[Control of Salmonella on dairy farms].
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Biomedical subjects
Publications and source records attributed to P Franken.
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To examine the relationship between sleep and brain temperature in the rat, the vigilance states, spectral power density of the electroencephalogram (EEG), hypothalamic temperature (T(hy)), and cortical temperature (Tcr) were recorded for 3 days. A 1-day rise of ambient temperature from 23 to 30 degrees C did not affect the percentage of waking, non-rapid eye movement sleep (NREMS), and rapid eye movement sleep (REMS), but increased EEG slow-wave activity in NREMS in the 12-h dark period. T(hy) was invariably higher than Tcr, but at 30 degrees C the difference diminished because of a rise in Tcr. In contrast to Tcr, T(hy) was only slightly increased at 30 degrees C and only during sleep and in the dark period. Although the temperatures changed largely in parallel at vigilance state transitions, Tcr rose more rapidly than T(hy) at NREMS-REMS transitions and more slowly at NREMS-waking transitions. T(hy) declined more rapidly than Tcr at waking-NREMS transitions and more slowly at REMS-NREMS transitions. The results are consistent with a central role of the hypothalamus in the activation and deactivation of the waking state.
To assess the influence of the photoperiod on sleep regulation, laboratory rats were adapted to a long photoperiod (LPP; 16:8-h light-dark cycle, LD 16:8) or a short photoperiod (SPP; LD 8:16). The electroencephalogram (EEG) and cortical temperature (TCRT) were continuously recorded for a baseline day, a 24-h sleep deprivation (SD) period, and a recovery day. Data obtained previously for LD 12:12 served for comparison. Whereas the photoperiod exerted a prominent effect on the 24-h sleep pattern, the 24-h baseline level of sleep and the response to SD were little affected. Recovery from SD was characterized by a marked rise in rapid eye movement sleep, a moderate rise in non-rapid eye movement sleep, and an initial enhancement of EEG slow-wave activity followed by a decrease below baseline. The amplitude and phase of the "unmasked" 24-h component of TCRT did not differ between LPP and SPP. Computer simulations demonstrated that the changes of TCRT and EEG slow-wave activity can be largely accounted for by the sequence of the vigilance states. We conclude that the photoperiod does not affect the basic processes underlying sleep regulation.
The use of 123I-labeled fatty acids is witnessing a resurgence of interest, primarily because of data from recent clinical protocols comparing regional myocardial uptake of 123I-labeled 15-(p-iodophenyl)-3-(R,S)-methylpentandecanoic acid (BMIPP) with flow tracers. Comparison of mismatches in BMIPP and flow tracer distribution (BMIPP < flow tracer) has demonstrated the usefulness of evaluating myocardial viability with BMIPP. BMIPP was introduced in 1993 as "Cardiodine" as an approved radiopharmaceutical in Japan by Nihon Medi-Physics, Inc. This article reviews the clinical use of BMIPP in the assessment of cardiomyopathy, myocardial infarction, ischemic heart disease and for the evaluation of myocardial viability in comparison with PET tracers. The results of two specific protocols demonstrating the utility of using BMIPP to detect viable myocardium are described in detail. The first study compares BMIPP and sestamibi uptake to wall motion and inotropic reserve after acute myocardial infarction in conjunction with two-dimensional echocardiography and low-dose dobutamine stimulation. The second example describes results of a triple SPECT technique using BMIPP reinjection for the assessment of ischemia.
Vigilance states, cortical temperature (TCRT), and electroencephalograph (EEG) slow-wave-activity (SWA, mean power density in the 0.75-4.0 Hz range) of ten rats were recorded continuously during a baseline day, and two recovery days (Recovery 1 and 2) after 24 h of sleep deprivation (SD). The short term changes of TCRT were analysed within episodes of nonrapid eye movement sleep (NREMS), REM sleep (REMS) and waking (W), and at transitions between vigilance states. SWA was analysed within NREMS episodes and at W to NREMS (WN) transitions. TCRT increased during episodes of W and REMS, and decreased during NREMS episodes. These changes were a function of episode duration, and, for W and NREMS, of TCRT at episode onset. In Recovery 1 the increase in TCRT at NREMS to REMS (NR) and NREMS to W (NW) transitions tended to be attenuated. SWA within NREMS episodes was enhanced after SD. Over all experimental days, the increase of SWA and the decrease of TCRT in NREMS episodes were not correlated. It is concluded that during recovery from SD the changes in TCRT at state transitions were little affected. The lack of a relationship between changes in TCRT and SWA indicates that separate mechanisms underlie the regulation of brain temperature and sleep intensity.
