Fetal spina bifida: What we tell the parents.

Worldwide, about 150 000 infants are born with spina bifida yearly, making this condition one of the most common fetal central nervous system anomalies compatible with life. Over the last decade, major changes have been introduced in the prenatal diagnosis and management of spina bifida. In this review, we provide a brief summary of the current management of fetal spina bifida and present essential information that should be provided to expecting parents when their fetus has been diagnosed with spina bifida. This information is focused around common parental questions, as encountered in our typical clinical practice, to facilitate knowledge translation.

Simulator Based Obstetric Ultrasound Training: A Prospective, Randomized Single-Blinded Study.

OBJECTIVE: To compare the use of simulator-based and patient-based obstetric ultrasound training. METHODS: This was a prospective, randomized, single-blinded trial. Eighteen consenting obstetric trainees with minimal previous ultrasound exposure were recruited. Enrolled patients were also fully consenting. Mid-trimester fetal brain anatomy in the standard planes (i.e., biparietal diameter and head circumference, cavum septum pellucidum, posterior fossa, and lateral ventricle) was chosen as a surrogate for all fetal anatomy ultrasound training. Trainees were randomized into two groups according to training method: simulator group (n = 9) or patient group (n = 9). All participating trainees went through the following sequence: a didactic session regarding the required planes; a "real" patient 15-minute pretest; a 45-minute training session with a dedicated ultrasound educator, using either a simulator or a "real" patient (according to the randomized group assignment); and a 15-minute post-test to obtain and label the standard four planes on a "real" patient. All images were stored and then scored by two blinded Maternal Fetal Medicine staff, according to 3 set criteria: image quality, landmarks, and measurements. Each criterion was scored 0 to 15 for a total score of 0 to 60. RESULTS: Pretest competence was similar between the two groups. For each of the two groups there was a significant score improvement following training: real patient (mean score pretest 13.3 vs. post-test 24.6; P < 0.04) and simulator group (mean score pretest 15.9 vs. post-test 28.9; P < 0.05). All trainees demonstrated significant overall score improvements (mean score pretest 14.6 vs. post-test 26.6; P < 0.04) regardless of training method. Trainees were further divided by their initial level of confidence (pretest score ≤5: very unconfident; pretest >5: unconfident). The improvement was similar for both groups, but "very unconfident" trainees' performance improved more in the simulator group (mean pretest vs. post-test score 3.5 to 35) compared with the patient group (mean pretest vs. post-test score 2.3 to 25.6) CONCLUSION: Simulator-based obstetric ultrasound training performed as well as real patient training and was found to be especially beneficial for beginner trainees. Simulator-based ultrasound training has a high rate of acceptance by trainees, does not require investment of patient or clinic resources, and warrants consideration as an educational tool for the safe and effective teaching of obstetric ultrasound.

Heparan sulfate side chains have a critical role in the inhibitory effects of perlecan on vascular smooth muscle cell response to arterial injury.

Perlecan is a proteoglycan composed of a 470-kDa core protein linked to three heparan sulfate (HS) glycosaminoglycan chains. The intact proteoglycan inhibits the smooth muscle cell (SMC) response to vascular injury. Hspg2(Δ3/Δ3) (MΔ3/Δ3) mice produce a mutant perlecan lacking the HS side chains. The objective of this study was to determine differences between these two types of perlecan in modifying SMC activities to the arterial injury response, in order to define the specific role of the HS side chains. In vitro proliferative and migratory activities were compared in SMC isolated from MΔ3/Δ3 and wild-type mice. Proliferation of MΔ3/Δ3 SMC was 1.5× greater than in wild type (P < 0.001), increased by addition of growth factors, and showed a 42% greater migratory response than wild-type cells to PDGF-BB (P < 0.001). In MΔ3/Δ3 SMC adhesion to fibronectin, and collagen types I and IV was significantly greater than wild type. Addition of DRL-12582, an inducer of perlecan expression, decreased proliferation and migratory response to PDGF-BB stimulation in wild-type SMC compared with MΔ3/Δ3. In an in vivo carotid artery wire injury model, the medial thickness, medial area/lumen ratio, and macrophage infiltration were significantly increased in the MΔ3/Δ3 mice, indicating a prominent role of the HS side chain in limiting vascular injury response. Mutant perlecan that lacks HS side chains had a marked reduction in the inhibition of in vitro SMC function and the in vivo arterial response to injury, indicating the critical role of HS side chains in perlecan function in the vessel wall.

Proteins mediating collagen biosynthesis and accumulation in arterial repair: novel targets for anti-restenosis therapy.

Events contributing to restenosis after coronary interventions include platelet aggregation, inflammatory cell infiltration, growth factor release, and accumulation of smooth muscle cells (SMCs) and extracellular matrix (ECM). The ECM is composed of various collagen subtypes and proteoglycans and over time constitutes the major component of the mature restenotic plaque. The pathophysiology of collagen accumulation in the ECM during arterial restenosis is reviewed. Factors regulating collagen synthesis and degradation, including various cytokines and growth factors involved in the process, may be targets for therapies aimed at prevention of in-stent restenosis.