金嘴蝎尾蕉花部维管束系统的解剖学研究

利用石蜡切片技术对蝎尾蕉科代表植物金嘴蝎尾蕉（Heliconia rostrata Ruiz＆Pavon）的花部维管束系统进行了解剖学研究。结果表明,心皮背束在延长部的基部分裂为内外2分支,内方分支与胎座维管束汇合后进入花柱,远轴面2枚外方分支在延长部的顶部分裂为2～4束进入远轴面2枚外轮雄蕊,而近轴面1枚外方分支则进入退化结构成为其中脉;隔膜束在延长部顶部亦分裂为3～5束,最终分别进入3枚内轮雄蕊;子房壁其它维管束最终进入花被片。本研究认为金嘴蝎尾蕉花部花瓣状退化结构与另外2枚外轮雄蕊具有完全相同的维管束系统来源,应属于雄蕊成员,且支持Kress关于蝎尾蕉科是姜群的姊妹群,区别于芭蕉群其它3科的观点。     

Architecture of the VE-cadherin hexamer

Vascular endothelial-cadherin (VE-cadherin) is the major constituent of the adherens junctions of endothelial cells and plays a key role in angiogenesis and vascular permeability. The ectodomains EC1-4 of VE-cadherin are known to form hexamers in solution. To examine the mechanism of homotypic association of VE-cadherin, we have made a 3D reconstruction of the EC1-4 hexamer using electron microscopy and produced a homology model based on the known structure of C-cadherin EC1-5. The hexamer consists of a trimer of dimers with each N-terminal EC1 module making an antiparallel dimeric contact, and the EC4 modules forming extensive trimeric interactions. Each EC1-4 molecule makes a helical curve allowing some torsional flexibility to the edifice. While there is no direct evidence for the existence of hexamers of cadherin at adherens junctions, the model that we have produced provides indirect evidence since it can be used to explain some of the disparate results for adherens junctions. It is in accord with the X-ray and electron microscopy results, which demonstrate that the EC1 dimer is central to homotypic cadherin interaction. It provides an explanation for the force measurements of the interaction between opposing cadherin layers, which have previously been interpreted as resulting from three different interdigitating interactions. It is in accord with observations of native junctions by cryo-electron microscopy. The fact that this hexameric model of VE-cadherin can be used to explain more of the existing data on adherens junctions than any other model alone argues in favour of the existence of the hexamer at the adherens junction. In the context of the cell-cell junction these cis-trimers close to the membrane, and trans-dimers from opposing membranes, would increase the avidity of the bond.     

Amyotrophic lateral sclerosis: all roads lead to Rome

Amyotrophic lateral sclerosis (ALS) is the most frequent adult-onset motor neuron disease characterized by degeneration of upper and lower motor neurons, generalized weakness and muscle atrophy. Most cases of ALS appear sporadically but some forms of the disease result from mutations in the gene encoding the antioxidant enzyme Cu/Zn superoxide dismutase (SOD1). Several other mutated genes have also been found to predispose to ALS including, among others, one that encodes the regulator of axonal retrograde transport dynactin. As all roads lead to the proverbial Rome, we discuss here how distinct molecular pathways may converge to the same final result that is motor neuron death. We critically review the basic research on SOD1-linked ALS to propose a pioneering model of a 'systemic' form of the disease, causally involving multiple cell types, either neuronal or non-neuronal. Contrasting this, we also postulate that other neuron-specific defects, as those triggered by dynactin dysfunction, may account for a primary motor neuron disease that would represent 'pure' neuronal forms of ALS. Identifying different disease subtypes is an unavoidable step toward the understanding of the physiopathology of ALS and will hopefully help to design specific treatments for each subset of patients.     

Transplantation of adipose stromal cells, but not mature adipocytes, augments ischemia-induced angiogenesis

Therapeutic angiogenesis has emerged as a promising therapy to treat patients with ischemic diseases. Transplantation of bone marrow cells (BMCs) is reported to augment collateral development in ischemic organs either by differentiating into vascular cells or by secreting angiogenic cytokines. Recent evidence suggests that adipose tissues secrete a number of humoral factors and contain pluripotent stem cells. Here, we evaluated the therapeutic potential of adipose tissue-derived cells to promote angiogenesis in a mouse model of hind limb ischemia. Stromal vascular fraction cells (SVFs) were isolated from inguinal adipose tissue. Endothelial-like cells or smooth muscle-like cells could be obtained from the culture of SVFs in the presence of growth factors. Freshly isolated BMCs, SVFs, or mature adipocytes were transplanted into the ischemic hind limb of mice. SVFs significantly augmented collateral development as determined by the restoration of blood perfusion and capillary density of the ischemic muscle. Angiogenic effects of SVFs were as potent as those of BMCs. Mature adipocytes showed no proangiogenic effects. The ischemic muscle contained endothelial cells or smooth muscle cells that derived from the transplanted SVFs and BMCs. These results suggest that SVFs might be used to promote angiogenesis in ischemic tissues.     

