[Drug induced changes of EEG vigilance and optimizing control behavior during car driving (author's transl)].
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Adult↗
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Severity of injuries in road crashes. A comparison of injured occupants of forward control vehicles and conventional passenger cars.
Light vans are being used increasingly as substitutes for conventional passenger cars in Australia. These "forward control" vans are not required to meet the same safety standards as passenger cars. A study group of 258 injured occupants of light vans was identified from the records of the Motor Accidents Board of Victoria. A comparison group of 3468 injured occupants of conventional cars was also identified. Both groups had been injured in accidents occurring in Victoria between 1980 and 1983. The injuries received by the van occupants were compared with those received by the car occupants. Van occupants injured in frontal crashes were more likely to have sustained leg injury, and were more likely to have sustained serious injury than were car occupants who were injured in frontal crashes. Forward control vans were found to lack protection for occupants in frontal crashes.
Accidents, Traffic↗
Effects of the reduced toxicity of car exhaust on accidental deaths: a comparison of the United States and Great Britain.
A study of the frequency of car exhaust as a cause of accidental death in the United States from 1968 to 1984 showed that the accidental death rate from car exhaust has declined during the same period during which the toxicity of car exhaust has been reduced through the imposition of emission controls. However, in Great Britain, where there are no emission controls on cars, the accidental death rate from car exhaust has risen slightly over the same period. Thus, the introduction of emission controls on cars to reduce pollution of the environment seems to have had incidental beneficial effects on mortality from accidental poisoning from car exhaust.
Automobiles↗
Purification and characterization of an arginine regulatory protein, ArgR, from Pseudomonas aeruginosa and its interactions with the control regions for the car, argF, and aru operons.
Pseudomonas aeruginosa ArgR, a regulatory protein that plays a major role in the control of certain biosynthetic and catabolic arginine genes, was purified to homogeneity. ArgR was shown to be a dimer of two equal subunits, each with a molecular mass of 37,000 Da. Determination of the amino-terminal amino acid sequence showed it to be identical to that predicted from the derived sequence for the argR gene. DNase I footprinting showed that ArgR protects a region of 45 to 47 bp that overlaps the promoters for the biosynthetic car and argF operons, indicating that ArgR exerts its negative control on the expression of these operons by steric hindrance. Studies were also carried out with the aru operon, which encodes enzymes of the catabolic arginine succinyl-transferase pathway. Quantitative S1 nuclease experiments showed that expression of the first gene in this operon, aruC, is initiated from an arginine-inducible promoter. Studies with an aruC::lacZ fusion showed that this promoter is under the control of ArgR. DNase I experiments indicated that ArgR protects two 45-bp binding sites upstream of aruC; the 3' terminus for the downstream binding site overlaps the -35 region for the identified promoter. Gel retardation experiments yielded apparent dissociation constants of 2.5 x 10(-11), 4.2 x 10(-12), and 7.2 x 10(-11) M for carA, argF, and aruC operators, respectively. Premethylation interference and depurination experiments with the car and argF operators identified a common sequence, 5'-TGTCGC-3', which may be important for ArgR binding. Alignment of ArgR binding sites reveals that the ArgR binding site consists of two half-sites, in a direct repeat arrangement, with the consensus sequence TGTCGCN8AAN5.
Arginine↗
The use of seat belts in cars with smart seat belt reminders--results of an observational study.
UNLABELLED: Recently, smart seat belt reminders (SBR) have been introduced in cars. By increasingly reminding drivers and passengers if they are not using the seat belt, the intention is to increase the belt use to almost 100%. OBJECTIVE: The objective was to study if there were differences in driver's seat belt use between cars with and without SBR. METHODS: Drivers of cars with and without SBR were observed concerning seat belt use. The case (cars with SBR) and the control group (cars without SBR) were similar in all major aspects except SBR. In all, more than 3,000 drivers were observed in five cities in Sweden. RESULTS: In cars without SBR, 82.3 percent of the drivers used the seat belt, while in cars with SBR, the seat belt use was 98.9 percent. The difference was significant. In cars with mild reminders, the use was 93.0 percent. CONCLUSION: It is concluded, that if the results can be generalised to the whole car population this would have a dramatic impact on the number of fatally and seriously injured car occupants.
