Reliability and validity of the Self-Reflection and Insight Scale for psychologists and the development and validation of the revised short version.

Self-reflection is broadly considered a core competency for psychologists; however, there is an absence of measures of self-reflection, limiting the extent to which self-reflection can be assessed in both research and practice contexts. Whilst the Self-Reflection and Insight Scale (Grant et al., 2002) has been validated in a range of formats with different populations, it has not yet been validated with psychologists. Further, the psychometric properties of a short version of the scale (Silvia, 2021) have not been examined for use with psychologists. This study tested the factor structure, internal consistency and convergent and divergent validity of the Self-Reflection and Insight Scale with registered psychologists (N = 123), finding both the full scale and short version to have sound psychometrics. However, as there were low loading items across both versions of the measure, and the short version also excluded high-loading items, the SRIS-Revised (SRIS-R) was formed through model improvement, retaining a total of 14 items. This revised version of the scale captures high loading items without redundancy of low-loading items, resulting in a measure that parsimoniously captures the construct of self-reflection as relevant to psychologists. The SRIS-R demonstrated good internal consistency (α = .882), convergent, divergent and construct validity. Scores on the SRIS-R were used to test whether there was a correlation between self-reflection and years of professional registration, with this not being significant.

Efficacy of single-dose intravenous phenylbutazone and flunixin meglumine before, during and after exercise in an experimental reversible model of foot lameness in horses.

REASONS FOR PERFORMING STUDY: Objective blinded efficacy data during exercise are lacking on the use of single-dose i.v. nonsteroidal anti-inflammatory drugs (NSAIDs) before, during and after exercise. HYPOTHESIS: Single i.v. doses of either phenylbutazone (PBZ) or flunixin meglumine (FM) would prove more efficacious than negative saline control (SAL) before, during and after exercise in a reversible model of foot lameness. METHODS: Six Quarter Horse mares had lameness induced by tightening a set screw against a heart bar shoe 1 h prior to treatment. Randomised blinded treatments included PBZ (4.4 mg/kg bwt i.v.), FM (1.1 mg/kg bwt i.v.), and SAL (1 ml/45 kg i.v.). Heart rate and lameness score (LS) were recorded at rest; every 20 min after lameness induction for 5 h and at the end of 2 min treadmill workloads of 2 and 4 m/s. Heart rate was also recorded from 0.5-60 min post exercise. Results were compared using RM ANOVA and Student-Newman-Keul's test (HR) and Wilcoxon signed rank test (%ΔLS) with significance set at P < 0.05. RESULTS: Pre-exercise mean HR was decreased for both NSAIDs compared to SAL from 1:20-4 h post treatment (P < 0.05). Pre-exercise mean %ΔLS was decreased for PBZ (1:20-4 h) and FM (1-4 h) compared to SAL (P < 0.01). With exercise, there were no HR differences between treatments (P > 0.05), but mean %ΔLS was decreased for both NSAIDs compared to SAL (P < 0.01). Mean recovery HR was decreased for PBZ and FM from 1-60 min compared to SAL (P < 0.05). CONCLUSIONS: PBZ and FM demonstrated definitive clinical efficacy after single i.v. doses before, during and after exercise. Use of single i.v. doses during competition may mask lameness and may affect the ability of judges in determining the soundness of horses in competition.

Thermal, but not mechanical, nociceptive behavior is altered in the Zucker Diabetic Fatty rat and is independent of glycemic status.

This study investigated the possible link between developing hyperglycemia and mechanical and/or thermal hyperalgesia in the Zucker Diabetic Fatty (ZDF) rat. When normoglycemic (nonfasting blood glucose levels of 6 mM), 6-week-old ZDF rats were glucose intolerant compared to the nondiabetic Zucker lean control (ZL) rats, but there was no difference in their response to a noxious mechanical (paw pressure test) or thermal (hot plate) stimulus (mechanical nociceptive thresholds: ZDF 176.7+/-14.4 g, ZL 161.7+/-13.3 g; latencies to response to the thermal stimulus: ZDF 13.1+/-1.6 sec, ZL 16.7+/-1.5 sec). Blood glucose levels in untreated ZDF rats increased to 28.4+/-2.9 mM by 20 weeks of age, while ZDF rats treated with the insulin sensitizer, rosiglitazone, and ZL rats remained normoglycemic (< or =8 mM) throughout the study. Hyperglycaemia in ZDF rats was not associated with mechanical hyperalgesia, as the nociceptive threshold remained constant in both the rosiglitazone-treated and untreated ZDF rats and in the ZL rats throughout the study. In contrast, the latency to response to the thermal stimulus increased with time in ZL rats, but remained constant in hyperglycaemic ZDF rats such that the difference reached significance by 9 weeks of age (ZDF 11.6+/-1.7 sec, ZL 21.8+/-2.7 sec, p<0.01) and is consistent with hyperalgesia in the ZDF phenotype. However, this difference was not moderated by maintaining normoglycaemia in rosiglitazone-treated ZDF rats (12.8+/-1.3 sec). Together, the data suggest that hyperglycemia does not play a central role in the development of hyperalgesia in the ZDF rat.

