桂西北喀斯特典型土壤有机碳矿化过程中微生物活性的变化

为了研究喀斯特地区典型土壤有机碳积累与转化过程,采取野外取样分析与室内培养相结合的方法,以红壤为对照,采集2种喀斯特典型土壤(即棕色石灰土和黑色石灰土),设置不添加外源物质(CK)、添加14C标记的稻草(T1)、添加碳酸钙粉末(T2)和同时添加14C标记的稻草与碳酸钙粉末(T3)4个处理,进行室内培养试验,以土壤微生物指标(微生物生物量碳、基础呼吸、微生物碳熵和代谢熵)指示土壤有机碳积累与转化过程。结果表明,土壤有机碳矿化过程中,土壤呼吸的累积量依次为黑色石灰土>棕色石灰土>红壤(P<0.05)。微生物碳熵随土壤有机碳矿化变化依次为黑色石灰土>棕色石灰土>红壤(P<0.05)。同时添加外源稻草和钙对提高土壤微生物碳稳定性的效果最强。桂西北喀斯特地区土壤微生物指标的变化因土壤类型不同而存在差异。利用微生物指标来衡量土壤有机碳稳定性较为可靠。     

棕色石灰土和红壤碳释放对添加矿物质(Fe(OH)_3和CaCO_3)的响应

为阐明喀斯特地区土壤演变过程(脱钙镁富铁铝化作用)中土壤特有矿物对碳释放的影响,本文以喀斯特区典型的高和低有机碳含量水平的棕色石灰土和红壤为研究对象,通过80 d室内培养试验,研究土壤碳释放(有机碳和无机碳)对添加土壤中特有矿物质(Ca14CO3和Fe(OH)3)的响应。结果表明:添加Ca14CO3和Fe(OH)3均对棕色石灰土和红壤中原有碳的释放有正激发效应,以前者(培养结束时土壤原有碳累积释放量为823.8~1367.2 mg·kg-1)显著大于后者(502.5~635.7 mg·kg-1),说明喀斯特地区土壤由富钙镁的石灰土向富铁铝的红壤演变过程可能是土壤碳库逐渐稳定的过程。添加Ca14CO3和Fe(OH)3后,土壤原有碳的累积释放量的大小与土壤有机碳本身含量水平密切相关,均以高量有机碳红壤低量有机碳红壤和石灰土高量有机碳石灰土(P0.05)。培养过程中,无论是添加Ca14CO3还是Fe(OH)3,土壤可溶性有机碳(DOC)含量与碳释放激发效应的变化趋势一致,表明DOC可用于指示棕色石灰土和红壤激发效应强弱。土壤微生物生物量碳与碳释放激发效应的变化趋势不一致,说明添加Ca14CO3或Fe(OH)3对土壤原有碳的激发效应主要源于外源物添加后改变了土壤物理和化学环境,而土壤微生物的贡献相对较少。     

红壤和风沙土添加不同化学结构有机碳对外源碳去向及累积贡献的影响

植物凋落物碳输入显著影响陆地生态系统土壤CO₂排放和有机碳(SOC)形成,然而,针对不同质地土壤添加不同化学结构外源碳去向依然不清楚。本研究将¹³C标记的葡萄糖、淀粉和纤维素添加至红壤和风沙土,比较2种质地土壤添加不同化学结构外源碳在土壤释放的CO₂、SOC、可溶性有机碳(DOC)和微生物生物量碳(MBC)库的净累积量、回收率及贡献比例上的差异。结果表明: 添加外源有机碳显著提高了CO₂、SOC、DOC和MBC的δ¹³C值,且随着外源有机碳化学结构复杂性的增加,CO₂的δ¹³C峰值依次延迟出现;外源有机碳种类、土壤类型和培养时间均显著改变外源碳去向及其在各碳库的贡献比例;在风沙土中,外源有机碳更多被矿化为CO₂,且CO₂库的外源碳净累积量和回收率大小依次为葡萄糖>淀粉>纤维素;红壤添加外源碳转变为SOC的累积量和回收率显著高于风沙土,且红壤SOC库的外源碳净累积量和回收率大小顺序也为葡萄糖>淀粉>纤维素。可见,外源有机碳化学结构和土壤质地共同调控外源碳去向及累积贡献。     

