首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   34篇
  免费   1篇
  2024年   2篇
  2022年   3篇
  2021年   4篇
  2020年   5篇
  2019年   3篇
  2018年   5篇
  2016年   3篇
  2015年   1篇
  2013年   2篇
  2012年   1篇
  2011年   2篇
  2010年   3篇
  2004年   1篇
排序方式: 共有35条查询结果,搜索用时 15 毫秒
31.
Therapeutic effects of saffron ingredients were studied in some diseases. The pharmacokinetics and pharmacodynamics of these ingredients were also studied, but their transport mechanism is not clearly known. Serum albumin has been known as the most important transporter of many drugs in the body that affects their disposition, transportation, and bioavailability. Here, we investigated the interaction of crocin (Cro) with HSA, for the first time, and compared with the crocetin (Crt)–HSA interaction. UV and fluorescence spectroscopy, circular dichroism (CD), and molecular docking was applied to investigate the possibility and mechanism of binding of HSA with these natural carotenoids. The gradually addition of Cro increased HSA absorbency at 278 nm, while Crt decreased it. Both of these changes induced HSA unfolding that was confirmed by the decreased α-helix content, as determined by the CD. Both carotenoids quenched HSA fluorescence emission, but with different mechanisms. The Stern–Volmer plots indicated a dynamic quenching of intrinsic emission of HSA due to Cro addition, while Crt quenching followed both static and dynamic quenching mechanisms. Docking results indicated binding of Cro/Crt in sub-domain IIA, Sudlow site I of HSA, which accompanied with the hydrogen bonding of Cro/Crt with Tyr138. The interaction of these ligands (Cro/Crt) caused HSA unfolding and affects the hydrophobic environment of Trp241, which result in the quenching of Trp fluorescence. The UV spectroscopy and fluorescence quenching data indicated the differences in the mechanisms of interaction of Cro/Crt with HSA, which is due to the differences in the structure and hydrophobicity of these ligands.  相似文献   
32.
Mechanical properties of the cell are important biomarkers for probing its architectural changes caused by cellular processes and/or pathologies. The development of microfluidic technologies has enabled measuring the cell’s mechanical properties at high throughput so that mechanical phenotyping can be applied to large samples in reasonable timescales. These studies typically measure the stiffness of the cell as the only mechanical biomarker and do not disentangle the rheological contributions of different structural components of the cell, including the cell cortex, the interior cytoplasm and its immersed cytoskeletal structures, and the nucleus. Recent advancements in high-speed fluorescent imaging have enabled probing the deformations of the cell cortex while also tracking different intracellular components in rates applicable to microfluidic platforms. We present a, to our knowledge, novel method to decouple the mechanics of the cell cortex and the cytoplasm by analyzing the correlation between the cortical deformations that are induced by external microfluidic flows and the nucleus displacements, induced by those cortical deformations, i.e., we use the nucleus as a high-throughput microrheological probe to study the rheology of the cytoplasm, independent of the cell cortex mechanics. To demonstrate the applicability of this method, we consider a proof-of-concept model consisting of a rigid spherical nucleus centered in a spherical cell. We obtain analytical expressions for the time-dependent nucleus velocity as a function of the cell deformations when the interior cytoplasm is modeled as a viscous, viscoelastic, porous, and poroelastic material and demonstrate how the nucleus velocity can be used to characterize the linear rheology of the cytoplasm over a wide range of forces and timescales/frequencies.  相似文献   
33.
MicroRNAs (miRNAs) play critical roles in cancer pathobiology, acting as regulators of gene expression and pivotal drivers of tumorigenesis. It is believed that miRNAs act through canonical mechanisms, involving the binding of mature miRNAs to target messenger RNAs (mRNAs) and subsequent repression of protein translation or degradation of target mRNAs. miR-142-3p/5p has been extensively studied and established as a key regulator in various malignancies. Recent discoveries have revealed miR-142-3p/5p serve as either oncogene or tumor suppressor in cancer. By targeting epigenetic factor and cancer-related signaling pathway, miR-142-3p/5p can regulate wide range of downstream genes. The immune modulatory role of miR-142-3p/5p has been shown in various cancers, which provides significant insight into immunosuppression and tumor escape from the immune response. Exosomes with miR-142-3p/5p facilitate cell communication and can affect cancer cell behavior, offering potential therapeutic, and diagnosis applications in cancer therapy. In this review, for the first time, we comprehensively summarize the current knowledge regarding mentioned functions of miR-142-3p/5p in cancer pathobiology.  相似文献   
34.
35.
Oil-polluted soils were sampled from National Iranian South Oil Company (NISOC) for isolation and screening of C–S and not C–C targeted Dibenzothiophene (DBT) degrading microorganisms. Microbacterium sp. NISOC-06, a C–S targeted DBT degrading bacterium, was selected and its desulfurization ability was studied in aqueous phase and water-gasoline biphasic systems. The 16srRNA gene was amplified using universal eubacteria-specific primers, PCR product was sequenced and the sequence of nearly 1,500 bp 16srDNA was studied. Based on Gas Chromatography results Microbacterium sp. NISOC-06 utilized 94.8% of 1 mM DBT during the 2 weeks of incubation. UV Spectrophotometry and biomass production measurements showed that the Microbacterium sp. NISOC-06 was not able to utilize DBT as a carbon source. There was no accumulation of phenolic compounds as Gibb’s assay showed. Biomass production in a biphasic system for which DBT-enriched gasoline was used as the sulfur source indicated the capability of Microbacterium sp. NISOC-06 to desulfurize gasoline.  相似文献   
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号