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At least 253 records · Page 14Linked to original sources
PubMed1998

Configuration options for intensity-modulated radiation therapy using multiple static fields shaped by a multileaf collimator. II: constraints and limitations on 2D modulation.

This paper addresses the technique of using multiple static multileaf-collimator-shaped field components to create a two-dimensional intensity-modulated beam (2D IMB). It addresses the physical constraints on the problem of determining the optimum field-component leaf configurations under the circumstances that (i) the static field components are shaped by leaves alone and (ii) the 2D intensity distribution is delivered by exactly N field components when there are N rising-intensity equal-fluence increments in the 1D channel containing the maximum fluence in the 2D IMB. This corresponds to the least inefficient delivery. In general it is noted that an optimum solution (set of field-component leaf configurations) with zero tongue-and-groove underdose may not exist (depending on the distribution) and an exhaustive search for the set of leaf configurations with the minimum tongue-and-groove underdose is impossible for realistically sized problems. Against this background iterative methods to examine a limited search space are shown to yield an optimum solution with zero tongue-and-groove underdose for certain intensity distributions. These searches are not robust and can be defeated. The problem of finding an optimum solution may be generally insoluble for some 2D IMBs under the conditions (i) and (ii). If, however, a larger number of field components is permitted and/or the accelerator jaws may also be used, in addition to the multileaves, then an optimum solution with zero tongue-and-groove underdose can always be found with lower efficiency.

Biophysical Phenomena↗
PubMed1994

Modulation of human P-glycoprotein epitope expression by temperature and/or resistance-modulating agents.

Three monoclonal antibodies (mAb), MRK16, MM4.17 and MC57, directed against distinct epitopes on the external domain of human P-glycoprotein (Pgp), were used to follow its expression on multidrug resistant (MDR)-cells. The linear MM4.17 epitope and conformational MRK16 epitope showed a 4-fold higher expression at 37 degrees C than at 4 degrees C, while the detection of the conformational MC57 epitope did not change. Inhibition of Pgp function, by a short pretreatment of the MDR-cells with resistance-modulating agents (RMA), such as SDZ PSC 833 and SDZ 280-446, could not be related to depletion of Pgp from the cell surface, since their expression of the MM4.17 and MRK16 epitopes was found unchanged. However, a substantially higher expression of MC57 epitopes was found on RMA-treated cells than on untreated ones. Since this effect correlated to the strength of different RMA in reversing the MDR phenotype, MC57 epitopes might be more efficiently expressed on inactivate(d) forms of the Pgp molecules, suggesting that RMA might inhibit Pgp function by disturbing the conformation of individual Pgp molecules, their topographical distribution or polymerization status in the membrane.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2000

Transverse modulation of an electron beam generated in self-modulated laser wakefield accelerator experiments

Low energy electron beams (E approximately 300 keV) generated in a self-modulated laser wakefield accelerator experiment were observed to filament and be deflected away from the laser axis forming radial jets in the electron beam profile. At higher energies (E>900 keV), the filamentation and jets were suppressed and smooth electron beams copropagating with the laser were observed. The observed electron beam filamentation likely results from laser beam filamentation in the plasma due to relativistic self-focusing effects. The radial jets of low energy electrons are likely caused by transverse ejection of the electrons due to the radial structure of the wakefield and space charge deflection of electrons as they exit the laser focus.

Journal Article↗
PubMed1994

Coordination of Chloroplastic Metabolism in N-Limited Chlamydomonas reinhardtii by Redox Modulation (II. Redox Modulation Activates the Oxidative Pentose Phosphate Pathway during Photosynthetic Nitrate Assimilation).

