Comparison of two noninvasive methods for measuring the pigment content in foliose macrolichens

Photosynthesis Research - Chlorophyll content in lichens is routinely used as an accurate indicator of lichen vigor, interspecific differences, and the effect of site-related environmental...     

胱氨酸/半胱氨酸调控活性氧代谢影响大肠杆菌耐药性

【背景】随着越来越多超级细菌出现和抗生素资源的渐渐枯竭,细菌耐药机制研究愈加重要。【目的】探讨大肠杆菌内源半胱氨酸推动Fenton反应,调控胞内的活性氧水平,从而影响细菌耐药性这一代谢途径。【方法】在贫硫的培养条件下,通过控制外源胱氨酸和抗生素浓度,研究了胱氨酸/半胱氨酸对大肠杆菌耐药性的影响。【结果】较低水平的半胱氨酸使大肠杆菌对抗生素的耐药性增强,RNA-Seq的结果证明了胱氨酸内流对Fur、CysB和SOS的调控作用。LC-MS对外流硫醇的分析显示,细胞会快速将过量内流的半胱氨酸泵出胞外。在抗生素一定浓度范围内,半胱氨酸外排泵AlaE表现出良好的细胞保护作用。【结论】大肠杆菌对不同作用机理抗生素硫酸庆大霉素、氨苄青霉素和诺氟沙星的耐药性均受内源半胱氨酸水平的影响。本文通过研究半胱氨酸调控活性氧代谢对大肠杆菌耐药性的影响,为探讨细菌耐药性机制提供新的理论依据。     

我国涉天鹅属鸟类死亡案件分析及防控对策研究

我国有分布的天鹅属所有种(Cygnusspp.)均为国家Ⅱ级重点保护野生动物,根据中华人民共和国刑法,非法猎捕、杀害珍贵濒危野生动物构成刑事犯罪。然而,天鹅死亡案件仍时有发生。本文分析2000至2016年有统计的我国天鹅死亡案件发现,每年11月至翌年1月是涉天鹅案件的高发时期;毒杀为致死主因;案件多发生于我国行政区划交界处。因此,应于迁徙越冬季节重点加强高案发地点的侦查监管;加强克百威(呋喃丹)为代表的高毒农药管控;建立迁徙季节多地区执法联动机制。     

Immune checkpoint blockade and its combination therapy with small-molecule inhibitors for cancer treatment

Initially understood for its physiological maintenance of self-tolerance, the immune checkpoint molecule has recently been recognized as a promising anti-cancer target. There has been considerable interest in the biology and the action mechanism of the immune checkpoint therapy, and their incorporation with other therapeutic regimens. Recently the small-molecule inhibitor (SMI) has been identified as an attractive combination partner for immune checkpoint inhibitors (ICIs) and is becoming a novel direction for the field of combination drug design. In this review, we provide a systematic discussion of the biology and function of major immune checkpoint molecules, and their interactions with corresponding targeting agents. With both preclinical studies and clinical trials, we especially highlight the ICI + SMI combination, with its recent advances as well as its application challenges.     

Potential roles and targeted therapy of the CXCLs/CXCR2 axis in cancer and inflammatory diseases

The chemokine receptor CXCR2 and its ligands are implicated in the progression of tumours and various inflammatory diseases. Activation of the CXCLs/CXCR2 axis activates multiple signalling pathways, including the PI3K, p38/ERK, and JAK pathways, and regulates cell survival and migration. The CXCLs/CXCR2 axis plays a vital role in the tumour microenvironment and in recruiting neutrophils to inflammatory sites. Extensive infiltration of neutrophils during chronic inflammation is one of the most important pathogenic factors in various inflammatory diseases. Chronic inflammation is considered to be closely correlated with initiation of cancer. In addition, immunosuppressive effects of myeloid-derived suppressor cells (MDSCs) against T cells attenuate the anti-tumour effects of T cells and promote tumour invasion and metastasis. Over the last several decades, many therapeutic strategies targeting CXCR2 have shown promising results and entered clinical trials. In this review, we focus on the features and functions of the CXCLs/CXCR2 axis and highlight its role in cancer and inflammatory diseases. We also discuss its potential use in targeted therapies.     

Blocking P2X7 receptor ameliorates oxidized LDL-mediated podocyte apoptosis

Molecular Biology Reports - The purpose of our research is to elucidate whether oxLDL activates P2X7R in cultured human podocytes and if the activation of P2X7R leads to podocyte apoptosis....     

Identification of amino acid residues critical for the B cell growth-promoting activity of HIV-1 matrix protein p17 variants

Background

HIV-1 matrix protein p17 variants (vp17s) detected in HIV-1-infected patients with non-Hodgkin's lymphoma (HIV-NHL) display, differently from the wild-type protein (refp17), B cell growth-promoting activity. Biophysical analysis revealed that vp17s are destabilized as compared to refp17, motivating us to explore structure-function relationships.

Comparative genomic analysis of Pseudomonas amygdali pv. lachrymans NM002: Insights into its potential virulence genes and putative invasion determinants

Pseudomonas amygdali pv. lachrymans is currently of important plant pathogenic bacteria that causes cucumber angular leaf spot worldwide. The pathogen has been studied for its roles in pathogenicity and plant inheritance resistance. To further delineate traits critical to virulence, invasion and survival in the phyllosphere, we reported the first complete genome of P. amygdali pv. lachrymans NM002. Analysis of the whole genome in comparison with three closely-related representative pathovars of P. syringae identified the conservation of virulence genes, including flagella and chemotaxis, quorum-sensing systems, two-component systems, and lipopolysaccharide and antiphagocytosis. It also revealed differences of invasion determinants, such as type III effectors, phytotoxin (coronatine, syringomycin and phaseolotoxin) and cell wall-degrading enzyme, which may contribute to infectivity. The aim of this study was to derive genomic information that would reveal the probable molecular mechanisms underlying the virulence, infectivity and provide a better understanding of the pathogenesis of the P. syringae pathovars.     

LncRNA FOXC2-AS1 protects cardiomyocytes from doxorubicin-induced cardiotoxicity through activation of WNT1-inducible signaling pathway protein-1

Doxorubicin (Dox) is an anthracycline antibiotic that has been used to treat different cancers. Dox-induced cardiotoxicity is common in clinical practice, while its mechanism is unknown. It has been proved that lncRNA FOXC2-AS1 may promote doxorubicin resistance and WNT1-inducible signaling pathway protein-1 (WISP1) blocks doxorubicin-induced cardiomyocyte death. Our study aimed to investigate the involvement of lncRNA FOXC2-AS1 and WISP1 in doxorubicin-induced cardiotoxicity and to explore their interactions. In our study we observed that FOXC2-AS1 and WISP1 mRNA were downregulated in heart tissues of mice with Dox-induced cardiotoxicity. FOXC2-AS1 and WISP1 mRNA expression were positively correlated in mice with Dox-induced cardiotoxicity but not in healthy mice. Overexpression of FOXC2-AS1 promoted to viability of mice cardiomyocytes under Dox treatment and also increased the expression level of WISP1. In contrast, WISP1 overexpression showed no significant effect on FOXC2-AS1. We therefore conclude that lncRNA FOXC2-AS1 may upregulate WISP1 to protect cardiomyocytes from doxorubicin-induced cardiotoxicity.