multicenter

谁知道CoQ10

硼、铝等原子的价电子数少于价轨道数，当它们形成化合物时，表现出明显的缺电子倾向。例如，在硼烷和烷基铝等化合物中，由于没有足够的价电子使所有两原子间的化学键都成为正常的两电子键，出现了多中心键。以乙硼烷B2H6为例，硼原子接近四面体构型，但它总共只有12个价电子。4个端梢的硼-氢键共用去8个价电子，剩下的4个价电子分配在两个硼-氢-硼桥键中，形成两个三中心-两电子的多中心键。在较复杂的硼烷中，还有三中心-两电子的硼-硼-硼桥键等形成的多中心键。

有关排球的知识英文带翻译

为虾米想问这么专业的词呀？我前年狂爱用Q10成分的东西。我对它的认识就是：能帮助收紧皮肤，抵抗衰老！

CoQ10是什么东西？

护心辅酶CoQ10是一种辅酶，所谓辅酶，本身并不是酶，但是许多酶的生化反应及生理效应却一定要在辅酶的存在下才能进行。

辅酶CoQ10其实存在动物体内的每个细胞中，主要的生理作用角色是在辅助催化线粒体中能量体ATP的磷酸还原作用，让细胞能量供应系统能够快速恢复活化。

现在更多的关于辅酶CoQ10的研究是围绕心脏病进行的，辅酶CoQ10的应用方面也更多的心肌保护方面。

CoQ10的应用

壹●前言

在这科技日新月异的时代,人对於健康的需求日渐增大,许多的药品和健康食品。

也陆续推出.而辅酶也就顺著潮流慢慢的显出他不可或缺的特殊功能;而辅酶之。

一～「CoQ10」正是目前炙手可热的新一代的科技产品. 。

一般而言,社会大众对於日常所见的抑或是未曾听说的科技药品通常都是一无所。

的盲目使用,甚至是盲目的被药品利用.如果对药品不熟悉而在一无所知的情。

况下使用,便容易造成一些意外,轻微者产生药物过敏,严重者则有丧命的危险.。

所以希望此篇报告能让读者可以进一部的了解一种少人知道却时常使用的药物. 。

辅酶是一种非蛋白质的维生素,金属离子或一种核苷酸.辅酶是一种分子极小的。

物质,能轻易渗透细胞的半透膜而且不容易被高温所破坏.在细胞的氧化还原的。

反应中,参与接受和供给氢与电子的工作,可决定催化作用速率的快慢.另外辅。

酶通常无专一性,也就是说一种辅酶可辅助多种的酶作用. 。

辅酶Q10(CoQ10)在一些需要高能量来运作的器官,如心脏,肾脏和肌。

肉在参与细胞的能量工厂-「粒线体」中电子传递及氧化作用的重要介质,尤其。

是心脏和肌肉需要额外的能量,CoQ10能适时参与能量产生;及紧急的能量。

供给.而且脂溶性CoQ10也具有抗氧化作用和抗自由基(Free Radicals)之特。

性.

贰●正文

一,CoQ10的发现及发展

辅酶Q10最早是在西元1957年由美国生化学家弗得瑞克(Frederick Crane)博。

士所发现,当时他是从牛心脏细胞的粒线体所分离出来.当时也由一位英国的科。

学家摩顿(Morton)教授把一种从缺乏vitamin A的老鼠肝脏提炼出的化合物定义。

为CoQ10,并正式确定它的化学结构将其命名为ubiquinone.1958年卡尔教授。

(Karl Folkers)和他的同事精确的确定了CoQ10的化学结构(dimethoxy-5 。

methyl-6 decaprenyl benzoquinone).而1960年代,日本的Yamamura教授,运用了C。

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oQ7(一种相关化合物)来治疗缺血性心脏衰竭,成为史上第一位用CoQ10。

来治疗人体疾病的人.1972义大利的 Gian Paolo Littarru 和Karl Folkers教。

授证明缺乏CoQ10会引起一种心脏病.1978年Peter Mitchell因为他对生物能。

量转移的chemiosmotic理论公式化的贡献,而获得了诺贝尔奖;内容提及了Co。

Q10在能量转移中扮演了的重要角色.而80年代至90年代后CoQ10逐。

渐成为抗氧化作用和自由基的主流. 。

二,CoQ10对於心脏疾病的帮助 。

在需要高能量来运作的心脏中CoQ10占有相当的地位.这也就是为什麼Co。

Q10一开始会使用在治疗心脏疾病上的原因.事实上,充血性的心力衰竭和血。

液中缺乏CoQ10有很大的关联;所以CoQ10似乎成为一种主要治疗心力。

衰竭的物质.

