'Getting control of Corona takes many angles': COVID-19 vaccine knowledge, attitudes and beliefs among refugee/immigrant/migrant communities in four US cities.

The objectives of the study were to (i) document refugee, immigrant and migrant (RIM) communities' knowledge, attitudes and beliefs (KABs) related to the Coronavirus disease (COVID-19) vaccine and (ii) identify best practices for developing and disseminating culturally and linguistically responsive health messaging addressing those KABs. Thirteen online focus groups (OFGs) in 10 languages were conducted. Each OFG was conducted in the participants' native language. OFGs were recorded, transcribed, translated and uploaded to qualitative software for coding. A thematic analysis was conducted. Results suggest that while there was some variation between different language groups (e.g. whether religious leaders were seen as trusted sources of information about COVID), there were also important commonalities. Most language groups (i) alluded to hearing about or having gaps in knowledge about COVID-19/the COVID-19 vaccine, (ii) reported hearing negative or conflicting stories about the vaccine and (iii) shared concerns about the negative side effects of the vaccine. There continues to be a need for health messaging in RIM communities that is culturally and linguistically concordant and follows health literacy guidelines. Message content about the COVID-19 vaccine should focus on vaccine importance, effectiveness and safety, should be multimodal and should be primarily delivered by healthcare professionals and community members who have already been vaccinated.

Public health crisis in the refugee community: little change in social determinants of health preserve health disparities.

Structural inequities and lack of resources put vulnerable refugee communities at great risk. Refugees flee their country of origin to escape persecution and flee from war, famine and torture. Resettled refugee communities become particularly vulnerable during times of crisis due to limited English proficiency and poor social determinants of health (SDOH), which create barriers to attaining and sustaining health and wellbeing for themselves and their families. The purpose of this case study was to evaluate SDOH among a refugee community in the Southeastern United States. We surveyed the community twice during a 1-year period to assess various elements of SDOH. Among a primarily African and Southeast Asian refugee community, 76% reported difficulty paying for food, housing and healthcare during the first round of surveys. During the second round of surveys at the beginning of the Coronavirus pandemic, 70% reported lost income; 58% indicated concern about paying bills. There was little change during the 12-month study period, showing that SDOH are an enduring measure of poor health and wellbeing for this vulnerable refugee community.

Dreamlike events are correlated with the length of sleep mentation reports.

We investigated the relationship between length and dreamlike quality in sleep mentation reports. Reports were obtained by waking subjects at sleep onset (SO) and at 5 and 10 minutes into the second (REMP2) and fourth REM periods (REMP4). Reports were recorded, transcribed, and scored blindly for total word count (TWC) and dreamlike quality as measured by a composite dream scale score (CDS). Dreamlike quality was strongly correlated with TWC; both CDS and TWC scores increased across successively later awakenings. Significant differences were found in both TWC and CDS between SO and REMP4 and also between REMP2 and REMP4; however, differences were not significant between SO and REMP2 or between the 5 and 10 minute awakenings in REMPs 2 and 4. These findings provide further evidence that the amount of dreamlike mentation is related to the within-sleep arousal level rather than to REMP duration and that the dreamlike quality of reports increases as they become longer.

Eye movement ativity during sleep and intellectual function in mental retardation.

A positive relation was found between the amount of eye movement during rapid-eye-movement or paradoxical sleep and estimates of intellectual level in a group of retarded adults. This result supports the hypothesis that during sleep the brain carries out processes important for cognitive function.

Absence of REM rebound after barbiturate withdrawal.

Administration of three different barbiturates reduced rapid eye movement (REM) sleep. Drug withdrawal led to a return to baseline REM] values without significant overshoot. Similar results are observed with administration of benzodiazepines in pharmacologically equivalent dosages; therefore, a distinction between these two drug classes on the basis of withdrawal effects on the sleep electroencephalogram appears unwarranted. Further investigation is required determine why high REM levels are sometimes associated with the withdrawal of sedative-hypnotic agents.

Computer-detected patterns of electroencephalographic delta activity during and after extended sleep.

