CO2激光照射对油菜种子活力指数的数学模拟

本试验采用多项式模拟方法,研究ＣＯ２激光对油菜种子活力指标的影响,分别得出了发芽种子的下胚轴长与ＣＯ２激光照射时间;发芽种子的胚根长与ＣＯ２激光照射时间;种子的发芽指数与ＣＯ２激光照射时间;萌动种子的过氧化氢酶活性与ＣＯ２激光照射时间;地上部鲜重与ＣＯ２激光照射时间;全株鲜重与ＣＯ２激光照射时间的数学模型。揭示了油菜种子活力与ＣＯ２激光照射时间的关系。     

CO2激光照射对石刁柏种子活力指标的数学模拟

本文在ＣＯ２激光对石刁柏种子活力影响的研究基础上,应用多项式回归对种子活力指标进行了数学模拟。分别得到了发芽种子的胚根长、下胚轴长、发芽率、发芽指数、活力指数、出苗率与ＣＯ２激光照射时间的数学模型。     

CO2激光辐照对酿酒酵母菌的诱变作用

应用红外ＣＯ２激光对甘蔗糖蜜工业性生产用酿酒酵母菌Ｓａｃｃｈａｒｏｍｙｃｅｓ ｃｅｒｅｖｉｓｉａｅ ＡＳ２．１１８９进行辐照处理,经酵母菌糖蜜酒精发酵试验,发现红外ＣＯ２激光对酿酒酵母菌具有诱变作用,并初步筛选到决乙醇含量有较大变化的辐照变异菌株;同时,通过对这些辐照变异菌株的乙醇脱氢酶同工酶的比较分析,进一步证实了红外ＣＯ２激光对酿酒酵母酶的诱变作用。从而为工业上利用红外ＣＯ２激光对酿酒酵母菌进     

激光对花生诱变效果的研究

Ｈｅ－ＮｅＹＡＧ和ＣＯ２激光对花生Ｌ１代幼苗期有刺激生长的作用,ＣＯ２激光对花生Ｌ１代的株高有较明显的抑制作用,ＣＯ２,Ｈｅ－Ｎｅ和ＹＡＧ激光对花生Ｌ１代植株的总果数,饱果数有一定的增多作用,且前者最明显,但Ｎ２激光对花生Ｌ１代植株的总果数,饱果数均有明显的减少作用;Ｈｅ－ＮｅＹＡＧ,Ｎ２和ＣＯ２激光均能诱发药生根尖细胞染色体畸变,且畸变率随辐照剂量的增大而上升,以上四种激光所诱发发生的变异性状是     

C02激光辐照对酿酒酵母菌的诱变作用

应用红外ＣＯ_２激光对甘蔗糖蜜工业性生产用酿酒酵母菌Ｓａｃｃｈａｒｏｍｙｃｅｓ ｃｅｒｅｖｉｓｉａｅ ＡＳ２．１１８９进行辐照处理,经酵母菌糖蜜酒精发酵试验,发现红外ＣＯ_２激光对酿酒酵母菌具有诱变作用,并初步筛选到产乙醇含量有较大变化的辐照变异菌株;同时,通过对这些辐照变异菌株的乙醇脱氢酶同工酶的比较分析,进一步证实了红外ＣＯ_２、激光对酿酒酵母菌的诱变作用．从而为工业上利用红外ＣＯ_２激光对酿酒酵母菌进行诱变育种展现新的前景。     

CO2激光辐射提高蔬菜种子活力的研究

本文总结了ＣＯ２激光辐射提高蔬菜种子活力的研究成果，适量ＣＯ２激光辐射蔬菜种子可增强种子活力，提高幼苗素质，增加产量，促进早熟，加强生物机能，改善解剖结构，提出一些需要解决的问题和对其进行的初步研究。     

CO2激光辐射黄瓜种子对种子活力影响的研究

采用功率密度为８９８ｍｗ／ｃｍ＾２的ＣＯ２激光对黄瓜子种子进行不同时间的照射处理,其结果表明,３ｓ－７ｓ均有不同程度的刺激效应,３０ｓ以上出现了不同程度的抑制作用和畸形芽,其中的９０ｓ组已达到了半致死剂量。     

CO2激光治疗慢性宫颈炎670例疗效观察

本文用ＣＯ２激光对６７０例慢性宫颈炎患者进行了治疗,经复查,治愈率９８％,有效率１００％。     

CO2激光对西瓜种子最佳辐射剂量的筛选及其数学模拟

采用功率密度为８９８ｍ ｗ ／ｃｍ ２ 的ＣＯ２ 激光对西瓜种子进行不同时间的辐射处理,筛选出了最佳刺激剂量,并应用多项式回归进行数学模拟,得到了比较理想的结论。     

