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Biomedical subjects

F Brady

Publications and source records attributed to F Brady.

At least 19 recordsLinked to original sources
PubMed2004

In vivo evaluation of [18F]fluoroetanidazole as a new marker for imaging tumour hypoxia with positron emission tomography.

Development of hypoxia-targeted therapies has stimulated the search for clinically applicable noninvasive markers of tumour hypoxia. Here, we describe the validation of [(18)F]fluoroetanidazole ([(18)F]FETA) as a tumour hypoxia marker by positron emission tomography (PET). Cellular transport and retention of [(18)F]FETA were determined in vitro under air vs nitrogen. Biodistribution and metabolism of the radiotracer were determined in mice bearing MCF-7, RIF-1, EMT6, HT1080/26.6, and HT1080/1-3C xenografts. Dynamic PET imaging was performed on a dedicated small animal scanner. [(18)F]FETA, with an octanol-water partition coefficient of 0.16+/-0.01, was selectively retained by RIF-1 cells under hypoxia compared to air (3.4- to 4.3-fold at 60-120 min). The radiotracer was stable in the plasma and distributed well to all the tissues studied. The 60-min tumour/muscle ratios positively correlated with the percentage of pO(2) values <5 mmHg (r=0.805, P=0.027) and carbogen breathing decreased [(18)F]FETA-derived radioactivity levels (P=0.028). In contrast, nitroreductase activity did not influence accumulation. Tumours were sufficiently visualised by PET imaging within 30-60 min. Higher fractional retention of [(18)F]FETA in HT1080/1-3C vs HT1080/26.6 tumours determined by dynamic PET imaging (P=0.05) reflected higher percentage of pO(2) values <1 mmHg (P=0.023), lower vessel density (P=0.026), and higher radiobiological hypoxic fraction (P=0.008) of the HT1080/1-3C tumours. In conclusion, [(18)F]FETA shows hypoxia-dependent tumour retention and is, thus, a promising PET marker that warrants clinical evaluation.

Animals↗
PubMed2003

In vitro selectivity, in vivo biodistribution and tumour uptake of annexin V radiolabelled with a positron emitting radioisotope.

The availability of a noninvasive method to detect and quantify apoptosis in tumours will enable tumour response to several cancer therapies to be assessed. We have synthesised two radiotracers, annexin V and the N-succinimidyl-3-iodobenzoic acid (SIB) derivative of annexin V, labelled with radio-iodine ((124)I and (125)I) and provided proof of the concept by assessing specific binding and biodistribution of these probes to apoptotic cells and tumours. We have also assessed the tumour uptake of [(124)I]annexin V in a mouse model of apoptosis. RIF-1 cells induced to undergo apoptosis in vitro showed a drug concentration-dependent increased binding of [(125)I]annexin V and [(125)I]SIB-annexin V. In the same model system, there was an increase in terminal deoxynucleotidyl transferase-mediated nick end labelling (TUNEL)-positive cells and a decrease in clonogenic survival. Radiotracer binding was completely inhibited by preincubation with unlabelled annexin V. In RIF-1 tumour-bearing mice, rapid distribution of [(125)I]SIB-annexin V-derived radioactivity to kidneys was observed and the radiotracer accumulated in urine. The binding of [(125)I]SIB-annexin V to RIF-1 tumours increased by 2.3-fold at 48 h after a single intraperitoneal injection of 5-fluorouracil (165 mg kg(-1) body weight), compared to a 4.4-fold increase in TUNEL-positive cells measured by immunostaining. Positron emission tomography images with both radiotracers demonstrated intense localisation in the kidneys and bladder. Unlike [(124)I]SIB-annexin V, [(124)I]annexin V also showed localisation in the thyroid region presumably due to deiodination of the radiolabel. [(124)I]SIB-annexin V is an attractive candidate for in vivo imaging of apoptosis by PET.

Animals↗
PubMed2002

Cancer Research UK procedures in manufacture and toxicology of radiotracers intended for pre-phase I positron emission tomography studies in cancer patients.

