on 15-Mar-2018 (Thu)

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要买车险或理赔的朋友一定要看（案例超强）。。。搬运

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前言：买车时，图省事，直接就在买车的地方上了保险。因为是新车，险种又上的全，所以花了不少钱，5000多。一年当中就出过一次险，900多元。那张保单除了前几天年检用上了，平常基本没什么用。眼看一年到了，该续保了，前卫想好好研究比较一下，尽量省点儿。

　　在JB搜了一下，没有特别完整和实用的贴子。网上网下收集了一堆资料，看了看，晕菜。前卫敢打赌99%的人没有完整的读过保单上的条款。不看了，直接找保险公司的人问，听人说比自己看明白得多。

　　一、选择保险公司。

　　国内开展车辆保险业务的保险公司有四家：中国人民保险公司(人保)、平安保险公司(平安)、太平洋保险公司(太保)、华泰保险公司(华泰)。

　　由于保监会1999年4月1日起统一了汽车保险的条款、费率和安返政策，所以各保险公司在价格上已没什么不同，他们的区别在于投保和理赔的服务上。前卫经比较之后仍旧选择了人保。主要考虑：

　　1、人保在北京汽车保险市场占有率约70%，有规模效益。
　　2、国有公司，理赔较松，经验丰富，操作规范。
　　3、在全国县级地区都有分支机构，如果车辆在外地出险，索赔方便。
　　4、上门办保险、上门送保险单、上门收保险费。
　　5、赠送玻璃单独破碎险和自然险。

　　二、选择代理。

　　人保北京分公司的各分支机构都是自主经营，互相竞争。这些分支机构大致可分为两大类：一类是人保北京分公司的直属营业部和城区支公司。这些分支机构被允许在本市跨区县开展业务，其中业绩较好的有东城支公司、海淀支公司、朝阳支公司等。一类是人保郊区支公司，自99年起已被禁止进入城区开展业务，目前在城区已接触不到这些分支公司。如果有在城区开展业务的，肯定是违规的，不能找他们投保。
　　前卫咨询比较了东城、朝阳、海淀的几个支公司，最后选定了一家代理。
　　主要考虑：

　　1、服务人员有服务意识，主动、耐心、细心、周到。
　　2、指定的大众专修厂位置好，交通方便。
　3、口头承诺专人负责、出现场、拖车、提供代步车等。虽是口头的，总比没有强，说明人家有这份心。

　　三、选择险种。

　　车险共有主险两种：车辆损失险、第三者责任险。

　　附加险九种：车上人员责任险、车上货物责任险、盗抢险、玻璃单独破碎险、停驶损失险、自燃损失险、车身划痕损失险、无过失责任险、不计免赔特约。
　　前卫结合自身实际，对这11项险种逐项分析：

　　*1、车辆损失险：就是自己开车碰了撞了，修车的钱保险公司给出。既然上保险，保的就是这个，怕的就是有个磕了碰了的，肯定得上。
　　*2、第三者责任险：就是自己开车碰了撞了别人，赔给别人的钱保险公司给出。这是强制必须上的，即使不强制，俺也得上，省得到时候麻烦。
　　*3、车上人员责任险：就是自己开车出了事，车上坐的人受伤，治疗花的钱保险公司给出。前卫自己有保险，可一想经常带家里人出来玩儿，得替他们想想，这得上。
　　4、车上货物责任险：就是自己开车出了事，车上拉的货的损失保险公司赔。俺又不是货车，能拉什么货？不上。
　　*5、盗抢险：这回不是自己开车磕了碰了，而是被坏蛋撬了偷了抢了破坏了，造成的损失，保险公司赔。嗯，自己小心可以，保不齐怀人惦记。上吧。
　　*6、玻璃单独破碎险：就是没发生碰撞，也没有坏人，玻璃自己破碎了，保险公司赔。这是他们送的。笑纳了。
　　7、停驶损失险：就是长时间不开车，车放着被人破坏了，或者自己坏了，保险公司管赔。前卫的二宝能闲着吗？不能吧。没用，不上。
　　*8、自燃损失险：就是车自己无缘无故的着了，烧坏了，保险公司管赔。JD不会吧？不过这是他们送的，笑纳。
　　9、车身划痕损失险：这可是新险种，150-200元保最多5000元，就是不小心弄的小划痕的修理费保险公司给出。有的代理这项险是赠送的。前卫咨询了一下，听说定损标准还不太明确，索赔可能比较麻烦。考虑对一年多的车来说划痕不是什么大不了的，决定不上了。
　　10、无过失责任险：就是别人骑车或走路碰了撞了你，人家受了伤，掰扯不清，非让你赔。你好心呀，赔吧，然后到保险公司报销去。前卫一想，凭什么呀？！要是俺不小心，有第三者险，要是别人不小心，俺不要它赔就不错了。不上。
　　*11、不计免赔特约：保险公司为了防止你上了保险就疯开乱开，规定了一个免配额，就是不管出什么事儿，你自己得承担20%，保险公司最多承担80%。你要想都让保险公司出，那就再花点儿钱，上这个附加险，这样甭管出什么事儿保险公司都100%承担。前卫怕麻烦，能省事儿就省事儿，上一个。