在早期CoQ10在心力衰竭和心脏肿大的人体进行实验,实验后发现:在食用。

高脂肪的食物后服用CoQ10胶囊后,心脏脉动数有明显的改善,而呼吸困。

难,胸口疼痛等心悸患者的症状也有逐步的改善.有些患者偶尔会发生剧烈程度。

的改善,使患者的心脏逐渐回复成类似正常的心脏大小和作用.而这些患著皆是。

在充血性心力衰竭发病后服用CoQ10;但是仅仅能改善病情却不能回复成正。

常的大小以及功能.

三,CoQ10的治疗事迹

现在国际上大概有九个关於CoQ10的研究场所:两个在日本,两个在美国,。

两个在义大利,两个在德国和一个在瑞典.临床研究的结论发现CoQ10能有。

效恢复心脏功能且不易和其他的药物起作用. 。

而最近最大的CoQ10临床实验是义大利的multicenter实验,2664位心力衰竭。

患者参与了此次实验,同时此实验也是有史以来最多位病患参与的CoQ10人。

体试验.

四,CoQ10其他的适用症状 。

CoQ10其实也被应用在治疗牙龈的疾病上,经研究发现不健康的牙龈的Co。

Q10含量比一般的健康牙龈的CoQ10含量低,由此可见CoQ10有助於。

牙龈的发展.

如之前所说的,CoQ10参与了细胞能量的产生,所以对於体力不佳的人适量。

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的投予CoQ10可促使患者体内的细胞产生能量. 。

五,CoQ10未来的应用

从前的医学主流都是在药物的发展或是病理学的修正,所以一些「新」的药物其。

实都是由一些许多年前「老」药物演变,转化而来.就如CoQ10一样,本来。

是治疗心脏疾病的药物,却经由近代的医学发现它具有强大的抗氧化作用及抗自。

由基作用的疗效,而渐渐的成为一种抗氧化作用及抗自由基作用的药物. 。

因为CoQ10对於各种类型的细胞都有容易吸收的特性,所以CoQ10能在。

细胞中有效率地进行反应,而且新陈代谢效率大的细胞对於CoQ10都有一定。

的敏感性,所以CoQ10拥有的抗氧化和抗自由基能力因为此种特性,能大量。

的减少组织的氧化和防止胆固醇的产生,甚至比维生素E更有效率,因为如此C。

oQ10在未来极可能成为抗氧化和抗自由基甚至抗癌的主要药物. 。

六,问题与讨论

辅酶为一种能促使酶产生反应的的非蛋白质,况且辅没并没有专一性～也就是说。

一种辅酶能加速许多种的酶产生反应,而CoQ10也是一种辅酶,所以如果将。

CoQ10使用在消化系统上是否也能治疗一些因缺少酶而产生的疾病呢 。

又因为CoQ10能防止细胞氧化和老化,所以说如果将CoQ10用於因细胞。

逐渐退化而产生的疾病上,像类似「运动神经元疾病」上,是否能也能产生治疗。

或是延缓的效果呢

而CoQ10除了能使用在人体上,说不定还能使用在植物上,利用CoQ10。

在细胞粒腺体所扮演的重要角色的特性,说不定能改造植物的细胞生长特性,藉。

此改变植物的成熟期,增加产量,你说有没有可能呢 。

参●结论

一些旧的药物在现代进步的科学下逐渐转变而成了拥有新功用的药物,而CoQ。

10也从原本的治疗心脏病的药物成为现代抗氧化,抗自由基的主流;又因为C。

oQ10拥有脂溶性,抗高温和易被人体吸收……等特点已逐渐取代了维他命E。

的地位.而关於CoQ10的主要抗氧化功用大致如下: 。

一,增加角化细胞glutathion浓度,增加皮肤细胞抗氧化能力. 。

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二,抑制细胞氧化作用.

三,抑制磷酸酪胺酸脢(Phosphatyrosin kinase)活性,防止黑色素行成,阻止黑斑。

产生.

