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Journal articles on the topic 'Halothane'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Raines, Douglas E., and Katie B. McClure. "Halothane Interactions with Nicotinic Acetylcholine Receptor Membranes." Anesthesiology 86, no. 2 (1997): 476–86. http://dx.doi.org/10.1097/00000542-199702000-00023.

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Background Although it has been suggested that anesthetics alter protein conformational states by binding to nonpolar sites within the interior regions of proteins, the rate and extent to which anesthetics penetrate membrane proteins has not been characterized. The authors report the use of steady-state and stopped-flow spectroscopy to characterize the interactions of halothane with receptor membranes. Methods Steady-state and stopped-flow fluorescence spectroscopy was used to characterize halothane quenching of nicotinic acetylcholine receptor (nAcChoR)-rich membrane intrinsic fluorescence an

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2

Williams, J. H., M. Holland, J. C. Lee, C. W. Ward, and K. P. Davy. "Effects of BAY K 8644, nifedipine, and low Ca2+ on halothane and caffeine potentiation." Journal of Applied Physiology 71, no. 2 (1991): 721–26. http://dx.doi.org/10.1152/jappl.1991.71.2.721.

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The purpose of this investigation was to examine the effects of the Ca2+ agonist BAY K 8644 and the Ca2+ antagonist nifedipine on halothane- and caffeine-induced twitch potentiation of mammalian skeletal muscle. Muscle fiber bundles were taken from normal Landrace pigs and exposed to BAY K 8644 (10 microM), nifedipine (1 microM), and low Ca2+ media administered alone and in combination with halothane (3%) or with increasing concentrations of caffeine (0.5–8.0 mM). Both BAY K 8644 and halothane potentiated twitches by approximately 80%; when they were administered in combination, twitch potenti

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3

Crowder, Michael C., Laynie D. Shebester, and Tim Schedl. "Behavioral Effects of Volatile Anesthetics in Caenorhabditis elegans." Anesthesiology 85, no. 4 (1996): 901–12. http://dx.doi.org/10.1097/00000542-199610000-00027.

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Background The nematode Caenorhabditis elegans offers many advantages as a model organism for studying volatile anesthetic actions. It has a simple, well-understood nervous system; it allows the researcher to do forward genetics; and its genome will soon be completely sequenced. C. elegans is immobilized by volatile anesthetics only at high concentrations and with an unusually slow time course. Here other behavioral dysfunctions are considered as anesthetic endpoints in C. elegans. Methods The potency of halothane for disrupting eight different behaviors was determined by logistic regression o

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Mason, Peggy, Casey A. Owens, and Donna L. Hammond. "Antagonism of the Antinocifensive Action of Halothane by Intrathecal Administration of GABA-A Receptor Antagonists." Anesthesiology 84, no. 5 (1996): 1205–14. http://dx.doi.org/10.1097/00000542-199605000-00023.

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Background The hind brain and the spinal cord, regions that contain high concentrations of gamma-aminobutyric acid (GABA) and GABA receptors, have been implicated as sites of action of inhalational anesthetics. Previous studies have established that general anesthetics potentiate the effects of gamma-aminobutyric acid at the GABAA receptor. It was therefore hypothesized that the suppression of nocifensive movements during anesthesia is due to an enhancement of GABAA receptor-mediated transmission within the spinal cord. Methods Rats in which an intrathecal catheter had been implanted 1 week ea

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Hemmings, Hugh C., and Anna I. B. Adamo. "Activation of Endogenous Protein Kinase C by Halothane in Synaptosomes." Anesthesiology 84, no. 3 (1996): 652–62. http://dx.doi.org/10.1097/00000542-199603000-00021.

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Background Protein kinase C is a signal transducing enzyme that is an important regulator of multiple physiologic processes and a potential molecular target for general anesthetic actions. However, the results of previous studies of the effects of general anesthetics on protein kinase C activation in vitro have been inconsistent. Methods The effects of halothane on endogenous brain protein kinase C activation were analyzed in isolated rat cerebrocortical nerve terminals (synaptosomes) and in synaptic membranes. Protein kinase C activation was monitored by the phosphorylation of MARCKS, a speci

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6

Alkire, Michael T., Chris J. D. Pomfrett, Richard J. Haier, et al. "Functional Brain Imaging during Anesthesia in Humans." Anesthesiology 90, no. 3 (1999): 701–9. http://dx.doi.org/10.1097/00000542-199903000-00011.