Radiolabelled compounds formulated for injection (radiopharmaceuticals), are increasingly being employed in drug development studies. These can be used in tracer amounts for either pharmacokinetic or pharmacodynamic studies. Such radiotracer studies can also be carried out early in man, even prior to conventional Phase I clinical testing. The aim of this document is to describe procedures for production and safety testing of oncology radiotracers developed for imaging by positron emission tomography in cancer patients. We propose strategies for overcoming the inability to produce compounds in sufficient quantities via the radiosynthetic routes for full chemical characterisation and toxicology testing including (i) independent confirmation as far as possible that the stable compound associated with the radiopharmaceutical is identical to the non-labelled compound, (ii) animal toxicity studies with > or = 10 times (typically 100 times) the intended tracer dose in humans scaled by body surface area, and (iii) patient monitoring during the radiotracer positron emission tomography clinical trial.

Animals↗
PubMed2001

Comparative biodistribution and metabolism of carbon-11-labeled N-[2-(dimethylamino)ethyl]acridine-4-carboxamide and DNA-intercalating analogues.

The tricyclic carboxamide N-[2-(dimethylamino)ethyl]acridine-4-carboxamide (DACA) is a DNA-intercalating agent capable of inhibiting both topoisomerases I and II and is currently in Phase II clinical trial. Many related analogues have been developed, but despite their potent in vitro cytotoxicities, they exhibit poor extravascular distribution. As part of an ongoing drug development program to obtain related "minimal intercalators" with lower DNA association constants, we have compared the biodistribution and metabolite profiles of the prototype compound, DACA, with three analogues to aid rational drug selection. All of these compounds share a common structural feature, N-dimethyl side chain, which was radiolabeled with the positron-emitting radioisotope, carbon-11. This strategy was selected because it allows promising candidates emerging from preclinical studies in animals to be evaluated rapidly in humans using positron emission tomography (PET). The acridine DACA, the phenazine SN 23490, the pyridoquinoline SN 23719, and the dibenzodioxin SN 23935 were found to be cytotoxic in in vitro assays with an IC50 of 1.4-1.8 microM, 0.4-0.6 microM, 1.3-1.6 microM, and 24-36 microM, respectively, in HT29, U87MG, and A375M cell lines. Ex vivo biodistribution studies with carbon-11 radiolabeled compounds in mice bearing human tumor xenografts showed rapid clearance of 11C-radioactivity (parent drug and metabolites) from blood and the major organs. Rapid hepatobiliary clearance and renal excretion were also observed. There was low [<5% of injected dose/gram (%ID/g)] and variable uptake of 11C-radioactivity in three tumor types for all of the compounds. Tumor (U87MG) to blood 11C-radioactivity for [11C]DACA, [11C](9-methoxyphenazine-1-carboxamide (SN 23490), [11C]2-(4-pyridyl)quinoline-8-carboxamide (SN 23719), and [11C]dibenzo[1,4]dioxin-1-carboxamide (SN 23935) at 30 min were 2.9 +/- 1.1, 2.3 +/- 0.6, 2.6 +/- 0.6, and 0.7 +/- 0.2, respectively. For SN 23719, the distribution of 11C-radioactivity in normal tissues and tumors determined ex vivo was in broad agreement with that determined in vivo by whole body PET scanning. [11C]DACA was rapidly and extensively metabolized to several plasma metabolites and a major tumor metabolite. In contrast, [11C]SN 23935, [11C]SN 23490, and [11C]SN 23719 showed less extensive metabolism. In the tumor samples, the parent [11C]DACA and [11C]SN 23935 represented between 0.3 and 1.5%ID/g, whereas [11C]SN 23490 and [11C]SN 23719 represented between 1.5 and 2.8%ID/g. In conclusion, by using a strategy with 11C-labeling, we have determined the tissue distribution and metabolic stability of novel tricyclic carboxamides with the view of selecting analogues with potentially better in vivo activity against solid tumors. SN 23490 and SN 23719 had more favorable distribution and metabolic stability compared with DACA and SN 23935 and may warrant further development. The radiolabeling strategy used allows ex vivo and in vivo evaluation of promising anticancer agents in animals and offers the potential of rapid translation to studies in humans using PET.

Acridines↗
PubMed2001

Pharmacokinetic evaluation of N-[2-(dimethylamino)ethyl]acridine-4-carboxamide in patients by positron emission tomography.

