由简单芳胺合成三苯二恶嗪荧光染料

以简单芳胺为原料合成了八个三苯二恶嗪型荧光染料，测定了它们在甲苯和ＤＭＦ中的吸收光谱和荧光光谱。结果表明，随着溶剂极性增大，荧光量子产率减少，而Ｓｔｏｋｅｓ位移增大。当在３－，１０－位引入－ＯＣＨ３时，甲苯中，染料荧光量子产率为７５％。     

Tbx6-dependent Sox2 regulation determines neural or mesodermal fate in axial stem cells

The classical view of neural plate development held that it arises from the ectoderm, after its separation from the mesodermal and endodermal lineages. However, recent cell-lineage-tracing experiments indicate that the caudal neural plate and paraxial mesoderm are generated from common bipotential axial stem cells originating from the caudal lateral epiblast. Tbx6 null mutant mouse embryos which produce ectopic neural tubes at the expense of paraxial mesoderm must provide a clue to the regulatory mechanism underlying this neural versus mesodermal fate choice. Here we demonstrate that Tbx6-dependent regulation of Sox2 determines the fate of axial stem cells. In wild-type embryos, enhancer N1 of the neural primordial gene Sox2 is activated in the caudal lateral epiblast, and the cells staying in the superficial layer sustain N1 activity and activate Sox2 expression in the neural plate. In contrast, the cells destined to become mesoderm activate Tbx6 and turn off enhancer N1 before migrating into the paraxial mesoderm compartment. In Tbx6 mutant embryos, however, enhancer N1 activity persists in the paraxial mesoderm compartment, eliciting ectopic Sox2 activation and transforming the paraxial mesoderm into neural tubes. An enhancer-N1-specific deletion mutation introduced into Tbx6 mutant embryos prevented this Sox2 activation in the mesodermal compartment and subsequent development of ectopic neural tubes, indicating that Tbx6 regulates Sox2 via enhancer N1. Tbx6-dependent repression of Wnt3a in the paraxial mesodermal compartment is implicated in this regulatory process. Paraxial mesoderm-specific misexpression of a Sox2 transgene in wild-type embryos resulted in ectopic neural tube development. Thus, Tbx6 represses Sox2 by inactivating enhancer N1 to inhibit neural development, and this is an essential step for the specification of paraxial mesoderm from the axial stem cells.     

The earliest thymic progenitors for T cells possess myeloid lineage potential

There exists controversy over the nature of haematopoietic progenitors of T cells. Most T cells develop in the thymus, but the lineage potential of thymus-colonizing progenitors is unknown. One approach to resolving this question is to determine the lineage potentials of the earliest thymic progenitors (ETPs). Previous work has shown that ETPs possess T and natural killer lymphoid potentials, and rare subsets of ETPs also possess B lymphoid potential, suggesting an origin from lymphoid-restricted progenitor cells. However, whether ETPs also possess myeloid potential is unknown. Here we show that nearly all ETPs in adult mice possess both T and myeloid potential in clonal assays. The existence of progenitors possessing T and myeloid potential within the thymus is incompatible with the current dominant model of haematopoiesis, in which T cells are proposed to arise from lymphoid-. Our results indicate that alternative models for lineage commitment during haematopoiesis must be considered.     

Cell fusion-independent differentiation of neural stem cells to the endothelial lineage

