A 19-Bit Small Absolute Matrix Encoder.

With the application of encoders in artificial intelligence and aerospace, the demand for the miniaturization and high measurement accuracy of encoders is increasing. To solve this problem, a new absolute matrix encoder is proposed in this paper, which can realize 19-bit matrix coding by engraving two circles of matrix code, and has the advantages of fewer circles of code disk engraving and higher measurement accuracy. This article mainly focuses on the design of a new matrix code disk, encoding and decoding methods, decoding circuit design, Matlab simulation analysis, and experimental error analysis. The experimental results show that the encoder designed in this paper achieves ultra-small volume Φ30 mm × 20 mm, and the angle measurement accuracy is 2.57".

Investigating the molecular mechanism of hydroxylated bromdiphenyl ethers to inhibit the thyroid hormone sulfotransferase SULT1A1.

Hydroxylated bromodiphenyl ethers (OH-BDEs) have raised great concern due to their potential endocrine disrupting effects on humans. In vitro experiments have indicated OH-BDEs can inhibit the activity of thyroid hormone (TH) sulfotransferases (SULTs); however, the molecular mechanism has not been investigated in depth. In this work, we employed 17 OH-BDEs with five or fewer Br atoms, and performed integrated computational simulations to unravel the possible inhibition mechanism of OH-BDEs on human SULT1A1. The molecular docking results demonstrate that OH-BDEs form hydrogen bonds with residues Lys106 and His108, and the neutral OH-BDEs show comparable binding energies with their anionic counterparts. The further hybrid quantum mechanical/molecular mechanical (QM/MM) calculations unravel a metabolic mechanism of OH-BDEs comprised by proton abstraction and sulfation steps. This mechanism is involved in the SULT1A1 inhibition by some OH-BDEs comprised of three or fewer Br atoms, while other OH-BDEs likely only form ternary complexes to competitively inhibit SULT1A1 activity. Moreover, the effect of the hydroxyl group of OH-BDEs on SULT1A1 inhibition potential follows the order of ortho-OH BDE > meta-OH BDE > para-OH BDE. These results provide an insight into the inhibition mechanism of OH-BDEs to SULT1A1 at the molecular level, which are beneficial in illuminating the molecular initiating events involved in the TH disruption of OH-BDEs.

Molecular Basis for Metabolic Regioselectivity and Mechanism of Cytochrome P450s toward Carcinogenic 4-(Methylnitrosamino)-(3-pyridyl)-1-butanone.

As an abundantly present tobacco component, carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) has also been detected in atmospheric particulate matter, suggesting the ineluctable exposure risk of this contaminant. NNK metabolic activation by cytochrome P450 enzymes (CYPs) is a prerequisite to exerting its genotoxicity, but the metabolic regioselectivity and mechanism are still unknown. Here the binding feature and regioselectivity of CYPs 1A1, 1A2, 2A6, 2A13, 2B6, and 3A4 toward NNK are unraveled through molecular docking and molecular dynamics (MD) simulations. Binding mode analyses reveal that 1A2 and 2B6 have definite preferences for NNK α-methyl hydroxylation, while the other four CYPs preferentially catalyze α-methylene hydroxylation. The binding affinities between NNK and CYPs evaluated by the binding free energies follow the order 2A13 > 2B6 > 1A2 > 2A6 > 1A1 > 3A4. Density functional theory (DFT) calculations are further performed to characterize the mechanism of NNK biotransformation. Results show that the α-hydroxyNNK generated from α-hydroxylation may undergo nonenzymatic decomposition to form genotoxic diazohydroxide and aldehyde, and further oxidation by P450 to yield nitrosamide, which mainly contributes to NNK toxification capacity. Meanwhile the pyridine N-oxidation and denitrosation of Cα-radical intermediate play an important role in detoxifying NNK. Overall, the present study provides the molecular basis for CYP-catalyzed regioselectivity and mechanism of NNK biotransformation, which can enable the identification of metabolites for assessing the health risk of individual NNK exposure.

