日本七鳃鳗胚胎发育及卵黄囊期仔鱼的异速生长

通过观察日本七鳃鳗Lampetra japonica (Martens, 1868)胚胎外部形态和内部组织结构变化, 描述受精卵从卵裂至器官形成以及仔鱼孵出的发育阶段, 采用实验生态学方法研究卵黄囊期仔鱼的异速生长模式。结果表明: 日本七鳃鳗卵子为乳白色, 呈卵圆形; 受精卵卵裂方式为全卵裂; 胚胎发育过程主要包括卵裂期、囊胚期、原肠胚期、神经胚期、头凸期、孵出前期和孵出期, 历时11—12d; 初孵仔鱼为乳白色, 全长约(3.41±0.24) mm, 体质量约为0.0006 g。日本七鳃鳗胚胎发育研究可为了解七鳃鳗胚胎发育过程, 早期脊椎动物的起源和发育进化研究提供参考。卵黄囊期内仔鱼身体各部分中, 头长和尾长均表现出快速生长, 同在7 日龄出现生长拐点, 且生长拐点后的生长速率都大于生长拐点前的生长速率; 而仔鱼体长在卵黄囊期内表现出慢速生长。在头部器官中, 吻长、鳃前长和鳃长均表现出快速生长现象, 吻长和鳃长分别在9日龄和8日龄出现生长拐点; 口笠长在3日龄时出现生长拐点, 在生长拐点前为等速生长, 而在生长拐点后表现出快速生长; 眼径和眼鳃间距则分别表现出等速生长和慢速生长。泄殖孔在卵黄囊期内未出现生长拐点, 生长速率相对于全长生长速率表现出快速生长现象。七鳃鳗卵黄囊期仔鱼的异速生长是在长期进化过程中, 适应早期生活环境和独特的生活方式而形成特有的发育机制。     

植物生长抽梢期和气候因子对株高生长影响

利用西双版纳热带植物园的热带植物物候观测资料和气候资料,通过对热带植物株高生长偏差、生长抽梢期和气候因子的分析,探讨了三者的关系。结果表明,热带植物生长抽梢期变长不一定影响株高生长,而且与株高生长偏差的关系也小于气候因子与株高生长偏差的关系。同时,热带植物生长抽梢期对气候因子和株高生长偏差之间关系的贡献很小。因此,可以认为热带植物的生长期对植被生产力的促进作用较弱。     

谈谈鱼类的补偿生长

简要介绍了鱼类的补偿生长现象,并根据补偿量的大小将鱼类的补偿生长划分为超补偿生长,完全补偿生长,部分补偿生长和不能补偿生长四类,同时根据饥饿或限食以及重喂时间的不同介绍了目前鱼类补偿生长实验设计的一般思路,最后对鱼类补偿生长在水产养殖和环境保护等方面的应用前景作了展望。     

木霉菌T25生物学特性的研究

温度对T25菌株菌丝生长和孢子产生影响显著,30℃时菌丝生长最快,25℃时产孢量最大。T25在pH值2~10范围内均可生长,pH值5~6时生长最快,pH值为6时孢子产生量最大。光照处理对菌丝生长影响显著,并且明显促进孢子产生。淀粉、蔗糖分别为菌丝生长和产孢的最佳碳源。硫酸铵和蛋白胨为菌丝生长和产孢的最佳氮源。不同维生素对菌丝生长和孢子产生的作用不同,VB1 VH、VB6对菌丝生长和产孢最有利。微量元素对菌丝生长有一定的促进作用,Ca2 有利于孢子的产生。     

广东黑石顶南亚热带常绿阔叶林树木生长研究(英文)

