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【简答题】
(a) IAS 8 Accounting Policies, Changes in Accounting Estimates and Errors contains guidance on the use of accounting policies and accounting estimates. Required: Explain the basis on which the management of an entity must select its accounting policies and distinguish, with an example, between changes in accounting policies and changes in accounting estimates. (5 marks) (b) The directors of Tunshill are disappointed by the draft profi t for the year ended 30 September 2010. The company’s assistant accountant has suggested two areas where she believes the reported profi t may be improved: (i) A major item of plant that cost $20 million to purchase and install on 1 October 2007 is being depreciated on a straight-line basis over a fi ve-year period (assuming no residual value). The plant is wearing well and at the beginning of the current year (1 October 2009) the production manager believed that the plant was likely to last eight years in total (i.e. from the date of its purchase). The assistant accountant has calculated that, based on an eight-year life (and no residual value) the accumulated depreciation of the plant at 30 September 2010 would be $7·5 million ($20 million/8 years x 3). In the fi nancial statements for the year ended 30 September 2009, the accumulated depreciation was $8 million ($20 million/5 years x 2). Therefore, by adopting an eight-year life, Tunshill can avoid a depreciation charge in the current year and instead credit $0·5 million ($8 million – $7·5 million) to the income statement in the current year to improve the reported profi t. (5 marks) (ii) Most of Tunshill’s competitors value their inventory using the average cost (AVCO) basis, whereas Tunshill uses the fi rst in fi rst out (FIFO) basis. The value of Tunshill’s inventory at 30 September 2010 (on the FIFO basis) is $20 million, however on the AVCO basis it would be valued at $18 million. By adopting the same method (AVCO) as its competitors, the assistant accountant says the company would improve its profi t for the year ended 30 September 2010 by $2 million. Tunshill’s inventory at 30 September 2009 was reported as $15 million, however on the AVCO basis it would have been reported as $13·4 million. (5 marks) Required: Comment on the acceptability of the assistant accountant’s suggestions and quantify how they would affect the fi nancial statements if they were implemented under IFRS. Ignore taxation. Note: the mark allocation is shown against each of the two items above.
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【简答题】航空像片比例尺、平均比例尺,引起比例尺变化的因素有哪些?
【简答题】何谓像片比例尺?如何求得像片比例尺?
【单选题】通过 协调多道程序之间的关系,解决对处理机实施分配调度策略、进行分配和回收等。
A.
进程管理
B.
存储管理
C.
设备管理
D.
文件管理
【单选题】有关航空像片比例尺的描述,正确的是
A.
是像片上两点间距离与地面上相应两点间实际距离之比;
B.
像片上的实际比例尺可以用焦距除以航高来计算;
C.
地形起伏会产生像点位移,但不影响图像上两点间比例尺计算;
D.
倾斜摄影不会引起像片比例尺变化。
【多选题】( )使非洲旅游业的发展具有巨大的潜力。
A.
丰富的历史文化遗迹
B.
迷人的自然风光
C.
奇异的野生动植物
D.
完善的基础设施建设
【多选题】影响航摄像片比例尺的因素有
A.
相机焦距
B.
航高
C.
像片尺寸
D.
地物高差
E.
相机视场角
【判断题】当航空摄影高度变化时,摄影像片的比例尺会随之发生变化。航高越小,像片比例尺越小。
A.
正确
B.
错误
【单选题】PPT2010演示文档的默认扩展名是( )
A.
.ppt
B.
.doc
C.
.pptx
D.
.docx
【简答题】讲依恋理论时提到了四种依恋类型,被提出分手后不断自我纠结的人属于四种依恋类型中的( )。
【多选题】Using leptin to explain the role of adipokines in metabolic and eating behavior regulation.
A.