5-HT4 receptor antagonism potentiates inhibition of intestinal allodynia by 5-HT3 receptor antagonism in conscious rats.

Acute levels of distension were applied by balloon to the colo-rectal region in conscious rats and visceromotor responses observed as abdominal muscle contraction; the threshold was typically between 10-40 mmHg. In saline-pretreated rats, the selective 5-HT3 (granisetron) and 5-HT4 (SB-207266) receptor antagonists had no effects on the visceromotor thresholds. 5-Hydroxytryptophan 10 mg/kg, subcutaneously (s.c.) decreased the distension threshold, indicating mechanical allodynia. This increased sensitivity was dose-dependently inhibited by granisetron but was unaffected by SB-207266 100 microg/kg, s.c., a dose which maximally and selectively antagonizes at 5-HT4 receptors. However, this dose of SB-207266 potentiated the inhibitory activity of submaximally-effective doses of granisetron, reducing the ED50 from 0.83 to 0.02 microg/kg, s.c., but without changing the maximum response or the bell-shaped nature of the dose-response curve for granisetron. These data suggest that 5-HT4 receptor activation enhances the ability of 5-HT3 receptor activation to induce intestinal allodynia.

SB-207266: 5-HT4 receptor antagonism in human isolated gut and prevention of 5-HT-evoked sensitization of peristalsis and increased defaecation in animal models.

SB-207266 is a new 5-HT4 receptor antagonist which in a pilot study reduced the symptoms of irritable bowel syndrome. To help validate this and further studies, we examined the ability of SB-207266 to antagonize at the human 5-HT4 receptor (human isolated intestine) and to affect the mechanisms of peristalsis (guinea-pig isolated ileum) and defaecation (conscious, fed mice). In the human intestine, the potency of 5-HT4 receptor antagonism (pKB 9.98) was similar to that previously demonstrated using a guinea-pig model of the receptor, validating the use of SB-207266 in clinical trials. In each of the animal models, SB-207266 did not affect normal patterns of intestinal motility measured in the absence of exogenous 5-HT. However, SB-207266 10-1000 pM concentration-dependently antagonized the ability of 5-HT (0.1 microM) to sensitize the peristaltic reflex and lower the distension threshold at which peristalsis was evoked. In mice, oral or subcutaneous (s.c.) doses of SB-207266 dose-dependently prevented the ability of the 5-HT precursor, 5-hydroxytryptophan (5-HTP, 10 mg kg-1 s.c.) to increase both the rate of defaecation of formed faecal pellets and their fluid content. SB-207266 was maximally active at 10 micrograms kg-1 s.c. and 1000 micrograms kg-1 p.o. SB-207266 may therefore represent a new class of therapeutic agent, capable of preventing the actions of an important sensitizer of gut function.

Increased defaecation caused by 5-HT4 receptor activation in the mouse.

The precursor to 5-hydroxytryptamine (5-HT), 5-hydroxytryptophan, (5-HTP, 5-50 mg.kg-1) administered subcutaneously (s.c.) to conscious, fed mice caused a dose dependent increase in faecal pellet and fluid output. To avoid provoking watery diarrhoea, all experiments were performed using 5-HTP at 10 mg.kg-1. This dose caused maximal increases in the fluid content (471 +/- 41%) and number of formed faecal pellets defaecated (328 +/- 13% n = 25), 10 and 20 min respectively after administration, when compared to saline-treated mice. In both saline- and 5-HTP-treated mice methiothepin, ketanserin, mianserin and granisetron reduced defaecation at high s.c. doses (100 micrograms.kg-1 or 1000 micrograms.kg-1). The 5-HT4 receptor antagonists, DAU 6285 (endo-6-methoxy-8-methyl-8-azabicyclo[3.2.1]oct-3-yl-2,3-dihydro-2-oxo-1 H-benzimidazole-1-carboxylate hydrochloride), SDZ 205-557 (2-methoxy-4-amino-5-chloro-benzoic acid 2-(diethylamino) ethyl ester) and SB 204070 ([1-butyl-4-piperidinylmethyl]-8-amino-7-chloro-1,4-benzodioxan -5- carboxylate), had no effects when administered s.c. to saline-treated mice, but dose-dependently inhibited the 5-HTP-evoked responses. Only SB 204070 at 1000 micrograms.kg-1 completely inhibited the responses to 5-HTP returning them to normal levels. We conclude that SB 204070 is a potent antagonist for the investigation of 5-HT4 receptor function in both normal and disturbed gastrointestinal activity.

5-Hydroxytryptamine3 receptor antagonism modulates a noxious visceral pseudoaffective reflex.

