WordNet

the property of being flexible; easily bent or shaped (同)flexibleness
the quality of being adaptable or variable; "he enjoyed the flexibility of his working arrangement" (同)flexibleness
wrap up in a cerecloth; "cere a corpse"
the fleshy, waxy covering at the base of the upper beak of some birds

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柔軟性,しなやかさ;適応性,融通性

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2021/03/17 17:35:38」(JST)

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Waxy flexibility is a psychomotor symptom of catatonia as associated with schizophrenia, bipolar disorder, or other mental disorders^[1] which leads to a decreased response to stimuli and a tendency to remain in an immobile posture.^[2] Attempts to reposition the patient are met by "slight, even resistance", and after being repositioned, the patient will typically remain in the new position.^[3] Waxy flexibility rarely occurs in cases of delirium.^[4] The presence of waxy flexibility along with at least two other catatonic symptoms such as stupor or negativism are enough to warrant a diagnosis of catatonia.^[5]

If one were to move the arm of someone with waxy flexibility, the patient would keep that arm where it had been positioned until moved again, as if positioning malleable wax. Further alteration of an individual's posture is similar to bending a candle.^[6] Although waxy flexibility has historically been linked to schizophrenia, there are also other disorders which it may be associated with, such as mood disorders with catatonic behaviour.^[7]

Electroconvulsive therapy is often used as a treatment for catatonia.^[8] A study has found that catatonic patients with waxy flexibility responded faster to electroconvulsive therapy, compared to patients with other symptoms of catatonia.^[9]

References

^ Ungvari GS, Goggins W, Leung SK, Lee E, Gerevich J (February 2009). "Schizophrenia with prominent catatonic features ('catatonic schizophrenia') III. Latent class analysis of the catatonic syndrome". Prog. Neuropsychopharmacol. Biol. Psychiatry. 33 (1): 81–5. doi:10.1016/j.pnpbp.2008.10.010. PMID 18992297.
^ Definition – Online Medical Dictionary
^ Barlow, D. H., & Durand, V. Mark. (2015). Abnormal Psychology: An Integrative Approach. Stamford, CT: Cengage Learning, p. 485
^ Regal, P. (2017). Malignant Catatonia Versus Delirium. American Journal of Medicine, 130(1), e33. doi:10.1016/j.amjmed.2016.07.033
^ Barlow, D. H., & Durand, V. Mark. (2015). Abnormal Psychology: An Integrative Approach. Stamford, CT: Cengage Learning, p. 485
^ Caroff, Stanley N.; Mann, Stephan C. (2007). Catatonia: From Psychopathology to Neurobiology. American Psychiatric Pub. p. 51. ISBN 9781585627127.
^ American Psychiatric Association (2000) Diagnostic and statistical manual of mental disorders (DSM-IV TR) 4th edition. USA: American Psychiatric Association
^ Raveendranathan, D., Narayanaswamy, J., & Reddi, S. (2012). Response rate of catatonia to electroconvulsive therapy and its clinical correlates. European Archives Of Psychiatry & Clinical Neuroscience, 262(5), 425.
^ Raveendranathan, D., Narayanaswamy, J., & Reddi, S. (2012). Response rate of catatonia to electroconvulsive therapy and its clinical correlates. European Archives Of Psychiatry & Clinical Neuroscience, 262(5), 429.

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English Journal

The potency and efficacy of anticholinergics to inhibit haloperidol-induced catalepsy in rats correlates with their rank order of affinities for the muscarinic receptor subtypes.