Automobile Driving↗
Rapid ventricular pacing induces delayed cardioprotection against myocardial stunning.
Tachycardia with rapid ventricular pacing induces delayed preconditioning against arrhythmias secondary to coronary artery occlusion (CAO) and reperfusion (CAR) but its effects on myocardial stunning remains unknown. Accordingly, we investigated whether delayed preconditioning with ventricular pacing develops against myocardial stunning and whether this phenomenon is triggered by reactive oxygen species. Eight chronically instrumented conscious dogs underwent three experimental sequences in a random order a week apart: (a) 10-min CAO (coronary occluder) followed by CAR, i.e. "Control" sequence; (b) pacing (right ventricular electrodes, 240 beats/min during 40 min) performed 24 h before the 10-min CAO, i.e. "PC" sequence; and (c) N-(2-mercaptopropionyl)-glycine (MPG, 100 mg/kg per h) administered concomitantly to pacing and 10-min CAO performed 24 h later, i.e. "PC+MPG" sequence. During "Control", left ventricular (LV) wall thickening (%, sonomicrometry) was dramatically reduced during CAO (-96 +/- 5% from 2.9 +/- 0.4 mm) and remained depressed during CAR demonstrating myocardial stunning. During "PC", LV wall thickening was not altered by pacing per se and was similarly decreased during CAO vs. "Control". However, during CAR, LV wall thickening was improved vs. "Control" (e.g. -24 +/- 5% and -8 +/- 4% from corresponding baseline for "PC" and "Control", respectively at 2 h-CAR; P<0.05), demonstrating delayed preconditioning. Administration of MPG during pacing (n=5) abolished the beneficial effects of pacing. Myocardial lactate extraction and transmural distribution of regional myocardial blood flow (fluorescent microspheres) were not modified, by pacing. In conclusion, tachycardia with rapid ventricular pacing induces delayed cardioprotection against myocardial stunning. The production of reactive oxygen species independently from ischemia appears to be a major trigger for this phenomenon.
Animals↗
Effects of pretreatment with 6-hydroxydopamine or noradrenergic receptor blockers on the clonidine-induced distruption of conditioned avoidance responding.
The effects of clonidine were assessed on conditioned avoidance responses (CAR) in control, 6-hydroxy-dopamine (6-OHDA)- and vehicle-treated rats, using a shuttle box device. Clonidine (100--400 micrograms/kg) produced a significant decrease of CAR in control and vehicle-treated animals. On the other hand, avoidance responding was only slightly inhibited in the 6-OHDA-lesioned rats. Pretreatment with the alpha-adrenergic blocking drugs yohimbine or phentolamine (1--8 mg/kg) prevented the CAR disrupting effects of clonidine. When animals were pretreated with the beta-adrenergic blocking agent propranolol (1--8 mg/kg) the ensuing injection of clonidine caused a greater CAR depression. Our results further support the hypothesis relating the conditioned performance depression observed after clonidine to the activation of a presynaptic negative feedback mechanism mediated by alpha-adrenoceptors. It is also suggested that propranolol increases the clonidine inhibition through the blockade of a positive feedback mechanism dependent on the activation of presynaptic beta-receptors.
Animals↗
Driver sleepiness and risk of serious injury to car occupants: population based case control study.
OBJECTIVES: To estimate the contribution of driver sleepiness to the causes of car crash injuries. DESIGN: Population based case control study. SETTING: Auckland region of New Zealand, April 1998 to July 1999. PARTICIPANTS: 571 car drivers involved in crashes where at least one occupant was admitted to hospital or killed ("injury crash"); 588 car drivers recruited while driving on public roads (controls), representative of all time spent driving in the study region during the study period. MAIN OUTCOME MEASURES: Relative risk for injury crash associated with driver characteristics related to sleep, and the population attributable risk for driver sleepiness. RESULTS: There was a strong association between measures of acute sleepiness and the risk of an injury crash. After adjustment for major confounders significantly increased risk was associated with drivers who identified themselves as sleepy (Stanford sleepiness score 4-7 v 1-3; odds ratio 8.2, 95% confidence interval 3.4 to 19.7); with drivers who reported five hours or less of sleep in the previous 24 hours compared with more than five hours (2.7, 1.4 to 5.4); and with driving between 2 am and 5 am compared with other times of day (5.6, 1.4 to 22.7). No increase in risk was associated with measures of chronic sleepiness. The population attributable risk for driving with one or more of the acute sleepiness risk factors was 19% (15% to 25%). CONCLUSIONS: Acute sleepiness in car drivers significantly increases the risk of a crash in which a car occupant is injured or killed. Reductions in road traffic injuries may be achieved if fewer people drive when they are sleepy or have been deprived of sleep or drive between 2 am and 5 am.
