An alternative method to restore endodontically treated teeth.
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Biomedical subjects
Publications and source records attributed to L Rosenthal.
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Two symptom clusters are prominent obstructive sleep apnea syndrome: excessive daytime sleepiness and neurocognitive difficulties. This article reviews studies that have attempted to determine the etiology and interrelation of these two symptom clusters. The research has clearly determined that the cause of the daytime sleepiness of obstructive sleep apnea syndrome is the fragmentation of sleep by the brief arousals that terminate each apneic event rather than the nocturnal hypoxemia that also occurs in obstructive sleep apnea syndrome. However, the daytime sleepiness and nocturnal hypoxemia appear to both contribute to the neurocognitive impairments of obstructive sleep apnea syndrome, and each seems to affect specific aspects of neurocognitive performance. The extent to which treatment reverses the neurocognitive impairments of obstructive sleep apnea syndrome is yet to be fully determined. The initial study suggests that the impairments are not completely reversed with treatment.
To study the short-term effects of theophylline on sleep and wakefulness, 24 healthy men and women, aged 21 to 35 years, received each of three doses, 0, 3, and 6 mg/kg, of theophylline double-blind in a Latin Square design, administered to 12 subjects at 9 AM and to the other 12 at 11 PM. After the daytime administration, sleep latency was tested at 10 AM, 12 Noon, 2 PM, and 4 PM and divided attention and auditory vigilance performance were tested at 10:30 AM and 2:30 PM. After the nighttime administration, a standard 8-h polysomnogram was collected. On a separate day all subjects received a single 6-mg/kg dose at 9 AM and blood samples were drawn at 8:30 and 10:30 AM, 12:30 PM, 2:30 PM, and 4:30 PM. The serum theophylline levels for the 6-mg/kg dose peaked at 11.0 micrograms/mL and declined to 8.1 micrograms/mL by 4:30 PM. In the daytime administration, daytime mean sleep latency was increased by both doses and performance was improved by the high dose but not the low dose. In the nighttime administration, nocturnal sleep onset was delayed and total wake time was increased by the high dose but not the low dose. The low dose increased the amount of light stage 1 sleep without producing wakefulness.
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The purpose of this study was to develop a valid multidimensional self-report measure of sleepiness. There were 554 subjects who completed the inventory. The structure of the Sleep-Wake Activity Inventory (SWAI) was derived from principal components analysis. The independent predictive strength of the factors was assessed by forward stepwise regression analysis with the average sleep latency on the Multiple Sleep Latency Test (MSLT) as the dependent variable. The scores on each of the factors were also compared by the level of sleepiness determined by the MSLT (pathological, diagnostic gray area, and normal). Factor analysis showed the existence of six factors on the SWAI (Excessive Daytime Sleepiness [EDS], Psychic Distress, Social Desirability, Energy Level, Ability to Relax and Nocturnal Sleep). The EDS factor was the best predictor of average MSLT. It was also able to differentiate pathological levels of sleepiness from both the diagnostic gray and normal levels of sleepiness. EDS factor scores were sensitive to changes in sleep physiology as improved scores followed normalization of sleep-disordered breathing. The SWAI was shown to be easy to complete, have a multi-dimensional structure, have a EDS factor useful in the prediction of average MSLT scores, be sensitive to differential levels of sleepiness, and change as a result of effective treatment.
The effects of various time in bed (TIB) conditions on daytime sleepiness and total sleep time (during a 24-hour enforced bedtime) were investigated. Thirty-two healthy male subjects participated in the study. Subjects were assigned to one of four groups to balance average screening multiple sleep latency tests (MSLT). Subjects were randomly assigned to spend 8, 6, 4 or 0 hours time in bed. They underwent the same TIB condition twice with at least 7 days between the two sessions. Following their assigned time in bed conditions, subjects were counterbalanced to have a standard MSLT and a 24-hour enforced bedtime protocol. To assess the effect of TIB on the MSLT, the sleep latencies were submitted to a four (TIB condition) by four (nap test) multivariate analysis of variance. The sleep latencies were shorter for those subjects in the 0-hours condition when compared to the other three conditions. Also, the sleep latencies of those subjects in the 4- and 6-hour conditions were comparable but different from those of subjects in the 8- and 0-hour TIB conditions. To assess the effect of TIB on the 24-hour enforced bedtime, the total sleep time during this period was submitted to a six (4-hour block) by four (TIB condition) multivariate analysis of variance. Subjects slept more following 0 hours TIB when compared to the other three conditions. There were no statistically significant differences between the 8-, 6- and 4-hour TIB conditions. Across conditions, subjects slept more during the first 4 hours when compared to blocks 2, 3, 4 and 5. Blocks 1 and 6 were comparable.(ABSTRACT TRUNCATED AT 250 WORDS)
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While the variety of responses of psychotherapy groups to new members is wide, this article addresses those that are treatment destructive, that is, murderous in that they are aimed at the elimination of a new sibling. A number of frequently encountered destructive response patterns to new members are illustrated and categorized. It is suggested that survival of the new member is best insured by adequate preparation of the group so that the nucleus of powerful feelings activated in this situation can be felt and expressed prior to the addition of the new member. A clinical example of appropriate preparation is offered, and the contributions of group therapists to new member casualties are noted.
