昆虫多样性三十年研究进展

当前, 全球昆虫数量和多样性均处于下降趋势, 而导致这一趋势的原因主要包括人为干扰及气候变化。本文基于森林、草地、农业、水生和土壤生态系统, 以植食性、访花、捕食性、寄生性、食果以及食腐昆虫为重点功能昆虫群, 综述了近三十年来国内外昆虫多样性研究领域的主要进展, 并分析了发展趋势。近年来, 昆虫多样性的研究维度不断拓展, 形态多样性研究不断深入, 系统发生多样性、功能多样性和遗传多样性等研究也显著加强。此外, 昆虫多样性研究的空间尺度也逐步扩大, 大尺度区域性研究甚至全球范围的调查持续增长。昆虫进化历史也被引入多样性格局研究中, 并随着系统发生信息学方法的普及而被整合到生态系统建成和生物多样性形成机制研究中。未来需要加强关键昆虫类群整合分类学研究、功能性状多样性、林冠昆虫多样性、互作网络结构等方向的研究。     

中国生物多样性核心监测指标遥感产品体系构建与思考

生物多样性的稳定维持关乎人类生存发展与地球健康。生物多样性核心监测指标(Essential Biodiversity Variables, EBVs)旨在结合地面调查与遥感技术, 为大尺度、长时间序列的生物多样性监测提供新的解决方案。然而, 目前学界仍然缺乏一套国家尺度标准化EBVs遥感监测产品数据集, 以进行生物多样性评估。本研究旨在对中国生物多样性核心监测指标遥感产品进行体系构建与思考, 首先综述了目前EBVs的遥感研究概况, 并根据EBVs研究文献的数量进行调研分析; 同时, 本文在已有遥感生物多样性产品优先标准的基础上, 添加了“可重复性”的新标准, 并据此构建了中国EBVs遥感产品体系与监测数据集的指标清单, 最终对中国EBVs遥感研究存在的问题进行思考与讨论。本研究可为中国的生物多样性遥感监测提供科学依据, 有望为中国生物多样性政策的制定提供支撑。     

天童山阔叶木本植物叶片大小与叶脉密度及单位叶脉长度细胞壁干质量的关系

叶片大小是植物生态策略中的一个关键性状, 而叶脉是叶内主要的支撑和输导结构, 对叶片的生长发育具有重要的影响。该研究以天童山38种阔叶木本植物为研究对象, 以叶片面积、干质量和周长表征叶片大小, 采用标准化主轴估计(SMA)方法和系统发育独立比较(PIC)分析主脉密度、细脉密度和总叶脉密度, 以及各级叶脉单位长度的细胞壁干质量与叶片大小之间的关系, 拟从叶片内部结构和资源分配策略的角度探明叶片大小与叶脉结构之间的变化关系及生态学意义。研究结果显示: (1)叶片大小与主脉密度极显著负相关, 细脉密度以及总叶脉密度与叶片大小关系不显著, 表明叶片越小, 主脉密度越高, 而细脉密度与叶片大小无关; (2)单位主脉长度的细胞壁干质量与叶片大小极显著正相关, 单位细脉和总叶脉长度的细胞壁干质量与叶片大小的相关性均不显著, 表明随着叶片的增大, 单位主脉长度的细胞壁干质量显著增加, 而细脉的细胞壁干质量与叶片大小无关; (3)主脉密度与单位主脉长度的细胞壁干质量之间是斜率显著大于-1的负异速生长关系, 表明主脉密度随单位主脉长度的细胞壁干质量增加而显著下降, 两者之间存在权衡关系, 而单位细脉长度的细胞壁干质量与细脉密度关系不显著。上述结果表明, 与大叶片相比, 小叶中通常具有较高的主脉密度, 这不仅是叶片发育过程中叶形变化调控的结果, 也是单位叶脉长度的细胞壁干质量调控的结果, 单位叶脉长度的细胞壁干质量是导致叶片大小与主、细脉密度之间不同变化关系的直接因素。该研究结果为我们理解全球范围内叶片大小变化的生物地理分布模式以及植物对环境的适应策略提供了参考。     

Retracted: Downregulated microRNA-224 aggravates vulnerable atherosclerotic plaques and vascular remodeling in acute coronary syndrome through activation of the TGF-β/Smad pathway