Delta (0.5 to 3 hertz) waves are the electroencephalographic hallmark of human sleep. We measured their rate of production during and following an extended night of sleep. On the extended night, we confirmed previous observations of a linear decline in delta wave production across the first four periods of non-rapid-eye-movement (non-REM) sleep. An asymptote was reached in the fifth non-REM period, perhaps signifying that sleep processes reached completion. On the day after the extended night, subjects were allowed to remain awake 3.6 hours less than normal. During the next sleep session, amplitude and number of delta waves in non-REM periods 1 and 3 were significantly reduced. These findings illustrate the value of computer analysis of electroencephalographic waveforms in sleep. Systematic measurement of the amount and distribution of these waveforms as a function of preceding waking duration should provide clues to the kinetics of the metabolic processes underlying sleep.

Flurazepam effects on slow-wave sleep: stage 4 suppressed but number of delta waves constant.

Repeated administration of flurazepam reduced stage 4 sleep (high delta-wave concentration) but produced a greater increase in stage 2 duration so that total sleep time was increased. Computer analysis revealed that the increased amount of stage 2 (low delta-wave concentration) sleep provided a number and duration of delta waves sufficient to offset the loss of delta activity in stage 4. However, the amplitude of the average delta wave was reduced. These results demonstrate the value of direct quantification of delta-wave activity, the variable that underlies visual classification of slow-wave sleep into stages 2 to 4. They also give rise to new hypotheses regarding the relative absence of side effects in spite of profound stage 4 suppression by flurazepam and the mechanisms by which total sleep time is increased by this drug.

Homeostatic behavior of fast Fourier transform power in very low frequency non-rapid eye movement human electroencephalogram.

Basic research shows that the physiological and molecular mechanisms of very low frequency (<1 Hz) electroencephalogram (EEG) waves of non-rapid eye movement (NREM) sleep differ from those of the higher (1-4 Hz) delta frequencies. Human studies show that the across-NREM period dynamics of very low frequency and 1-4 Hz EEG also differ. These differences and the reported failure of very low frequency EEG power to increase after a night of total sleep deprivation raise the question of whether very low frequency EEG shows the other homeostatic properties established for higher delta frequencies. Here we tested the relation of very low frequency EEG power density to prior waking duration across a normal day and whether these low frequencies meet another criterion for homeostatic sleep EEG: conservation of power across a late nap and post-nap sleep. Data from 19 young adults recorded in four separate sessions of baseline, daytime nap and post-nap sleep were analyzed. Power density in very low frequency NREM EEG increased linearly when naps were taken later in the day (i.e. were preceded by longer waking durations). In the night following an 18:00 h nap, very low frequency power was reduced by roughly the amount of power in the nap. Thus, very low frequency EEG meets two major homeostatic criteria. We hypothesize that these low frequencies reflect the executive rather than the functional processes by which NREM sleep reverses the effects of waking brain activity.

Further evidence of abnormal non-rapid-eye-movement sleep in schizophrenia.

Very low levels of visually scored stage 4 sleep are found in 40% to 50% of acute and chronic schizophrenics. Stage 4 is a visual estimate of high-amplitude delta (0.5 to 3 Hz) electroencephalographic waves; these waves can now be measured directly and reliably by computer. In this pilot study, we carried out such measurement in the successive non-rapid-eye-movement periods (NREMPs). We also sampled and measured visually sleep spindles by NREMP; spindles constitute a second distinctive feature of the NREM electroencephalogram. In five unmedicated, recently rehospitalized schizophrenic patients we found reduced delta amplitude and abundance (and increased spindle density) in NREMP1 (also called "REM latency") as compared with ambulatory normal controls. NREMP1 was also abnormally short with an average length similar to that reported for major depression. These striking abnormalities of NREM sleep may underlie the abnormal rapid eye movement distributions sometimes found in schizophrenic and depressed patients. Further studies are required to evaluate the relation of these NREM abnormalities to psychopathology (and hence their utility as biological "markers") and to rule out confounding effects of hospitalization or undetected napping.

Flurazepam effects on sleep EEG. Visual, computer, and cycle analysis.

