catena-Poly[[tetra­aqua­zinc(II)]-μ-2,2′-dihydr­oxy-5,5′-diazenediyldibenzoato]

In the title compound, [Zn(C14H8N2O6)(H2O)4]n, the 2,2′-dihydr­oxy-5,5′-diazenediyldibenzoate ligand acts as a carboxyl­ate bridge, leading to the formation of a polymeric chain running along the [10] direction. The ZnII atom is hexa-coordinated in a distorted octa­hedral geometry by six O atoms [Zn—O = 2.055 (4)–2.132 (3) Å] from two carboxylate ligands and four water mol­ecules. The crystal packing is stabilized by inter­molecular O—H⋯O, O—H⋯N and C—H⋯O hydrogen bonds, and two π–π inter­actions. The centroid–centroid distances are 3.803 (16) and 3.804 (17) Å

Plasma level of M-CSF was independently related to 30-day survival in patients with suspected sepsis, and correlated to pathogen load: A prospective cohort study.

The purpose of our study was to screen the plasma cytokines to find possible indicators of disease progression and prognosis of patients with infection. With a prospective cohort study, selected patients were divided into sepsis group and non-sepsis group. Demographic and clinical information were collected. Blood samples were tested for the levels of plasma cytokines and metagenomic next-generation sequencing (mNGS). 30-day follow-up information was recorded, and data was analyzed by SPSS22.0 (SPSS Inc, Chicago, IL). A total of 95 patients were selected. After propensity score matching of age and gender, 36 patients with sepsis and 36 with non-sepsis were enrolled. 30-day follow-up data exhibited that 41 patients died and 31 survived. Patients with sepsis and 30-day death had higher plasma levels of cytokines, including macrophage-stimulating factor (M-CSF), monocyte chemoattractant protein-3 (MCP-3), etc., than patients with non-sepsis and 30-day survival, respectively. M-CSF > 8.21pg/ml was an independent risk factor for 30-day death, and the reads of pathogens in mNGS reports was positively correlated with the plasma concentrations of various cytokines, including M-CSF

6′,7′-Dimeth­oxy-1′,2′-dihydro­spiro­[cyclo­hexane-1,2′-quinazolin]-4′(3′H)-one

In the title compound, C15H20N2O3, prepared from the reaction of 2-amino-4,5-dimeth­oxy­benzonitrile and cyclo­hexa­none, the six-membered diaza ring assumes an envelope conformation. In the crystal, inversion dimers are formed by pairs of N—H⋯O hydrogen bonds. Futher N—H⋯O hydrogen bonds link the dimers into a two-dimensional structure parallel to (001)

Effect of ligustrazine injection on the change of oxidative stress system during renal ischemia reperfusion injury in rabbits