用测树器和年轮解析法 ,测定了广东黑石顶南亚热带常绿阔叶林的立木和幼树的径向生长和高生长。年轮解析法测得立木的年直径生长量在 0 .1～ 0 .5cm之间 ,一些立木的直径生长呈现出生长快的年份 ( 1～ 3a)和生长慢的年份 ( 1～ 3a)交替的节律。测树器测得立木 5a的年平均直径生长量为0 .0 74cm,5年期间测得有 1 7.6%的个体直径为零增长或负增长。立木的年高增长量为 1 0～ 50 cm,高生长高峰期通常在 1 0～ 30年龄。在树木生长的早期 ,高度的生长优于直径的生长 ,而在树木生长的中、后期 ,直径的生长逐渐优于高度的生长。用游标卡尺和卷尺测得幼树 (通常 1～ 3m高 )的直径和高度 5a的平均生长量分别为 0 .1 0 7cm和 4.76cm。 5a间没有幼树的直径生长为零增长或负增长 ,但约有 9%的个体的高度生长为零增长或负增长。     

3种四照花一年生播种苗生长规律初探

为揭示3种四照花的苗期生长规律,对1a生大花四照花(Cornusflorida)、香港四照花(C.hongkongensis)和东京四照花(C. hongkongensis subsp. tonkinensis)幼苗的年生长节律进行了观测分析。结果表明,根据拟合的Logistic方程生长模型(R~20.98,P 0.01),可将3种四照花苗期的苗高和地径年生长进程划分为生长初期、生长盛期、生长后期3个时期。其中,生长盛期的苗高和地径的生长量分别占全年的55.23%～59.06%和59.46%～60.71%。大花四照花的年生长积累均大于2种东亚类常绿四照花,而香港四照花和东京四照花的苗高和地径生长相似;大花四照花的生长初期和生长盛期的启动时间早于2种东亚类四照花,但持续时间最短。3种1 a生四照花的苗高和地径生长呈现出"慢-快-慢"的生长节律,符合"S"型生长曲线;且地径和苗高呈现出异速生长现象。这为四照花栽培推广、引种驯化提供了理论依据。     

玉米幼苗叶片生长部位和瞬时生长速率的测定

研究植物生长不但需要知道生长的部位,更需测定其生长速率。过去曾用“等距线条或方格”、“水平显微镜”、“生长自动记录仪”以及直接度量生长器官等方法,测定植物生长部位和生长速率。本文介绍另一种测定玉米等单子叶植物叶片生长部位及生长速率的方法。 1.叶片生长部位的测定单子叶植物     

祁连山不同植被类型的物候变化及其对气候的响应

基于1982—2006年GIMMS NDVI和2000—2014年MODIS NDVI遥感数据,利用double logistic拟合方法提取了1982—2014年祁连山区不同植被的生长季始期、生长季末期和生长季长度3个重要的物候参数,分析了不同植被物候期的时间变化趋势、空间分异特征及对气候因子的响应。结果表明:(1)祁连山区不同植被的生长季始期和生长季末期随年际变化表现出波动提前或推迟,其中沼泽植被的变化波动最大;草甸植被、灌丛植被、阔叶林植被和栽培植被生长季长度出现延长趋势;(2)祁连山区植被生长季始期集中在5月初,其中阔叶林植被生长季开始最早,荒漠植被生长季开始最晚,植被生长季末期集中在9月,栽培植被生长季结束较早,荒漠植被、沼泽植被生长季结束较晚,植被生长季长度集中在110—140 d,其中阔叶林植被、针叶林植被生长季长度较长,而荒漠植被、高山植被生长季长度较短;(3)祁连山植被物候期变化趋势的空间分布表明植被生长季始期、生长季末期主要表现为提前不明显和推迟不明显,生长季长度主要表现为缩短不明显和延长不明显;(4)物候要素与气候要素相关性表明前期温度的积累有利于植被的开始生长,但当年3月的降水量对植被生长季始期同样有重要作用,不同植被生长季末期与8月、9月温度相关性较大,而与10月、11月降水的相关性较大。     

长白山阔叶红松林3个常见树种径向生长的影响因素

为探究树木径向生长的影响因子,基于对长白山阔叶红松林25 hm²样地中3个常见树种红松、紫椴、蒙古栎连续5年的生长环监测数据,分析各树种的季节生长变化,比较树种间的生长速率差异,并分析初始径级、邻体树木竞争、土壤、地形因素等对不同树种径向生长的作用.结果表明: 3个树种径向生长的季节变化趋势一致,树木于5月末开始生长,7月是生长旺盛期,8月底生长开始减缓,于10月中下旬停止生长.3个树种的径向相对生长率存在显著差异,蒙古栎相对径向生长率显著高于红松和紫椴,该差异在小、中径级个体中表现更为显著.3个树种径向生长的主要影响因子不同,邻体树木的竞争显著抑制了红松和蒙古栎的径向生长,而紫椴的径向生长主要受初始径级、土壤和地形等因子的影响.     

