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Biomedical subjects

J M Fry

Publications and source records attributed to J M Fry.

35 records · Page 2Linked to original sources
PubMed1986

Problems in the interpretation of nocturnal penile tumescence studies: disruption of sleep by occult sleep disorders.

A review of the sleep of 31 patients 45 years old or older undergoing nocturnal penile tumescence studies showed that 19 had a previously undiagnosed sleep disorder. Of the patients 9 had periodic leg movements in sleep, 9 had sleep apnea and 1 had both disorders. In 10 of these patients the sleep disorders affected nocturnal penile tumescence by disrupting sleep and causing brief periods of detumescence, movement artifacts and delays in the tumescing phase of nocturnal penile tumescence. These disruptions resulted in an apparently abnormal nocturnal penile tumescence that appeared as if the patient had difficulty in achieving or maintaining an erection. The nocturnal penile tumescence disruptions may have reflected only a disruption of the necessary conditions for normal nocturnal penile tumescence to occur, namely adequate sleep and rapid eye movement sleep. The results strongly suggest that failure to measure concurrent sleep parameters and screen for occult sleep disorders could result in the incorrect diagnosis of abnormal nocturnal penile tumescence.

Aged↗
PubMed1986

Senile miosis: the possible contribution of disordered sleep and daytime sleepiness.

The contribution of disordered sleep and daytime sleepiness to senile miosis was investigated in 23 participants aged 60 to 80 years and 12 participants aged 21 to 40 years. All participants filled out questionnaires and were interviewed about their health, sleep, and daytime alertness. On this basis the older group was subdivided into a group of 13 participants with sleep disorders or daytime sleepiness and 10 participants without. All participants were studied with a computerized infrared television pupillometry system for 15 s in ambient lighting, 15 s after 5 min dark adaptation and with 5 light flashes. Pupil diameter after dark adaptation was significantly larger in the older group without sleep disorders than in the older group with sleep disorders (5.94 +/- .73 mm vs. 4.49 +/- .62 mm, M +/- SD, p less than .001). Significant partial correlation coefficients controlled for age were found between pupillary diameter and a variety of sleep variables. The data suggest that occult sleep disorders and daytime sleepiness may contribute to senile miosis.

Adult↗
PubMed1986

Treatment of narcolepsy with codeine.

The effectiveness of codeine as a treatment for the excessive daytime sleepiness of narcolepsy was studied in two experimental trials. In an open trial of codeine in five narcoleptic subjects, dramatic clinical improvement was reported. However, all-night polysomnography and maintenance of wakefulness tests before and after codeine showed no significant differences. A double-blind placebo-codeine trial was conducted in which eight narcoleptic subjects received codeine for 1 week and placebo for 1 week in a random order. During the week they kept a diary, and on the sixth evening and for 10 h following awakening on the seventh day they were monitored by radiotelemetry in the sleep laboratory for electroencephalogram, electro-oculogram, and electromyogram. The results were analyzed for sleep stages as well as four levels of wakefulness. The results showed no significant differences in any of the objective sleep or wakefulness parameters. However, the diaries showed significantly fewer naps during the week on codeine as compared with the placebo week. Eighteen of 27 narcoleptic patients treated with codeine report clinical improvement. Codeine consistently results in subjective clinical improvement. However, this is not reflected in the objective measures generally used to assess daytime sleepiness.

Adult↗
PubMed1986

Effects of low-dose naloxone on subjective alertness and pupil diameter in normal and narcoleptic subjects.

Recent evidence suggests that endogenous opiates may be involved in the pathophysiology of narcolepsy. To test this theory, the effect of 0.8 mg naloxone hydrochloride on pupil size and subjective alertness was measured in normal and narcoleptic subjects. Naloxone resulted in significant pupillary constriction in the normal but not in the narcoleptic subjects. The extent of contraction of the pupil light reflex was reduced significantly in the narcoleptic but not in the normal subjects. There was no effect on subjective ratings of alertness on the Stanford Sleepiness Scale or the visual analogue scale in either group. The naloxone-related miosis in the normal group confirms that naloxone is not a pure opiate antagonist. The lack of naloxone-related miosis in the narcoleptics suggests that narcoleptic individuals do not respond to naloxone as do normal individuals. However, this difference can not be definitely attributed to the antagonism of endogenous opiates. The reduction of the extent of contraction of the light reflex suggests that naloxone caused an increase in supranuclear inhibition of parasympathetic pupil reflex activity. However, this finding may have resulted from mechanical limitations of a small pupil or technical limitations of the recording equipment. This study does not support previous reports that naloxone causes an increase in subjective alertness in narcoleptics.

Adult↗
PubMed1979

Antiserum induced myelination inhibition in vitro without complement.

Exposure of neonatal rat cerebellum cultures to antiserum to whole spinal cord or galactocerebroside inhibited myelin formation regardless of whether guinea pig serum was added fresh or after heating to 56 degrees C for 1 h in order to achieve complete removal of hemolytic complement activity. Myelination followed removal of antisera from the culture media. This suggests that the inhibition of primary myelination by anti-CNS tissue antiserum occurs through some mechanism other than as the result of a cytotoxic reaction against oligodendrocytes mediated via the complement system.

Animals↗
PubMed1976

Serological techniques for detection of antibody to galactocerebroside.

Two serological techniques were developed for the detection of antibody to galactocerebroside using liposomes as a carrier for the lipid hapten. One assay is a radioimmunoprecipitation test employing [3H] cholesterol as a marker in the galactocerebroside-liposomes. The other is a less sensitive but quick and easy galactocerebroside-liposome agglutination assay. Specificity is demonstrated by comparison of titers when other lipid haptens replace galactocerebroside in the liposomes, and when other anti-glycolipid antisera are reacted with galactocerebroside-liposomes.

Agglutination Tests↗
PubMed1974

Cerebroside antibody inhibits sulfatide synthesis and myelination and demyelinates in cord tissue cultures.

Antiserum to cerebroside was prepared in rabbits by injection of cerebroside together with bovine serum albumin in complete Freund's adjuvant. When applied to cultures of embryo mouse spinal cord at explantation, this antiserum inhibited sulfatide synthesis and myelination; when applied to myelinated cultures it inhibited sulfatide synthesis and produced demyelination. Complement fixation assays also show antibody to cerebroside in serums from rabbits with experimental allergic encephalomyelitis induced by injection of whole white matter. Absorption of such serum with cerebroside abolishes the inhibiting and demyelinating activities.

Animals↗
PubMed1972

Sulfatide synthesis: inhibition by experimental allergic encephalomyelitis serum.

The rate of (35)S incorporation into cerebroside sulfate in cultures of embryo mouse spinal cord shows a rapid acceleration at the time of myelin formation. Exposure of cultures to dilute serum from rabbits with experimental allergic encephalomyelitis results in almost complete inhibition of sulfatide synthesis. Within 24 hours after replacement of inhibiting medium with normal medium there is an increase in sulfatide synthesis followed by myelination.

Animals↗