　　这样，前卫一共上了7项，其中主险2项，附加险3项，赠送的附加险2项。(加*号的)

　　四、费用比较。
　　选好了险种，开始逐项比价钱。每一项都有一个特罗嗦的计算公式，前卫懒的算，找了几个代理，让他们分别直接报算好并且打完折的价：(为便于查阅，序号与上一条一致)

　　*1、车辆损失险：一年的JettaGix按最低12万保额计算。你可以要求保得更高，那样保费也高，实际没必要。因为车价是不断降低的，等你索赔的时候价格肯定更低，而保险公司将会按当时的市价再减去折旧赔给你，所以上高了没用。这一项的报价在1200-2100之间。
　　*2、第三者责任险：前卫按10万元保险金额上的，比5万多不了多少。这一项报价在700-1300之间。
　　*3、车上人员责任险：前卫自己有寿险，想只上四个乘客险。一打听，按每人1万元投保，上1-4个人，每人70元，共280元。而如果5个座位全上，批发价，250元。嘿！那还不如全上呢。
　　*5、盗抢险：也按12万算，在800-1100之间。
　　*6、玻璃单独破碎险：赠送。
　　*8、自燃损失险：赠送。
　　*11、不计免赔特约：根据两项主险保费之和计算，在400-700之间。

　　各代理在各险种之间价格互有高低，没有一家是全都最低的。所以最后一总计，价格都在3500元左右。前卫选定的那家代理的报价居中。得，就他了。

　　五、办手续。
　　都定好了，电话跟业务员逐项核对，确认。他们打好单子，问前卫哪天送方便。前卫让他们在保单生效那天(去年保单到期那一天的次日)送。外勤送来保单，前卫上人保网站电子商务平台核实了保单的有效性，没问题，交钱，然后微笑着换名片握手再见。
　　需要说明的是，保单生效后才能在人保网站或打电话核实，所以如果小心的话，在那一天之后交钱最好。
　　以上是针对那些真的想上保险的DX。如果你确信自己的技术和车车没问题，可以不上。但年检时必须有第三者责任险的保单，为此，你可以在年检前一个月上3个月的第三者责任险就行了。不过这样一来你可要担很大的风险啊。前卫不鼓励这样做。：) 保险攻略

保险公司的条文晦涩难懂，这篇文章深入浅出的教你如何与保险公司周旋

（一）车损，第三者
（二）丢车
（三）撞车
（四）索赔

保险条款精解（一）- 车损，第三者

咱们先说说最主要的车损险和三责险。
车损险和三责险是车辆保险的基本险，主要赔偿被保险车辆的损失以及由被保险车辆在使用中给第三者带来的损失！
您大概觉得即使是自然灾害造成的车辆损失，保险公司也照赔不误！
这话对了一半，大部分的自然灾害造成的损失都赔，惟独一样除外--------地震！！！！

案例1：如果您的车有幸在地震中被建筑物砸到的话，哈哈
应对方法：等地震过后几天再申请赔偿
出险陈述：大概由于地震造成墙体松动，终于在某一天倒下了（不要提及地震时出险）★★

案例2：如果您的爱车在一次急刹车中，车里的东东飞到了风挡上造成玻璃破裂。您该怎么说呢？
你老老实实的对保险公司说：“我的纸巾盒飞起来打中了玻璃，“哗。。。。。。”（内功够高，呵呵）”
你惨了。。。。。。那个理赔员会指着自己的嘴：“请看我的口型---------no！！！！！！”
正确的应对方法：小小的改变一下事实
出险陈述：我的一个练过铁头功的朋友在刹车时撞碎了风挡，ok！
记住，受车内物品的撞击所受损失，保险公司不赔的！！！！！！★★★★★

案例3：您如果在拖车时与别的车发生了碰撞时
应对方法：忽略一些事实存在的东西
出险陈述：别提你在拖带车辆或者被别人拖带，否则不管你有没有事故责任，保险公司一律不赔★

案例4：如果你在事故时，打破了自己的玻璃...

Krebs cycle or the citric acid cycle) plays several roles in metabolism. It is the final pathway where the oxidative metabolism of carbohydrates, amino acids, and fatty acids converge, their carbon skeletons being converted to CO 2 .