四,预防因紫外线UVA照射所引起之表皮细胞DNA之破坏,防止皮肤癌. 。

五,减低皱纹深度,改善皮肤暗沈. 。

六,抑制胶原蛋白脢(collagenase mRAN)活性,促进胶原蛋白增生. 。

七,减低角质细胞(coryneocyte)直径大小,减少皮肤老化. 。

,增加玻尿酸浓度(Hyaluronic acid)提高肌肤含水量. 。

虽说CoQ10现今主要是对於抗氧化和抗自由基这两方面在研发,但仍然不改。

它在其他疾病方面的地位,像是在心脏,牙龈相关的疾病仍然有相当的重要性,。

也因为CoQ10拥有相当高的易吸收度,也可用於补充体力上;况且CoQ1。

0还有增强抵抗力的功能,更重要的是它原本就是存在於人体细胞的物质,所以。

CoQ10对於人体并不会有排斥的行为或过敏的情形产生. 。

对於CoQ10大家一定还是有许多的不了解,应该是因为CoQ10是在这几。

年前才提出的关系,我个人在此提出一些一般人时常问的问题来使大家能更了解。

CoQ10的特性和相关知识: 。

一,什麼是CoQ10

其实CoQ10只不过是一种辅酶,它大量的存在於心脏的细胞中可与细胞中的。

粒腺体产生能量ATP,而且近代的科学发现脂溶性的CoQ10拥有比维他命。

E更高效率的抗氧化及抗自由基的能力.CoQ10能从一些食物中取得,像是。

心脏,肝脏,肾脏,沙丁鱼,鲭鱼,花生都能摄取少量的CoQ10. 。

二,为何CoQ10会用於保养品上 。

因为脂溶性的CoQ10具有能直接从皮肤吸收的特性,而且因为是脂溶性不溶。

於水并不会经由水分代谢掉,况且因为CoQ10原本就是从细胞内的粒腺体所。

生产的,所以并不会和身体产生抗拒.。

帮帮翻译成中文，谢谢大家，

Volleyball development。

1. Volleyball originated in which year? The current chairman of the international amiss? Chairman of the Asian union?。

In 1895, Wei Jizhong Russell。

2. The principle of revise the rules of volleyball and what is the trend?。

1. To ensure that the rules simple 2. Keep the relative balance of offensive and defensive contradictions 3. Maintain the continuous 4. Race against time television broadcasts controllable 5 to 3. What is the development trend of modern volleyball tactics?。

1. Multicenter fast-break tactics 2. Development and changes of the defensive tactics。

Volleyball technology。

1. What is the definition of a volleyball?。

Volleyball technology refers to the athletes under the condition of the rules of the game allows use of reasonable hitting the floorboard of the action and cooperate with the action. Volleyball has two kinds: one kind is with the ball technology, one kind is no ball technology。

2. The main mechanical factors affect how starting which three?。

1. The size of the stability in starting direction Angle 2. The size of the support reaction (3) the size of the seed。

3. The main mechanical factors affect how brake which three?。

1) the size of the support reaction (2) the size of the supporting force and the Angle of the ground 4. What is the definition of a whip?。

Arm waving shots to arm can drive the forearm, drive strokes of the wrist, forearm called whip.。

Angle of the passing lanes and net easy spiking in what condition, passing the target far, passing pay attention to?。

6. Self cover spiking definition, it is divided into several? 1. Time difference attack 2. Poor position attack 7. Blocking the air moving arm。

Air moving arm, is in order to improve the success rate of blocking. 1) along the ball shift to intercept (2) a diversion to intercept 3. Attack to intercept two arms。

Step 8. Set up, adjust fofao, what is the definition of a fly before?。

Players forward or to the side across the step mat ball method called step mat. Will pass does not reach the designated position and far away from net ball to facilitate attacking the location and height of the rap, called a setter adjustment. Before flying: player button is short term rapid take-off point do feint, using inertia of jump forward, make the body horizontal displacement in the air near the Williams team, buckle air ball 9. What are the definitions of sway the?。

Jump do drop shot, suddenly setter to attack the ball companion, this setter is called sway。

What are the main types of 10. Spiking technique changes?。

1. Swivel spiking 2. Turn the wrist smash 3 thugs out 4. Super hand drop shot 5. 6. The light spiking drop spike the ball。

11. Please list the single block is easy to make mistakes and correct method four columns? P140。

12. Are you ready to teaching steps through which help beginners to master positive mat ball, frontal spiking, positive overhand pass, positive, single blocking technology? P110 13. Blocking takeoff time cook according to what?。

Blocking the takeoff time according to the situation of the second pass and smash the action characteristics of to decide.。

14. What kind of hands against the ball the shape of the hand are there?。

Has two kinds: one kind is fuels type, and the other is a palm. 15. The control point of service include? To find weak areas serve, look for a person to serve. 16. What are the individual tactical smash?。

Route change 2. Weight change 3. Super hand and thugs 4. Left and right hand smash。

17. Smash role in the game and smash the development of the technology in different s P113/114 18. Positive cushion the ball, the ball is easy to make mistakes and correct method? P94/113 19 offensive serve mainly reflected in what respect?。

On the basis of guarantee the accurate, as far as possible speed, strong strength, rotating, radian aggressive driving.。

20. The ball should be and what the size of the force into positive and negative than?。

Mat ball should match the size of the force to force is inversely proportional to, with pad out the ball and radian is proportional to the distance.。

21. A separate overhand positive, positive overhand floater serve the difference of the techniques of P60。

physical

1. The development of the volleyball players should strength include what? General strength, power, and strength endurance (2) speed can be divided into what kind?。

1. Reaction speed 2. Movement speed 3. Movement speed。

3. What is power? Please list the six development of volleyball athletes practicing ways of the upper limb muscles around the waist strength。

