In-utero stenting: development of a low-cost high-fidelity task trainer.

OBJECTIVE: To develop an in-utero stent placement training model. METHODS: The in-utero stent task trainer was constructed using a formalin-preserved gravid pig uterus. Altering the size of the uterine segment, changing the fluid level in the uterus and addition of a large Ziploc freezer bag variably filled with differing amounts of ultrasound gel can vary the procedural skill required. RESULTS: Thoracoamniotic and vesicoamniotic shunts can be simulated using this life-like model. The cost of eight to 10 learning stations is approximately US $ 60. Fetal position, maternal size and amniotic fluid status can be altered rapidly to increase the complexity of the procedure. CONCLUSIONS: This low-cost and realistic task trainer can provide the opportunity to practice in-utero shunt procedures in a non-clinical environment. This model should enhance learning and reinforce acquired skills.

Continued Validation of Ultrasound Guidance Targeting Tasks: Assessment of Internal Structure.

RATIONALE AND OBJECTIVES: We previously demonstrated validity evidence for our novel ultrasound-guided invasive procedure targeting tasks in the content, response process, relations with other variables, and consequences validity domains. Here, we investigate their internal structure by assessing their interrater, intrarater, and test-retest reliability. METHODS: In this Institutional Review Board approved nonrandomized interventional trial first year medical students performed our previously described dowel and straw ultrasound guidance targeting tasks as a pretest. Afterward, the training group had four weekly 1-hour training sessions. The control group had no further training. Both groups then had a posttest for both tasks. The training group was re-evaluated 2 and 5 months later. Completion time in seconds, errors, and error adjusted time (5 seconds penalty/error) were recorded. Pretest and posttest performance was compared within groups, and the amount of improvement from pretest to posttest was compared between groups. Interrater, intrarater, and test-retest interclass correlation coefficients (ICC) were calculated. RESULTS: Although some improvements from pretest to posttest were seen in both groups, greater improvements were seen in the training group. This skill was retained for at least several months. The interrater and intrarater ICCs were excellent (range 0.83-0.93). The test-retest ICCs were good to excellent in all but one performance measure (0.50-0.78). CONCLUSION: Student performance on the targeting tasks improved markedly after training and persisted for several months. The interrater and intrarater reliability were excellent, while the test-retest reliability was good. This provides additional validity evidence for our novel ultrasound-guided invasive procedure targeting curriculum.

Retention of supraspinal delta-like analgesia and loss of morphine tolerance in delta opioid receptor knockout mice.

Gene targeting was used to delete exon 2 of mouse DOR-1, which encodes the delta opioid receptor. Essentially all 3H-[D-Pen2,D-Pen5]enkephalin (3H-DPDPE) and 3H-[D-Ala2,D-Glu4]deltorphin (3H-deltorphin-2) binding is absent from mutant mice, demonstrating that DOR-1 encodes both delta1 and delta2 receptor subtypes. Homozygous mutant mice display markedly reduced spinal delta analgesia, but peptide delta agonists retain supraspinal analgesic potency that is only partially antagonized by naltrindole. Retained DPDPE analgesia is also demonstrated upon formalin testing, while the nonpeptide delta agonist BW373U69 exhibits enhanced activity in DOR-1 mutant mice. Together, these findings suggest the existence of a second delta-like analgesic system. Finally, DOR-1 mutant mice do not develop analgesic tolerance to morphine, genetically demonstrating a central role for DOR-1 in this process.

Expression of functional mu-opioid receptors during T cell development.

We have examined the chemotactic responsiveness of thymocytes to selective mu-, kappa-, and delta-opioid agonists. Our results show that developing T cells migrate in response to mu-, but not kappa- or delta-opioids. The mu-opioid response appears to be dependent on the classical mu-opioid receptor (MOR-1) since the chemotactic response is blocked by a selective mu-opioid antagonist, and is absent in thymocytes from MOR-1-deficient mice. Flow cytometric analysis of the mu-opioid responsive cells shows that these cells consist predominantly of highly immature CD4- CD8- T cells. These results represent the first demonstration of the functional expression of mu-opioid receptors by developing T cells.

Rocket immunoelectrophoresis of C4 and C4d. A simple sensitive method for detecting complement activation in plasma.

Activation of complement component C4 has recently been measured by the quantitation of C4 and C4d (a cleavage fragment of C4) by electroimmunodiffusion in gels containing specific precipitating antibodies for C4 and C4d (Rocket immunoelectrophoresis, RIE). Quantitative measurements of the complement component C4 and its fragment C4d were determined in rocket immunoelectrophoresis (RIE) and compared with measurements of total hemolytic complement activity (CH50) or concentrations of C4 as determined by single radial immunodiffusion (RID). This newly developed RIE assay shows activation of the classical complement pathway and involves electroimmunodiffusion in gels containing specific precipitating antibodies for C4 and its cleavage fragment, C4d. In 37 plasma samples, excellent correlation was demonstrated between the C4 in RIE and CH50 (r = .70) and C4 by RID (r = .87). In vivo activation of C4 was determined by measuring the ratio of C4d to C4; 21 of the plasma samples assayed had ratios greater than 1.1 indicating activation of C4. In 13 of the plasma samples there were correspondingly low CH50 values, whereas 8 had normal CH50 levels. Therefore, activation can be detected in those instances when other measurements (CH50 and C4 quantitation) are normal. Thus the RIE assay for plasma C4 activation appears to be the most sensitive method available for assessing in vivo activation of the classical pathway of complement.