The relationship between the time course of cortical temperature (TCRT) and sleep-wake alternation was investigated by correlation analyses and a computer simulation. The data for these analyses were collected in 10 rats in a 4-day experiment (LD 12:12), during which vigilance states and TCRT were determined for consecutive 8-sec epochs. On day 1 baseline recordings were obtained; on day 2 the animals were sleep-deprived; and days 3 and 4 served as recovery days. The correlation analyses revealed that the alternation of sleep and waking accounted for 84% of the variance of TCRT when analyzed for hourly intervals. The residual variance displayed a 24-hr periodicity with an amplitude of 0.15 degrees C. Similar results were obtained in a separate data set of a 2-day experiment, which consisted of a baseline day (LD 12:12) and a day with constant darkness. The periodicity of the residual variance of TCRT can therefore be considered to represent the circadian temperature rhythm not masked by the vigilance states. In the computer simulation, the time course of TCRT was simulated on the basis of the sequence of the vigilance states with an 8-sec time resolution. It was assumed that TCRT increases during waking and rapid-eye-movement (REM) sleep according to an exponential saturating function, and decreases exponentially during non-REM sleep. The simulations could account for 88-93% of the variance of TCRT. We conclude that in the rat, the major part of the variation of TCRT is accounted for by vigilance states, whereas a minor part can be attributed to a direct effect of the circadian pacemaker.
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According to the two-process model of sleep regulation, a homeostatic Process S increases during waking and declines during sleep. For humans, the time course of S has been derived from the changes in EEG slow-wave activity (SWA; spectral power density in the 0.75-4.0 Hz range) during sleep. We tested the applicability of the model to sleep in the rat. The simulation was based on the vigilance states for consecutive 8-s epochs of a 96-h experiment in 9 animals. The level of S was made to decrease in epochs of non-REM sleep (NREMS), and to increase in epochs of waking or REM sleep according to exponential functions. By optimizing the initial value and the time constants of S, a close fit between the hourly values of SWA in NREMS and of S was obtained. The biphasic time course of SWA during baseline, its enhancement in the initial recovery period after 24-h sleep deprivation, and its subsequent prolonged undershoot were present in the simulation. We conclude that sleep homeostasis as conceptualized in the two-process model may be a general property of mammalian sleep.
To investigate the influence of light on sleep and the electroencephalogram (EEG), chronically implanted rats were continuously recorded during a baseline day under 12-h light-12-h dark (LD 12:12) conditions, and an experimental day with short LD (LD 1:1) cycles. The percentage of non-REM sleep (NREMS) was higher and the percentage of REM sleep (REMS) lower in the 1-h light [corrected] intervals than in the 1-h dark intervals. The maximum of NREMS induction by 1-h light occurred in the habitual 12-h dark period (activity period), while the largest enhancement of REMS by 1-h darkness occurred in the second half of the habitual 12-h light period (rest period). The EEG of waking, NREMS and REMS was subjected to spectral analysis to determine the power density of the frequency components in the range of 0.25-25.0 Hz. The overall 24-h time course of the EEG-spectra in NREMS was similar under baseline and experimental conditions. Nevertheless, the spectra were modified by the short LD-cycle. In NREMS, the values in the middle and high frequencies (greater than 6 Hz in the rest period; greater than 11 Hz in the activity period) were lower in the 1-h light intervals than in the 1-h dark intervals. In contrast, activity in some frequency bands during waking and REMS was higher in the light than in the dark intervals. It is concluded that the short LD-cycle modulates the vigilance states and induces state-specific changes in the EEG, whereas circadian aspects of sleep are little affected.
Two chalcone synthase genes in maize have been cloned and molecularly characterized to be the C2 and the Whp (white pollen) locus. The two genes have highly homologous exon sequences but differ considerably in sequences 5' upstream and 3' downstream of the coding region, as well as in their introns. Northern and Western experiments of chalcone synthase expression in various tissues and in different genotypes indicated that C2 and Whp are differently regulated. The expression of Whp in maize aleurone is dependent on the presence of the recessive allele of the gene intensifier (in). The regulatory effect of in on Whp expression is not detectable at the transcriptional level, but seems to take place during translation.
Vigilance states, electroencephalogram (EEG) power spectra (0.25-25.0 Hz), and cortical temperature (TCRT) of 10 rats were obtained during a baseline day, a 24-h sleep deprivation (SD) period, and 2 days of recovery (recoveries 1 and 2). EEG power density in waking gradually increased in most frequencies during the SD period. Non-rapid-eye-movement (NREM) sleep was enhanced on both recovery days, and rapid-eye-movement sleep was enhanced only on recovery 1. In the initial 4 h of recovery 1, EEG slow-wave activity (SWA; mean power density 0.75-4.0 Hz) in NREM sleep was elevated relative to baseline, and the number of brief awakenings (nBA) was reduced. In the dark period of recovery 1 and the light period of recovery 2, SWA was below baseline, and nBA was increased. During the entire recovery period, SWA and nBA, both expressed as deviation from baseline values, were negatively correlated. During the SD period, TCRT was above baseline, and in the initial 16 h of recovery 1 it was below baseline. Whereas TCRT was negatively correlated with NREM sleep, no significant correlation was found between TCRT and SWA within NREM sleep. It is concluded that SD causes a short-lasting intensification of sleep, as indicated by the enhanced SWA and the reduced nBA, and a long-lasting increase in sleep duration. The different time courses of SWA and TCRT suggest that variations in NREM sleep intensity are not directly related to changes in TCRT.