Accidents, Traffic↗
The serotonin 5-HT2A receptors antagonist M100907 prevents impairment in attentional performance by NMDA receptor blockade in the rat prefrontal cortex.
We investigated whether 5-HT2A receptors contribute to the control of attentional performance by glutamate NMDA receptor mechanisms in the medial prefrontal cortex (mPFC). We examined the effects of NMDA receptor blockade in the mPFC on attentional performance by infusing a competitive glutamate NMDA receptor antagonist, 3-(R)-2-carboxypiperazin-4-propyl-1-phosphonic acid (CPP) into the mPFC of rats performing a task of divided and sustained visual attention. The five-choice serial reaction time task provides indices of attentional functioning (% correct responses), executive control (measured by anticipatory and perseverative responses) and speed. A dose of 10 ng CPP injected bilaterally into the mPFC increased anticipatory and perseverative responding; 50 ng reduced accuracy. Increasing the stimulus duration alleviated the CPP-induced accuracy deficit but did not reduce its effects on anticipatory and perseverative responses. CPP at 50 ng caused motor hyperactivity whereas lower doses had no effect. [R-(+)-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidine-methanol] (M100907) (M100907), a 5-HT2A receptor antagonist, injected subcutaneously at 10 and 40 microg/kg, had no effect on accuracy but dose dependently reversed the impairment induced by 50 ng CPP. Both doses of M100907 completely abolished CPP-induced anticipatory but not perseverative over-responding. At the dose of 40 microg/kg M100907 reversed CPP-induced motor hyperactivity. This study provides evidence that the prefronto-cortical glutamate NMDA system may make an important contribution to the control of attention and executive functions. It also indicates that 5-HT2A receptors may serve to optimize attentional selectivity and improve some aspects of executive control.
Animals↗
Apical localization of the coxsackie-adenovirus receptor by glycosyl-phosphatidylinositol modification is sufficient for adenovirus-mediated gene transfer through the apical surface of human airway epithelia.
In well-differentiated human airway epithelia, the coxsackie B and adenovirus type 2 and 5 receptor (CAR) resides primarily on the basolateral membrane. This location may explain the observation that gene transfer is inefficient when adenovirus vectors are applied to the apical surface. To further test this hypothesis and to investigate requirements and barriers to apical gene transfer to differentiated human airway epithelia, we expressed CAR in which the transmembrane and cytoplasmic tail were replaced by a glycosyl-phosphatidylinositol (GPI) anchor (GPI-CAR). As controls, we expressed wild-type CAR and CAR lacking the cytoplasmic domain (Tailless-CAR). All three constructs enhanced gene transfer with similar efficiencies in fibroblasts. In airway epithelia, GPI-CAR localized specifically to the apical membrane, where it bound adenovirus and enhanced gene transfer to levels obtained when vector was applied to the basolateral membrane. Moreover, GPI-CAR facilitated gene transfer of the cystic fibrosis transmembrane conductance regulator to cystic fibrosis airway epithelia, correcting the Cl(-) transport defect. In contrast, when we expressed wild-type CAR it localized to the basolateral membrane and failed to increase apical gene transfer. Only a small amount of Tailless-CAR resided in the apical membrane, and the effects on apical virus binding and gene transfer were minimal. These data indicate that binding of adenovirus to an apical membrane receptor is sufficient to mediate effective gene transfer to human airway epithelia and that the cytoplasmic domain of CAR is not required for this process. The results suggest that targeting apical receptors in differentiated airway epithelia may be sufficient for gene transfer in the genetic disease cystic fibrosis.
3T3 Cells↗
An experimental model of tennis elbow in rats: a study of the contribution of the nervous system.