改变施肥管理后不同肥力稻田土壤CO2排放特征

利用一个长达30a水稻土长期定位试验,在保证原有定位试验继续正常开展的前提下,将原化肥处理改施有机肥,原有机肥处理改施化肥或者增施有机肥。通过观测田间试验2012—2013年双季稻轮作周期内不同肥力水平稻田土壤施肥管理改变后的土体CO2排放通量(FCO2),研究不同后续施肥管理对不同肥力红壤性水稻土CO2排放的影响。结果表明:变更施肥能明显改变CO2排放动态变化,其中长期施用有机肥处理改施化肥后其FCO2明显减小,长期施用化肥或有机肥处理增施有机肥后其FCO2显著增大。有机肥和土壤有机碳均可促进土体CO2排放,有机肥处理有机物料碳添加量与CO2-C年排放量呈极显著的正相关关系(r=0.9015**,n=21),单施化肥处理土壤有机碳含量与土体CO2-C年排放量符合线性方程:y=10.962x-68.86(R2=0.7507,n=9,P0.01)。长期施用有机肥土壤改施化肥会导致其有机碳矿化损失,土壤有机碳含量越高,矿化损失量越多,最终其有机碳水平将与长期施用化肥的土壤有机碳平衡值一致;长期施用化肥或有机肥土壤改施或增施有机肥可促进土壤有机碳积累,外源添加碳越多,土壤积累碳越多;相同有机肥施用量下土壤有机碳含量越高,有机物料表观分解率越大,积累于土壤中的有机碳越少,不同有机碳水平土壤在相同有机肥管理下其有机碳最终会达到相同的平衡值。在有机碳水平较低(20.46 g/kg)红壤稻田上增施有机肥是提升已培肥水稻土有机碳含量的可持续发展措施,而在有机碳水平较高(14.45 g/kg)红壤稻田上应避免改施化肥。总之,在有机碳含量较高或者较低的中国南方红壤性水稻土上,持续的有机肥施用是保持或者提高其有机碳水平的必要措施。     

秸秆还田配施中微量元素对农田土壤有机碳固持的影响

为研究秸秆还田配施中量元素(S)和微量元素(Fe和Zn)对粮田土壤有机碳固持的影响,进行了为期52 d的室内玉米秸秆腐解培养试验. 结果表明:秸秆腐解过程中分别添加S、Fe和Zn元素,均提高了微生物生物量碳(MBC)及土壤CO₂-C矿化速率,52 d腐解培养结束后,CO₂-C的累积矿化量显著提高,但土壤有机碳含量并未显著降低;3种元素中,添加Fe或Zn的处理提高了土壤惰性碳库、惰性碳库比例及土壤有机碳表观平衡,有利于土壤有机碳固持,而添加S的处理却降低了惰性有机碳比例及土壤有机碳表观平衡,不利于有机碳固持. 因此,在施N、P肥基础上,秸秆还田添加S、Fe或Zn均能促进土壤有机碳的矿化进程,但添加Fe或Zn可使更多有机碳固持于土壤中,添加S不利于土壤有机碳的固持.     

不同环境因子对樟子松人工林土壤有机碳矿化的影响

土壤有机碳矿化是土壤向大气释放CO2的最大净输出途径,其与植被的净初级生产力的差值是判断生态系统碳源或碳汇的关键。本研究以科尔沁沙地10年生樟子松人工林生态系统为研究对象,采用室内培养实验方法,测定了不同温度、土壤含水量以及碳、氮添加条件下土壤有机碳矿化的速率。结果表明：土壤有机碳矿化速率随温度和土壤含水量的升高分别呈指数和线性增长,不同的土壤水分条件下土壤有机碳矿化的温度敏感性不同;在土壤含水量最小时（田间持水量的10％）,土壤有机碳矿化的温度敏感性最低;土壤有机碳矿化对水分的敏感性在低温条件下（10℃）显著低于在适温和高温条件下（20℃～30℃）。土壤中有机碳含量的增加显著提高土壤碳矿化速率,氮的添加对土壤有机碳矿化没有显著影响,但随着土壤有机碳含量的增加,土壤氮素含量对土壤碳矿化速率产生影响。     

