Functions of VEGF in female reproductive system

As a homodimeric glycoprotein,vascular endothelial growth factor(VEGF)is a highly specific mitogen of vascular endothelial cells.It can induce proliferation and migration,and inhibit apoptosis of endothelial cell.VEGF is involved in many processes in the female reproductive system,such as ovulation,periodical changes of endometrium,embryo implantation and development,VEGF plays important roles in some reproductive diseases,including preeclampsia and fetal hypoevolutism in uterus.Based on our studies on angiogenesis and its relevant factors in the female reproductive system these years,the functions of VEGF in female reproductive system are reviewed,and the research prospect and application of VEGF are also discussed.     

Nitric oxide as an inhibitory non-adrenergic non-cholinergic neurotransmitter

Inhibitory non-adrenergic non-cholinergic (NANC) nerves are thought to be important in the autonomic innervation of the gastrointestinal tract and other organ systems. The nature of their neurotransmitter is still debated. Speculation that nitric oxide (NO), formed from L-arginine in neuronal structures and other cells, could act as a neurotransmitter, is not yet supported by demonstration of its release upon nerve stimulation. Using a superfusion bioassay, we report the release of a vasorelaxant factor upon stimulation of the NANC nerves in the canine ileocolonic junction. Several pieces of evidence, including the selectivity of the bioassay tissues, chemical instability, inactivation by superoxide anion and haemoglobin, inhibition by NG-nitro-L-arginine (L-NNA) and potentiation by L-arginine all indicated that NO accounted for the biological activity of this transferable NANC factor.     

Nitric oxide damages neuronal mitochondria and induces apoptosis in neurons

The cytotoxic effect of nitric oxide on primarily cultured rat cerebellar granule cells was studied, and the mechanisms were discussed. The results showed that nitric oxide donor S-nitroso-N-acetyl-penicillamine (SNAP; 500 μmol/L) could induce apoptosis in immature cultures of cerebellar granule cells. Flow cytometry and HPLC analyses revealed that after treatment with SNAP, the mitochondrial transmembrane potential and the cellular ATP content decreased significantly. Nitric oxide scavenger hemoglobin could effectively prevent the neuronal mitochondria from dysfunction and attenuate apoptosis. The results suggested that nitric oxide activated the apoptotic program by inhibiting the activity of mitochondrial respiratory chain and thus decreasing the cellular ATP content.     

Nitric oxide regulates the heart by spatial confinement of nitric oxide synthase isoforms

Subcellular localization of nitric oxide (NO) synthases with effector molecules is an important regulatory mechanism for NO signalling. In the heart, NO inhibits L-type Ca2+ channels but stimulates sarcoplasmic reticulum (SR) Ca2+ release, leading to variable effects on myocardial contractility. Here we show that spatial confinement of specific NO synthase isoforms regulates this process. Endothelial NO synthase (NOS3) localizes to caveolae, where compartmentalization with beta-adrenergic receptors and L-type Ca2+ channels allows NO to inhibit beta-adrenergic-induced inotropy. Neuronal NO synthase (NOS1), however, is targeted to cardiac SR. NO stimulation of SR Ca2+ release via the ryanodine receptor (RyR) in vitro, suggests that NOS1 has an opposite, facilitative effect on contractility. We demonstrate that NOS1-deficient mice have suppressed inotropic response, whereas NOS3-deficient mice have enhanced contractility, owing to corresponding changes in SR Ca2+ release. Both NOS1-/- and NOS3-/- mice develop age-related hypertrophy, although only NOS3-/- mice are hypertensive. NOS1/3-/- double knockout mice have suppressed beta-adrenergic responses and an additive phenotype of marked ventricular remodelling. Thus, NOS1 and NOS3 mediate independent, and in some cases opposite, effects on cardiac structure and function.     

青海沙蜥雌性生殖对策及进化

青海沙蜥是分布于青藏高原的卵胎生蜥蜴 ,雌性性成熟的最小 SVL是 5 0 .0 mm.窝卵数 1～ 5枚 ,平均 2 .74± 0 .86枚 (n=2 3) ,常见窝卵数 2～ 3枚 ,窝卵数随 SVL的增加而明显增加 (r=0 .70 30 ,P<0 .0 0 2 ) .单卵干重 0 .10～ 0 .2 0 g,平均 0 .14± 0 .0 0 5 g,随窝卵数的增加而显著变轻 (r=- 0 .70 77,P<0 .0 0 2 ) .窝卵干重 0 .2 0～ 0 .5 5 g,平均 0 .38± 0 .0 0 7g,随窝卵数和 SVL的增加而增加 (r=0 .8730 ,P<0 .0 0 1;r=0 .8776,P<0 .0 0 1) .与其卵生的近缘种相比 ,青海沙蜥雌性发育缓慢 ,性成熟较晚 ,年产单窝和较多窝卵数 .其生殖对策及进化是高寒环境选择的结果 .     

