Histone acetyltransferases and histone deacetylases (HDACs) determine the acetylation status of histones, regulating gene transcription. Decidualization is the progestin-induced differentiation of estrogen-primed endometrial stromal cells (ESCs), which is crucial for implantation and maintenance of pregnancy. We here show that trichostatin A (TSA), a specific HDAC inhibitor, enhances the up-regulation of decidualization markers such as insulin-like growth factor binding protein-1 (IGFBP-1) and prolactin in a dose-dependent manner that is directed by 17␤-estradiol (E 2 ) plus progesterone (P 4 ) in cultured ESCs, but not glandular cells, both isolated from human endometrium. Morphological changes resembling decidual transformation were also augmented by co-addition of TSA. Acid urea triton gel analysis and immunoblot using acetylated histone typespecific antibodies demonstrated that treatment with E 2 plus P 4 significantly increased the levels of acetylated H3 and H4 whose increment was augmented by cotreatment with TSA. Chromatin immunoprecipitation assay revealed that treatment with E 2 plus P 4 increased the amount of proximal progesterone-responsive region of IGFBP-1 promoter associated with acetylated H4, which was dramatically enhanced by co-addition of TSA. Taken together, our results suggest that histone acetylation is deeply involved in differentiation of human ESCs and that TSA has a potential as an enhancer of decidualization through promotion of progesterone action.

Only 20.5% to 61.6% of abstracts presented at biomedical meetings are subsequently published as full-length articles. The aim of this study was to analyze the abstract-to-publication rate of International Liver Transplantation Society (ILTS) meeting abstracts. Abstracts presented at 5 consecutive annual ILTS meetings (2004)(2005)(2006)(2007)(2008) were included to ensure a minimum follow-up period of 4 years. For each abstract, a PubMed Central search was conducted with the first author's name and affiliation along with keywords from the title. The following abstract characteristics were examined and used to obtain the abstractto-publication rate: (1) the year of presentation, (2) the presentation category (plenary session, concurrent oral presentation, or poster presentation), (3) the type of study (randomized clinical study, case report, other clinical study, or basic science study), (4) the first author's discipline (surgery, medicine, anesthesiology/critical care medicine, pathology, radiology, or pharmacology), and (5) the location of the authors (ie, an English-speaking or non-English-speaking country). A total of 2345 abstracts (469 6 144 abstracts per meeting) were presented, and 913 of those abstracts (38.9%) were expanded into fulllength publications. It took 46 months for 90% of the abstracts to be published as full-length journal articles. The abstract-topublication rates differed with the year of abstract presentation (50.2% in 2004, 45.9% in 2005, 47.6% in 2006, 30.6% in 2007, and 30.3% in 2008; P < 0.001), with the presentation category (49.6% for plenary sessions, 48.5% for concurrent oral presentations, and 34.8% for poster presentations; P < 0.001), and with the type of study (66.7% for randomized clinical studies, 63.1% for basic science studies, 36.7% for other clinical studies, and 35.0% for case reports; P < 0.001). Abstracts from authors from non-English-speaking countries had a higher publication rate (41.1% versus 33.6%, P < 0.001). No differences were found between first authors' disciplines. Liver Transpl 20:355-360, 2014. V C 2014 AASLD.Received November 5, 2013; accepted November 24, 2013.Presenting abstracts at national meetings allows researchers to share their scientific discoveries with a large audience, and this should lead them to submit their findings as full-length manuscripts to peerreviewed journals for publication. Unfortunately, not all researchers follow through with this process after the presentation of their abstracts. This failure to publish abstract data in full-length articles limits the dissemination of knowledge, the opportunity for more rigorous peer review of the findings, and ultimately could indicate the need to improve society meetings and their related specialties. The abstract to peerreviewed publication rate has been reported to be 20.5% to 61.6% for various medical specialties. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] In the field of liver transplantation, the annual meeting of the International Liver Transplantation Socie...