Recent studies have shown that circulating microRNAs (miRNA) play a critical role in diagnosing acute coronary syndrome (ACS). This study aims to investigate the effect of miR-224 on atherosclerotic plaques forming and vascular remodeling in ACS and its relationship with TGF-β/Smad pathway. Myocardial infarction (MI) rat model was established and lentivirus vector of miR-224 inhibitor was prepared for investigating the effect of downregulated miR-224 on the contents of nitric oxide (NO) and endothelin-1 (ET-1), blood lipid levels and inflammatory factor levels in serum as well as the TGF-β/Smad pathway. The rats suffering from MI had decreased survival rates and exhibited reduced levels of NO, high-density lipoprotein cholesterol, and lumen diameter, and Smad7 messenger RNA (mRNA) and protein expression; while had significantly increased ratio of heart weight or body weight, levels of ET-1, inflammatory factors, blood lipid indexes, vascular remodeling indexes, collagen volume fraction, vulnerable atherosclerotic plaque area, VCAM-1 and MMP-2 protein expression, TGF-β, Smad2, Smad3, and Smad4 mRNA and protein expression. After inhibiting the TGF-β/Smad pathway, the rats suffering from MI showed notably opposite trend. In conclusion, downregulation of miR-224 expression promotes the formation of vulnerable atherosclerotic plaques and vascular remodeling in ACS through activation of the TGF-β/Smad pathway. Therefore, this study provides a new therapeutic target for ACS.     

Promoter methylation as biomarkers for diagnosis of melanoma: A systematic review and meta-analysis

Melanoma is one of the most common skin cancer that is characterized by rapid growth, early metastasis, high malignant, and mortality. Accumulating evidence demonstrated that promoter methylation of tumor-suppressor genes is implicated in the pathogenesis of melanoma. In the current study, we performed a meta-analysis to identify promising methylation biomarkers in the diagnosis of melanoma. We carried out a systematic literature search using Pubmed, Embase, and ISI web knowledge database and found that gene promoter methylation of 50 genes was reported to be associated with the risk of melanoma. Meta-analysis revealed that hypermethylation of claudin 11 (CLDN11; odds ratio [OR], 16.82; 95% confidence interval [CI], 1.97–143.29; p = 0.010), O-6-methylguanine-DNA methyltransferase (MGMT; OR, 5.59; 95% CI, 2.51–12.47; p < 0.0001), cyclin-dependent kinase inhibitor 2A (p16; OR, 6.57; 95% CI, 2.19–19.75; p = 0.0008), retinoic acid receptor β (RAR-β2; OR, 24.31; 95% CI, 4.58–129.01; p = 0.0002), and Ras association domain family member (RASSF1A; OR, 9.35; 95% CI, 4.73–18.45; p < 0.00001) was significantly higher in melanoma patients compared with controls. CLDN11 (OR, 14.52; 95% CI, 1.84–114.55; p = 0.01), MGMT (OR, 8.08; 95% CI, 1.84–35.46; p = 0.006), p16 (OR, 9.44; 95% CI, 2.68–33.29; p = 0.0005), and RASSF1A (OR, 7.72; 95% CI, 1.05–56.50; p = 0.04) hypermethylation was significantly increased in primary melanoma compared with controls. Methylation frequency of CLDN11 (OR, 25.56; 95% CI, 2.32–281.66; p = 0.008), MGMT (OR, 4.64; 95% CI, 1.98–10.90; p = 0.0004), p16 (OR, 4.31; 95% CI, 1.33–13.96; p = 0.01), and RASSF1A (OR, 10.10; 95% CI, 2.87–35.54; p = 0.0003) was significantly higher in metastasis melanoma compared with controls. These findings indicated that CLDN11, MGMT, p16, RAR-β2, and RASSF1A hypermethylation is a risk factor and a potential biomarker for melanoma. CLDN11, MGMT, p16, and RASSF1A promoter methylation may take part in the development of melanoma and become useful biomarkers in the early diagnosis of the disease.     

LncRNA SLC8A1-AS1 protects against myocardial damage through activation of cGMP-PKG signaling pathway by inhibiting SLC8A1 in mice models of myocardial infarction

