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Drastic ecological restructuring, species redistribution and extinctions mark the Pleistocene-Holocene transition, but an insufficiency of numbers of well-dated large mammal fossils from this transition have impeded progress in understanding the various causative links. Here I add many new radiocarbon dates to those already published on late Pleistocene fossils from Alaska and the Yukon Territory (AK-YT) and show previously unrecognized patterns. Species that survived the Pleistocene, for example, bison (Bison priscus, which evolved into Bison bison), wapiti (Cervus canadensis) and, to a smaller degree, moose (Alces alces), began to increase in numbers and continued to do so before and during human colonization and before the regional extinction of horse (Equus ferus) and mammoth (Mammuthus primigenius). These patterns allow us to reject, at least in AK-YT, some hypotheses of late Pleistocene extinction: 'Blitzkrieg' version of simultaneous human overkill, 'keystone' removal, and 'palaeo-disease'. Hypotheses of a subtler human impact and/or ecological replacement or displacement are more consistent with the data. The new patterns of dates indicate a radical ecological sorting during a uniquely forage-rich transitional period, affecting all large mammals, including humans.

Island colonization and subsequent dwarfing of Pleistocene proboscideans is one of the more dramatic evolutionary and ecological occurrences, especially in situations where island populations survived end-Pleistocene extinctions whereas those on the nearby mainland did not. For example, Holocene mammoths have been dated from Wrangel Island in northern Russia. In most of these cases, few details are available about the dynamics of how island colonization and extinction occurred. As part of a large radiocarbon dating project of Alaskan mammoth fossils, I addressed this question by including mammoth specimens from Bering Sea islands known to have formed during the end-Pleistocene sea transgression. One date of 7,908 +/- 100 yr bp (radiocarbon years before present) established the presence of Holocene mammoths on St Paul Island, a first Holocene island record for the Americas. Four lines of evidence--265 accelerator mass spectrometer (AMS) radiocarbon dates from Alaskan mainland mammoths, 13 new dates from Alaskan island mammoths, recent reconstructions of bathymetric plots and sea transgression rates from the Bering Sea--made it possible to reconstruct how mammoths became stranded in the Pribilofs and why this apparently did not happen on other Alaskan Bering Sea islands.

About 70% of North American large mammal species were lost at the end of the Pleistocene epoch. The causes of this extinction--the role of humans versus that of climate--have been the focus of much controversy. Horses have figured centrally in that debate, because equid species dominated North American late Pleistocene faunas in terms of abundance, geographical distribution, and species variety, yet none survived into the Holocene epoch. The timing of these equid regional extinctions and accompanying evolutionary changes are poorly known. In an attempt to document better the decline and demise of two Alaskan Pleistocene equids, I selected a large number of fossils from the latest Pleistocene for radiocarbon dating. Here I show that horses underwent a rapid decline in body size before extinction, and I propose that the size decline and subsequent regional extinction at 12,500 radiocarbon years before present are best attributed to a coincident climatic/vegetational shift. The present data do not support human overkill and several other proposed extinction causes, and also show that large mammal species responded somewhat individualistically to climate changes at the end of the Pleistocene.

Different physiologic measures during EEG sleep periods in preterm neonates are postulated to change with maturation and reflect functional brain development. Forty-three healthy preterm neonates received 3-h EEG sleep studies in an environmentally controlled setting. Postconceptional ages of neonates at each recording session ranged from 28 to 35 wk. Minute-by-minute analyses of EEG discontinuity, motility, arousals, and REM were performed. Eight phasic events and continuity measures of sleep were tabulated. Data were analyzed using Spearman rank order correlation coefficients. Increases in arousal numbers (p < 0.001) and durations (p < 0.001) were noted with age only during continuous periods of EEG activity (i.e. active sleep). REM also increased with corrected age during indeterminate or transitional sleep (p < 0.002) and decreased during quiet sleep (p < 0.01). Decreases in small body movements per minute (p = 0.02) and large body movements per minute (p < 0.001) occurred only during discontinuous periods of EEG activity (i.e. quiet sleep). Sleep efficiency (p < 0.001), maintenance (p < 0.001), and latency (p = 0.01) also decreased with increasing postconceptional age. Cycle length between two segments of continuous EEG with an intervening period of EEG discontinuity also lengthened with maturation (p < 0.001). These findings are discussed in the context of previously reported differences in phasic and continuity measures noted between preterm and full-term infants at matched full-term postconceptional ages. Changes in phasic and continuity measures with increasing postconceptional ages reflect maturation of specific neuronal processes of the CNS within a rudimentary sleep cycle of the preterm neonate.

