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Placenta previa presents a highest risk to pregnancy, and placenta accreta is the most serious. Placenta accreta requires cesarean delivery and often results in massive obstetric hemorrhage and higher maternal morbidity. Challenges associated with cesarean delivery techniques may contribute to increased maternal blood loss and morbidity rates. Several recent obstetric studies reported the usefulness of transverse uterine fundal incision for managing placenta accreta. We present a case of placenta percreta that was treated by a transverse fundal incision. We successfully avoided cutting through the placenta and helped decrease maternal blood loss. After delivery, the patient underwent a cesarean hysterectomy. Postoperative day 48, she experienced watery discharge and was diagnosed with vaginal fistula. We present our case and review the literature.

The rate of cesarean delivery was higher in patients with a fetus in cephalic presentation after a successful external cephalic version (ECV) [1,2]. However, other studies do not support those results [3,4]. This controversy is most likely the result of the heterogeneity of the study population. The aim of the present study was to evaluate whether patients who had undergone successful ECV at term were at a higher risk of cesarean section in Japanese population. The present study was performed on patients who were delivered in Osaka University Hospital between 1995 and 2004. Inclusion criteria for ECV

Background: Platinum drugs are often used for the postoperative adjuvant therapy or treatment in advanced and recurrent ovarian cancer. We have previously reported that ovarian clear cell carcinoma (CCC) has increased expression of Annexin A4 (Anx A4) in comparison with other subtype of ovarian cancer. Enhanced expression of Anx A4 has been shown to induce chemoresistance via extracellular efflux of carboplatin. Purpose: To identify the domain of Anx A4 relevant to chemoresistance. Materials and methods: Anx A4 possesses the NH2-terminal domain and four annexin repeat domains with one Ca2+-binding site in each domain. Deleting annexin repeat domains one by one from C-terminal site, we generated four deletion mutants of Anx A4 named R1, 2, 3, and 4 (arabic figure shows the number of annexin repeat domains). Stable cell lines overexpressing each deletion mutants were established in NUGC3 cells. Chemosensitivity to platinum drugs was evaluated using the MTT assay. Results. Compared with mock transfected cells, all the four deletion mutants induced chemoresistance to both cisplatin and carboplatin. Conclusions. The deletion derivative covering only one annexin repeat domain can induce chemoresistance to platinum drugs. Further study is underway to determine the specific site for chemoresistance of Anx A4. Citation Format: Akiko Morimoto, Takayuki Enomoto, Shinya Matsuzaki, Kousuke Hiramatsu, Yutaka Ueda, Kiyoshi Yoshino, Masami Fujita, Takuhei Yokoyama, Satoshi Serada, Tetsuji Naka, Tadashi Kimura. Functional domain of Annexin A4: which domain is indispensable for chemoresistance to platinum drugs. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4057. doi:10.1158/1538-7445.AM2013-4057

Because platinum drugs are often used for the chemotherapy of human cancers, when platinum resistance occurs it is a major issue. We recently reported that enhanced expression of Annexin A4 (Anx A4) increases chemoresistance to Carboplatin via increased extracellular efflux of the drug. However, the precise mechanisms of that chemoresistance, and the relationship of Anx A4 to platinum resistance in vivo, remain unclear. In this report we investigate in vitro the mechanism of platinum resistance induced by Anx A4 in endometrial carcinoma cells (HEC1 cells) which normally have a low level of expression of Anx A4. Forced expression of Anx A4 in HEC1 cells resulted in chemoresistance to platinum drugs. In addition, we compared HEC1 control cells with Anx A4-overexpressing HEC1 cells when both were xenografted to mice, Anx A4-overexpressing xenografted mice presented with significantly greater chemoresistance to Cisplatin in vivo. By immunofluorescence analysis we found that exposure to platinum drugs induced relocation of Anx A4 from the cytoplasm to the cellular membrane, where it became co-localized with ATP7A, a copper transporter also well known to be a platinum effluxer. When the expression of ATP7A was suppressed by small interfering RNA in HEC1 control cells, they showed no change of chemosensitivity to platinum drugs. However, suppressed ATP7A in Anx A4 overexpressing platinum-resistant cells, they showed improved chemosensitivity to platinum drugs, to a level comparable of that of control cells. Our results indicate that enhanced expression of Anx A4 confers platinum resistance by promoting efflux of platinum drugs via ATP7A. Citation Format: Shinya Matsuzaki, Akiko Morimoto, Satoshi Serada, Takuhei Yokoyama, Toshihiro Kimura, Eiji Kobayashi, Yutaka Ueda, Kiyoshi Yoshino, Masami Fujita, Takayuki Enomoto, Tetsuji Naka, Tadashi Kimura. Annexin A4-conferred platinum resistance is mediated by the copper transporter ATP7A. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4059. doi:10.1158/1538-7445.AM2013-4059