侧柏幼树不同生长阶段对水分的敏感性与蒸腾效率

通过旱棚人工控水,对不同生长阶段谐变供水条件下,供水量与供水方式对侧柏幼树蒸腾耗水、水分利用效率的影响、幼树不同生长阶段对水分的敏感性等问题进行了研究。结果表明,幼树总耗水量随年均土壤供水能力和幼树各生长阶段供水模式的不同而变化。在平均有效水供给能力较低或单一阶段土壤相对含水率不超过87.84 %时,幼树蒸腾耗水量随中后期——生长盛期和生长后期供水量的增加而增大;相反,在平均有效水供给能力较高或单一阶段土壤相对含水率超过87.84 %时,幼树蒸腾耗水量则随着中前期——生长前期和生长盛期供水量的增加而增大。在年均土壤供水能力基本相同时,不同生长阶段供水量的分配对侧柏幼树蒸腾耗水有较大影响。综合分析表明,生长盛期供水对蒸腾耗水的贡献最大,生长后期次之,生长前期最小。侧柏幼树不同生长阶段对水分的敏感性,以生长盛期和生长前期最大,生长后期较低。但生长后期适度减少水分供应,具有一定的促长作用。使侧柏幼树达到最佳水分利用效率的土壤供水水平为:生长前期土壤相对含水率75 .96 % ,生长盛期73.76 % ,生长后期6 9.5 2 %。并建立了侧柏幼树的时间水分生产函数     

Down-regulation of Id-1 expression is associated with TGF beta 1-induced growth arrest in prostate epithelial cells

Transforming growth factor beta1 (TGF beta 1) plays important roles in the regulation of cell growth and differentiation in both normal and malignant prostate epithelial cells. Although certain pathways have been suggested, the mechanisms responsible for the action of TGF beta 1 are not well understood. In the present study, using a human papilloma virus 16 E6/E7 immortalized prostate epithelial cell line, HPr-1, we report that TGF beta 1 was able to suppress the expression of Id-1, a helix-loop-helix (HLH) protein, which plays important roles in the inhibition of cell differentiation and growth arrest. In addition, a decrease at both Id-1 mRNA and protein expression levels was associated with TGF beta 1-induced growth arrest and differentiation, indicating that Id-1 may be involved in TGF beta 1 signaling pathway. The fact that up-regulation of p21(WAF1), one of the downstream effectors of Id-1, was observed after exposure to TGF beta 1 further indicates the involvement of Id-1 in the TGF beta 1-induced growth arrest in HPr-1 cells. However, increased expression of p27(KIP1) was also observed in the TGF beta 1-treated cells, suggesting that in addition to down-regulation of Id-1, other factors may be involved in the TGF beta 1-induced cell growth arrest and differentiation in prostate epithelial cells. Our results provide evidence for the first time that TGF beta 1 may be one of the upstream regulators of Id-1.     

Chondrocyte integrin expression and function

The extracellular matrix (ECM) is an "information rich" environment and interactions between the chondrocyte and ECM regulate many biological processes important to cartilage homeostasis and repair including cell attachment, growth, differentiation, and survival. The integrin family of cell surface receptors appears to play a major role in mediating cell-matrix interactions that are important in regulating these processes. Chondrocytes have been found to express several members of the integrin family which can serve as receptors for fibronectin (alpha 5 beta 1), types II and VI collagen (alpha 1 beta 1, alpha 2 beta 1, alpha 10 beta 1), laminin (alpha 6 beta 1), and vitronectin and osteopontin (alpha V beta 3). Integrin expression can be regulated by growth factors including IGF-I and TGF-beta. By providing a link between the ECM and the cytoskeleton, integrins may be important transducers of mechanical stimuli. Integrin binding stimulates intracellular signaling which can affect gene expression and regulate chondrocyte function. Further studies are needed to more clearly define the role of integrins in cartilage.     

