Assessment of uterine and ovarian arteries before uterine artery embolization: advantages conferred by unenhanced MR angiography.

PURPOSE: To clarify the benefits of unenhanced magnetic resonance (MR) angiography in planning uterine artery embolization (UAE). MATERIALS AND METHODS: This retrospective study was approved by the institutional review board, and the informed consent requirement was waived. Fifty-five consecutive women (mean age, 42 years; age range, 26-52 years) who underwent UAE for symptomatic uterine fibroids were placed chronologically into groups 1, 2, or 3, which were composed of 20, 22, and 13 patients, respectively. Digital subtraction angiography was performed in groups 1 and 2 but not in group 3. In the 35 patients in groups 2 and 3, unenhanced MR angiography was performed before UAE, and two independent radiologists assessed the results. The parameters indicating performance of UAE were compared among the three groups with the Tukey test. RESULTS: Forty-five patients underwent routine UAE (19, 16, and 10 patients in groups 1, 2, and 3, respectively). Sixty-eight (97%) of 70 uterine artery origins were demonstrated clearly at MR angiography. Among five ovarian arteries detected at MR angiography, collateral supply was confirmed in four (80%). The assessment of MR angiographic results and discontinuation of digital subtraction angiography led to a reduction in the mean performance time (from 96.2 minutes to 51.9 minutes [P = .004]), fluoroscopy time (from 28.5 minutes to 17.8 minutes [P = .036]), dose-area product (from 109.8 Gy.cm(2) to 25.4 Gy.cm(2) [P < .001]), and contrast medium volume (from 103.8 mL to 40.8 mL [P < .001]). CONCLUSION: Unenhanced MR angiography provides useful information regarding uterine and ovarian arteries before UAE.

High prevalence of intrapelvic parasitic arteries in patients with placenta accreta spectrum: A case-control study using unenhanced magnetic resonance angiography.

PURPOSE: To compare the prevalence of enlarged ovarian and intrapelvic parasitic arteries to the gravid uterus between cases of placenta accreta spectrum (PAS) and those with normal placentation using unenhanced magnetic resonance (MR) angiography. METHODS: Unenhanced time-of-flight MR angiography was performed in 12 consecutive women with PAS (mean age, 34 years; range, 23-42 years) and 24 women with normal placentation (mean age, 31 years; range, 24-42 years) in their third trimester and reviewed by two independent observers. The consensus reading served as the reference standard. Findings of pelvic arteriography performed at cesarean hysterectomy were reviewed in all cases of PAS. The prevalence of enlarged ovarian and intrapelvic parasitic arteries was compared using Fisher's exact test. The interobserver agreement was assessed with Kappa statistics. RESULTS: The prevalence of enlarged ovarian arteries was not significantly different between cases of PAS and normal placentation (17% [4/24 pelvic sides] vs. 4% [2/48 pelvic sides], P = .091). The prevalence of intrapelvic parasitic arteries was significantly higher in cases of PAS than in those with normal placentation (67% [16/24 pelvic sides] vs. 0% [0/48 pelvic sides], P < .0001). On a patient-by-patient basis, the intrapelvic parasitic artery was frequently present in women with PAS (92% [11/12 patients]). The Kappa values were 0.915 and 0.852 for detecting enlarged ovarian and intrapelvic parasitic arteries, respectively, indicating excellent interobserver agreement. CONCLUSIONS: The development of intrapelvic parasitic arteries was an anomalous phenomenon observed on unenhanced MR angiography in the majority of women with PAS but was not observed in those with normal placentation.

Influence of irradiation time on volumetric shrinkage and flexural properties of flowable resins.

The purpose of this study was to evaluate the influence of irradiation time on volumetric change and flexural properties of flowable resins. Four commercially available flowable resins were employed. For volumetric shrinkage measurement, resin pastes were inserted into a mold (2 mm in height, 4 mm in diameter) and put into a water-filled dilatometer. This was followed by light irradiation for 10, 20, or 30 seconds at 600 mW/cm2. Volumetric shrinkage of the specimens was then determined from the change in the height of water meniscus, and the percentage volumetric change thereof was calculated. For flexural strength measurement, resin pastes were filled into a stainless steel mold (25 x 2 x 2 mm), and the middle one-third of the specimen was first irradiated. The remaining two-thirds were irradiated under the same irradiation conditions as volumetric shrinkage measurement. After 24-hour storage in 37 degrees C water, three-point flexural tests were performed with a span length of 20 mm at a crosshead speed of 1.0 mm/min. One-way ANOVA followed by Tukey's HSD test were used for statistical analysis. For all materials tested except Estelite Flow Quick, both volumetric shrinkage and flexural strength increased with longer light irradiation time. Results of this study indicated that both volumetric shrinkage and flexural properties were influenced by light irradiation time and resin composite type.

Primary structures of guinea pig high- and low-molecular-weight kininogens.

Guinea pig high-molecular-weight and low-molecular-weight (HMW and LMW) kininogen cDNA were amplified from liver mRNA by RT-PCR. Their nucleotide sequences were analyzed and deduced to amino acid sequences. The HMW kininogen, composed of 607 amino acid residues with a 18-residue signal sequence, possessed the cysteine protease inhibitor domains I and II, the bradykinin domain, the histidine-rich region, and the prekallikrein-binding region. The amino acid sequence preceding the bradykinin domain was found not to be -Leu-Met-Lys- but -Leu-Thr-Arg-. Therefore, kallidin (Lys-bradykinin) and Met-kallidin are not liberated from the guinea pig kininogens. We purified the HMW kininogen protein from plasma and prepared the kinin-free form using guinea pig plasma kallikrein. Although the amino-terminal of the HMW kininogen was modified, the 25 amino-terminal residues of the light chain of the kinin-free kininogen corresponded to the deduced sequence just after the bradykinin moiety of the HMW kininogen. With regard to the LMW kininogen, the nucleotide sequence down to T(1200) as well as the amino acid sequence till Thr(382) was identical to that of the HMW kininogen. We also examined the localization of the guinea pig kininogen gene on the prometaphase lymphocyte chromosomes by fluorescence in situ hybridization method. Two pair signals were observed on a pair of homologous chromosomes, each of which is composed of two chromatids. Based on these findings, we concluded that HMW and LMW kininogens are produced from the single kininogen gene in guinea pig as in the cases of the other mammalian species reported so far.