Most of the body's catabolic pathways converge on the TCA cycle (Figure 9.1). Reactions such as the catabolism of some amino acids generate intermediates of the cycle and are called anaplerotic reactions. The citric acid cycle also supplies intermediates for a number of important synthetic reactions. For exam- ple, the cycle functions in the formation of glucose from the carbon skeletons of some amino acids, and it provides building blocks for the synthesis of some amino acids (see p. 267) and heme (see p. 278). Therefore, this cycle should not be viewed as a closed circle, but instead as a traffic circle with compounds entering and leaving as required.

n the TCA cycle, oxaloacetate is first condensed with an acetyl group from acetyl coenzyme A (CoA), and then is regenerated as the cycle is completed (Figure 9.1). Thus, the entry of one acetyl CoA into one round of the TCA cycle does not lead to the net production or consump- tion of intermediates. [Note: Two carbons entering the cycle as acetyl CoA are balanced by two CO 2 exiting.]

Once in the matrix, pyruvate is converted to acetyl CoA by the pyruvate dehydrogenase complex , which is a multienzyme complex.

Their physical association links the reactions in proper sequence without the release of intermediates. In addition to the enzymes participating in the conversion of pyruvate to acetyl CoA, the complex also contains two tightly bound regula- tory enzymes, pyruvate dehydrogenase kinase and pyruvate dehydrogenase phosphatase .

The PDH complex contains five coenzymes that act as carriers or oxidants for the intermediates of the reactions shown in Figure 9.2. E 1 requires thiamine pyro phos phate (TPP), E 2 requires lipoic acid and CoA, and E 3 requires FAD and NAD + .

This is because brain cells are unable to produce suffi- cient ATP (via the TCA cycle) if the PDH complex is inactive. Wernicke-Korsakoff,

Covalent modification by the two regulatory enzymes that are part of the complex alternately activate and inactivate E 1 ( PDH )

The kinase itself is allosterically acti- vated by ATP, acetyl CoA, and NADH. There fore, in the presence of these high-energy signals, the PDH complex is turned off. Pyruvate is a potent inhibitor of PDH kinase . Therefore, if pyruvate concentrations are elevated, E 1 will be maximally active. Calcium is a strong activator of PDH phosphatase , stimulating E 1 activity. This is particularly important in skeletal muscle, where release of Ca 2+ during contraction stimulates the PDH complex , and thereby energy production. [Note: Although covalent regulation by the kinase and phosphatase is key, the complex is also subject to product (NADH, acetyl CoA) inhibition.

The condensation of acetyl CoA and oxaloacetate to form citrate (a tricarboxylic acid) is catalyzed by citrate synthase (Figure 9.4). This aldol condensation has an equilibrium far in the direction of citrate synthesis.

In humans, citrate synthase is not an allosteric enzyme. It is inhibited by its product, citrate. Substrate availability is another means of regulation for citrate synthase . The binding of oxaloacetate causes a conformational change in the enzyme that generates a binding site for acetyl CoA. [Note: Citrate, in addition to being an intermediate in the TCA cycle, provides a source of acetyl CoA for the cytosolic synthesis of fatty acids (see p. 183).

Citrate also inhibits phosphofructokinase , the rate-limiting enzyme of glycolysis (see p. 99), and activates acetyl CoA carboxylase (the rate-limiting enzyme of fatty acid synthesis; see p. 183).]

Oxidation and decarboxylation of isocitrate Isocitrate dehydrogenase catalyzes the irreversible oxidative decar- boxylation of isocitrate, yielding the first of three NADH molecules produced by the cycle, and the first release of CO 2 (see Figure 9.4). This is one of the rate-limiting steps of the TCA cycle. The enzyme is allosterically activated by ADP (a low-energy signal) and Ca 2+ , and is inhibited by ATP and NADH, whose levels are elevated when the cell has abundant energy stores.

The conversion of α-ketoglutarate to succinyl CoA is catalyzed by the α-ketoglutarate dehydrogenase complex , a multimolecular aggregate of three enzymes (Figure 9.5). The mechanism of this oxidative decarboxylation is very similar to that used for the conver- sion of pyruvate to acetyl CoA by the PDH complex . The reaction releases the second CO 2 and produces the second NADH of the cycle. The coenzymes required are thiamine pyrophosphate, lipoic acid, FAD, NAD + , and CoA. Each functions as part of the catalytic mechanism in a way analogous to that described for the PDH complex (see p. 110). The equilibrium of the reaction is far in the direction of succinyl CoA—a high-energy thioester similar to acetyl CoA. α-Ketoglutarate dehydrogenase complex is inhibited by its products, NADH and succinyl CoA, and activated by Ca 2+ . However, it is not regulated by phosphorylation/dephosphorylation reactions as described for PDH complex . [Note: α-Ketoglutarate is also pro- duced by the oxidative deamination (see p. 252) or transamination of the amino acid, glutamate (see p. 250).]