排球发展

1. 排球的起源于哪年？现任国际排联主席？亚洲联主席？

1895年 魏继忠 拉塞尔 。

2. 排球规则修改的原则和趋势是什么？

1.保证规则的简洁 2.保持攻防矛盾的相对平衡 3.维护比赛的持续性 4.争取比赛时间的可控性 5有利于电视转播 3. 现代排球战术发展趋势是什么？

1.多中心的快攻战术 2.发展与变化的防守战术 。

排球技术

1. 排球技术的定义是什么？

排球技术是指运动员在比赛规则允许的条件下采用的各种合理的击球动作和配合动作的总称。排球技术有两种：一种是有球技术，一种是无球技术 。

2. 影响起动快慢的力学因素主要哪三个？

1.在起动方向上稳定角的大小 2.支撑反作用力的大小 3.蹬地角的大小 。

3. 影响制动快慢的力学因素主要哪三个？

1.支撑反作用力的大小 2.支撑作用力与地面的夹角的大小 4. 鞭打动作的定义是什么？

手臂挥动击球时，以大臂带动小臂，小臂带动手腕的击球动作，称为鞭打动作。

5. 传球路线与网的夹角处于什么情况下易扣球，传球目标远时，传球注意什么？

6. 自我掩护扣球定义，它分为哪几种？ 1.时间差进攻 2.位置差进攻 7. 拦网时手臂空中移动拦截 。

手臂空中移动拦截，是为了提高拦网的成功率。 1.随球转移拦截 2.声东击西拦截 3.两臂夹击拦截 。

8. 跨步垫球，调整二传，前飞的定义是什么？

队员向前或向侧跨出一步的垫球方法称为跨步垫球。将一传不到位且离网较远的球传至便于进攻队员扣击的位置及高度，称为调整二传。前飞：队员在扣短平快的起跳点上做佯攻，利用向前冲跳的惯性，使身体在空中水平位移到二传队员附近，扣半空球 9. 晃传的定义是什么？

跳起做扣球动作，突然改为二传把球传给同伴进攻，这种二传称为晃传 。

10. 扣球技术变化主要有哪几种？

1.转体扣球 2.转腕扣球 3.打手出界 4.超手扣球 5.轻扣球 6.轻吊球 。

11. 请列举单人拦网易犯错误及纠正方法4列？P140 。

12. 你准备通过哪些教学步骤使初学者掌握正面垫球、正面扣球、正面传球、正面上手发球、单人拦网技术？P110 13. 拦网起跳时间熬根据什么来确定？

拦网的起跳时间要根据二传球的情况和扣球人的动作特点来决定。

14. 双手挡球的手型有哪几种？

有两种：一种是抱拳式，另一种是并掌式。 15. 控制落点的发球包括什么？ 找薄弱区域的发球、找人发球。 16. 扣球的个人战术有哪些？

1.路线变化 2.轻重变化 3.超手和打手 4.左、右手扣球 。

17. 扣球在比赛中的作用及扣球技术在不同年代的发展过程P113/114 18. 正面垫球、传球易犯错误及纠正方法？P94/113 19. 攻击性发球主要体现在哪些方面？