BACKGROUND: Platinum drugs play the key role for postoperative adjuvant therapy and treatment in progress and recurrent ovarian cancer. We have previously reported that ovarian clear cell carcinoma (CCC) has increased expression of Annexin A4 (Anx A4) in comparison with other subtypes of ovarian cancer. Enhanced expression of Anx A4 has been shown to induce chemoresistance via extracellular efflux of carboplatin. However, it remains unclear whether targeting Anx A4 is effective for improving the sensitization against chemotherapy, like platinum drugs. The aim of this study was to evaluate the role of Anx A4 in chemoresistance in ovarian CCC. MATERIAL AND METHODS: RMG-I cell lines were used to establish the stable knockdown of Anx A4. Plasmids encoding short hairpin RNAs (shRNAs) targeting Anx A4 were transfected. Chemoresistance was assessed by IC50 value in various drugs. RESULTS: Compared with control cells, knockdown of Anx A4 gene expression in RMG-I cells induced chemosentisitzation around 2-fold to cisplatin (IC50: 11.2 μM to 5.8 μM, P Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4225. doi:1538-7445.AM2012-4225

Background. Endometrial cancer is one of the most common malignancies of the female genital tract. The identification of proteins for prognostic assessment and therapeutic targets in this disease is of significant clinical importance. Quantitative proteomic analysis provides a powerful approach in screening for alterations in protein levels and post-translational modifications that are associated with tumors. To date, proteomic studies of cancer have focused particularly on sub-cellular compartments or post-translational modifications. An analysis of the differential expression of cell-surface membrane proteins would be of particular interest, since these proteins play key roles in cell function including cell migration and drug resistance. Purpose of study. To identify membrane proteins overexpressed in endometrial cancer which may represent novel biomarkers of disease and therapeutic targets. Procedures. We developed a biotinylation-based approach for cell membrane enrichment combined with iTRAQ (isobaric tags for relative and absolute quantitation) technology using nano-LC-MS/MS analysis, to identify cell surface proteins overexpressed in seven endometrial cancer cell lines compared with a control normal endometrial cell line. Results. 365 proteins were identified, of which, 65 proteins (18%) possessed a trans-membrane domain. We identified overexpression of 24 membrane proteins in endometrial cancer cell lines compared with a normal endometrial cell line. By this proteomic approach, we identified several tumor antigens which included antigens previously associated with endometrial cancer and antigens not previously reported in this disease. Tumorigenic proteins such as neural cell adhesion molecule L1 (NCAML1), previously reported to be overexpressed in endometrial cancer, were identified. Interestingly we also identified Claudin-4, a protein associated with poor prognosis in various cancers, but not previously reported in the pathogenesis of cancer. In addition, we also successfully identified novel antigens associated with endometrial cancer. Conclusions. We developed a high throughput cell-surface membrane proteomic analysis combining biotinylation of cell-surface membrane protein and iTRAQ technology. In addition to the identification of previously reported tumor antigens such as NCAML1 and Claudin-4, we also identified novel tumor antigens in endometrial cancer by this methodology. This iTRAQ based quantitative proteomic analysis represented a useful approach in screening for novel disease biomarkers and therapeutic targets. Further studies on the physiological role of novel tumor antigens overexpressed in endometrial cancer and their application as biomarkers/therapeutic targets are underway. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5108. doi:10.1158/1538-7445.AM2011-5108

