Rapid and Direct Detection of Trimethylamine N-oxide Using an Off-Chip Capacitance Biosensor with Readout SoC for Early-Stage Thrombosis and Cardiovascular Disease.

A demonstration of an off-chip capacitance array sensor with a limit of detection of 1 µM trimethylamine N-oxide (TMAO) to diagnose a chronic metabolism disease in urine is presented. The improved Cole-Cole model is employed to determine the parameters of R_catalyzed, C_catalyzed, and Rp_catalyzed, enabling the prediction of the catalytic resistance of enzyme, reduction effects of the analyte, and characterize the small signal alternating current properties of ionic strength caused by catalysis. Based on the standard solutions, we investigate the effects of pixel geometry parameters, driving electrode width, and sensing electrode width on the electrical field change of the off-chip capacitance sensor; the proposed off-chip sensor with readout system-on-chip exhibits a high sensitivity of 21 analog-to-digital converter counts/µM TMAO (or 2.5 mV/µM TMAO), response time of 1 s, repetition of 98.9%, and drift over time of 0.5 mV. The proposed off-chip sensor effectively discriminates TMAO in a phosphate-buffered saline solution based on minute changes in capacitance induced by the TorA enzyme, resulting in a discernible 2.15% distinction. These measurements have been successfully corroborated using the conventional cyclic voltammetry method, demonstrating a mere 0.024% variance. The off-chip sensor is crafted with a specific focus on detecting TMAO, achieved by excluding any reduction reactions between the TMAO-specific enzyme TorA and the compounds creatine and creatinine present in urine. This deliberate omission ensures that the sensor's attention remains solely on TMAO, thereby enhancing its precision in achieving accurate and reliable TMAO detection.

Enantioselective Synthesis of Nabscessin C.

Enantioselective synthesis of nabscessin C (1), an aminocyclitol amide with antimicrobial activity, is reported. Starting from myo-inositol, (+)-nabscessin C was synthesized in 12 isolation steps. Desymmetrization of 2-deoxygenated 4,6-dibenzylinositol was achieved using lipase from porcine pancreas (PPL), and the stereochemistry was established by X-ray crystallography. This method has the potential for synthesizing other cyclitol-derived compounds.

Self-referencing biosensors using Fano resonance in periodic aluminium nanostructures.

Surface plasmon resonance (SPR) is an important technique for real-time and label-free detection of specific binding biomolecules. However, conventional SPR signals come from both the surface binding biomolecules and the variation in the bulk refractive index. This work demonstrates that Fano resonance in an aluminum capped nanoslit array has the ability to remove the signal of bulk refractive index changes from the SPR signal. As compared to gold nanostructures, the aluminum nanostructure provides an asymmetrical Fano resonance with clear peak and dip wavelengths. The peak wavelength is close to the grating resonance condition. The evanescent depth at the peak wavelength is up to several microns. The dip wavelength comes from the SPR effect. The evanescent depth at the dip wavelength is about 300 nm. By simultaneously measuring the shifts of peaks and the dip wavelengths, the variation in the bulk refractive index can be removed and only the biolayer thickness is measured. The finite-difference time-domain calculation shows that the 470 nm-period nanoslit array with 90 and 70 nm slit depths has the optimal thickness sensitivity. In this experiment, a simple multispectral imaging system is developed for multiple bio-interaction measurements. The measured results verify that the bulk refractive index changes can be removed and the surface biomolecular interactions can be directly obtained without the need of a reference channel.

Effects of oral zinc supplementation on patients with noise-induced hearing loss associated tinnitus: A clinical trial.

BACKGROUND: Zinc plays a vital antioxidant role in human metabolism. Recent studies have demonstrated a correlation between noise-induced hearing loss (NIHL) and oxidative injury; however, no investigation has focused specifically on the subgroup of NIHL associated tinnitus patients. We aimed to evaluate the effectiveness of zinc supplementation in treating NIHL associated tinnitus. METHODS: Twenty patients with tinnitus and a typical NIHL audiogram (38 ears) were included in this study. Another 20 healthy subjects were used as the control group. A full medical history assessment was performed, and each subject underwent an otoscopic examination, basic audiologic evaluation, distortion product otoacoustic emissions (DPOAEs), tinnitus-match testing, Tinnitus Handicap Inventory (THI) and serum zinc level analyses. After 2 months of treatment with zinc, all tests were repeated. RESULTS: There was a significant difference between pretreatment and post-treatment within the tinnitus group (73.6 vs. 84.6 µg/dl). The pre- and post-treatment difference in serum zinc was significantly higher in the young group (≦50 years) compared to the old group (19.4 ± 11.4 vs. 2.6 ± 9.2 µg/dl, respectively; p = 0.002). There were no statistically significant differences in hearing thresholds, speech reception thresholds, or tinnitus frequency and loudness results before and after treatment. In addition, 17 patients (85%) showed statistically significant improvement of THI-total scores post-treatment, from 38.3 to 30 (p = 0.024). CONCLUSIONS: Zinc oral supplementation elevated serum zinc levels, especially in younger patients. THI scores improved significantly following zinc treatment in patients with NIHL associated tinnitus. However, no improvements in objective hearing parameters were observed.

