitized speech production device for producing instructions facilitates testing of illiterate subjects, use of auditory stimulus materials, and relatively easy translation of the testing instructions to other languages. Use of a pen-based notebook computer enables responding by the subject in a manner that is both natural and analogous to that used in existing paper-and-pencil testing instruments. Five neuropsychological tests were developed to cover a range of cognitive domains: 1) verbal list learning and recognition memory, 2) visual memory span, 3) conceptual and motor tracking, 4) psychomotor speed and accuracy, and 5) delayed verbal recognition. The screening instrument has been pilot-tested for feasibility of use among outpatients at an occupational medicine clinic and among community-dwelling older adults. This instrument is intended to provide a standardized efficient, cost-effective method for widespread use in occupational medicine and public health to detect and track subclinical neurotoxic effects and to prevent additional harmful exposure. Additional aspects of development of the computer-based testing system are discussed.

Adult↗

PubMedDate not supplied

Placebos in clinical trials in Alzheimer disease: an international discussion.

Explore the source record for details and available documents.

Alzheimer Disease↗

PubMedDate not supplied

Noninvasive measurement of cardiac pressures by induced ventricular wall resonance: preliminary results in the dog.

Experiments in the excised dog heart and in live dogs are presented wherein a method of induced right ventricular wall resonance has been utlized to estimate the pressure in the right ventricle of the heart. Externally induced cardiac wall vibrations produced low frequency signals which, when subjected to spectrum analysis and coherent signal processing, permitted close approximation of static pressures and wave forms in the right ventricle at normal and hypertensive levels.

Animals↗

PubMedDate not supplied

Kindling susceptibility and genetic seizure predisposition in inbred mice.

Olfactory bulb kindling rates were studied in two inbred strains of genetically seizure-prone mice (DBA/2 and El) and in three non-epileptic inbred strains [C57BL/6 (B6), ddY, and C3H/He (C3H)]. None of the DBA/2 mice had been stimulated to seizure before or during the kindling and all mice were studied at 4-6 weeks of age, before development of spontaneous or movement-induced seizure activity in the El strain. The audiogenically seizure-susceptible DBA/2 mice required the fewest number of stimulations to reach stage 5 seizure (mean +/- SE = 4.0 +/- 0.6). The nonepileptic C3H mice required the most stimulations to reach stage 5 seizures (22.6 +/- 1.4). Kindling rates for B6 (9.6 +/- 0.6), El (14.8 +/- 1.1), and ddY (18.5 +/- 1.0) strains were intermediate, and the kindling rate for each strain was significantly different from that of the other strains. These findings show that the seizure-susceptible El mouse kindles more rapidly than the genetically similar but nonepileptic ddY control and suggest that an inherited seizure susceptibility accelerates the kindling rate. Nonepileptic B6 mice kindled more rapidly than El mice, however, suggesting that genetic factors other than those that influence seizure susceptibility are of primary importance in the determination of the kindling rate.

Acoustic Stimulation↗

PubMedDate not supplied

Olfactory bulb kindling in mice susceptible and resistant to ethanol withdrawal.

The relation between kindling and susceptibility to ethanol withdrawal seizures was investigated using withdrawal seizure-prone (WSP) and withdrawal seizure-resistant (WSR) mice. These lines were developed by selective breeding to be prone and resistant, respectively, to handling-induced convulsions after chronic exposure to ethanol. Development of kindled seizures in response to electrical stimulation of the olfactory bulb was investigated in mice aged 2 and 8 months with no exposure to ethanol. Older WSP mice kindled more slowly than older WSR mice, requiring significantly more stimulations to reach the first stage 3 and the first stage 5 seizures. In younger mice, there was no significant difference between the two lines in the rate of kindling. The lower kindling rate in mature WSP mice is in contrast to their higher sensitivity to handling-induced convulsions on withdrawal from ethanol and other agents. This finding suggests that separate genetic factors underlie these two models of mouse seizures.

Age Factors↗