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51.
参照植物根尖细胞学研究的方法标准,对香薷属3种(5个居群)植物进行核形态学分析。结果表明:(1)从染色体数目看,密花香薷2居群染色体数目2n=16;野苏子2居群染色体数目2n=20,染色体数目和倍性与前人报道的一致;毛穗香薷染色体数目2n=10为首次报道。(2)聚类分析结果显示,3种(5居群)植物中野苏子和密花香薷亲缘关系较近;结合现有报道数据分析表明,该属植物仅有2种倍性(二倍体和四倍体),且二倍体占主导地位。(3)核型参数分析表明:密花香薷的稻城无名山居群1核型公式为2n=2x=16=14m+2sm,居群2为2n=2x=16=16m,着丝粒指数(CI)分别为39.57和42.32,不对称系数AI值分别为2.75和2.87,核型不对称性都为1A型;毛穗香薷的核型公式为2n=2x=10=10m,着丝粒指数(CI)为41.76,不对称系数AI值为5.25,核型不对称性为1B型;野苏子的昆明西山居群核型公式为2n=2x=20=14m+6sm,聂拉木樟木沟居群为2n=2x=20=16m+4sm,着丝粒指数(CI)分别为38.49和40.97,不对称系数AI值为4.20和4.30,核型不对称性为1B型和2B型。 相似文献
52.
为了解渐危植物新疆野核桃的病害情况,在新疆野核桃自然保护区调查不同坡向、不同龄级野核桃4种病害的患病比例,分析病害种类、病害等级与野核桃胸径及坡向的相关关系。结果表明: 保护区野核桃的主要病害为核桃褐斑病(95.8%)、核桃枯枝病(90.5%)、核桃黑斑病(74.4%)和核桃腐朽病(7.7%)。4个坡向的野核桃均易患核桃褐斑病,阴坡和半阴坡的野核桃易患核桃枯枝病,阳坡和阴坡的野核桃易患核桃黑斑病,半阳坡和半阴坡的野核桃相对易患核桃腐朽病。4个坡向野核桃的4种病害均随病害等级(1~4级)的增加而病株比例减小。4个坡向核桃枯枝病、核桃黑斑病、核桃褐斑病均以中龄树比例最大,其次是老龄树,再次是小树,未见幼苗患病;核桃腐朽病仅发生在老龄树。核桃枯枝病、核桃腐朽病、核桃黑斑病、核桃褐斑病与野核桃的胸径呈显著正相关,核桃黑斑病与坡向呈显著负相关,核桃枯枝病、核桃腐朽病、核桃黑斑病的不同病害等级与胸径和坡向存在相关性。 相似文献
53.
Cyanobacterium Anacystis nidulans R2, Synechocystis sp. PCC 6803 (wild-type strain and mutants Delta2 and Delta3 lacking PSII and PSI, respectively), and Synechocystis sp. BO 9201 synthesize the pigment--protein complex CP36 (CPIV-4, CP43') under iron deficiency in the medium. Accumulation of CP36 is accompanied by structural reorganizations in the photosynthetic membranes. Integrating mean times of excitation relaxation (quenching) are 2.2 nsec (CP36), 1 nsec (PSI), and 420 psec (PSII in Fm state). The energy migration between CP36 and the photosystems can be described by a model of a one-layer ring of CP36 around core-complexes. The excitation from CP36 to PSI is transferred within <10 psec. The energy transfer from CP36 to PSII occurs during 170 psec. Cells with low content of CP36 probably contain only a latent fraction of unbound to phycobilisomes PSII which is the analog of PSIIbeta of higher plants. In PSI there are four binding sites for CP36 monomers per RC. PSII can bind up to 32 molecules of CP36 per RC. Cells with a large amount of CP36 contain monomer form of PSII core-complex which can bind eight tetramers of CP36 (8 binding sites). In conditions of iron deficiency only one monomer of a dimer PSII core-complex is destroyed and released chlorophyll is accumulated in CP36. Accumulation of CP36 in A. nidulans cells can be accompanied by membrane stacking which is similar to the stacking in chlorophyll b-containing organisms. The stacking can occur in the region of localization of PSII latent fraction bound to CP36. The membrane stacking shields PSII stromal surfaces from the aqueous phase for activation of electron transfer on the acceptor side of PSII. 相似文献
54.