Transforming growth factor-beta bound to soluble derivatives of the beta amyloid precursor protein of Alzheimer's disease

Transforming growth factors beta (TGF beta) are multifunctional polypeptides that participate in regulation of growth, differentiation and function of many cell types. The mature TGF beta molecule is a 25 kDa protein composed of two 12.5 kDa monomers linked by disulfide bonds. Human glioblastoma cells secrete biologically active TGF beta 2. Here we report that in addition to the free form of TGF beta 2, a stable complex between a approximately 110 kDa binding protein and TGF beta 2 was isolated from glioblastoma cell supernatant. This binding protein was purified and was found to show sequence identity to part of the beta amyloid precursor protein (beta APP), to be specifically labeled by several different antisera to beta APP, and to be affinity labeled with TGF beta by crosslinking. The complex formation between TGF beta and beta APP may have important implications in regulation of biological activity of the two proteins and in delivery or clearance of TGF beta and beta APP in the brain and other compartments.     

Gastrin and interleukin-1beta stimulate growth factor secretion from cultured rabbit gastric parietal cells

The hormone gastrin stimulates proliferation of the gastric mucosa. Inflammation of the stomach is also associated with increased proliferation. The proliferative response is important in the reparative response to injury but can be deleterious by predisposing to the development of cancer. Parietal cells, but not the cells in the proliferative zone of the gastric glands, express the appropriate gastrin receptor. Parietal cells may mediate the trophic effects of gastrin by secreting other growth factors. The role of parietal cells in the proliferative responses has been examined in this study. Rabbit parietal cells were cultured with gastrin or the cytokine interleukin-1beta for 18 hours. The conditioned medium from gastrin or IL-1beta stimulated parietal cells increased proliferation of HeLa cells in an epidermal growth factor-receptor dependant manner. Gastrin and IL-1beta stimulated the secretion of heparin-binding epidermal growth factor and amphiregulin but not transforming growth factor-alpha from parietal cells. Combinations of gastrin and IL-1beta on growth factor secretion were synergistic. The protein kinase C inhibitor staurosporine abolished these stimulatory effects of gastrin and IL-1beta. Divergent effects on histamine-stimulated acid secretion were observed; 18 hours pre-treatment with gastrin enhanced acid secretion by 50% but IL-1beta inhibited acid secretion in both control and gastrin pre-treated parietal cells. The acid-secreting parietal cell plays a central role in the regulation of mucosal proliferation in gastric inflammation. Secretion of paracrine growth factors by parietal cells may be an important point of integration between the endocrine and inflammatory stimuli in determining mucosal responses to injury and inflammation.     

Effects of Transforming Growth Factor β1 on Astroglial Cells in Culture

The effects of transforming growth factor beta 1 (TGF beta 1) on DNA synthesis and functional differentiation of astroglial cells cultured in serum-free medium were investigated. TGF beta 1 diminished and delayed the peak of DNA synthesis induced by serum. TGF beta 1-treated cells were larger than control cells. This factor delayed the appearance of process-bearing cells induced by acidic fibroblast growth factor treatment and also affected the astrocyte-specific enzyme glutamine synthetase (GS), whose accumulation is under hydrocortisone (HC) control. TGF beta 1 inhibited the induction of GS activity by HC in a dose- and time-dependent manner. Moreover, pretreatment with TGF beta 1 for 4 h maintained the inhibition of GS activity for approximately 16 h after removal of this factor from culture medium. These results suggest that TGF beta 1 may be an important regulator of astrocyte growth and differentiation.     