Adipokines may act locally (autocrine and paracrine action) or systemically (endocrine action), carrying information about the adequacy of the energy reserves (TAGs) stored in adipose tissue to other tissues and to the brain. Normally, adipokines produce changes in fuel metabolism and feeding behavior that reestablish adequate fuel reserves and maintain body mass. When adipokines are over- or underproduced, the resulting dysregulation may result in life-threatening disease.
B.
Leptin is an adipokine (167 amino acid residues) that, on reaching the brain, acts on receptors in the hypothalamus to curtail appetite. Leptin was first identified as the product of a gene designated OB (obese) in laboratory mice. Mice with two defective copies of this gene ( ob / ob genotype) show the behavior and physiology of animals in a constant state of starvation: their plasma cortisol levels are elevated; they exhibit unrestrained appetite, are unable to stay warm, grow abnormally large, and do not reproduce.
C.
A second mouse gene, designated D B (diabetic), also has a role in appetite regulation. Mice with two defective copies ( db / db ) are obese and diabetic. The D B gene encodes the leptin receptor. When the receptor is defective, the signaling function of leptin is lost. The leptin receptor is expressed primarily in regions of the brain known to regulate feeding behavior—neurons of the arcuate nucleus of the hypothalamus. Leptin carries the message that fat reserves are sufficient, and it promotes reduction of fuel intake and increase in expenditure of energy. Leptin-receptor interaction in the hypothalamus alters the release of neuronal signals to the region of the brain that affects appetite.
D.
Leptin also stimulates the sympathetic nervous system, increasing blood pressure, heart rate, and thermogenesis by uncoupling the mitochondria of brown adipocytes. Recall that the uncoupling protein UCP1 forms a channel in the inner mitochondrial membrane that allows protons to reenter the mitochondrial matrix without passing through the ATP synthase complex. This permits constant oxidation of fuel (fatty acids in a brown or beige adipocyte) without ATP synthesis, dissipating energy as heat and consuming dietary calories or stored fats in potentially very large amounts.
相关题目:
【多选题】Using leptin to explain the role of adipokines in metabolic and eating behavior regulation.
A.
Adipokines may act locally (autocrine and paracrine action) or systemically (endocrine action), carrying information about the adequacy of the energy reserves (TAGs) stored in adipose tissue to other tissues and to the brain. Normally, adipokines produce changes in fuel metabolism and feeding behavior that reestablish adequate fuel reserves and maintain body mass. When adipokines are over- or underproduced, the resulting dysregulation may result in life-threatening disease.
B.
Leptin is an adipokine (167 amino acid residues) that, on reaching the brain, acts on receptors in the hypothalamus to curtail appetite. Leptin was first identified as the product of a gene designated OB (obese) in laboratory mice. Mice with two defective copies of this gene ( ob / ob genotype) show the behavior and physiology of animals in a constant state of starvation: their plasma cortisol levels are elevated; they exhibit unrestrained appetite, are unable to stay warm, grow abnormally large, and do not reproduce.
C.
A second mouse gene, designated D B (diabetic), also has a role in appetite regulation. Mice with two defective copies ( db / db ) are obese and diabetic. The D B gene encodes the leptin receptor. When the receptor is defective, the signaling function of leptin is lost. The leptin receptor is expressed primarily in regions of the brain known to regulate feeding behavior—neurons of the arcuate nucleus of the hypothalamus. Leptin carries the message that fat reserves are sufficient, and it promotes reduction of fuel intake and increase in expenditure of energy. Leptin-receptor interaction in the hypothalamus alters the release of neuronal signals to the region of the brain that affects appetite.
D.
Leptin also stimulates the sympathetic nervous system, increasing blood pressure, heart rate, and thermogenesis by uncoupling the mitochondria of brown adipocytes. Recall that the uncoupling protein UCP1 forms a channel in the inner mitochondrial membrane that allows protons to reenter the mitochondrial matrix without passing through the ATP synthase complex. This permits constant oxidation of fuel (fatty acids in a brown or beige adipocyte) without ATP synthesis, dissipating energy as heat and consuming dietary calories or stored fats in potentially very large amounts.
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