Infants' Dermatitis Quality of Life Index: a decade of experience of validation and clinical application.

The Infants' Dermatitis Quality of Life Index (IDQoL) is a questionnaire completed by parents to assess the impact of atopic dermatitis on the quality of life of infants aged 0-3 years. The aim was to review all clinical and psychometric data on the use of the IDQoL from its inception in 2001 until November 2012, to serve as a single reference source. A literature search was carried out using Medline, PubMed, EBSCOhost, Science Direct and Google Scholar. Articles and abstracts that described the clinical use of the IDQoL and those that investigated its psychometric properties were included. Articles not in English were excluded. Fifty-one publications were identified, of which 46 fulfilled the inclusion criteria. IDQoL data relating to psychometric, descriptive and clinical practice research, drug trials and therapeutic interventions were extracted. The IDQoL has been translated into 21 languages and used in 18 countries, including two multinational studies. Thirty-one studies demonstrated its psychometric properties, such as test-retest reliability, internal consistency, validity, responsiveness to change and interpretability. No studies investigated dimensionality, carried out factor analysis or described the minimal clinically important difference of the tool. Eight studies used the IDQoL to assess the effectiveness of therapeutic interventions such as education programmes, consultations and wet-wrap therapy, while seven studies described the use of IDQoL in topical interventions. When deciding whether to use the IDQoL, researchers and clinicians should consider the validation data, the relevant comparative clinical data available and the potential burden on the respondents.

Carcinoma of the breast wire localisation post nuclear medicine sentinel lymph node imaging. Are radiologists receiving a significant dose?

OBJECTIVE: To assess the radiation dose received by the radiologist when performing wire localisation for axillary radio-isotope sentinel node imaging-guided biopsy in patients with impalpable breast cancers treated with breast-preserving excision. When wire placement follows radio-isotope sentinel node imaging (RSNI) the radiologist is exposed to a radiation risk that has never been previously assessed. METHODS: Radiation doses to radiologists performing ultrasound-guided localisation following nuclear medicine sentinel node imaging were measured for procedures on the day of surgery (20 MBq) and also on the day before surgery (40 MBq). These measurements were compared with theoretically calculated doses. RESULTS: Twelve patients showed comparable results between measurements and estimated doses. The mean measured dose was 1.8 muSv (estimated 1.8 muSv) for same-day and 4.8 muSv (estimated 3.4 muSv) for next-day surgery cases. At worst, radiologists who perform 36 wire localisations per year immediately following RSNI receive a radiation dose of 0.17 mSv. CONCLUSIONS: This study highlights the need to inform radiologists of the relative risk when performing pre-surgical localisation after RSNI. This risk should be justified locally in accordance with the total dose received by the localising radiologist. Particular consideration should be given to pregnant staff and the possibility of performing wire localisations before radio-isotope injection.

Head-twitch response induced by ergometrine in mice: behavioural evidence for direct stimulation of central 5-hydroxytryptamine receptors by ergometrine.

Ergometrine (2.5-80 mg/kg IP) induced head twitches in mice. Pretreatment with cyproheptadine (1.5 and 3 mg/kg), methysergide (5 and 10 mg/kg) and (-)-propranolol (2.5 and 5 mg/kg) significantly decreased the number of head twitches induced by ergometrine. Pretreatment with p-chlorophenylalanine (100 mg/kg/day X 4 days) and clomipramine (5 and 10 mg/kg) significantly decreased the number of head twitches induced by fenfluramine (10 mg/kg) and p-chloramphetamine (5 mg/kg) but had no significant effect on the number of head twitches induced by ergometrine. The results indicate that ergometrine induces head twitches in mice by directly stimulating central 5-hydroxytryptamine receptors.

Small doses of apomorphine induce catalepsy and antagonize methamphetamine stereotypy in rats.

Small doses of apomorphine (AP, 31.25-125 micrograms/ kg IP) induced dose-dependent catalepsy in rats. However, unlike the stereotyped behavior induced by high doses of AP which has a rapid onset and is short-lasting, the cataleptic effect induced by small doses of AP was evident 30 min after AP injection and was unusually long-lasting. Further, AP (31.25-125 micrograms/kg) administered 60 min before methamphetamine was found to significantly antagonize the methamphetamine-induced stereotyped behavior. Pretreatment with molindone (0.45 and 0.8 mg/kg IP), in doses reported to selectively block the presynaptic DA receptors, not only decreased the cataleptic effect of AP but also reversed the AP antagonism of methamphetamine stereotypy. The results suggest that small doses of AP induce catalepsy and antagonize methamphetamine stereotypy probably by an action at presynaptic DA receptor sites.

Effect of ergometrine on methamphetamine and apomorphine stereotypy in the guinea-pig.

Pretreatment with the DAi receptor antagonist ergometrine (10, 20 mg kg-1 i.p.) significantly potentiated methamphetamine stereotypy and facilitated the induction of biting, gnawing or licking behaviour by amantadine. However, ergometrine (5-20 mg kg-1) did not significantly influence the stereotyped behaviour induced by the DAe receptor agonist apomorphine. The results suggest that the DAi antagonist ergometrine is effective in modifying the behaviours induced by methamphetamine and amantadine, agents which through released DA simultaneously activate both DAe and DAi receptors, but fails to modify the stereotyped behaviour induced by apomorphine which specifically activates only DAe receptors. However, the possibility that ergometrine might have potentiated methamphetamine stereotypy and facilitated the induction of biting, gnawing or licking behaviour by amantadine through modulation of the activity of the central noradrenergic and 5-hydroxytryptaminergic systems, which are reported to influence DA-mediated behaviours, also needs to be considered.