To determine the association of HLA DR2 in patients with narcolepsy without cataplexy, a case-control study was performed. Patients receiving the diagnosis of narcolepsy without cataplexy had excessive daytime sleepiness (EDS) and polysomnographic findings consistent with narcolepsy but no clinical evidence of cataplexy. Of 28 patients identified, 12 agreed to return for HLA typing. Respondents did not differ from nonrespondents in demographic, clinical, or sleep laboratory data. The comparison group was 503 individuals, those 30 years and older, on the Michigan Kidney Transplant Registry. The odds ratio obtained from logistic regression indicated a strong association between narcolepsy without cataplexy and HLA DR2. To control for potential confounding variables, multivariate models were constructed to explore the joint effects of HLA DR2 and each one of the covariates (age, sex, and race), their possible combinations, and the effect of all three covariates. The odds ratios decreased minimally and the association between the disease and HLA DR2 remained significant.
Connexins are protein subunits that constitute gap junction channels. Two members of this gene family, connexin43 (Cx43) and connexin32 (Cx32), are abundantly expressed in the heart and liver, respectively. Human genomic DNA analysis revealed the presence of two loci for Cx43: an expressed gene and a processed pseudogene. The expressed gene (GJA1) was mapped to human chromosome 6 and the pseudogene (GJA1P) to chromosome 5. To determine whether Cx32 was linked to Cx43, somatic cell hybrids were analyzed by polymerase chain reaction and hybridization, resulting in the assignment of the gene for Cx32 (GJB1) to the X chromosome at Xp11----q22. Comparison of the structures of connexin genes suggests that members of this multigene family arose from a single precursor, but evolved to distinct chromosomal locations.
The pattern of recovery sleep after sleep deprivation was investigated in healthy young adults. Six subjects experienced three experimental conditions (0, 24, and 48 hr sleep deprivation) in a Latin Square design. The recovery period consisted of a 24-hr enforced time in bed during which subjects were polysomnographically recorded beginning at 0800. To assess the differential effects of the deprivation conditions, the total sleep time on the 24-hr recordings was submitted to a six (4-hr block) by three (deprivation condition) multivariate analysis of variance. Subjects slept more following the 24- and 48-hr conditions when compared to the 0-hr condition. Across conditions, subjects slept more during the first 4 hr when compared to the remaining five blocks. Importantly, there was a significant interaction of sleep deprivation by 4-hr block. In block 1 sleep was differentially recovered between each condition with more sleep being recorded following longer hours of deprivation. In block 2 subjects in the 24- and 48-hr conditions slept comparable amounts and significantly more than those in the 0-hr condition. In blocks 3 and 4 only the 48-hr condition exhibited significantly more sleep than the 0-hr condition. However, significantly less sleep was found in block 6 following the 48-hr condition. Overall, subjects recovered 72% and 42% of the total amount of sleep lost during the 24- and 48-hr conditions, respectively.
To assess the alerting effects of caffeine after normal and restricted nocturnal sleep, 36 healthy, nonsmoking men, 19 to 35 years old, who reported normal sleep and daytime alertness received 0, 75, or 150 mg caffeine twice daily after 8 and 5 hours in bed the previous night. Sleep restriction reduced average daily sleep latency measured by the Multiple Sleep Latency Test (MSLT) and slowed auditory vigilance reaction time in the latter half of the 40-minute task. Caffeine (75 and 150 mg) increased average daily sleep latency and improved vigilance reaction time. However, sleep restriction did not alter the alerting effects of caffeine. The data show that, unlike ethanol, basal level of sleepiness/alertness does not interact with the effects of caffeine.
alpha-Latrotoxin causes a massive release of endogenous glutamate from guinea-pig cerebrocortical synaptosomes. There appear to be two components to the release. In the first 2 min following addition of 1.3 nM alpha-latrotoxin, glutamate release is largely energy dependent. Superimposed upon this release is a more slowly developing but ultimately much more extensive release of cytoplasmic glutamate together with gamma-aminobutyric acid and nonvesicular amino acids such as aspartate and alpha-aminoisobutyrate. In parallel with this cytoplasmic release there is an extensive depletion of ATP, a massive rise in cytoplasmic free Ca2+ concentration, and a severe restriction of synaptosomal respiratory capacity. The cytoplasmic release is only partially Na+ dependent, eliminating a simple reversal of the plasma membrane acidic amino acid carrier. It is concluded that alpha-latrotoxin releases both transmitter and cytoplasmic pools of amino acids in synaptosomes and causes a major disruption of terminal integrity.