The food-web structure of the Arctic deep Canada Basin was investigated in summer 2002 using carbon and nitrogen stable isotope tracers. Overall food-web length of the range of organisms sampled occupied four trophic levels, based on 3.8 trophic level enrichment (15N range: 5.3–17.7). It was, thus, 0.5–1 trophic levels longer than food webs in both Arctic shelf and temperate deep-sea systems. The food sources, pelagic particulate organic matter (POM) (13C=–25.8, 15N=5.3) and ice POM (13C=–26.9, 15N=4.1), were not significantly different. Organisms of all habitats, ice-associated, pelagic and benthic, covered a large range of 15N values. In general, ice-associated crustaceans (15N range 4.6–12.4, mean 6.9) and pelagic species (15N range 5.9–16.5, mean 11.5) were depleted relative to benthic invertebrates (15N range 4.6–17.7, mean 13.2). The predominantly herbivorous and predatory sympagic and pelagic species constitute a shorter food chain that is based on fresh material produced in the water column. Many benthic invertebrates were deposit feeders, relying on largely refractory material. However, sufficient fresh phytodetritus appeared to arrive at the seafloor to support some benthic suspension and surface deposit feeders on a low trophic level (e.g., crinoids, cumaceans). The enriched signatures of benthic deposit feeders and predators may be a consequence of low primary production in the high Arctic and the subsequent high degree of reworking of organic material. 相似文献
55.
比格犬MC4R基因多态性与体重相关性的研究 总被引:11,自引:3,他引:8
为了分析比格犬黑素皮质素受体-4基因多态性与犬体重的关系, 根据犬MC4R基因DNA外显子序列, 设计MC4R基因特异PCR引物1对, 犬DNA经PCR扩增, 克隆和测序, 寻找和确定犬MC4R基因的多态性位点, 分析多态性与犬体重的关系。结果在比格犬MC4R基因中发现2处单碱基缺失突变, 1个单碱基颠换变异, 存在Psh AⅠ酶切位点, 并基于PshAⅠ酶切位点建立了PCR-RFLP技术。统计分析显示犬MC4R基因型与体重显著相关, 可以考虑将MC4R基因作为犬体重的候选基因。 相似文献
56.
Emma?L. Baple Reza Maroofian Barry?A. Chioza Maryam Izadi Harold?E. Cross Saeed Al-Turki Katy Barwick Anna Skrzypiec Robert Pawlak Karin Wagner Roselyn Coblentz Tala Zainy Michael?A. Patton Sahar Mansour Phillip Rich Britta Qualmann Matt?E. Hurles Michael?M. Kessels Andrew?H. Crosby 《American journal of human genetics》2014,94(1):87-94
The proper development of neuronal circuits during neuromorphogenesis and neuronal-network formation is critically dependent on a coordinated and intricate series of molecular and cellular cues and responses. Although the cortical actin cytoskeleton is known to play a key role in neuromorphogenesis, relatively little is known about the specific molecules important for this process. Using linkage analysis and whole-exome sequencing on samples from families from the Amish community of Ohio, we have demonstrated that mutations in KPTN, encoding kaptin, cause a syndrome typified by macrocephaly, neurodevelopmental delay, and seizures. Our immunofluorescence analyses in primary neuronal cell cultures showed that endogenous and GFP-tagged kaptin associates with dynamic actin cytoskeletal structures and that this association is lost upon introduction of the identified mutations. Taken together, our studies have identified kaptin alterations responsible for macrocephaly and neurodevelopmental delay and define kaptin as a molecule crucial for normal human neuromorphogenesis. 相似文献
57.
目的:探讨MR弥散加权成像(DWI)鉴别诊断良恶性椎体压缩性骨折的临床价值。方法:对57 例经临床或病理证实的椎体
良恶性压缩性骨折患者行矢状位T1WI、T2WI、T2WI/FS 及DWI扫描,研究其在常规序列和DWI序列上的表现,将常规MR 序列
和DWI序列检出率进行比较,测量正常椎体及病变椎体的表观弥散系数(ADC)值,并进行统计学分析。结果:(1)MR 常规序列和
DWI序列(b=500s/mm2)表现:良性椎体压缩性骨折呈长T1 长或等T2 改变,T2WI/FS 呈高信号,DWI 可以呈高信号、等信号及低
信号;恶性椎体压缩性骨折呈长T1 长T2 信号,大部分病灶T2WI/FS 及DWI呈高信号,少数变现为低信号;(2)MR 常规序列和
DWI 序列(b=500s/mm2)病灶检出率的比较:T1WI、T2WI/FS 及DWI序列病灶检出率均高于T2WI 序列,其间的差别有显著性意
义(P<0.01),T1WI、T2WI/FS 及DWI序列病灶检出率之间无显著性差异(P>0.01);(3)ADC 值比较:在DWI(b=500 s/mm2)上,良性组
ADC 值为(2.03± 0.83)× 10-3mm2/s,恶性组ADC 值为(1.37 ± 0.75)× 10-3mm2/s,正常组ADC值为(0.36± 0.21)× 10-3mm2/s,成像条
件相同时,良性组高于恶性组,两组间有明显的统计学意义(P<0.05)。结论:DWI可较好的反映椎体的弥散特征,ADC值作为量化
指标可对良恶性椎体压缩性骨折进行可靠鉴别。 相似文献
58.
