The beta decay of N-21

The beta-delayed neutron and gamma energy spectra taken from the decay of neutron-rich nucleus N-21 were measured by using the beta - gamma and beta - n coincidence detection method. Thirteen new neutron groups ranging from 0.28MeV to 4.98 MeV and with a total branching ratio of 88.7 +/- 4.2% were observed and presented. One gamma transition with an energy of 1222 keV emitted from the excited state of O-21, and four gamma transitions with energies of 1674, 2397, 2780, and 3175 keV emitted from the excited states of O-20 were identified in the 3 decay chain of N-21. The beta decay half-life for N-21 is determined to be 82.9 +/- 1.9 ms. The uncertainty of half-life is much smaller than the previous result.

Cells deficient in the base excision repair protein, DNA polymerase beta, are hypersensitive to oxaliplatin chemotherapy

A significant proportion of human cancers overexpress DNA polymerase beta (Pol beta), the major DNA polymerase involved in base excision repair. The underlying mechanism and biological consequences of overexpression of this protein are unknown. We examined whether Pol beta, expressed at levels found in tumor cells, is involved in the repair of DNA damage induced by oxaliplatin treatment and whether the expression status of this protein alters the sensitivity of cells to oxaliplatin. DNA damage induced by oxaliplatin treatment of HCT116 and HT29 colon cancer cells was observed to be associated with the stabilization of Pol beta protein on chromatin. In comparison with HCT116 colon cancer cells, isogenic oxaliplatin-resistant (HCT-OR) cells were found to have higher constitutive levels of Pol beta protein, faster in vitro repair of a DNA substrate containing a single nucleotide gap and faster repair of 1,2-GG oxaliplatin adduct levels in cells. In HCT-OR cells, small interfering RNA knockdown of Pol beta delayed the repair of oxaliplatin-induced DNA damage. In a different model system, Pol beta-deficient fibroblasts were less able to repair 1,2-GG oxaliplatin adducts and were hypersensitive to oxaliplatin treatment compared with isogenic Pol beta-expressing cells. Consistent with previous studies, Pol beta-deficient mouse fibroblasts were not hypersensitive to cisplatin treatment. These data provide the first link between oxaliplatin sensitivity and DNA repair involving Pol beta. They demonstrate that Pol beta modulates the sensitivity of cells to oxaliplatin treatment. Oncogene (2010) 29, 463-468; doi:10.1038/onc.2009.327; published online 19 October 2009

Investigation of add-back effects in a segmented Clover detector

The resolution and the summing characteristics of an EXOGAM segmented Clover germanium detector has been studied for use it in gamma spectroscopic experiments. The measurements have been performed with standard radioactive sources of Eu-152, Ba-133 and beta-delayed gamma-rays from Ir-176 decay. The data analytic results, realized by software, are presented in this paper.

Observation of a Possible New Isomer in Ir-175

The neutron deficient nuclide Ir-175 was produced by irradiation of Nd-146 with 210 MeV Cl-35 via a fusion-evaporation reaction channel. The reaction products were transported to a low-background location using a helium-jet recoil fast-moving tape-transport system for measurement. The experimental devices and data analysis method are introduced. Based on the decay-curve fitting of the beta-delayed gamma ray from Ir-175, realized by the least-square method, a new long-lived isomeric state of Ir-175 is proposed and briefly discussed.

丰中子新核素238Th的合成、鉴别和230Ac b 延发裂变的观测

新核素的合成及衰变性质的研究一直是核物理科学的前沿领域，它对于人类拓广对原子核运动规律的认识有着十分重要的意义。本文首先概述了新核素合成的意义、方法，并简要阐述了一种奇异的衰变方式—β~-延发裂变，为实验部分的论述提供理论基础。在实验部分，本文阐述了用放射化学方法研究了钍、钡、镭等复杂反应产物的化学分离。通过在Th的分离中引用PMBP萃取和反萃体系，并采用氧化还原体系有效地去除了绝大多数杂质元素，特别是非常好的去除了碘和溴离子的沾污，较好地完成了Th与其它反应产物的分离。对Ba、Ra的分离主要采用快速的阳离子交换流程，达到了满意的分离效果。对用中能~(18)O离子束照射铀、钍的反应产物进行分离，对分离出的钍、钡、镭样品进行了γ（X）单谱和时间序列谱测量。并对记录下来的样品的谱图进行了分析。使用上述方法，我们在兰州重离子加速器（HIRFL）上用~(18)O离子照射重铀酸铵靶，通过多核子转移反应，首次合成并鉴别了新核素不相识~(238)Th。 同时通过不同的反应道产生~(237)Th，并对~(237)Th的半衰期进行了测定；在HIRFL上用~(18)O离子照射氧化钍靶对~(230)Ra的子体~(230)Ac的β~-延发裂变现象进行了观测，在被Ra样品爆光的云母径迹探测器上观察到了两个裂变径迹，从ThO_2靶中用三次BaCl_2沉淀法分离出钡、使用γ谱学这技术测定了十多个Ba的放射性同位素的截面。

