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Biomedical subjects

K McCulloch

Publications and source records attributed to K McCulloch.

At least 19 recordsLinked to original sources
PubMed2005

Countermeasures to driver fatigue: a review of public awareness campaigns and legal approaches.

OBJECTIVE: Driver fatigue accounts for 10-40% of road crashes and is a critical area for public health. As other major road safety issues are more successfully managed, driver fatigue becomes proportionately more important. Both public awareness and legal developments have been slow to reach the same levels as for other road safety risks. The aim of this article is to review countermeasures for non-commercial drivers that are designed to reduce the likelihood of fatigue-related crashes through education and legislation. METHODS: This review outlines information from a wide variety of sources including governments, road safety groups and the scientific literature. Educational and legislative approaches are discussed in terms of both their effectiveness and the associated implications for public health. CONCLUSIONS: Areas for improvement in education include personalising the risk to drivers and developing simple metrics for the self-assessment of fatigue. Legal implications should be more clearly defined and specific laws are needed to more effectively prosecute fatigued drivers who cause crashes. Additional research is needed to further investigate the efficacy of available countermeasures. IMPLICATIONS: Increasingly, road traffic injury is being discussed more broadly as a public health issue. However, the specific issue of driver fatigue still receives less attention than other main causes of road crashes, despite making a significant and comparable contribution to crash rates. Countries such as Australia and New Zealand have a responsibility to counter driver fatigue, as well as other causes of road crashes, and to further pursue improvements for the benefit of public health.

Accidents, Traffic↗
PubMed2003

The impact of a week of simulated night work on sleep, circadian phase, and performance.

AIMS: To investigate factors that may contribute to performance adaptation during permanent night work. METHODS: Fifteen healthy subjects participated in an adaptation and baseline night sleep, directly followed by seven simulated eight-hour night shifts (2300 to 0700 hours). At the end of each shift they were taken outside and exposed to natural light for 20 minutes. They then slept from approximately 0800 hours until they naturally awoke. RESULTS: There was a significant increase in mean performance on a visual psychomotor vigilance task across the week. Daytime sleep quality and quantity were not negatively affected. Total sleep time (TST) for each of the daytime sleeps was reduced, resulting in an average cumulative sleep debt of 3.53 hours prior to the final night shift. TST for each of the daytime sleep periods did not significantly differ from the baseline night, nor did TST significantly vary across the week. There was a significant decrease in wake time after sleep onset and sleep onset latency across the week; sleep efficiency showed a trend towards greater efficiency across the consecutive daytime sleeps. Hours of wakefulness prior to each simulated night shift significantly varied across the week. The melatonin profile significantly shifted across the week. CONCLUSIONS: Results suggest that under optimal conditions, the sleep debt that accumulates during consecutive night shifts is relatively small and does not exacerbate decrements in night-time performance resulting from other factors. When sleep loss is minimised, adaptation of performance during consecutive night shifts can occur in conjunction with circadian adaptation.

Adaptation, Physiological↗
PubMed2001

Role of C chemokine lymphotactin in mediating recruitment of antigen-specific CD62L(lo) cells in vitro and in vivo.

In this study we investigated whether T cells expressing high or low levels of CD62L were differentially susceptible to the T cell chemokine lymphotactin. We found that lymphotactin induced preferential migration of antigen-specific (CD62L(lo)) T cells over the nonspecific (CD62L(hi)) T cells in vitro and in vivo. The differing migratory abilities correlated with higher levels of mRNA encoding the lymphotactin receptor (XCR1) on the CD62L(lo) cells compared to the CD62L(hi) cells. Thus, we have identified a coupling mechanism between the activation of T cells and acquisition of new homing properties, in this case conferred by XCR1 expression. These data confirm that at least one function of lymphotactin includes mediating the recruitment of recently activated antigen-specific T cells.

Animals↗
PubMed2001

Performance, sleep and circadian phase during a week of simulated night work.

