中国野生牡丹研究（一）芍药属牡丹组新分类群

牡丹为我国特产珍贵花树和药用树种,已有1500余年栽培历史,建国以来,各地栽培品种已达500余个。 有关牡丹分类的主要研究成果多为西方科学家根据18—19世纪从我国引种到英、美、法等国的栽培牡丹和腊叶标本加以描述和定名。 作者近几年来在安徽、河南、湖南、山西、陕西、甘肃、四川、云南等地对我国野生牡丹进行了较广泛的调查和研究。 本文发表3个新种和1个新等级,这对研究我国栽培牡丹的起源和栽培品种的自然分类,发掘、保护、利用我国珍稀野生牡丹基因资源,培育新品种,扩大牡丹栽培地区等方面提供了科学理论依据。     

Yersiniae in pond water and snails

A Yersinia enterocolitica serotype 9 was isolated from pond water; Y. enterocolitica-like bacteria were also isolated from pond water and from three species of snails (Lymnaea palustris elodes, Helisoma sp., Oxyloma retusa) from the Edwin S. George Reserve in southeastern Michigan. There was evidence for biochemical stability among some of the organisms over a period of years. There also was evidence of transmission of these organisms to snails from the water.     

CD36 aggravates podocyte injury by activating NLRP3 inflammasome and inhibiting autophagy in lupus nephritis

A major cause of proteinuria in lupus nephritis (LN) is podocyte injury, and determining potential therapeutic targets to prevent podocyte injury is important from a clinical perspective in the treatment of LN. CD36 is involved in podocyte injury in several glomerulopathies and was reported to be a vital candidate gene in LN. Here, we determined the role of CD36 in the podocyte injury of LN and the underlying mechanisms. We observed that CD36 and NLRP3 (NLR family pyrin domain containing 3) were upregulated in the podocytes of lupus nephritis patients and MRL/lpr mice with renal impairment. In vitro, CD36, NLRP3 inflammasome, and autophagy were elevated accompanied with increased podocyte injury stimulated by IgG extracted from lupus nephritis patients compared that from healthy donors. Knocking out CD36 with the CRISPR/cas9 system decreased the NLRP3 inflammasome levels, increased the autophagy levels and alleviated podocyte injury. By enhancing autophagy, NLRP3 inflammasome was decreased and podocyte injury was alleviated. These results demonstrated that, in lupus nephritis, CD36 promoted podocyte injury by activating NLRP3 inflammasome and inhibiting autophagy by enhancing which could decrease NLRP3 inflammasome and alleviate podocyte injury.Subject terms: Mechanisms of disease, Inflammasome, Lupus nephritis, Autophagy     

耦合生态系统服务供需的生态安全格局构建——以苏南地区为例

生态系统服务供需平衡是保障生态安全的基础,将生态系统服务供需作用流动机制融入生态安全格局构建对保障区域生态安全和提升人类生态福祉具有重要意义。基于景观生态学原理,提出耦合生态系统服务供需的生态安全格局构建逻辑方法,以苏南地区为研究区构建了景观生态安全格局和社会生态安全格局。研究结果表明:(1)耦合生态系统服务供需的生态安全格局应以维系区域生态安全和保障区域人类生态福祉为构建目标。其中,生态安全以生态系统服务与生态风险为核心关注对象,人类生态福祉的实现依赖于人类主动获取与生态系统服务流;(2)苏南地区生态系统服务供需间存在错配格局,在此基础上分别识别生态源地与需求源地4247.46km²、1882.16km²,生态廊道与供需廊道1614.02km、1915.82km,生态夹点29处、生态障碍点23处、生态供需节点20处;(3)形成"三区四带两组团"的社会-景观生态安全格局优化布局方案,并在此基础上提出针对性保护修复策略,推动经济-生态空间协同发展。研究可为丰富区域生态安全格局构建理论和方法、推动国土空间优化与管控提供参考借鉴。     

