Spectral Decomposition of the Tent Map with Varying Height

The generalized spectral decomposition of the Frobenius-Perron operator of the tent map with varying height is determined at the band-splitting points. The decomposition includes both decay onto the attracting set and the approach to the asymptotically periodic state on the attractor. Explicit compact expressions for the polynomial eigenstates are obtained using algebraic techniques.Comment: 39 pages, 7 figures, in LATeX with embedded PS figure

Backward whirl in a simple rotor supported on hydrodynamic bearings

The asymmetric nature of the fluid film stiffness and damping properties in rotors supported on fluid film bearings causes a forward or a backward whirl depending on the bearing parameters and the speed of the rotor. A rotor was designed to exhibit backward synchronous whirl. The rotor-bearing system exhibited split criticals, and a backward whirl was observed between the split criticals. The orbital diagrams show the whirl pattern

H-E-Super Magic Decomposition of Graphs

An H-magic labeling in an H-decomposable graph G is a bijection f:V(G) U E(G) --> {1,2, … ,p+q} such that for every copy H in the decomposition, $\sum\limits_{v\in V(H)} f(v)+\sum\limits_{e\in E(H)} f(e)$ is constant. The function f is said to be H-E-super magic if f(E(G)) = {1,2, … ,q}. In this paper, we study some basic properties of m-factor-E-super magic labelingand we provide a necessary and sufficient condition for an even regular graph to be 2-factor-E-super magic decomposable. For this purpose, we use Petersen\u27s theorem and magic squares

STRUCTURE OF BENZ[A]ANTHRACENE-7,12-DIONE

C18H1002, monoclinic, C2/c, a = 10.918 (1), b = 11.369(1), c = 19.850(1)A, /~= 97.224(7) ° , U = 2444.4 A 3, Z = 8, D,n = 1.41 (2), D c = 1.403 Mg m -3, F(000) = 1072, 2(CuKa) = 1.5418/~, ~t = 0.742 mm -1. 2253 reflections were measured, of which 1039 had significant intensities. Refinement converged to a final R of 0.045. The molecule is approximately planar. Ring C is significantly non-delocalized. Bonds C(3)-C(4) and C(5)-C(6) are short, and indicate pronounced olefinic character for these bonds

Germline PTPRD mutations in Ewing sarcoma: biologic and clinical implications.

Ewing sarcoma occurs in children, adolescents and young adults. High STAT3 levels have been reported in approximately 50% of patients with Ewing sarcoma, and may be important in tumorigenesis. Protein tyrosine phosphatase delta (PTPRD) is a tumor suppressor that inhibits STAT3 activation. To date, while somatic mutations in PTPRD have been reported in diverse tumors, germline mutations of PTPRD have not been investigated in Ewing sarcoma or other cancers. We identified a novel germline mutation in the PTPRD gene in three of eight patients (37.5%) with metastatic Ewing sarcoma. Although the functional impact in two of the patients is unclear, in one of them the aberration was annotated as a W775stop germline mutation, and would be expected to lead to gene truncation and, hence, loss of the STAT3 dephosphorylation function of PTPRD. Since STAT3 is phosphorylated after being recruited to the insulin growth factor receptor (IGF-1R), suppression of IGF-1R could attenuate the enhanced STAT3 activation expected in the presence of PTPRD mutations. Of interest, two of three patients with germline PTPRD mutations achieved durable complete responses following treatment with IGF-1R monoclonal antibody-based therapies. Our pilot data suggest that PTPRD germline mutations may play a role in the development of Ewing sarcoma, a disease of young people, and their presence may have implications for therapy

インドにおけるオープンアクセスと機関リポジトリ

DRFIC2008 Session 1. Open Access and Institutional Repository in Asia-PacificDRFIC2008 セッション1:アジア・環太平洋地域におけるオープンアクセスと機関リポジトリ 報告

Targeted therapy of advanced gallbladder cancer and cholangiocarcinoma with aggressive biology: eliciting early response signals from phase 1 trials.

PurposePatients with advanced cholangiocarcinoma (CC) and gallbladder carcinoma (GC) have few therapeutic options for relapsed disease. methods: Given the overall poor prognosis in this population and the availability of novel targeted therapies, we systematically analyzed the characteristics and outcomes for GC and CC patients treated on phase I trials with an emphasis on targeted agents and locoregional therapies.ResultsOf 40 treated patients (GC=6; CC=34; median age, 60 years), 8 (20%) had stable disease (SD) > 6 months, 3 (8%) partial response (PR), on protocols with hepatic arterial drug infusion and anti-angiogenic, anti-HER-2/neu or novel MAPK/ERK kinase (MEK) inhibitors. Median progression-free survival (PFS) on phase I trials was 2.0 months (95% CI 1.7, 2.8) versus 3.0 months (95% CI 2.4, 5.0), 3.0 months (95% CI 2.3, 4.6), and 3.0 months (95% CI 2.4, 3.9) for their first-, second-, and last-line FDA-approved therapy. In univariate analysis, >3 metastatic sites, elevated alanine aminotransferase (ALT) (>56IU/L), serum creatinine (>1.6mg/dL), and CA19-9 (>35U/mL) were associated with a shorter PFS. Mutational analysis revealed mutation in the KRAS oncogene in 2 of 11 patients (18%). The SD >6 months/PR rate of 28% was seen with hepatic arterial infusion of oxaliplatin, and inhibitors of angiogenesis, HER-2/neu or MEK.ConclusionsThe PFS in phase I trials was similar to that of the first, second, and last-line therapy (P=0.95, 0.98, 0.76, respectively) with FDA-approved agents given in the advanced setting, emphasizing a role for targeted agents in a clinical trials setting as potentially valuable therapeutic options for these patients

Novel secondary somatic mutations in Ewing's sarcoma and desmoplastic small round cell tumors.

