Pelvimetry in nulliparous and primiparous women using 3 Tesla magnetic resonance imaging.

AIMS: To perform pelvimetry in nulliparous and primiparous women using 3 Tesla magnetic resonance imaging (3T MRI). METHODS: Twenty-five nulliparous volunteers and 25 primiparous women underwent pelvic 3T MRI within one week after vaginal childbirth in a prospective clinical single-center trial. The pelvimetric parameters interspinous distance (ISD), intertuberous distance (ITD), sagittal outlet (SO), obstetric conjugate (OC), and coccygeal curved length (CCL) were adapted from anthropometric measurements as well as from sonographic and computed tomography-based pelvimetry performed on high-resolution T2-weighted images. We compared the results of the two study groups to one another, recent literature and postpartum-diagnosed levator ani muscle (LAM) injuries. RESULTS: The mean values for primipara/nullipara were ISD 107 ± 8.3/105 ± 8.4 mm, ITD 119.8 ± 10.2/118.4 ± 13.1 mm, OC 129.4 ± 10/130.8 ± 6.9 mm, SO 114.3 ± 7.8/112.5 ± 8.9 mm, and CCL 37.3 ± 7.4/39 ± 8 mm. Significant differences (P < 0.05) were found between the results for OC, SO, and CCL (primipara) and ISD, ITD and OC (nullipara) and the values in the literature. No significant difference in pelvimetric values was found between the groups. A significant correlation was found between the pelvimetric parameters and five types of LAM injuries. CONCLUSIONS: Two-dimensional 3T MRI combines high-resolution images with objective pelvimetric measurements applicable in a postpartum setting. Our results provide a good foundation for further MRI-based studies evaluating the bony pelvis and its relation to LAM injuries during vaginal childbirth.

3 T MRI-based measurements for the integrity of the female pelvic floor in 25 healthy nulliparous women.

AIMS: Measurements indicating a loss of integrity of the levator ani muscle, which is an integral part of the pelvic floor, have been subject of recent studies using translabial ultrasound and 3D-MRI-models. We transferred these measurements into 2D-3 T-MR-images for clinical routine, as it is objective and does not need exhaustive post-processing. METHODS: The trial was accepted by the local ethics committee. 25 healthy volunteers fulfilled the inclusion criteria and gave written informed consent. Using high-resolution T2-weighted images (TE 5030-7810 ms, TR 88-112 ms, matrix 512, FOV 280-300 mm, ST 2-3 mm), measurements of anteroposterior hiatus (APH), laterolateral hiatus (LLH), hiatal area (HA), hiatal circumference (HC), levator area (LA), maximum muscle thickness (MMT) and levator urethra gap (LUG) were transferred from ultrasound, iliococcygeus width (IW), puborectalis attachment width (PAW), and levator symphysis gap (LSG) were transferred from 3D-MRI-models. We compared our results to previous studies in the literature. RESULTS: Mean value was 52.22 ± 6.97 mm for APH, 33.15 ± 4 mm for LLH, 13.22 ± 3.05 cm(2) for HA, 14.19 ± 1.61 cm for HC, 7.14 ± 1.85 cm(2) for LA, 6.45 ± 2.07 mm for MMT, 19.47 ± 2.38 mm for LUG, 45 ± 3.97 mm for IW, 33.94 ± 3.34 mm for PAW, 20.54 ± 5.29 mm for LSG. Our results for APH, HA, LUG, and with limitations LA, were comparable to the literature, while HC, LLH, and MMT showed anatomical variances. Results for IW and LSG were comparable, but challenging to measure. We newly proposed a cutoff value for PAW. CONCLUSIONS: 2D-3 T-MRI combines high-resolution images with objective measurements of parameters regarding pelvic floor integrity, without resorting to exhaustive post-processing methods. Our results may provide a good foundation for further 2D-MR-studies.

CD19-independent instruction of murine marginal zone B-cell development by constitutive Notch2 signaling.

B cell-specific gene ablation of Notch2 results in the loss of the marginal zone (MZ) B-cell lineage. To analyze the effects of constitutive Notch2 signaling in B cells, we have generated a transgenic mouse strain that allows the conditional expression of a constitutively active, intracellular form of Notch2 (Notch2IC). Expression of Notch2IC at the earliest developmental stages of the B-cell lineage completely abolished B-cell generation and led to the development of ectopic T cells in the bone marrow (BM), showing that Notch2IC is acting redundantly with Notch1IC in driving ectopic T-cell differentiation. In B cells clearly committed to the B-cell lineage induction of Notch2IC drove all cells toward the MZ B-cell compartment at the expense of follicular B cells. Notch2IC-expressing B cells reflected the phenotype of wild-type MZ B cells for their localization in the MZ, the expression of characteristic surface markers, their enhanced proliferation after stimulation, and increased basal activity of Akt, Erk, and Jnk. Notch2IC-driven MZ B-cell generation in the spleen was achieved even in the absence of CD19. Our results implicate that a constitutive Notch2 signal in transitional type 1 B cells is sufficient to drive MZ B-cell differentiation.

Notch1, Notch2, and Epstein-Barr virus-encoded nuclear antigen 2 signaling differentially affects proliferation and survival of Epstein-Barr virus-infected B cells.

The canonical mode of transcriptional activation by both the Epstein-Barr viral protein, Epstein-Barr virus-encoded nuclear antigen 2 (EBNA2), and an activated Notch receptor (Notch-IC) requires their recruitment to RBPJ, suggesting that EBNA2 uses the Notch pathway to achieve B-cell immortalization. To gain further insight into the biologic equivalence between Notch-IC and EBNA2, we performed a genome-wide expression analysis, revealing that Notch-IC and EBNA2 exhibit profound differences in the regulation of target genes. Whereas Notch-IC is more potent in regulating genes associated with differentiation and development, EBNA2 is more potent in inducing viral and cellular genes involved in proliferation, survival, and chemotaxis. Because both EBNA2 and Notch-IC induced the expression of cell cycle-associated genes, we analyzed whether Notch1-IC or Notch2-IC can replace EBNA2 in B-cell immortalization. Although Notch-IC could drive quiescent B cells into the cell cycle, B-cell immortalization was not maintained, partially due to an increased apoptosis rate in Notch-IC-expressing cells. Expression analysis revealed that both EBNA2 and Notch-IC induced the expression of proapoptotic genes, but only in EBNA2-expressing cells were antiapoptotic genes strongly up-regulated. These findings suggest that Notch signaling in B cells and B-cell lymphomas is only compatible with proliferation if pathways leading to antiapototic signals are active.