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We present a detailed study on the temperature-dependent THz spectra of the polycrystalline amino acids, L-serine and L-cysteine, for wavenumbers from 20 to 120 cm−1 and temperatures from 4 to 300 K. Even though the structure of these two amino acids is very similar, with a sulfur atom in the side chain of cysteine instead of an oxygen atom in serine, the excitation spectra are drastically different. Obviously, the vibrational dynamics strongly depend on the ability of cysteine to form sulfur–hydrogen bonds. In addition, cysteine undergoes an order–disorder type phase transition close to 80 K, documented by additional specific heat experiments, with accompanying anomalies in the THz results. On increasing temperatures, well-defined vibrational excitations exhibit significant shifts in the eigenfrequencies with concomitant line-broadening yielding partly overlapping modes. Interestingly, several modes completely lose all their dipolar strength and are unobservable under ambient conditions. Comparing the recent results to the published work utilizing THz, Raman, and neutron-scattering techniques, as well as with ab initio simulations, we aim at a consistent analysis of the results ascribing certain eigenfrequencies to distinct collective lattice modes. We document that THz spectra can be used to fine-tune the parameters of model calculations and as fingerprint properties of certain amino acids. In addition, we analyzed the low-temperature heat capacity of both the compounds and detected strong excess contributions compared to the canonical Debye behavior of crystalline solids, indicating soft excitations and a strongly enhanced phonon-density of states at low frequencies. [ABSTRACT FROM AUTHOR]

Finding low-energy structures of ligand-protected clusters is challenging due to the enormous conformational space and the high computational cost of accurate quantum chemical methods for determining the structures and energies of conformers. Here, we adopted and utilized a kernel rigid regression based machine learning method to accelerate the search for low-energy structures of ligand-protected clusters. We chose the Au25(Cys)18 (Cys: cysteine) cluster as a model system to test and demonstrate our method. We found that the low-energy structures of the cluster are characterized by a specific hydrogen bond type in the cysteine. The different configurations of the ligand layer influence the structural and electronic properties of clusters. [ABSTRACT FROM AUTHOR]

[Display omitted] Advanced multi-functional epoxy coating with physical barrier/shielding against corrosive species, self-repairing-capability/active anti-corrosive behavior, abrasion resistance, and thermomechanical durability was established in this study. For this purpose, zinc/ l -cysteine (ZC) inbuilt pH-sensitive covalent organic framework (COF) decorated two dimensional (2D) layered amino-functionalized (Si) oxidized hexagonal boron nitride (ZC-COF-Si-Oh-BN) container was prepared. Different analyses such as FT-IR, XRD, BET, XPS, TGA, TEM, and FE-SEM were utilized to evaluate the synthesized containers and pristine materials. To figure out the function of entry of the ZC-COF-Si-Oh-BN container into the epoxy coating (EC/ZC-COF-Si-Oh-BN), the EIS, salt spray (SS), cathodic disbondement (CD), pull-off adhesion, Taber abrasion, and dynamic mechanical thermal analysis (DMTA) tests were employed. The results revealed that the introduction of the ZC-COF-Si-Oh-BN container into the neat epoxy polyamide coating (EC) improved the physical barrier protection with a value of log |Z| 10mHz equal to 10.22 even after too long soaking time of 112 days in the saline solution (3.5 wt% of sodium chloride), and recovery-capability/active anti-corrosive behavior with 20.6 % healing degree after 7 h of soaking time. The abrasion weight loss for the EC and EC/ZC-COF-Si-Oh-BN coatings after 2000 abrasion cycles was about 4.8, and 4.1 mg, respectively, with 14.5 % improvement in abrasion resistance. [ABSTRACT FROM AUTHOR]