In silico study for inhibiting thyroid hormone sulfotransferase activity by halogenated phenolic chemicals.

Thyroid hormones (THs) are essential to proper growth and development of human bodies. Inhibiting the sulfation metabolism of THs has been demonstrated to be an important way for some environmental pollutants, such as halogenated phenolic compounds, to interfere THs homeostasis, thereby causing health problems. However, the important property characteristics that govern the sulfation inhibition of these chemicals are not well understood, and the experimental data on inhibition potential is limited. In this work, an in silico approach was developed to investigate the structure-activity relationship for their sulfotransferases (SULTs) inhibition. A series of quantum chemical descriptors that quantify the electronic and energy properties of 22 halogenated phenolic compounds have been calculated to establish a predictive model and analyzed their corresponding contributions to SULTs inhibition. Density functional theory (DFT) B3LYP/6-31G** has been employed to optimize molecular geometries to obtain a total of 15 descriptors for every compound. The implementation of linear regression shows three descriptors that represent molecular mass, positive charges on hydrogen atoms, and energy of frontier orbitals strongly correlate with SULTs inhibition potential. This indicates molecular size, hydrogen-bond strength, and nucleophilic-electrophilic reactivity may play important roles in SULTs inhibition. The derived regression model has good statistical performance (r2 = 0.84, rms = 0.35), and different validation strategies indicate it can serve as an efficient predictive tool for other chemicals in application domain but with no experimental data, consequently assisting in their THs sulfation inhibition and health risk assessment.

Massive Cerebrospinal Fluid Replacement Reduces Delayed Cerebral Vasospasm After Embolization of Aneurysmal Subarachnoid Hemorrhage.

BACKGROUND Delayed cerebral vasospasm (DCVS) following aneurismal subarachnoid hemorrhage (SAH) is a leading cause of poor prognosis and death in SAH patients. Effective management to reduce DCVS is needed. A prospective controlled trial was conducted to determine if massive cerebrospinal fluid (CSF) replacement (CR) could reduce DCVS occurrence and improve the clinical outcome after aneurysmal SAH treated with endovascular coiling. MATERIAL AND METHODS Patients treated with endovascular coiling after aneurysmal SAH were randomly divided into a control group receiving regular therapy alone (C group, n=42) and a CSF replacement group receiving an additional massive CSF replacement with saline (CR group, n=45). CSF examination, head CT, DCVS occurrence, cerebral infarction incidence, Glasgow Outcome Scale prognostic score, and 1-month mortality were recorded. RESULTS The occurrence of DCVS was 30.9% in the C group and 4.4% in the CR group (P<0.005). The cerebral infarction incidences in the C and CR groups were 19.0% and 2.2% (P<0.05), respectively, 1 month after the treatments. Mortality was not significantly different between the 2 groups during the follow-up period. CONCLUSIONS Massive CR after embolization surgery for aneurysmal SAH can significantly reduce DCVS occurrence and effectively improve the outcomes.

Acute carotid artery dissection treated with stenting and hematoma aspiration guided by ultrasonography.

We report the successful treatment of dissection with stenosis of the carotid artery by stenting and aspiration of hematoma. A male patient, presenting with acute blurred vision and weakness and numbness of the right side of his body, was diagnosed with common carotid artery (CCA) dissection and severe stenosis of the internal carotid artery and CCA by digital subtraction arteriography and color Doppler ultrasonography (CDU). Two stents were separately implanted into the left internal carotid artery and CCA to restore blood flow and seal the opening of the dissection. The hematoma inside the CCA dissection was transcutaneously aspirated under CDU guidance after thrombolysis with tissue plasminogen activator. Three days after the operation, the dissection was still sealed. The patient was discharged 1 week later without any signs or symptoms. Follow-up examination at 70 days confirmed complete healing of the CCA dissection. Transcutaneous intradissection hematoma aspiration with CDU guidance may be applicable in treating arterial dissection, especially when conservative treatments cannot be expected to improve severe flow disturbances.