The contribution of the sensory and autonomic nervous system to experimentally induced tennis elbow or lateral epicondylalgia was investigated by analyses of the release of neuropeptides from sensory (substance P, SP, neurokinin A, NKA, calcitonin gene-related peptide, CGRP) and sympathetic (neuropeptide Y, NPY) nerves. SP, CGRP, NKA, NPY-like immunoreactivity (-LI) was studied in rats cerebrospinal fluid (CSF), plasma and perfusates (PF) from the enthesis of the extensor carpi radialis brevis (ECRB) of the right elbow at 2, 6 and 24 h following 0.01 ml injection of either complete Freund adjuvans (FA) or 2% Carrageenan (CAR). The control group was injected with 0.01 ml saline. In general the changes of neuropeptide-LI in the CSF and plasma were similar for both treated groups compared with the controls, but they were more pronounced in the FA group than the CAR. SP-, NKA-, CGRP- and NPY-LI were significantly increased to a similar degree in the perfusates of the ECRBs of the treated groups with a greater increase in SP-LI in the FA than the CAR group compared with controls. When comparing the neuropeptide-LI in the CSF, plasma and PF between the 2 treated groups, there were thus few differences found. Generally a unilateral injection with either FA or CAR into the rat ECRB induced a similar alteration in the concentration of SP-, NKA-, CGRP- and NPY-LI in the CSF, plasma and PF at 2, 6 and 24 h following injection. However, the most pronounced changes in neuropeptide-LI occurred locally in the elbow ECRBs PF in both treated groups.
Animals↗
Isoflurane inhaled at the onset of reperfusion potentiates the cardioprotective effect of ischemic postconditioning through a NO-dependent mechanism.
Postconditioning (PCD) is known to reduce infarct size (IS). Here, we investigated whether isoflurane, which is known to potentiate preconditioning, also potentiates PCD and whether NO is involved. Accordingly, open-chest rabbits underwent 30-minute coronary artery occlusion (CAO) followed by 3-hour coronary artery reperfusion (CAR). In control and postconditioned (4 cycles of 30s-CAR/30s-CAO after the 30-min CAO), rabbits were anesthetized with pentobarbital alone or in combination with isoflurane inhaled (i) throughout the experiment or (ii) only during CAR. With pentobarbital alone, PCD significantly reduced IS versus control (39 +/- 7% vs. 55 +/- 4% of the risk zone, respectively, P < 0.05). Isoflurane--0.5% throughout the experiment did not alter IS in both control and PCD groups. Isoflurane--2% throughout the experiment reduced IS in control (37 +/- 8%, P < 0.05 vs. pentobarbital alone) and enhanced the protective effect of PCD (IS = 21 +/- 3%, P < 0.05 vs. both control and PCD under pentobarbital alone). When isoflurane--2% was administered only during reperfusion, IS was not changed in control (53 +/- 3%) but combination with PCD reduced IS to 23 +/- 4% (P < 0.05 vs. both control and PCD under pentobarbital alone). L-arginine analog N-nitro-L-arginine methyl ester administered before reperfusion did not properly alter IS (53 +/- 6%) but abolished the effect of PCD alone (IS = 47 +/- 7%) or in combination with isoflurane--2% during reperfusion (55 +/- 3%). Thus, isoflurane potentiates PCD at reperfusion through a NO-dependent mechanism.
Administration, Inhalation↗
Changing rates of suicide by car exhaust in men and women in the United States after car exhaust was detoxified.
The rates of men and women committing suicide by using car exhaust responded differently to the imposition of emission controls on cars. The male rate dropped immediately after emission controls were imposed, whereas that of females continued to rise. Eventually both rates dropped until the early 1980s, whereupon they began to rise again slightly. The implications of these findings are discussed.
Carbon Monoxide Poisoning↗
Human-factors engineering for smart transport: design support for car drivers and train traffic controllers.