The current study investigated changes in night-time performance, daytime sleep, and circadian phase during a week of simulated shift work. Fifteen young subjects participated in an adaptation and baseline night sleep, directly followed by seven night shifts. Subjects slept from approximately 0800 hr until they naturally awoke. Polysomnographic data was collected for each sleep period. Saliva samples were collected at half hourly intervals, from 2000 hr to bedtime. Each night, performance was tested at hourly intervals. Analysis indicated that there was a significant increase in mean performance across the week. In general, sleep was not negatively affected. Rather, sleep quality appeared to improve across the week. However, total sleep time (TST) for each day sleep was slightly reduced from baseline, resulting in a small cumulative sleep debt of 3.53 (SD = 5.62) hours. Finally, the melatonin profile shifted across the week, resulting in a mean phase delay of 5.5 hours. These findings indicate that when sleep loss is minimized and a circadian phase shift occurs, adaptation of performance can occur during several consecutive night shifts.

Adolescent↗
PubMed2001

Daytime cardiac autonomic activity during one week of continuous night shift.

Shift workers encounter an increased risk of cardiovascular disease compared to their day working counterparts. To explore this phenomenon, the effects of one week of simulated night shift on cardiac sympathetic (SNS) and parasympathetic (PNS) activity were assessed. Ten (5m; 5f) healthy subjects aged 18-29 years attended an adaptation and baseline night before commencing one week of night shift (2300-0700 h). Sleep was recorded using a standard polysomnogram and circadian phase was tracked using salivary melatonin data. During sleep, heart rate (HR), cardiac PNS activity (RMSSD) and cardiac SNS activity (pre-ejection period) were recorded. Night shift did not influence seep quality, but reduced sleep duration by a mean of 52 +/- 29 min. One week of night shift evoked a small chronic sleep debt of 5 h 14 +/- 56 min and a cumulative circadian phase delay of 5 h +/- 14 min. Night shift had no significant effect on mean HR, but mean cardiac SNS activity during sleep was consistently higher and mean cardiac PNS activity during sleep declined gradually across the week. These results suggest that shiftwork has direct and unfavourable effects on cardiac autonomic activity and that this might be one mechanism via which shiftwork increases the risk of cardiovascular disease. It is postulated that sleep loss could be one mediator of the association between shiftwork and cardiovascular health.

Adolescent↗
PubMed2001

A week of simulated night work delays salivary melatonin onset.

In most studies, the magnitude and rate of adaptation to various night work schedules is assessed using core body temperature as the marker of circadian phase. The aim of the current study was to assess adaptation to a simulated night work schedule using salivary dim light melatonin onset (DLMO) as an alternative circadian phase marker. It was hypothesised that the night work schedule would result in a phase delay, manifest in relatively later DLMO, but that this delay would be somewhat inhibited by exposure to natural light. Participants worked seven consecutive simulated 8-hour night shifts (23:00-07:00 h). By night 7, there was a mean cumulative phase delay of 5.5 hours, equivalent to an average delay of 0.8 hours per day. This indicates that partial circadian adaptation occurred in response to the simulated night work schedule. The radioimmunoassay used in the current study provides a sensitive assessment of melatonin concentration in saliva that can be used to determine DLMO, and thus provides an alternative phase marker to core body temperature, at least in laboratory studies.

Adaptation, Physiological↗
PubMed2000

Prevalence of SIDS risk factors: before and after the "Back to Sleep" campaign in North Dakota Caucasian and American Indian infants.

The objective of this study was to compare rates of infant sleeping position and other risk factors for sudden infant death syndrome from 1991 before the "Back to Sleep" campaign to rates in 1998 after the campaign. We used a cross-sectional risk factor prevalence study of risk factors for the years 1991 and 1998. In North Dakota the prevalence rates of prone sleeping declined 72% for American Indian infants and 62% for Caucasian infants. We were unable to identify a corresponding decline in SIDS in North Dakota for this time period. The relationship between sleeping position and SIDS may be more complex in rural and frontier settings and in American Indian populations than in urban and majority populations. The generalizability of this study is limited by the rural setting and small sample size. Longer term surveillance and additional reports from sites with pre "Back to Sleep" data as a baseline for both SIDS rates and sleeping position will be important to clarify the rate of prone sleeping position and SIDS.

