典型气候条件下东北地区生态系统水源涵养功能特征

东北地区是我国重要的生态功能区,其包含的典型生态系统具有独特的水源涵养功能,在防洪减灾,保障生态安全和人居安全中发挥着关键作用。以往有关水源涵养功能的研究主要是依托不同水文模型方法,从单一年份或多个年份的角度进行研究,较少考虑不同气候条件下水源涵养功能的空间分异特征。采用标准化降水蒸散发指数(Standardized Precipitation Evapotranspiration Index,SPEI)划分研究区的典型气候年份(干旱、正常和湿润);基于水量平衡法,结合SCS-CN模型以及Penman-Monteith方程对东北地区典型气候条件下生长季内的水源涵养功能进行研究。结果表明:(1)研究区水源涵养功能在不同气候条件下差异明显,三个典型气候年份生长季内的水源涵养总量分别为:干旱年(SPEI=-1.26)为2214.64亿m~3、正常年(SPEI=-0.22)为3231.49亿m~3和湿润年(SPEI=1.05)为3969.33亿m~3。(2)水源涵养功能空间变异突出,但在三种典型气候条件下呈现出一致变化,均表现为长白山地区水源涵养量最大,大小兴安岭地区次之,水源涵养量最低的地方主要出现在呼伦贝尔以西的草原地区,在东北平原的部分地区也有低值的出现,如白城、通辽、鸡西等地区,水源涵养量较一般的地方出现在东北平原大部分以农田为主的地区。(3)水源涵养功能除受气候因素的影响外,还取决于土地利用类型的变化,对于整个东北地区来讲,水源涵养总量表现为林地农田草地湿地,单位面积水源涵养量在干旱年和正常年表现为林地农田湿地草地,在湿润年份表现为林地湿地农田草地。研究结果揭示了东北地区三种典型气候条件下重要生态系统的水源涵养功能大小、空间分布特征及其主要驱动因素,可为区域生态空间规划和生态系统管理提供科学指导。     

基于土地利用及植被覆盖变化的黄河源区生境质量时空变化特征

位于青藏高原腹地的黄河源地区生态环境脆弱,面临生物多样性锐减、生态系统退化等问题,黄河源区生态系统保护及其高质量发展已成为国家的重点战略之一。土地利用与植被覆盖是影响生境质量的重要因素,定量化土地利用方式、强度及格局和植被覆盖格局对生态质量影响的研究越来越受到关注,但其对黄河源区生态质量的耦合效应尚不明确。基于2000年和2015年黄河源区土地利用类型及生长季归一化植被指数（NDVI）,采用InVEST模型探究了不同时期黄河源区生境质量时空变化,并采用地理加权回归（GWR）模型揭示了生境质量对土地利用和植被覆盖变化的空间响应特征。结果表明,2000年与2015年土地利用类型变化主要为未利用土地向草地的转移。植被覆盖变化方面,源区生长季NDVI整体上升。从生境质量的空间分布来看,黄河源区生境质量总体呈现南高北低的空间格局,高值分布在南部及中部地区,低值分布在北部布青山、东北部高海拔区及黄河乡的黄河沿岸。相较于2000年,2015年黄河源区生境质量平均提高11.47%。草地面积和NDVI与生境质量均呈显著正相关关系,其中NDVI是提高黄河源区生境质量的重要驱动因子。研究结果突出了NDVI对提高黄河源区生境质量的主导作用,可为未来源区生态保护提供借鉴。     

TBK1 Facilitates GLUT1-Dependent Glucose Consumption by suppressing mTORC1 Signaling in Colorectal Cancer Progression

