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A Lie derivation is called standard if it is a sum of a derivation and a linear map with image in the center vanishing on commutators. In this paper we show that Lie derivations of a reflexive algebra AlgL on a Banach space are standard if L is a nest, or has the non-trivial smallest element, or has the non-trivial greatest element. (2000). Primary 47L35; Secondary 17B40, 17B60. Mathematics Subject Classification

Endotoxins and other harmful substances may cause an increase in permeability in endothelial cells (ECs) monolayers, as well as ECs shrinkage and death to induce lung damage. Lipopolysaccharide (LPS) can impair endothelial progenitor cells (EPCs) functions, including proliferation, migration, and tube formation. EPCs can migrate to the damaged area, differentiate into ECs, and participate in vascular repair, which improves pulmonary capillary endothelial dysfunction and maintains the integrity of the endothelial barrier. Hydrogen (H2) contributes to the repairment of lung injury and the damage of ECs. We therefore speculate that H2 protects the EPCs against LPS-induced damage, and it’s mechanism will be explored. The bone marrow-derived EPCs from ICR Mice were treated with LPS to establish a damaged model. Then EPCs were incubated with H2, and treated with PI3K inhibitor LY294002 and endothelial nitric oxide synthase (eNOS) inhibitor L-NAME. MTT assay, transwell assay and tube formation assay were used to detect the proliferation, migration and angiogenesis of EPCs. The expression levels of target proteins were detected by Western blot. Results found that H2 repaired EPCs proliferation, migration and tube formation functions damaged by LPS. LY294002 and L-NAME significantly inhibited the repaired effect of H2 on LPS-induced dysfunctions of EPCs. H2 also restored levels of phosphor-AKT (p-AKT), eNOS and phosphor-eNOS (p-eNOS) suppressed by LPS. LY294002 significantly inhibited the increase of p-AKT and eNOS and p-eNOS expression exposed by H2. L-NAME significantly inhibited the increase of eNOS and p-eNOS expression induced by H2. H2 repairs the dysfunctions of EPCs induced by LPS, which is mediated by PI3K/AKT/eNOS signaling pathway.

Sapylin (OK‐432) revealed biological properties in cancers. In this study, the effect of sapylin on lung cancer cell A549 was investigated. A549 cell lines were treated with sapylin (0.1, 0.5, and 1 KE/mL) for different time intervals. A549 cell proliferation and apoptosis was determined using 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐2H‐tetrazolium bromide/Ki67 assay and flow cytometry, respectively. Western blot was used to determine the expressions of proteins involved in proliferation, apoptosis, and phosphoinositide 3‐kinase/serine/threonine kinase (PI3K/AKT), Wnt3a/β‐catenin signaling pathway. Level of intracellular reactive oxygen species (ROS) was insured by using the ROS kit. Sapylin inhibited A549 cell viability and the expressions of proliferation‐related proteins (cyclin E1 and D1) in dose‐ and time‐dependent manners. Sapylin promoted apoptosis in a dose‐ and time‐dependent manners. Sapylin also promoted the expressions of apoptotic proteins (cleaved caspase‐3 and 8) in dose‐ and time‐dependent manners. Furthermore, sapylin increased the intracellular concentration of ROS in a dose‐dependent manner. Besides, the high expression of ROS level might induce inhibition of cell viability and increase cell apoptosis. The mechanistic study revealed that sapylin inactivated the PI3K/AKT and Wnt3a/β‐catenin signaling pathways. Our findings suggest that sapylin inhibits proliferation and promotes apoptosis in lung cancer cells, thus providing a new theoretical basis for the treatment of lung cancer.

The present study aimed to discuss and compare the effects and expenses of different antibiotic regimens in the treatment of lower respiratory tract infection (LRTI). A retrospective analysis was performed on 200 patients diagnosed with LRTI and treated at the Department of Respiratory Medicine of Dongying People's Hospital from February 2015 to May 2017. The patients were randomly divided into Group A, Group B, Group C and Group D, with 50 cases in each group, and were treated with ceftriaxone sodium, ceftizoxime sodium, levofloxacin and azithromycin, respectively. Venous blood of patients was collected. White blood cells (WBC) of venous blood were detected using a hematology analyzer and C-reactive protein (CRP) was tested with latex immunoturbidimetry. Moreover, therapeutic effects and drug costs of four different antibiotics were compared. No adverse reactions occurred to patients in the four groups during the treatment process. The value at each time point after treatment was significantly decreased compared with that at the previous time point before treatment within the group (P<0.01). The treatment expenses of patients in Group A, Group B and Group D were significantly increased compared with those in Group C (P<0.01), the treatment expenses of patients in Group B and Group D were significantly increased compared with those in Group A (P<0.01) and the treatment expenses of patients in Group D were significantly increased compared with those in Group B (P<0.01). Ceftriaxone sodium, ceftizoxime sodium, levofloxacin and azithromycin all have a good antimicrobial efficacy. The treatment condition of LRTI can be dynamically monitored by WBC and CRP which can accurately reflect the progression condition of patients' illness and the treatment effect. In economic terms, the treatment cost of levofloxacin is the lowest; thus, it is worthy of clinical popularization and application.

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Let X be a Banach space of dimension greater than 1. We prove that if a map δ :for any A, B ∈ B( X), then δ = D + τ , where D is an additive derivation of B( X) and the map τ : B( X) → FI vanishes at commutators [A, B].