Cross-Sectional Studies↗
PubMed2000

A prevalence methodology for mental illness and developmental disorders in rural and frontier settings.

A prevalence study methodology developed for use in rural and frontier settings is described. The general method was developed over a 15 year period and has been successfully adapted and used in studies of 14 different childhood onset developmental disorders. Subjects were the 168,000 school aged children from North Dakota who were first surveyed for cases of autism--pervasive developmental disorders in 1985 and 1986. The results of the prevalence study were compared with the results of a 12-year ongoing surveillance of the cohort. The 12-year ongoing surveillance identified one case missed by the original prevalence study. Thus the original prevalence study methodology identified 98% of the cases of autism-pervasive developmental disorder in the population. This methodology may also be useful for studies of other developmental disorders in rural and frontier settings.

Adolescent↗
PubMed1995

Somatostatin in preterm infants: postnatal changes and response to stress.

To determine the chronology of postnatal somatostatin (SRIF) changes in preterm infants and the relationship of SRIF levels to respiratory and gastrointestinal complications, we evaluated sequential SRIF levels in 62 preterm infants in the first month of life. Weekly preprandial plasma samples were obtained and analyzed for SRIF using a radioimmunoassay. Additional blood samples were obtained at the time of abdominal events. Somatostatin levels were highest in week 2 and gradually declined in weeks 3 and 4 (mean +/- SD pmol/l, SRIF = 92.3 +/- 30.3 in week 2 vs. 79.8 +/- 33.9 in week 3 and 69.7 +/- 54.4 in week 4, p < 0.03). Birth weight, gestational age and sex were not related to initial SRIF levels. Infants with respiratory distress requiring assisted ventilation had significantly higher week 1 SRIF levels compared to infants without respiratory problems (97.9 +/- 22.7 vs. 74.9 +/- 21 pmol/l, p < 0.02). Twenty-one of the 62 infants had gastrointestinal complications. Somatostatin levels preceding (89.0 +/- 25.9 pmol/ 1), during (91.0 +/- 13.3) and after (79.3 +/- 28.6) the gastrointestinal events were not significantly different, nor were they different from SRIF concentrations of age-matched preterm infants without gastrointestinal complications. The results suggest that in preterm infants, postnatal SRIF changes follow a definite pattern with peak concentrations in week 2. Respiratory distress is associated with a significant increase in SRIF. However, subsequent gastrointestinal events do not lead to an increase in SRIF. This lack of SRIF response in gastrointestinal stress may play a role in the pathogenesis of gut injury in the premature neonate.

Aging↗
PubMed1993

Dexamethasone treatment suppresses collagen synthesis in infants with bronchopulmonary dysplasia.

Collagen is an essential component of connective tissue and is present in the pulmonary interstitium. Collagen deposition is known to increase in many acquired chronic diseases, including bronchopulmonary dysplasia (BPD). Urinary excretion of hydroxyproline has been used as a specific index of collagen synthesis. Many studies have demonstrated that dexamethasone therapy is associated with respiratory improvement in infants with BDP but the mechanism of this effect is not well understood. We postulated that in infants with BDP who receive dexamethasone, suppression of collagen synthesis may cause respiratory improvement. Therefore, we studied the effect of dexamethasone on respiratory status and urinary excretion of hydroxyproline in 14 ventilator-dependent infants with BDP. Infants received 0.5 mg/kg/day dexamethasone, tapered by half every 3 days to complete a 12 day course. Eleven of the 14 infants were extubated at a mean +/- SD of 8.7 +/- 4.9 days after starting dexamethasone. Mean urinary hydroxyproline/creatinine ratios at 3, 6, 9, and 12 days of dexamethasone therapy were significantly lower than the mean pretreatment value, but after discontinuation rapidly rose toward baseline values. Decreased urinary excretion of hydroxyproline indicates that dexamethasone suppressed collagen synthesis in these infants. We speculate that suppression of collagen synthesis reduced pulmonary inflammation and fibrosis, resulting in respiratory improvement.

Bronchopulmonary Dysplasia↗
PubMed1989

Oleic acid lung injury increases plasma prostaglandin levels.