Succinate thiokinase (also called succinyl CoA synthetase —named for the reverse reaction) cleaves the high-energy thioester bond of succinyl CoA (see Figure 9.5). This reaction is coupled to phospho- rylation of guanosine diphosphate (GDP) to guanosine triphosphate (GTP). GTP and ATP are energetically interconvertible by the nucleo side diphosphate kinase reaction: GTP + ADP GDP + ATP The generation of GTP by succinate thiokinase is another example of substrate-level phosphorylation (see p. 102). [Note: Succinyl CoA is also produced from propionyl CoA derived from the metabolism of fatty acids with an odd number of carbon atoms (see p. 193), and from the metabolism of several amino acids (see pp. 265–266).]

Succinate is oxidized to fumarate by succinate dehydrogenase , as FAD (its coenzyme) is reduced to FADH 2 (see Figure 9.5). Succinate dehydrogenase is the only enzyme of the TCA cycle that is embed- ded in the inner mitochondrial membrane. As such, it functions as Complex II of the electron transport chain (see p. 75). [Note: FAD, rather than NAD + , is the electron acceptor because the reducing power of succinate is not sufficient to reduce NAD + .

Fumarate is hydrated to malate in a freely reversible reaction cat- alyzed by fumarase (also called fumarate hydratase , see Figure 9.5). [Note: Fumarate is also produced by the urea cycle (see p. 254), in purine synthesis (see p. 294), and during catabolism of the amino acids, phenylalanine and tyrosine (see p. 263).]

Malate is oxidized to oxaloacetate by malate dehydrogenase (Figure 9.6). This reaction produces the third and final NADH of the cycle. The ΔG 0 of the reaction is positive, but the reaction is driven in the direction of oxaloacetate by the highly exergonic citrate synthase reaction. [Note: Oxaloacetate is also produced by the transamination of the amino acid, aspartic acid (see p. 250).]

Two carbon atoms enter the cycle as acetyl CoA and leave as CO 2 . The cycle does not involve net consumption or production of oxaloac- etate or of any other intermediate. Four pairs of electrons are trans- ferred during one turn of the cycle: three pairs of electrons reducing three NAD + to NADH and one pair reducing FAD to FADH 2 . Oxidation of one NADH by the electron transport chain leads to formation of approximately three ATP, whereas oxidation of FADH 2 yields approxi- mately two ATP (see p. 77). The total yield of ATP from the oxidation of one acetyl CoA is shown in Figure 9.7. Figure 9.8 summarizes the reactions of the TCA cycle.

Pyruvate is oxidatively decarboxylated by pyruvate dehydrogenase (PDH) complex , producing acetyl CoA, which is the major fuel for the tricarboxylic acid cycle

This multienzyme com- plex requires five coenzymes: thiamine pyrophosphate, lipoic acid, FAD, NAD + , and coenzyme A. PDH complex is regulated by covalent modification of E 1 (pyruvate dehydrogenase, PDH) by PDH kinase and PDH phosphatase: phosphorylation inhibits PDH.

PDH kinase is allosterically activated by ATP, acetyl CoA, and NADH and inhibited by pyruvate; the phosphatase is activated by Ca 2+ .

Citrate is synthesized from oxaloacetate and acetyl CoA by citrate synthase. This enzyme is subject to product inhibition by citrate.

Citrate is isomerized to isoci- trate by aconitase. Isocitrate is oxidized and decarboxylated by isoci- trate dehydrogenase to α-ketoglutarate , producing CO 2 and NADH. The enzyme is inhibited by ATP and NADH, and activated by ADP and Ca 2+ .

α-Ketoglutarate is oxidatively decarboxylated to succinyl CoA by the α-ketoglutarate dehydrogenase complex , producing CO 2 and NADH. The enzyme is very similar to pyruvate dehydrogenase and uses the same coenzymes. α-Ketoglutarate dehydrogenase complex is activated by calcium and inhibited by NADH and succinyl CoA, but is not covalently regulated.

Succinyl CoA is cleaved by succinate thioki- nase (also called succinyl CoA synthetase), producing succinate and GTP. This is an example of substrate-level phosphorylation. Succinate is oxidized to fumarate by succinate dehydrogenase, pro- ducing FADH 2 . Fumarate is hydrated to malate by fumarase (fumarate hydratase), and malate is oxidized to oxaloacetate by malate dehydro- genase , producing NADH. Three NADH, one FADH 2 , and one GTP (whose terminal phosphate can be transferred to ADP by nucleoside diphosphate kinase, producing ATP) are produced by one round of the TCA cycle. The generation of acetyl CoA by the oxidation of pyruvate via the PDH complex also produces an NADH. Oxidation of these NADHs and FADH 2 by the electron transport chain yields 14 ATP. An additional ATP (GTP) comes from substrate level phosphorylation in the TCA cycle. Therefore, a total of 15 ATPs are produced from the complete mitochondrial oxidation of pyruvate to CO 2