AbstractParkinson’s disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra. Recently, disorders in metabolism of metals, including copper (Cu) and iron (Fe), have been reported to be linked to the pathogenesis of PD. We previously demonstrated that 6-hydoroxydopamine (6-OHDA), a neurotoxin used for the production of PD model animals, decreases Atox1, a Cu chaperone, and ATP7A, a Cu transporter, and disrupts intracellular Cu metabolism in human neuroblastoma SH-SY5Y cells. However, the exact mechanisms remain unclear. Meanwhile, intracellular Fe modulates 6-OHDA-induced cellular responses. In this study, we investigated whether Fe participates in 6-OHDA-induced abnormality in Cu metabolism. 6-OHDA-induced reactive oxygen species (ROS) production and cellular injury were suppressed by Fe chelators, deferoxamine and 2,2’-bipyridyl (BIP). These chelators also restored 6-OHDA-induced degradation of Atox1 and ATP7A proteins and subsequent Cu accumulation, indicating that intracellular Fe is involved in the disruption of Cu homeostasis associated with 6-OHDA. Atox1 has redox-sensitive cysteine (Cys) residues in its Cu-binding site. The Cys residues of Atox1 were oxidized by 6-OHDA, and BIP suppressed their oxidation. Moreover, the replacement of Cys with histidine in the Cu-binding site conferred resistance to 6-OHDA-induced Atox1 degradation. These results suggest that oxidized modification of Atox1 by 6-OHDA is likely to accelerate its degradation. Thus, we conclude that Fe and Cu metabolisms are closely related to each other in the pathogenesis of PD. [ABSTRACT FROM AUTHOR]

Cysteine (Cys) is closely associated with many physiological and pathological processes in organisms and cells. The establishment of a molecular tool for the rapid and simple selective recognition of Cys would be of great benefit in the diagnosis and prevention of related diseases. In this paper, we developed a turn-on fluorescent probe BMBA, 3-(benzo[d]thiazol-2-yl)-4′-morpholino-[1,1′-biphenyl]-4-yl acrylate, designed with an acryloyl ester group to initiate the reaction and a benzothiazole moiety serving as the fluorescent component. Compared with other biological thiols, the probe BMBA possessed exceptional sensitivity and specificity for detecting Cys, boasting a low detection limit at 28.6 nM and a response duration of merely 5 min. The single-crystal data for the probe BMBA and compound 2 were successfully obtained and the recognition mechanism of Cys was investigated by FTIR spectroscopy and 1H NMR. Most importantly, we effectively utilized BMBA for the detection of Cys in calf serum and living cells. [ABSTRACT FROM AUTHOR]

Introduction: Chronic kidney disease of unknown etiology (CKDu) is an epidemic which is increasingly prevalent among agricultural workers and nearby communities, particularly those involved in the harvest of sugarcane. While CKDu is likely multifactorial, occupational exposure to silica nanoparticles (SiNPs), a major constituent within sugarcane ash, has gained increased attention as a potential contributor. SiNPs have high potential for generation of reactive oxygen species (ROS), and their accumulation in kidney could result in oxidative stress induced kidney damage consistent with CKDu pathology. Methods: In order to characterize the impact of sugarcane ash derived (SAD) SiNPs on human kidney proximal convoluted tubule (PCT) cells and identify potential mechanisms of toxicity, HK-2 cells were exposed to treatments of either pristine, manufactured, 200 nm SiNPs or SAD SiNPs and changes to cellular energy metabolism and redox state were determined. To determine how the cellular redox environment may influence PCT cell function and toxicity, the redox proteome was examined using cysteine-targeted click chemistry proteomics. Results: Pristine, 200 nm SiNPs induced minimal changes to energy metabolism and proteomic profiles in vitro while treatment with SAD SiNPs resulted in mitochondrial membrane hyperpolarization, inhibited mitochondrial respiration, increased reactive oxygen species generation, and redox proteomic trends suggesting activation of aryl hydrocarbon receptor (AHR) and other signaling pathways with known roles in mitochondrial inhibition and CKD progression. Conclusion: Results suggest that PCT cell exposure to SAD SiNPs could promote glycolytic and fibrotic shifts consistent with CKDu pathology via oxidative stress-mediated disruption of redox signaling pathways. [ABSTRACT FROM AUTHOR]