253 research outputs found
Search for the Decays B^0 -> D^{(*)+} D^{(*)-}
Using the CLEO-II data set we have searched for the Cabibbo-suppressed decays
B^0 -> D^{(*)+} D^{(*)-}. For the decay B^0 -> D^{*+} D^{*-}, we observe one
candidate signal event, with an expected background of 0.022 +/- 0.011 events.
This yield corresponds to a branching fraction of Br(B^0 -> D^{*+} D^{*-}) =
(5.3^{+7.1}_{-3.7}(stat) +/- 1.0(syst)) x 10^{-4} and an upper limit of Br(B^0
-> D^{*+} D^{*-}) D^{*\pm} D^\mp and
B^0 -> D^+ D^-, no significant excess of signal above the expected background
level is seen, and we calculate the 90% CL upper limits on the branching
fractions to be Br(B^0 -> D^{*\pm} D^\mp) D^+
D^-) < 1.2 x 10^{-3}.Comment: 12 page postscript file also available through
http://w4.lns.cornell.edu/public/CLNS, submitted to Physical Review Letter
Production in Two-Photon Interactions at CLEO
Using the CLEO detector at the Cornell storage ring, CESR, we study
the two-photon production of , making the first
observation of . We present the
cross-section for as a function of
the center of mass energy and compare it to that predicted by
the quark-diquark model.Comment: 10 pages, postscript file also available through
http://w4.lns.cornell.edu/public/CLN
Observation of the Decay
Using e+e- annihilation data collected by the CLEO~II detector at CESR, we
have observed the decay Ds+ to omega pi+. This final state may be produced
through the annihilation decay of the Ds+, or through final state interactions.
We find a branching ratio of [Gamma(Ds+ to omega pi+)/Gamma(Ds+ to eta
pi+)]=0.16+-0.04+-0.03, where the first error is statistical and the second is
systematic.Comment: 9 pages, postscript file also available through
http://w4.lns.cornell.edu/public/CLN
CCR3 and Choroidal Neovascularization
Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly in industrialized countries. The “wet” AMD, characterized by the development of choroidal neovacularization (CNV), could result in rapid and severe loss of central vision. The critical role of vascular endothelial growth factor A (VEGF-A) in CNV development has been established and VEGF-A neutralization has become the standard care for wet AMD. Recently, CCR3 was reported to play an important role in CNV development and that CCR3 targeting was reported to be superior to VEGF-A targeting in CNV suppression. We investigated the role of CCR3 in CNV development using the Matrigel induced CNV and found that in both rats and mice, CNV was well-developed in the control eyes as well as in eyes treated with CCR3 antagonist SB328437 or CCR3 neutralizing antibodies. No statistically significant difference in CNV areas was found between the control and SB328437 or CCR3-ab treated eyes. Immunostaining showed no specific expression of CCR3 in or near CNV. In contrast, both VEGF-A neutralizing antibodies and rapamycin significantly suppressed CNV. These results indicate that CCR3 plays no significant role in CNV development and question the therapeutic approach of CCR3 targeting to suppress CNV. On the other hand, our data support the therapeutic strategies of VEGF-A and mTOR (mammalian target of rapamycin) targeting for CNV
Angiopoietin-1 inhibits tumour growth and ascites formation in a murine model of peritoneal carcinomatosis
Angiopoietin-1 is an important regulator of endothelial cell survival. Angiopoietin-1 also reduces vascular permeability mediated by vascular endothelial growth factor. The effects of angiopoietin-1 on tumour growth and angiogenesis are controversial. We hypothesised that angiopoietin-1 would decrease tumour growth and ascites formation in peritoneal carcinomatosis. Human colon cancer cells (KM12L4) were transfected with vector (pcDNA) alone (control) or vector containing angiopoietin-1 and injected into the peritoneal cavities of mice. After 30 days, the following parameters were measured: number of peritoneal nodules, ascites volume, and diameter of the largest tumour. Effects of angiopoietin-1 on vascular permeability were investigated using an intradermal Miles assay with conditioned media from transfected cells. Seven of the nine mice in the pcDNA group developed ascites (1.3±0.5 ml (mean±s.e.m.)), whereas no ascites was detectable in the angiopoietin-1 group (0 out of 10) (P<0.01). Number of peritoneal metastases (P<0.05), tumour volume, (P<0.05), vessel counts (P<0.01), and tumour cell proliferation (P<0.01) were significantly reduced in angiopoietin-1-expressing tumours. Conditioned medium from angiopoietin-1-transfected cells decreased vascular permeability more than did conditioned medium from control cells (P<0.05). Our results suggest that angiopoietin-1 is an important mediator of angiogenesis and vascular permeability and thus could theoretically serve as an anti-neoplastic agent for patients with carcinomatosis from colorectal cancer
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