在保证准确的基础上，尽可能的发出速度快、力量大、旋转强、弧度平的攻击性发球。

20. 垫球用力的大小应与什么成正反比？

垫球用力的大小应与来球力量的成反比，同垫出球的距离和弧度成正比。

21. 分别列出正面上手发球、正面上手飘球的技术动作不同点P60 。

体能

1. 排球运动员需发展的力量包括哪些？ 一般力量、爆发力和力量耐力 2. 速度可分为哪些类？

1.反应速度 2.动作速度 3.移动速度 。

3. 何谓力量？请列举6个发展排球运动员上肢肌肉群腰部力量的练习方法。

卡瑞利珠单抗说明书中重点的注意事项有哪些，我记下来？

INTRODUCTION

Much progress has been made in our understanding of the role of nutritional factors in the pathogenesis of liver disease and its treatment. The basic concept has been that some nutrients are essential because they cannot be synthesized endogenously in the mammalian body and therefore must be provided exogenously in the diet. A classic example is that of the amino acids, 9 of which are essential and therefore are mandatory constituents of any diet. An important one is methionine. Its requirements have been established and its key role in a score of vital functions has been well chartered, as reviewed in the introduction to this symposium (1) and elsewhere (2). In addition, to this traditional concept, a new approach has emerged that has changed the use of some of the essential nutrients in pathologic conditions. Indeed, many of these nutrients, including methionine, must first be activated in the liver or in other tissues before they can exert their key functions. This activating process, however, is altered by liver disease and, as a consequence, nutritional requirements change. For instance, methionine has to be converted to S-adenosyl-L-methionine (SAMe) before it can act as the main cellular methyl donor (Figure 1). This function of SAMe is important for the metabolism of nucleic acids and for the structure and function of membranes and many other cellular constituents. These are often disturbed in various liver diseases but cannot be restored by the simple administration of methionine. Indeed, experimentally, it has been shown that even a 7-fold increase in the normal dietary methionine content failed to significantly alter hepatic SAMe (3). This is exacerbated when there is significant liver disease, which is commonly associated with impairment of the enzyme activating methionine to SAMe (4). Therefore, supplementation with methionine is useless in most such circumstances and may even result in toxicity because of its accumulation as a result of nonutilization. Indeed, elevated concentrations of circulating methionine in patients with liver disease have been reported (5–7), and excess methionine was shown to have toxic effects (3), including a decrease in hepatic ATP (8). Accordingly, one must bypass the enzyme deficiency due to liver disease and provide the product of the defective reaction, namely SAMe, which becomes crucial for the functioning of the cell under these pathologic conditions. Thus, SAMe then becomes the essential nutrient instead of methionine. It is a typical example of a "conditional essential amino acid" (9) and what is now also called a supernutrient, namely an activated nutrient that must be provided to meet the normal cellular requirements when its endogenous synthesis from a nutritional precursor becomes insufficient because of an impairment in the activation process secondary to a pathologic state. Because the essential supernutrient SAMe is key to many basic cellular functions, it is not surprising that its lack is associated with many pathologic manifestations of liver diseases and that these can be corrected by simply providing the missing supernutrient (10). 。

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FIGURE 1. . Lipid peroxidation and other adverse effects resulting from alcoholic liver disease and from free radical generation and acetaldehyde production by ethanol-induced microsomes and associated cytochrome P4502E1 (CYP2E1) up-regulation. Metabolic blocks caused by liver disease (a and b) or folate (c), vitamin B-12 (c), or vitamin B-6 (d) deficiencies result in corresponding depletions in S-adenosyl-L-methionine, phosphatidylcholine, and glutathione (GSH). New therapeutic approaches include the down-regulation of microsomal enzyme induction, 1, especially of CYP2E1; the trapping of free radicals with antioxidants, 2; the replenishment of S-adenosyl-L-methionine, 3; and the replenishment of phosphatidylcholine, 4. ADH, alcohol dehydrogenase (EC 1.1.1.1). Reprinted with permission from reference 2. 。

BENEFICIAL EFFECTS OF SAMe ON BASIC MANIFESTATIONS OF LIVER DISEASE 。

Role of SAMe on oxidative stress。

As reviewed elsewhere (11), oxidative stress was shown to play a major pathogenic role in multiple disease states ranging from the hepatotoxicity of alcohol (and other xenobiotics) to the carcinogenicity of many compounds. The major natural defense mechanism against oxidative stress is reduced glutathione, which traps the excess of free radicals (Figure 1). Glutathione is a tripeptide, the rate-limiting amino acid being cysteine (12), and SAMe plays a fundamental role in the formation of cysteine. 。

Role of SAMe in transmethylation and transsulfuration reactions。

Another basic cellular activity of SAMe is its role as a methyl donor and enzyme activator in the transmethylation and transsulfuration reactions key to membrane structure and function. For example, SAMe is essential for the transport processes and signal transmission across membranes. One of the important consequences of the failure of these functions is insufficiency of bile formation, a key aspect of many diseases of the liver, resulting in a pathologic state called cholestasis. SAMe opposes successfully many of the cholestatic states, as reviewed elsewhere (13). Given either orally or parenterally, SAMe improves both the pruritus and the biochemical indexes of cholestasis, such as serum bilirubin, alkaline phosphatase (EC 3.1.3.1), and -glutamyltransferase (EC 2.3.2.2). It is noteworthy that in a prospective, multicenter, double-blind, placebo-controlled trial performed in 220 inpatients with chronic liver disease (chronic active hepatitis and cirrhosis, including primary biliary cirrhosis), serum markers of cholestasis and subjective symptoms (eg, pruritus and fatigue) significantly improved after SAMe treatment (14). Cholestasis is not only an important manifestation of various liver disorders, but it also may complicate physiologic states such as pregnancy. SAMe was shown to be a useful therapy for cholestasis during pregnancy (15) and for cholestasis that is sometimes associated with parenteral nutrition (16). 。

Role of SAMe in opposing fibrosis。

The leading cause of morbidity and mortality in all major liver diseases is an inappropriately excessive healing process with uncontrolled scarring or fibrosis culminating in cirrhosis. Indeed, fibrosis can be viewed as an initially beneficial scarring process that has escaped control and results ultimately in cirrhosis. SAMe was shown to be therapeutically useful in alleviating this process experimentally (17) and for improving the outcome clinically (18). 。