To determine whether lung injury causes increased plasma prostaglandin (PG) levels, 35 rabbits received oleic acid and 35 served as controls. Half of each group also received 4 ml/kg of Intralipid over one hour and at least five in each subgroup received indomethacin 7.5 mg/kg. Arterial and venous plasma concentrations of PGE2, 6-keto-PGF1 alpha, and PGF2 alpha-M were measured. Venous PGE2 was significantly higher in the oleic acid-injured than in the normal lung group, 1560 +/- 270 (Mean +/- SEM) versus 880 +/- 140 pg/ml (p less than .05). Plasma levels were reduced by 50% with indomethacin, but PGE2 levels remained significantly higher than in the normal lung group, 850 +/- 180 versus 480 +/- 60 for arterial (p less than .05) and 820 +/- 140 versus 480 +/- 80 for venous (p less than .05), respectively. PGF2 alpha-M levels were significantly higher in the lung injury group, 240 +/- 50 versus 50 +/- 40 pg/ml for arterial (p less than .05) and 220 +/- 50 versus 95 +/- 40 for venous (p less than .05), respectively. These lung injury-related increases in PGE2 and PGF2 alpha-M appear related both to increased pulmonary production and to decreased pulmonary clearance. With Intralipid infusion, however, arterial PGE2 increased by 500 +/- 260 pg/ml compared to baseline (p less than .05) with no change in venous PGE2, indicating in this instance that the increase in arterial PGE2 levels is related to increased pulmonary production.

Animals↗
PubMed1988

Comparison of auditory brainstem responses and pneumograms in intensive care nursery infants.

Central slowing of auditory brainstem responses (ABRs) and excessive breathing irregularity on pneumogram recordings indicate dysfunction in central auditory pathways and brainstem respiratory control mechanisms, respectively. These centers are anatomically proximate within the brainstem so that ABR slowing and respiratory instability might be expected to occur concomitantly, reflecting overall dysfunction of this part of the central nervous system. To examine the relationship between these two assessments, testing results were compared for 15 infants in the intensive care nursery who had ABRs and 12-hour pneumograms performed at about the same age for separate clinical indications. Wave V latency at 70 dB was found to correlate significantly with three pneumogram measurements of breathing irregularity: the density of short apneas during sleep (p less than 0.01), the number of episodes of periodic breathing per 100 minutes of sleep (p less than 0.05), and the percentage of sleep time spent in periodic breathing (p less than 0.05). Interwave interval I-V correlated significantly with the density of short apneas during sleep (p less than 0.01). The auditory brainstem response and the pneumogram appeared to serve as related indicators of brainstem function in these infants.

Brain Stem↗
PubMed1988

Neonatal problems in twins.

Twins have higher rates of perinatal mortality, prematurity and its complications, low birth weight, intrauterine growth retardation, congenital anomalies, and long-term developmental morbidity. Monozygotic twins have lower birth weights and higher rates of congenital anomalies than dizygotic twins, which suggests that the etiology of these problems may be related to the monozygotic twinning process. Monochorionic twins have higher rates of perinatal mortality, intrapair birth weight discrepancies, and intrauterine growth retardation than dichorionic twins, which suggests that these complications may be related to placental vascular anastomoses. Monochorial vascular communications also can be responsible for twin transfusion syndrome, disseminated intravascular coagulation at birth and disruptive structural defects. Followup studies indicate that twins remain at a disadvantage for subsequent physical growth and intellectual achievement. The management of twins is challenging and fascinating because of the wide range of perinatal, neonatal, developmental, and parenting problems that can occur.

Congenital Abnormalities↗
PubMed1986

Infantile apnea.

Infants who are found apneic, limp and cyanotic or pale and who require resuscitation must be hospitalized for cardiorespiratory monitoring and medical evaluation. If no cause is found, the diagnosis of idiopathic infantile apnea is made. The impedance pneumocardiogram is often helpful in diagnosis and management. Home monitoring limits asphyxia and may prevent death in infants thought to be at risk for recurrent apnea.

Apnea↗
PubMed1983

Intralipid alterations in pulmonary prostaglandin metabolism and gas exchange.