Phosphorylation at threonine 288 by cell cycle checkpoint kinase 2 (CHK2) controls human monopolar spindle 1 (Mps1) kinetochore localization.

Human Mps1 (hMps1) is a mitotic checkpoint kinase responsible for sensing the unattached and tensionless kinetochore. Despite its importance in safeguarding proper chromosome segregation, how hMps1 is recruited to the kinetochore remains incompletely understood. Here, we demonstrate that phosphorylation at Thr-288 by the cell cycle checkpoint kinase CHK2 is involved in this process. We discovered that the phosphorylation-deficient T288A mutant has an impaired ability to localize to the kinetochore and cannot reestablish the mitotic checkpoint in hMps1-depleted cells. In support, we found that nocodazole induced hMps1 phosphorylation at the previously identified CHK2 site Thr-288 and that this could be detected at the kinetochore in a CHK2-dependent manner. Mechanistically, phosphorylation at Thr-288 promoted the interaction with the KMN (KNL1-Mis12-Ndc80 network) protein HEC1. Forced kinetochore localization corrected the defects associated with the T288A mutant. Our results provide evidence of a newly identified hMps1 phosphorylation site that is involved in the mitotic checkpoint and that CHK2 contributes to chromosomal stability through hMps1.

Bis[µ-N-(pyridin-2-yl)methane-sulfon-amido-κ(2) N:N']silver(I).

In the title compound, [Ag2(C6H7N2O2S)2], the Ag(I) atom is coordinated by two N atoms from two N-(pyridin-2-yl)methane-sulfonamidate anions in a slightly bent linear geometry [N-Ag-N = 166.03 (7)°]. The Ag(I) atoms are bridged by the N-(pyridin-2-yl)methane-sulfonamidate anions, forming a centrosymmetric dinuclear mol-ecule, in which the Ag⋯Ag distance is 2.7072 (4) Å.

Bis(2-amino-pyrimidin-1-ium) sulfate.

In the title compound, 2C(4)H(6)N(3) (+)·SO(4) (2-), the cations are each essentially planar with r.m.s. deviations of the fitted atoms of 0.008 and 0.002 Å. In the crystal, adjacent ions are linked by N-H⋯O, C-H⋯O and C-H⋯N hydrogen bonds, forming a three-dimensional network.

Tetra-kis[µ-1,3-bis-(4,5-dihydro-1,3-oxazol-2-yl)benzene-κ(2)N:N']tris-ilver(I) tris-(hexa-fluoridophosphate).

In the title compound, [Ag(3)(C(12)H(12)N(2)O(2))(4)](PF(6))(3), one Ag(I) ion, lying on a twofold rotation axis, is coordinated by four N atoms from four 1,3-bis-(4,5-dihydro-1,3-oxazol-2-yl)benzene (L) ligands in a distorted tetra-hedral geometry and the other Ag(I) ion is coordinated by two N atoms from two L ligands in a bent arrangement [N-Ag-N = 169.03 (17)°]. Two L ligands adopt a syn conformation, while the other two adopt an anti conformation. They bridge adjacent Ag(I) ions, forming a trinuclear complex. One of the PF(6) (-) anions is half-occupied, with the P atom located on a twofold rotation axis. The PF(6) (-) anions link the complex mol-ecules via Ag⋯F inter-actions [2.80 (2) and 2.85 (2) Å] into a polymeric chain along [100].

Poly[[µ-(3-amino-pyridine)-κ(2)N:N'-µ-chlorido-chlorido(N,N'-dimethyl-formamide-κO)nickel(II)] N,N'-dimethyl-formamide monosolvate].

The title compound, {[NiCl(2)(C(5)H(6)N(2))(C(3)H(7)NO)]·C(3)H(7)NO}(n), is a two-dimensional polymer in which the Ni(II) atom is coordinated by two N atoms from two 3-amino-pyridine ligands, one O atom from a dimethyl-formamide (DMF) group, one terminal Cl and two bridging Cl atoms in a distorted octa-hedral geometry. The Ni(II) atoms are bridged by the 3-amino-pyridine ligands [Ni⋯N = 6.7048 (3) Å] and Cl(-) atoms [Ni⋯N = 3.5698 (3) Å], forming (4,4) two-dimensional nets. The DMF solvent mol-ecule and the non-bridged Cl(-) ions participate in N-H⋯O and N-H⋯Cl hydrogen bonds with the amino groups.