Somatic stem cells have been claimed to possess an unexpectedly broad differentiation potential (referred to here as plasticity) that could be induced by exposing stem cells to the extracellular developmental signals of other lineages in mixed-cell cultures. Recently, this and other experimental evidence supporting the existence of stem-cell plasticity have been refuted because stem cells have been shown to adopt the functional features of other lineages by means of cell-fusion-mediated acquisition of lineage-specific determinants (chromosomal DNA) rather than by signal-mediated differentiation. In this study we co-cultured mouse neural stem cells (NSCs), which are committed to become neurons and glial cells, with human endothelial cells, which form the lining of blood vessels. We show that in the presence of endothelial cells six per cent of the NSC population converted to cells that did not express neuronal or glial markers, but instead showed the stable expression of multiple endothelial markers and the capacity to form capillary networks. This was surprising because NSCs and endothelial cells are believed to develop from the ectoderm and mesoderm, respectively. Experiments in which endothelial cells were killed by fixation before co-culture with live NSCs (to prevent cell fusion) and karyotyping analyses, revealed that NSCs had differentiated into endothelial-like cells independently of cell fusion. We conclude that stem-cell plasticity is a true characteristic of NSCs and that the conversion of NSCs to unanticipated cell types can be accomplished without cell fusion.     

Cell lineage analysis reveals multipotency of some avian neural crest cells

A major question in developmental biology is how precursor cells give rise to diverse sets of differentiated cell types. In most systems, it remains unclear whether the precursors can form many or all cell types (multipotent or totipotent), or only a single cell type (predetermined). The question of cell lineage is central to the neural crest because it gives rise to numerous and diverse derivatives including peripheral neurons, glial and Schwann cells, pigment cells, and cartilage. Although the sets of derivatives arising from different populations of neural crest cells have been well-documented, relatively little is known about the developmental potentials of individual neural crest cells. We have iontophoretically microinjected the vital dye, lysinated rhodamine dextran (LRD) into individual dorsal neural tube cells to mark unambiguously their descendants. Many of the resulting labelled clones consisted of multiple cell types, as judged by both their location and morphology. Cells as diverse as sensory neurons, presumptive pigment cells, ganglionic supportive cells, adrenomedullary cells and neural tube cells were found within individual clones. Our results indicate that at least some neural crest cells are multipotent before their departure from the neural tube.     

Receptors for B-cell stimulatory factor-1 expressed on cells of haematopoietic lineage

B-cell stimulatory factor-1 (BSF-1) is a T-cell product of relative molecular mass 20,000 (Mr, 20K) initially described as a cofactor required for DNA synthesis by resting mouse B cells stimulated with low concentrations of anti-IgM antibodies. It acts on resting B cells to enhance the expression of class II major histocompatibility complex (MHC) molecules, to prepare these cells to respond more promptly to subsequent stimuli, such as anti-IgM antibodies, and causes the secretion of IgG1 and IgE by B cells stimulated with lipopolysaccharide (LPS). BSF-1 has been shown to stimulate T cell lines, resting T cells and some mast cell lines. Recently, the designation interleukin-4 (IL-4) has been suggested for BSF-1. We report here the existence of high-affinity cell-surface receptors specific for BSF-1 on both B and T lymphocytes, and on cells of several other haematopoietic lineages, including mast cell, macrophage and undifferentiated haematopoietic cell lines. Resting B and T lymphocytes express receptors, which increase in number upon activation of B cells with LPS or anti-IgM, and of T cells with concanavalin A. Cross-linking of 125I-labelled-BSF-1 to its receptors creates a complex of Mr approximately 80,000.     

PTEN maintains haematopoietic stem cells and acts in lineage choice and leukaemia prevention

Haematopoietic stem cells (HSCs) must achieve a balance between quiescence and activation that fulfils immediate demands for haematopoiesis without compromising long-term stem cell maintenance, yet little is known about the molecular events governing this balance. Phosphatase and tensin homologue (PTEN) functions as a negative regulator of the phosphatidylinositol-3-OH kinase (PI(3)K)-Akt pathway, which has crucial roles in cell proliferation, survival, differentiation and migration. Here we show that inactivation of PTEN in bone marrow HSCs causes their short-term expansion, but long-term decline, primarily owing to an enhanced level of HSC activation. PTEN-deficient HSCs engraft normally in recipient mice, but have an impaired ability to sustain haematopoietic reconstitution, reflecting the dysregulation of their cell cycle and decreased retention in the bone marrow niche. Mice with PTEN-mutant bone marrow also have an increased representation of myeloid and T-lymphoid lineages and develop myeloproliferative disorder (MPD). Notably, the cell populations that expand in PTEN mutants match those that become dominant in the acute myeloid/lymphoid leukaemia that develops in the later stages of MPD. Thus, PTEN has essential roles in restricting the activation of HSCs, in lineage fate determination, and in the prevention of leukaemogenesis.     