The most common liver disease for which SAMe has been shown to be useful therapeutically is alcoholic liver injury, which encompasses all the pathologic manifestations discussed above, namely a deficiency in the activation of methionine to SAMe, in the pathogenic role of oxidative stress and glutathione deficiency, in complications of cholestasis, and in the devastating consequences of excessive liver fibrosis (leading to cirrhosis). 。

SAMe AND THE PATHOGENESIS OF ALCOHOLIC LIVER INJURY 。

Alcohol causes liver disease through a variety of pathogenic mechanisms that were reviewed in detail elsewhere (19–21). The major mechanisms include interactions with nutrition and toxic manifestations through generation of oxidative stress and production of the toxic metabolite acetaldehyde. 。

Interactions of alcohol with nutrition。

In addition to its pharmacologic action, alcohol (ethanol) has a considerable energy content (7.1 kcal/g). Thus, its consumption may cause primary malnutrition by displacing other nutrients in the diet because of the high energy content of the alcoholic beverages or because of associated socioeconomic and medical disorders. Secondary malnutrition may result from either maldigestion or malabsorption of nutrients caused by gastrointestinal complications associated with alcoholism. Alcohol also promotes nutrient degradation or impaired activation (see below). Whereas it continues to be important to replenish nutritional deficiencies, it is crucial to recognize that, because of the alcohol-induced disease process, some nutritional requirements change. 。

Methionine and its utilization in liver diseases。

In rats, alcohol consumption is associated with impaired methionine conservation. Consequently, methionine supplementation has been proposed for the treatment of liver diseases, especially the alcoholic variety, but some difficulties have been encountered, which are reviewed in detail elsewhere (22). Indeed, fatty liver and cirrhosis were not prevented in baboons given liberal amounts of methionine and other lipotropes (23, 24), and excess methionine was shown in various studies to have some adverse effects (see above). Whereas in some patients with alcoholic liver disease, circulating methionine concentrations may be normal or even low (25), elevated concentrations have been reported in others (see above). Furthermore, there was a delay in the clearance of plasma methionine after its systemic administration to patients with liver damage (26). Similarly, the blood clearance of methionine after an oral load of this amino acid was slowed (27). Because about one-half of methionine is metabolized by the liver, the above observations suggest the impaired hepatic metabolism of this amino acid. Indeed, Duce et al (4) reported a decrease in SAMe-synthetase activity in cirrhotic livers. As a consequence, methionine supplementation may be ineffective in alcoholic liver disease and SAMe depletion ensues, as was verified in nonhuman primates after long-term ethanol consumption (28). Additional factors that contribute to the decrease in hepatic SAMe are increased glutathione utilization secondary to enhanced free radical and acetaldehyde generation by the induced microsomal ethanol-oxidizing system (see below). 。

Microsomal ethanol-oxidizing system and SAMe。

The microsomal ethanol-oxidizing system has been the subject of extensive research, and is reviewed in detail elsewhere (29, 30). With the use of Western blot technique with specific antibodies against cytochrome P4502E1 (CYP2E1), a 4-fold induction of CYP2E1 was found in liver biopsy samples from recently drinking subjects (31). CYP2E1 activates some xenobiotics (such as acetaminophen) to toxic metabolites (29). It also generates several species of active oxygen (Figures 2 and 3). Glutathione provides one of the cell’s fundamental mechanisms for the scavenging of toxic free radicals (Figure 1), but the generation of active oxygen species by CYP2E1 may overwhelm this antioxidant system with pathogenic consequences requiring new therapeutic approaches (32). Furthermore, acute ethanol administration also inhibits glutathione synthesis and produces an increased loss from the liver (33). Indeed, rats fed ethanol chronically have significantly increased rates of glutathione turnover (34). Such an increased glutathione turnover was also shown indirectly by an increase in -amino-N-butyrate (Figure 1), which has been shown in both nonhuman primates and in humans (35). A depletion in the steady state concentrations of hepatocellular glutathione, in synergy with other conditions, leads to hepatocellular necrosis and liver injury (36). Glutathione is selectively depleted in the mitochondria (37) and may contribute to the striking alcohol-induced alterations of that organelle. In addition, -tocopherol, the major antioxidant in the membranes, is depleted in patients with cirrhosis (38). This deficiency in the defense systems, coupled with increased oxygen and other free radical generation (by the ethanol-induced microsomes; see above) and with acetaldehyde production (see below), may contribute to liver damage not only via lipid peroxidation but also by enzyme inactivation (39). Replenishment of glutathione can be achieved in acute situations (such as acetaminophen poisoning) by administration of precursors of cysteine (one of the amino acids of glutathione), such as acetylcysteine, or in chronic conditions by SAMe (10, 28). Beneficial effects of SAMe on glutathione were also observed in humans (40, 41). Moreover, experimentally, the ethanol-induced increase in fluidity of mitochondrial membranes was prevented by SAMe but not by N-acetylcysteine supplementation (42). 。

