80 research outputs found
Road Environment and Driver Fatigue
No full textSummary: We distinguish between fatigue caused by the demands of the driving task itself (see Hancock & Desmond, 2001) from the standard traditional approach that links fatigue predominately to the lack of sleep. Fatigue can be caused by two sources: (1) the driver’s initial state before starting the drive, or (2) the characteristics of the drive and the road environment; both sources can have a cumulative effect. It is not clear what principles are involved in making one road environment more prone to inducing driver fatigue than another. For the purpose of the current presentation we provide empirical data on road environment and driver fatigue summarized from a series of three experiments that the first author has conducted at Ben-Gurion University (see Oron-Gilad, 2003; Oron-Gilad, et al., 2001). Those are examined in relation to the Hancock and Warm (1989) model of adaptability. The most significant and consistent findings of the three experiment is in the way that fatigue is reflected in driving performance across different road environments. These findings suggest that drivers are flexible in the way they handle fatigue over the course of time. They can adopt different strategies to compensate for their performance decrement, by focusing efforts on critical elements of each different type of roadway. Understanding of this dependency of fatigue symptoms on road conditions is of especial relevance to designers of technological fatigue countermeasures as well as those of future roadway systems
Neurotransmitter-caused increase in [3H]inositol incorporation into phosphatidylinositol de novo synthesis vs exchange
No full textAbstract[3H]inositol and 32Pi were simultaneously incorporated into rat parotid phosphatidylinositol. The ratio of [3H]/32Pi incorporation dropped dramatically following stimulation with muscarinic or α-adrenergic agonists and returned to control values following the addition of appropriate antagonists. The drop in [3H]/32Pi ratio can be explained by a rapid increase in de- novo synthesis of phosphatidylinositol following its receptor-mediated breakdown. The change in this ratio also provided evidence for the existence of CDP-DG + inositol ⇄ phosphatidylinositol exchange reaction in the intact tissue
Acetylcholine- and inositol 1,4,5-trisphosphate-induced calcium mobilization in Xenopus laevis oocytes
No full textAbstractAcetylcholine induces a complex electrical membrane response in Xenopus laevis oocytes. This response is mimicked, and probably mediated by injected inositol 1,4,5-trisphosphate. Oocytes prelabelled with 45Ca released calcium in two phases, the second, slow phase exhibiting first order kinetics of release. Brief exposure of prelabelled oocytes to acetylcholine resulted in a significant increase in the rate of calcium release that returned to control values 2-3 min following the removal of the neurotransmitter. Intracellular injection of inositol 1,4,5-trisphosphate resulted in increased rate of calcium release similar to, but longer than that caused by acetylcholine. Experiments conducted on single oocytes permitted the investigation of the relationship between acetylcholine-induced and inositol 1,4,5-trisphosphate-induced calcium mobilization and the resulting electrical membrane response. Our data reinforce our previous suggestion that inositol 1,4,5-trisphosphate is the intracellular second messenger of the muscarinic membrane electrical response in Xenopus oocytes
Gα11 and Gαq guaninine nucleotide regulatory proteins differentially modulate the response to thyrotropin-releasing hormone in Xenopus oocytes
No full textAbstractXenopus oocytes that express mouse thyrotropin-releasing hormone receptors (TRH-Rs) after injection if RNA transcribed from TRH-R cDNA respond to THR by a depolarizing current. This response is transducer by activation of phosphoinositide-specific phospholipase C and utilizes an as yet unidentified endogenous guanine nucleotide-binding regulatory (G) protein(s). The α subunit of G11 and Gq have recently been shown to couple receptors to activation of phospholipase C. To determine whether there are functional differences between these proteins, we have co-expressed the TRH-R with either α11 or αq, α11 potentiated the response to TRH (by 61±16%), while αq inhibited the response (by 37±9%). The changes in amplitudes were accompanied by inverse changes in response latencies. These data show that α11 and αq differentially modulate signal transduction in Xenopus oocytes
Prolonged, repetitive calcium transients in rat oocytes fertilized in vitro and in vivo
No full textAbstractZona-free rat oocytes inseminated with capacitated sperm, under conditions that allow polyspermic fertilization, exhibited a rapid, transient elevation of cellular calcium (from 147 ± 10 to 607 ± 55 nM, n = 19, measured by Fura 2 fluorescence ratio imaging) immediately after sperm attachment. This peak was followed by a series of dramatic calcium transients of high amplitude (maximal 847 ± 32 nM) and frequency (range 2.1 ± 0.07–3.9 ± 0.07 min), which continued for several hours. A similar pattern was seen also in zona-free oocytes fertilized with low sperm density (i.e. producing mainly monospermic attachment) and in zona-enclosed oocytes fertilized in vitro. Moreover, single or repetitive calcium transients were observed in rat oocytes fertilized in vivo. These findings indicate that in normal fertilization in vivo, sperm-oocyte interaction initiates a prolonged train of cyclical calcium changes in the oocyte. This activity may be necessary for the early events in the fertilization process
Hemispheric asymmetry of rapid chloride responses to inositol trisphosphate and calcium in Xenopus oocytes
No full textAbstractShallow injection of inositol 1,4,5-trisphosphate (IP3) near the animal pole of the Xenopus oocyte resulted in a large depolarizing current that decayed rapidly. A similar injection near the vegetal pole produced a much smaller response characterized by a significantly slower rate of decay. Injection of CaCl2 near the animal pole of the oocyte resulted in a large depolarizing current characterized by rapid rise and decay times. Injection near the vegetal pole of the cell produced responses that exhibited similar amplitudes but much longer rise and decay times. The protein kinase C (PK-C) activator, β-phorbol 12-myristate 13-acetate (PMA), significantly enhanced the rapid responses to IP3 injections at either hemisphere but did not affect the amplitudes of the responses to CaCl2. The PK-C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) had no effect on the responses to CaCl2. These results imply an asymmetric distribution of calcium stores and chloride channels between the two hemispheres of the oocyte
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