PURPOSE: To evaluate tumor, normal tissue, and plasma pharmacokinetics of N-[2-(dimethylamino)ethyl]acridine-4-carboxamide (DACA). The study aimed to determine the pharmacokinetics of carbon-11-labeled DACA ([11C]DACA) and evaluate the effect of pharmacologic doses of DACA on radiotracer kinetics. PATIENTS AND METHODS: [11C]DACA (at 1/1,000 phase I starting dose) was administered to 24 patients with advanced cancer (pre-phase I) or during a phase I trial of DACA in five patients. Positron emission tomography (PET) was performed to assess pharmacokinetics and tumor blood flow. Plasma samples were analyzed for metabolite profile of [11C]DACA. RESULTS: There was rapid systemic clearance of [11C]DACA over 60 minutes (1.57 and 1.46 L x min(-1) x m(-2) in pre-phase I and phase I studies, respectively) with the production of several radiolabeled plasma metabolites. Tumor, brain, myocardium, vertebra, spleen, liver, lung, and kidneys showed appreciable uptake of 11C radioactivity. The area under the time-versus-radioactivity curves (AUC) showed the highest variability in tumors. Of interest to potential toxicity, maximum radiotracer concentrations (Cmax) in brain and vertebra were low (0.67 and 0.54 m(2) x mL(-1), respectively) compared with other tissues. A moderate but significant correlation was observed for tumor blood flow with AUC (r = 0.76; P =.02) and standardized uptake value (SUV) at 55 minutes (r = 0.79; P =.01). A decrease in myocardial AUC ( P =.03) and splenic and myocardial SUV ( P =.01 and.004, respectively) was seen in phase I studies. Significantly higher AUC, SUV, and Cmax were observed in tumors in phase I studies. CONCLUSION: The distribution of [11C]DACA and its radiolabeled metabolites was observed in a variety of tumors and normal tissues. In the presence of unlabeled DACA, pharmacokinetics were altered in myocardium, spleen, and tumors. These data have implications for predicting activity and toxicity of DACA and support the use of PET early in drug development.

Acridines↗
PubMed2001

Two routes to [11C-carbonyl]organo-isocyanates utilizing [11C]phosgene ([11C]organo-isocyanates from [11C]phosgene).

Two generic radiosynthetic routes for the preparation of [11C-carbonyl]isocyanates have been developed. Reaction of N-organo-sulfinylamines; RNSO, (R = Me, Et, allyl, cyclohexyl and phenyl) with [11C]phosgene gave the corresponding [11C-carbonyl]isocyanates in good radiochemical yield (53-68%) from [11C]phosgene (decay corrected) in ca 16 min from EOB. Alternatively, the reaction of [11C]phosgene with N,N'-organo-ureas; (RNH)(2)CO, (R = Me, Et, Pr and phenyl) also gave the corresponding [11C-carbonyl]isocyanates in moderate radiochemical yield (9-37%) from [11C]phosgene (decay corrected) in ca 16 min from EOB. For identification, the [11C-carbonyl]organo-isocyanates were derivatized with 1-(2-methoxyphenyl)piperazine in situ to [11C-carbonyl]carboxamides and the position of radiolabelling in the carbonyl group confirmed by [11/13C]co-labeling and subsequent carbon-13 NMR spectroscopy.

Carbon Radioisotopes↗
PubMed2001

Radiolabelled tracers and anticancer drugs for assessment of therapeutic efficacy using PET.

Positron Emission Tomography (PET) has the potential to improve efficacy of established and novel cancer therapies and to assist more rapid and rational progression of promising novel therapies into the clinic. This is due to PET's unrivalled sensitivity and ability to monitor the pharmacokinetics and pharmacodynamics of drugs and biochemicals radiolabelled with short -lived positron emitting radioisotopes. PET is a multidisciplinary science which employs chemists, biologists, mathematical modellers, pharmacologists as well as clinicians. Clinical research questions in oncology determine the methodological challenges faced by these other disciplines. Within this context we focus on the developments of the radiolabelled compounds that have underpinned the clinical work in oncology for monitoring tumour and normal tissue pharmacokinetics, assessment of tumour response, cell proliferation, gene expression, hypoxia, multidrug resistance and status of receptors on tumours.

Animals↗
PubMed2000

Modulation of fluorouracil tissue pharmacokinetics by eniluracil: in-vivo imaging of drug action.

