闽三角城市群生态安全格局构建及城镇扩展模拟

在快速城镇化背景下,构建生态安全格局并探讨城镇用地扩展格局已成为保障区域生态安全和缓解生态保护与土地开发矛盾的重要手段。以闽三角城市群为例,基于景观安全格局原理和ArcGIS空间分析法,从综合水安全、生物保护安全、地质灾害安全以及游憩安全四个方面叠加构建"底线安全格局-缓冲安全格局-最优安全格局"三种不同安全水平的综合生态安全格局;然后结合SLEUTH模型,将不同生态安全格局情景作为约束条件融入其排除图层,对研究区2015—2030年的城镇用地空间扩展进行多情景模拟。研究表明:(1)底线安全格局、缓冲安全格局以及最优安全格局的面积为9305.51、7576.28、3482.73 km²,分别占闽三角城市群总面积的36.89%、30.03%、13.81%;(2)三种生态安全格局情景模拟下城镇用地均呈增长趋势,但增长速度均小于历史用地的增长速度,高安全格局约束下的新增城镇用地面积和增长速度均最小,表明将生态安全格局作为城镇发展的约束条件,在城镇土地开发中能够增强对生态空间的保护力度,维护区域生态安全,控制城镇蔓延。相关研究成果可为城镇开发边界管控与国土空间规划的编制提...     

5种东北红豆杉植物群丛及其物种多样性的比较

东北红豆杉(Taxus cuspidata)是我国数量极少的珍贵濒危树种, 了解其天然群落的组成和特征对东北红豆杉种群的保护利用和恢复有重要意义。本文对吉林省天然东北红豆杉群落进行调查, 根据物种组成进行系统聚类分析。将20块40 m × 40 m样地划分为5种群丛类型, 分别以优势种进行命名, 即: Ⅰ. 舞鹤草-五味子+狗枣猕猴桃-紫椴+臭冷杉群丛; II. 东北羊角芹-狗枣猕猴桃-臭冷杉群丛; III. 盾叶唐松草-狗枣猕猴桃-臭冷杉群丛; IV. 舞鹤草-软枣猕猴桃-红松+紫椴+臭冷杉群丛; V. 舞鹤草-软枣猕猴桃-紫椴+臭冷杉群丛。对群丛的物种组成、群落结构和群丛类型、物种多样性进行了分析。物种多样性选用Menhinick丰富度指数、Pielou均匀度指数、Simpson优势度指数以及Shannon-Wiener多样性指数, 对比分析不同群丛特征。结果显示: 东北红豆杉植物群落组成中蔷薇科的种和属数所占比例最大; 5个群丛的多样性指数顺序为群丛V > 群丛III > 群丛IV > 群丛II > 群丛Ⅰ; 群丛Ⅰ和II具有较低的多样性和较高的优势度, 群丛II和群丛III的乔木层的多样性指数差异不明显, 但其丰富度指数和优势度指数却呈现了相反的特征; 群丛II丰富度低而优势度高, 而群丛III丰富度高而优势度低; 群丛III中的草本层的多样性高于乔木层, 群落郁闭度较低; 群丛IV和群丛V均位于和龙市荒沟林场, 随着海拔上升, 其物种多样性随之下降。结果表明, 不同物种组成的东北红豆杉植物群丛的群落特征存在显著差异。     

Anti-Human α-Synuclein N-Terminal Peptide Antibody Protects against Dopaminergic Cell Death and Ameliorates Behavioral Deficits in an AAV-α-Synuclein Rat Model of Parkinson’s Disease

The protein α-synuclein (α-Syn) has a central role in the pathogenesis of Parkinson’s disease (PD) and immunotherapeutic approaches targeting this molecule have shown promising results. In this study, novel antibodies were generated against specific peptides from full length human α-Syn and evaluated for effectiveness in ameliorating α-Syn-induced cell death and behavioral deficits in an AAV-α-Syn expressing rat model of PD. Fisher 344 rats were injected with rAAV vector into the right substantia nigra (SN), while control rats received an AAV vector expressing green fluorescent protein (GFP). Beginning one week after injection of the AAV-α-Syn vectors, rats were treated intraperitoneally with either control IgG or antibodies against the N-terminal (AB1), or central region (AB2) of α-Syn. An unbiased stereological estimation of TH+, NeuN+, and OX6 (MHC-II) immunostaining revealed that the α-Syn peptide antibodies (AB1 and AB2) significantly inhibited α-Syn-induced dopaminergic cell (DA) and NeuN+ cell loss (one-way ANOVA (F (3, 30) = 5.8, p = 0.002 and (F (3, 29) = 7.92, p = 0.002 respectively), as well as decreasing the number of activated microglia in the ipsilateral SN (one-way ANOVA F = 14.09; p = 0.0003). Antibody treated animals also had lower levels of α-Syn in the ipsilateral SN (one-way ANOVA F (7, 37) = 9.786; p = 0.0001) and demonstrated a partial intermediate improvement of the behavioral deficits. Our data suggest that, in particular, an α-Syn peptide antibody against the N-terminal region of the protein can protect against DA neuron loss and, to some extent behavioral deficits. As such, these results may be a potential therapeutic strategy for halting the progression of PD.     