Analysis of sleep effects of flurazepam hydrochloride on four normal subjects confirmed that this drug substantially suppresses both REM and stage 4 sleep. Computer analysis disclosed that delta wave amplitude was greatly reduced by flurazepam. However, low density delta wave activity (ie, stage 2 sleep, which was increased in duration beyond the reduction in stage 4), permitted the number of delta waves and the time they occupied per night to remain at baseline levels. This finding suggests that sedative-hypnotics increase total sleep time by slowing the metabolic processes of sleep so that a longer sleep duration is required for the same biological effects. New observations on the induction times of REM and stage 4 effects are also presented. In general, the distortions in sleep EEG produced by flurazepam qualitatively resemble, but are quantitatively greater than, those produced by barbiturates in equivalent hypnotic doses.

High internight reliability of computer-measured NREM delta, sigma, and beta: biological implications.

BACKGROUND: Computer analysis of the sleep electroencephalogram (EEG) waveforms is widely employed, but there have been no systematic studies of its reliability. METHODS: The most commonly used computer methods are power spectral analysis with the fast-Fourier transform (FFT) and period amplitude analysis (PAA) with zero cross or zero first derivative half-wave measurement. We applied all three computer methods to the digitized EEG of 16 normal subjects who underwent 5 consecutive nights of baseline (placebo) recording. We evaluated the internight reliability of three non-rapid eye movement (NREM) frequency bands of special importance to sleep research: delta (0.3-3 Hz), sigma (12-15 Hz), and beta (15-23 Hz). RESULTS: Both FFT and the two methods of PAA gave excellent internight reliability for delta and sigma. Even a single night of recording correlated highly (r >.9) with the 5-night mean. Beta reliability was lower but still highly significant for both the PAA and the FFT measures. CONCLUSIONS: Computer-analyzed sleep EEG data are highly reliable. Period amplitude methods demonstrate that wave incidence and period as well as amplitude are reliable, indicating that the reliability of composite measures (FFT power, PAA integrated amplitude) is not solely based on individual differences in EEG amplitude. The high internight stability of NREM delta indicates that it possesses traitlike characteristics and is relatively independent of day-to-day variations in state.

Effects of high dosage delta-9-tetrahydrocannabinol on sleep patterns in man.

Electroencephalographic readings and eye movement were recorded in experienced marijuana users under placebo and tetrahydrocannabinol (THC). Four subjects were studied for 3 baseline nights, 3 nights under initial dosage of 70 mg/day, the last 3 nights of a 2-wk period of 210 mg/day, and the first 3 nights of withdrawal. Three other subjects were studied only during the latter 2 conditions. Administration of THC significantly reduced eye movement activity during sleep with rapid eye movements (REM) and, to a lesser extent, the duration of REM itself. Withdrawal led to increases above baseline in both measures but the "rebound" effect was greater for eye movement. Stage 4 sleep tended to increase on drug, but this effect was not statistically significant. On withdrawal, stage 4 sleep decreased significantly; this change was marked only on the first withdrawal night. The functional or biological significance of these changes is unclear. Nevertheless, these are the most marked effects of THC on brain electrical activity demonstrated thus far. Since its pattern of effects on sleep appears unique to THC, this drug may prove to be a valuable tool in the elucidation of the pharmacology of sleep. Possible relations between effects on sleep pattern and on behavior are discussed.

Effects of marijuana extract and tetrahydrocannabinol on electroencephalographic sleep patterns.

Marijuana extract, given in daily doses containing 70 to 210 mg delta-9-tetrahydrocannabinol (THC), induced effects on sleep that were virtually identical to those produced by the same doses of relatively pure (96%) THC. Both drugs reduced eye movements density with some tolerance developing to this effect. Stage 4 tendend to increase with drug administration. Abrupt withdrawal led to extremely high densities of eye movement, increased rapid eye movement (REM) durations, and a sharp but transient fall in stage 4 to baseline levels. These effects may be useful in the elucidation of the pharmacology of sleep. The effects on sleep of THC administration (but not withdrawal) closely resemble those induced by lithium. For this reason, we suggest further studies of THC in affective disorders. Evidence available thus far suggests that THC produces dysphoric symptoms in unipolar but not in bipolar depressed patients; these differences in response may prove of diagnostic value. An adequate therapeutic trial of THC in bipolar depressed patients has not yet been carried out.

Ketamine administration during waking increases delta EEG intensity in rat sleep.