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Background Propofol and isoflurane anesthesia were studied previously with functional brain imaging in humans to begin identifying key brain areas involved with mediating anesthetic-induced unconsciousness. The authors describe an additional positron emission tomography study of halothane's in vivo cerebral metabolic effects. Methods Five male volunteers each underwent two positron emission tomography scans. One scan assessed awake-baseline metabolism, and the other scan assessed metabolism during halothane anesthesia titrated to the point of unresponsiveness (mean +/- SD, expired = 0.7+/-0.2%

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7

VARMA, R. R., R. C. WHITESELL, and M. M. ISKANDARANI. "Halothane Hepatitis Without Halothane." Survey of Anesthesiology 30, no. 4 (1986): 205. http://dx.doi.org/10.1097/00132586-198608000-00027.

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8

Conn, Harold O., and Jonas Skornicki. "Halothane hepatitis sans halothane." Hepatology 5, no. 6 (1985): 1238–40. http://dx.doi.org/10.1002/hep.1840050631.

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9

SATHER, A. P., A. L. SCHAEFER, A. K. W. TONG, C. GARIÉPY, and S. M. ZAWADSKI. "MUSCLE AND RECTAL TEMPERATURE RESPONSE CURVES TO A SHORT-TERM HALOTHANE CHALLENGE IN EIGHT-WEEK-OLD PIGLETS WITH KNOWN GENOTYPE AT THE HALOTHANE LOCUS." Canadian Journal of Animal Science 70, no. 1 (1990): 9–14. http://dx.doi.org/10.4141/cjas90-002.

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Each of the three genotypes (NN: normal, halothane negative; Nn: carrier, halothane negative; nn: halothane sensitive) at the halothane locus had a significantly different muscle temperature response curve to a 3-min halothane challenge, while only halothane positive (H+) and negative H−) phenotypes could be distinguished on the basis of the rectal temperature response curves. However, the among animal variation precludes its use as a diagnostic tool for the identification of heterozygous and homozygous normal among halothane negative pigs. Key words: Temperature, halothane gene, swine, genoty

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10

Spencer, G. E., N. I. Syed, K. Lukowiak, and W. Winlow. "Halothane-induced synaptic depression at both in vivo and in vitro reconstructed synapses between identified Lymnaea neurons." Journal of Neurophysiology 74, no. 6 (1995): 2604–13. http://dx.doi.org/10.1152/jn.1995.74.6.2604.

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1. In the present study we tested the ability of the general anesthetic, halothane, to affect synaptic transmission at in vivo and in vitro reconstructed peptidergic synapses between identified neurons of Lymnaea stagnalis. 2. An identified respiratory interneuron, visceral dorsal 4 (VD4), innervates a number of postsynaptic cells in the central ring ganglia of Lymnaea. Because VD4 has previously been shown to exhibit immunoreactivity for FMRFamide-related peptides, it was hypothesized that these peptides may be utilized by VD4 during synaptic transmission. In the intact, isolated CNS of Lymna

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11

&NA;. "Halothane see Enflurane/halothane/isoflurane." Reactions Weekly &NA;, no. 351 (1991): 6. http://dx.doi.org/10.2165/00128415-199103510-00028.

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12

Staunton, Michael, Cathy Drexler, Phillip G. Schmid, Heather S. Havlik, Antal G. Hudetz, and Neil E. Farber. "Neuronal Nitric Oxide Synthase Mediates Halothane-induced Cerebral Microvascular Dilation." Anesthesiology 92, no. 1 (2000): 125. http://dx.doi.org/10.1097/00000542-200001000-00023.

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Background The causes of volatile anesthetic-induced cerebral vasodilation include direct effects on smooth muscle and indirect effects via changes in metabolic rate and release of mediators from vascular endothelium and brain parenchyma. The role of nitric oxide and the relative importance of neuronal and endothelial nitric oxide synthase (nNOS and eNOS, respectively) are unclear. Methods Rat brain slices were superfused with oxygenated artificial cerebrospinal fluid. Hippocampal arteriolar diameters were measured using computerized videomicrometry. Vessels were preconstricted with prostaglan

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13

Hassall, Eric, David M. Israel, Thirumazhisai Gunasekaran, and David Steward. "Halothane Hepatitis in Children." Journal of Pediatric Gastroenterology and Nutrition 11, no. 4 (1990): 553–57. http://dx.doi.org/10.1002/j.1536-4801.1990.tb10165.x.

