This paper reexamines recent epidemiologic and molecular genetic studies on the genetic basis of Alzheimer's Disease (AD). Careful analysis of the available epidemiologic data strongly suggests that at least a proportion of AD results from the inheritance of an autosomal dominant gene defect. However, studies of isolated families, of concordance rates in twins, and of risk for AD in relatives of AD probands yield conflicting data. While it is likely that much of the conflict can be ascribed to methodologic differences, it remains premature to conclude that all AD is transmitted as an autosomal dominant trait. Molecular genetic techniques hold the promise of isolation and characterization of the genetic defect(s) in familial AD (FAD). Recently, chromosome 21 has been implicated as the potential site of an autosomal dominant defect in some but not necessarily all FAD pedigrees. However, the results of recent genetic epidemiologic studies suggest that progress in the molecular genetic approach to AD will be difficult.

Adult↗

PubMedDate not supplied

The use of the Cape Minor ventilator with the circle absorber system.

Various methods by which the Cape Minor ventilator may be used in the circle absorber system are described and the problems of the circuits described are considered. A new valve system is described which overcomes most of the problems encountered with other circuits. The economic advantages of an inexpensive ventilator and absorber system which is economical are obvious.

Humans↗

PubMedDate not supplied

A study of the thermogenic effect of ethanol in the hypothermic rat.

1. The hypothesis that ethanol may exert a thermogenic effect in cold environments was studied by infusing ethanol, dextrose or saline into hypothermic rats and observing the rate of rewarming in each group. 2. No difference was found in the rate of heat gain in any of the three groups.

Animals↗

PubMedDate not supplied

Naloxone does not reverse ethanol analgesia in man.

The effects of intravenously administered ethanol and morphine on pain threshold, reaction time, motor skills and short-term memory were investigated, and the ability of naloxone to reverse any changes was studied. Morphine (loading dose 0.2 mg/kg with an infusion of 0.004 mg/kg per min) and ethanol (loading dose 0.75 ml/kg with an infusion of 0.0025 ml/kg per min) produced a similar increase in pain threshold of 6.3 (s.e.m. = 1.5, n = 8) pain units and 7.7 (s.e.m. = 1.9, n = 8) pain units, respectively. Naloxone 0.015 mg/kg produced a significant reduction in pain threshold in the morphine group, but not in the ethanol group, and there was a significant difference between the groups following naloxone (P less than 0.05, t-test, 7 d.f.). Ethanol produced a significantly greater deterioration in motor skills than did morphine (P less than 0.05, t-test, 7 d.f.) and performance in both groups was improved following naloxone (P less than 0.05, t-test, 7 d.f.). There was no significant change in the other modalities studied. It is concluded that the reversal of ethanol effects by naloxone is probably due to a non-specific analeptic action rather than blockade of opioid receptors.

Analgesics↗

PubMedDate not supplied

[Metabolism of morphine, its analgesic activity and adverse reactions during prolonged administration by various routes].

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Drug Administration Schedule↗