The ATLAS collaboration has recently reported an excess of about 2.5 $\sigma$ global significance at around 2 TeV in the diboson channel with the boson-tagged fat dijets, which may imply a new resonance beyond the standard model. We provide a possible explanation of the excess as the isospin-triplet technivector mesons (technirhos, denoted as $\rho_\Pi^{\pm,3}$) of the walking technicolor in the case of the one-family model as a benchmark. As the effective theory for the walking technicolor at the scales relevant to the LHC experiment, we take a scale-invariant version of the hidden local symmetry model so constructed as to accommodate technipions, technivector mesons, and the technidilaton in such a way that the model respects spontaneously broken chiral and scale symmetries of the underlying walking technicolor. In particular, the technidilaton, a (pseudo) Nambu-Goldstone boson of the (approximate) scale symmetry predicted in the walking technicolor, has been shown to be successfully identified with the 125 GeV Higgs. Currently available LHC limits on those technihadrons are used to fix the couplings of technivector mesons to the standard-model fermions and weak gauge bosons. We find that the technirho's are mainly produced through the Drell-Yan process and predominantly decay to the dibosons, which accounts for the currently reported excess at around 2 TeV. The consistency with the electroweak precision test and other possible discovery channels of the 2 TeV technirhos are also addressed., Comment: 8 pages, 4 eps figures, latex; version to appear in PLB

A new particle at around 125 GeV has been observed at the LHC, which we show could be identified with the techni-dilaton (TD) predicted in the walking technicolor and thus should be an evidence of walking technicolor. The TD is a pseudo Nambu-Goldstone boson for the approximate scale symmetry spontaneously broken by techni-fermion condensation, with its lightness being ensured by the approximate scale invariance of the walking technicolor. We test the goodness-of-fit of the TD signatures using the presently available LHC data set, and show that the 125 GeV TD is actually favored by the current data to explain the reported signal strengths in the global fit as well as in each channel including the coupling properties, most notably the somewhat large diphoton event rate., 2 eps figures, 5 pages, latex; typos fixed, version published in PLB

We propose a new dark matter candidate, {\it light decoupled techni-dilaton}, which arises from the almost scale-invariant/conformal (walking) technicolor. We investigate its characteristic nature and discuss several cosmological and astrophysical constraints. It turns out that techni-dilatons are extremely weakly interacting and produced dominantly by the non-thermal mechanism to be the main component of dark matter with mass range between around 0.01 eV and 500 eV for typical walking technicolor scenarios., Comment: 6 pages, 2 figures; version to appear in PLB

Clear cell adenocarcinoma (CCC) is generally thought to originate from ovarian, endometrial, or renal tissue. A CCC of the peritoneum (CCAP) is an extremely rare medical condition and is associated with a poor prognosis. To date, only 10 cases of CCAP have been reported, of which half resulted in death or recurrence within 6 months after initial treatment because CCAP is commonly resistant to multiple drugs. In this report, we present a case of CCAP of the pouch of Douglas coexisting with an endometriosis and we offer a review of the related literature.

In this paper we compute the the one-loop chiral logarithmic corrections to the S and T parameters in a highly deconstructed Higgsless model with only three sites. In addition to the electroweak gauge bosons, this model contains a single extra triplet of vector states (which we denote \rho^{\pm} and \rho^0), rather than an infinite tower of "KK" modes. We compute the corrections to S and T in 'tHooft-Feynman gauge, including the ghost, unphysical Goldstone-boson, and appropriate "pinch" contributions required to obtain gauge-invariant results for the one-loop self-energy functions. We demonstrate that the chiral-logarithmic corrections naturally separate into two parts, a model-independent part arising from scaling below the \rho mass, which has the same form as the large Higgs-mass dependence of the S or T parameter in the standard model, and a second model-dependent contribution arising from scaling between the \rho mass and the cutoff of the model. The form of the universal part of the one-loop result allows us to correctly interpret the phenomenologically derived limits on the S and T parameters (which depend on a "reference" Higgs-boson mass) in this three-site Higgsless model. Higgsless models may be viewed as dual to models of dynamical symmetry breaking akin to "walking technicolor", and in these terms our calculation is the first to compute the subleading 1/N corrections to the S and T parameters. We also discuss the reduction of the model to the ``two-site'' model, which is the usual electroweak chiral lagrangian, noting the ``non-decoupling'' contributions present in the limit as M_\rho goes to infinity., Comment: 58 pages; uses JHEP and axodraw. Extensively corrected to incorporate consistent perturbative expansion, additional pinch contributions, and running of delocalization parameter. Footnotes added