Intestinal inflammation is a vital precipitating factor of colorectal cancer (CRC), but the underlying mechanisms are still elusive. TANK-binding kinase 1 (TBK1) is a core enzyme downstream of several inflammatory signals. Recent studies brought the impacts of TBK1 in malignant disease to the forefront, we found aberrant TBK1 expression in CRC is correlated with CRC progression. TBK1 inhibition impaired CRC cell proliferation, migration, drug resistance and tumor growth. Bioinformatic analysis and experiments in vitro showed overexpressed TBK1 inhibited mTORC1 signaling activation in CRC along with elevated GLUT1 expression without inducing GLUT1 translation. TBK1 mediated mTORC1 inhibition induces intracellular autophagy, which in turn decreasing GLUT1 degradation. As a rescue, blocking of autophagosome and retromer respectively via autophagy-related gene 7 (ATG7) or TBC1 Domain Family Member 5 (TBC1D5) silence diminished the regulation of TBK1 to GLUT1. GLUT1 staining presented that TBK1 facilitated GLUT1 membrane translocation which subsequently enhanced glucose consumption. Inhibitor of TBK1 also decreased GLUT1 expression which potentiated drug-sensitivity of CRC cell. Collectively, TBK1 facilitates glucose consumption for supporting CRC progression via initiating mTORC1 inhibition induced autophagy which decreases GLUT1 degradation and increases GLUT1 membrane location. The adaptive signaling cascade between TBK1 and GLUT1 proposes a new strategy for CRC therapy.     

Intravital lipid droplet labeling and imaging reveals the phenotypes and functions of individual macrophages in vivo

Macrophages play pivotal roles in the maintenance of tissue homeostasis. However, the reactivation of macrophages toward proinflammatory states correlates with a plethora of inflammatory diseases, including atherosclerosis, obesity, neurodegeneration, and bone marrow (BM) failure syndromes. The lack of methods to reveal macrophage phenotype and function in vivo impedes the translational research of these diseases. Here, we found that proinflammatory macrophages accumulate intracellular lipid droplets (LDs) relative to resting or noninflammatory macrophages both in vitro and in vivo, indicating that LD accumulation serves as a structural biomarker for macrophage phenotyping. To realize the staining and imaging of macrophage LDs in vivo, we developed a fluorescent fatty acid analog-loaded poly(lactic-co-glycolic acid) nanoparticle to label macrophages in mice with high efficiency and specificity. Using these novel nanoparticles, we achieved in situ functional identification of single macrophages in BM, liver, lung, and adipose tissues under conditions of acute or chronic inflammation. Moreover, with this intravital imaging platform, we further realized in vivo phenotyping of individual macrophages in the calvarial BM of mice under systemic inflammation. In conclusion, we established an efficient in vivo LD labeling and imaging system for single macrophage phenotyping, which will aid in the development of diagnostics and therapeutic monitoring. Moreover, this method also provides new avenues for the study of lipid trafficking and dynamics in vivo.Supplementary key words: macrophage, inflammation, lipid droplet, nanoparticle delivery, in vivo imaging, fatty acid analog, bone marrow, systemic inflammation, lipid trafficking, biomarker