Cardiorespiratory behavior during sleep has been investigated by comparing visually analyzed minutes of EEG sleep with the digitized values of these two physiologic variables for each corresponding minute. Continuous 3-h nighttime sleep studies on 37 full-term and preterm neonates at comparable postconceptional term ages were acquired under controlled conditions, using a 24-channel computerized monitoring system and an automated event-marker program. Five thousand, two hundred ninety-four minutes were assigned an EEG state by traditional criteria. Eighteen preterm infants were compared with 19 full-term infants with respect to six cardiac and six respiratory measures: two nonspectral calculations (i.e. average per minute and variance of the means) and four spectral calculations of the cardiorespiratory signal (i.e. bandwidth, spectral edge, mean frequency, and ratio of harmonics). The relative capabilities of these measures to predict a sleep state change were investigated using discriminant analysis. A stepwise selection algorithm in discriminant analysis was used to identify the order of significance for the remaining variables. Eight cardiorespiratory measures were then submitted to multivariate analysis of variance to assess sleep state or preterm-full-term differences: mean frequency, bandwidth, average per minute, and ratio of harmonics for cardiac signals; and spectral edge, mean frequency, logarithm of variance, and ratio of harmonics for respiratory signals. Differences among the sleep states and between neonatal groups were highly significant (p < 0.0001). Interaction between sleep state and neonatal group was also significant (p < 0.034). Two variables differentiated preterm from full-term respiratory behavior: ratio (p < or = 0.001) and mean frequency (p < or = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

We examined the centroid frequency (Fc) of the electromyogram power-frequency spectra from the costal (EMGco) and crural (EMGcr) diaphragms at functional residual capacity and at reduced end-expiratory lung volume (EELV) (induced by abdominal banding) in six anesthetized newborn piglets. EMGco and EMGcr were recorded from bipolar electrodes embedded in the costal and crural diaphragms respectively. A fast Fourier transformation of ECG free EMGco and EMGcr was used to compute the power-frequency spectra and calculate the Fc of EMGco and EMGcr. The nitrogen washout technique was used to measure EELV. Abdominal banding induced a reduction in EELV of 30.6% functional residual capacity (range 22-39%). The mean Fc of EMGcr was not significantly altered by the reduction in EELV, whereas the mean Fc of the EMGco fell in every animal at reduced EELV by 13 +/- 8% of baseline Fc (p less than 0.05). We conclude that alterations in lung volume alone can determine changes in the EMGco power spectrum and Fc. Investigators performing EMGco power spectral analysis should consider EELV status when interpreting their findings.

The steady state ventilatory response to inhaled CO2 was measured in eleven unanesthetized premature Macaca nemestrina during the first 3 wk of life in different steady state background O2 mixtures hypoxia (FIO2 = 0.08 or 0.12), normoxia (FIO2 = 0.21) and hyperoxia (FIO2 = 0.96). Hyperoxic delta VI/delta PACO2 and delta P0.2/ delta PACO2 were significantly greater than hypoxic delta VI/ delta PACO2 and delta P0.2/delta PACO2, respectively, at both 2 and 21 days postnatal age by the Mann Whitney test of nonparametric ranking (2 days: 89.. and 80.2 degrees versus 88.7 and 56.4 degrees, respectively; 21 days: 89.3 and 76.6 degrees versus 50.2 and 57.1 degrees, respectively; p less than 0.05). Hypoxic delta VI/delta PACO2 was significantly depressed compared to normoxic delta VI/ delta PACO2 only at 21 days of age (50.2 versus 89.4 degrees, respectively; p less than 0.05); hyperoxic CO2 sensitivity and normoxic CO2 sensitivity did not differ at either age. The ventilatory interaction between O2-CO2 in the neonatal primate appears to be the inverse of the typical adult ventilatory interaction. It is hypothesized that differential changes in brain stem blood flow between neonates and adults might explain this difference in O2-CO2 ventilatory interaction.