Heteroclinic orbits indicate overexploitation in predator-prey systems with a strong Allee effect

Species establishment in a model system in a homogeneous environment can be dependent not only on the parameter setting, but also on the initial conditions of the system. For instance, predator invasion into an established prey population can fail and lead to system collapse, an event referred to as overexploitation. This phenomenon occurs in models with bistability properties, such as strong Allee effects. The Allee effect then prevents easy re-establishment of the prey species. In this paper, we deal with the bifurcation analyses of two previously published predator-prey models with strong Allee effects. We expand the analyses to include not only local, but also global bifurcations. We show the existence of a point-to-point heteroclinic cycle in these models, and discuss numerical techniques for continuation in parameter space. The continuation of such a cycle in two-parameter space forms the boundary of a region in parameter space where the system collapses after predator invasion, i.e. where overexploitation occurs. We argue that the detection and continuation of global bifurcations in these models are of vital importance for the understanding of the model dynamics.     

Load application induces changes in the expression levels of Sox-9, FGFR-3 and VEGF in condylar chondrocytes

Experimental and clinical observations have proven the modulatory effects of mechanical loading on the development and maintenance of cartilage architecture. Here we examined the involvement of Sox-9, FGFR-3 and VEGF (pivotal factors controlling cartilage development and growth) in the mechano-transduction pathway of mandibular condylar cartilage by changing the dynamics of the transmitted load via changes in food hardness. To this end, condyle cartilage tissue of rats fed with hard or soft food was analyzed immunohistochemically at various time points. Our findings demonstrate that different mechanical loading conditions in condylar chondrocytes trigger differentiation-/maturation-related processes by affecting the expression levels of these factors, ultimately influencing condylar cartilage growth.     

Actions of TGF-β as tumor suppressor and pro-metastatic factor in human cancer

Transforming growth factor-β (TGF-β) is a secreted polypeptide that signals via receptor serine/threonine kinases and intracellular Smad effectors. TGF-β inhibits proliferation and induces apoptosis in various cell types, and accumulation of loss-of-function mutations in the TGF-β receptor or Smad genes classify the pathway as a tumor suppressor in humans. In addition, various oncogenic pathways directly inactivate the TGF-β receptor-Smad pathway, thus favoring tumor growth. On the other hand, all human tumors overproduce TGF-β whose autocrine and paracrine actions promote tumor cell invasiveness and metastasis. Accordingly, TGF-β induces epithelial–mesenchymal transition, a differentiation switch that is required for transitory invasiveness of carcinoma cells. Tumor-derived TGF-β acting on stromal fibroblasts remodels the tumor matrix and induces expression of mitogenic signals towards the carcinoma cells, and upon acting on endothelial cells and pericytes, TGF-β regulates angiogenesis. Finally, TGF-β suppresses proliferation and differentiation of lymphocytes including cytolytic T cells, natural killer cells and macrophages, thus preventing immune surveillance of the developing tumor. Current clinical approaches aim at establishing novel cancer drugs whose mechanisms target the TGF-β pathway. In conclusion, TGF-β signaling is intimately implicated in tumor development and contributes to all cardinal features of tumor cell biology.     

Uterine epithelial changes during placentation in the viviparous skink Eulamprus tympanum