BACKGROUND: Fluorouracil is widely used for chemotherapy of gastrointestinal cancer, but response rates are poor. Eniluracil is being developed as an inactivator of dihydropyrimidine dehydrogenase, the enzyme that brings about first-pass degradation of fluorouracil. We studied the mechanism of action of eniluracil by measuring with positron emission tomography (PET) the effect of eniluracil on tumour and normal-tissue pharmacokinetics of fluorine-18-labelled fluorouracil. METHODS: Six patients with advanced gastrointestinal cancers were studied. PET scanning was done after injection of oxygen-15-labelled water to assess tissue blood flow, followed by 1 mg/m2 18F-fluorouracil. We compared the pharmacokinetics of 18F-fluorouracil when the patients had not received eniluracil, during a 4-day course of oral eniluracil, and during a 28-day course of oral fluorouracil plus eniluracil. FINDINGS: In eniluracil-naïve patients, 18F-fluorouracil localised more strongly (mean 0.0234% [SE 0.0019] of injected activity per mL tissue at 11 min) in liver than in tumours (0.0032% [0.0004]). There was substantial inhibition, after eniluracil administration, of radiotracer uptake and retention in normal liver (mean area under the time versus radioactivity curve 0.927 [SE 0.086] vs 1.857 [0.169] m2 mL(-1) s) and kidneys (1.096 [0.048] vs 5.043 [0.915] m2 mL(-1) s). There was also an increase in plasma uracil and unmetabolised 18F-fluorouracil and an increase in the radiotracer half-life in tumours (2.3 h to >4.0 h). INTERPRETATION: Two events strongly suggested increased exposure of 18F-fluorouracil and its anabolites in the tumours, consistent with the inactivation of dihydropyrimidine dehydrogenase: a selective decrease in radiotracer exposure in normal liver and kidneys compared with tumours; and an increase in radiotracer half-life in tumours.

Administration, Oral↗
PubMed2000

Intermolecular O-H.O hydrogen bonding in the three independent molecules of (2S)-3-(4-hydroxyphenyl)-2-(1-oxoisoindolin-2-yl)propanoic acid.

The title compound, C(17)H(15)NO(4), derived from L-tyrosine, crystallizes with three independent molecules which differ in the conformation of the asymmetric unit: the N-C-C-C(ipso) torsion angles are -71.7 (5), -63.6 (6) and -52.5 (5) degrees, respectively. Deformations in the phenol ring hydroxy O-C-C angles of 116.5 (4)/123.9 (4), 121.7 (5)/118.1 (4) and 122.4 (5)/118.6 (5) degrees, respectively, result from their respective intermolecular hydrogen-bonding environments. Intermolecular O(acid)-H.O=C(indole), O(phenol)-H.O-H(phenol) and O(phenol)-H.O=C(indole) hydrogen bonds, with O.O distances in the range 2.607 (4)-2.809 (4) A, are present in combination with C-H.O and C-H.pi(arene) interactions. The primary hydrogen-bonding systems assemble with graph sets R(3)(3)(8) and R(3)(2)(22).

Journal Article↗
PubMed1999

An automated radiosynthesis of 2-[11C]thymidine using anhydrous [11C]urea derived from [11C]phosgene.

2-[11C]Thymidine has been produced from [11C]methane via [11C]phosgene and [11C]urea. Anhydrous [11C]urea was prepared from [11C]phosgene by reaction with liquid ammonia. This novel approach avoids the problems associated with the synthesis of anhydrous [11C]urea from [11C]cyanide. A fully automated system based on a modular approach and under PLC control has been developed. The system provides 2-[11C]thymidine reliably and reproducibly for clinical PET studies. The radiosynthesis takes 45-50 min from [11C]methane and the average yield was 1.5-3.3 GBq (40-90 mCi). The specific radioactivity was typically in the range 29.6-51.8 GBq mumol-1 (0.8-1.4 Ci mumol-1) at EOS corresponding to 6-12 micrograms of stable thymidine. The radiochemical yield of 2-[11C]thymidine was ca. 14% from [11C]methane.

Carbon Radioisotopes↗
PubMed1999

Tumor, normal tissue, and plasma pharmacokinetic studies of fluorouracil biomodulation with N-phosphonacetyl-L-aspartate, folinic acid, and interferon alfa.

