catena-Poly[[(1,10-phenanthroline-κ2 N,N′)zinc]-μ-4-sulfonato­benzo­triazolido-κ3 N 3,O:N 1]

In the title complex, [Zn(C6H3N3O3S)(C12H8N2)]n, the Zn2+ cation is coordinated by two N atoms from two 4-sulfonato­benzotriazolide dianions, two N atoms from a 1,10-phenanthroline mol­ecule and a sulfonate O atom from a 4-sulfonato­benzotriazolide anion, displaying a distorted ZnN4O trigonal–bipyramidal geometry. Each 1,10-phenanthroline ligand displays a bidentate chelating coordinating mode and the 4-sulfonato­benzotriazolide ions act as μ2-bridges, linking different Zn2+ cations into a chain along the b axis. The crystal structure is consolidated by C—H⋯O hydrogen-bonding inter­actions

Bis(1H-benzotriazole-7-sulfonato-κO)bis­(1,10-phenanthroline-κ2 N,N′)cadmium dihydrate

In the title complex, [Cd(C6H4N3O3S)2(C12H8N2)2]·2H2O, the Cd2+ cation is located on an inversion center and is coordinated by four N atoms from two symmetry-related 1,10-phenanthroline ligands and two sulfonate O atoms from two benzotriazole-7-sulfonate anions, displaying a distorted CdN4O2 octa­hedral geometry. In the crystal, O—H⋯N, O—H⋯O, N—H⋯O, C—H⋯N and C—H⋯O hydrogen bonds occur. The lattice water mol­ecules and sulfonate O atoms as donor or acceptor atoms play important roles in the formation of these inter­actions

Bis(1H-benzotriazole-4-sulfonato-κ2 N 3,O)(2,2′-bipyridyl-κ2 N,N′)cadmium

In the title complex, [Cd(C6H4N3O3S)2(C10H8N2)], the Cd2+ cation is located on a twofold rotation axis and is coordinated by two N and two O atoms from two symmetry-related benzotriazole-4-sulfonate anions and two N atoms from a 2,2-bipyridyl ligand, displaying a distorted CdN4O2 octa­hedral geometry. The crystal structure is stabilized by N—H⋯O and C—H⋯O hydrogen-bonding inter­actions

Geometric bionics: Lotus effect helps polystyrene nanotube films get good blood compatibility

Various biomaterials have been widely used for manufacturing biomedical applications including artificial organs, medical devices and disposable clinical apparatus, such as vascular prostheses, blood pumps, artificial kidney, artificial hearts, dialyzers and plasma separators, which could be used in contact with blood^1^. However, the research tasks of improving hemocompatibility of biomaterials have been carrying out with the development of biomedical requirements^2^. Since the interactions that lead to surface-induced thrombosis occurring at the blood-biomaterial interface become a reason of familiar current complications with grafts therapy, improvement of the blood compatibility of artificial polymer surfaces is, therefore a major issue in biomaterials science^3^. After decades of focused research, various approaches of modifying biomaterial surfaces through chemical or biochemical methods to improve their hemocompatibility were obtained^1^. In this article, we report that polystyrene nanotube films with morphology similar to the papilla on lotus leaf can be used as blood-contacted biomaterials by virtue of Lotus effect^4^. Clearly, this idea, resulting from geometric bionics that mimicking the structure design of lotus leaf, is very novel technique for preparation of hemocompatible biomaterials

2-Chloro-4-(3,3-dichloro­all­yloxy)-1-nitro­benzene

In the crystal structure of the title compound, C9H6Cl3NO3, mol­ecules are connected by C—H⋯O hydrogen bonds, forming chains along the b axis. The dihedral angle between the benzene ring and the plane of the nitro group is 16.2 (1)° and that between the benzene ring and the plane of the dichloro­allyl group is 10.2 (1)°

The correlation between the severity of radiotherapy-induced glossitis and endothelial cell injury in local tissues in a rat model