The onset of photosynthetic NO3- assimilation in N-limited Chlamydomonas reinhardtii increased the initial extractable activity of the glucose-6-phosphate dehydrogenase (G6PDH), the key regulatory step of the oxidative pentose phosphate pathway. The total activated enzyme activity did not change upon NO3- resupply. The higher activity, therefore, represents activation of existing enzyme. No activation occurred during NH4+ assimilation. Incubation of extracts with DTT reversed the NO3- stimulation of G6PDH activity, indicating that the activation involved redox modulation of G6PDH. Phosphoribulosekinase, an enzyme activated by thioredoxin reduction, was inhibited at the onset of NO3- assimilation. A 2-fold stimulation of O2 evolution and a 70% decrease in the rate of photosynthetic CO2 assimilation accompanied the enzyme activity changes. There was an immediate drop in the NADPH and an increase in NADP upon addition of NO3-, whereas NH4+ caused only minor fluctuations in these pools. The response of C. reinhardtii to NO3- indicates that the oxidative pentose phosphate pathway was activated to oxidize carbon upon the onset of NO3- assimilation, whereas reduction of carbon via the reductive pentose phosphate pathway was inhibited. This demonstrates a possible role for the Fd-thioredoxin system in coordinating enzyme activity in response to the metabolic demands for reducing power and carbon during NO3- assimilation.

Journal Article↗
PubMed1992

Phenylalanine positively modulates the cAMP-dependent phosphorylation and negatively modulates the vasopressin-induced and okadaic-acid-induced phosphorylation of phenylalanine 4-monooxygenase in intact rat hepatocytes.

The state of phosphorylation of phenylalanine hydroxylase was determined in isolated intact rat hepatocytes. 32P-labeled phenylalanine hydroxylase was immunoisolated from cells loaded with 32Pi or from cell extracts 'back-phosphorylated' with [gamma-32P]ATP by cAMP-dependent protein kinase. The rate of phenylalanine hydroxylase phosphorylation in cells with elevated cAMP was similar to that observed for the isolated enzyme phosphorylated by homogeneous cAMP-dependent protein kinase. The phosphorylation rate in cAMP-stimulated cells was increased up to four times (reaching 0.018 s-1) by the presence of phenylalanine, the phosphate content (mol/mol hydroxylase) increasing to 0.5 from the basal level (0.17) in 50 s. The half maximal effect of phenylalanine was obtained at a physiologically relevant concentration (110 microM). The synthetic phenylalanine hydroxylase cofactor dimethyltetrahydropterin also enhanced the cAMP-stimulated phosphorylation of phenylalanine hydroxylase, presumably by displacing the endogenous cofactor, tetrahydrobiopterin. Phenylalanine was a negative modulator of the phosphorylation of phenylalanine hydroxylase induced by incubating cells with vasopressin or with the phosphatase inhibitor okadaic acid. The same site on the phenylalanine hydroxylase was phosphorylated in response to these two agents as in response to elevated cAMP. The available evidence suggested that not only vasopressin, but also okadaic acid, acted by stimulating the multifunctional Ca2+/calmodulin-dependent protein kinase II or a kinase with closely resembling properties.

Amino Acid Sequence↗
PubMed1989

Prejunctional modulation of acetylcholine release from the skeletal neuromuscular junction: link between positive (nicotinic)- and negative (muscarinic)-feedback modulation.

1. Presynaptic receptor-mediated modulation of stimulation-evoked [3H]-acetylcholine[( 3H]-ACh) release from the neuromuscular junction was studied in the region of the mouse hemidiaphragm which contains the motor endplates, and which can easily be loaded with [3H]-choline. This method made it possible to detect exclusively the [Ca2+]0-dependent, quantal release of [3H]-ACh in response to axonal stimulation. 2. Atropine enhanced, and non-depolarizing muscle relaxants [+)-tubocurarine, pancuronium and pipecuronium) reduced, the release of [3H]-ACh evoked by high frequency trains of stimulation (50 Hz, 40 shocks) of the phrenic nerve. The effect of (+)-tubocurarine was frequency-dependent as at 5 Hz (40 shocks) it was less effective than at 50 Hz. The resting release of [3H]-ACh was not affected by these compounds. These findings indicate that ACh released into the synaptic gap by axonal firing reaches a concentration sufficient to influence its own release by a prejunctional effect. 3. The anticholinesterase, physostigmine sulphate, enhanced the release of [3H]-ACh in a concentration-dependent manner. This effect was mediated via prejunctional nicotinic receptor stimulation: (+)-tubocurarine, pancuronium and pipecuronium completely prevented the effect of physostigmine. 4. When the prejunctional nicotinic and muscarinic receptors were stimulated by a high concentration of extracellular ACh which had accumulated in the junctional gap in the presence of physostigmine, atropine did not influence the evoked release of [3H]-ACh. However, when the effect of endogenous ACh on nicotinic receptors was prevented by (+)-tubocurarine, atropine enhanced the release. 5. It is concluded that quantally-released ACh from motor endplates is subject to prejunctional automodulation: (a) ACh facilitates its own release via an effect on prejunctional nicotinic receptors (positive feedback), (b) ACh release is reduced by an action on muscarinic receptors. When the nicotinic receptor-mediated facilitation is fully operative, the muscarinic receptor-mediated negative feedback is much less effective. It is supposed that there is a link between the two feedback mechanisms possibly at the level of the second messenger system(s).