用共聚焦显微镜观察ACh及ATP对豚鼠耳蜗外毛细胞Ca^2＋的调控

用激光扫描共聚焦显微镜研究了一般公认的耳蜗传出神经递质乙酰胆碱（ＡＣｈ）和三磷酸腺苷（ＡＴＰ）对豚鼠耳蜗外毛细胞（ＯＨＣｓ）胞内游离Ｃａ＾２＋浓度（Ｃａ＾２＋）的作用,ＯＨＣｓ用Ｃａ＾２＋敏感荧光染料Ｆｌｕｏ－３着色,胞内Ｃａ＾２＋的分布以细胞底部稍强。ＡＣｈ在ＯＨＣ底部引起Ｃａ＾２＋的缓慢上长并维持在一个较高水平。ＡＴＰ在整个ＯＨＣ引起一个急剧的Ｃａ＾２＋升高,升高幅度在ＯＨＣ顶部最大。随着ＡＴ     

Vulva morphogenesis involves attraction of plexin 1-expressing primordial vulva cells to semaphorin 1a sequentially expressed at the vulva midline

Vulva development in C. elegans involves cell fate specification followed by a morphogenesis phase in which homologous mirror image pairs within a linear array of primordial vulva cells form a crescent shape as they move sequentially towards a midline position within the array. The homologous pairs from opposite half vulvae in fixed sequence fuse with one another at their leading tips to form ring-shaped (toroidal) cells stacked in precise alignment one atop the other. Here, we show that the semaphorin 1a SMP-1, and its plexin receptor PLX-1, are required for the movement of homologous pairs of vulva cells towards this midline position. SMP-1 is upregulated on the lumen membrane of each primordial vulva cell as it enters the forming vulva and apparently attracts the next flanking homologous PLX-1-expressing vulva cells towards the lumen surface of the ring. Consequently, a new ring-shaped cell forms immediately ventral to the previously formed ring. This smp-1- and plx-1-dependent process repeats until seven rings are stacked along the dorsoventral axis, creating a common vulva lumen. Ectopic expression of SMP-1 suggests it has an instructive role in vulva cell migration. At least two parallel acting pathways are required for vulva formation: one requires SMP-1, PLX-1 and CED-10; and another requires the MIG-2 Rac GTPase and its putative activator UNC-73.     

Vulva formation in Pristionchus pacificus relies on continuous gonadal induction

One of the best known features of vulva development in Caenorhabditis elegans is the induction of vulval precursor cells by the gonadal anchor cell. Induction is crucial for the initiation of pattern formation within the C. elegans vulva equivalence group, and it is therefore surprising to find that this aspect of vulva formation, in particular, varies greatly among nematodes. In some species which form vulvae in the posterior body region, no gonadal signal is necessary for vulva induction. In other nematodes, such as Panagrolaimus, Oscheius, and Rhabditella, vulva formation depends on two temporally distinct gonadal inductions which specify the different cell fates. Here we report our analysis of vulva induction in Pristionchus pacificus, a specieswhich has recently been used as a genetic system to analyze the evolution of vulva development. Cell ablation studies in P. pacificus show that another mode of vulva induction exists. P. pacificus vulva formation depends on a continuous gonadal induction that starts several hours after hatching and continues until the birth of the anchor cell, some 20 h later. Mutations defective in gonadal induction result in the absence of vulva differentiation, suggesting that only one signaling system is involved in the gonadal-epidermal interaction. This new mode adds further to the great variety of gonadal inductions among nematode species. Received: 25 February 1999 / Accepted: 20 April 1999     

lin-17/Frizzled and lin-18 regulate POP-1/TCF-1 localization and cell type specification during C. elegans vulval development

The Caenorhabditis elegans vulva is comprised of highly similar anterior and posterior halves that are arranged in a mirror symmetric pattern. The cell lineages that form each half of the vulva are identical, except that they occur in opposite orientations with respect to the anterior/posterior axis. We show that most vulval cell divisions produce sister cells that have asymmetric levels of POP-1 and that the asymmetry has opposite orientations in the two halves of the vulva. We demonstrate that lin-17 (Frizzled type Wnt receptor) and lin-18 (Ryk) regulate the pattern of POP-1 localization and cell type specification in the posterior half of the vulva. In the absence of lin-17 and lin-18, posterior lineages are reversed and resemble anterior lineages. These experiments suggest that Wnt signaling pathways reorient cell lineages in the posterior half of the vulva from a default orientation displayed in the anterior half of the vulva.     

Formation of <Emphasis Type="Italic">Yersinia pseudotuberculosis</Emphasis> biofilms on multiple surfaces on <Emphasis Type="Italic">Caenorhabditis elegans</Emphasis>

Summary A liquid-based assay was used to evaluate the ability of Yersinia pseudotuberculosis to form a bacterial biofilm on the nematode Caenorhabditis elegans. After 3 days of incubation in the liquid assay a biofilm was clearly visible by light microscopy on both the head and vulva region of the worms. At times, the biofilm formation on the vulva appeared to prevent the laying of eggs by the adult hermaphrodite; the eggs would later hatch inside of the worm. One possible explanation for the biofilm formation observed on the vulva may be the increased motion of the cuticle surrounding the vulva when the worm is immersed in a liquid culture. This is the first report of biofilm formation on the vulva of C. elegans.     

