Delay Of Several Seconds Research Articles

Performance evaluation of radio link control protocol using stop-and-wait arq in mobile radio systems

In land mobile data transmission, the error control by FEC and ARQ generally is employed to improve the reliability of transmission. In the control signal transmission for the radio link control in the mobile communication system, the error usually is detected by FEC, and the reliability is improved by ARQ. Under the condition of motion velocity of 40 to 50 km/h and the tolerable transmission delay of several seconds, the transmission characteristics of ARQ depend greatly on the short-term median variation of the received level of the retransmitted signal, together with the packet signal transmission characteristics under the instantaneous received level variation due to fading. No evaluation has been presented for the transmission characteristics of ARQ considering such a median variation. This paper considers the stop-and-wait (SAW) ARQ where the number of retransmissions is limited to a finite value, and presents an evaluation of the transmission characteristics considering the correlation of the short-term median variation of the retransmitted signal. Numerical examples are presented. Assuming that SAW-ARQ is applied to the transmission protocol of the common control channel, the blocking probability is examined, together with numerical examples.

Chloride current activated by cyclic AMP and parathyroid hormone in rat osteoblasts

In primary cultures of rat osteoblasts, studied with the whole-cell configuration of the patch-clamp technique, 8-bromo-cyclic AMP (8BrcAMP) forskolin (FS) and 1-34 parathyroid hormone (PTH) were shown to activate a Cl conductance. This conductance shows a pronounced outward rectification, even with symmetrical Cl concentrations. It is blocked partially and reversibly by 4,4'-diisothiocyanatostilbene 2,2'-disulfonic acid (DIDS) or diphenylcarboxylate (DPC). The blockade induced by DIDS is time- and voltage-dependent. The Cl responses to FS and PTH develop slowly, after a delay of several seconds and are very slowly reversible. These responses were observed only in a fraction of the cells tested and their detection was favoured by cell dialysis. This Cl current should be taken into account for studying possible modulations of the voltage-gated Ca currents of osteoblasts. It is suggested that its physiological role may be related to the well-known morphological changes induced by PTH in osteoblasts. The cyclic AMP-sensitivity, the outward rectification and the sensitivity to dialysis of this Cl current are reminiscent of the properties of the cystic fibrosis-sensitive Cl channels of epithelial cells.

Cell calcium and its regulation in smooth muscle

Two novel methods used to study smooth muscles-electron probe X-ray microanalysis and Ca2+-sensitive indicators (which are used for resolving, respectively, the spatial distribution and temporal distribution of calcium)-are briefly reviewed and the major findings obtained are summarized. In smooth muscle the sarcoplasmic reticulum is the major intracellular source of Ca2+; mitochondria do not play a significant role in the physiological regulation of [Ca2+]i. Under pathological conditions mitochondria can reversibly accumulate large amounts of calcium. Resting [Ca2+]i generally ranges from 80 to 200 nM, and is lower in phasic than in tonic smooth muscles. Removal of extracellular Ca2+ and Ca2+ entry blockers can reduce [Ca2+]i, but the effects of beta-adrenergic agents are variable. Increases in [Ca2+]i are triggered by electrical stimulation, depolarization with high K+, and excitatory agonists. Stretch, after a delay of several seconds, can cause an increase in [Ca2+]i in some smooth muscles. There is also a delay of approximately 200-400 ms between the initiation of the rise of Ca2+ and contraction that follows spontaneous action potentials or electrical stimulation. Agonist-induced Ca2+ release, a major mechanism of pharmacomechanical coupling, has been demonstrated in smooth muscles depolarized with high K; evidence suggests that it is mediated by G proteins that couple receptors to phospholipase C. Ca2+ release can be triggered directly in permeabilized smooth muscle with inositol 1,4,5-trisphosphate. Even though Ca2+ is the major physiological regulator of contraction, Ca2+ sensitivity of the regulatory-contractile apparatus differs in different (phasic and tonic) smooth muscles, and can be modulated in a given smooth muscle. The force [Ca2+]i ratio is higher during agonist-stimulated than during high K+-induced contractions, owing to agonist-induced increases in Ca2+ sensitivity mediated by G proteins. In some phasic smooth muscles (guinea pig ileum), the time course of the initial myosin light chain phosphorylation is extremely rapid and returns to basal levels while force remains elevated. In these smooth muscles there is also a marked decrease in the Ca2+ sensitivity of the regulatory-contractile apparatus during maintained depolarization in Ca2+-free or low Ca2+ solutions. It has been suggested that regulation of myosin light chain phosphatase plays a major role in the modulation of the Ca2+ sensitivity manifested as either potentiation or desensitization to [Ca2+]i.