Irradiation to the immature brain attenuates neurogenesis and exacerbates subsequent hypoxic‐ischemic brain injury in the adult

Cranial radiotherapy is common in pediatric oncology. Our purpose was to investigate if irradiation (IR) to the immature brain would increase the susceptibility to hypoxic‐ischemic injury in adulthood. The left hemisphere of postnatal day 10 (P10) mice was irradiated with 8 Gy and subjected to hypoxia‐ischemia (HI) on P60. Brain injury, neurogenesis and inflammation were evaluated 30 days after HI. IR alone caused significant hemispheric tissue loss, or lack of growth (2.8 ± 0.42 mm³, p < 0.001). Tissue loss after HI (18.2 ± 5.8 mm³, p < 0.05) was synergistically increased if preceded by IR (32.0 ± 3.5 mm³, p < 0.05). Infarct volume (5.1 ± 1.6 mm³) nearly doubled if HI was preceded by IR (9.8 ± 1.2 mm³, p < 0.05). Pathological scoring revealed that IR aggravated hippocampal, cortical and striatal, but not thalamic, injury. Hippocampal neurogenesis decreased > 50% after IR but was unchanged by HI alone. The number of newly formed microglia was three times higher after IR + HI than after HI alone. In summary, IR to the immature brain produced long‐lasting changes, including decreased hippocampal neurogenesis, subsequently rendering the adult brain more susceptible to HI, resulting in larger infarcts, increased hemispheric tissue loss and more inflammation than in non‐irradiated brains.     

SlERF52 regulates SlTIP1;1 expression to accelerate tomato pedicel abscission

Abscission of plant organs is induced by developmental signals and diverse environmental stimuli and involves multiple regulatory networks, including biotic or abiotic stress-impaired auxin flux in the abscission zone (AZ). Depletion of auxin activates AZ ethylene (ETH) production and triggers acceleration of abscission, a process that requires hydrogen peroxide (H₂O₂). However, the interaction between these networks and the underlying mechanisms that control abscission are poorly understood. Here, we found that expression of tonoplast intrinsic proteins, which belong to the aquaporin (AQP) family in the AZ was important for tomato (Solanum lycopersicum) pedicel abscission. Liquid chromatography–tandem mass spectrometry and in situ hybridization revealed that SlTIP1;1 was most abundant and specifically present in the tomato pedicel AZ. SlTIP1;1 localized in the plasma membrane and tonoplast. Knockout of SlTIP1;1 resulted in delayed abscission, whereas overexpression of SlTIP1;1 accelerated abscission. Further analysis indicated that SlTIP1;1 mediated abscission via gating of cytoplasmic H₂O₂ concentrations and osmotic water permeability (P_f). Elevated cytoplasmic levels of H₂O₂ caused a suppressed auxin signal in the early abscission stage and enhanced ETH production during abscission. Furthermore, we found that increasing P_f was required to enhance the turgor pressure to supply the break force for AZ cell separation. Moreover, we observed that SlERF52 bound directly to the SlTIP1;1 promoter to regulate its expression, demonstrating a positive loop in which cytoplasmic H₂O₂ activates ETH production, which activates SlERF52. This, in turn, induces SlTIP1;1, which leads to elevated cytoplasmic H₂O₂ and water influx.

A SlERF52-SlTIP1;1 regulatory module accelerates pedicel abscission by increasing cytoplasmic hydrogen peroxide contents and osmotic water permeability.     

Vangl2 limits chaperone-mediated autophagy to balance osteogenic differentiation in mesenchymal stem cells

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Construction and screening of a multi-point site-specific mutant library of subtilisin E with a set of oligonucleotides

A mutant library of subtilisin E containing random combinations of various mutagenized sites was constructed by one-round mutagenesis with 15 mutagenic oligonucleotides. Mutants were screened through dot blot hybridization and DNA sequencing. A single-point mutant (Met 222Ala) and a three-point (Asn 76Asp/Asn109Ser/ I le 205/Cys) mutant gene from the library were expressed. The mutant proteins exhibited conspicuously improved resistance to oxidation and heat treatment, as reported before. The results show that the library is reliable and very useful for protease subtilisin E engineering.     

Atg7 is required for acrosome biogenesis during spermatogenesis in mice

The acrosome is a specialized organelle that covers the anterior part of the sperm nucleus and plays an essential role in the process of fertilization. The molecular mechanism underlying the biogenesis of this lysosome-related organelle (LRO) is still largely unknown. Here, we show that germ cell-specific Atg7-knockout mice were infertile due to a defect in acrosome biogenesis and displayed a phenotype similar to human globozoospermia; this reproductive defect was successfully rescued by intracytoplasmic sperm injections. Furthermore, the depletion of Atg7 in germ cells did not affect the early stages of development of germ cells, but at later stages of spermatogenesis, the proacrosomal vesicles failed to fuse into a single acrosomal vesicle during the Golgi phase, which finally resulted in irregular or nearly round-headed spermatozoa. Autophagic flux was disrupted in Atg7-depleted germ cells, finally leading to the failure of LC3 conjugation to Golgi apparatus-derived vesicles. In addition, Atg7 partially regulated another globozoospermia-related protein, Golgi-associated PDZ- and coiled-coil motif-containing protein (GOPC), during acrosome biogenesis. Finally, the injection of either autophagy or lysosome inhibitors into testis resulted in a similar phenotype to that of germ cell-specific Atg7-knockout mice. Altogether, our results uncover a new role for Atg7 in the biogenesis of the acrosome, and we provide evidence to support the autolysosome origination hypothesis for the acrosome.