Erosa-Rivero HB1, Bata-García JL1, Alvarez-Cervera FJ1, Heredia-López FJ1, Góngora-Alfaro JL2.Author information 1Departamento de Neurociencias, Centro de Investigaciones Regionales "Dr. Hideyo Noguchi", Universidad Autónoma de Yucatán, CIR-UADY, Avenida Itzáes No. 490 × 59, Mérida, Yucatán 97000, Mexico.2Departamento de Neurociencias, Centro de Investigaciones Regionales "Dr. Hideyo Noguchi", Universidad Autónoma de Yucatán, CIR-UADY, Avenida Itzáes No. 490 × 59, Mérida, Yucatán 97000, Mexico. Electronic address: jlgongoralf@gmail.com.AbstractExtrapyramidal syndromes (EPS) caused by antipsychotic therapy are currently treated with anticholinergics that lack selectivity for the five muscarinic receptor subtypes. Since these receptors are heterogeneously expressed among the different classes of striatal neurons and their afferents, it can be expected that their simultaneous blockade will cause distinct, sometimes opposed, effects within the striatal circuitry. In order to test the hypothesis that the differential blockade of the muscarinic receptor subtypes would influence their potency and efficacy to prevent EPS, here we tested four anticholinergics with varying order of affinities for the muscarinic receptor subtypes, and compared their dose-response curves to inhibit haloperidol-induced catalepsy in male rats. Drugs were applied into the lateral ventricle 15 min before haloperidol (2 mg/kg, s.c.). Catalepsy was measured in the bar test at 15 min intervals during 5 h. The preferential M1/M4 antagonist pirenzepine (3, 10, 30, 100, and 300 nmol) caused a dose-dependent inhibition of catalepsy intensity: ED50 = 5.6 nmol [95% CI, 3.9-8.1], and latency: ED50 = 5.6 nmol [95% CI, 3.7-8.6]. Pirenzepine had the steepest dose-response curve, producing maximal inhibition (84 ± 5%) at the dose of 10 nmol, while its effect tended to reverse at higher doses (62 ± 11%). The purported M1/M3 antagonist 4-DAMP (30, 100, and 300 nmol) also caused a dose-dependent inhibition of catalepsy intensity: ED50 = 29.5 nmol [95% CI, 7.0 to 123.0], and latency: ED50 = 28.5 nmol [95% CI, 2.2 to 362.0]. However, the curve for 4-DAMP had a less pronounced slope, reaching its maximal effect (63 ± 14%) at the dose of 300 nmol. The M2/M4 antagonist AF-DX 116 (10, 30, and 300 nmol) only caused a partial inhibition of catalepsy (30 ± 11%) at the dose of 30 nmol, but this changed to a non-significant increment (15 ± 10%) at the dose of 100 nmol. The alleged M4 antagonist tropicamide (30, 100, 300, and 600 nmol) produced a partial inhibition of catalepsy (36 ± 12%) at the dose of 300 nmol, but lacked effect at higher or lower doses. Concurrent treatment with pirenzepine (10 nmol) and tropicamide (300 nmol) produced an effect similar to that of tropicamide alone. The greater potency and efficacy of pirenzepine for catalepsy inhibition could be due to its higher affinity for M1 receptors and, to a lesser extent, for M4 receptors. It is suggested that selective M1 antagonists would be more effective than M2, M3 or M4 antagonists to prevent EPS caused by antipsychotic drugs.
Neuropharmacology.Neuropharmacology.2014 Jun;81:176-87. doi: 10.1016/j.neuropharm.2014.02.005. Epub 2014 Feb 15.
Extrapyramidal syndromes (EPS) caused by antipsychotic therapy are currently treated with anticholinergics that lack selectivity for the five muscarinic receptor subtypes. Since these receptors are heterogeneously expressed among the different classes of striatal neurons and their afferents, it can
PMID 24534110

TRR469, a potent A1 adenosine receptor allosteric modulator, exhibits anti-nociceptive properties in acute and neuropathic pain models in mice.