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Halothane hepatitis is now a well‐recognized distinct entity in adults, but there prevails an often‐taught “axiom” that halothane hepatitis “does not occur” in children. We describe 2 children who developed cholestatic hepatitis following halothane anesthesia. The first patient had no antecedent liver disease, and presented with anorexia, abdominal pain and delayed onset of jaundice after multiple halothane exposures. Halothane‐specific antibodies were positive, and liver tests resolved completely. The second patient had antecedent liver disease and presented with delayed onset of unexplained

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14

Sudo, Roberto T., Gisele Zapata, and Guilherme Suarez-Kurtz. "Studies of the halothane-cooling contractures of skeletal muscle." Canadian Journal of Physiology and Pharmacology 65, no. 4 (1987): 697–703. http://dx.doi.org/10.1139/y87-115.

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The characteristics of transient contractures elicited by rapid cooling of frog or mouse muscles perfused in vitro with solutions equilibrated with 0.5–2.0% halothane are reviewed. The data indicate that these halothane-cooling contractures are dose dependent and reproducible, and their amplitude is larger in muscles containing predominantly slow-twitch type fibers, such as the mouse soleus, than in muscles in which fast-twitch fibers predominate, such as the mouse extensor digitorum longus. The halothane-cooling contractures are potentiated in muscles exposed to succinylcholine. The effects o

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15

Schmidt, Ulrich, Robert H. G. Schwinger, and Michael Bohm. "Interaction of Halothane with Inhibitory G-proteins in the Human Myocardium." Anesthesiology 83, no. 2 (1995): 353–60. http://dx.doi.org/10.1097/00000542-199508000-00016.

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Background Halothane has been reported to possess a catecholamine-sensitizing effect in laboratory animals and in anesthetized patients and to enhance the positive inotropic effect of isoproterenol in human papillary muscle strips. The current study was designed to investigate further the underlying subcellular mechanisms on human myocardium, in particular the mechanism of action of halothane on G-proteins. Methods To investigate the effect of halothane on adenylyl cyclase activity, isoproterenol-, guanylylimidodiphosphate (Gpp(NH)p)-, and forskolin-activated enzyme activities were studied alo

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16

SATHER, A. P., and A. C. MURRAY. "THE DEVELOPMENT OF A HALOTHANE-SENSITIVE LINE OF PIGS." Canadian Journal of Animal Science 69, no. 2 (1989): 323–31. http://dx.doi.org/10.4141/cjas89-036.

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A halothane-sensitive line of pigs was developed from a Pietrain-Lacombe synthetic line through selection of breeding stock based on their sensitivity to a 4 min, 4.5% halothane challenge. It appears that halothane sensitivity is inherited by a single, autosomal recessive allele (n), that is essentially fully penetrant (0.98) in halothane-sensitive pigs (nn). The gene was fixed within four cycles of selection. Segregation at the halothane locus among the two sexes provided no evidence to suggest differential mortality between the sexes and fit inheritance patterns typical of an autosomal locus

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17

Diaz-Sylvester, Paula L., Maura Porta, and Julio A. Copello. "Halothane modulation of skeletal muscle ryanodine receptors: dependence on Ca2+, Mg2+, and ATP." American Journal of Physiology-Cell Physiology 294, no. 4 (2008): C1103—C1112. http://dx.doi.org/10.1152/ajpcell.90642.2007.

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Malignant hyperthermia (MH) susceptibility is a genetic disorder of skeletal muscle associated with mutations in the ryanodine receptor isoform 1 (RyR1) of sarcoplasmic reticulum (SR). In MH-susceptible skeletal fibers, RyR1-mediated Ca2+ release is highly sensitive to activation by the volatile anesthetic halothane. Indeed, studies with isolated RyR1 channels (using simple Cs+ solutions) found that halothane selectively affects mutated but not wild-type RyR1 function. However, studies in skeletal fibers indicate that halothane can also activate wild-type RyR1-mediated Ca2+ release. We hypothe

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18

Gallant, Esther M., and William E. Rempel. "Porcine malignant hyperthermia: False negatives in the halothane test." American Journal of Veterinary Research 48, no. 3 (1987): 488–91. https://doi.org/10.2460/ajvr.1987.48.03.488.