Properties of membrane ion conductances evoked by hormonal stimulation of guinea-pig and rabbit isolated hepatocytes

Membrane conductance changes evoked in isolated guinea-pig or rabbit hepatocytes by hormonal stimulation were studied with the whole-cell patch clamp technique. In Cl-containing solutions, noradrenaline (NA), ATP or angiotensin II (AII) evoked an increase of conductance to both K (GK) and Cl (GCl) ions. Activation of GK occurred after a delay of several seconds and was sustained in the presence of hormone. Activation of GCl was transient, lasting several seconds, and arose either at the same time or shortly after the increase in GK. Conductances showed an initial rapid rise and slow oscillatory changes during maintained hormone application. The NA-induced current reversed at -19 mV in Cl solutions, between the equilibrium potentials for chloride (ECl = 0 mV) and potassium ions (EK = -85 mV), and at -75 mV, near EK, in Cl-free solution. In both conditions whole-cell current-voltage curves were linear in the range -100 mV to +40 mV. The conductance increase produced by NA to Cl- ions was about 50 nS, that to K+ ions was 6 nS. The potassium conductance increase was abolished by the polypeptide toxin apamin (50 nM). An increase in membrane current noise was associated with NA-evoked outward K+ current and blocked by apamin. Spectral analysis gave estimates of the elementary K channel conductance of 1.7 pS. Power spectra were fitted by two Lorentzian components, with average half-power frequencies of 2 and 190 Hz. These results are discussed in relation to the single-channel properties and indicate that the open probability of K channels during the NA response is high. In Cl solutions, with apamin to block the K conductance, no increase in current noise was detected during the large Cl conductance evoked by NA. This suggests either that Cl channels are of very low unitary conductance (less than 1 pS) or that Cl transport is due to a membrane carrier. The complex time-course of hormonally evoked conductances is not due to the properties of ion conductances per se but probably to underlying changes of intracellular second-messenger concentration.

Dynamical aspects of laser generating luminescence centers in (Al,Ga)As

Luminescence measurements performed during pulsed laser irradiation indicate a two step mechanism for the formation of new luminescence centers: First, nonradiative recombination centers appear in the focal zone. Then, after a delay of several seconds, new luminescence centers are created on a microsecond time scale. The delay depends exponentially on the optically generated carrier density which is typically 8·1018cm-3. The luminescence centers act predominately as nonradiative recombination centers under laser processing conditions (0.5 MW/cm2). At lower excitation densities they exhibit a high luminescence efficiency at temperatures of up to 400 °K.

Nonlinear model of tectonic release from underground explosions

Reversal of teleseismic Rayleigh wave polarity has been observed for some underground explosions in eastern Kazakh. Furthermore, the reversed-polarity Rayleigh waves are observed to be time-delayed by several seconds. We analyze two-dimensional, nonlinear numerical simulations of underground explosions to examine the hypothesis that these phase reversals and apparent time delays result from the action of tectonic prestress on the explosion-created nonlinear volume (the shatter zone model of tectonic release). We conclude that tectonic shear stress exceeding about 10 MPa (100 bars) is sufficient to reverse the Rayleigh wave polarity and cause an apparent time delay of several seconds, even in the absence of triggered strain release on faults. Shear stresses of this magnitude are plausible at several hundred meters depth, in that they do not exceed strength bounds for a fractured rock mass, as estimated from Byerlee's law. The nonlinear model predictions imply that if tectonic release is modeled elastically as the relaxation of the deviatoric part of the prestress into a spherical cavity, the appropriate cavity radius is approximately 80 per cent of the explosion elastic radius. The apparent time delays result from interference between the explosion and tectonic source functions, and can be quantitatively related to the presence of overshoot in the isotropic part of the explosion moment rate tensor. It is therefore conceivable that careful observations of Rayleigh wave phase for the anomalous events (relative to nearby unreversed events) could help constrain the amount of overshoot in the explosion source function, even though the overshoot occurs on a time scale of a few tenths of a second and has a negligible effect on Rayleigh wave spectral amplitudes.