- Why did scientists in the past believe that excessive gastric
acid secretion was the cause of gastric ulcers?
- In the 1980s, based on what observations did Barry Marshall
consider Helicobacter pylori to be a more plausible cause of gastric
ulcers?
- Among his patients, Helicobacter pylori was detected in the
stomachs of all those with gastric ulcers. Can this observation
conclusively prove that Helicobacter pylori is definitely the cause of
gastric ulcers? Why or why not?
- If not, suggest other possible sources of error.
- To prove that Helicobacter pylori causes gastric ulcers, what
should the experimental and control groups be?
- What is the prediction of this experiment?
- What is the independent variable in this experiment?
- What is the dependent variable in this experiment?
- What is the assumption of this experimental design (if any)?
- What are the control variables in this experimental design?
- Since mental stress and chronic stress may also cause gastric
ulcers, how can the experiment prevent participants from developing ulcers
due to stress after knowing they have ingested Helicobacter pylori?
- In reality, it is difficult to find participants for the
experimental group. Suggest possible reasons for this.
- Some people ingested Helicobacter pylori but did not develop
gastric ulcers. Suggest possible reasons for this.
- Using humans as test subjects can lead to significant errors.
Identify possible sources of error and suggest ways to reduce them.
- In the end, only one person (Barry Marshall) participated in
the experimental group. Is this experimental result credible? What methods
could be used to address this?
- Was this scientist risking his life to conduct this experiment?
Comment on this approach.
- What tests should this scientist have conducted beforehand to
mitigate health risks?
- As early as the late 19th and early 20th centuries,
Helicobacter pylori had been discovered on the gastric mucosa of ulcer
patients, yet scientists did not believe there was a connection between
Helicobacter pylori and gastric ulcers. How did they explain these
findings?
1.
胃酸是鹽酸,屬強酸,可破壞細胞。身體是如何防止胃壁受到破壞的?
2.
根據以上的機制,胃潰瘍(即胃壁損傷和出血)的可能成因是甚麼?
3.
從前的科學家為何認為過量的胃酸分泌是導致胃潰瘍的成因?
4.
於1980年代,Barry Marshall憑甚麼觀察認為螺旋桿菌是更合理導致胃潰瘍的成因?
5.
已知他的病人中,患有胃漬瘍的患者胃部皆可檢測出螺旋桿菌。但這觀察能否推論出胃漬瘍的成因一定是因為螺旋桿菌? 為甚麼?
6.
如不能的話,試提出其他可能的誤差。
7.
要證明幽門螺旋菌引致胃漬瘍的話,實驗組及對照組分別應是甚麼?
8.
這實驗的預測是甚麼?
9.
這實驗的自變量是甚麼?
10. 這實驗的因變量是甚麼?
11. 這實驗驗設計的假設是甚麼? (如有的話)
12. 這實驗設計的控制變量是甚麼?
13. 已知精神緊張及長期壓力也可能引致胃潰瘍。進行實驗時如何避免實驗者因知道服食了幽門螺旋菌而導致緊張,從而引致胃潰瘍?
14. 現實上,很難找到實驗組所需的參加者。試估計其原因。
15. 有人服食了幽門螺旋菌,但卻沒有患上胃潰瘍。試估計可能的原因。
16. 使用人作為測試對象,誤差會很大。試指出可能出現誤差的原因。並指出如何減少誤差?
17. 這實驗最終祇有一人(即Barry Marshall)參與實驗組。哪這實驗結果是否可信? 有甚麼方法可解決?
18. 這科學家是否在冒死進行這實驗? 試評論這做法。
19. 試估計這科學家事前應進行甚麼測試,以降低自己的健康風險?
20. 其實早於19世紀末20世紀初時,胃潰瘍患者胃黏膜上已發現螺旋桿菌, 但科學家並不認為胃潰瘍跟螺旋桿菌有關。哪他們如何解釋這些發現?
21. 嚴格來說,胃酸分泌過多並不是全錯的成因。試加以解釋。
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