PURPOSE: To evaluate the effect of N-phosphonacetyl-L-aspartate (PALA), folinic acid (FA), and interferon alfa (IFN-alpha) biomodulation on plasma fluorouracil (5FU) pharmacokinetics and tumor and liver radioactivity uptake and retention after [18F]-fluorouracil (5-[18F]-FU) administration. PATIENTS AND METHODS: Twenty-one paired pharmacokinetic studies were completed on patients with colorectal, gastric, and hepatocellular cancer, utilizing positron emission tomography (PET), which allowed the acquisition of tumor, normal tissue, and plasma pharmacokinetic data and tumor blood flow (TBF) measurements. The first PET study was completed when the patient was biomodulator-naive and was repeated on day 8 after the patient had been treated with either PALA, FA, or IFN-alpha in recognized schedules. RESULTS: TBF was an important determinant of tumor radioactivity uptake (r = .90; P < .001) and retention (r = .96; P < .001), for which radioactivity represents a composite signal of 5-[18F]-FU and [18F]-labeled metabolites and catabolites. After treatment with PALA, TBF decreased (four of four patients; P = .043), as did tumor radioactivity exposure (five of five patients; P = .0437), with no change in plasma 5FU clearance. With FA treatment, there were no differences observed in whole-body metabolism, plasma 5FU clearance, or tumor and liver pharmacokinetics. IFN-alpha had measurable effects on TBF and 5-[18F]-FU metabolism but had no apparent affect on liver blood flow. CONCLUSION: The administration of PALA and IFN-alpha produced measurable changes in plasma, tumor, and liver pharmacokinetics after 5-[18F]-FU administration. No changes were observed after FA administration. In vivo effects may negate the anticipated therapeutic advantage of 5FU biomodulation with some agents.

Adult↗
PubMed1998

Specific T cell recognition of peptides derived from prostate-specific antigen in patients with prostate cancer.

OBJECTIVES: To determine if proteins known to be expressed by both benign and malignant prostate epithelium can be recognized by T cells from patients with prostate cancer. We examined 7 HLA-A2 patients with prostate cancer for evidence of T cell reactivity with prostate-specific antigen (PSA). METHODS: Four peptides derived from PSA were chemically synthesized and shown to bind to HLA-A2. As a control, we also examined the immunogenic influenza matrix peptide Flu58-66 that binds to HLA-A2. These peptides were used to stimulate peripheral blood lymphocytes by in vitro stimulation. RESULTS: In 1 patient, specific recognition of peptide PSA141-150 was observed. The remaining 6 patients had no reactivity with any PSA-derived peptide. The T cell line with specific recognition of peptide PSA141-150 failed to recognize an autologous B cell blast line expressing endogenous PSA following infection with a recombinant PSA vaccinia virus construct. Three of the 7 patients demonstrated specific reactivity with Flu58-66. CONCLUSIONS: We found specific recognition of one PSA-derived peptide in 1 patient of 7 with prostate cancer. The peptide-specific lymphocyte cell line did not recognize endogenous PSA, suggesting that the peptide may not be produced by prostate cancer cells producing PSA. Specific recognition of PSA peptides was not common in our patients with prostate cancer. Whether such activity can be induced by vaccination strategies or can be therapeutic in men with established prostate cancer remains to be demonstrated.

Antigen-Antibody Reactions↗
PubMed1997

Studies on the metabolism of the novel antitumor agent [N-methyl-11C]N-[2-(dimethylamino)ethyl]acridine-4-carboxamide in rats and humans prior to phase I clinical trials.

