文献翻译

中国的利率市场化

Tarhan Feyzio?lu, Nathan Porter, and El?d Takáts*著作

奈杰尔·乔克授权

20xx年x月

摘要

本作不代表IMF的观点。表示该工作文件中的观点是作者的,并不一定代表IMF或IMF的政策。工作论文描述的研究由作者的完成,公布并征求意见和进一步讨论。 中国利率市场自由化对中介和资本成本的影响有多大?虽然贷款利率经常调整但在中国最具约束力的利率管制是对存款利率上限的管制。通过案例研究和基于模型的模拟,我们发现,自由化可能会导致更高的利率,抑制投资边际效用,提高中介和货币政策传导的有效性,提高服务部门的金融准入水平。这可能会连续的发生。国际经验表明,然而,实现这些好处不需要不必要的不稳定手段,只需要严谨的监督,治理,和货币政策,以及灵活的政策工具。

JEL分类编号:D43,E43,E58,G14,G18。

关键词:利率自由化,金融管制的解除,利率市场化,中国

一、引言

利率自由化可以提供很多好处。通过允许资本和风险定价更自由化,改善投资的配置效率。 较大份额的仲裁会更有效也更好地评估银行承担的风险。更多的信用也会填补先前的不足。 金融产品的范围应扩大,让企业和集团更好地管理风险,并为他们提供多元化的投资组合的机会。然而,如果试图过早进行自由化,可能使金融部门的脆弱性被暴露,抑制仲裁和创造经济波动。在本文中,我们问什么影响利率自由化,很可能是银行系统更宽广的金融自由化的核心部分。中国已经在开放金融市场取得了实质性的进展,特别是它的利率。然而经过多年的改革,仍然存在银行贷款利率的下限和存款利率的上限。特别是似乎被绑定了的存款利率上限,存款利率一直聚集在他们的基准,而实际存款利率平均为零。利率管制严重扭曲了中国经济。首先,家庭是不适当地补偿他们的储蓄,他们的财政收入占总收入的份额仍然是世界上最低的。其次,大量的行政决定的利率提供小的激励银行更加高效的完善仲裁和风险定价。第三,信贷约束将限制信贷增长(因为利率为函数)创建一个银行渠道资金和人脉广泛的大型企业密切相关,而不是中小型企业和家庭的环境。第四,缺乏市场化的利率抢劫了中国人民银行宏观经济和流动性状况的重要信息。我们通过两个不同的方法来探究改革可能带来的影响。首先,我们建立并校准的银行系统的寡头垄断模型(第II部分)。利用这个模型,我们研究了解除利率管制可能产生的影响(第三)。类似的基于模型的方法已被应用到其他市场解除管制的研究(见布什内尔,曼苏尔,和萨拉维亚,20xx;和kopsangas萨沃莱恩,20xx,电力改革的例子)。模型模拟表明,自由化

产生了在一个更高的资本成本,较低的贷款额,和更有效的货币政策。所有这一切的发生都很可能不损害银行业的稳健运行,并且确实提高了系统的整体效率。特别是规模较小的银行,从自由化中获益。通过开放更深层次的竞争渠道,小银行能够吸引到更多的存款,并扩展其业务。大银行随着资金成本上升而缩减存款。自由存款利率也提高了对给定目标银行同业存款利率和贷款利率的变化,以及对仲裁活动的影响。银行系统在面对自由化之后更大的竞争时仍保持稳健尽管有着长期的存款利差。我们的第二个方法讨论了一系列的案例研究,关于中国能从其他国家利率市场化经验中吸取到的经验(第四部分)。其他国家改革的经验强调改革成功了一些先决条件,包括宏观经济的稳定,良好的银行治理和监督,以及面对改革后面临着国度需求所要做出适当的货币政策。当监督管理结合的较少时,自由化可能会更容易,而且改革后私营部门的信贷需求不太可能大幅度震荡。这些情况似乎更容易在中国发生。尽管如此,银行监管与货币政策需要保持警惕,特别是在自由化的早期阶段。由于堆存借款控制的丧失,中国人民银行不得不更多的依赖间接的调整货币政策手段。