稻田土壤有机碳矿化及其激发效应对磷添加的响应

采用室内模拟培养和¹³C同位素标记技术相结合的研究方法,探讨了在葡萄糖与无机氮肥共施的条件下,土壤有机碳矿化及其激发效应对外源磷添加的响应,以揭示土壤有机碳矿化的碳磷耦合调控机制.结果表明:外源磷的输入加快了CO_2的释放,但抑制了CH_4的释放;在整个土壤淹水培养期间,磷添加抑制了土壤碳矿化释放CH_4总量的53.1%,其中外源葡萄糖-¹³C矿化成¹³CH_4的总量降低了70.5%;磷添加促使通过微生物转化的葡萄糖-¹³C向易利用态碳库的分配比例增加了3.6%,显著提高土壤有机碳快库矿化速率,缩短土壤碳矿化周期.土壤培养前期,外源有机质的添加表现为短暂的负激发效应;随着葡萄糖不断矿化分解,CO_2累积激发效应(PE_{CO_2})总体上呈现先增加后下降的趋势,而CH_4累积激发效应(PE_{CH_4})稳步增加最终保持基本稳定状态;培养结束时(100 d),在磷添加条件下,PE_{CO_2}增强32.3%,PE_{CH_4}显著降低93.4%.冗余分析和Pearson分析表明,电导率、氧化还原电位和溶解有机碳对稻田土壤碳矿化的影响最为显著;速效磷与¹³CH_4、PE_{CH_4}呈极显著负相关.在外源有机质添加条件下,磷的添加能够抑制CH_4排放及其激发效应,促进土壤有机质的矿化和养分释放,提高土壤原有有机碳的可利用性,促进稻田土壤有机碳循环.     

常绿阔叶林与杉木林的土壤碳矿化潜力及其对土壤活性有机碳的影响

采用室内土壤培养法,比较分析了湖南省会同地区常绿阔叶林、杉木纯林土壤有机碳的矿化速率和累计矿化量,分析了有机碳矿化量与土壤活性有机碳初始含量的关系。结果表明:常绿阔叶林土壤有机碳矿化速率和累计矿化量均显著高于杉木纯林。在培养的第21天,在培养温度为9℃和28℃条件下,常绿阔叶林0～10和10～20cm土层的土壤有机碳累计矿化量为杉木纯林的1.7～2.7倍。常绿阔叶林土壤有机碳矿化释放的CO2-C分配比例高于杉木纯林。林地土壤有机碳矿化量受土壤微生物碳、可溶性有机碳初始含量的影响(P<0.01)。土壤有机碳矿化使土壤微生物碳增加而可溶性有机碳下降,但变化幅度均不大。温度从9℃升高到28℃后,林地土壤有机碳矿化速率提高3.1～4.5倍;2林地有机碳矿化对温度的敏感性无显著差异。     

不同坡向亚高山草甸土壤有机碳光降解特征及其对铁添加的响应

在全球中波紫外辐射(UVB)增加的背景下,土壤有机碳(SOC)矿化速率增强是多数陆地生态系统正在经历的重要生态学过程。铁氧化物可以通过吸附或共沉淀作用,影响土壤有机碳的稳定性,在调节碳循环过程起到重要作用。以历山舜王坪亚高山草甸东南坡与西北坡表层土壤为对象,通过为期50 d的室内培养实验,研究铁添加对土壤有机碳光降解的影响机制。结果表明：不同坡向亚高山草甸表层SOC矿化特征不相同,西北坡的SOC累积矿化量和矿化速率均显著高于东南坡,主要是因为西北坡土壤中非晶形铁(Feo-p)含量显著低于东南坡,对SOC保护力较弱;在UVB辐射下,表层土壤有机碳发生了光降解作用,促进了土壤有机碳的矿化。UVB辐射下西北坡的矿化量以及矿化速率增加幅度(即光引发作用)显著高于东南坡;外源添加铁抑制了土壤有机碳矿化,显著降低了土壤碳的累积矿化量和矿化效率,也显著了降低土壤碳的光降解;在未来UVB辐射持续增强下,西北坡向土壤有机碳有较强的光降解潜力,外源添加铁可以在一定程度上缓解表层土壤有机碳光降解作用。本文可为气候变化背景下深入理解亚高山草甸表层土壤有机碳固持机制提供理论依据。     

