Studies of the Decay B+- -> D_CP K+-

We report studies of the decay B+- -> D_CP K+-, where D_CP denotes neutral D mesons that decay to CP eigenstates. The analysis is based on a 29.1/fb data sample of collected at the \Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric e+ e- storage ring. Ratios of branching fractions of Cabibbo-suppressed to Cabibbo-favored processes involving D_CP are determined to be B(B- -> D_1 K-)/B(B- -> D_1 pi-)=0.125 +- 0.036 +- 0.010 and B(B- -> D_2 K-)/B(B- -> D_2 pi-)=0.119 +- 0.028 +- 0.006, where indices 1 and 2 represent the CP=+1 and CP=-1 eigenstates of the D0 - anti D0 system, respectively. We also extract the partial rate asymmetries for B+- -> D_CP K+-, finding A_1 = 0.29 +- 0.26 +- 0.05 and A_2 = -0.22 +- 0.24 +- 0.04.Comment: 10 pages, 2 figures, submitted to Physical Review Letter

Chitohexaose Activates Macrophages by Alternate Pathway through TLR4 and Blocks Endotoxemia

Sepsis is a consequence of systemic bacterial infections leading to hyper activation of immune cells by bacterial products resulting in enhanced release of mediators of inflammation. Endotoxin (LPS) is a major component of the outer membrane of Gram negative bacteria and a critical factor in pathogenesis of sepsis. Development of antagonists that inhibit the storm of inflammatory molecules by blocking Toll like receptors (TLR) has been the main stay of research efforts. We report here that a filarial glycoprotein binds to murine macrophages and human monocytes through TLR4 and activates them through alternate pathway and in the process inhibits LPS mediated classical activation which leads to inflammation associated with endotoxemia. The active component of the nematode glycoprotein mediating alternate activation of macrophages was found to be a carbohydrate residue, Chitohexaose. Murine macrophages and human monocytes up regulated Arginase-1 and released high levels of IL-10 when incubated with chitohexaose. Macrophages of C3H/HeJ mice (non-responsive to LPS) failed to get activated by chitohexaose suggesting that a functional TLR4 is critical for alternate activation of macrophages also. Chitohexaose inhibited LPS induced production of inflammatory molecules TNF-α, IL-1β and IL-6 by macropahges in vitro and in vivo in mice. Intraperitoneal injection of chitohexaose completely protected mice against endotoxemia when challenged with a lethal dose of LPS. Furthermore, Chitohexaose was found to reverse LPS induced endotoxemia in mice even 6/24/48 hrs after its onset. Monocytes of subjects with active filarial infection displayed characteristic alternate activation markers and were refractory to LPS mediated inflammatory activation suggesting an interesting possibility of subjects with filarial infections being less prone to develop of endotoxemia. These observations that innate activation of alternate pathway of macrophages by chtx through TLR4 has offered novel opportunities to cell biologists to study two mutually exclusive activation pathways of macrophages being mediated through a single receptor

Role of Sphingosine Kinase 1 and Sphingosine-1-Phosphate Axis in Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC) is primarily diagnosed in the latter stages of disease progression and is the third leading cause of cancer deaths worldwide. Thus, there is a need to find biomarkers of early HCC as well as the development of more effective treatments for the disease. Sphingosine-1-phosphate (S1P) is a pleiotropic lipid signaling molecule produced by two isoforms of sphingosine kinase (SphK1 and SphK2) that is involved in regulation of many aspects of mammalian physiology and pathophysiology, including inflammation, epithelial and endothelial barrier function, cancer, and metastasis, among many others. Abundant evidence indicates that SphK1 and S1P promote cancer progression and metastasis in multiple types of cancers. However, the role of SphK/S1P in HCC is less well studied. Here, we review the current state of knowledge of SphKs and S1P in HCC, including evidence for the correlation of SphK1 expression and S1P levels with progression of HCC and negative outcomes, and discuss how this information could lead to the design of more effective diagnostic and treatment modalities for HCC

Observation of Ds+K- and evidence for D-s(+)pi(-) final states in neutral B decays

We report the first observation of a B meson decay that is not accessible by a direct spectator process. The channel (B) over bar (0)-->Ds+K- is found in a sample of 85x10(6) B (B) over bar events, collected with the Belle detector at KEKB, with a branching fraction B((B) over bar (0)-->Ds+K-)=(4.6(-1.1)(+1.2)+/-1.3)x10(-5). We also obtain evidence for the B-0-->D(s)(+)pi(-) decay with branching fraction B(B-0-->D(s)(+)pi(-))=(2.4(-0.8)(+1.0)+/-0.7)x10(-5). This value may be used to extract a model-dependent value of \V-ub\

Upper bound on the decay tau ->mu gamma from the Belle detector

We have performed a search for the lepton-flavor-violating decay tau-->mugamma using a data sample of 86.3 fb(-1) accumulated by the Belle detector at KEK. No evidence for a signal is seen, and we set an upper limit for the branching fraction of B(tau-->mugamma) < 3.1x10(-7) at the 90% confidence level

Measurement of the B-0-(B)over-bar(0) mixing parameter Delta m(d) using semileptonic B-0 decays

We present a measurement of the B-0-(B-0) over bar mixing parameter Deltam(d) using neutral B meson pairs in a 29.1 fb(-1) data sample collected at the Y(4S) resonance with the Belle detector at the KEKB asymmetric-energy e(+)e(-) collider. We exclusively reconstruct one neutral B meson in the semileptonic B-0-->D*-.(+)nu decay mode and identify the flavor of the accompanying B meson from its decay products. From the distribution of the time intervals between the two flavor-tagged B meson decay points, we obtain Deltam(d)=(0.494+/-0.012+/-0.015) ps(-1), where the first error is statistical and the second error is systematic

Observation of B -> K(*)l(+)l(-)

We report the observation of the flavor-changing neutral current decay B-->K*l(+l-) and an improved measurement of the decay B-->Kl(+l-), where l represents an electron or a muon, with a data sample of 140 fb(-1) accumulated at the Y(4S) resonance with the Belle detector at KEKB. The results for the branching fractions are B(B-->K*l(+l-))=(11.5(-2.4)(+2.6)+/-0.8+/-0.2)x10(-7) and B(B-->Kl(+l-))=(4.8(-0.9)(+1.0)+/-0.3+/-0.1)x10(-7), where the first error is statistical, the second is systematic and the third is from model dependence

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