Ketamine is known to increase the metabolic rate of limbic brain structures. We exploited this action to test a hypothesis of the homeostatic model of delta sleep: that an increase in the waking metabolic rate of plastic neuronal systems would increase delta electroencephalographic (EEG) intensity in subsequent nonrapid-eye-movement (NREM) sleep. In separate experiments, we gave intraperitoneal injections of ketamine to Sprague-Dawley rats of either 15, 25, or 50 mg/kg (0.055, 0.091, 0.18 mmol/kg) three times, at approximately hourly intervals, during the dark (waking) period; the last dose was given 4 to 5 hours before onset of the light (sleep) period. After ketamine, both NREM duration and delta EEG intensity (amplitude and incidence) increased significantly over control (saline injections) levels. The magnitude of this increase places it among the largest pharmacologically induced stimulations of delta sleep yet observed. The interpretation of this effect is complicated by the fact that ketamine produces widespread metabolic changes throughout the brain and it also acts on several receptor classes. However, since ketamine's major action is noncompetitive blockade of the cation channel gated by the N-methyl-D-aspartate receptor, our data join recent observations that suggest that excitatory amino acid receptor systems are involved in sleep regulation.

Beta (20-28 Hz) and delta (0.3-3 Hz) EEGs oscillate reciprocally across NREM and REM sleep.

Across-night oscillations of beta (20-28 Hz) and delta (0.3-3 Hz) electroencephalograms (EEGs) were examined with spectral analysis in 10 normal young adult subjects (Ss). In each S, power densities of beta were found to oscillate reciprocally with delta power density across both nonrapid eye movement (NREM) and rapid eye movement (REM) sleep. Linear correlation coefficients between log power density of delta vs. beta were significant (p less than 0.0001) for each S. An incidental observation was that beta power within REM was reliably lower in epochs with more eye movement activity. The reciprocal relationship between beta and delta holds implications for sleep physiology and supplements our earlier finding that sigma (12-15 Hz) oscillates reciprocally with delta within NREM sleep. These descriptions of the continuously varying EEG across sleep provide information not available when EEG measures are tabulated by discrete NREM periods and REM periods.

Comparison of MK-801 and sleep deprivation effects on NREM, REM, and waking spectra in the rat.

In previous studies, we showed that blockade of the cation channel gated by NMDA glutamate receptors with ketamine or MK-801 massively stimulates NREM delta. We now test whether this NREM delta stimulation is physiological by comparing the EEG response following MK-801 to the EEG response following sleep deprivation (SD). Our previous studies measured only NREM 1-4 Hz EEG with period-amplitude analysis (PAA). Here we extended the analysis of MK-801 effects on sleep EEG by applying power spectral analysis (PSA) to examine delta and higher frequency spectra (.2-100 Hz) in NREM and by including REM and waking spectra. The changes in EEG spectra following MK-801 and SD were remarkably similar. Both SD and MK-801 produced their largest changes in NREM delta and REM 10-20 Hz power. There were some differences in the high frequency EEG, but the overall similarity of the PSA spectra in all three vigilance states after MK-801 and SD supports the possibility that MK-801 stimulated physiologic sleep, perhaps by increasing the need for homeostatic recovery from the metabolic effects of NMDA channel blockade.

Precise conservation of NREM period 1 (NREMP1) delta across naps and nocturnal sleep: implications for REM latency and NREM/REM alternation.

The delta integrated amplitude (DIA) in nonrapid eye movement period 1 (NREMP1) of daytime naps was precisely subtracted from the NREMP1s of ensuing nocturnal sleep, indicating that the brain can retain a record of DIA expressed in sleep episodes initiated 12.5 and 8.5 hours before nocturnal sleep onset. The DIA subtraction was primarily accomplished by reduced NREMP1 duration [earlier rapid eye movement (REM) onset], suggesting that the timing of REM period 1 (REMP1) onset is controlled by delta need. This result is consistent with the hypothesis that REM sleep occurs when a stimulus for NREM has been partially depleted.

Acute deprivation of the terminal 3.5 hours of sleep does not increase delta (0-3-Hz) electroencephalograms in recovery sleep.

