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We describe a novel surgical technique in 31 women with histopathologically confirmed placenta accreta spectrum (PAS) disorders managed by a multidisciplinary team using a prophylactic infrarenal abdominal aortic cross‐clamping technique during caesarean hysterectomy. We conclude that this new surgical procedure is a relatively safe technique to potentially control operative blood loss. Our work may stimulate others to develop protocols assessing this innovative technique to improve the surgical outcome of PAS disorders. [ABSTRACT FROM AUTHOR]

Among several surgical techniques for the aforementioned conditions, the first strategy is a primary caesarean hysterectomy and partial cystectomy for scenario 1 and an extended hysterectomy with radical parametrectomy procedure for scenario 2. Authors' response Re: Some concerns regarding aortic cross-clamping in caesarean hysterectomy for placenta accreta spectrum (Re: Vascular control by infrarenal aortic cross-clamping in placenta accreta spectrum disorders: description of technique; something old, something new & something borrowed) I Sir, i We thank Matsubara and Fox for their insightful comments1,2 on our article.3 We agree with their point that the infrarenal aortic cross-clamping technique for placenta accreta spectrum (PAS) disorder ideally should be evaluated by well-designed, high-quality, prospective randomised controlled studies. [Extracted from the article]

Balloon occlusion of the infrarenal abdominal aorta theoretically provides the same level of pelvic perfusion blockage as our approach.3 A major disadvantage of this procedure is that the catheter must be placed before commencing the surgery,3 which may not be possible if a prenatal diagnosis of PAS disorder has not been made. I Sir, i We thank Nieto-Calvache et al. for their insightful comments1 on our article.2 We agree with their point that the choice of vascular control techniques should be determined by the topography and severity of placenta accreta spectrum (PAS) disorders. Authors' reply re: Vascular control by infrarenal aortic cross-clamping in placenta accreta spectrum disorders: description of technique. [Extracted from the article]

ABSTRACT A case of fetal axillary hemangiolymphangioma coexisting with intralesional hemorrhage is presented. At 27 weeks’ gestation, the fetus was found to have a 52 × 43-mm left axillary multilocular cystic mass which showed no signals on color Doppler. The mass was composed mostly of sonolucent spaces. At 29 weeks’ gestation, an arterial flow signal (15 cm/s) was detected within the mass. In addition, two low-density echogenic cystic spaces with bidirectional flow waveforms were found, which raised the suspicion of intratumoral bleeding. Two weeks later, a fine-needle aspiration of the mass revealed both straw-colored and chocolate-colored fluid. The tumor size increased from 52 × 43 mm at 27 weeks to 100 × 79 mm at 37 weeks. Blood clots developed gradually in the hemorrhagic spaces. The pregnancy proceeded smoothly to term and at 38 weeks an elective Cesarean section was performed. After a surgical excision of the mass at the age of 4 days, a mixed cavernous hemangioma and cystic lymphangioma with secondary intralesional hemorrhage was confirmed histopathologically. [ABSTRACT FROM AUTHOR]

A case of mixed intrahepatic arteriovenous shunts in a fetus diagnosed at 35 weeks' gestation is presented. Color Doppler ultrasonography in the fetal liver demonstrated complicated vascular connections fed by the hepatic arterial branches and drained into the portal and middle hepatic veins. Pulsed Doppler ultrasonography identified a high cardiac output state by the detection of increased flow velocities of the great vessels. The contribution of Doppler ultrasonography to hemodynamic changes is highlighted. The management is briefly discussed. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented about a case of a 29-year-old woman who is diagnosed with an asymptomatic uterine rupture in a twin pregnancy.

Fetal cardiac hemangioma is rarely diagnosed prenatally. We present here a fetus with such a tumor diagnosed at 28 weeks' gestation. With the use of fetal echocardiography, a mixed echogenic mass protruding outward from the right atrial wall was observed. Moderate amounts of pericardial effusion were also found. Although no apparent blood flow signal was detected in the mass, fetal echocardiography showed signs suggestive of a hemangioma. Differential diagnosis, management and prognosis are discussed. [ABSTRACT FROM AUTHOR]

Describes a case of Krukenberg tumor secondary to gastric carcinoma in which the prenatal diagnosis was made using color Doppler sonography. Malignancy rate of ovarian tumors in pregnancy; Percentage of the symptoms and signs of Krukenberg tumor attributed to abdominal pain and mass; Description of the characteristic ultrasonographic appearance of Krukenberg tumor.