230Ac的 b 延发裂变的观测及新核素合成

第一部分：β延发裂变（βDF）是一种稀有的核衰变模式,它在天体物理学和研究中具有重要价值;为研究远离β稳定线核素提供了可能性,是研究新核素合成的新台阶.第二部分：采用放射化学分离法从中能<'18>O离子辐照过的天然铀靶以及钍靶中分离出放射性Ba同位素,用高分辨的HPGe探测器测量Ba部分的γ射线谱,对测得的时间累计谱进行分析,用常规的计算产额生成截面的方法得到了Ba同位素的生成截面,并对其中的一些截面数据进行了讨论.第三部分：在中子发生器上用14-15MeV的中子轰击天然白金箔,通过<'198>Pt(n,2p）反应产生<'197>Os.使用两台HPGe探测器做γ（X）单谱和X-γ-t符合测量.对测得的数据进行了分析,结果显示我们合成并鉴定了新丰中子同位素<'197>Os,确定它的半衰期为2.8±0.5min.第四部分：用<'133>Ba作示踪剂对Ba在不锈钢片上的分子镀进行了研究.对在异丙醇溶液中的影响Ba分子镀的因素：电镀时间和电流密度等做了条件实验.在电流密度为4.0～6.0mA/cm<'2>,沉积时间30min的实验条件下,可在不锈钢片上获得厚度为0.5～1.0mg/cm<'2>的Ba镀层,也确定了Ba的电镀效率.

First Results with the RISING active stopper

This paper outlines some of the physics opportunities available with the GSI RISING active stopper and presents preliminary results from an experiment aimed at performing beta-delayed gamma-ray spectroscopic studies in heavy-neutron-rich nuclei produced following the projectile fragmentation of a 1 GeV per nucleon 208Pb primary beam. The energy response of the silicon active stopping detector for both heavy secondary fragments and beta-particles is demonstrated and preliminary results on the decays of neutron-rich Tantalum (Ta) to Tungsten (W) isotopes are presented as examples of the potential of this technique to allow new structural studies in hitherto experimentally unreachable heavy, neutron-rich nuclei. The resulting spectral information inferred from excited states in the tungsten daughter nuclei are compared with results from axially symmetric Hartree–Fock calculations of the nuclear shape and suggest a change in ground state structure for the N = 116 isotone 190W compared to the lighter isotopes of this element.

New insights into the structure of exotic nuclei using the RISING active stopper

This conference paper outlines the operation and some of the preliminary physics results using the GSI RISING active stopper. Data are presented from an experiment using combined isomer and beta‐delayed gamma‐ray spectroscopy to study low‐lying spectral and decay properties of heavy‐neutron‐rich nuclei around A∼190 produced following the relativistic projectile fragmentation of 208Pb primary beam. The response of the RISING active stopper detector is demonstrated for both the implantation of heavy secondary fragments and in‐situ decay of beta‐particles. Beta‐delayed gamma‐ray spectroscopy following decays of the neutron‐rich nucleus 194Re is presented to demonstrate the experimental performance of the set‐up. The resulting information inferred from excited states in the W and Os daughter nuclei is compared with results from Skyrme Hartree‐Fock predictions of the evolution of nuclear shape.

Aplicação do Método de Monte Carlo no estudo da atividade obtida em sistema de coincidências 4π(β,EC)-γ pelo Método da Discriminação com reposição

Dissertação (Mestrado em Tecnologia Nuclear)

Glial cell line-derived neurotrophic factor but not transforming growth factor beta 3 prevents delayed degeneration of nigral dopaminergic neurons following striatal 6-hydroxydopamine lesion.

Glial cell line-derived neurotrophic factor (GDNF) and transforming growth factor beta 3 (TGF-beta 3) are members of the TGF-beta superfamily with high neurotrophic activity on cultured nigral dopamine neurons. We investigated the effects of intracerebral administration of GDNF and TGF-beta 3 on the delayed cell death of the dopamine neurons in the rat substantia nigra following 6-hydroxydopamine lesions of dopaminergic terminals in the striatum. Fluorescent retrograde tracer injections and tyrosine hydroxylase immunocytochemistry demonstrated nigral degeneration with an onset 1 week after lesion, leading to extensive death of nigral neurons 4 weeks postlesion. Administration of recombinant human GDNF for 4 weeks over the substantia nigra at a cumulative dose of 140 micrograms, starting on the day of lesion, completely prevented nigral cell death and atrophy, while a single injection of 10 micrograms 1 week postlesion had a partially protective effect. Continuous administration of TGF-beta 3, starting on the day of lesion surgery, did not affect nigral cell death or atrophy. These findings support the notion that GDNF, but not TGF-beta 3, is a potent neurotrophic factor for nigral dopamine neurons in vivo.