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FIGURE 2. . Pathogenesis of hepatic, nutritional, and metabolic abnormalities after ethanol abuse. Malnutrition, whether primary or secondary, can be differentiated from metabolic changes or direct toxicity, resulting partly from redox changes mediated by alcohol dehydrogenase (ADH; EC 1.1.1.1) or effects secondary to microsomal induction, including increased acetaldehyde production. L-FABP, L-fatty acid binding protein; FA, fatty acid; GSH, glutathione; MEOS, microsomal ethanol-oxidizing system; 4A1, cytochrome P4504A1. Reprinted with permission from reference 2. 。

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FIGURE 3. . Physiologic and toxic roles of cytochrome P4502E1 (CYP2E1), the main cytochrome P450 of the microsomal ethanol-oxidizing system. Many endogenous and xenobiotic compounds are substrates for CYP2E1 and induce its activity through various mechanisms, resulting in an array of beneficial as well as harmful effects. Reprinted with permission from reference 30. 。

Toxicity of acetaldehyde。

Acetaldehyde, the product of all pathways of ethanol oxidation, is highly toxic (18) and is rapidly metabolized to acetate, mainly by a mitochondrial aldehyde dehydrogenase, the activity of which is significantly reduced by chronic ethanol consumption (43). The decreased capacity of mitochondria in alcoholfed subjects to oxidize acetaldehyde, associated with unaltered or even enhanced rates of ethanol oxidation (and therefore acetaldehyde generation because of the induction of the microsomal ethanol-oxidizing system; see above), results in an imbalance between the production and disposition of acetaldehyde. The latter causes the elevated acetaldehyde concentrations observed after chronic ethanol consumption in baboons (44) and humans (45). 。

Acetaldehyde’s toxicity is due, in part, to its capacity to form protein adducts, which results in antibody production, enzyme inactivation, and decreased DNA repair (19). Moreover, acetaldehyde promotes lipid peroxidation (Figure 1); one mechanism that promotes lipid peroxidation is glutathione depletion. The binding of acetaldehyde with cysteine, glutathione, or both (Figure 1) may contribute to a decrease in liver glutathione (46). Acetaldehyde adducts also promote collagen production because collagen synthesis by liver stellate cells is released from the feedback inhibition produced by the carboxy terminal propeptide of procollagen through adduct formation of acetaldehyde with the latter (47). Thus, acetaldehyde toxicity plays a fundamental role in alcohol-induced liver injury, and glutathione is a key defense mechanism by inactivating the free radicals generated by acetaldehyde and by binding to acetaldehyde itself (Figure 1). SAMe, in turn, serves as the main support for the maintenance of adequate glutathione concentrations. 。

BENEFICIAL EFFECTS OF SAMe IN ALCOHOLIC LIVER DISEASE 。

Experimental studies。

Although it has been claimed that the liver does not take up SAMe from the bloodstream, other results indicate its uptake by isolated hepatocytes; results in baboons (28) also clearly showed hepatic uptake of exogenous SAMe in vivo, associated with beneficial effects on liver function and structure. In these baboons, correction of the ethanol-induced hepatic SAMe depletion with oral SAMe administration (28) resulted in a corresponding attenuation of ethanol-induced liver injury, as shown by a less-striking glutathione depletion and lesser increases in plasma aspartate transaminase (EC 2.6.1.1). The number of alcohol-induced megamitochondria (documented by electron microscopy) was markedly reduced (28). The latter was associated with a lesser leakage of the mitochondrial enzyme glutamic dehydrogenase into the bloodstream. In rats, SAMe also decreased ethanol-induced fat accumulation (48). Thus, SAMe was shown to be useful for opposing the oxidative stress and the alcohol-induced liver injury. 。

Membrane alterations are common in alcoholic liver injury and are also associated with a decrease in phosphatidylcholine, the backbone of the membranes. One pathway for the maintenance and preservation of adequate phosphatidylcholine concentrations in the liver membranes is the methylation of phosphatidylethanolamine to phosphatidylcholine through the action of SAMe (Figure 1). This vital function is impaired in alcoholic liver disease because, under these conditions, the activity of phosphatidylethanolamine methyltransferase (EC 2.1.1.17) is depressed (4, 49). This deficiency is exacerbated if SAMe is depleted (Figure 1). These metabolic considerations may explain, at least in part, some of the beneficial effects of SAMe on alcohol-induced liver injury in baboons (28) through the restoration of some of the phosphatidylcholine production or through the positive effects of the supplementation with phosphatidylcholine (50), the depleted product of the reaction (Figure 1). 。

Clinical trial

A significant therapeutic success in alcoholic liver disease was achieved in a recent long-term randomized, placebo-controlled, double-blind, multicenter clinical trial of SAMe in patients with alcoholic liver cirrhosis in whom SAMe improved survival or delayed liver transplantation (18). 。

