[reaction: see text] A new sensing mechanism based on C=N isomerization, which shows a very significant fluorescence enhancement to the metal cations in a simple and efficient way, is demonstrated. A coumarin derivative (L) containing a C=N group was designed as an example for illustration. The free ligand L is almost nonfluorescent due to the isomerization of C=N double bond in the excited state. However, the solution of ligand shows about a 200-fold increase of fluorescence quantum yield (about 30%) upon addition of Zn(ClO4)2.

A ratiometric fluorescence sensor based on pyrene was designed for selective detection of heparin in HEPES (N-(2-hydroxyethyl)piperazine-N'-ethanesulfonic acid) buffer and serum sample. Pyrene and long-chain alkanes were linked through bisquaternary functionality in the sensor which could interact with heparin via supramolecular assembly. A ratiometric fluorescent signal change of the sensor can be observed because of the specific monomer-excimer conversion of pyrene which is modulated by the supramolecular self-assembly of sensor and heparin. Upon addition of heparin, the excimer emission of the sensor at 489 nm is observed and the monomer emission intensity at 395 nm decreases concomitantly. Addition of heparin derivatives with very similar structure such as chondroitin 4-sulfate or hyaluronic acid to the same sensor solution only leads to very smaller changes in intensity ratios probably because of lower charge density and more distant spatial distribution of anions (or disadvantageous spatial orientation of anions) as compared to those of heparin. The novel sensor can effectively differentiate heparin from its derivatives with relatively low background interference and wide linear response in HEPES and serum. A linear calibration curve is obtained from 0 to 3.4 μM for heparin quantification in serum.

A naphthalimide-based colorimetric fluorescent probe containing a disulfide group was designed and synthesized, which could detect the physiological level of GSH quantitatively by a ratiometric fluorescence method and was successfully applied to the imaging of thiols in living HeLa cells.

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A coumarin-derived complex, Hg(2)L(2), was reported as a highly sensitive and selective probe for the detection of mercapto biomolecules in aqueous solution. The addition of Cys to a 99% aqueous solution of Hg(2)L(2) resulted in rapid and remarkable fluorescence OFF-ON (emission at 525 nm) due to the ligand-exchange reaction of Cys with L coordinated to Hg(2+). The increased fluorescence can be completely quenched by Hg(2+) and recovered again by the subsequent addition of Cys. Such a fluorescence OFF-ON circle can be repeated at least 10 times by the alterative addition of Cys and Hg(2+) to the solution of Hg(2)L(2), indicating that it can be used as a convertible and reversible probe for the detection of Cys. The interconversion of Hg(2)L(2) and L via the decomplexation/complexation by the modulation of Cys/Hg(2+) was definitely verified from their crystal structures. Other competitive amino acids without a thiol group cannot induce any fluorescence changes, implying that Hg(2)L(2) can selectively determine mercapto biomolecules. Using confocal fluorescence imaging, L/Hg(2)L(2) as a pair of reversible probes can be further applied to track and monitor the self-detoxification process of Hg(2+) ions in SYS5 cells.

A new quinine derivative PQ, bearing pyrenyl as a fluorophore, was prepared to recognize heparin in aqueous solution. PQ exhibits good selectivity and sensitivity for heparin over other biological molecules. Upon binding with heparin, PQ shows a typical excimer emission peaked at 489 nm along with a weak monomer emission at 376 nm. Moreover, PQ also shows good performance to detect the heparin in serum.

No abstract

Rationale: Olfactory ensheathing cell (OEC) transplantation has emerged as a promising therapy for spinal cord injury (SCI) repair. In the present study, we explored the possible mechanisms of OECs transplantation underlying neuroinflammation modulation. Methods: Spinal cord inflammation after intravenous OEC transplantation was detected in vivo and ex vivo by translocator protein PET tracer [ 18 F]F-DPA. To track transplanted cells, OECs were transduced with enhanced green fluorescent protein (eGFP) and HSV1-39tk using lentiviral vector and were monitored by fluorescence imaging and [ 18 F]FHBG study. Protein microarray analysis and ELISA studies were employed to analyze differential proteins in the injured spinal cord after OEC transplantation. The anti-inflammation function of the upregulated protein was also proved by in vitro gene knocking down experiments and OECs/microglia co-culture experiment. Results: The inflammation in the spinal cord was decreased after OEC intravenous transplantation. The HSV1-39tk-eGFP-transduced OECs showed no accumulation in major organs and were found at the injury site. After OEC transplantation, in the spinal cord tissues, the interleukin-1 receptor antagonist (IL-1Ra) was highly upregulated while many chemokines, including pro-inflammatory chemokines IL-1α, IL-1β were downregulated. In vitro studies confirmed that lipopolysaccharide (LPS) stimulus triggered OECs to secrete IL-1Ra. OECs significantly suppressed LPS-stimulated microglial activity, whereas IL-1Ra gene knockdown significantly reduced their ability to modulate microglial activity. Conclusion: The OECs that reached the lesion site were activated by the release of pro-inflammatory cytokines from activated microglia in the lesion site and secreted IL-1Ra to reduce neuroinflammation. Intravenous transplantation of OECs has high therapeutic effectiveness for the treatment of SCI via the secretion of IL-1Ra to reduce neuroinflammation.