Growth factors and beta cell replication

Recent studies have demonstrated that human islet allograft transplantation can be a successful therapeutic option in the treatment of patients with Type I diabetes. However, this impressive recent advance is accompanied by a very important constraint. There is a critical paucity of pancreatic islets or pancreatic beta cells for islet transplantation to become a large-scale therapeutic option in patients with diabetes. This has prompted many laboratories around the world to invigorate their efforts in finding ways for increasing the availability of beta cells or beta cell surrogates that potentially could be transplanted into patients with diabetes. The number of studies analyzing the mechanisms that govern beta cell proliferation and growth in physiological and pathological conditions has increased exponentially during the last decade. These studies exploring the role of growth factors, intracellular signaling molecules and cell cycle regulators constitute the substrate for future strategies aimed at expanding human beta cells in vitro and/or in vivo after transplantation. In this review, we describe the current knowledge on the effects of several beta cell growth factors that have been shown to increase beta cell proliferation and expand beta cell mass in vitro and/or in vivo and that they could be potentially deployed in an effort to increase the number of patients transplanted with islets. Furthermore, we also analyze in this review recent studies deciphering the relevance of these specific islet growth factors as physiological and pathophysiological regulators of beta cell proliferation and islet growth.     

Mutations in Elongation Factor 1β, a Guanine Nucleotide Exchange Factor, Enhance Translational Fidelity

Translation elongation factor 1beta (EF-1beta) is a member of the family of guanine nucleotide exchange factors, proteins whose activities are important for the regulation of G proteins critical to many cellular processes. EF-1beta is a highly conserved protein that catalyzes the exchange of bound GDP for GTP on EF-1alpha, a required step to ensure continued protein synthesis. In this work, we demonstrate that the highly conserved C-terminal region of Saccharomyces cerevisiae EF-1beta is sufficient for normal cell growth. This region of yeast and metazoan EF-1beta and the metazoan EF-1beta-like protein EF-1delta is highly conserved. Human EF-1beta, but not human EF-1delta, is functional in place of yeast EF-1beta, even though both EF-1beta and EF-1delta have previously been shown to have guanine nucleotide exchange activity in vitro. Based on the sequence and functional homology, mutagenesis of two C-terminal residues identical in all EF-1beta protein sequences was performed, resulting in mutants with growth defects and sensitivity to translation inhibitors. These mutants also enhance translational fidelity at nonsense codons, which correlates with a reduction in total protein synthesis. These results indicate the critical function of EF-1beta in regulating EF-1alpha activity, cell growth, translation rates, and translational fidelity.     

Functional role of beta 1 integrin-mediated signalling in the human hair follicle

Integrins are transmembrane adhesion proteins that convey critical topobiological information and exert crucial signalling functions. In skin and hair follicle biology, beta1 integrins and their ligands are of particular interest. It is not yet known whether beta1 integrins play any role in the regulation of human hair growth and the expression pattern of beta1 integrin in the human pilosebaceous unit remains ill-defined. Here, we show that pilosebaceous immunoreactivity for beta1 integrin is most prominent in the outermost layer of the outer root sheath and the surrounding connective tissue sheath of human scalp hair follicles in situ and in vitro. Sites of beta1 integrin immunoreactivity co-express fibronectin and tenascin-C. Contrary to previous reports, beta1 integrin immunoreactivity in situ was not significantly upregulated in the human bulge region. Functionally, two beta1 integrin-activating antibodies (12G10, TS2/16) and ligand-mimicking RGD peptides promoted the growth of microdissected, organ-cultured human scalp hair follicles in vitro and inhibited spontaneous hair follicle regression. This supports the concept that beta1 integrin-mediated signalling is also important in human hair growth control. The physiologically relevant organ culture assay employed here is a potential research tool for exploring whether targeted stimulation of beta1 integrin-mediated signalling is a suitable candidate for human hair loss management.     

Integrated genomics of chemotherapy resistant ovarian cancer: A role for extracellular matrix,TGFbeta and regulating microRNAs

Epithelial ovarian cancer is the sixth most common cancer in women worldwide and the most important cause of death from gynaecological cancers in the Western world.Our explorative pathway analysis on seven published gene-sets associated with platinum resistance in ovarian cancer reveals TP53 and transforming growth factor beta as key genes. Furthermore, the extracellular matrix was associated with chemotherapy resistance in ovarian cancer as well as endocrine resistance in breast cancer. Pathway analysis again revealed transforming growth factor beta as a key gene regulating extracellular matrix gene expression. A model is presented based on literature linking transforming growth factor beta, extracellular matrix, integrin signalling, epithelial to mesenchymal transition and regulating microRNAs with a (bivalent) role in chemotherapy response.