Unenhanced MR angiography of uterine and ovarian arteries after uterine artery embolization: differences between patients with incomplete and complete fibroid infarction.

PURPOSE: To compare the status of uterine and ovarian arteries after uterine artery embolization (UAE) in patients with incomplete and complete fibroid infarction via unenhanced 3D time-of-flight magnetic resonance (MR) angiography. MATERIALS AND METHODS: Thirty-five consecutive women (mean age 43 years; range 26-52 years) with symptomatic uterine fibroids underwent UAE and MR imaging before and within 2 months after UAE. The patients were divided into incomplete and complete fibroid infarction groups on the basis of the postprocedural gadolinium-enhanced MR imaging findings. Two independent observers reviewed unenhanced MR angiography before and after UAE to determine bilateral uterine and ovarian arterial flow scores. The total arterial flow scores were calculated by summing the scores of the 4 arteries. All scores were compared with the Mann-Whitney test. RESULTS: Fourteen and 21 patients were assigned to the incomplete and complete fibroid infarction groups, respectively. The total arterial flow score in the incomplete fibroid infarction group was significantly greater than that in the complete fibroid infarction group (P=0.019 and P=0.038 for observers 1 and 2, respectively). In 3 patients, additional therapy was recommended for insufficient fibroid infarction. In 1 of the 3 patients, bilateral ovarian arteries were invisible before UAE but seemed enlarged after UAE. CONCLUSION: The total arterial flow from bilateral uterine and ovarian arteries in patients with incomplete fibroid infarction is less well reduced than in those with complete fibroid infarction. Postprocedural MR angiography provides useful information to estimate the cause of insufficient fibroid infarction in individual cases.

S19 ribosomal protein dimer augments metal-induced apoptosis in a mouse fibroblastic cell line by ligation of the C5a receptor.

To analyze the role of S19 ribosomal protein (RP S19) in apoptosis, murine NIH3T3 were transfected with either hemagglutinin peptide-tagged (HA) wild-type human RP S19 or a mutant (Gln137Asn) that is resistant to transglutaminase-catalyzed cross-linked-dimerization. Transfection with the mutant HA-RP S19 inhibited manganese (II) (Mn II)-induced apoptosis whereas the wild-type HA-RP S19 augmented apoptosis and a mock transfection had no effect. Release of the wild-type HA-RP S19 dimer but not the mutant HA-RP S19 was observed during the apoptosis. The reduced rate of apoptosis of the cells transfected with the mutant HA-RP S19 was overcome by addition of extracellular wild-type RP S19 dimer. The apoptosis rates in cells transfected with either form of human HA-RP S19 and in mock transfectants were reduced to about 40% by the presence of anti-RP S19 antibody in the culture medium. Immunofluorescence staining and fluorescence-activated cell sorting (FACS) analysis showed that the cell surface expression of the receptor for cross-linked RP S19 dimer, C5a receptor, increased during apoptosis, concomitant with phosphatidylserine exposure. The expression of the C5a receptor gene also increased twofold. Apoptosis rates in the transfected and control cell lines were also reduced by the presence of an anti-mouse C5a receptor monoclonal antibody or of a peptide C5a receptor antagonist. These results indicated the presence of an RP S19 dimer- and C5a receptor-mediated autocrine-type augmentation mechanism during Mn II-induced apoptosis in the mouse fibroblastic cell line. In contrast to the RP S19 dimer, C5a actually inhibited apoptosis, suggesting that signaling through the C5a receptor varies depending on the ligand bound.

Switch moiety in agonist/antagonist dual effect of S19 ribosomal protein dimer on leukocyte chemotactic C5a receptor.

The cross-linked homodimer of S19 ribosomal protein (RP S19) induces monocyte predominant infiltration due to a dual effect on the C5a receptor in leukocyte chemotaxis, agonistic to monocytes and antagonistic to polymorphonuclear leukocytes (PMN) (H. Nishiura, Y. Shibuya, T. Yamamoto, Lab Invest 1998, 78:1615-1623). The agonistic ligand moiety was recently determined to be -Leu131-Asp132-Arg133- (Y. Shibuya et al, Am J Pathol 2001, 159:2293-2301). In this study we determined the moiety responsible for the antagonistic function. A C-terminal analogue peptide of RP S19, with 18 residues containing the agonistic ligand moiety as a part, reproduced the dual function in the leukocyte chemotaxis. A C5a analogue peptide attracted PMN as well as monocytes. When C-terminal 12 residues of RP S19 after the agonistic moiety, IAGQVAAANKKH, were connected to the C5a peptide, the chimeric peptide newly obtained the dual function, indicating that the C-terminal portion of RP S19 functions as a converter from the agonist to the antagonist. C-terminal truncation analyses indicated that the C-terminal His was not essential but the next Lys was necessary for the converter function. The homodimer of a mutant RP S19 that was truncated for the C-terminal 4 residues lost the monocyte selectivity in the leukocyte infiltration in vivo as in the case of the leukocyte chemotaxis in vitro. These results indicated that the conversion of the RP S19 dimer from agonist to antagonist of C5a receptor is attributed to the IAGQVAAANKK moiety between Ile134 and Lys144.