Vincenzi F1, Targa M1, Romagnoli R2, Merighi S1, Gessi S1, Baraldi PG2, Borea PA1, Varani K3.Author information 1Department of Medical Sciences, Pharmacology Section, University of Ferrara, via Fossato di Mortara 17/19, 44121 Ferrara, Italy.2Department of Pharmaceutical Sciences, University of Ferrara, via Fossato di Mortara 17/19, 44121 Ferrara, Italy.3Department of Medical Sciences, Pharmacology Section, University of Ferrara, via Fossato di Mortara 17/19, 44121 Ferrara, Italy. Electronic address: vrk@unife.it.AbstractA1 adenosine receptors (ARs) have been identified as a potential target for the development of anti-nociceptive compounds. The present study explores the analgesic effects of a novel A1AR positive allosteric modulator, TRR469, in different models of acute and chronic pain in mice. To evaluate the allosteric enhancement, in vitro binding experiments were performed. The anti-nociceptive properties were investigated in formalin and writhing tests, and in the streptozotocin-induced diabetic neuropathic pain model. Rotarod and catalepsy tests were used to identify potential side effects, while the functional effect of TRR469 was studied using [(3)H]-d-aspartate release from synaptosomes. TRR469 effectively inhibited nociceptive responses in the formalin and writhing tests, with effects comparable to those of the reference analgesic morphine. Isobolographic analysis of the combination of TRR469 and morphine revealed an additive interaction. TRR469 was anti-allodynic in the neuropathic pain model and did not display locomotor or cataleptic side effects. TRR469 enhanced the binding of the agonist radioligand [(3)H]-CCPA and induced a 33-fold increase of adenosine affinity in spinal cord membranes. In mouse spinal cord synaptosomes, TRR469 enhanced the inhibitory effect of A1AR activation on [(3)H]-d-aspartate release, a non-metabolizable analogue of glutamate. In conclusion, this research demonstrates the anti-nociceptive effect of the novel compound TRR469, one of the most potent and effective A1AR positive allosteric modulators so far synthesized. The use of TRR469 allows for the possibility of exploiting analgesic properties of endogenous adenosine, with a minor potential to develop the various side effects often associated with the use of direct receptor agonists.
Neuropharmacology.Neuropharmacology.2014 Jun;81:6-14. doi: 10.1016/j.neuropharm.2014.01.028. Epub 2014 Jan 31.
A1 adenosine receptors (ARs) have been identified as a potential target for the development of anti-nociceptive compounds. The present study explores the analgesic effects of a novel A1AR positive allosteric modulator, TRR469, in different models of acute and chronic pain in mice. To evaluate the al
PMID 24486382

Actions of the dual FAAH/MAGL inhibitor JZL195 in a murine inflammatory pain model.

Anderson WB1, Gould MJ2, Torres RD2, Mitchell VA2, Vaughan CW2.Author information 1Pain Management Research Institute, Kolling Institute of Medical Research, Northern Clinical School, University of Sydney at Royal North Shore Hospital, St Leonards, NSW 2065, Australia. Electronic address: wayne.anderson@sydney.edu.au.2Pain Management Research Institute, Kolling Institute of Medical Research, Northern Clinical School, University of Sydney at Royal North Shore Hospital, St Leonards, NSW 2065, Australia.AbstractThe analgesic efficacy of cannabinoids in chronic pain models is limited by side-effects. It has been proposed that this might be overcome by using agents which indirectly activate the endocannabinoid system. We examined the analgesic and side-effect profile of the dual FAAH/MAGL inhibitor JZL195 in an inflammatory pain model. The effect of systemic injections of a range of doses of JZL195 and the pan-cannabinoid receptor agonist WIN55212 were performed 1 day following intraplantar injection of CFA in C57BL/6 mice. JZL195 and WIN55212 both reduced mechanical allodynia and thermal hyperalgesia, and produced catalepsy and sedation in a dose dependent manner. Unlike WIN55212, JZL195 reduced allodynia at doses below those at which side-effects were observed. The effects of JZL195 and WIN55212 were abolished by co-application with the CB1 antagonist AM251. The CB2 antagonist also reduced the JZL195 anti-allodynia, and reversed the WIN55212 anti-allodynia. The reduction in allodynia produced by JZL195 was greater than that produced individually by the FAAH and MAGL inhibitors, URB597 and JZL184. These findings suggest that JZL195 reduces inflammation induced allodynia at doses below those which produce side-effects, and displays greater efficacy that FAAH or MAGL inhibitors. Thus, dual FAAH/MAGL inhibition has the potential to alleviate inflammatory pain with reduced cannabinoid-like side-effects.
Neuropharmacology.Neuropharmacology.2014 Jun;81:224-30. doi: 10.1016/j.neuropharm.2013.12.018. Epub 2013 Dec 30.
The analgesic efficacy of cannabinoids in chronic pain models is limited by side-effects. It has been proposed that this might be overcome by using agents which indirectly activate the endocannabinoid system. We examined the analgesic and side-effect profile of the dual FAAH/MAGL inhibitor JZL195 in
PMID 24384256

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