We studied the crystallization kinetics in a diblock copolymer system exhibiting different mesophase structures in the melt. A symmetric poly(ethylene oxide)-block-poly(1,4-butadiene) (PEO-b-PB) was blended with a low molecular weight PB homopolymer to yield the block copolymer blends containing lamellar, cylindrical, and spherical PEO microdomains. The crystallization kinetics of PEO blocks in these nanoscaled microdomains was then studied by monitoring the development of crystallinity in the course of isothermal crystallization. In the lamellar melt, crystallization could occur at the normal undercooling, and its kinetics closely followed the classical Avrami model found in the spherulitic crystallization of homopolymers. Crystallinity developments in the cylindrical and spherical morphology obeyed a simple exponential function prescribed by the first-order kinetics. This first-order kinetic behavior along with the exceedingly large undercooling verified the homogeneous nucleation controlled kinetics in these two types of mesophases. Crystallization in the lamellar melt transformed the melt structure into a highly interconnected lamellar morphology due to the ability of the crystal growth fronts to repeatedly thrust into the microdomains yet to be crystallized. For the crystallization condition chosen (i.e., cooling at −5 °C/min from the melt), the melt structures associated with the cylindrical and spherical morphology were not totally disrupted and transformed into one-dimensionally stacked lamellae upon crystallization. The melt mesophases were not fully preserved either, suggesting that some intermediate structures may have been formed through the crystallization.

The complex phenotypes of eukaryotic cells are controlled by decision-making circuits and signaling pathways. A key obstacle to implementing artificial connections in signaling networks has been the lack of synthetic devices for efficient sensing, processing and control of biological signals. By extending sgRNAs to include modified riboswitches that recognize specific signals, we can create CRISPR-Cas9-based 'signal conductors' that regulate transcription of endogenous genes in response to external or internal signals of interest. These devices can be used to construct all the basic types of Boolean logic gates that perform logical signal operations in mammalian cells without needing the layering of multiple genetic circuits. They can also be used to rewire cellular signaling events by constructing synthetic links that couple different signaling pathways. Moreover, this approach can be applied to redirect oncogenic signal transduction by controlling simultaneous bidirectional (ON-OFF) gene transcriptions, thus enabling reprogramming of the fate of cancer cells.

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Bladder cancer is one of the most common malignancies worldwide. Long non-coding RNAs (lncRNAs) are a class of non-coding RNAs that play crucial roles in diverse biological processes. The pseudogene-expressed lncRNA is one major type of lncRNA family. Small ubiquitin-like modifier (SUMO) 1 pseudogene 3, (SUMO1P3) is a novel indentified lncRNA that was previously reported to be up-regulated in gastric cancer. However, we know nothing about the biological function and underlying mechanism of SUMO1P3 in tumor. Furthermore, the relationship between SUMO1P3 and bladder cancer is completely unknown. We hypothesized that SUMO1P3 also have roles in bladder cancer.In this study, we found that SUMO1P3 was significantly up-regulated in bladder cancer tissues compared with paired-adjacent nontumorous tissues in a cohort of 55 bladder cancer patients. Moreover, up-regulated SUMO1P3 expression was positively correlated with greater histological grade (P<0.05) and advanced TNM stage (P<0.05). Furthermore, we found cell proliferation / migration inhibition and apoptosis induction were also observed in SUMO1P3 siRNA-transfected bladder cancer cells. Our data suggest that SUMO1P3 plays oncogenic roles in bladder cancer and can be used as a potential prognostic and therapeutic target.