Nitric oxide produced by cumulus cells stimulates maturation of mouse oocytes

In recent years, embryo engineering concerning animal cloning, animal transgene and bioreactor technique has been developed rapidly. Since the operation of each of these techniques needs matured mammalian oocytes, the demand for highly qualified oocytes is expanding. On the other hand, various factors existing in follicle might be involved in oocyte meiotic maturation, and the process involved is extremely complex and inadequately defined. As a result, the mechanism of oocyte maturation regula…     

Nitric oxide produced by cumulus cells stimulates maturation of mouse oocytes

The effect of sodium nitroprusside (SNP), a donor of nitric oxide, on meiotic maturation of mouse oocytes was studied by injecting N^w-nitro-L-arginine methyl ester (L-NAME) intra-peritoneal (ip), a nitric oxide synthase inhibitor, or culturing oocytes in the medium supplemented with L-NAME or hypoxanthine (HX) to arrest the spontaneous oocyte maturation in vitro. The results showed that the inhibitory effect of L-NAME by injecting 10 mg/kg ip on extrusion of the first polar body only could be reversed by injecting 2.5 mg/kg SNP with L-NAME simultaneously (P < 0.05). Half an hour later ten mice died when given 10 mg/kg SNP ip. The treatment of some concentrations of SNP (10^–7, 10^–6, 10^–5mol/L) significantly stimulated meiotic maturation to metaphase Ⅱ stages in cumulus enclosed oocytes in the presence of HX. However, other concentrations of SNP (10^–8, 10^–4, 10^–3 mol/L) had no effect on HX-arrested oocyte meiotic maturation. The optimal concentration of SNP on CEOs had no effect on DOs. The dose of 10^–3 mol/LL-NAME demonstrated a significant suppression in formation of PB₁, but not in GVBD. This inhibition was reversed by the addition of SNP. These results indicated that the physiological levels of NO produced by cumulus cells could stimulate meiotic maturation of mouse oocytes both in vivo and in vitro.     

Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor

Endothelium-derived relaxing factor (EDRF) is a labile humoral agent which mediates the action of some vasodilators. Nitrovasodilators, which may act by releasing nitric oxide (NO), mimic the effect of EDRF and it has recently been suggested by Furchgott that EDRF may be NO. We have examined this suggestion by studying the release of EDRF and NO from endothelial cells in culture. No was determined as the chemiluminescent product of its reaction with ozone. The biological activity of EDRF and of NO was measured by bioassay. The relaxation of the bioassay tissues induced by EDRF was indistinguishable from that induced by NO. Both substances were equally unstable. Bradykinin caused concentration-dependent release of NO from the cells in amounts sufficient to account for the biological activity of EDRF. The relaxations induced by EDRF and NO were inhibited by haemoglobin and enhanced by superoxide dismutase to a similar degree. Thus NO released from endothelial cells is indistinguishable from EDRF in terms of biological activity, stability, and susceptibility to an inhibitor and to a potentiator. We suggest that EDRF and NO are identical.     

Nitric oxide release from a single cell measured in situ by a porphyrinic-based microsensor.

Nitric oxide is an important bioregulatory molecule, being responsible, for example, for activity of endothelium-derived relaxing factor (EDRF). Acute hypertension, diabetes, ischaemia and atherosclerosis are associated with abnormalities of EDRF. Nitric oxide is thought to be a retrograde messenger in the central nervous system. The technology is not yet available for rapid detection of NO released by a single cell in the presence of oxygen and/or nitrite, so the release, distribution and reactivity of endogenous NO in biological systems cannot be analysed. Here we describe a porphyrinic microsensor that we have developed and applied to monitoring NO release in a microsystem. We selectively measured in situ the NO released from a single cell with a response time of less than 10 ms. The microsensor consists of p-type semiconducting polymeric porphyrin and a cationic exchanger (Nafion) deposited on a thermally sharpened carbon fibre with a tip diameter of approximately 0.5 microns. The microsensor, which can be operated in either the amperometric or voltammetric mode, is characterized by a linear response up to 300 microM and a detection limit of 10 nM. Nitric oxide at the level of 10(-20) mols can be detected in a single cell.     

Nitric oxide involved in signal transduction of Jasmonic acid-induced stomatal closure of Vicia faba L.