Psychopharmacological investigation of the monoamine oxidase inhibitory activity of molindone, a dihydroindolone neuroleptic.

24 h pretreatment with molindone enhanced the behavioural effects of L-dopa and 5-HTP, precursors of biogenic amines (catecholamines and 5-HT respectively) preferentially deaminated by MAO-A, confirming that a metabolite of molindone inhibits MAO-A. 24 h pretreatment with molindone enhanced the behavioural effects of tryptamine and antagonized reserpine-induced ptosis, and in molindone-pretreated rats L-tryptophan induced behavioural effects, probably because of the MAO-A inhibitory activity exerted by a metabolite of molindone. Since 24 h pretreatment with molindone, unlike 30 min pretreatment with clomipramine, failed to antagonize fenfluramine and p-chloramphetamine-induced behavioural syndromes, it suggests that molindone and/or its metabolites most probably do not exert 5-HT neuronal uptake blocking activity and the potentiation of 5-HTP-induced behavioural syndrome is due to a metabolite's MAO-A inhibitory activity. As 2 h pretreatment with molindone induced catalepsy and antagonized apomorphine-induced climbing behaviour in mice and stereotypy in rats, while 24 h pretreatment failed to induce catalepsy and to antagonize apomorphine-induced behaviour, it appears that, at 24 h, the tissue levels of molindone are inadequate to block postsynaptic striatal and mesolimbic DA receptors and that, though a metabolite of molindone is biologically active so far as inhibition of MAO-A is concerned, the metabolites are devoid of neuroleptic activity. Further, since 2 h pretreatment with molindone failed to enhance the behavioural effects of L-dopa, it suggests that at 2 h the degree of MAO-A inhibition induced by molindone and/or the metabolite is not sufficient to counteract the neuroleptic activity of the parent compound.

Antagonism of apomorphine-induced cage climbing behaviour and methamphetamine stereotypy by fenfluramine in mice.

Pretreatment with fenfluramine (5 and 10 mg/kg, ip) in doses which induced head twitches was found to antagonize apomorphine-induced cage climbing behaviour and methamphetamine stereotypy in mice. Since fenfluramine (5 and 10 mg/kg) did not induce catalepsy it indicates that fenfluramine lacks postsynaptic striatal and mesolimbic dopamine receptor blocking activity and it is possible that the fenfluramine-induced enhancement of central 5-hydroxytryptamine neuronal transmission may be responsible for its antagonistic effect on apomorphine-induced climbing behaviour and methamphetamine stereotypy.

Effect of alpha-methyl-p-tyrosine on neuroleptic-induced catalepsy in rat.

Pretreatment with alpha-methyl-p-tyrosine, a tyrosine hydroxylase inhibitor, was found to increase the intensity of catalepsy induced by haloperidol, chlorpromazine and molindone. The drug probably decreases the synthesis of dopamine and makes less dopamine available for release and to compete with the neuroleptic for the postsynaptic striatal dopamine receptor sites with resultant potentiation of the neuroleptic-induced catalepsy.

Antagonism of bromocriptine-induced cage climbing behaviour in mice by the selective D-2 dopamine receptor antagonists, metoclopramide and molindone.

Bromocriptine (5-30 mg/kg, ip), 2 hr after administration, induced cage climbing behaviour in mice. Pretreatment with haloperidol, an antagonist of both D-1 and D-2 dopamine receptors, metoclopramide and molindone, the selective D-2 dopamine receptor antagonists, effectively antagonised bromocriptine-induced climbing behaviour. The results indicate that bromocriptine most probably induces climbing behaviour in mice by stimulating the postsynaptic striatal D-2 dopamine receptors.

Variation of mesorectal volume with abdominal fat volume in patients with rectal carcinoma: assessment with MRI.

The purpose of this study was to assess the variability in the volume of the mesorectum in patients with rectal carcinoma. A retrospective review was made of pelvic MRI studies in 30 patients (mean age 64 years, range 34-88 years, 18M:12F) with histologically proven rectal carcinomas that were confined to the mesorectum. The outer low signal margin of the mesorectum was traced, over at least 10 consecutive 10 mm contiguous slices, until its disappearance. The visceral fascial compartment, body cross-sectional area and body mass index were measured, on a solitary slice, at the level of the L5/S1 disc. Linear regression was calculated for independent determinants of the mesorectal volume. Mean mesorectal volume in males was 227.5 cm3 (95%CI 191.6-263.4), and in females was 157.5 cm3 (95%CI 129.3-185.7). The difference in mesorectal volume between men and women was statistically significant (p<0.001). Mean visceral compartment area in males was 18.4 cm2 (95%CI 16.3-20.5) and in females was 14.6 cm2 (95%CI 12.8-16.4). Visceral compartment area correlated with mesorectal area and volume in females (p<0.05), and extremely well in males (p<0.005). Body cross-sectional area, body mass index and age did not correlate with mesorectal size. The correlation of visceral compartment area with mesorectal volume and mean area suggests that the mesorectum is determined in a similar way to other body fat compartments, with a similar anatomical variation. This significant variation in size and volume may have an important prognostic implication in patients with rectal carcinoma. This volume can be measured and reported on pre-operative MRI scanning and may be communicated to surgeons and radiotherapists.