二.中国银行业的模型部分 在这一节中我们建立了一个模型来了解中国银行业的主要特点。这个模型允许银行在存款和贷款方面有着不同的规模,它还允许银行经营和规模报酬增加和减少而有不同的盈利水平。这些假设是由银行间的自由竞争组成的。特别是我们将银行模拟成寡头垄断,在这个模型中,每个银行选择贷款和存款的活动中的方式类似于古诺竞争的产业组织常用的描述(见Freixas和Rochet,20xx,一个更广泛的处理银行业模型)。

A. 基线寡头模型 我们假设有n个银行,并且每个银行的贷款(Li)与存款(Di)数额都是由我规定的。与存款银行必须要有一定的储备金不同,这些银行有着遵从供给曲线和需求曲线的贷款和存款,并与存贷款的利率关系密切。 对存款和贷款需求曲线总供给曲线表示为RD

(D)和RL(L)

 

第二篇:文献翻译

Monosodium glutamate-induced damage in liver and kidney:a morphological and biochemical approach 在肝和肾脏中的感应谷氨酸钠的损坏:一个形态学和

生物化学的方法

Abstract

It has been demonstrated that high concentrations of monosodium glutamate in the central nervous system induce neuronal necrosis and damage in retina and circumventricular organs. In this model, the monosodium glutamate is used to induce an epileptic state; one that requires highly concentrated doses. The purpose of this study was to evaluate the toxic effects of the monosodium glutamate in liver and kidney after an intra-peritoneal injection. For the experiment, we used 192 Wistar rats to carry out the following assessments: a) the quantification of the enzymes alanine aminotransferase and aspartate aminotransferase, b) the quantification of the lipid peroxidition products and c) the morphological evaluation of the liver and kidney. During the experiment, all of these assessments were carried out at 0, 15, 30 and 45 min after the intraperitoneal injection. In the rats that received monosodium glutamate, we observed increments in the concentration of alanine aminotransferase and aspartate aminotransferase at 30 and 45 min. Also, an increment of the lipid preoxidition products, in kidney, was exhibited at 15, 30 and 45 min while in liver it was observed at 30 and 45 min. Degenerative changes were observed (edema-degeneration-necrosis) at 15, 30 and 45 min.

摘要

它已经被证明,中枢神经系统在高浓度的谷氨酸钠环境下引起视网膜神经细胞坏死和心室周围的器官损害。在这种模式下,谷氨酸钠是被用来诱发一个需要高度集中的剂量的癫痫状态。这研究的目的将评估一个腹膜内注入谷氨酸钠后的

肝和肾脏中的毒性效应。在实验中,我们用192只大鼠进行以下评估:a)定量化的谷丙转氨酶和天冬氨酸转氨酶。b)对脂质过氧化产物的定量和c)肝脏和肾脏的形态学评价。

在实验过程中,所有这些评估在腹腔注射后的第0,15,30,45分钟时进行。在大鼠接受味精,我们观察到在30和45分钟的谷丙转氨酶和天冬氨酸转氨酶的浓度在曾加。此外,在肾脏中,脂质过氧化产物的增加在15,30和45分钟被发现,而在肝脏中只有30和45分钟才能观察出来。变性的变化(水肿-退化-坏死)在第 15, 30 和第 45 分钟被观察到了。

Introduction

L-glutamate is an excitatory neurotransmitter in the central nervous system (CNS) of mammals. Glutamate is present in high levels in the brain and select groups of neurons. The endogenous L-glutamate, as the derived L-glutamate of exogenous precursors, is liberated in a Ca2+-dependent way after a depolarizing stimulus in the CNS.

Early studies in the 70’s, demonstrated that the administration of high concentrations of glutamate and other excitatory amino acids to the nervous system, produced degeneration and neuronal death in certain cerebral regions and that these effects are related to the excitotoxicity or neuronal damage due to excessive neuronal excitation through a specific on-activation of their ionotropic receptors.

Two different groups of receptors, ionotropic and metabotropic, have been described for glutamate in the CNS. The ionotropic receptors are those that include; the N-methyl-D-aspartate (NMDA) type, the non-NMDA, the kainic receptor (KA) and the propionic alfa-amino-3-hydroxy-5-methyl-4-isoxasol(AMPA). The metabotropic receptors are present in the presynaptic membrane and do not form ion channels; they are associated with G proteins and respond to the stimulus of second intracellular messengers.