Objectives: To explore the correlation between the severity of radiotherapy-induced glossitis (RTG) and endothelial cell injury in local tissues in a rat model. Study Design: The RTG animal model was designed and used by our team. The Oral mucositis index(OMI) was documented daily. Immunohistochemistry (IHC) Staining of CD34 was utilized to identify endothelial cells in the RTG tissues. Apoptosis of endothelial cells in local lesions due to RTG was detected by the TUNEL assay. The dynamic relationship between the OMI and apoptotic endothelial cells was statistically analyzed by time. Results and Conclusions: The injury and apoptosis of endothelial cells were observed 3 day post-irradiation. The vascular lumens of the post-irradiation tongue lesions were irregular; thrombosis formation in the center of the lumens, unsmooth lumen walls and vasodilated vessels were observed. Also, endothelial cells detached from the basal membrane and were found in the lumens. The percentages (%) of apoptotic endothelial cells were 78.3±0.31 (5 day); 89.3±0.83 (8 day); 83.5±0.41 (14 day); 69.3±0.57 (21 day); and 47.3±0.59 (28 day). The OMI was correlated with the percentage of apoptotic endothelial cells (R=0.67, P=0.034). Summary, endothelial cell injury was correlated with the pathogenic condition of RTG. © Medicina Oral S. L

An adaptive working state iterative calculation method of the power battery by using the improved Kalman filtering algorithm and considering the relaxation effect.

The battery modeling and iterative state calculation in the battery management system is very important for the high-power lithium-ion battery packs, the accuracy of which affects its working performance and safety. An adaptive improved unscented Kalman filtering algorithm is developed to realize the iterative calculation process, aiming to overcome the rounding error in the numerical calculation treatment when it is used to estimate the nonlinear state value of the battery pack. As the sigma point is sampled in the unscented transform round from the unscented Kalman filter algorithm, an imaginary number appears that results in the working state estimation failure. In order to solve this problem, the decomposition is combined with the calculation process. Meanwhile, an adaptive noise covariance matching method is implied. Experiments show that the proposed method can guarantee the semi-positive and numerical stability of the state covariance, and the estimation accuracy can reach the third-order precision. The estimation error remains 1.60% under the drastic voltage and current change conditions, which can reduce the estimation error by 1.00% compared with the traditional method. It can provide a theoretical safety protection basis of the energy management for the lithium-ion battery pack

Ulinastatin attenuates oxidation, inflammation and neural apoptosis in the cerebral cortex of adult rats with ventricular fibrillation after cardiopulmonary resuscitation

OBJECTIVE: The role of Ulinastatin in neuronal injury after cardiopulmonary resuscitation has not been elucidated. We aim to evaluate the effects of Ulinastatin on inflammation, oxidation, and neuronal injury in the cerebral cortex after cardiopulmonary resuscitation. METHODS: Ventricular fibrillation was induced in 76 adult male Wistar rats for 6 min, after which cardiopulmonary resuscitation was initiated. After spontaneous circulation returned, the rats were split into two groups: the Ulinastatin 100,000 unit/kg group or the PBS-treated control group. Blood and cerebral cortex samples were obtained and compared at 2, 4, and 8 h after return of spontaneous circulation. The protein levels of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were assayed using an enzyme-linked immunosorbent assay, and mRNA levels were quantified via real-time polymerase chain reaction. Myeloperoxidase and Malondialdehyde were measured by spectrophotometry. The translocation of nuclear factor-κB p65 was assayed by Western blot. The viable and apoptotic neurons were detected by Nissl and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). RESULTS: Ulinastatin treatment decreased plasma levels of TNF-α and IL-6, expression of mRNA, and Myeloperoxidase and Malondialdehyde in the cerebral cortex. In addition, Ulinastatin attenuated the translocation of nuclear factor-κB p65 at 2, 4, and 8 hours after the return of spontaneous circulation. Ulinastatin increased the number of living neurons and decreased TUNEL-positive neuron numbers in the cortex at 72 h after the return of spontaneous circulation. CONCLUSIONS: Ulinastatin preserved neuronal survival and inhibited neuron apoptosis after the return of spontaneous circulation in Wistar rats via attenuation of the oxidative stress response and translocation of nuclear factor-κB p65 in the cortex. In addition, Ulinastatin decreased the production of TNF-α, IL-6, Myeloperoxidase, and Malondialdehyde