Sleep electroencephalograms (EEG) and electrooculograms were recorded in nine young adult males on a baseline night, a night in which they were deprived of an average of 3 hr 27 min of sleep by early awakening, and on a recovery night. Records were analyzed by visual sleep stage scoring and period-amplitude analysis; the results of both were tabulated by successive nonrapid eye movement periods (NREMPs) and rapid eye movement (REM) periods. Neither visually scored delta nor REM measures were affected by this substitution of waking for sleep. Although there was a significant increase in the 0-3-Hz time/epoch on the recovery night, this finding was not confirmed in the accompanying report. These results, taken in association with data from previous studies, are consistent with the hypothesis that, in an acute experiment, visually scored delta and computer-measured 0-3-Hz EEGs increase above the baseline levels only if there has been loss of stage 3/4 EEG (or of sleep) from the first two NREMPs. The findings here are inconsistent with older reports and indicate that further parametric data are required to construct a quantitative model of the relation of sleep EEG waveforms to the duration of prior waking.

Response of delta (0-3 Hz) EEG and eye movement density to a night with 100 minutes of sleep.

In one of a series of experiments aimed at gathering the empirical data required to formulate mathematically our recovery model of sleep, we recently (1) measured the increase in delta electroencephalogram (EEG) following one night of total sleep deprivation (TSD). We found that the delta rebound was confined to the first non-rapid eye movement period (NREM-P1) of recovery sleep; this unexpected result was documented with direct computer measurement of 0-3 Hz EEG, as well as with visual scoring of stages 3 and 4. We also found a robust decrease in eye movement density during the second and third REM periods, which we hypothesized to be due to the increased depth of recovery sleep. In the present experiment, we awakened young adult subjects after 100 min of sleep, a duration that includes the first cycle for this age group, and analyzed visual and computer measures of delta and eye movement density during recovery sleep. We again found eye movement density to be significantly reduced in REM-P2 and P3, but to a lesser degree than after total sleep deprivation, a condition that may be presumed to produce a greater increase in sleep depth. Delta increases were again limited to the first cycle, although all subjects completed this cycle on the 100-min night. The major difference between recovery sleep patterns following the total deprivation and the 100-min sleep conditions was that 0-3-Hz wave amplitude increased significantly after the former, but not after the latter. In both studies, recovery sleep showed increased 0-3-Hz wave density. The neurophysiological implications of a response of EEG amplitude as opposed to wave density are briefly considered; separate measurement of these variables is more readily accomplished with period-amplitude than with spectral analysis. Our results further illustrate the importance of measuring sleep by physiological units, such as the successive NREMPs and REMPs. They also support other data that indicate that NREM-P1 plays a special role in human sleep: it responds selectively to sleep deprivation, shows the greatest ontogenetic variation across the human lifespan, and is the component of sleep that is most frequently abnormal in psychiatric patients. As we have long argued, it is inappropriate to conceptualize this high priority component of NREM sleep as "REM latency" and as a measure of REM "pressure" exclusively.

Acute deprivation of the terminal four hours of sleep does not increase delta (0-3-Hz) electroencephalograms: a replication.

This experiment evaluated further our previous finding that substitution of waking for the terminal 3-4 hr of sleep produces little or no increase in either visually scored or computer measures of delta sleep. Eleven young adults (mean age 24.5 yr) were studied on a baseline night, a night with sleep limited to an average of 188 min, and a recovery night. Visually scored sleep stages, eye movement activity and computer measures of 0-3 Hz were analyzed by nonrapid eye movement periods (NREMPs) and for all recorded sleep in each condition. In addition, we measured the heights, durations and areas under the curve manifested by the cyclic waxing and waning of 0-3-Hz integrated amplitude across sleep. Acute loss of 3.9 hr of sleep did not increase either visual or computer measures of delta electroencephalograms (EEG) on the recovery night, essentially confirming our previous findings. We hypothesize that augmentation of delta EEG above baseline levels after acute (one night's) sleep loss requires that disruption or loss of sleep from the first two NREMPs (or delta cycles). Rapid eye movement (REM) sleep durations on the recovery night were unaffected by the marked loss of REM sleep caused by partial deprivation. Although eye movements as well as stage REM were lost in the deprivation condition, eye movement density was significantly reduced rather than increased on the recovery night. This reduction is consistent with the hypothesis that REM activity varies inversely with sleep depth (or directly with central arousal level). The observations here, taken in association with previous results, suggest that a threshold for eye movement suppression by sleep deprivation in young adults lies in the range of 3-4 hr of prior sleep loss.