Haemonectin, a bone marrow adhesion protein specific for cells of granulocyte lineage

There is substantial evidence that the haematopoietic microenvironment is crucial to the growth and differentiation of haematopoietic cells. This microenvironment is composed of stromal cells, soluble factors and extracellular matrix (ECM). We have shown that a complex extract of bone marrow ECM can stimulate the growth and differentiation of haematopoietic cells in vitro. Furthermore, the use of inhibitors or stimulators of ECM synthesis in long-term marrow culture affects cell proliferation. On a molecular level, however, the interactions between ECM and haematopoietic cells are not well understood. We have investigated the adhesion between specific bone marrow ECM components and haematopoietic cells, and found a protein, 'haemonectin', of relative molecular mass 60,000 in bone marrow ECM which is a lineage- and organ-specific attachment molecule for cells of granulocyte lineage. This specificity distinguishes haemonectin from previously described adhesion proteins which have a wider tissue distribution and cell type specificity.     

雌激素对缺氧/复氧心肌钙离子的影响

雌激素对心肌细胞缺氧/复氧损伤具有保护作用,但其保护机制尚未完全阐明.缺氧/复氧可引起心肌细胞损伤,其中发生钙超载是心肌损伤的一个重要因素.进行了雌激素对缺氧/复氧心肌细胞内钙离子浓度的影响研究.结果显示:心肌细胞缺氧/复氧后细胞内钙离子浓度明显升高,呈复氧时间依赖性增加.雌激素有抑制缺氧/复氧心肌细胞内钙离子浓度升高...     

Cloning of cDNA for the major DNA-binding protein of the erythroid lineage through expression in mammalian cells

Genes expressed in erythroid cells contain binding sites for a cell-specific factor believed to be an important regulator for this haematopoietic lineage. Using high-level transient expression in mammalian cells, we have identified complementary DNA encoding the murine protein. The factor, a new member of the zinc-finger family of DNA-binding proteins, is restricted to erythroid cells at the level of RNA expression and is closely homologous between mouse and man.     

Induction of a novel epidermal growth factor-secreting cell lineage by mucosal ulceration in human gastrointestinal stem cells

Epidermal growth factor, and its human homologue urogastrone (EGF/URO), are secreted by the gut-associated salivary and Brunner's glands. Recombinant EGF/URO is a powerful stimulator of cell proliferation and differentiation in the rodent and neonatal human intestine. But EGF/URO is not absorbed from the adult gut and has no action when given through the gut lumen; thus the role of secreted EGF/URO is unknown. We now report that ulceration of the epithelium anywhere in the human gastrointestinal tract induces the development of a novel cell lineage from gastrointestinal stem cells. This lineage initially appears as a bud from the base of intestinal crypts, adjacent to the ulcer, and grows locally as a tubule, ramifying to form a new small gland, and ultimately emerges onto the mucosal surface. The lineage produces neutral mucin, shows a unique lectin-binding profile and immunophenotype, is nonproliferative, and contains and secretes abundant immunoreactive EGF/URO. We propose that all gastrointestinal stem cells can produce this cell lineage after mucosal ulceration, secreting EGF/URO to stimulate cell proliferation, regeneration and ulcer healing. This cell lineage is very commonly associated with gastrointestinal mucosal ulceration, and we conclude that a principal in vivo role for EGF/URO is to stimulate ulcer healing throughout the gut through induction of this cell lineage in the adjacent mucosa.     