The neurotoxicity that is induced by an on-activation of these glutamatergic receptors has been associated with diverse neurodegenerative diseases, as well as the

excitotoxicity by nutritious ingestion of glutamate in the form of monosodic salts when consumed in high concentrations. It has also been demonstrated that the administration of monosodium glutamate(MSG) to immature animals induces destruction in certain regions of the brain that lack a blood–brain barrier, such as the arcuatus nucleus of the hypothalamus that is involved in the regulation of neuroendocrine functions. However, these demonstrations have ignored the effects of the systemic administration of MSG that can develop high concentrations in organs such as liver and kidney; even when the presence of glutamatergicreceptors has been demonstrated outside the CNS. These sub-types of receptors have been observed as the NMDA-R1, GluR 2/3 and mGluR 2/3 in liver, kidney,lungs, spleen and testicles.

前言

L-氨酸盐是在哺乳动物的中枢神经系统 (CNS)中的一个有刺激性的神经传递素。谷氨酸在脑中和选择神经元组中是高水平的存在。内源性L -谷氨酸,作为派生L-谷氨酸的外源前体是一种钙离子依赖性的方式解放之后,在中枢神经系统中去极化刺激。

在xx年代早期的研究中,我们证明了施用高浓度的谷氨酸和其他兴奋性氨基酸的神经系统会产生变性和在某些脑区的神经细胞死亡,而这些影响都与兴奋性中毒神经元由于过多神经元的激发在这些亲离子受体一个特有的命令执行期间的受损有关

两个不同群体的受体,离子型和代谢型,被描述为在中枢神经系统中谷氨酸。离子型受体的是那些N-甲基- D-天冬氨酸(NMDA)型,非NMDA受体,红藻受体(KA)和丙酸α-氨基- 3 -羟基- 5 -甲基- 4 - isoxasol(AMPA).代谢型受体在突触前膜目前并没有形成离子通道,它们都与G蛋白和回应第二细胞内的信使的刺激有关。

一个被谷氨酸受体的激活引导的神经毒性与不同的神经退化性疾病有关,以及营养的摄取谷氨酸的兴奋毒性以monosodic盐形式在高浓度下被消耗。它也已

经被证明,对味精(MSG)的处理诱导未成熟动物的大脑某些区域的破坏,缺乏血脑屏障,像是如丘脑弓状核的是在参与调节神经内分泌功能。然而,这些示范已经忽略能在像是肝和肾脏等器官中高浓度的味精的被吸收的效应,甚至当谷氨酸受体的存在被表明是中枢神经系统外。这些受体亚型一直被视为对NMDA- R1的,GluR2 / 3的和代谢型谷氨酸受体2 / 3在肝,肾,肺,脾和睾丸中。 Discussion

MSG, a dose of 4 mg/g of body weight administered by intra-peritoneal injection to rats, is toxic for the liver and the kidney.

In this study,starting from 15 min post injection, we ob-served high levels of ALAT and ASAT (Fig. 1a, b), which indicate that the serum concentration of these enzymes fluctuates with the hepatic damage. The localization of ALAT and ASAT in the hepatocyte is cytoplasmatic; the MSG cytotoxic effect induced tissue damage and enzyme release increasing their serum levels.

The circulating MSG was dissociated in sodium (Na+) and L-glutamate. The L-glutamate crosses the mesothelial peritoneal cells and arrives at the bloodstream by means of a transport system using ATP. A part of the L-glutamate in the cell conjugates,in order to be eliminated, and another part is transformed into glutamine. When this occurs, the cells try to repair some of the damages by using enzymes that are present in the smooth endoplasmic reticulum but the cell is not able to completely remove the excess glutamine. Probably, for this reason, the liver (15 min) presented cloudy swelling (turbid swelling) at 30 min. It is possible to observe vesicular degeneration and necrosis at 45 min.

When the L-glutamate arrives in high concentrations through the renal artery,the kidney tries to excrete it. The renal corpuscle receives the L-glutamate through the afferent arteriole, it is absorbed, filtrated, and crosses the membrane damaging the cell. The convoluted proximal tubules were more susceptible to damage in comparison to the distal convoluted tubules.The kidney at 15, and 30 min exhibited edema; hydropic degeneration and necrosis were observed at 45 min.

