Synergistic therapeutic effect of arsenic trioxide and radiotherapy in BALB/C nude mice bearing nasopharyngeal carcinoma xenografts

It has been shown that arsenic trioxide (ATO) induced apoptosis in human nasopharyngeal carcinoma cells and inhibited the growth of nasopharyngeal carcinoma xenografts (NPCX) in nude mice. Aim: The present study was designed to determine whether ATO at the non-toxic dose level could potentiate the therapeutic effectiveness of radiation therapy in nasopharyngeal carcinoma, using a BALB/C nude mouse xenograft model. Methods: The mice bearing NPCX were treated with radiation alone (2, 4, and 6 Gy), ATO alone (4 mg/kg/day x 6 days), and ATO plus radiation at the same dosage levels. Time of tumor growth delay (defined as the time necessary for the tumor to grow four-fold of its initial volume after, compared with untreated tumors) and toxic effects were determined. Results: The low dose ATO alone has no pronounced effects on tumor growth delay compared to untreated control. However, compared with radiation alone, the combined regimen delayed the tumor growth by 2–10 days and had no significant toxic effects such as the liver function damage. Conclusions: Combination of ATO at non-toxic dose level and radiation has synergistic effects on tumor growth inhibition in vivo and is well tolerated.Установлено, что триоксид мышьяка (ТОМ) индуцирует апоптоз в клетках карциномы носоглотки человека и ингибирует рост ксенографта карциномы носоглотки у атимических мышей. Цель работы — установить терапевтическую эффективность радиотерапии в комбинации ТОМ в нетоксичной дозе мышам линии BALB/ с ксенографтом карциномы носоглотки. Методы: животные с ксенографтом карциномы носоглотки получали либо только радиотерапию (2, 4 и 6 Гр) или ТОМ (4 мг/кг/день в течение 6 дней), или их комбинацию в тех же режимах и дозах. Задержку роста опухоли определяли как различие во времени, необходимом для достижения опухолью 4-кратного объема по сравнению с начальным объемом в опытной группе versus такового в контрольной группе. Результаты: введение ТОМ в низкой дозе не оказывало выраженного влияния на рост опухоли по сравнению с показателями в конт­рольной группе, а в комбинации с облучением приводило к задержке роста опухоли на 2–12 сут по сравнению с показателями у животных, получавших только лучевую терапию при отсутствии выраженных побочных эффектов. Выводы: комбинация ТОМ в нетоксической дозе и лучевой терапии приводит к ингибированию роста опухоли in vivo и не вызывает побочных эффектов. Ключевые слова: триоксид мышьяка, радиотерапия, ксенографт карциномы носоглотки

Measurements of J/psi Decays into 2(pi+pi-)eta and 3(pi+pi-)eta

Based on a sample of 5.8X 10^7 J/psi events taken with the BESII detector, the branching fractions of J/psi--> 2(pi+pi-)eta and J/psi-->3(pi+pi-)eta are measured for the first time to be (2.26+-0.08+-0.27)X10^{-3} and (7.24+-0.96+-1.11)X10^{-4}, respectively.Comment: 11 pages, 6 figure

BESII Detector Simulation

A Monte Carlo program based on Geant3 has been developed for BESII detector simulation. The organization of the program is outlined, and the digitization procedure for simulating the response of various sub-detectors is described. Comparisons with data show that the performance of the program is generally satisfactory.Comment: 17 pages, 14 figures, uses elsart.cls, to be submitted to NIM

Measurement of branching fractions for the inclusive Cabibbo-favored ~K*0(892) and Cabibbo-suppressed K*0(892) decays of neutral and charged D mesons

The branching fractions for the inclusive Cabibbo-favored ~K*0 and Cabibbo-suppressed K*0 decays of D mesons are measured based on a data sample of 33 pb-1 collected at and around the center-of-mass energy of 3.773 GeV with the BES-II detector at the BEPC collider. The branching fractions for the decays D+(0) -> ~K*0(892)X and D0 -> K*0(892)X are determined to be BF(D0 -> \~K*0X) = (8.7 +/- 4.0 +/- 1.2)%, BF(D+ -> ~K*0X) = (23.2 +/- 4.5 +/- 3.0)% and BF(D0 -> K*0X) = (2.8 +/- 1.2 +/- 0.4)%. An upper limit on the branching fraction at 90% C.L. for the decay D+ -> K*0(892)X is set to be BF(D+ -> K*0X) < 6.6%

Study of J/ψ→ωK+K−J/\psi \to \omega K^+K^-

New data are presented on $J/\psi \to \omega K^+K^-$ from a sample of 58M $J/\psi$ events in the upgraded BES II detector at the BEPC. There is a conspicuous signal for $f_0(1710) \to K^+K^-$ and a peak at higher mass which may be fitted with $f_2(2150) \to K\bar K$. From a combined analysis with $\omega \pi ^+ \pi ^-$ data, the branching ratio $BR(f_0(1710)\to\pi\pi)/BR(f_0(1710) \to K\bar K)$ is $< 0.11$ at the 95% confidence level.Comment: 11 pages, 5 figures. Submitted to Phys. Lett.

Measurements of Cabibbo Suppressed Hadronic Decay Fractions of Charmed D0 and D+ Mesons

Using data collected with the BESII detector at $e^{+}e^{-}$ storage ring Beijing Electron Positron Collider, the measurements of relative branching fractions for seven Cabibbo suppressed hadronic weak decays $D^0 \to K^- K^+$, $\pi^+ \pi^-$, $K^- K^+ \pi^+ \pi^-$ and $\pi^+ \pi^+ \pi^- \pi^-$, $D^+ \to \bar{K^0} K^+$, $K^- K^+ \pi^+$ and $\pi^- \pi^+ \pi^+$ are presented.Comment: 11 pages, 5 figure

Direct Measurement of the Pseudoscalar Decay Constant fD+

The absolute branching fraction of $D^+ \to \mu^+ \nu$ has been directly measured by an analysis of a data sample of about 33 ${\rm pb^{-1}}$ collected around $\sqrt{s}=3.773$ GeV with the BES-II at the BEPC. At these energies, $D^-$ meson is produced in pair as $e^+e^-\to D^{+} D^{-}$. A total of $5321 \pm 149 \pm 160$ $D^-$ mesons are reconstructed from this data set. In the recoil side of the tagged $D^-$ mesons, $2.67\pm1.74$ purely leptonic decay events of $D^+ \to \mu^+ \nu$ are observed. This yields a branching fraction of $BF(D^+ \to \mu^+ \nu_{\mu}) = (0.122^{+0.111}_{-0.053}\pm 0.010)$, and a corresponding pseudoscalar decay constant $f_{D^+}=(371^{+129}_{-119}\pm 25)$ MeV.Comment: 7 pages, 8 figures, Submitted to Physics Letters B in October, 200

The Pediatric Cell Atlas: defining the growth phase of human development at single-cell resolution

Single-cell gene expression analyses of mammalian tissues have uncovered profound stage-specific molecular regulatory phenomena that have changed the understanding of unique cell types and signaling pathways critical for lineage determination, morphogenesis, and growth. We discuss here the case for a Pediatric Cell Atlas as part of the Human Cell Atlas consortium to provide single-cell profiles and spatial characterization of gene expression across human tissues and organs. Such data will complement adult and developmentally focused HCA projects to provide a rich cytogenomic framework for understanding not only pediatric health and disease but also environmental and genetic impacts across the human lifespan