Acetylcholine↗
PubMed2025

The SlGRAS9-SlMYC1 regulatory module controls glandular trichome formation and modulates resilience to pest in tomato.

Trichomes of aerial plant organs contribute to adaptive responses to abiotic and biotic stresses. In horticultural plants, increasing glandular trichome density is an effective breeding strategy to enhance resistance to herbivores through promoting the capacity to produce specialized metabolites. The regulatory mechanisms controlling multicellular trichome formation are only partially understood. In this study, we reveal that SlGRAS9 and SlMYC1 transcription factors form a regulatory module controlling glandular trichome formation in multiple tissues. Knockout of SlGRAS9 or overexpression of SlMYC1 in tomato leads to an increased number of type VI glandular trichomes and to higher terpenoid accumulation in leaves, petals, sepals, and fruits. Conversely, knockout of SlMYC1 results in reduced type VI glandular trichomes number and terpenoid levels. Promoter-binding and genetic interaction experiments revealed that SlGRAS9 negatively regulates the transcription of SlMYC1, indicating that the regulation of glandular trichome formation by SlGRAS9 is dependent, at least partly, on SlMYC1. Consistently, both SlGRAS9 knockout and SlMYC1 overexpression result in higher tolerance of tomato plants to spider mites and aphids. In addition to adding some of the missing components to the mechanisms controlling formation of type VI glandular trichome, our findings also uncover new targets for breeding strategies aimed at improving crop protection against pest invasion, thus ensuring crop yield resilience to climate change.

Trichomes↗
PubMedDate not supplied

A cosine modulation artifact in modulation transfer function computations caused by the misregistration of line spread profiles.

Modulation transfer functions (MTFs) are used to analyze the spatial frequency transfer characteristics of medical imaging systems. By definition, accurate MTFs should not include the effects of image noise and they should not be aliased. Therefore, many techniques used to compute MTFs register and average together multiple profiles to improve both signal to noise and/or eliminate aliasing. It is demonstrated that improper registration of individual profiles can cause errors of up to 100% in the MTF. Computer modelling shows that a maximum allowable error of 2% in the MTF requires a registration precision of +/- 1/9 of a pixel for each profile, if the profile was sampled at twice the cutoff frequency of the MTF. One suggested registration method, demonstrated with experimental magnetic resonance image data, is 1.5 times more accurate than the minimum requirement.

Algorithms↗
PubMed1997

The perception of frequency peaks and troughs in wide frequency modulations. IV. Effects of modulation waveform.

This work extends previous studies on the perceptual asymmetry between the local maxima and minima of wide frequency modulations (FMs) [L. Demany and K. I. McAnally, J. Acoust. Soc. Am. 96, 706-715 (1994); L. Demany and S. Clément, J. Acoust. Soc. Am. 97, 2454-2459 (1995); L. Demany and S. Clément, J. Acoust. Soc. Am. 98, 2515-2523 (1995)]. In experiment 1, subjects had to discriminate frequency shifts in the temporally central vertex of V- and A-shaped FMs imposed on 200-ms sinusoidal tone bursts. The precise shapes of these FMs varied in eight steps from quasi-triangles (with a durationless central vertex) to quasi-squares (with a long-duration central vertex). The central vertex was either a minimum or a maximum, but in each case the corresponding frequency was near 1000 Hz and the FM span was about 0.5 oct. For each FM shape, the discrimination threshold was lower when the vertex was a maximum than when it was a minimum, but (in four subjects out of five) this difference decreased monotonically as the FM became less and less triangular. FM shape had a remarkably small effect on the discrimination of the maxima, and the thresholds measured for the sharpest maxima were unexpectedly low. In subsequent experiments, subjects had to discriminate frequency shifts in the starting point or the final point of unidirectional FMs (tone glides) that spanned about 0.5 oct in 100 ms. The relevant frequency extremum was near 1000 Hz in each condition. At the final point of the glides, discrimination was better for rising glides than for falling glides. At the starting point of the glides, discrimination was better for falling glides than for rising glides. Thus discrimination was always better when the relevant frequency extremum was a maximum than when it was a minimum, and this effect was produced both "forward" and "backward." The latter fact suggests that the perceptual asymmetry of FM originates at least partly from central factors.

