Simultaneous coupling of metal removal and visual detection by nature-inspired polyphenol-amine surface chemistry.

The interplay between polyphenols, amines, and metals has broad implications for surface chemistry, biomaterials, energy storage, and environmental science. Traditionally, polyphenol-amine combinations have been recognized for their ability to form adhesive, material-independent thin layers that offer a diverse range of surface functionalities. Herein, we demonstrate that a coating of tannic acid (TA) and polyethyleneimine (PEI) provides an efficient platform for capturing and monitoring metal ions in water. A unique feature of our PEI/TA-coated microbeads is the 'Detection-Capture' (Detec-Ture) mechanism. The galloyl groups in TA coordinate with Fe(III) ions (capture), initiating their oxidation to gallol-quinone. These oxidized groups subsequently react with PEI amines, leading to the formation of an Fe(II/III)-gallol-PEI network that produces a vivid purple color, thereby enabling visual detection. This mechanism couples metal capture directly with detection, distinguishing our approach from existing studies, which have either solely focused on metal removal or metal detection. The metal capturing capacity of our materials stands at 0.55 mg g-1, comparable to that of established materials like alginate and wollastonite. The detection sensitivity reaches down to 0.5 ppm. Our findings introduce a novel approach to the utility of metal-polyphenol-amine networks, presenting a new class of materials suited for simultaneous metal ion detection and capture in environmental applications.

Material-Selective Polydopamine Coating in Dimethyl Sulfoxide.

Polydopamine coating is known to be performed in a material-independent manner and has become a popular tool when designing a surface-functionalization strategy of a given material. Studies to improve polydopamine coatings have been reported, aiming to reduce the coating time (by transition metals, oxidants, applied voltages, or microwave irradiation), control surface roughness using catechol derivatives, and vary the ad-layer molecules formed on an underlying polydopamine layer. However, none of the techniques have changed the most important intrinsic property of polydopamine, the surface-independent coating. Currently, no method has been reported to modify this property to create a material-selective 'smart' polydopamine coating. Herein, we report a method with polydopamine to differentiate the chemistry of surfaces. We found that the polydopamine coating was largely inhibited on silicon-containing surfaces such as Si wafers and quartz crystals in a dimethyl sulfoxide (DMSO)/phosphate-buffered saline (PBS) cosolvent, while the coating properties on other materials remained mostly unchanged. Among the various interface bonding mechanisms of coordination, namely, cation-π, π-π stacking, and hydrogen-bonding interactions, the DMSO/PBS cosolvent effectively inhibits hydrogen-bond formation between catechol and SiO2, resulting in surface-selective 'smart' polydopamine coatings. The new polydopamine coating is useful for functionalizing patterned surfaces such as Au patterns on SiO2 substrates. Considering that Si wafer is the most widely used substrate, the surface-selective polydopamine coating technique described herein opens up a new direction in surface functionalization and interface chemistry.

The effect of gonadotrophin-releasing hormone agonist treatment over 3 years on bone mineral density and body composition in girls with central precocious puberty.

OBJECTIVE: Puberty is a period characterized by growth spurt and rapid change in body composition. The effect of GnRH agonist therapy for central precocious puberty on bone mineral density is unclear. We demonstrated changes in bone mineral density in subjects with central precocious puberty, who were treated with GnRH agonist for more than 3 years. DESIGN: The changes in bone mineral density and body compositions were tested with analysis of variance with repeated measures to identify statistical significance over the treatment period. PATIENTS: One hundred ninety-five Korean girls with central precocious puberty were treated with GnRH agonist, and among these subjects, 39 patients were treated for more than 3 years. MEASUREMENTS: Dual-energy X-ray absorptiometry was performed on the subjects at the initial evaluation and once yearly thereafter while on the treatment. RESULTS: The bone mineral density parameters for chronological age tended to decrease near the mean for the treatment period; however, they increased significantly for bone age excluding bone mineral apparent density. An increment of the BMI was not significant for the chronological age. CONCLUSIONS: Three-year treatment with GnRH agonist in central precocious puberty patients did not impair bone maturation. GnRH agonist could be effectively commenced in girls with precocious puberty from an early age.

Manganese superoxide dismutase induced by TNF-beta is regulated transcriptionally by NF-kappaB after spinal cord injury in rats.

Antioxidant enzymes including superoxide dismutase (SOD) may play a role in the mechanism by which cells counteract the deleterious effects of reactive oxygen species (ROS) after spinal cord injury (SCI). Cu/Zn and MnSOD are especially potent scavengers of superoxide anion and likely serve important cytoprotective roles against cellular damage. We investigated expression of SOD after SCI to address its role during the early stages of injury. MnSOD activity was increased 4 h after SCI and persisted at elevated levels up to 24-48 h; by contrast, Cu/ZnSOD activity was not changed. RT-PCR and Western blot analyses showed increased levels of MnSOD mRNA and protein, respectively, by 4 h and reached maximum levels by 24-48 h. Double immunostaining revealed that MnSOD protein was localized within neurons and oligodendrocytes. Tumor necrosis factor-alpha (TNF-alpha) was administered locally into uninjured spinal cords to examine potential mechanisms for MnSOD induction after injury. TNF-alpha administered exogenously increased MnSOD expression in uninjured spinal cords. Western blot and immunostaining also revealed that a transcription factor, NF-kappaB, was activated and translocated into the nuclei of neurons and oligodendrocytes. By contrast, administration of neutralizing antibody against TNF-alpha into injured spinal cords attenuated the increase in MnSOD expression and activation of NF-kappaB. Double immunostaining revealed that MnSOD was co-localized with NF-kappaB in neurons and oligodendrocytes after SCI. These results suggest that TNF-alpha may be an inducer of NF-kappaB activation and MnSOD expression after SCI and that MnSOD expression induced by TNF-alpha is likely mediated through activation of NF-kappaB.