棉秆炭特性及其对灰漠土土壤有机碳矿化的效应

生物炭具有提高土壤肥力和减缓温室气体排放的作用,但其对土壤有机碳矿化的作用效应存在争议。以新疆灰漠土为研究对象,采用300℃和600℃制备的棉花秸秆炭(棉杆炭)为试材,在25℃、75%的土壤饱和含水量条件下,通过100 d的室内培养,研究了不同比例的棉杆炭添加(0、0.1%、0.5%、1.0%、2.0%和100%,以质量计)对土壤有机碳矿化的效应。结果表明:1)高温制备的棉杆炭,孔隙结构排列整齐,表面光滑,孔隙度和比表面积大,芳香化程度增强;2)棉杆炭的有机碳矿化速率与时间呈乘幂关系(P0.05),300℃棉杆炭相比600℃棉杆炭的累积矿化量和累积矿化率分别提高了318%和87.06%;高温炭化抑制了有机碳矿化;与对照相比,添加300℃棉杆炭增加了土壤有机碳累积矿化量(0.1%处理除外,降低了7.22%),并随棉杆炭添加量而增加,土壤有机碳累积矿化量提高幅度在3.05%—35.28%,而添加600℃棉杆炭降低了土壤有机碳累积矿化量,降低幅度为6.11%—10.79%;3)培养前期(0—20 d)300℃棉杆炭对灰漠土土壤原有有机碳矿化为正激发效应(0.1%处理除外),后期为负激发效应,整个培养期内为负激发效应;600℃棉杆炭培养前期(0—5 d)对土壤原有有机碳激发效应微小,主要表现为负激发效应。由此可见,低温制备的棉杆炭能提高土壤有机碳矿化,而高温制备棉杆炭则抑制了土壤有机碳矿化,棉杆炭添加对土壤原有有机碳矿化具有负激发效应,能够促进土壤有机碳积累。     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

我国葫芦科植物离体培养研究进展

葫芦科植物包括多种瓜类蔬菜,对其进行离体培养研究具有重要的理论和实践意义。综述了国内在葫芦科植物器官培养、体细胞胚胎发生、花药培养、原生质体培养和体细胞杂交及离体遗传转化等方面取得的研究进展,并对葫芦科植物离体培养、遗传转化与育种的前景作了展望。     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.     

2018年中国植物科学若干领域重要研究进展

2018年中国植物科学继续呈现快速发展的态势, 我国科学家在国际植物科学主流学术刊物发表论文数量大幅增加, 取得了多项具有重要影响的成果。调控植物生长-代谢平衡实现可持续农业发展入选2018年度中国科学十大进展; 中国被子植物区系进化历史研究入选2018年度中国生命科学十大进展。以水稻为代表的农作物和果蔬等经济作物研究在国际上已呈现出明显的优势, 若干领域已从“追赶”状态跨越到“领跑”地位。该文对2018年中国科学家在植物科学若干领域取得的重要研究成果进行了概括性评述, 旨在全面追踪和报道当前中国植物科学领域的发展前沿和热点, 展示中国科学家所取得的杰出成就。     

2018年中国植物科学若干领域重要研究进展

2018年中国植物科学继续呈现快速发展的态势, 我国科学家在国际植物科学主流学术刊物发表论文数量大幅增加, 取得了多项具有重要影响的成果。调控植物生长-代谢平衡实现可持续农业发展入选2018年度中国科学十大进展; 中国被子植物区系进化历史研究入选2018年度中国生命科学十大进展。以水稻为代表的农作物和果蔬等经济作物研究在国际上已呈现出明显的优势, 若干领域已从“追赶”状态跨越到“领跑”地位。该文对2018年中国科学家在植物科学若干领域取得的重要研究成果进行了概括性评述, 旨在全面追踪和报道当前中国植物科学领域的发展前沿和热点, 展示中国科学家所取得的杰出成就。     

2017年中国植物科学若干领域重要研究进展

2017年中国植物科学继续保持高速发展态势, 重大成果频出, 具体表现在中国植物学家在国际顶级学术期刊发表的文章数量平稳上升。中国植物科学领域的研究工作者成果精彩纷呈, 如新型广谱抗病机制的发现、水稻广谱抗病遗传基础及机制和疫霉菌诱发病害成灾机制研究等。2017年中国生命科学领域十大进展评选中, 有两项植物科学领域的研究成果入选。水稻生物学、进化与基因组学和激素生物学等领域学科发展突出。另外, 值得一提的是, 长期从事高等植物与代谢途径调控分子网络研究和水稻品种设计育种的李家洋院士的研究成果“水稻高产优质性状形成的分子机理及品种设计”荣获2017年国家自然科学一等奖。这一具有重大国际影响的开创性贡献标志着中国植物科学在该领域的国际科学前沿居于引领和卓越地位。该文对2017年中国本土科学家在植物科学若干领域取得的重要研究成果进行了系统梳理, 旨在全面追踪和报道当前中国植物科学领域发展的最新前沿动态, 与广大读者共同分享我国科学家所取得的辉煌成就。     

我国葫芦科植物离体培养研究进展

葫芦科植物包括多种瓜类蔬菜,对其进行离体培养研究具有重要的理论和实践意义.综述了国内在葫芦科植物器官培养、体细胞胚胎发生、花药培养、原生质体培养和体细胞杂交及离体遗传转化等方面取得的研究进展,并对葫芦科植物离体培养、遗传转化与育种的前景作了展望.     

