scholarly journals The polyacrylic acid/modified chitosan capsules with tunable release of small hydrophobic probe and drug

Author(s):  
Lucia Ya. Zakharova ◽  
Elmira A. Vasilieva ◽  
Gulnara A. Gaynanova ◽  
Alla B. Mirgorodskaya ◽  
Alsu R. Ibragimova ◽  
...  
TAPPI Journal ◽  
2009 ◽  
Vol 8 (6) ◽  
pp. 29-35 ◽  
Author(s):  
PEDRAM FATEHI ◽  
LIYING QIAN ◽  
RATTANA KITITERAKUN ◽  
THIRASAK RIRKSOMBOON ◽  
HUINING XIAO

The application of an oppositely charged dual polymer system is a promising approach to enhance paper strength. In this work, modified chitosan (MCN), a cationic polymer, and carboxymethyl cellulose (CMC), an anionic polymer, were used sequentially to improve paper strength. The adsorption of MCN on cellulose fibers was analyzed via polyelectrolyte titration. The formation of MCN/CMC complex in water and the deposition of this complex on silicon wafers were investigated by means of atomic force microscope and quasi-elastic light scattering techniques. The results showed that paper strength was enhanced slightly with a layer-by-layer assembly of the polymers. However, if the washing stage, which was required for layer-by-layer assembly, was eliminated, the MCN/CMC complex was deposited on fibers more efficiently, and the paper strength was improved more significantly. The significant improvement was attributed to the extra development of fiber bonding, confirmed further by scanning electron microscope observation of the bonding area of fibers treated with or without washing. However, the brightness of papers was somewhat decreased by the deposition of the complex on fibers. Higher paper strength also was achieved using rapid drying rather than air drying.


2010 ◽  
Vol 7 (6) ◽  
pp. 458-464
Author(s):  
Xiao-Li WU ◽  
Can ZHANG ◽  
Qi-Neng PING

2019 ◽  
Vol 20 (11) ◽  
pp. 1091-1111 ◽  
Author(s):  
Maryam Zanjirband ◽  
Soheila Rahgozar

MDM2 protein is the core negative regulator of p53 that maintains the cellular levels of p53 at a low level in normal cells. Mutation of the TP53 gene accounts for 50% of all human cancers. In the remaining malignancies with wild-type TP53, p53 function is inhibited through other mechanisms. Recently, synthetic small molecule inhibitors have been developed which target a small hydrophobic pocket on MDM2 to which p53 normally binds. Given that MDM2-p53 antagonists have been undergoing clinical trials for different types of cancer, this review illustrates different aspects of these new cancer targeted therapeutic agents with the focus on the major advances in the field. It emphasizes on the p53 function, regulation of p53, targeting of the p53-MDM2 interaction for cancer therapy, and p53-dependent and -independent effects of inhibition of p53-MDM2 interaction. Then, representatives of small molecule MDM2-p53 binding antagonists are introduced with a focus on those entered into clinical trials. Furthermore, the review discusses the gene signatures in order to predict sensitivity to MDM2 antagonists, potential side effects and the reasons for the observed hematotoxicity, mechanisms of resistance to these drugs, their evaluation as monotherapy or in combination with conventional chemotherapy or with other targeted therapeutic agents. Finally, it highlights the certainly intriguing questions and challenges which would be addressed in future studies.


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