Methyl 4-[N-(5-bromo-pyrimidin-2-yl)carbamo-yl]benzoate.

In the title compound, C(13)H(10)BrN(3)O(3), the pyrimidine and benzene rings are twisted with an inter-planar angle of 58.4 (1)°. The secondary amide group adopts a cis conformation with an H-N-C-O torsion angle of 14.8 (1)°. In the crystal, mol-ecules are connected into inversion dimers via pairs of N-H⋯N hydrogen bonds, generating an R(2) (2)(8) motif. The dimers are further connected through a C-Br⋯O inter-action [3.136 (1) Šand 169.31 (1)°] into a chain along [110]. Weak C-H⋯N hydrogen bonds between the methyl benzoate groups and pyrimidine rings are also observed in the crystal structure.

Poly[(µ(3)-quinoline-6-carboxyl-ato-κ(3)N:O:O')silver(I)].

In the title coordination polymer, [Ag(C(10)H(6)NO(2))](n), the Ag(I) cation is coordinated by two O atoms and one N atom from three 6-quinoline-carboxyl-ate anions in a distorted T-shaped AgNO(2) geometry, in which the O-Ag-O angle is 160.44 (9)°. The 6-quinoline-carboxyl-ate anion bridges three Ag(+) cations, forming a nearly planar polymeric sheet parallel to (101). The distance between Ag(+) cations bridged by the carboxyl group is 2.9200 (5) Å. In the crystal, π-π stacking is observed between parallel quinoline ring systems, the centroid-centroid distance being 3.7735 (16) Å.

catena-Poly[[silver(I)-µ-1,2-bis-(4,4-dimethyl-4,5-dihydro-1,3-oxazol-2-yl)ethane-κ(2)N:N'] perchlorate hemihydrate].

In the title coordination polymer, {[Ag(C(12)H(20)N(2)O(2))]ClO(4)·0.5H(2)O}(n), the Ag(I) cation is coordinated by two N atoms from two 1,2-bis-(4,4-dimethyl-4,5-dihydro-1,3-oxazol-2-yl)ethane (L) ligands in a nearly linear geometry [N-Ag-N = 171.07 (8)°]. The L ligand bridges adjacent Ag(+) cations, forming a polymeric chain running along the c axis. The lattice water mol-ecule is situated on a twofold rotation axis, and links to the perchlorate anion via an O-H⋯O hydrogen bond. The long Ag⋯O separation of 3.200 (4) Šindicates a weak inter-action between the perchlorate anion and the Ag(I) cation. Weak C-H⋯O hydrogen bonding occurs between the chain and the lattice water mol-ecule and between the chain and perchlorate anions. Both five-membered rings of the L ligand display envelope conformations; in one five-membered ring, the flap C atom is disordered on opposite sides of the ring with occupancies of 0.65 and 0.35.

2-Amino-4,6-dimethyl-pyrimidin-1-ium chloride.

In the title compound, C6H10N3(+)·Cl(-), the cation is essentially planar with an r.m.s. deviations of the fitted atoms of 0.008 Å. In the crystal, adjacent ions are linked by weak N-H⋯Cl hydrogen bonds involving the pyrimidine and amine N atoms, forming a three-dimensional network. C-H⋯π inter-actions between the methyl and pyrimidine groups and π-π stacking [centroid-centroid distance = 3.474 (1) Å] between parallel pyrimidine ring systems are also observed.

Tetra-kis[µ-1,4-bis-(4,5-dihydro-1,3-oxazol-2-yl)benzene-κN:N']tetra-kis-(µ-methano-lato-κO:O)bis-(µ-perchlorato-κO:O')tetra-copper(II) bis-(perchlorate).