Nitric oxide (NO) and Jasmonic acid (JA) are two key signaling molecules involved in many and diverse biological pathways in plants. Growing evidence suggested that NO signaling interacts with JA signaling. In this work, Our experiment showed that NO exists in guard cell of Vicia faba L., and NO is involved in signal transduction of JAinduced stomata closuring: ( i ) JA enhances NO synthesis in guard cell; ( ii ) both JA and NO induced stomatal closure, and had dose response to their effects; ( iU ) there are synergetic correlation between JA and lower NO concentration in regulation of stomatal movement; (iV) JA-induced stomatal closure was largely prevented by 2-phenyl-4,4,5,5-tetramethylimidazoline-l-oxyl-3-oxide (PTIO), a specific NO scavenger. An inhibitor of NO synthase (NOS) in mammalian cells, N^G-nitro-L-Arg-methyl eater (L-NAME) also inhibits plant NOS, repressing JA-induced NO generation and JA-induced stomatal closure. We presumed that NO mainly comes from NOS after JA treatment.     

静脉注射海洛因对一氧化氮及红细胞免疫功能的影响

目的 :探讨静脉注脉射海洛因者血中一氧化氮、一氧化氮合酶与红细胞免疫功能变化的关系。方法 :检测静脉注射海洛因者血中一氧化氮、一氧化氮合酶及红细胞 C3b受体活性等水平。结果 :静脉注射海洛因者血中一氧化氮及一氧化氮合酶的含量显著高于对照组 ,治疗组与非治疗组亦存在显著性差异 ,红细胞C3b受体活性明显下降且与一氧化氮含量呈负相关 ,治疗组一氧化氮及红细胞 C3b受体活性等指标有所恢复。结论 :静脉注射海洛因影响血中一氧化氮及一氧化氮合酶的含量 ,高浓度的一氧化氮 ,可能是红细胞免疫功能低下的重要原因之一 ,戒毒有望恢复其红细胞免疫功能。     

湖南平江棘胸蛙两性异形和雌性个体生育力

测定了湖南平江棘胸蛙成体的体长、体质量、头长、头宽、前肢长、后肢长等形态指标以及雌体的怀卵数量．结果表明：棘胸蛙雄体体长和体质量显著大于雌体．以体长为协变量的多元方差分析表明,雌雄两性在局部形态上不存在显著差异．各局部形态特征指标与体长呈正相关,它们随体长的增长速率在雌雄间无显著差异．棘胸蛙雌体怀卵量与体长和体质量皆成正相关关系,表明棘胸蛙通过增加个体的大小增加繁殖输出．     

Nitric oxide suppresses stomatal opening by inhibiting inward-rectifying K_(in)~ channels in Arabidopsis guard cells

We explore nitric oxide (NO) effect on K in channels in Arabidopsis guard cells. We observed NO inhib- ited K in currents when Ca2 chelator EGTA (Ethylene glycol-bis(2-aminoethylether)-N,N,N′,N′-tetraacetic acid) was not added in the pipette solution; K in currents were not sensitive to NO when cytosolic Ca2 was chelated by EGTA. NO inhibited the Arabidopsis stomatal opening, but when EGTA was added in the bath solution, inhibition effect of NO on stomatal opening vanished. Thus, it implies that NO ele- vates cytosolic Ca2 by activating plasma membrane Ca2 channels firstly, then inactivates K in chan- nels, resulting in stomatal opening suppressed subsequently.     

ZnO微粉在水体系中的分散性能

以质量分数为10%的ZnO水悬浮液为研究对象,采用机械搅拌与分散剂分散相结合的方法,以重力沉降法为表征手段,研究不同工艺参数对ZnO微粉分散效果的影响,并初步探讨了作用机理.实验结果表明:当分散时间为1h,分散速度3000r/min,pH为11时均能得到较好的分散效果.对比3种不同类型的分散剂发现,加入质量分数为0.1%的阴离子表面活性剂十二烷基苯磺酸钠(SDBS)时,悬浮液的稳定性最佳.通过激光粒度仪分析得出,较未分散的ZnO微粉,颗粒的平均粒径从16.191μm降低到0.311μm,颗粒尺寸较小,团聚现象得到明显的改善.     

Nitric oxide:A potential key point of the signaling network leading to plant secondary metabolite biosynthesis

The endogenous signaling network of plants plays important roles in mediating the exogenous factor-induced biosynthesis of secondary metabolites. Nitric oxide (NO) has emerged as a key signaling molecule in plants recently. Numerous studies demonstrated that the main signaling molecules such as salicylic acid (SA), jasmonic acid (JA), reactive oxygen species (ROS), and NO were not only involved in regulating plant secondary metabolite biosynthesis but also interacted to form a complex signaling network by mutual inhibition and/or synergy. The recent progress in the signal network of plant secondary metabolite biosynthesis has been discussed in this paper. Furthermore, we propose a hypothetical model to show that NO might act as a potential molecular switch in the signaling network leading to plant secondary metabolite biosynthesis.