The theme Smart Transport can be described as adequate human-system symbiosis to realize effective, efficient and human-friendly transport of goods and information. This paper addresses how to attune automation to human (cognitive) capacities (e.g. to take care of information uncertainty, operator trust and mutual man-machine adaptations). An introduction to smart transport is presented, including examples of best practice for engineering human factors in the vehicle ergonomics and train traffic control domain. The examples are representative of an ongoing trend in automation and they show how the human role changes from controller to supervisor. Section 2 focuses on the car driver and systems that support, or sometimes even take over, critical parts of the driving task. Due to the diversity of driver ability, driving context and dependence between driver and context factors, there is a need for personalised, adaptive and integrated support. Systematic research is needed to establish sound systems. Section 3 focuses on the train dispatcher support systems that predict train movements, detect potential conflicts and show the dispatcher the possibilities available to solve the detected problems. Via thorough analysis of both the process to be controlled and the dispatcher's tasks and cognitive needs, support functions were developed as part of an already very complex supervision and control system. The two examples, although from a different field, both show the need for further development in cognitive modelling as well as for the value of sound ergonomics task analysis in design practice.
Accidents, Traffic↗
A serious case of radiofrequency EMI, when an ICD wearer manipulated a remote control of a toy car.
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Artifacts↗
From the Centers for Disease Control and Prevention. Fatal car trunk entrapment involving children--United States, 1987-1998.
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Accidents↗
Inverse association of cell adhesion regulator messenger RNA expression with metastasis in human colorectal cancer.
Alterations in several classes of adhesion molecules have been implicated in the progression of colorectal cancer. Cell adhesion regulator (CAR) has been identified as a regulator molecule of integrin-dependent cell adhesion. We have explored a possible involvement of the CAR gene in colorectal cancer. Reverse transcription-PCR revealed that CAR expression was detected in normal colonic cells, whereas it was decreased or undetectable in 6 of 13 (46.2%) human colon cancer cell lines. To further study the biological significance of CAR expression in colon cancer cells, a CAR expression vector was introduced into HT-29 cells, in which CAR is not expressed. Adhesion of HT-29 cells to extracellular matrix components was up-regulated by the introduction of CAR. In spite of similar growth properties with the controls, CAR-transfected HT-29 cells showed a significantly reduced spontaneous metastatic potential in nude mice. To determine whether these experimental results are of relevance with respect to actual human tumors, we investigated CAR expression in 30 surgical specimen pairs of human colorectal cancer and adjacent noncancerous tissue using semiquantitative reverse transcription-PCR. In 14 of 30 cases (46.7%), CAR expression in cancer was less than one-tenth of that in matched noncancerous tissue. The tumor:normal ratio of CAR expression was significantly lower in patients with lymph node metastasis than in those without it (P < 0.01) and in patients with distant metastasis than in those without it (P < 0.05). CAR expression was significantly lower in more advanced Dukes' stage tumors (P < 0.05). Our results suggest that down-regulation of CAR expression may play an important role in the progression and metastasis of colorectal cancer.
ATPases Associated with Diverse Cellular Activitie↗
The driver's role in fatal two-car crashes: a paired "case-control" study.
This population-based study examines drivers' characteristics associated with driving errors that resulted in fatal motor vehicle crashes. Routinely collected data from the Fatal Accident Reporting System were used to assess whether a driver initiated the crash (case) or was passively involved (control) in 6,506 two-car collisions (81% of 7,993 eligible events). A paired comparison of cases and controls avoided confounding by environmental factors, exposure to traffic, and differences in case fatality. The strongest predictor of crash initiation is alcohol (odds ratio (OR) = 11.5; 95% confidence interval (CI) 9.57-13.9). Odds ratios are elevated even at the lowest blood alcohol concentration levels and increase dramatically as alcohol levels rise. Drivers aged 40-49 years are least likely to initiate crashes; odds ratios rise in a U-shaped manner to 3.35 in teenagers (95% CI 2.72-4.13) and to 22.1 in drivers over 80 years (95% CI 14.2-34.5). Other risk factors for initiating a fatal crash are the following: not wearing a seat belt (OR = 1.54; 95% CI 1.35-1.75), driving without a valid driver's license (OR = 2.16; 95% CI 1.72-2.73), and having had a crash within the last year (OR = 1.21; 95% CI 1.07-1.38). Driving errors leading to fatal crashes do not occur at random, but are associated with specific driver characteristics. The risk factors for crash initiation among crash-involved drivers are similar to risk factors for crash involvement found in other studies. These findings suggest that driving errors often explain high rates of crash involvement, invite further use of crash initiation in traffic injury research, and underscore the value of population-based registries for analytic epidemiology.
Accidents, Traffic↗