SP-10 is a sperm intra-acrosomal protein, specific to the testis, that is believed to play an important role in egg-sperm binding. While the molecular characterization of the SP-10 protein has been clarified, little is yet known of its functional role in fertilization. We therefore established a monoclonal antibody (mAb pep-SP10) against a peptide (pep-SP10) that included the most hydrophilic portion of human SP-10 between the 135th and 149th amino acids. Human SP-10 was found to be localized in the equatorial region of acrosome-reacted sperm by immunofluorescent staining using our mAb pep-SP10. Monoclonal Ab pep-SP10 inhibited sperm-oolemma binding in the zona-free hamster egg penetration test, but it did not inhibit sperm-zona binding in the hemizona assay. Furthermore, we demonstrated that the oolemmal ligands of human SP-10 did not include beta(1) integrins, the most promising candidates for oocyte ligands involved in sperm-oolemma binding, based on the findings of a human sperm-cultured cell binding assay using F9 mouse embryonal carcinoma cells and F9-transformed cells lacking beta(1) integrins. In conclusion, our present data suggest that human SP-10, expressed on the equatorial region of acrosome-reacted sperm, indeed mediates sperm-oolemma binding in a beta(1) integrin-independent manner, but not sperm-zona binding.

AimsLeiomyosarcomas (LMSs) occur in various tissues and harbour potential for metastases. The genomic landscape of LMS is poorly understood. In an effort to improve understanding of the LMS genome, we analysed 11 LMSs of somatic soft tissue including matching tissue of normal phenotype.MethodsDNA derived from microdissected tumour domains and matching normal tissue underwent amplicon sequencing of 409 tumour suppressors and oncogenes using the Ion Torrent Comprehensive Cancer Panel.ResultsGenomic changes were heterogeneous with few recurrent abnormalities detected. Coding variants were identified in genes involved in signal transduction, transcriptional regulation and DNA repair. There were variants in several genes related to angiogenesis and GPR124 variants (TEM5) were confirmed by immunohistochemical analysis of a LMS tissue microarray. Surprisingly, there were shared coding variants in tumour and corresponding normal tissue.ConclusionsLMSs are a very heterogeneous population lacking recurrent somatic abnormalities. The presence of damaging mutations in normal tissue may reflect either a germline predisposition or field effect rather than tissue contamination. Hopeful therapeutic targets appear to be those related to AKT/MTOR pathway.

Reversible protein tyrosine phosphorylation, coordinately controlled by protein tyrosine kinases and phosphatases, is a critical element in signal transduction pathways regulating a wide variety of biological processes, including cell growth, differentiation, and tumorigenesis. We have previously reported that c-Src belonging to the Src family tyrosine kinase (SFK) becomes dephosphorylated at tyrosine 530 (Y530) and thereby activated during progestin-induced differentiation of human endometrial stromal cells (i.e., decidualization). In this study, to elucidate the role of decidual c-Src activation, we examined whether 4-amino-5-(4-methylphenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP1) and 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2), both potent and selective SFK inhibitors, affected the ovarian steroid-induced decidualization in vitro. Unexpectedly, PP1 paradoxically increased the kinase activity of decidual c-Src together with dephosphorylation of Y530 in the presence of ovarian steroids. Concomitantly, PP1 enhanced morphological and functional decidualization, as determined by induction of decidualization markers, such as insulin-like growth factor binding protein-1 and prolactin. PP2 also advanced decidualization along with up-regulation of the active form of c-Src whose Y-530 was dephosphorylated. In contrast to PP1 and PP2, herbimycin A, a tyrosine kinase inhibitor with less specificity for SFKs, showed little enhancing effect on the expression of both IGFBP-1 and active c-Src. These results suggest that SFKs, including c-Src, may play a significant role in stromal cell differentiation, providing a clue for a possible therapeutic strategy to modulate endometrial function by targeting signaling pathway(s) involving SFKs.