To assess the role of Intralipid as a prostaglandin (PG) precursor, we infused Intralipid into 40 rabbits with long-term arterial and venous catheters; 24 other rabbits received a control saline infusion. One-half of the rabbits in both experimental and control groups had oleic acid-damaged lungs, and at least 5 in each of the 4 groups (Intralipid/saline in normal/damaged lungs) received indomethacin. Two vasodilating PGs (E2 and 6KF1 alpha) and one vasoconstricting PG (F2 alpha) were measured. Triglyceride levels increased significantly in all Intralipid groups, averaging 580 mg/dl. Intralipid-related alterations in PG levels and arterial oxygen tension (PaO2) were significant only in the lung-damaged group. The mean (+/- sem) decrease in PaO2 was 12 +/- 1.5 torr (p less than .001). For both vasodilating PGs, Intralipid infusion increased the pulmonary arteriovenous gradients for PG E2 and PG 6KF1 alpha by 960 pg/ml (p less than .05) and 697 pg/ml (p less than .10), respectively. Both the PaO2 decrease and the vasodilating PG increases were blocked by indomethacin. In summary, Intralipid infusion in lung-damaged rabbits increased pulmonary production of vasodilating PGs and associated hypoxemia, presumably caused by an unblocking of hypoxic vasoconstriction and resultant increase in intrapulmonary right-to-left shunt.

Animals↗
PubMed1982

Arousal responses in near-miss sudden infant death syndrome and in normal infants.

Hypercarbic and hypoxic arousal responses were measured in 22 normal and 11 near-miss sudden infant death syndrome infants during natural sleep. End-tidal PCO2, (PACO2), transcutaneous PO2, electrocardiogram and heart rate, and thoracic and abdominal circumference were continuously recorded. The essential behavioral criteria for arousal were eye opening and crying. For each hypercarbic arousal test, step increases in FICO2 were made until arousal occurred or until PACO2 reached 65 mm Hg. For each hypoxic arousal, step decreases in FIO2 were made until arousal occurred or until FIO2 = 0.15 had been maintained for 20 minutes. The hypercarbic arousal threshold was significantly higher in near-miss SIDS than in normal infants, 54.9 +/- 2.3 vs 48.4 +/- 1.4, respectively ((P less than 0.05). An arousal response to hypoxia occurred in only 9% of near-miss SIDS infants compared to 70% of normal infants (P less than 0.01). The level of respiratory chemostimulation required to produce an arousal response from sleep is significantly greater in near-miss SIDS than in normal infants. We speculate that deficient arousal responsiveness, especially to hypoxia, may prevent potential SIDS victims from responding appropriately to apneic asphyxia.

Arousal↗
PubMed1981

Diminished hypoxic ventilatory responses in near-miss sudden infant death syndrome.

The ventilatory response to hypoxia and to hypercarbia was assessed in 36 near-miss sudden infant death syndrome (N.M SIDS) and 23 control infants. Base-line measurements during non-REM sleep documented no significant difference in respiratory frequency, alveolar CO2 and O2 partial pressure (PAco2 and PAo2) or tidal volume between the N-M SIDS and control infants. In the N.M SIDS group, mean inspiratory flow and minute ventilation (VI) were significantly lower than in the control group (p less than 0.001 and p less than 0.01, respectively), and the slope of the ventilatory response to hypercarbia ((delta VI/Torr Paco2) was only 21 +/- 1.9 (SE) ml.kg-1 min-1 Torr PAco2 compared with 62 +/- 3.5 in controls (p less than 0.001). For both groups, the increase in ventilation with hypoxia appeared linear within the PAo2 range assessed (65-115 Torr) and was therefore expressed as the slope of the delta VI/PAo2 plot (ml.kg-1 min-1 per Torr PAo2). The slope of the hypoxic ventilatory response was significantly less in the N-M SIDS than in the control group, -8.3 +/- 1.0 VS. -19.9 +/- 1.5, respectively (p less than 0.001). In summary, in comparison to control infants, N-M SIDS infants as a group have a significantly smaller increase in VI in response to hypoxia as well as to hypercarbia.

Arousal↗