This study reports on the biodistribution and metabolism of the 11C-labeled novel antitumor agent N-[2-(dimethylamino)ethyl]acridine-4-carboxamide (DACA) (also known as NSC 601316) in rats (plasma and tissues) and humans (plasma). Information on plasma metabolites was uniquely obtained in humans prior to Phase I clinical trial following i.v. injection of [11C]DACA at tracer dose. DACA was labeled in the N-methyl position using no-carrier-added [11C]iodomethane. Rapid high-performance liquid chromatography methods were developed for metabolite analysis of [11C]DACA. The metabolism of [11C]DACA was investigated in patients by plasma sampling. The biodistribution and metabolism of [11C]DACA was investigated in rats by plasma sampling, sacrifice experiments with tissue analyses, and imaging using positron emission tomography scanning. Analysis of human plasma demonstrated rapid and extensive metabolism of [11C]DACA. The levels of [11C]DACA changed from 77 +/- 8% (SD) at 5 min to 25 +/- 5% at 45 min postinjection. Seven radioactive metabolites were observed in human plasma, and one was identified as [11C]DACA-N-oxide. Rapid clearance of 11C radioactivity from rat blood, plasma, and major organs was observed. The half-life of 11C radioactivity clearance in rat blood between 15 and 90 min was calculated to be 3.2 h; the levels of [11C]DACA in rat plasma decreased from 69 +/- 3% (SD) at 2 min to 29 +/- 1.5% at 25 min. The number of radioactive metabolites in rat plasma was the same as in human plasma except that the proportions differed. Again, one metabolite was identified as the [11C]DACA-N-oxide. Analysis of rat tissues showed rapid and extensive metabolism in tissues, particularly liver and kidney; however, [11C]DACA (i.e., the parent compound) was the major radioactive component in the lung, heart, and brain over 40 min. Positron emission tomography scanning using [11C]DACA in the rat showed little retention of 11C radioactivity in major organs with rapid excretion via gut and kidney. The rat data were consistent with animal (mouse and rat) preclinical data obtained with preexisting techniques with longer-lived isotopes. Labeling of potential anticancer drugs with positron-emitting radionuclides and performing in vivo preclinical evaluation at tracer doses in animals and humans prior to Phase I clinical trials provides unique information that could speed up the assessment of the drug and could potentially assist drug development programs. In this example, there was no unexpected interspecies difference in metabolism of DACA that would have alerted us to make a change in the planned Phase I study.

Acridines↗
PubMed1997

Autoimmune prostatitis: evidence of T cell reactivity with normal prostatic proteins.

OBJECTIVES: To determine whether men with chronic prostatitis/chronic pelvic pain syndrome have evidence of an autoimmune response to prostatic proteins. We examined men with a history of chronic prostatitis/ chronic pelvic pain syndrome for evidence of T lymphocyte reactivity to seminal plasma. METHODS: Patients underwent automated leukopheresis to obtain peripheral blood mononuclear cells. We performed a recall antigen proliferation assay to detect specific proliferation of peripheral helper T lymphocytes in men. with chronic prostatitis/chronic pelvic pain syndrome and compared the results with those of normal men. The antigen for these studies consisted of seminal plasma from normal donors and men with seminal vesicle atresia. RESULTS: A specific recall proliferative response to seminal plasma was observed in 3 of 10 men with a history of chronic prostatitis/chronic pelvic pain syndrome compared with none of 15 normal men. The CD4 T cell proliferative response to seminal plasma was statistically significant when compared with medium alone in men with a history of chronic prostatitis/chronic pelvic pain syndrome but it was not statistically significant in normal men. The recall responses of both the chronic prostatitis/chronic pelvic pain syndrome group and normal subjects to the recall antigens tetanus toxoid and Candida extract were equivalent. CONCLUSIONS: The data represent the first direct evidence that some men with chronic prostatitis/chronic pelvic pain syndrome have an autoimmune component to their disease. Autoimmunity is a potential etiology for chronic nonbacterial prostatitis.

Adult↗
PubMed1997

Carbon-11 labelling of the antitumour agent N-[2-(dimethylamino)ethyl]acridine-4-carboxamide (DACA) and determination of plasma metabolites in man.

The potential anti-cancer agent N-[2-(dimethylamino)ethyl] acridine-4-carboxamide, DACA has been labelled with carbon-11. N-[2-11C-methyl]DACA was produced in 73% radiochemical yield from [11C]iodomethane in 40 min from EOB. The average radiochemical yield was 3.2 GBq with specific radioactivity of 41.5 GBq mumol-1 at EOS, corresponding to 24 micrograms of stable DACA. The position of labelling was confirmed by co-labelling with [11/13C]iodomethane. PET studies in patients have been performed prior to Phase I trial of DACA and during Phase I trial of DACA. Analysis of serial plasma samples showed that the metabolism of N-[2-11C-methyl]DACA is rapid and extensive in patient plasma.

Acridines↗
PubMed1997

Contextual interference and teaching golf skills.

This study was designed to examine the contextual interference effect on teaching golf skills in a naturalistic setting to 2 groups of 18 novice golfers who as undergraduate students practiced four foundational skills under conditions of low and high contextual interference, respectively. A t test for independent samples indicated no significant differences between groups. Findings are discussed and recommendations for research are made.

Adult↗