典型海湾与海岛近海脉红螺碳、氮稳定同位素特征差异

为深入了解不同大小脉红螺(Rapana venosa)的碳、氮稳定同位素特征,探究其在典型海湾和海岛水域生态系统所处营养位置,于2022年春季和夏季在胶州湾和长岛近海通过拖网和潜水采集160个脉红螺样本,详细分析了不同体长、体重脉红螺的δ¹³C和δ¹⁵N变化,并计算各研究区域的脉红螺核心生态位宽度及相关参数。结果显示,脉红螺δ¹³C值范围在-22.12‰--16.63‰,四组数据均值为-19.74‰--17.42‰,δ¹⁵N值范围在8.77‰-13.48‰,均值为9.64‰-12.81‰,各组数据营养级均值在2.63-3.57;胶州湾春季脉红螺δ¹³C值与体长、体重呈显著负相关,夏季呈显著正相关,长岛近海区域无明显变化,表明不同季节和不同区域的食物多样性水平存在差异, 胶州湾脉红螺δ¹³C、δ¹⁵N的变化更为突出;两个研究区域δ¹⁵N值和营养级与体长、体重呈显著正相关,主要由于脉红螺摄食偏好性差异,较大的脉红螺倾向于摄食高营养级生物,造成营养级较高。此外,胶州湾脉红螺营养级高于长岛近海,表明其¹⁵N来源更为广泛。营养生态位总面积、δ¹⁵N差值、δ¹³C差值、校正后标准椭圆面积等评价指标,揭示了不同区域、不同季节的脉红螺稳定同位素营养生态位的显著差异,反映了区域地理位置与食物来源对脉红螺δ¹³C和δ¹⁵N的影响。上述研究结果为近海生态系统食物网的构建提供了重要数据,并为区域生物资源的管理和生态系统修复工作提供了科学支撑。     

Long noncoding RNA lncMREF promotes myogenic differentiation and muscle regeneration by interacting with the Smarca5/p300 complex

Long noncoding RNAs (lncRNAs) play important roles in the spatial and temporal regulation of muscle development and regeneration. Nevertheless, the determination of their biological functions and mechanisms underlying muscle regeneration remains challenging. Here, we identified a lncRNA named lncMREF (lncRNA muscle regeneration enhancement factor) as a conserved positive regulator of muscle regeneration among mice, pigs and humans. Functional studies demonstrated that lncMREF, which is mainly expressed in differentiated muscle satellite cells, promotes myogenic differentiation and muscle regeneration. Mechanistically, lncMREF interacts with Smarca5 to promote chromatin accessibility when muscle satellite cells are activated and start to differentiate, thereby facilitating genomic binding of p300/CBP/H3K27ac to upregulate the expression of myogenic regulators, such as MyoD and cell differentiation. Our results unravel a novel temporal-specific epigenetic regulation during muscle regeneration and reveal that lncMREF/Smarca5-mediated epigenetic programming is responsible for muscle cell differentiation, which provides new insights into the regulatory mechanism of muscle regeneration.     

DNASE1L3 inhibits proliferation,invasion and metastasis of hepatocellular carcinoma by interacting with β‐catenin to promote its ubiquitin degradation pathway

As a member of the deoxyribonuclease 1 family, DNASE1L3 plays a significant role both inside and outside the cell. However, the role of DNASE1L3 in hepatocellular carcinoma (HCC) and its molecular basis remains to be further investigated. In this study, we report that DNASE1L3 is downregulated in clinical HCC samples and evaluate the relationship between its expression and HCC clinical features. In vivo and in vitro experiments showed that DNASE1L3 negatively regulates the proliferation, invasion and metastasis of HCC cells. Mechanistic studies showed that DNASE1L3 recruits components of the cytoplasmic β‐catenin destruction complex (GSK‐3β and Axin), promotes the ubiquitination degradation of β‐catenin, and inhibits its nuclear transfer, thus, decreasing c‐Myc, P21 and P27 level. Ultimately, cell cycle and EMT signals are restrained. In general, this study provides new insight into the mechanism for HCC and suggests that DNASE1L3 can become a considerable target for HCC.

Decreased expression of DNASE1L3 is associated with poor prognosis in patients with HCC DNASE1L3 inhibits the proliferation and cell cycle of HCC cells in vitro and promotes the invasion and metastasis of HCC cells DNASE1L3 inhibits the tumorigenicity and metastasis of HCC cells in vivo DNASE1L3 interacts with β‐catenin and promotes its binding to the β‐catenin destroying complex DNASE1L3 interacts with P21 and stabilizes P21 by mediating the deubiquitin activity