Macrophages, a type of immune cells, almost reside in all tissues of body, from the skin to the bone marrow (BM) (1). Macrophages have remarkable plasticity, and they can be activated into specific subtypes by modifying their physiology and functions in response to local environmental cues. Activated macrophages are commonly divided into proinflammatory killing subtype and anti-inflammatory repairing subtype. Proinflammatory macrophages responding to bacteria, IFN-γ, and lipopolysaccharide (LPS) are involved in host defense and inflammation, whereas anti-inflammatory macrophages responding to interleukin-4 (IL-4), IL-10, and IL-13 play a pivotal role in tissue homeostasis and remodeling (2). Increasing evidence indicates that the reactivation of macrophages toward proinflammatory states under diverse kinds of stress is correlated with a plethora of inflammatory diseases, such as atherosclerosis, diabetes, obesity, rheumatoid arthritis, neurodegeneration, and BM failure syndromes (3, 4). Thus, characterization of macrophage activation status and the underlying molecular mechanism in situ will help elucidate their functions in these diseases; however, in vivo analysis of the macrophage activation status in their native multicellular microenvironment is challenging.Although lipid droplets (LDs) have been initially described as intracellular fat storage organelles in adipocytes, increasing studies indicate that myeloid cells also form LDs under inflammation and stress (5, 6). Macrophages, as the effector cells of innate immunity, are found to form LDs to support their host defense when exposed to pathogens, such as parasites, bacteria, and viruses (7, 8, 9, 10, 11). However, abnormal LD accumulation in tissue-resident macrophages correlates with the pathogenesis of various inflammatory diseases. For instance, foam cells in atherosclerotic lesions can maintain the local inflammatory response by secreting proinflammatory cytokines (12, 13, 14). Moreover, LD-accumulating microglia contribute to neurodegeneration by producing high levels of reactive oxygen species (ROS) and secreting proinflammatory cytokines (15). These findings indicate that LD accumulation might be a hallmark of macrophages with proinflammatory functions.In this study, based on the typical activation of in vitro BM-derived macrophages, we find that proinflammatory M_{(LPS + IFN-γ)} macrophages are characterized by LD accumulation, whereas resting macrophages and anti-inflammatory M_(IL-4) and M_(IL-10) macrophages do not contain any LDs. These features also hold for Matrigel plug-recruited macrophages and tissue-resident macrophages in mice. These findings demonstrate that LD accumulation could serve as a morphological index to distinguish proinflammatory macrophages from others.It is feasible to distinguish LD-containing cells using imaging techniques, which has translational potential for identification of proinflammatory macrophages in vivo. However, current techniques for LD visualization are traditional in vitro staining method, and in vivo staining and imaging of LD in individual macrophages remains a challenge. Through nanocarrier screening, we selected the poly(lactic-co-glycolic acid) (PLGA) nanoparticles (NPs) as nanocarrier to deliver the lipophilic carbocyanine dye (DiI_C18(5) solid (1,1''-dioctadecyl-3,3,3'',3''-tetramethylindodicarbocyanine, 4-chlorobenzenesulfonate salt) [DiD]) and lipid staining dye (C1-BODIPY 500/510-C12) into macrophages. Using these dual fluorescence-labeled PLGA NPs, we achieved in situ and in vivo functional identification of single macrophages in various tissues under systemic or local inflammatory stress. Collectively, this study establishes an efficient in vivo labeling and imaging system of intracellular LDs for phenotyping the activation status and functions of individual macrophages in their dynamic niche, which is pivotal for disease diagnosis and preclinical research.     

烷烃溶剂对耐有机溶剂极端微生物地衣芽孢杆菌YP1产胞外蛋白酶的影响

考察了添加5%(V/V)浓度的正庚烷、正辛烷、正癸烷、十二烷、十四烷、十六烷等烷烃溶剂对耐有机溶剂极端微生物地衣芽孢杆菌(Bacillus licheniformis)YP1的生长及产胞外蛋白酶的影响.结果表明5%(V/V)浓度的各种烷烃溶剂对YP1蛋白酶的稳定性及菌体生物量均无显著影响,正庚烷、正辛烷、正癸烷等溶剂显著抑制YP1产蛋白酶,而十二烷、十四烷,十六烷能提高YP1产蛋白酶1倍以上.发酵液中十四烷的浓度(1%-8%,VIV)与蛋白酶的活力呈正相关性,添加十四烷后发酵过程中蛋白酶活力的显著增加出现在菌体生长的对数后期.培养过程中添加十四烷能导致YP1菌体形态显著变小.首次报道了烷烃溶剂对极端微生物产蛋白酶的影响.     

太湖流域丘陵区两种土地利用类型土壤水分分布控制因素

为探究太湖流域丘陵区典型土地利用类型(如竹林地和茶园)土壤水分的控制因素,在不同深度土壤水分定期观测的基础上,根据前7d降雨量将研究时段划分为干旱状态和湿润状态,利用分类与回归树(CART)方法得出不同干湿状态下土壤水分分布的主控因子,并借助典范对应分析(CCA)定量分析不同土地利用类型、不同土壤深度土壤水分格局与环境因子关系。结果表明:(1)高程、土地利用类型和土层厚度对土壤水分分布的相对贡献率最大,但在不同干湿状态下其影响程度存在差异;(2)干旱状态时土壤水分主要受高程、坡度、地形湿度指数(TWI)和剖面曲率等地形因素的作用,而土层厚度和粘粒也分别为0—20 cm和20—40 cm深度土壤水分的主控因子;(3)在湿润状态下,茶园0—20 cm土壤水分的主控因素为地形因子,在20—40 cm则以土壤性质为主,竹林地两个深度的土壤水分受地形和土壤性质的作用都很强,其中20—40 cm深度土壤水分与环境因子的关系较0—20 cm深度更为复杂。