Ureteral injuries are uncommon but serious complications of laparoscopically-assisted vaginal hysterectomy. The ureter is particularly at risk for inadvertent injury when the cardinal-uterosacral ligament complex is coagulated and divided below the uterine vessels. We present two recent cases which describe the application of transabdominal ultrasound including color Doppler mapping in the diagnosis of ureteral injury after laparoscopically-assisted vaginal hysterectomy. Transabdominal ultrasound including color Doppler mapping has great diagnostic potential as a method for non-invasive evaluation of post-operative ureteral conditions. Ultrasonic triads (absence of a ureteric jet, ascites, and the presence or absence of hydronephrosis) are capable of differentiating diagnosis of complete, partial, or nonobstructive surgical ureteral injuries. [ABSTRACT FROM AUTHOR]

Antiphase domains are seen in single crystal gamma lithium aluminate (γ-LiAlO2) with 16.7 nm periodicity in the <110> direction. Alternate domains have a 12 [001] shift. Beta phase lithium aluminate (β-LiAlO2) is seen to form on the surface of the as-received wafers with an epitaxial strain limited relationship with the bulk γ phase. The orthorhombic β phase aligns with the a and b axes (0.528 and 0.630 nm) matching with the tetragonal γ phase’s a and c axes (0.5168 and 0.6268 nm). The γ and β phases are seen to have different etch rates. The β phase converts back to the γ phase above 450 °C. [ABSTRACT FROM AUTHOR]

Photoconduction (PC) properties in the ZnO films with the (110) nonpolar surface (a-plane) epitaxially grown by chemical vapor deposition on the LiGaO2 (010) substrates with low lattice mismatches (4.0% along the c-axis and 3.8% along the m-axis) have been studied. The structural and optical qualities of the epitaxial films have been characterized using theta-two theta and phi scans, X-ray diffraction, rocking curve, and photoluminescence measurements. The nonpolar ZnO film exhibits a near visible-blind ultraviolet photoresponse. The optimal photocurrent to dark current ratio (i.e., sensitivity) can reach 13360%. The responsivity of the a-plane ZnO photoconductor-type detector can also reach 1%7 AW-1, which is two to four orders of magnitude higher than those of the m-plane, a-plane, and r-plane photodiodes based on ZnO/ZnMgO quantum wells. The normalized gain at 2.%9 cm2V-1%, of the nonpolar film is also comparable with the optimal recorded value of the ZnO nanowires. In addition, the PC mechanism has also been investigated by the power-dependent and time-resolved photoconductivity measurements. The power-sensitive responsivity can be attributed to the effect of light intensity on carrier lifetime and quantum efficiency. The photovoltaic effect of the surface depletion region is inferred to be the reason resulting in the anomalous powerdependent quantum efficiency. [ABSTRACT FROM AUTHOR]

The NF-κB transcription factor has a central role in diverse processes, including inflammation, proliferation and cell survival, and its activity is dysregulated in diseases such as autoimmunity and cancer. We recently identified the TRE17/ubiquitin-specific protease 6 (USP6) oncogene as the first de-ubiquitinating enzyme to activate NF-κB. TRE17/USP6 is translocated and overexpressed in aneurysmal bone cyst (ABC), a pediatric tumor characterized by extensive bone degradation and inflammatory recruitment. In the current study, we explore the mechanism by which TRE17 induces activation of NF-κB, and find that it activates the classical NF-κB pathway through an atypical mechanism that does not involve IκB degradation. TRE17 co-precipitates with IκB kinase (IKK), and IKK activity is augmented in stable cell lines overexpressing TRE17, in a USP-dependent manner. Optimal activation of NF-κB by TRE17 requires both catalytic subunits of IKK, distinguishing its mechanism from the classical and non-canonical pathways, which require either IKKβ or IKKα, respectively. TRE17 stimulates phosphorylation of p65 at serine 536, a modification that has been associated with enhanced transcriptional activity and nuclear retention. Induction of S536 phosphorylation by TRE17 requires both IKKα and IKKβ, as well as the IKKγ/NEMO regulatory subunit of IKK. We further demonstrate that TRE17(long) is highly tumorigenic when overexpressed in NIH3T3 fibroblasts, and that inhibition of NF-κB significantly attenuates tumor formation. In summary, these studies uncover an unexpected signaling mechanism for activation of classical NF-κB by TRE17. They further reveal a critical role for NF-κB in TRE17-mediated tumorigenesis, and suggest that NF-κB inhibitors may function as effective therapeutic agents in the treatment of ABC. [ABSTRACT FROM AUTHOR]