5-Hydroxytryptamine (5-HT) receptor agonists and antagonists were dosed intravenously (i.v.) and studied for their effects on the depressor cardiovascular pseudoaffective reflex evoked by acute noxious colo-rectal distension in the anaesthetized rat. Methiothepin (100 micrograms kg-1) caused an initial, unsustained blockade of evoked depressor responses whilst ketanserin (100 micrograms kg-1) was without effect. By comparison, ondansetron dose dependently inhibited evoked depressor responses and was maximally active at 100 micrograms kg-1, causing a 57.5 +/- 0.9% reduction. An ID50 value of 36.7 micrograms kg-1 was estimated by regression analysis. In contrast, granisetron caused complete blockade of the depressor response with an ID50 of 0.4 microgram kg-1. Bell-shaped dose-effect curves were demonstrated for both granisetron and ondansetron. Intrathecal dosing with granisetron (100 ng) into the thoracolumbar region of the spinal cord prevented the depressor response to colo-rectal distension, suggesting a spinal site of action. The pseudoaffective depressor responses were not facilitated by pre-dosing with the 5-HT receptor agonists, 8-OH DPAT, alpha-methyltryptamine or 1-phenyl-biguanide. However, 8-OH DPAT (100 micrograms kg-1) facilitated pressor responses. It is suggested that 5-HT3-like receptors may have a role in modulating depressor responses to visceral pain and that in this action different 5-HT3 receptor antagonists are not necessarily equi-effective.

Differences between 5-HT3 receptor antagonists in modulation of visceral hypersensitivity.

1. Noxious colo-rectal distension was applied in conscious rats by acute balloon inflation and the effects observed as abdominal muscle contraction with the threshold typically between 10-40 mmHg. The effects of 5-HT3 receptor antagonists on responses to noxious colo-rectal distension were then studied in both normal rats and those pretreated with 5-hydroxytryptophan (5-HTP). 2. Granisetron and ondansetron (10 micrograms kg-1 and 1 mg kg-1, s.c.) had no effect on visceromotor thresholds to colo-rectal distension in normal rats. 3. Hypersensitivity of the colo-rectum was achieved by systemic administration of a low dose of 5-HTP (10 mg kg-1, s.c.) which lowered the distension pressure required to induce the visceromotor reflex; analysis of variance showed a highly significant treatment effect (F1,11 = 84.26, P < 0.001). 4. Granisetron, zatosetron, bemesetron and renzapride equi-potently increased the threshold values at which distension evoked a visceromotor reflex after dosing with 5-HTP, with a maximal response 3.6 to 4.2 fold above saline controls, at 10 micrograms kg-1, s.c. Metoclopramide (10 micrograms kg-1) also raised the level of distension required to elicit a response. By comparison, tropisetron caused a small, non-significant increase in visceromotor threshold values and only at high doses (1 mg kg-1), whilst ondansetron and BRL 46470 had no significant effects at doses up to 10 mg kg-1. 5. The response to granisetron (10 micrograms kg-1, s.c.) in 5-HTP-treated rats was unaltered by pre-administration of naloxone (5 mg kg-1, s.c.). 6. These results suggest that a 5-HT3-like receptor modulates 5-HTP- evoked visceral hypersensitivity.However, the rank order of antagonist potency does not correlate with their order of potency against the classically defined 5-HT3 receptor.

Effects of FMRFamide-related peptides and morphine on the isolated foregut of the locust Schistocerca gregaria.

1. Morphine and YAGFMamide were the most effective potentiators of 5-hydroxytryptamine (5-HT)-induced relaxation of the isolated foregut. 2. Morphine had no effect on proctolin-induced tissue contraction which was inhibited by YGGFMamide and YFMRFamide. 3. The differing potency of FaRPs and morphine to potentiate 5-HT effects and reduce proctolin responses suggests that there are two separate FaRP receptor sub types. 4. This proposal is supported by the observation that, while naloxone (10(-5) M) is a relatively potent antagonist of FaRP induced inhibition of proctolin contraction, it has less effect on FaRP-induced potentiation of 5-HT-induced relaxation.

Tyramine antagonizes proctolin-induced contraction of the isolated foregut of the locust Schistocerca gregaria by an interaction with octopamine2 receptors.

1. Octopamine (OA) (10(-7)-10(-5) M) relaxed isolated foreguts. Tyramine mimicked the effects of OA but was 64x less potent. 2. Proctolin (10(-8) M to 10(-6) M) induced contraction of isolated foreguts was antagonised non competitively by tyramine. 3. Mianserin (10(-6) M) was a non competitive antagonist of relaxation caused by tyramine but was without effect on proctolin induced contraction. 4. Caffeine (1 microM and 2 microM) caused non competitive inhibition of proctolin-induced tissue contraction. 5. It is concluded that tyramine antagonises proctolin-induced contraction of the foregut by activating an adenylate cyclase-linked OA2 receptor.