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SUMMARY Purebred Pietrain pigs presumed (on the basis of pedigree) to be homozygous for malignant hyperthermia (mh) susceptibility were subjected to a 3% halothane challenge test. A few (6%) pigs that should have been mh susceptible on the basis of parental genotype did not develop muscle rigidity in response to repeated halothane tests. Three of these animals were brought into the laboratory, and muscle biopsy specimens were obtained for in vitro analysis. Bundles of intact muscle cells dissected from biopsy specimens were electrically stimulated, and mechanical responses were monitored durin

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19

Awad, Joseph A., Jean-Louis Horn, L. Jackson Roberts II, and John J. Franks. "Demonstration of Halothane-induced Hepatic Lipid Peroxidation in Rats by Quantification of Flourine2-Isoprostanes." Anesthesiology 84, no. 4 (1996): 910–16. http://dx.doi.org/10.1097/00000542-199604000-00019.

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Background Halothane can be reductively metabolized to free radical intermediates that may initiate lipid peroxidation. Hypoxia and phenobarbital pretreatment in Sprague-Dawley rats increases reductive metabolism of halothane. F(2)-isoprostanes, a novel measure of lipid peroxidation in vivo, were used to quantify halothane-induced lipid peroxidation in rats. Methods Rats were exposed to 1% halothane or 14% O(2) for 2 h. Pretreatments included phenobarbital, isoniazid, or vehicle. Rats also were exposed to halothane, enflurane, and desflurane at 21% O(2). Lipid peroxidation was assessed by mass

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20

Akata, Takashi, and Walter A. Boyle. "Dual Actions of Halothane on Intracellular Calcium Stores of Vascular Smooth Muscle." Anesthesiology 84, no. 3 (1996): 580–95. http://dx.doi.org/10.1097/00000542-199603000-00014.

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Background Halothane has been reported to affect the integrity of intracellular Ca2+ stores in a number of tissues including vascular smooth muscle. However, the actions of halothane on intracellular Ca2+ stores are not yet fully understood. Methods Employing the isometric tension recording method, the action of halothane in isolated endothelium-denuded rat mesenteric arteries under either intact or beta-escinmembrane-permeabilized conditions was investigated. Results Halothane (0.125-5%) produced concentration-dependent contractions in Ca2+ free solution in both intact and membrane-permeabili

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21

Keifer, J. C., H. A. Baghdoyan, and R. Lydic. "Pontine Cholinergic Mechanisms Modulate the Cortical Electroencephalographic Spindles of Halothane Anesthesia." Anesthesiology 84, no. 4 (1996): 945–54. http://dx.doi.org/10.1097/00000542-199604000-00023.

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Background Halothane anesthesia causes spindles in the electroencephalogram (EEG), but the cellular and molecular mechanisms generating these spindles remain incompletely understood. The current study tested the hypothesis that halothane-induced EEG spindles are regulated, in part, by pontine cholinergic mechanisms. Methods Adult male cats were implanted with EEG electrodes and trained to sleep in the laboratory. Approximately 1 month after surgery, animals were anesthetized with halothane and a microdialysis probe was stereotaxically placed in the medial pontine reticular formation (mPRF). Si

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22

&NA;. "Halothane." Reactions Weekly &NA;, no. 721 (1998): 8. http://dx.doi.org/10.2165/00128415-199807210-00024.

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&NA;. "Halothane." Reactions Weekly &NA;, no. 1145 (2007): 11. http://dx.doi.org/10.2165/00128415-200711450-00034.

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&NA;. "Halothane." Reactions Weekly &NA;, no. 445 (1993): 8. http://dx.doi.org/10.2165/00128415-199304450-00034.

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&NA;. "Halothane." Reactions Weekly &NA;, no. 446 (1993): 10. http://dx.doi.org/10.2165/00128415-199304460-00039.

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&NA;. "Halothane." Reactions Weekly &NA;, no. 367 (1991): 8. http://dx.doi.org/10.2165/00128415-199103670-00038.

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&NA;. "Halothane." Reactions Weekly &NA;, no. 401 (1992): 8. http://dx.doi.org/10.2165/00128415-199204010-00032.