Crosby AH Patel H Chioza BA Proukakis C Gurtz K Patton MA Sharifi R Harlalka G Simpson MA Dick K Reed JA Al-Memar A Chrzanowska-Lightowlers ZM Cross HE Lightowlers RN 《American journal of human genetics》2010,87(5):655-660
In human mitochondria, polyadenylation of mRNA, undertaken by the nuclear-encoded mitochondrial poly(A) RNA polymerase, is essential for maintaining mitochondrial gene expression. Our molecular investigation of an autosomal-recessive spastic ataxia with optic atrophy, present among the Old Order Amish, identified a mutation of MTPAP associated with the disease phenotype. When subjected to poly(A) tail-length assays, mitochondrial mRNAs from affected individuals were shown to have severely truncated poly(A) tails. Although defective mitochondrial DNA maintenance underlies a well-described group of clinical disorders, our findings reveal a defect of mitochondrial mRNA maturation associated with human disease and imply that this disease mechanism should be considered in other complex neurodegenerative disorders. 相似文献
59.
目的:探究高血压脑出血患者术后重症监护治疗与早期(24 h内)再出血的相关因素。方法:回顾性分析2014年1月至2018年10月于中山大学附属第一医院及中山市人民医院行手术治疗并进行重症监护的高血压脑出血患者的相关资料,记录术后早期发生再出血情况,比较其相关因素,包括年龄、性别、术前格拉斯哥昏迷量表(GCS)评分、出血量、术前收缩压、术后收缩压、镇静时间、插管时间、有无使用止血药、血压波动、血压差、有无镇痛情况,分析术后早期再出血的影响因素。结果:本研究共纳入465例患者,其中术后早期再出血患者44例,未再出血患者421例,再出血发生率为9.46%(44/465)。高血压脑出血术后早期再出血患者的术后收缩压、有无镇痛、血压差、血压波动与未再出血患者比较差异具有统计学意义(P0.05)。术后早期再出血患者的年龄、性别及术前GCS评分、出血量、术前收缩压、镇静时间、插管时间、有无使用止血药与未再出血患者比较差异无统计学意义(P0.05)。多因素Logistic回归分析显示,患者血压波动大是术后早期再出血的危险因素,手术前后血压差大、术后使用镇痛治疗是其保护因素。结论:高血压脑出血患者术后血压波动、手术前后血压差及术后镇痛治疗均是早期再出血的影响因素,合理降压及镇痛治疗可减少脑出血术后早期再出血的发生。 相似文献
60.
Deficiency of terminal ADP‐ribose protein glycohydrolase TARG1/C6orf130 in neurodegenerative disease
Reza Sharifi Rosa Morra C Denise Appel Michael Tallis Barry Chioza Gytis Jankevicius Michael A Simpson Ivan Matic Ege Ozkan Barbara Golia Matthew J Schellenberg Ria Weston Jason G Williams Marianna N Rossi Hamid Galehdari Juno Krahn Alexander Wan Richard C Trembath Andrew H Crosby Dragana Ahel Ron Hay Andreas G Ladurner Gyula Timinszky R Scott Williams Ivan Ahel 《The EMBO journal》2013,32(9):1225-1237
Adenosine diphosphate (ADP)‐ribosylation is a post‐translational protein modification implicated in the regulation of a range of cellular processes. A family of proteins that catalyse ADP‐ribosylation reactions are the poly(ADP‐ribose) (PAR) polymerases (PARPs). PARPs covalently attach an ADP‐ribose nucleotide to target proteins and some PARP family members can subsequently add additional ADP‐ribose units to generate a PAR chain. The hydrolysis of PAR chains is catalysed by PAR glycohydrolase (PARG). PARG is unable to cleave the mono(ADP‐ribose) unit directly linked to the protein and although the enzymatic activity that catalyses this reaction has been detected in mammalian cell extracts, the protein(s) responsible remain unknown. Here, we report the homozygous mutation of the c6orf130 gene in patients with severe neurodegeneration, and identify C6orf130 as a PARP‐interacting protein that removes mono(ADP‐ribosyl)ation on glutamate amino acid residues in PARP‐modified proteins. X‐ray structures and biochemical analysis of C6orf130 suggest a mechanism of catalytic reversal involving a transient C6orf130 lysyl‐(ADP‐ribose) intermediate. Furthermore, depletion of C6orf130 protein in cells leads to proliferation and DNA repair defects. Collectively, our data suggest that C6orf130 enzymatic activity has a role in the turnover and recycling of protein ADP‐ribosylation, and we have implicated the importance of this protein in supporting normal cellular function in humans. 相似文献