Differential Threshold↗
PubMed2002

Modulation of mouse and human phenobarbital-responsive enhancer module by nuclear receptors.

The constitutive androstane receptor (CAR) regulates mouse and human CYP2B genes through binding to the direct repeat-4 (DR4) motifs present in the phenobarbital-responsive enhancer module (PBREM). The preference of PBREM elements for nuclear receptors and the extent of cross-talk between CAR and other nuclear receptors are currently unknown. Our transient transfection and DNA binding experiments indicate that binding to DR4 motifs does not correlate with the activation response and that mouse and human PBREM are efficiently 'insulated' from the effects of other nuclear receptors despite their substantial affinity for DR4 motifs. Certain nuclear receptors that do not bind to DR4 motifs, such as peroxisome proliferator-activated receptor-alpha and farnesoid X receptor, can suppress PBREM function via a coactivator-dependent process that may have relevance in vivo. In competition experiments, mouse PBREM is clearly more selective for CAR than human PBREM. Pregnane X, vitamin D, and thyroid hormone receptors can potentially compete with human CAR on human PBREM. In contrast to the selective nature of PBREM, CYP3A enhancers are highly and comparably responsive to CAR, pregnane X receptor, and vitamin D receptor. In addition, the ligand specificities of human and mouse CAR were defined by mammalian cotransfection and yeast two-hybrid techniques. Our results provide new mechanistic explanations to several previously unresolved aspects of CYP2B and CYP3A gene regulation.

Animals↗
PubMed1994

Modulation of insulin signalling in non-insulin-dependent diabetes mellitus: significance of altered receptor isoform patterns and mechanisms of glucose-induced receptor modulation.

Insulin resistance in skeletal muscle plays a key role in the development of the metabolic-endocrine syndrome and its further progression to non-insulin-dependent diabetes mellitus (NIDDM). Available data suggest that insulin resistance is caused by impaired signalling from the insulin receptor to the glucose transport system and to glycogen synthase. The impaired response of the insulin receptor tyrosine kinase, which is found in NIDDM, appears to contribute to the pathogenesis of the signalling defect. The reduced kinase activation is not caused by mutation of the receptor. Two potential mechanisms were investigated that might be relevant to the abnormal function of the insulin receptor in NIDDM. That is, changes of the receptor isoforms and the effect of hyperglycaemia. The insulin receptor is expressed in two different isoforms (HIR-A and HIR-B). HIR-B expression in skeletal muscle is increased in NIDDM. Characterization of the functional properties of HIR-B, however, revealed that increased HIR-B expression did not cause impaired tyrosine kinase activity, but more probably represented a compensatory event. In contrast, hyperglycaemia is able to inhibit insulin receptor function. In a rat-1 fibroblast cell line overexpressing human insulin receptor, inhibition of the tyrosine kinase activity of the receptor can be induced by high glucose levels. This effect appears to be mediated through activation of certain protein kinase C isoforms, which are able to form stable complexes with the insulin receptor and modulate its tyrosine kinase activity through serine phosphorylation of the receptor beta-subunit. This mechanism might also be relevant in human skeletal muscle and thereby contribute to the pathogenesis of insulin resistance.

Animals↗
PubMed2005

Modulation of Tenoxicam release from hydrophilic matrix: modulator membrane versus rate-controlling membrane.