The 24-hr sleep-wake distribution and power spectra of the electroencephalogram were determined in rabbits that had been implanted with cortical and hippocampal electrodes. A diurnal preference for sleep was observed. The spectral power density in nonrapid eye movement sleep (NREM sleep) of the cortex showed a decreasing trend in most frequencies within the 12-hr light period. In the 12-hr dim period no clear trend was present. Most hippocampal EEG frequencies decreased in NREM sleep in the first two hours of the light period, and thereafter stayed on a constant level. Sleep deprivation elicited the following changes: a prolonged increase of NREM sleep and a short increase of REM sleep; in the cortex, an increase of slow-wave activity (SWA; power density in the 0.25-2.0 Hz frequency band) in NREM sleep, which declined in the course of recovery; an enhancement of slow-wave (1.25-3 Hz) and theta (6.25-7 Hz) activity in REM sleep. The hippocampus showed an increase in NREM sleep power density in almost all frequencies. In REM sleep the hippocampus exhibited an increase in power density in the 6.25-7 Hz and 12.25-13 Hz bands, whereas in the 7.25-8 Hz band the values were below baseline. The results show that SWA in NREM sleep and theta activity in REM sleep are enhanced by sleep deprivation, as has been observed in other mammalian species. The EEG changes in the hippocampus resembled those in the cortex.
In this paper the symptomatology, epidemiology, and diagnosis of Leptospira interrogans serovar hardjo infections in cattle are reviewed. The possibilities on monitoring and control of this disease in both foreign countries and the Netherlands are discussed. Special attention is paid to the zoonotic aspects of the infection (dairy fever).
In a subacute experiment the authors studied the effects of a fourteen -day treatment with nebivolol, 5 mg once a day, in 10 healthy male volunteers with a mean age of thirty-one, twenty-five to thirty-nine years, by comparing the results of the resting ratio of the preejection period (PEP) to the left ventricular ejection time (LVET), as measured by systolic time intervals (STI), with the results obtained by equilibrium radionuclide angiocardiography (ERNA), using technetium 99m-labeled autologous red blood cells as a marker. A submaximal treadmill exercise test performed before and during treatment demonstrated that nebivolol significantly (p less than 0.01) reduced peak exercise heart rate and systolic blood pressure from a mean value of 158 +/- 5.4 bpm to 131 +/- 4.3 bpm and from 171 +/- 4.9 mmHg to 144 +/- 4.5 mmHg respectively. The data from the STI and ERNA were calculated and analyzed independently by two observers. A highly significant (r = 0.8182, p = 0.0038) correlation was found between the changes of stroke volume (SV) and PEPc/LVETc during treatment with nebivolol. Furthermore end-diastolic volume significantly(p = 0.03) increased from a mean value of 177 +/- 10.1 ml to 198 +/- 6 ml and stroke volume significantly (p = 0.01) increased from 120 +/- 6.8 ml to 136 +/- 6.3 ml. Systemic vascular resistance tended to decrease from a mean value of 11.4 +/- 1.28 units to 10.6 +/- 1.10 units. No changes could be observed either in ejection fraction or in cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)
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Seventy-eight Friesian bull calves were purchased in a cattle market and housed in a veal calf unit. There was a correlation between the risk of enteric disorders and the quantity of milkreplacer supplied during the first fortnight. The risk of respiratory disease did not show significant correlation with- and globulin levels and with serum protein and IgG1 levels at the time of purchase. No significant relationship could be shown to be present between growth and serum protein, IgG1, or globulin levels. Calves with diarrhoea during the first three weeks showed an average decrease in growth of 1.6 kg during the first ten weeks (p greater than 0.1), and calves with respiratory disease showed an average reduction of growth of 5.4 kg during the period from 0 to 10 weeks (p less than 0.01). There was no evidence to suggest that the low serum protein levels during the first six weeks of the fattening period are affected by a lower of higher feed intake during the first fortnight.
1099 female cattle from 35 farms in the provinces of North Brabant, Gelderland and Overijssel were examined for the presence of antibodies against Bovine Virus Diarrhoea (BVD) and Infectious Bovine Rhinotracheitis (IBR) by serum neutralisation tests. One of the farms examined was seronegative for BVD and 11 farms were seronegative for IBR. On the seropositive farms about 50% of cattle carrying their first calf had not experienced infection i.e. were seronegative (BVD 51.2%, IBR 48.3%). After calving the percentages of seronegative cows were considerably lower (BVD 19.6%, IBR 28.6%). The cause, implications, and prospects of prevention (vaccination) of the diseases are discussed.
The results of a bacteriological and serological study of the presence of L. hardjo on a dairy farm in view of a case of milk fever in a farmer are reviewed. In addition, the epidemiology, prevention and possible treatment of the infection on the dairy farm are discussed.