1997的粤东海域棕囊藻赤潮原因种18SrDNA基因分析

近年来,随着沿海城市工农业的高速发展,大量含有氮、磷等营养元素的污水排入大海,导致海水富营养化的加剧,有毒藻类赤潮分布范围及出现频率明显增加.1997年7～12月我国东南沿海水面首次发生大规模的棕囊藻类(Ｐｈａｅｏｃｙｓｔｉｓ)有毒赤潮,其持续时间长,危害大,给水产...     

骨髓间质干细胞横向分化为心肌细胞的机制和诱导因素

心血管疾病严重威胁着人类的健康，近年来，随着对干细胞多向分化潜能研究的进展，其在心血管疾病方面的应用也引起了关注，而骨髓间质干细胞（MSC）以其横向分化潜能在治疗心血管疾病方面显示了巨大潜力。不少研究已证实MSC在体内、外均可分化为心肌细胞，然而其分化为心肌细胞的机制，诱导分化的相关因素和如何定向诱导，如何提高其分化效率等均为人们所关注，本文就此作一综述。     

SM-18E及MA-18A降凝剂的合成与评价

以苯乙烯、马来酸酐、甲基丙烯酸脂为原料,合成了苯乙烯—马来酸酐-十八醇酯共聚物(SM-18E)和甲基丙烯酸十八脂——丙烯酰胺共聚物(MA-18A)。并对这两种聚合物对原油的降凝效果作了评价实验,结果表明:在添加量为 2000ppm的情况下,原油的凝固点分别下降11.5C(SM-18E)和15.5(MA-18A)。     

快速复极化电流对心肌细胞电生理特征的影响

针对增大快速复极化电流对心肌细胞动作电位、钾离子浓度及电生理特征的影响问题,沿用毕勒-路特心肌细胞数理模型,以一阶龙格-库达法进行计算,研究心肌细胞外加刺激使动作电位、钾离子浓度呈现周期性,结果更具有实际意义.研究结果表明,增大复极化电流使动作电位短期内出现震荡,钾离子电流密度初期减小,心肌细胞兴奋性、传导性、自律性降低,进而诱发心律失常.     

莎士比亚十四行诗Sonnet 18译文比较研究

在英国乃至世界十四行诗的创作中,莎士比亚十四行诗是一座高峰,有着崇高的地位。很多国内学者都尝试翻译过莎士比亚的十四行诗。本文以许渊冲先生诗歌翻译的三美原则为分析框架,从意美、音美和形美三个层面上比读和分析莎士比亚十四行诗中脍炙人口的Sonnet 18的3篇译文,说明三篇译文虽各有轩轾,但未见完美。在诗歌翻译中应将三美有机结合,在最大程度上体现诗歌的整体美。     

Haematopoietic stem cells do not transdifferentiate into cardiac myocytes in myocardial infarcts

The mammalian heart has a very limited regenerative capacity and, hence, heals by scar formation. Recent reports suggest that haematopoietic stem cells can transdifferentiate into unexpected phenotypes such as skeletal muscle, hepatocytes, epithelial cells, neurons, endothelial cells and cardiomyocytes, in response to tissue injury or placement in a new environment. Furthermore, transplanted human hearts contain myocytes derived from extra-cardiac progenitor cells, which may have originated from bone marrow. Although most studies suggest that transdifferentiation is extremely rare under physiological conditions, extensive regeneration of myocardial infarcts was reported recently after direct stem cell injection, prompting several clinical trials. Here, we used both cardiomyocyte-restricted and ubiquitously expressed reporter transgenes to track the fate of haematopoietic stem cells after 145 transplants into normal and injured adult mouse hearts. No transdifferentiation into cardiomyocytes was detectable when using these genetic techniques to follow cell fate, and stem-cell-engrafted hearts showed no overt increase in cardiomyocytes compared to sham-engrafted hearts. These results indicate that haematopoietic stem cells do not readily acquire a cardiac phenotype, and raise a cautionary note for clinical studies of infarct repair.