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&NA;. "Halothane." Reactions Weekly &NA;, no. 405 (1992): 10. http://dx.doi.org/10.2165/00128415-199204050-00040.

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&NA;. "Halothane." Reactions Weekly &NA;, no. 1217 (2008): 17. http://dx.doi.org/10.2165/00128415-200812170-00054.

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&NA;. "Halothane." Reactions Weekly &NA;, no. 1255 (2009): 17. http://dx.doi.org/10.2165/00128415-200912550-00048.

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&NA;. "Halothane." Reactions Weekly &NA;, no. 298 (1990): 5. http://dx.doi.org/10.2165/00128415-199002980-00024.

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&NA;. "Halothane." Reactions Weekly &NA;, no. 333 (1991): 7. http://dx.doi.org/10.2165/00128415-199103330-00035.

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&NA;. "Halothane." Reactions Weekly &NA;, no. 338 (1991): 5. http://dx.doi.org/10.2165/00128415-199103380-00025.

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&NA;. "Halothane." Reactions Weekly &NA;, no. 363 (1991): 6. http://dx.doi.org/10.2165/00128415-199103630-00025.

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35

ATLEE, JOHN L. "Halothane." Anesthesiology 67, no. 5 (1987): 617–18. http://dx.doi.org/10.1097/00000542-198711000-00001.

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&NA;. "Halothane." Reactions Weekly &NA;, no. 1071 (2005): 9. http://dx.doi.org/10.2165/00128415-200510710-00026.

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37

&NA;. "Halothane." Reactions Weekly &NA;, no. 483 (1994): 7. http://dx.doi.org/10.2165/00128415-199404830-00027.

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38

ASSCHER, A. W. "HALOTHANE." British Journal of Anaesthesia 60, no. 4 (1988): 479. http://dx.doi.org/10.1093/bja/60.4.479.

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39

SPENCE, A. A. "HALOTHANE." British Journal of Anaesthesia 60, no. 4 (1988): 479–80. http://dx.doi.org/10.1093/bja/60.4.479-a.

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ASSCHER, A. W. "HALOTHANE." British Journal of Anaesthesia 61, no. 1 (1988): 123–24. http://dx.doi.org/10.1093/bja/61.1.123-a.

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SPENCE, A. A. "HALOTHANE." British Journal of Anaesthesia 61, no. 1 (1988): 124. http://dx.doi.org/10.1093/bja/61.1.124.

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42

Summers, Frank W. "Halothane." International Anesthesiology Clinics 36, no. 4 (1998): 83–96. http://dx.doi.org/10.1097/00004311-199803640-00009.

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Ball, C., and R. N. Westhorpe. "Halothane." Anaesthesia and Intensive Care 35, no. 2 (2007): 3. http://dx.doi.org/10.1177/0310057x0703500201.

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&NA;. "Halothane see Fentanyl/halothane/vecuronium bromide." Reactions Weekly &NA;, no. 367 (1991): 8. http://dx.doi.org/10.2165/00128415-199103670-00039.

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45

Ludders, John W., Gordon S. Mitchell, and Susan L. Schaefer. "Minimum anesthetic dose and cardiopulmonary dose response for halothane in chickens." American Journal of Veterinary Research 49, no. 6 (1988): 929–32. https://doi.org/10.2460/ajvr.1988.49.06.929.

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SUMMARY The minimum anesthetic dose (mad) and the cardiopulmonary dose-response for halothane were determined in male chickens. The mad for halothane was 0.85 ± 0.09% (mean ± sd), with a range of 0.75% to 0.98%. There was a significant (P < 0.002) positive correlation between increasing concentrations of halothane and Paco2, and significant negative correlations of halothane concentration with respiratory rate (P < 0.04), arterial blood pH (P < 0.008), and mean arterial blood pressure P < 0.008). A significant correlation was not found between halothane concentration and heart rate

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46

Pabelick, Christina M., Yedatore S. Prakash, Mathur S. Kannan, David O. Warner, and Gary C. Sieck. "Effects of Halothane on Sarcoplasmic Reticulum Calcium Release Channels in Porcine Airway Smooth Muscle Cells." Anesthesiology 95, no. 1 (2001): 207–15. http://dx.doi.org/10.1097/00000542-200107000-00032.