CONCLUSIONS

Liver disorders, including alcoholic liver disease, are associated with and result in part from impaired activation of methionine to SAMe or from alcohol-induced oxidative stress, which results in the increased utilization of SAMe, a key precursor of cysteine—the rate-limiting amino acid of the tripeptide glutathione. Depletion of SAMe, the main methylating agent of the liver, and associated liver pathology can be corrected by the administration of this safe, yet therapeutically effective nutrient.。

其实，对于这些药物的使用，最重要最需要注意的就是副作用对于身体的影响，但是随着医疗水平的逐渐进步，缓解的方式也越来越多，参百益辅助就是其中之一，缓解副作用提高免疫力。

卡瑞利珠单抗副作用：

副作用叙述了在临床实验中观查到的分辨为可能与卡瑞利珠单抗有关的副作用的类似发病率。因为临床实验是在不一样标准下开展的，不一样临床实验中观查到的副作用的发病率不可以立即较为，也可能不可以体现临床护理中的具体发病率。忌讳：对特异性成分或(成分)列出的一切辅材存有超敏反应的病人。

再分享一下

抗癌的食物有什么吧：

1、山芋

山芋一般全是南方地区种植比较多，其丰富多彩的营养成分，具备提高身体的免疫功能的功效。可做为预防癌症肿瘤的常见养生药膳正餐。其丰富多彩的维他命可以激话身体体细胞，加快基础代谢，进而做到减肥瘦身的目地。

2、马齿笕

这类菜全是天然的的，没有为什么说去专业种马齿笕的，但是吃这类菜的群体也很少，一般全是60岁以上的才会吃，年青人如今非常少有些人吃完。马齿笕带有丰富多彩的类胡萝卜素、维生素E和硒元素，可以合理的延缓衰老，抗氧化性，抑止肝癌、淋巴癌的产生。

3、辣椒

辣椒别名青柿椒、柿子椒、青椒等，是饭桌上的普遍菜式。它的维他命C成分是西红柿的7~15倍，在蔬菜水果中占第一位。它独有的味儿有刺激性唾沫代谢的功效;含有的辣椒素能提高胃口，促进消化，避免便秘。这一成份还是是一种抗氧化性物质，可阻拦相关体细胞的基础代谢，进而停止体细胞组织的病变全过程，减少癌症体细胞的发病率。

4、霍山铁皮石斛

霍山铁皮石斛具备提高机体免疫功能和防癌功效 ，临床医学上常见于恶变肿瘤的辅助医治 。霍山铁皮石斛能改进肿瘤病人的病症 ,缓解放疗化疗造成的副作用 ,增强免疫作用 ,提升存活品质 ,增加存活时间。

5、番茄

番茄是一种蔬菜水果类发食材，它的营养成分十分的丰富多彩。番茄里边有一个物质它叫番茄素，番茄素是一种强抗氧剂，此外它也有贝塔 胡罗卜素，维C这种营养元素加起来它的防癌实际效果更强。

6、西蓝花

西蓝花带有很多的“惊喜原素”— 硒，从而被《时代》杂志期刊选举为十大身心健康食品之一。硒具备防癌、耐老化、提高免疫力功效。另外，它带有很多的萝卜硫素，能抵制多种多样恶变肿瘤的产生。

7、荔技

荔技是一种具备强防癌实际效果的新鲜水果。用这类新鲜水果做成的水果汁能够合理抵抗肿瘤细胞。而这类水果汁不但口感好，并且还不容易像放疗那般产生负面信息影响。

8、山楂果

山楂果能活血化淤、温胃化滞、健脾开胃助消化，另外还带有复合的维他命C.中医学认为，癌症肿瘤为实性硬块，具备气虚血瘀状况，由于山楂果能活血化瘀、善消肉积，又能按捺肿瘤细胞的进度，因此适宜多种多样癌症肿瘤病人的医治。

9、猴头菇

猴头菇是很好的健康养生食物，不但能够延缓衰老还能防癌，猴头菇含有多种多样矿物和维他命，是优良的滋补养生食品，对消化道溃疡有优良功效。此外猴头菇带有核甘酸等防癌活性物质，能提高机体抗病能力，推动抗原的转化成，对肝癌、淋巴癌、直肠癌拥有非常好的防止和抵御实际效果。

10、无花果

无花果也是一种碱性食品，生津解渴，老少两相宜。果子奶水对肉瘤、乳瘤、腺癌、败血症、淋巴肉瘤均有抑制效果。未熟果子的乳浆中带有补骨脂素、佛柑内酯等特异性成份，其完善果子的水果汁中可获取一种芬芳物质苯甲醛，二者都具备抗癌防癌、提高机体抗病性工作能力的功效，能够防止多种多样癌症的产生，减缓可移植性腺癌、淋巴肉瘤的发展趋势，促进其衰退，并对一切正常体细胞不容易造成危害。

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