This paper describes the preparation of two layered device comprising of tenoxicam containing layer and a drug free membrane layer based on Geomatrix Technology. Our device based on bilaminated films which produced by a casting/solvent evaporation technique. The drug-hydroxypropyl methylcellulose (HPMC) layer was covered by drug free membrane layer composed of a mixture of different ratios of HPMC and ethyl cellulose (EC). The prepared devices were evaluated for thickness, weight, drug content uniformity, water absorption capacity and in-vitro drug release. The films were also evaluated for appearance, smoothness and transparency. The influence of drug free membrane layer composition and thickness on the drug release pattern was studied on 12 devices (D1 to D12). The results indicate that, the release of drug from HPMC matrixes without the drug free membrane layer was fast and follows diffusion controlled mechanism. The release of drug from the devices D1, D4, D9 and D12 follow the same mechanism, while the release of drug from other devices become linear with time (zero order) and extended for long time especially when thickness and the ratio of EC was increased in the drug free membrane layer. From this study it is concluded that, changing the geometry of drug layer by addition of drug free membrane layer and changing its composition and thickness plays an important role in determining whether the drug free membrane layer is rate-controlling or modulator membrane. Hence it can facilitate the development of different pharmaceutical products with different release pattern.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2005

Polarization properties of a nematic liquid-crystal spatial light modulator for phase modulation.

The polarization properties of a nematic zero-twist liquid-crystal (NLC) spatial light modulator (SLM) were studied. A large ratio between the liquid-crystal (LC) layer thickness and the pixel pitch combined with spatial variations in the applied electric field causes fringing fields between pixels. Depending on the LC alignment, the electric field components within the LC layer can result in a twist deformation. The produced inhomogeneous optical anisotropy affects the polarization of light propagating through the device. We experimentally examined polarization effects in different diffraction orders for both binary and blazed phase gratings. Simulations of the LC deformation together with finite-difference time-domain simulations for the optical propagation were used to calculate the corresponding far-field intensities. It was demonstrated how rigorous simulations of the NLC SLM properties can be used to understand the polarization features of different diffraction orders.

Journal Article↗
PubMed1992

Mechanism for ganglioside-mediated modulation of a calmodulin-dependent enzyme. Modulation of calmodulin-dependent cyclic nucleotide phosphodiesterase activity through binding of gangliosides to calmodulin and the enzyme.

Gangliosides were recently shown to bind to calmodulin (Higashi, H., Omori, A., and Yamagata, T. (1992) J. Biol. Chem. 267, 9831-9838). This prompted us to investigate the effects of gangliosides on the calmodulin-dependent enzyme, cyclic nucleotide phosphodiesterase. Several species of gangliosides competitively inhibited calmodulin-stimulated phosphodiesterase activity, with GD1b, GT1b, and GD1a being noted to do so particularly (group 1). GM1, GQ1b, and GM2 (group 2) were less inhibitory, and GM3, GM3(NeuGc), GalCer, sulfatide, GgOse4Cer, and oligosaccharide portions of inhibitory gangliosides showed no inhibition in accordance with the binding specificity of calmodulin to gangliosides. Trypsin-activated phosphodiesterase was inhibited by gangliosides with similar specificity, indicating interactions of gangliosides with the enzyme. Inhibition, however, was less than that of calmodulin-dependent activity by these compounds and, in both cases, was eliminated by excess calmodulin. In the absence of calmodulin, group 1 gangliosides at lower concentrations activated the intact enzyme but inhibited it over a certain range of increase in concentration. Ganglioside-dependent modulation of calmodulin-dependent phosphodiesterase activity is thus shown to be due to interactions of gangliosides with both calmodulin and the enzyme, and consequently, ganglioside-calmodulin binding is likely the mechanism for regulation of the enzyme.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1990

Modulation of CALLA (CD10) antigen on cultured ALL (REH) cells: effect of various modulators.

Phorbol ester (TPA)-induced down-regulation of the common ALL (CALLA) antigen was studied by continuous flow immunocytometry with the aid of several CD10 monoclonal antibodies, including a new CD10 monoclonal antibody (DGH-10-1-A9), shown to be of IgG1 isotype, recognizing a 100 kDa cell surface protein and effectively inhibited by a series of reference CD10 monoclonal antibodies. The TPA-induced down-regulation of CALLA on REH cells was demonstrated with the aid of the following CD10 monoclonal antibodies: J-5, VIL-A1 and DGH-10-1-A9. No major modulations in cell surface expression of CALLA on REH cells were observed after induction with 1,25-(OH)2 vitamin D3, retinoic acid, recombinant interferon (IFN) alpha 2a and recombinant interleukin 2.

Antibodies, Monoclonal↗
PubMed1982

Opioids modulate intestinal peristalsis at a site of action additional to that modulating acetylcholine release.