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Background Volatile anesthetics relax airway smooth muscle (ASM) by altering intracellular Ca2+ concentration ([Ca2+]i). The authors hypothesized that relaxation is produced by decreasing sarcoplasmic reticulum Ca2+ content via increased Ca2+ "leak" through both inositol trisphosphate (IP3) and ryanodine receptor channels. Methods Enzymatically dissociated porcine ASM cells were exposed to acetylcholine in the presence or absence of 2 minimum alveolar concentration (MAC) halothane, and IP3 levels were measured using radioimmunoreceptor assay. Other cells were loaded with the Ca2+ indicator flu

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Minoda, Yuko, and Evan D. Kharasch. "Halothane-dependent Lipid Peroxidation in Human Liver Microsomes Is Catalyzed by Cytochrome P4502A6 (CYP2A6)." Anesthesiology 95, no. 2 (2001): 509–14. http://dx.doi.org/10.1097/00000542-200108000-00037.

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Background Halothane is extensively (approximately 50%) metabolized in humans and undergoes both oxidative and reductive cytochrome P450-catalyzed hepatic biotransformation. Halothane is reduced under low oxygen tensions by CYP2A6 and CYP3A4 in human liver microsome to an unstable free radical, and then to the volatile metabolites chlorodifluoroethene (CDE) and chlorotrifluoroethane (CTE). The free radical is also thought to initiate lipid peroxidation. Halothane-dependent lipid peroxidation has been shown in animals in vitro and in vivo but has not been evaluated in humans. This investigation

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48

Rezaiguia-Delclaux, Saida, Christian Jayr, Deng Feng Luo, Nor-Eddine Saidi, Michel Meignan, and Philippe Duvaldestin. "Halothane and Isoflurane Decrease Alveolar Epithelial Fluid Clearance in Rats." Anesthesiology 88, no. 3 (1998): 751–60. http://dx.doi.org/10.1097/00000542-199803000-00027.

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Background Active sodium transport is the primary mechanism that drives alveolar fluid clearance. In the current study, the effects of exposure to halothane and isoflurane on alveolar fluid clearance in rats were evaluated. Methods Rats were exposed to either halothane (0.4% for 6 h or 2% for 2 h) or isoflurane (0.6% for 6 h or 2.8% for 2 h). Reversibility of halothane effects was assessed after 2 h of exposure to 2% halothane. Alveolar and lung liquid clearance were measured by intratracheal instillation of a 5% albumin solution with 1.5 microCi of 125I-albumin, during mechanical ventilation

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Matsumoto, Mishiya, Yasuhiko Iida, Takafumi Sakabe, Takanobu Sano, Toshizo Ishikawa, and Kazuhiko Nakakimura. "Mild and Moderate Hypothermia Provide Better Protection than a Burst-suppression Dose of Thiopental against Ischemic Spinal Cord Injury in Rabbits." Anesthesiology 86, no. 5 (1997): 1120–27. http://dx.doi.org/10.1097/00000542-199705000-00016.

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Background Controversy exists over the efficacy of different methods for protecting the spinal cord against experimental ischemic injury. Therefore, the authors compared the protective effects of thiopental with those of hypothermia (35 degrees C and 32 degrees C) on hindlimb motor functions and histopathology after transient spinal cord ischemia. Methods Twenty-seven New Zealand white rabbits were assigned to one of the four groups: a thiopental-normothermia group (burst-suppression dose of thiopental; esophageal temperature = 38 degrees C; n = 7), a halothane-mild hypothermia group (halothan

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50

Grosenbaugh, D. A., and W. W. Muir. "Cardiorespiratory effects of sevoflurane, isoflurane, and halothane anesthesia in horses." American Journal of Veterinary Research 59, no. 1 (1998): 101–6. http://dx.doi.org/10.2460/ajvr.1998.59.01.101.

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SUMMARY Objective To determine and compare cardiorespiratory and recovery effects of sevoflurane, isoflurane, and halothane in horses. Animals 8 clinically normal horses (4 mares, 4 geldings), 5 to 12 years old. Procedure Inhalation anesthesia was maintained for 90 minutes with sevoflurane, isoflurane, or halothane. Anesthesia depth was maintained at 1.5 minimum alveolar concentration of halothane, isoflurane, and sevoflurane, then was reduced at 30 and 60 minutes. A surgical plane of anesthesia was reinduced by administration of ketamine or thiopental or by increasing the fractional inspired

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