We used scanning electron microscopy (SEM) and transmission electron microscopy (TEM) to describe the complete ontogeny of simple placentation and the development of both the yolk sac placentae and chorioallantoic placentae from nonreproductive through postparturition phases in the maternal uterine epithelium of the Australian skink, Eulamprus tympanum. We chose E. tympanum, a species with a simple, noninvasive placenta, and which we know, has little net nutrient uptake during gestation to develop hypotheses about placental function and to identify any difference between the oviparous and viviparous conditions. Placental differentiation into the chorioallantoic placenta and yolk sac placenta occurs from embryonic Stage 29; both placentae are simple structures without specialized features for materno/fetal connection. The uterine epithelial cells are not squamous as previously described by Claire Weekes, but are columnar, becoming increasingly attenuated because of the pressure of the impinging underlying capillaries as gestation progresses. When the females are nonreproductive, the luminal uterine surface is flat and the microvillous cells that contain electron-dense vesicles partly obscure the ciliated cells. As vitellogenesis progresses, the microvillous cells are less hypertrophied than in nonreproductive females. After ovulation and fertilization, there is no regional differentiation of the uterine epithelium around the circumference of the egg. The first differentiation, associated with the chorioallantoic placentae and yolk sac placentae, occurs at embryonic Stage 29 and continues through to Stage 39. As gestation proceeds, the uterine chorioallantoic placenta forms ridges, the microvillous cells become less hypertrophied, ciliated cells are less abundant, the underlying blood vessels increase in size, and the gland openings at the uterine surface are more apparent. In contrast, the yolk sac placenta has no particular folding with cells having a random orientation and where the microvillous cells remain hypertrophied throughout gestation. However, the ciliated cells become less abundant as gestation proceeds, as also seen in the chorioallantoic placenta. Secretory vesicles are visible in the uterine lumen. All placental differentiation and cell detail is lost at Stage 40, and the uterine structure has returned to the nonreproductive condition within 2 weeks. Circulating progesterone concentrations begin to rise during late vitellogenesis, peak at embryonic Stages 28-30, and decline after Stage 35 in the later stages of gestation. The coincidence between the time of oviposition and placental differentiation demonstrates a similarity during gestation in the uterus between oviparous and simple placental viviparous squamates.     

环加氧酶-2抑制剂尼美舒利通过改善内皮功能和增加NO含量对抗大鼠心肌氧化应激损伤

本文旨在研究冠状动脉内皮和NO在选择性环加氧酶2（cyclooxygenase2,COX-2）抑制剂尼美舒利（nimesulide）对抗心肌氧化损伤中的作用。离体大鼠心脏行Langendorff灌流,给予H2O2（140Bmol／L）观察心脏收缩功能。用U-46619灌流心脏,使冠状动脉预收缩后,观察冠状动脉对内皮依赖性舒张因子5-HT和内皮非依赖性舒张因子硝普钠（sodiumnitroprusside,SNP）的反应。结果显示：（1）与空白对照组（100％）相比,H202灌流20min后,左心室发展压[left ventriculardevelo pedpressure,LVDP,（54．8±4．0）％],和心室内压最大变化速率【±dp／dtmax（50．8±3．1）％和（46．2±2．9）％]明显降低。H2O2灌流前尼美舒利（5μmol/L）预处理10min,能够显著抑制H2O2引起的LVDP和μdp/dtmax下降[（79．9±2．8）％,（80．3±2．6）％和（81．4±2．6）％,P〈0．0l]。（2）与空白对照组相比,H2O2灌流后,5-HT和SNP引起内皮依赖性和内皮非依赖性血管舒张功能均明显下降;而尼美舒利预处理10min能明显对抗内皮依赖性血管舒张功能的下降[（-22．2±4．2）％vsH2O2组（-6．0±2．5）％,P〈0．0l],但对其内皮非依赖性血管舒张功能的下降没有明显作用[（-2．0±1．8）％vsH202组（-7．0±3．5）％,P〉0．05]。（3）一氧化氮合酶（nitric oxide synthase,NOS）抑制剂L-NAME能够部分取消尼美舒利预处理对H20,应激心脏心功能指标的改善作用ILVDP和±dp/dtmax分别为（60．2±2．1）％,（63．9±2．4）％和（63．1±2．9）％,P〈0．01]。同时尼美舒利预处理10min能使H202应激心肌NO含量增加[（2．63±0．40）vs（1．36±0．23）nmol／gprotein,P〈0．051,而L-NAME抑制此作用。（4）选择性COX-1抑制剂吡罗昔康（piroxicam）预处理不能抑制H202引起的LVDP和±dp/dtmax下降,但促进左心室舒张末压（1eftventricular end diastolicpressure,LVEDP）升高;吡罗昔康对H202引起的内皮依赖性和内皮非依赖性血管舒张功能下降无显著作用。以上结果提示,选择性COX-2抑制剂尼美舒利能够对抗大鼠离体心肌氧化应激损伤,其机制可能是通过改善内皮依赖性血管舒张功能和增加心肌NO含量起作用。