301 research outputs found

    Nucleotide polymorphisms of the bovine growth hormone secretagogue receptor 1a (GHSR1a) gene and their association with growth and carcass traits in Japanese Black cattle

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    Ghrelin growth hormone secretagogue receptor 1a (GHSR1a) is involved in many important functions, including growth hormone secretion and food intake (Howard et al. 1996). To the best of our knowledge, there have been no reports to date on nucleotide polymorphisms from the 5’-flanking region to the 3’-UTR nor on the transcriptional analysis of the 5’-UTR of the GHSR1a gene in cattle. In our previous study (Malau-Aduli et al. (2005)), the GHSR1a gene was reported as a potential candidate gene when we detected growth trait QTLs in Japanese Black cattle using microsatellite DNA markers and half-sib regression analysis. Here we describe (1) all possible nucleotide polymorphisms from the 5’-flanking region to the 3’-UTR of the GHSR1a gene, (2) the transcript sequences of the 5’-UTR of the gene, which allows one to determine whether the microsatellite locus has been transcribed, and (3) an association between nucleotide polymorphisms of the gene and growth and carcass traits in Japanese Black cattle (Komatsu et al. (2010)). Finally, we propose a hypothesis that the association is due to differences in RNA secondary structure of the GHSR 1b mRNA

    Effect of the adenovirus E1A gene on nitric oxide production in alveolar epithelial cells

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    ABSTRACTThis study determined the effect of the adenovirus E1A gene on nitric oxide (NO) production in alveolar epithelial (A549) cells. E1A-positive A549 cells (E1A transfectants), E1A-negative A549 cells (control transfectants) and untransfected A549 cells were placed in 96-well tissue culture plates. After stimulation with lipopolysaccharide (LPS) or cytokine mixture (CM), the biochemical reaction products of NO (nitrite and nitrate) in the culture medium were measured by chemiluminescence. The inducible (iNOS) and the endothelial (eNOS) isoforms of nitric oxide synthase (NOS) protein expression were examined by Western blotting. iNOS mRNA expression was examined by Northern blotting and RT-PCR. CM-induced NO production by E1A-positive A549 cells was significantly lower than that of E1A-negative cells (p < 0.0001). LPS stimulation failed to enhance NO production in both cell types. CM induced iNOS protein expression in E1A-negative A549 cells, but not in E1A-positive cells. eNOS protein expression was constitutive and was not affected by CM stimulation, LPS stimulation or E1A. CM induced iNOS mRNA expression in E1A-negative A549 cells, but not in E1A-positive cells. In conclusion, the adenovirus E1A gene suppressed NO production through transcriptional control of the iNOS gene in A549 cells. This inhibition of NO production may enable the virus to persist in human tissue, since NO is an antiviral effector of the innate immune system

    Photo-production of neutral kaons on 12C in the threshold region

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    Kaon photo-production process on 12^{12}C has been studied by measuring neutral kaons in a photon energy range of 0.8-1.1 GeV. Neutral kaons were identified by the invariant mass constructed from two charged pions emitted in the KS0π+πK^{0}_{S}\to\pi^{+}\pi^{-} decay channel. The differential cross sections as well as the integrated ones in the threshold photon energy region were obtained. The obtained momentum spectra were compared with a Spectator model calculation using elementary amplitudes of kaon photo-production given by recent isobar models. Present result provides, for the first time, the information on n(γ,K0)Λn(\gamma,K^{0})\Lambda reaction which is expected to play an important role to construct models for strangeness production by the electromagnetic interaction. Experimental results show that cross section of 12C(γ,K0)^{12}{\rm C}(\gamma,K^0) is of the same order to that of 12C(γ,K+)^{12}{\rm C}(\gamma,K^+) and suggest that slightly backward K0K^0 angular distribution is favored in the γnK0Λ\gamma n\to K^0\Lambda process.Comment: 6 pages, 8 figure

    Implementing Grover Oracles for Quantum Key Search on AES and LowMC

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    Grover's search algorithm gives a quantum attack against block ciphers by searching for a key that matches a small number of plaintext-ciphertext pairs. This attack uses O(N)O(\sqrt{N}) calls to the cipher to search a key space of size NN. Previous work in the specific case of AES derived the full gate cost by analyzing quantum circuits for the cipher, but focused on minimizing the number of qubits. In contrast, we study the cost of quantum key search attacks under a depth restriction and introduce techniques that reduce the oracle depth, even if it requires more qubits. As cases in point, we design quantum circuits for the block ciphers AES and LowMC. Our circuits give a lower overall attack cost in both the gate count and depth-times-width cost models. In NIST's post-quantum cryptography standardization process, security categories are defined based on the concrete cost of quantum key search against AES. We present new, lower cost estimates for each category, so our work has immediate implications for the security assessment of post-quantum cryptography. As part of this work, we release Q# implementations of the full Grover oracle for AES-128, -192, -256 and for the three LowMC instantiations used in Picnic, including unit tests and code to reproduce our quantum resource estimates. To the best of our knowledge, these are the first two such full implementations and automatic resource estimations.Comment: 36 pages, 8 figures, 14 table

    Aldo-keto reductases are biomarkers of NRF2 activity and are co-ordinately overexpressed in non-small cell lung cancer

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    BACKGROUND: Although the nuclear factor-erythroid 2-related factor 2 (NRF2) pathway is one of the most frequently dysregulated in cancer, it is not clear whether mutational status is a good predictor of NRF2 activity. Here we utilise four members of the aldo-keto reductase (AKR) superfamily as biomarkers to address this question. METHODS: Twenty-three cell lines of diverse origin and NRF2-pathway mutational status were used to determine the relationship between AKR expression and NRF2 activity. AKR expression was evaluated in lung cancer biopsies and Cancer Genome Atlas (TCGA) and Oncomine data sets. RESULTS: AKRs were expressed at a high basal level in cell lines carrying mutations in the NRF2 pathway. In non-mutant cell lines, co-ordinate induction of AKRs was consistently observed following activation of NRF2. Immunohistochemical analysis of lung tumour biopsies and interrogation of TCGA data revealed that AKRs are enriched in both squamous cell carcinomas (SCCs) and adenocarcinomas that contain somatic alterations in the NRF2 pathway but, in the case of SCC, AKRs were also enriched in most other tumours. CONCLUSIONS: An AKR biomarker panel can be used to determine NRF2 status in tumours. Hyperactivation of the NRF2 pathway is far more prevalent in lung SCC than previously predicted by genomic analyses
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