Good results for early treatment of clinically isolated syndrome prior to multiple sclerosis with interferon beta-1b and glatiramer

Background: The first sign of developing multiple sclerosis is a clinically isolated syndrome that resembles a multiple sclerosis relapse. Objective/methods: The objective was to review the clinical trials of two medicines in clinically isolated syndromes (interferon β and glatiramer acetate) to determine whether they prevent progression to definite multiple sclerosis. Results: In the BENEFIT trial, after 2 years, 45% of subjects in the placebo group developed clinically definite multiple sclerosis, and the rate was lower in the interferon β-1b group. Then all subjects were offered interferon β-1b, and the original interferon β-1b group became the early treatment group, and the placebo group became the delayed treatment group. After 5 years, the number of subjects with clinical definite multiple sclerosis remained lower in the early treatment than late treatment group. In the PreCISe trial, after 2 years, the time for 25% of the subjects to convert to definite multiple sclerosis was prolonged in the glatiramer group. Conclusions: Interferon β-1b and glatiramer acetate slow the progression of clinically isolated syndromes to definite multiple sclerosis. However, it is not known whether this early treatment slows the progression to the physical disabilities experienced in multiple sclerosis.

Transforming growth factor -beta signaling through Smad3 in allergy : Studies in the mechanisms of asthma, atopic dermatitis and allergic contact reactions

Transforming growth factor β signalling through Smad3 in allergy Allergic diseases, such as atopic dermatitis, asthma, and contact dermatitis are complex diseases influenced by both genetic and environmental factors. It is still unclear why allergy and subsequent allergic disease occur in some individuals but not in others. Transforming growth factor (TGF)-β is an important immunomodulatory and fibrogenic factor that regulates cellular processes in injured and inflamed skin. TGF-β has a significant role in the regulation of the allergen-induced immune response participating in the development of allergic and asthmatic inflammation. TGF-β is known to be an immunomodulatory factor in the progression of delayed type hypersensitivity reactions and allergic contact dermatitis. TGF-β is crucial in regulating the cellular responses involved in allergy, such as differentiation, proliferation and migration. TGF-β signals are delivered from the cytoplasm to the nucleus by TGF-β signal transducers called Smads. Smad3 is a major signal transducer in TGF-β -signalling that controls the expression of target genes in the nucleus in a cell-type specific manner. The role of TGF-β-Smad3 -signalling in the immunoregulation and pathophysiology of allergic disorders is still poorly understood. In this thesis, the role of TGF-β-Smad -signalling pathway using Smad3 -deficient knock out mice in the murine models of allergic diseases; atopic dermatitis, asthma and allergic contact reactions, was examined. Smad3-pathway regulates allergen induced skin inflammation and systemic IgE antibody production in a murine model atopic dermatitis. The defect in Smad3 -signalling decreased Th2 cytokine (IL-13 and IL-5) mRNA expression in the lung, modulated allergen induced specific IgG1 response, and affected mucus production in the lung in a murine model of asthma. TGF-β / Smad3 -signalling contributed to inflammatory hypersensitivity reactions and disease progression via modulation of chemokine and cytokine expression and inflammatory cell recruitment, cell proliferation and regulation of the specific antibody response in a murine model of contact hypersensitivity. TGF-β modulates inflammatory responses - at least partly through the Smad3 pathway - but also through other compensatory, non-Smad-dependent pathways. Understanding the effects of the TGF-β signalling pathway in the immune system and in disease models can help in elucidating the multilevel effects of TGF-β. Unravelling the mechanisms of Smad3 may open new possibilities for treating and preventing allergic responses, which may lead to severe illness and loss of work ability. In the future the Smad3 signalling pathway might be a potential target in the therapy of allergic diseases.

轻核区质子滴线附近奇异核#beta#延迟质子衰变研究

远离#beta#稳定线的原子核所具有的特性是否与稳定区附近的核的性质相同，一直是核物理学家所关注的问题，实验上通过对缺中子区奇异核#beta#~+延迟粒子衰变的研究，可以精确测定与核性质有关的各个参数，这将对核结构理论研究产生重要的影响。本论文将首先介绍奇异核#beta#~+延迟粒子衰变研究的历史及其理论，接着介绍关于此研究的实验技术，最后详尽阐述对~(19)Na、~(65)Se和~(20)Na的研究