How does a cell anchor and invade an organ?

In multicellular organisms, most cells are confined to a particular tissue. However, some cells invade organs during normal development and in diseases (e.g., angiogenesis and cancer). Recent studies reveal a fascinating step-by-step process in which specific vulval cells induce and attract a single gonadal cell to invade an epithelial tubular organ in order to connect the uterus to the vulva in C. elegans.     

Wnt signaling induces vulva development in the nematode Pristionchus pacificus

The Caenorhabditis elegans vulva is induced by a member of the epidermal growth factor (EGF) family that is expressed in the gonadal anchor cell, representing a prime example of signaling processes in animal development. Comparative studies indicated that vulva induction has changed rapidly during evolution. However, nothing was known about the molecular mechanisms underlying these differences. By analyzing deletion mutants in five Wnt pathway genes, we show that Wnt signaling induces vulva formation in Pristionchus pacificus. A Ppa-bar-1/beta-catenin deletion is completely vulvaless. Several Wnt ligands and receptors act redundantly in vulva induction, and Ppa-egl-20/Wnt; Ppa-mom-2/Wnt; Ppa-lin-18/Ryk triple mutants are strongly vulvaless. Wnt ligands are differentially expressed in the somatic gonad, the anchor cell, and the posterior body region, respectively. In contrast, previous studies indicated that Ppa-lin-17, one of the Frizzled-type receptors, has a negative role in vulva formation. We found that mutations in Ppa-bar-1 and Ppa-egl-20 suppress the phenotype of Ppa-lin-17. Thus, an unexpected complexity of Wnt signaling is involved in vulva induction and vulva repression in P. pacificus. This study provides the first molecular identification of the inductive vulva signal in a nematode other than Caenorhabditis.     

PAR-1 is required for morphogenesis of the Caenorhabditis elegans vulva

The Caenorhabditis elegans vulva provides a simple model for the genetic analysis of pattern formation and organ morphogenesis during metazoan development. We have discovered an essential role for the polarity protein PAR-1 in the development of the vulva. Postembryonic RNA interference of PAR-1 causes a protruding vulva phenotype. We found that depleting PAR-1 during the development of the vulva has no detectable effect on fate specification or precursor proliferation, but instead seems to specifically alter morphogenesis. Using an apical junction-associated GFP marker, we discovered that PAR-1 depletion causes a failure of the two mirror-symmetric halves of the vulva to join into a single, coherent organ. The cells that normally form the ventral vulval rings fail to make contact or adhere and consequently form incomplete toroids, and dorsal rings adopt variably abnormal morphologies. We also found that PAR-1 undergoes a redistribution from apical junctions to basolateral domains during morphogenesis. Despite a known role for PAR-1 in cell polarity, we have observed no detectable differences in the distribution of various markers of epithelial cell polarity. We propose that PAR-1 activity at the cell cortex is critical for mediating cell shape changes, cell surface composition, or cell signaling during vulval morphogenesis.     

The nematode even-skipped homolog vab-7 regulates gonad and vulva position in Pristionchus pacificus

In free-living nematodes, developmental processes like the formation of the vulva, can be studied at a cellular level. Cell lineage and ablation studies have been carried out in various nematode species and multiple changes in vulval patterning have been identified. In Pristionchus pacificus, vulva formation differs from Caenorhabditis elegans with respect to several autonomous and conditional aspects of cell fate specification. To understand the molecular basis of these evolutionary changes, we have performed a genetic analysis of vulva formation in P. pacificus. Here, we describe two mutants where the vulva is shifted posteriorly, affecting which precursor cells will form vulval tissue in P. pacificus. Mutant animals show a concomitant posterior displacement of the gonadal anchor cell, indicating that the gonad and the vulva are affected in a similar way. We show that mutations in the even-skipped homolog of nematodes, vab-7, cause these posterior displacements. In addition, cell ablation studies in the vab-7 mutant indicate that the altered position of the gonad not only changes the cell fate pattern but also the developmental competence of vulval precursor cells. Investigation of Cel-vab-7 mutant animals showed a similar but weaker vulva defective phenotype to the one described for Ppa-vab-7.     

The SynMuv genes of Caenorhabditis elegans in vulval development and beyond

For a nonessential diminutive organ comprised of only 22 nuclei, the Caenorhabditis elegans vulva has done very well for itself. The status of the vulva as an overachiever is in part due to its inherent structural simplicity as well as to the intricate regulation of its induction and development. Studies over the past twenty years have shown the vulva to be a microcosm for organogenesis and a model for the integration of complex signaling pathways. Furthermore, many of these signaling molecules are themselves associated with cancer in mammals. This review focuses on what is perhaps the most intriguing and complex story to emerge from these studies thus far, the role of the Synthetic Multivulval (SynMuv) genes in controlling vulval cell-fate adoption. Recent advances have led to a greater mechanistic understanding of how these genes function during vulval development and have also identified roles for these genes in diverse developmental processes.