Glutamate, a major excitatory amino acid neurotransmitter is also an endogenous

excitotoxin. The effects of the glutamate excitotoxicity in different brain regions, and lipid peroxidation are well documented.

In this study, the increase of lipid peroxidation products(MDA and 4-OH alkenals) was the response of the liver and kidney damage. At the same times, there were observed increases in malonaldehyde and 4-OH alkenals as well as ALAT and ASAT enzymes. The morphology of the damage shows a correlation between the progressive damage and the lipid peroxidation products, especially during the 30 and 45 min after glutamate administration. In liver the steatosis and necrosis were observed with high levels of malonaldehyde and 4-OH alkenals. In kidney, very similar responses were exhibited with hydropic degeneration and necrosis. All of these data could be explained by the excitotoxic role of the glutamate.

Finally, relatively little attention has been paid to functional expression of glutamate signaling molecules in peripheral tissues.Evidence is emerging for a role of glutamate as an extra-cellular signal mediator in several organs and systems, in addition to an excitatory amino acid neurotransmitter role in the CNS .

The results of this study provide strong motivation to investigate the systemic effects of the MSG. It is clear that this model induced neuroexcitotoxic damage, as well as exhibiting a strong and diffuse peripheral damage, probably in all the organs and systems.

结果讨论

味精,以每4mg/g体重的剂量对大鼠体腹腔注射给药,对肝脏和肾脏是有毒害作用的。

在这项研究中,注射后15分钟开始,我们观察到高水平ALAT和ASAT(图1a,b)项,这表明酶的血清浓度的波动伴随着肝脏的损害。ALAT和ASAT在肝细胞中的定位是细胞质多角体病毒;味精的细胞毒作用是诱导组织损伤和酶的释放,以提高他们的血清水平。

味精是分离的循环中钠(Na +)和L -谷氨酸。在L -谷氨酸穿过间皮腹腔细胞,并消耗ATP通过运输系统到达血液中。在细胞结合物中的一部分L-谷氨酸

为了被淘汰和另一部分转化成谷氨酰胺。当发生这种情况,细胞尝试用酶去修复一些存在于滑面内质网但细胞无法完全去除多余的谷氨酰胺的损害。也许,因为这个原因,肝脏(15分钟)在30分钟时颁发细胞肿胀(浑浊肿胀)。也许在45分钟时能观察到水泡变性和坏死.

当L-谷氨酸达到高浓度时通过肾动脉,肾尝试排泄它。肾小体,通过输入小动脉接收L-谷氨酸,它被吸收,过滤,并穿过细胞膜破坏细胞。该曲肾小管上皮细胞相比末梢的曲细精管更容易受到损害。肾脏在15和30分钟展示水肿;在45分钟的时候观察到水样变性,坏死。

一个主要的兴奋性氨基酸类神经递质,也是一种内源性兴奋性毒素。 谷氨酸,

在不同的脑区谷氨酸和脂质过氧化作用的影响是有据可查的。

在这项研究中,脂质过氧化产物丙二醛(MDA和4- OH的烯烃)的增加是肝脏和肾脏损伤反应。与此同时,有观察到丙二醛和4- OH 烯烃以及ALAT和ASAT酶在增加。损害的形态显示出累进损害和脂质过氧化产物之间的相关性,特别是在谷氨酸施用后的30和45分钟期间。在肝脏中的脂肪变性和坏死是伴随着丙二醛和4- OH的烯烃的高水平被观察到。在肾脏,也显现出了非常相似的水样变性,坏死反应。这些数据都可以被解释为对谷氨酸兴奋毒性作用。 最后,相对很少关注到谷氨酸的信号分子在周边组织的功能表达。越来越多的证据为谷氨酸是一种在一些器官和系统中作为信号中间人的作用,除了一种兴奋性氨基酸在中枢神经系统神经递质的作用。

本研究结果为调查味精的内吸收的副作用提供了强大的动力,很明显,这种模型引起神经兴奋毒性损伤,以及表现出强烈的和弥漫的周边破坏,或许在所有的器官和系统。

相关推荐