目的  通过由兔肾脏缺血/再灌注损伤（IRI）导致的氧化应激体系中的变化，研究中药川芎嗪对IRI干预下的作用机制。方法  建立持续性阻断兔双侧肾动脉血流1h，再灌注5h的肾IRI动物模型。日本大耳兔32只，随机分成3组（n=10）：假手术组(sham，S组)，缺血/再灌注组(ischemia-reperfusion，IR组)，川芎嗪干预缺血/再灌注组（ligustrazine+ ischemia-reperfusion，LZ组），另外两只作为补充实验中意外死亡之用。于缺血前、缺血1h、再灌注1h、3h和5h依次经颈总动脉抽血用以检测超氧化物歧化酶（SOD）活力、黄嘌呤氧化酶（XO）活力以及丙二醛（MDA）含量。在实验结束后取兔肾组织依次检测SOD、XO活力以及MDA含量，并对其进行电镜观察。结果  随着肾缺血和再灌注时间的增加，IR组和LZ组血浆中的XO活力和MDA含量逐渐呈上升趋势，但同时间点LZ组较于IR组明显降低（均P<0.01）；SOD活力随着肾缺血和再灌注时间的增加而逐渐呈下降趋势，但同时间点下，LZ组较于IR组均明显偏高（均P<0.01）。IR组和LZ组相较于S组，肾组织XO活力、MDA含量均明显升高，SOD活力均明显降低（均P<0.01）；而LZ组肾组织中的XO活力、MDA含量均显著低于IR组，SOD活力均显著高于IR组，差异有非常显著性（均P<0.01），LZ组肾组织细胞的超微结构异常改变较IR组显著减轻。结论  川芎嗪能够使氧自由基水平降低，氧化应激损伤减轻，具有保护肾缺血/再灌注损伤的作用。Objective: To investigate the change of oxidative stress system during renal ischemia-reperfusion injury, and to study the mechanism of Ligustrazine on IRI under the intervention. Methods: Establish the IRI animal model by persistent blocking rabbits’ bilateral renal artery blood flow for 1 hour, then reperfusion for another 5 hours. Japanese big ear rabbits, 32, were randomly divided into three groups (n=10): sham operation group (group S), ischemia/reperfusion group (group IR), the effect of ligustrazine on ischemia/ reperfusion group (LZ group), the other two being added in the experiment for accidental death. In 1 hour before ischemia, ischemia, reperfusion 1h, 3h and 5h in turn to check the enzyme activity of superoxide dismutase (SOD), xanthine oxidase (XO) and the content of malondialdehyde (MDA) by getting the blood from common carotid artery. At the end of the experiment, the rabbit’s kidney was used to check the enzyme activity of XO, SOD and the content of MDA, then to observe the morphological changes under the electron microscopy. Results: With the increase of renal ischemia and reperfusion time, XO activity and MDA content of IR group and LZ group in plasma gradually up, they were significantly lower in LZ group than in IR group at same time point (all P<0.01), the activity of SOD in plasma was shown a time-dependent decline in both IR group and LZ group, whereas it was significant higher in LZ group compared with IR group at same time point during ischemia reperfusion (all P<0.01). SOD activity gradually decreased with the increase of renal ischemia and reperfusion time, but at the same time point, LZ group compared with IR group were significantly higher (P<0.01), however, for LZ group, as compared with IR group, activity of XO, content of MDA were increased remarkably while activity of SOD was decreased significantly in kidney tissue (all P<0.01) the abnormal changes of ultrastructure were mitigated significantly. Conclusion: Ligustrazine may attenuate renal ischemia-reperfusion injury by dropping oxygen free radical generation and enhancing oxygen free radical scavenge so that it can antagonize oxidative stress

Enhancement of polar phases in PVDF by forming PVDF/SiC nanowire composite

Different contents of silicon carbide (SiC) nanowires were mixed with Poly(vinylidene fluoride) (PVDF) to facilitate the polar phase crystallization. It was shown that the annealing temperature and SiC content affected on the phase and crystalline structures of PVDF/SiC samples. Furthermore, the addition of SiC nanowire enhanced the transformation of non-polar α phase to polar phases and increased the relative fraction of β phase in PVDF. Due to the nucleating agent mechanism of SiC nanowires, the ion-dipole interaction between the negatively charged surface of SiC nanowires and the positive CH2 groups in PVDF facilitated the formation of polar phases in PVDF

Adaptation Mechanism and Tolerance of \u3cem\u3eRhodopseudomonas palustris\u3c/em\u3e PSB-S Under Pyrazosulfuron-Ethyl Stress

Background: Pyrazosulfuron-ethyl is a long lasting herbicide in the agro-ecosystem and its residue is toxic to crops and other non-target organisms. A better understanding of molecular basis in pyrazosulfuron-ethyl tolerant organisms will shed light on the adaptive mechanisms to this herbicide. Results: Pyrazosulfuron-ethyl inhibited biomass production in Rhodopseudomonas palustris PSB-S, altered cell morphology, suppressed flagella formation, and reduced pigment biosynthesis through significant suppression of carotenoids biosynthesis. A total of 1127 protein spots were detected in the two-dimensional gel electrophoresis. Among them, 72 spots representing 56 different proteins were found to be differently expressed using MALDI-TOF/TOF-MS, including 26 up- and 30 down-regulated proteins in the pyrazosulfuron-ethyl-treated PSB-S cells. The up-regulated proteins were involved predominantly in oxidative stress or energy generation pathways, while most of the down-regulated proteins were involved in the biomass biosynthesis pathway. The protein expression profiles suggested that the elongation factor G, cell division protein FtsZ, and proteins associated with the ABC transporters were crucial for R. palustris PSB-S tolerance against pyrazosulfuron-ethyl. Conclusion: Up-regulated proteins, including elongation factor G, cell division FtsZ, ATP synthase, and superoxide dismutase, and down-regulated proteins, including ALS III and ABC transporters, as well as some unknown proteins might play roles in R. palustris PSB-S adaptation to pyrazosulfuron-ethyl induced stresses. Functional validations of these candidate proteins should help to develope transgenic crops resistant to pyrazosulfuron-ethyl