The nature of the interaction between cholinergic and opioid mechanisms controlling peristalsis in the intact segment of the guinea-pig ileum was examined. The induction of rhythmic peristaltic activity by acetylcholine was dose dependently inhibited and facilitated by preapplication of, respectively, normorphine and naloxone. The action of intestinal opioids occurs, at least partially, at a site of action differing from that modulating the release of acetylcholine from the myenteric plexus. Interruption of the peristaltic reflex by hexamethonium, atropine, tetrodotoxin or desensitization of the segments to serotonin also strongly impaired or abolished the initiation of circular muscle contractions produced by naloxone. Therefore, no indication could be found for a direct action of naloxone upon the circular muscle. Rather, intestinal opioids appear to be involved in regulating the activity of the reflex arc.

Acetylcholine↗
PubMed1995

Modulation of Tax and PKA-mediated expression of HTLV-I promoter via cAMP response element binding and modulator proteins CREB and CREM.

Nuclear proteins of the human peripheral blood T lymphocytes that bind to the CREs located within three 21-bp repeat enhancers of the HTLV-I promoter belong to the CREB/CREM family of bZIP transcription factors. It has been shown previously that Tax enhances transactivation of these CREs by direct interactions with the bZIP domain of the transcription factors to stabilize DNA-binding. We show that CREB and CREM bind all three CRE sequences of the HTLV-I promoter which are important determinants in Tax-elicited transactivation as well as PKA-mediated activation of the HTLV-I promoter. Tax and PKA activate transcription from a HTLV-I-LTR CAT reporter plasmid transfected to NIH 3T3 cells, and CREM attenuates the activation. In the context of a GAL4 CREB fusion protein in which the DNA-binding bZIP domain of CREB is replaced by GAL4 binding domain, a single amino acid substitution of serine-133, phosphorylated by PKA and critical for the transactivation function of CREB, attenuates both Tax and PKA-mediated transcriptional responses. These observations suggest that Tax enhances CREB-mediated transactivation of the HTLV-I promoter by a mechanism apart from, and/or in addition to, the reported stabilization of DNA-binding by interaction with the bZIP domain of CREB.

3T3 Cells↗
PubMed1995

Modulation of basal and stress-induced release of acetylcholine and dopamine in rat brain by abecarnil and imidazenil, two anxioselective gamma-aminobutyric acidA receptor modulators.

The effects of imidazenil (6-(2-bromophenyl)-8-fluoro-4-H-imidazo[1-5-a][1-4]benzodiazepine-3- carboxamide) and abecarnil (isopropyl-6-benzyloxy-4-methoxymethyl-beta-carboline-3-carboxylate), new partial and selective benzodiazepine recognition site agonists, respectively, on basal and stress-induced hippocampal acetylcholine and cortical dopamine release were determined with the microdialysis technique in freely moving rats. The actions of these new anxioselective and anticonvulsant drugs were compared with those of diazepam and midazolam, two classical benzodiazepine full agonists. Abecarnil (0.05-1 mg/kg i.p.), imidazenil (0.05-1 mg/kg i.p.), diazepam (2.5-10 mg/kg i.p.) and midazolam (2.5-10 mg/kg i.p.) inhibited basal hippocampal acetylcholine release in a dose-dependent manner. In contrast, whereas diazepam and midazolam significantly decreased dopamine release in the prefrontal cortex, abecarnil and imidazenil had no effect on basal dopamine output. The effects of these drugs on both acetylcholine and dopamine release were antagonized by the benzodiazepine receptor antagonist flumazenil (1 mg/kg i.p.). Foot-shock stress (0.2 mA for 500 msec/sec) delivered for 8 min induced a rapid and marked (+75%) increase in hippocampal acetylcholine output that persisted for approximately 40 min. Foot-shock stress also increased dopamine release in the cerebral cortex; the effect was maximal (+90%) after 20 min and persisted for approximately 30 min. Prior administration of abecarnil or imidazenil at a dose (0.05 mg/kg) that did not significantly affect the basal release of either acetylcholine or dopamine completely prevented the effect of stress on the output of these neurotransmitters, an effect mimicked by higher doses of diazepam (2.5 mg/kg) and midazolam (2.5 mg/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