BackgroundEwing's sarcoma (ES) and desmoplastic small round cell tumors (DSRCT) are small round blue cell tumors driven by an N-terminal containing EWS translocation. Very few somatic mutations have been reported in ES, and none have been identified in DSRCT. The aim of this study is to explore potential actionable mutations in ES and DSRCT.MethodologyTwenty eight patients with ES or DSRCT had tumor tissue available that could be analyzed by one of the following methods: 1) Next-generation exome sequencing platform; 2) Multiplex PCR/Mass Spectroscopy; 3) Polymerase chain reaction (PCR)-based single- gene mutation screening; 4) Sanger sequencing; 5) Morphoproteomics.Principal findingsNovel somatic mutations were identified in four out of 18 patients with advanced ES and two of 10 patients with advanced DSRCT (six out of 28 (21.4%));KRAS (n = 1), PTPRD (n = 1), GRB10 (n = 2), MET (n = 2) and PIK3CA (n = 1). One patient with both PTPRD and GRB10 mutations and one with a GRB10 mutation achieved a complete remission (CR) on an Insulin like growth factor 1 receptor (IGF1R) inhibitor based treatment. One patient, who achieved a partial remission (PR) with IGF1R inhibitor treatment, but later developed resistance, demonstrated a KRAS mutation in the post-treatment resistant tumor, but not in the pre-treatment tumor suggesting that the RAF/RAS/MEK pathway was activated with progression.ConclusionsWe have reported several different mutations in advanced ES and DSRCT that have direct implications for molecularly-directed targeted therapy. Our technology agnostic approach provides an initial mutational roadmap used in the path towards individualized combination therapy

Development of self-repair nano-rod scaffold materials for implantation of osteosarcoma affected bone tissue

Osteosarcoma is the most widely recognized fatal bone disease in children and young adults. The osteosarcoma affected places of bone implant materials lose their activity after a period of time due to the possibility of regenerating sarcoma cells. Hence, the complete recovery of this disease is very challenging. Subsequently, new helpful methodologies, including natural antioxidant loaded bone implant materials, are effectively used to treat osteosarcoma cells. In this regard, nano-hydroxyapatite reinforced with a xylitol based poly(xylitol sebacate) PXS co-polymer together with a capsaicin loaded scaffold was investigated on osteosarcoma cells. The physicochemical properties of the scaffold were evaluated by FT-IR (Fourier transform infrared spectroscopy), SEM (scanning electron microscopy), TEM (transmission electron microscopy), and XRD (X-ray diffraction). The in vitro release and antioxidant activity of the capsaicin loaded nHAP/PXS/CAP scaffold were evaluated by UV-Visible spectroscopy. Cytotoxicity against the Saos-2 cancer line and cell viability in the osteoblast cell MG63 are reported. Eventually, the composite enlarges the creation of reactive oxygen species (ROS) in Saos-2 cells

Phase I dose-escalation study of the mTOR inhibitor sirolimus and the HDAC inhibitor vorinostat in patients with advanced malignancy.

Preclinical models suggest that histone deacetylase (HDAC) and mammalian target of rapamycin (mTOR) inhibitors have synergistic anticancer activity. We designed a phase I study to determine the safety, maximum tolerated dose (MTD), recommended phase II dose (RP2D), and dose-limiting toxicities (DLTs) of combined mTOR inhibitor sirolimus (1 mg-5 mg PO daily) and HDAC inhibitor vorinostat (100 mg-400 mg PO daily) in patients with advanced cancer. Seventy patients were enrolled and 46 (66%) were evaluable for DLT assessment since they completed cycle 1 without dose modification unless they had DLT. DLTs comprised grade 4 thrombocytopenia (n = 6) and grade 3 mucositis (n = 1). Sirolimus 4 mg and vorinostat 300 mg was declared RP2D because MTD with sirolimus 5 mg caused significant thrombocytopenia. The grade 3 and 4 drug-related toxic effects (including DLTs) were thrombocytopenia (31%), neutropenia (8%), anemia (7%), fatigue (3%), mucositis (1%), diarrhea (1%), and hyperglycemia (1%). Of the 70 patients, 35 (50%) required dose interruption or modification and 61 were evaluable for response. Partial responses were observed in refractory Hodgkin lymphoma (-78%) and perivascular epithelioid tumor (-54%), and stable disease in hepatocellular carcinoma and fibromyxoid sarcoma. In conclusion, the combination of sirolimus and vorinostat was feasible, with thrombocytopenia as the main DLT. Preliminary anticancer activity was observed in patients with refractory Hodgkin lymphoma, perivascular epithelioid tumor, and hepatocellular carcinoma