Aneurysmal bone cyst (ABC) is an aggressive, pediatric bone tumor characterized by extensive destruction of the surrounding bone. Although first described over 60 years ago, its molecular etiology remains poorly understood. Recent work revealed that ABCs harbor translocation of TRE17/USP6, leading to its transcriptional upregulation. TRE17 encodes a ubiquitin-specific protease (USP), and a TBC domain that mediates binding to the Arf6 GTPase. However, the mechanisms by which TRE17 overexpression contributes to tumor pathogenesis, and the role of its USP and TBC domains, are unknown. ABCs are characterized by osteolysis, inflammatory recruitment and extensive vascularization, the processes in which matrix proteases have a prominent role. This led us to explore whether TRE17 regulates the production of matrix metalloproteinases (MMPs). In this study we show that TRE17 is sufficient to induce expression of MMP-9 and MMP-10, in a manner requiring its USP activity, but not its ability to bind Arf6. TRE17 induces transcription of MMP-9 through activation of nuclear factor-κB (NF-κB), mediated in part by the GTPase RhoA and its effector kinase, ROCK. Furthermore, xenograft studies show that TRE17 induces formation of tumors that reproduce multiple features of ABC, including a high degree of vascularization, with an essential role for the USP domain. In sum, these studies reveal that TRE17 is sufficient to initiate tumorigenesis, identify MMPs as novel TRE17 effectors that likely contribute to ABC pathogenesis and define the underlying signaling mechanism of their induction. [ABSTRACT FROM AUTHOR]

Background:Visfatin is an adipokine that is highly expressed in visceral fat. Plasma levels of visfatin have been reported to be higher in subjects with obesity and/or type 2 diabetes mellitus. However, the role of visfatin in endothelial dysfunction has been largely unexplored.Objectives:We investigated the possible pathogenic role of visfatin in endothelial dysfunction, particularly focusing on its effect on inflammatory mediators.Design:Primary human umbilical vein endothelial cells (HUVECs) pretreated with visfatin (1, 10 and 50 ng ml−1) were used to study the relationship between visfatin and endothelium dysfunction. Expressions of adhesion molecules (ICAM-1, VCAM-1 and E-selectin) and cytokines (interleukin (IL)-6 and IL-8) affected by visfatin were investigated by enzyme-linked immunosorbent assay, flow cytometry and real-time PCR. Activity of nuclear factor (NF)-κB was examined by electrophoretic mobility shift assay.Results:At a visfatin concentration of 50 ng ml−1, significant increases in IL-6, IL-8, ICAM-1, VCAM-1 and E-selectin gene expression along with increased IL-6, IL-8 and sE-selectin protein levels in the conditioned medium were detected. Flow cytometry showed that the addition of visfatin significantly increased ICAM-1 expression and VCAM-1 expression (10 and 50 ng ml−1, respectively). Electrophoretic mobility shift assay confirmed that visfatin increased the DNA-binding activity of NF-κB. In addition, pretreatment with visfatin (10 and 50 ng ml−1) increased human monocyte cell line THP-1 adhesion to HUVECs.Conclusions:Our findings suggest that visfatin causes endothelial dysfunction by increasing inflammatory and adhesion molecule expression at least partly through the upregulation of NF-κB activity.International Journal of Obesity (2009) 33, 465–472; doi:10.1038/ijo.2009.24; published online 17 February 2009 [ABSTRACT FROM AUTHOR]