Extensive investigations into long noncoding RNAs (lncRNAs) in various diseases and cancers, including acute myocardial infarction (AMI) have been conducted. The current study aimed to investigate the role of lncRNA solute carrier family 8 member A1 antisense RNA 1 (SLC8A1-AS1) in myocardial damage by targeting solute carrier family 8 member A1 (SLC8A1) via cyclic guanosine 3′,5′-monophosphate-protein kinase G (cGMP-PKG) signaling pathway in AMI mouse models. Differentially expressed lncRNA in AMI were initially screened and target relationship between lncRNA SLC8A1-AS1 and SLC8A1 was then verified. Infarct size, levels of inflammatory factors, biochemical indicators, and the positive expression of the SLC8A1 protein in AMI were subsequently determined. The expression of SLC8A1-AS1, SLC8A1, PKG1, PKG2, atrial natriuretic peptide, and brain natriuretic peptide was detected to assess the effect of SLC8A1-AS1 on SLC8A1 and cGMP-PKG. The respective contents of superoxide dismutase, lactate dehydrogenase (LDH), and malondialdehyde (MDA) were detected accordingly. Microarray data GSE66360 provided evidence indicating that SLC8A1-AS1 was poorly expressed in AMI. SLC8A1 was verified to be a target gene of lncRNA SLC8A1-AS1. SLC8A1-AS1 upregulation decreased levels of left ventricular end-systolic diameter, −dp/ dt _max, interleukin 1β (IL-1β), IL-6, transforming growth factor α, nitric oxide, inducible nitric-oxide synthase, endothelial nitric-oxide synthase, infarct size, LDH activity and MDA content, and increased IL-10, left ventricular end-diastolic pressure and + dp/ dt _max. Furthermore, the overexpression of SLC8A1-AS1 was noted to elicit an inhibitory effect on the cGMP-PKG signaling pathway via SLC8A1. In conclusion, lncRNA SLC8A1-AS1, by downregulating SLC8A1 and activating the cGMP-PKG signaling pathway, was observed to alleviate myocardial damage, inhibit the release of proinflammatory factors and reduce infarct size, ultimately protecting against myocardial damage.     

Retracted: Impaired Th17 cell proliferation and decreased pro-inflammatory cytokine production in CXCR3/CXCR4 double-deficient mice of vulvovaginal candidiasis

Vulvovaginal candidiasis (VVC) is a common observed infection, affecting approximately 75% of women of reproductive age. Drug resistance represents a troublesome stumbling block associated with VVC therapy. Thus the aim of the present study was to provide information regarding the selection of potential drug targets for VVC. CXCR3-, CXCR4-, or CXCR/CXCR4 double-deficient mouse models of VVC were subsequently established, with changes to the load of Candida Albicans evaluated accordingly. The biological behaviors of the vaginal epithelial cells were characterized in response to the CXCR3-, CXCR4-, or CXCR3/CXCR4 double-knockout in vivo. Our initial observations revealed that in mice with VVC, CXCR3-, CXCR4-, or CXCR3 - CXCR4 double-knockout resulted in a decreased load of C. Albicans as well as reduced levels and proportion of Th17 cells. Proinflammatory cytokine production was found to be inhibited by CXCR3-, CXCR4-, or CXCR3/CXCR4 double-knockout whereby the mRNA and protein expressions CXCR3, CXCR4, IL-17, IL-6, and TNF-α exhibited decreased levels. CXCR3-, CXCR4-, or CXCR3/CXCR4 double-knockout appeared to function as positive proliferation factors, while playing a negative role in the processes of apoptosis and the cell cycle of vaginal epithelial cells. Taken together, the key findings of the study suggested that CXCR3/CXCR4 double-knockout could act to hinder the progression of VVC, highlighting its promise as a novel therapeutic target in the treatment of VVC. CXCR3 and CXCR4 genes may regulate Th17/IL-17 immune inflammatory pathways to participate in antifungal immunity.     

Identification and validation of key genes associated with non-small-cell lung cancer

Non-small-cell lung cancer (NSCLC) is one of the main causes of death induced by cancer globally. However, the molecular aberrations in NSCLC patients remain unclearly. In the present study, four messenger RNA microarray datasets (GSE18842, GSE40275, GSE43458, and GSE102287) were downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) between NSCLC tissues and adjacent lung tissues were obtained from GEO2R and the overlapping DEGs were identified. Moreover, functional and pathway enrichment were performed by Funrich, while the protein–protein interaction (PPI) network construction were obtained from STRING and hub genes were visualized and identified by Cytoscape software. Furthermore, validation, overall survival (OS) and tumor staging analysis of selected hub genes were performed by GEPIA. A total of 367 DEGs (95 upregulated and 272 downregulated) were obtained through gene integration analysis. The PPI network consisted of 94 nodes and 1036 edges in the upregulated DEGs and 272 nodes and 464 edges in the downregulated DEGs, respectively. The PPI network identified 46 upregulated and 27 downregulated hub genes among the DEGs, and six (such as CENPE, NCAPH, MYH11, LRRK2, HSD17B6, and A2M) of that have not been identified to be associated with NSCLC so far. Moreover, the expression differences of the mentioned hub genes were consistent with that in lung adenocarcinoma and lung squamous cell carcinoma in the TCGA database. Further analysis showed that all the six hub genes were associated with tumor staging except MYH11, while only the upregulated DEG CENPE was associated with the worse OS of patients with NSCLC. In conclusion, the current study showed that CENPE, NCAPH, MYH11, LRRK2, HSD17B6, and A2M might be the key genes contributed to tumorigenesis or tumor progression in NSCLC, further functional study is needed to explore the involved mechanisms.