The effect of acute graded hypoxemia on the electroencephalogram (EEG) of five prematures and five full term Macaca nemestrina in the neonatal period was determined using power spectral analysis--a technique that obviates the limitations of visual inspection. The EEG of selected epochs was analyzed by a Fast Fourier Transform program (POWER) during the 20 min of each trial of hypoxemia and compared with simultaneous arterial oxygen tensions. Levels of hypoxemia were graded as profound (PaO2=15-25 Torr); severe (PaO2=26-35 Torr), moderate (PaO2=36-50 Torr), or mild (PaO2=51-75 Torr). The EEG during normoxemia had a band width of 0.5 to 10 Hz and a peak power at 1-3 Hz. During mild hypoxemia, an increase in power in the delta range (0-3.5 Hz) occurred in the oldest animals. At moderate hypoxemia, the youngest animals showed a depression of absolute power in the delta band. A slowing of the EEG and decrease in power in the theta frequency range (4-8 Hz) followed when severe hypoxemic levels are reached. During profound hypoxemia, all animals at each postnatal age exhibited a significant decrease in EEG power at the delta and theta frequencies (P less than 0.025) except 3-wk-old full term animals in which there was no significant change in the delta band. These results clarify and extend previously reported effects of hypoxemia on the neonatal EEG.

The sustained increase in ventilation (V1) that occurs during acute hypoxemia in adults is not characteristic of the neonate as V1 falls to or below baseline values soon after onset of the hypoxic stimulus. Associated with this decline in V1 is a decrease in tidal volume, lung compliance, inspiratory duration, and an increase in functional residual capacity and respiratory frequency. We hypothesized that hypoxemia induced small airway constriction and pulmonary time constant inequalities resulting in a frequency dependent fall in lung compliance and tidal volume and retention of lung volume. In seven newborn subhuman primates, responses to acute hypoxemia were measured prior to and after administration of atropine methyl bromide to prevent vagally mediated narrowing of peripheral airways. The increase in frequency and fall in inspiratory duration characteristic of the ventilatory decline during hypoxemia was eliminated by the drug but functional residual capacity and lung compliance were unaffected. Also, the initial rise in V1 was blunted or blocked in all subjects. Bilateral vagotomy caused V1 to fall significantly requiring oxygen supplementation but responses to hypoxemia were still biphasic in nature. These findings suggest that cholinergically mediated mechanisms in the airways do not alter effective lung distensibility related to respiratory rate. Acetylcholine may be important at the peripheral chemosensor since cholinergic blockade eliminated the initial ventilatory increase.(ABSTRACT TRUNCATED AT 250 WORDS)

The hypoxic ventilatory response was determined in twelve unanesthetized newborn monkeys, Macaca nemestrina. Measurements of blood gases and ventilation were made during normoxia and hypoxia at the postnatal ages of 2, 7, and 21 days. Data were collected during quiet sleep. The infant monkey demonstrated a definite but transient hyperventilatory response following exposure to a FiO2 of 0.12 or 0.14 on the second day of life. Baseline ventilation increased 15% (Fi02=0.14) and 28% (Fi02=0.12) after 1 minute of hypoxia; p less than 0.05 in both instances. Return to baseline ventilation occurred between 3 and 5 minutes after hypoxic stimulus onset. This biphasic response to hypoxia converted to an adult-like, sustained hyperventilation during the ensuing three weeks of postnatal maturation. Episodes of periodic breathing and/or apnea were noted to occur during the induced hypoxemia. These data demonstrate that the infant subhuman primate has a ventilatory response to hypoxia that is similar to that of the human infant and is an excellent model for the study of the maturation of the respiratory control system.

Comparison between 21 2-day-old infant monkeys and 17 21-day-old infants during non-rapid eye movement sleep demonstrated that minute ventilation (VI) increased from 141 +/- 30 to 257 +/- 65 ml/min secondary to elevations in tidal volume (VT) and mean inspiratory flow (VT/Ti) with little change in respiratory timing. These volumetric parameters of ventilation as well as functional residual capacity remained significantly augmented when standardized for gain in body weight. Dynamic lung compliance increased from 0.69 +/- 0.19 to 0.89 +/- 0.39 ml/cm H2O with age while inspiratory pulmonary resistance did not change. Effective elastance fell significantly with maturation (5.27 +/- 1.51 cm H2O/ml on day 2 versus 4.15 +/- 1.35 cm H2O/ml on day 21) while effective impedance was elevated postnatally. The postnatal ventilatory gain (80% increase in VI) was attributable to increases both in dynamic lung compliance (30%) and inspiratory effort (50%) as determined by esophageal pressure changes. Isometric occlusion pressures (P0.1, P0.2 . . . Pmax) also significantly increased during this time span, suggesting that the increased ventilation resulted from an elevated respiratory drive.