Changes in aquatic vegetation in Rhine floodplain streams in Alsace in relation to disturbance

Abstract. Changes are described in aquatic vegetation in oligotrophic, groundwater-fed Rhine floodplain streams in Alsace (eastern France), resulting from disturbance. Disturbance factors include changes in nutrients, either permanent ones - effluent from a waste water treatment plant or trout hatcheries - or periodic ones: flooding. Regular inputs of high levels of phosphate and ammonia modified the macrophyte vegetation in these streams. The floristic composition, which was characteristic of oligotrophic waters upstream of the eutrophicated sector, changed to that of a eutrophic situation as originally found downstream. Periodic disturbance by floods which normally occur once a year, irregularly eutrophicates the small streams, causing the development of a mixture of eutrophic and oligotrophic species. Six macrophyte communities are distinguished, indicating different trophic levels. The aquatic vegetation is adapted to the variations of phosphate and ammonia levels. Hence, aquatic macrophytes can be used as bio-indicators of fluctuations in water nutrient levels in relation to the type of disturbance.     

Morphine-potentiated platelet aggregation in in vitro and platelet plug formation in in vivo experiments

The detailed mechanisms underlying morphine-signaling pathways in platelets remain obscure. Therefore, we systematically examined the influence of morphine on washed human platelets. In this study, washed human platelet suspensions were used for in vitro studies. Furthermore, platelet thrombus formation induced by irradiation of mesenteric venules with filtered light in mice pretreated with fluorescein sodium was used for an in vivo thrombotic study. Morphine concentration dependently (0.6, 1, and 5 microM) potentiated platelet aggregation and the ATP release reaction stimulated by agonists (i.e., collagen and U46619) in washed human platelets. Yohimbine (0.1 microM), a specific alpha(2)-adrenoceptor antagonist, markedly abolished the potentiation of morphine in platelet aggregation stimulated by agonists. Morphine also potentiated phosphoinositide breakdown and intracellular Ca(2+) mobilization in human platelets stimulated by collagen (1 microg/ml). Moreover, morphine (0.6-5 microM) markedly inhibited prostaglandin E(1) (10 microM)-induced cyclic AMP formation in human platelets, while yohimbine (0.1 microM) significantly reversed the inhibition of cyclic AMP by morphine (0.6 and 1 microM) in this study. The thrombin-evoked increase in pH(i) was markedly potentiated in the presence of morphine (1 and 5 microM). Morphine (2 and 5 mg/g) significantly shortened the time require to induce platelet plug formation in mesenteric venules. We concluded that morphine may exert its potentiation in platelet aggregation by binding to alpha(2)-adrenoceptors in human platelets, with a resulting inhibition of adenylate cyclase, thereby reducing intracellular cyclic AMP formation followed by increased activation of phospholipase C and the Na(+)/H(+) exchanger. This leads to increased intracellular Ca(2+) mobilization, and finally potentiation of platelet aggregation and of the ATP release reaction.     

Apoptosis in experimental myocardial infarction in situ and in the perfused heart in vitro

We report the appearance of apoptotic cells in experimental myocardial infarction (rabbit heart) in in situ and in vitro preparations. Apoptosis was recognized by intravital staining with Hoechst 33342 (Ho342), by nick-end labeling (TUNEL) and by DNA laddering. A steady rise in the relative number of apoptotic cardiomyocytes (apoptotic index) was noted in in situ preparations. Apoptosis was first noted 6 h after the onset of ischemia with its highest value occurring after 72 h. Apoptotic nuclei were absent in remote areas of the left and right ventricles. Apoptotic nuclei within the infarcted area showed diminished intensity of Ho342 fluorescence. Three days after ischemia, a border zone adjacent to the infarcted area consisting of apoptotic macrophages was recognized. A novel finding was the appearance of apoptotic cardiomyocytes in the isolated perfused ischemic heart. Occurring as early as 50 min after the onset of ischemia, a high apoptotic index was present adjacent to the ligature placed around the coronary artery. This observation provides the opportunity to selectively examine factors leading to apoptosis in the ischemic heart under controlled experimental conditions.