Contrast-enhanced voiding urosonography (ceVUS) is a dynamic imaging technique that makes it possible to study the structure of the urinary tract after the administration of intravesical contrast material. Initially, ceVUS was indicated mainly to study vesicoureteral reflux (VUR); however, since the ability of ceVUS to depict the structure of the urethra was demonstrated in both sexes, ceVUS is now indicated for examination of the entire urinary tract. The main benefit of ceVUS is that it does not use ionizing radiation. In recent years, fundamental changes have occurred in the understanding of VUR. The lessening effect of VUR and the low rate of occurrence of urethral pathologic conditions have given rise to changes in the indications for tests for these conditions. In addition to being able to help confirm a diagnosis of VUR, the ceVUS technique can be used to depict obstructive and nonobstructive urethral pathologic conditions, as well as normal variants, on high-quality images. Furthermore, ceVUS enables real-time assessment of voiding function. For these reasons, ceVUS should be not only an alternative to voiding cystourethrography, but also the technique of choice for the study of the entire urinary tract in pediatric patients. Online supplemental material is available for this article. RSNA, 2017.

In genetically-modified Lmx1bf/f/p mice, selective deletion of LMX1B in Pet-1 expressing cells leads to failure of embryonic development of serotonin (5-HT) neurons. As adults, these mice have a decreased hypercapnic ventilatory response and abnormal thermoregulation. This mouse model has been valuable in defining the normal role of 5-HT neurons, but it is possible that developmental compensation reduces the severity of observed deficits. Here we studied mice genetically modified to express diphtheria toxin receptors (DTR) on Pet-1 expressing neurons (Pet-1-Cre/Floxed DTR or Pet1/DTR mice). These mice developed with a normal complement of 5-HT neurons. As adults, systemic treatment with 2 – 35 μg diphtheria toxin (DT) reduced the number of tryptophan hydroxylase immunoreactive (TpOH-ir) neurons in the raphe nuclei and ventrolateral medulla by 80%. There were no effects of DT on baseline ventilation (VE) or the ventilatory response to hypercapnia or hypoxia. At an ambient temperature (TA) of 24°C, all Pet1/DTR mice dropped their body temperature (TB) below 35°C after DT treatment, but the latency was shorter in males than females (3.0 ± 0.37 vs 4.57 ± 0.29 days, respectively; p < 0.001). One week after DT treatment, mice were challenged by dropping TA from 37°C to 24°C, which caused TB to decrease more in males than in females (29.7 ± 0.31°C vs 33.0 ± 1.3°C, p < 0.01). We conclude that the 20% of 5-HT neurons that remain after DT treatment in Pet1/DTR mice are sufficient to maintain normal baseline breathing and a normal response to CO2, while those affected include some essential for thermoregulation, in males more than females. In comparison to models with deficient embryonic development of 5-HT neurons, acute deletion of 5-HT neurons in adults leads to a greater defect in thermoregulation, suggesting that significant developmental compensation can occur.

Pregnant women with IDDM who have a positive test for TPO-Abs before gestation have poorer glucose control and a high prevalence of hypothyroidism. Therefore we recommend that prepregnant IDDM patients be screened for anti-TPO-Abs. Those with a positive result should be followed with serial monitoring of free T4 and TSH levels during each trimester as well as the postpartum period.