scholarly journals Absolute requirement of GDNF for adult catecholaminergic neuron survival

2008 ◽  
Vol 11 (7) ◽  
pp. 755-761 ◽  
Author(s):  
Alberto Pascual ◽  
María Hidalgo-Figueroa ◽  
José I Piruat ◽  
C Oscar Pintado ◽  
Raquel Gómez-Díaz ◽  
...  
2015 ◽  
Vol 18 (3) ◽  
pp. 319-322 ◽  
Author(s):  
Jaakko Kopra ◽  
Carolina Vilenius ◽  
Shane Grealish ◽  
Mari-Anne Härma ◽  
Kärt Varendi ◽  
...  

2015 ◽  
Vol 18 (3) ◽  
pp. 322-323 ◽  
Author(s):  
Alberto Pascual ◽  
José López-Barneo

Author(s):  
Kaldius Ndruru ◽  
Putri Ramadhani

Security of data stored on computers is now an absolute requirement, because every data has a high enough value for the user, reader and owner of the data itself. To prevent misuse of the data by other parties, data security is needed. Data security is the protection of data in a system against unauthorized authorization, modification, or destruction. The science that explains the ways of securing data is known as cryptography, while the steps in cryptography are called critical algorithms. At this time, there are many cryptographic algorithms whose keys are weak especially the symmetric key algorithm because they only have one key, the key for encryption is the same as the decryption key so it needs to be modified so that the cryptanalysts are confused in accessing important data. The cryptographic method of Word Auto Key Encryption (WAKE) is one method that has been used to secure data where in this case the writer wants to maximize the encryption key and description of the WAKE algorithm that has been processed through key formation. One way is to apply the algebraic pascal triangle method to maximize the encryption key and description of the WAKE algorithm, utilizing the numbers contained in the columns and rows of the pascal triangle to make shifts on the encryption key and the description of the WAKE algorithm.Keywords: Cryptography, WAKE, pascal


EMBO Reports ◽  
2008 ◽  
Vol 9 (10) ◽  
pp. 1041-1047 ◽  
Author(s):  
Epaminondas Doxakis ◽  
Laura Howard ◽  
Hermann Rohrer ◽  
Alun M Davies

Author(s):  
Jan J Sixma ◽  
Kjell S Sakariassen ◽  
Piet A Bolhuis

The relation between the VWF-A of F VIII-VWF and its multimeric structure was studied in an annular perfusion chamber according to Baumgartner, with a steady flow system. 51Cr-labelled aspirin treated human platelets and human post mortem renal arteries were employed. F VIII-VWF was purified from cryoprecipitate by agarose gel chromatography and radiolabelled by the lactoperoxydase method. The multimeric distribution was determined by SDS-agarose electrophoresis. Five different commercial high purity concentrates contained multimers between 0.5 and 3.5 x 106 mol wt. None of these concentrates had VWF-A at ristocetin cofactor activities (RIC0F-A) of 1.0 u/ml. A low potency concentrate with mul- timers in the same mol wt range had normal VWF-A. Mild reduction (dithioerythritol-DTE ≤ 2mM) caused a shift in , mol wt range from 3.0 - 20.0 × 106 towards 0.5 - 2.0 × 106 with little decrease in RIC0F-A and VWF-A. Reduction with 10 mM DTE produced multimers of 1.5 and 0.5 × 106 without RICOF-A and VWF-A, but binding normally to the vessel wall. The void volume peak of 125I-VIII-VWF was rechromatographed on Sepharose-2B and arbitrarily divided in fractions A: mol wt 8,0 - 18.0 × 106 ;B: mol wt 4.5 - 11.0 × 106 ; and C: mol wt 2.5 - 6.5 × 106 . Binding of 125I-VIII-VWF to the subendothelium was highest for A, intermediate for B and lowest for C. Correction for mean mol wt showed that almost equal numbers of molecules bound from all three fractions. When the quantity of bound VIII-VWF was thus expressed, all fractions had a similar relative VWF-A.These data indicate that high purity concentrates do not correct the bleeding time at normal RICOF-levels, because they lack VWF-A. Multimers of high mol wt normally carry both RICOF-A and VWF-A, but the high mol wt is no absolute requirement. These data are in agreement with the notion that VWF-A resides on a specific polypeptide chain in the molecule.


1999 ◽  
Vol 19 (4) ◽  
pp. 2828-2834 ◽  
Author(s):  
Kazumi Nakagawa ◽  
Yoichi Taya ◽  
Katsuyuki Tamai ◽  
Masaru Yamaizumi

ABSTRACT Microinjection of the restriction endonuclease HaeIII, which causes DNA double-strand breaks with blunt ends, induces nuclear accumulation of p53 protein in normal and xeroderma pigmentosum (XP) primary fibroblasts. In contrast, this induction of p53 accumulation is not observed in ataxia telangiectasia (AT) fibroblasts. HaeIII-induced p53 protein in normal fibroblasts is phosphorylated at serine 15, as determined by immunostaining with an antibody specific for phosphorylated serine 15 of p53. This phosphorylation correlates well with p53 accumulation. Treatment with lactacystin (an inhibitor of the proteasome) or heat shock leads to similar levels of p53 accumulation in normal and AT fibroblasts, but the p53 protein lacks a phosphorylated serine 15. Following microinjection of HaeIII into lactacystin-treated normal fibroblasts, lactacystin-induced p53 protein is phosphorylated at serine 15 and stabilized even in the presence of cycloheximide. However, neither stabilization nor phosphorylation at serine 15 is observed in AT fibroblasts under the same conditions. These results indicate the significance of serine 15 phosphorylation for p53 stabilization after DNA double-strand breaks and an absolute requirement for ATM in this phosphorylation process.


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