18 research outputs found
Spallation reactions. A successful interplay between modeling and applications
The spallation reactions are a type of nuclear reaction which occur in space
by interaction of the cosmic rays with interstellar bodies. The first
spallation reactions induced with an accelerator took place in 1947 at the
Berkeley cyclotron (University of California) with 200 MeV deuterons and 400
MeV alpha beams. They highlighted the multiple emission of neutrons and charged
particles and the production of a large number of residual nuclei far different
from the target nuclei. The same year R. Serber describes the reaction in two
steps: a first and fast one with high-energy particle emission leading to an
excited remnant nucleus, and a second one, much slower, the de-excitation of
the remnant. In 2010 IAEA organized a worskhop to present the results of the
most widely used spallation codes within a benchmark of spallation models. If
one of the goals was to understand the deficiencies, if any, in each code, one
remarkable outcome points out the overall high-quality level of some models and
so the great improvements achieved since Serber. Particle transport codes can
then rely on such spallation models to treat the reactions between a light
particle and an atomic nucleus with energies spanning from few tens of MeV up
to some GeV. An overview of the spallation reactions modeling is presented in
order to point out the incomparable contribution of models based on basic
physics to numerous applications where such reactions occur. Validations or
benchmarks, which are necessary steps in the improvement process, are also
addressed, as well as the potential future domains of development. Spallation
reactions modeling is a representative case of continuous studies aiming at
understanding a reaction mechanism and which end up in a powerful tool.Comment: 59 pages, 54 figures, Revie
State of the art review on the socio-economics of the bamboo and rattan sector in Southeast Asia
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Not AvailableInitially, a preliminary study was conducted to assess the variation of grain zinc (Zn) and iron (Fe) content of 10 basmati rice cultivars. Thereafter, comprehensive study was conducted to enhance the Zn density in grain using three cultivars (CSR 30, Pusa Basmati-6 and PusaSugandh 5) selected from the preliminary study, using three diverse soil types (Inceptisols of IARI, New Delhi; Inceptisols of farmer’s field, Karnal; and Alfisols of CRIDA, Hyderabad) and six zinc nutrient management treatments including control. The results in the preliminary study indicated that the Zn content in rice grain (after hulling) varied from 13.3 to 22.5 mg kg−1 with mean of 18.8 mg kg−1, while Fe content varied from 8.3 to 14.3 mg kg−1 with mean of 10.7 mg kg−1. In the comprehensive study, the highest Zn content in grain (21.2 mg kg−1) and straw (33.2 mg kg−1) was observed in CSR-30 Cultivar. Among the soil types, Alfisols of CRIDA, Hyderabad maintained significantly highest Zn content in grains and straw. Among the Zn containing nutrient management treatments, application of 5 mg Zn kg−1 (basal) + foliar spray of 0.5% ZnSO4 (bi-weekly) maintained significantly highest Zn content in grain (21.9 mg kg−1) and straw (41.3 mg kg−1). Further, based on the assumption that when an individual consumes rice @ 200 g day−1, his daily dietary intake of Zn would be 3.53 mg day−1 in control (without Zn application) as compared to 4.38 mg day−1 with the rice grown with soil and foliage application of ZnNot Availabl
Familial cancer associated with a polymorphism in ARLTS1.
The finding of hemizygous or homozygous deletions at band 14 on chromosome 13 in a variety of neoplasms suggests the presence of a tumor-suppressor locus telomeric to the RB1 gene. METHODS: We studied samples from 216 patients with various types of sporadic tumors or idiopathic pancytopenia, peripheral-blood samples from 109 patients with familial cancer or multiple cancers, and control blood samples from 475 healthy people or patients with diseases other than cancer. We performed functional studies of cell lines lacking ARLTS1 expression with the use of both the full-length ARLTS1 gene and a truncated variant. RESULTS: We found a gene at 13q14, ARLTS1, a member of the ADP-ribosylation factor family, with properties of a tumor-suppressor gene. We analyzed 800 DNA samples from tumors and blood cells from patients with sporadic or familial cancer and controls and found that the frequency of a nonsense polymorphism, G446A (Trp149Stop), was similar in controls and patients with sporadic tumors but was significantly more common among patients with familial cancer than among those in the other two groups (P=0.02; odds ratio, 5.7; 95 percent confidence interval, 1.3 to 24.8). ARLTS1 was down-regulated by promoter methylation in 25 percent of the primary tumors we analyzed. Transfection of wild-type ARLTS1 into A549 lung-cancer cells suppressed tumor formation in immunodeficient mice and induced apoptosis, whereas transfection of truncated ARLTS1 had a limited effect on apoptosis and tumor suppression. Microarray analysis revealed that the wild-type and Trp149Stop-transfected clones had different expression profiles. CONCLUSIONS: A genetic variant of ARLTS1 predisposes patients to familial cancer. Copyright 2005 Massachusetts Medical Society
Familial cancer associated with a polymorphism in ARLTS1
BACKGROUND: The finding of hemizygous or homozygous deletions at band 14 on chromosome 13 in a variety of neoplasms suggests the presence of a tumor-suppressor locus telomeric to the RB1 gene. METHODS: We studied samples from 216 patients with various types of sporadic tumors or idiopathic pancytopenia, peripheral-blood samples from 109 patients with familial cancer or multiple cancers, and control blood samples from 475 healthy people or patients with diseases other than cancer. We performed functional studies of cell lines lacking ARLTS1 expression with the use of both the full-length ARLTS1 gene and a truncated variant. RESULTS: We found a gene at 13q14, ARLTS1, a member of the ADP-ribosylation factor family, with properties of a tumor-suppressor gene. We analyzed 800 DNA samples from tumors and blood cells from patients with sporadic or familial cancer and controls and found that the frequency of a nonsense polymorphism, G446A (Trp149Stop), was similar in controls and patients with sporadic tumors but was significantly more common among patients with familial cancer than among those in the other two groups (P=0.02; odds ratio, 5.7; 95 percent confidence interval, 1.3 to 24.8). ARLTS1 was down-regulated by promoter methylation in 25 percent of the primary tumors we analyzed. Transfection of wild-type ARLTS1 into A549 lung-cancer cells suppressed tumor formation in immunodeficient mice and induced apoptosis, whereas transfection of truncated ARLTS1 had a limited effect on apoptosis and tumor suppression. Microarray analysis revealed that the wild-type and Trp149Stop-transfected clones had different expression profiles. CONCLUSIONS: A genetic variant of ARLTS1 predisposes patients to familial cancer