We report the observation of two narrow structures in the mass spectra of the π(±)Υ(nS) (n=1, 2, 3) and π(±)h(b)(mP) (m=1, 2) pairs that are produced in association with a single charged pion in Υ(5S) decays. The measured masses and widths of the two structures averaged over the five final states are M(1)=(10,607.2±2.0)  MeV/c2, Γ(1)=(18.4±2.4)  MeV, and M(2)=(10,652.2±1.5)  MeV/c2, Γ(2)=(11.5±2.2)  MeV. The results are obtained with a 121.4  fb(-1) data sample collected with the Belle detector in the vicinity of the Υ(5S) resonance at the KEKB asymmetric-energy e+ e- collider.

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We report preliminary results on the analysis of the three-body Υ( 10860) → B Bπ, Υ(10860) → [B B * + c.c.]π and Υ(10860) → B * B * π decays including an observation of the Υ(10860) → Z ± b (10610)π ∓ → [B B * + c.c.] ± π ∓ and Υ(10860) → Z ± b (10650)π ∓ → [B * B * ] ± π ∓ decays as intermediate channels. We measure branching fractions of the three-body decays to be B(Υ(10860) → [B B * + c.c.] ± π ∓ ) = (28.3 ± 2.9 ± 4.6) × 10 −3 and B(Υ(10860) → [B * B * ] ± π ∓ ) = (14.1 ± 1.9 ± 2.4) × 10 −3 and set 90% C.L. upper limit B(Υ(10860) → [B B] ± π ∓ ) < 4.0 × 10 −3 . We also report results on the amplitude analysis of the three-body Υ(10860) → Υ(nS)π + π − , n = 1, 2, 3 decays and the analysis of the internal structure of the three-body Υ(10860) → h b (mP )π + π − , m = 1, 2 decays. The results are based on a 121.4 fb −1 data sample collected with the Belle detector at a center-of-mass energy near the Υ(10860).

Nijmegen breakage syndrome (NBS) is a chromosomal instability syndrome associated with cancer predisposition, radiosensitivity, microcephaly, and growth retardation. The NBS gene product, NBS1 (p95) or nibrin, is a part of the hMre11 complex, a central player associated with double strand break repair. We previously demonstrated that c-Myc directly activates NBS1 expression. Here we have shown that constitutive expression of NBS1 in Rat1a and HeLa cells induces/enhances their transformation. Repression of endogenous NBS1 levels using short interference RNA reduces the transformation activity of two tumor cell lines. Increased NBS1 expression is observed in 40 -52% of non-small cell lung carcinoma, hepatoma, and esophageal cancer samples. NBS1 overexpression stimulates phosphatidylinositol (PI) 3-kinase activity, leading to increased phosphorylation levels of Akt and its downstream targets such as glycogen synthase kinase 3␤ and mammalian target of rapamycin in different cell lines and tumor samples. Transformation induced by NBS1 overexpression can be inhibited by a PI3-kinase inhibitor (LY294002). Repression of endogenous Akt expression by short interference RNA decreases the transformation activity of Rat1a cells overexpressing NBS1. These results indicate that overexpression of NBS1 is an oncogenic event that contributes to transformation through the activation of PI3-kinase/Akt. Nijmegen breakage syndrome (NBS)3 is an autosomal recessive hereditary disorder characterized by microcephaly, a "bird-like" facial appearance, growth retardation, immunodeficiency, radiosensitivity, chromosomal instability, and predisposition to tumor formation (1-3). The gene defective in NBS has been cloned, and the gene product, NBS1 (p95, nibrin), is a member of the DNA double strand break repair complex (hMre11 complex) including hMre11, hRad50, and NBS1 (1, 3). Increased radiation sensitivity and radioresistant DNA synthesis of NBS fibroblasts are similar to the cellular features of AT (ataxia-telangiectasis) cells (2, 4), demonstrated by the recent results that ATM (ataxiatelangiectasis-mutated) protein phosphorylates NBS1 (5-7), linking these two proteins in the same pathway. NBS1 is a putative tumor suppressor gene as shown by the existence of NBS patients and some mutations discovered in different tumors (1, 2). However, NBS1 is expressed in highly proliferating tissues developmentally (8) and is located at sites of DNA synthesis through interaction with E2F (9). In addition, Mre11 complex is able to prevent double strand break accumulation during chromosomal DNA synthesis to ensure cell cycle progression (10). Nbs1 knock out in mouse embryonic stem cells shows the phenotype of diminished expansion of the inner cell mass of mutant blastocysts (Nbs1 null) (11, 12). Cellular proliferation defects are shown in Nbs1 m/m mouse embryonic fibroblasts (13). Obviously, the roles of NBS1 are multiple, and some of them are still subject to intensive investigation.Phosphatidylinositol (PI) 3-kinase is a major signaling component downs...