The title tetra-nuclear Cu(II) complex, [Cu(4)(C(12)H(12)N(2)O(2))(4)(CH(3)O)(4)(ClO(4))(2)](ClO(4))(2), is located around an inversion center. Each Cu(II) atom is coordinated by two cis-O atoms from two bridging methano-late anions and two cis-N atoms from two bridging 1,4-bis-(4,5-dihydro-1,3-oxazol-2-yl)benzene (L) ligands in the basal plane, and is further coordinated by one O atom of the bridging perchlorate anion, forming a distorted square-pyramidal geometry. The Cu⋯Cu separations in the recta-ngular core are 2.9878 (11) and 6.974 (1) Å. In the asymmetric unit, there are two L ligands with a syn conformation. In one L ligand, the dihedral angles between the central benzene ring and the terminal 4,5-dihydro-1,3-oxazol-2-yl mean planes are 22.1 (4) and 33.1 (4)°, and in the other L ligand the corresponding dihedral angles are 29.3 (4) and 29.9 (4)°. The uncoordinated perchlorate anion is linked with the complex mol-ecules via weak C-H⋯O hydrogen bonds.

catena-Poly[(µ-2-amino-1,3,4-thia-diazole-κN:N)di-µ-chlorido-cadmium].

In the title coordination polymer, [CdCl(2)(C(2)H(3)N(3)S)](n), the Cd(II) cation is coordinated by four Cl(-) anions and two N atoms from two trans 2-amino-1,3,4-thia-diazole (L) ligands in a distorted octa-hedral geometry. The L ligand and Cl(-) anions bridge adjacent Cd cations, forming a polymeric chain along the b axis; the separation between adjacent Cd cations is 3.619 (1) Å. In the crystal, the polymeric chains are inter-linking through N-H⋯Cl hydrogen bonds between the L ligands and Cl(-) anions.

Poly[[µ(2)-1,4-bis-(4,5-dihydro-1,3-oxazol-2-yl)benzene-κN:N']di-µ(2)-chlorido-cadmium].

In the title coordination polymer, [CdCl(2)(C(12)H(12)N(2)O(2))](n), the Cd(II) ion, situated on an inversion center, is coordinated by four bridging Cl atoms and two N atoms from two 1,4-bis-(4,5-dihydro-1,3--oxazol-2-yl)benzene (L) ligands in a distorted octa-hedral geometry. Each L ligand also lies across an inversion center and bridges two Cd(II) ions, forming infinite two-dimensional recta-ngular layers running parallel to (010).

Poly[[µ-1,4-bis-(4,5-dihydro-1,3-oxazol-2-yl)benzene-κN:N']di-µ-bromido-cadmium].

In the title coordination polymer, [CdBr(2)(C(12)H(12)N(2)O(2))](n), the Cd(II) ion, situated on an inversion centre, is coordinated by four bridging Br atoms and two N atoms from two 1,4-bis-(4,5-dihydro-1,3-oxazol-2-yl)benzene (L) ligands in a distorted octa-hedral geometry. The L ligand, which also lies across an inversion centre, bridges two Cd(II) ions, forming layers parallel to (010).

Methyl 4-[(5-chloro-pyrimidin-2-yl)carbamo-yl]benzoate.

Mol-ecules of the title compound, C(13)H(10)ClN(3)O(3), form centrosymmetric dimers via inter-molecular N-H⋯N hydrogen bonds generating an R(2) (2)(8) motif. The dimers are further connected through an O⋯Cl-C halogen bond [O⋯Cl = 3.233 (1) Šand O⋯Cl-C = 167.33 (1)°] into a chain along [110]. The secondary amide group adopts a cis conformation. Weak C-H⋯N hydrogen bonds among the methyl benzoate and pyrimidyl rings are also observed in the crystal structure.

4-Methyl-N-[(Z)-3-(4-methyl-phen-ylsulfon-yl)-1,3-thia-zolidin-2-yl-idene]benzene-sulfonamide.

In the crystal structure of the title compound, C(17)H(18)N(2)O(4)S(3), mol-ecules are connected into centrosymmetric dimers via weak inter-molecular C-H⋯π inter-actions. These dimers are further connected through a series of weak C-H⋯O hydrogen bonds, while futher C-H⋯π inter-actions involving the phenyl and thia-zoline rings are also observed. The thia-zolidine ring is twisted from the benzene rings rings by dihedral angles of 79.1 (1) and 85.0 (1)°, while the dihedral angle between two benzene rings is 76.0 (1)°.

catena-Poly[[bis-(nitrato-κO)copper(II)]-µ-1,4-bis-(4,5-dihydro-1,3-oxazol-2-yl)-benzene-κN:N'].

In the title coordination polymer, [Cu(NO(3))(2)(C(12)H(12)N(2)O(2))](n), the Cu(II) ion, situated on an inversion center, is coordinated by two O atoms from two nitrate anions and two N atoms from two 1,4-bis-(4,5-dihydro-1,3-oxazol-2-yl)benzene (L) ligands in a distorted square-planar geometry. Each L ligand also lies across an inversion center and bridges two Cu(II) ions, forming a polymeric chain running along the [101] direction. The three O atoms of the nitrate group are disordered over two positions in a 3:2 ratio.