A botanist is trying to see the effects of temperature on a certain plant species. She prepares four identical plots of soil and runs a heating element through the soil so she can vary the temperature of each plot. After one month she harvests all of the plant biomass and records the temperature of each plot along with the biomass collected. The data are given in the table below.

Suppose the experimenter prepares four more plots, each with a constant soil temperature of , but each plot is equipped with misters to vary the humidity levels. Below are the data for the biomass yield for four different humidity levels. 

Based on the information above, which of the following is closest to the humidity level of Plots A, B, C and D?

A botanist is trying to see the effects of temperature on a certain plant species. She prepares four identical plots of soil and runs a heating element through the soil so she can vary the temperature of each plot. After one month she harvests all of the plant biomass and records the temperature of each plot along with the biomass collected. The data are given in the table below.

After the experiment, the botanist noticed that the heating element was not calibrated properly and displayed a temperature 3 degrees lower than it actually was. The botanist repeats the experiment, this time with the correct heating element. In this repeated experiment, the heating element now displays 22 degrees Celsius for plot A. Which of the plots would you expect to have the highest yield in the repeated experiment?

Three different species of bacteria were grown in the laboratory. The experiment measured the effect of pH on the concentration of the three species of bacteria. The graphs below show the concentration of bacteria at different pH levels. Figure 2 shows the effect of pH on the concentration of a third bacterial strain, bacteria C.

Oceans on Planet XYZ have been determined by scientists as being highly alkeline. Based on figures 1, 2 and 3 which species of bacteria would have the highest chance of surviving on this planet's oceans?

The population of two different sparrow varieties were recorded from spring 1992 to fall 1996 and displayed below in the form of a graph.

During the period this experiment was taking place, the area where the sparrow populations were being recorded suffered from a forest fire. From studying the data presented in the graph, when would the forest fire have most likely occurred?

An undergraduate biology student working in a lab was reading about the latest health epidemic in the United States concerning obesity. He recently learned in his biology class that an enzyme called fatty acid synthase (FAS) catalyzes the formation of fatty acids. Accumulation of these fatty acids then creates the adipose fatty tissue that individuals typically see in their belly or side-regions. He hypothesizes that by decreasing the rate that this enzyme produces fatty acids by administering an inhibitor will aid in reducing the storage of fats, helping to alleviate obesity. After gaining approval from the university's clinical trials and ethics committee, he gathered a group of 20 test subjects. With the help of his research director, he measured the baseline rate of FAS activity for all test subjects and the averaged rate after oral administrators of a placebo and three types of inhibitors at a concentration of 0.6M to four equally-sized groups. The data is shown in Table 1.                      

Table 1.

The student then wonders if a mixture of different inhibitors were to increase the effect in the subject. He again measured the averaged baseline FAS level of the subjects and then attempted administering a placebo and three different combinations of inhibitors to subjects in a second trial. The results are shown in Table 2.

Table 2. 

A colleague of the researcher interpreted the results from Table 1 and 2 and suggested a third trial which would track the averaged weight change of the subjects over a 6-month period. The results are shown in Table 3.

Table 3.

According to the data tables presented, if the researcher instead gave the subjects an inhibitor of concentration 1.15 M, how would the FAS activity change?

An undergraduate biology student working in a lab was reading about the latest health epidemic in the United States concerning obesity. He recently learned in his biology class that an enzyme called fatty acid synthase (FAS) catalyzes the formation of fatty acids. Accumulation of these fatty acids then creates the adipose fatty tissue that individuals typically see in their belly or side-regions. He hypothesizes that by decreasing the rate that this enzyme produces fatty acids by administering an inhibitor will aid in reducing the storage of fats, helping to alleviate obesity. After gaining approval from the university's clinical trials and ethics committee, he gathered a group of 20 test subjects. With the help of his research director, he measured the baseline rate of FAS activity for all test subjects and the averaged rate after oral administrators of a placebo and three types of inhibitors at a concentration of 0.6M to four equally-sized groups. The data is shown in Table 1.                      

Table 1.

The student then wonders if a mixture of different inhibitors were to increase the effect in the subject. He again measured the averaged baseline FAS level of the subjects and then attempted administering a placebo and three different combinations of inhibitors to subjects in a second trial. The results are shown in Table 2.

Table 2. 

A colleague of the researcher interpreted the results from Table 1 and 2 and suggested a third trial which would track the averaged weight change of the subjects over a 6-month period. The results are shown in Table 3.

Table 3.

What is a plausible explanation for why the placebo group gained less in weight than the group not given any drug?

An undergraduate biology student working in a lab was reading about the latest health epidemic in the United States concerning obesity. He recently learned in his biology class that an enzyme called fatty acid synthase (FAS) catalyzes the formation of fatty acids. Accumulation of these fatty acids then creates the adipose fatty tissue that individuals typically see in their belly or side-regions. He hypothesizes that by decreasing the rate that this enzyme produces fatty acids by administering an inhibitor will aid in reducing the storage of fats, helping to alleviate obesity. After gaining approval from the university's clinical trials and ethics committee, he gathered a group of 20 test subjects. With the help of his research director, he measured the baseline rate of FAS activity for all test subjects and the averaged rate after oral administrators of a placebo and three types of inhibitors at a concentration of 0.6M to four equally-sized groups. The data is shown in Table 1.                      

Table 1.

The student then wonders if a mixture of different inhibitors were to increase the effect in the subject. He again measured the averaged baseline FAS level of the subjects and then attempted administering a placebo and three different combinations of inhibitors to subjects in a second trial. The results are shown in Table 2.

Table 2. 

A colleague of the researcher interpreted the results from Table 1 and 2 and suggested a third trial which would track the averaged weight change of the subjects over a 6-month period. The results are shown in Table 3.

Table 3.

A novel inhibitor, Inhibitor C, was found to bind to and increase the rate of Enzyme Y that acted as a strict agonist to FAS. What would be predicted to occur if Inhibitor C was given to all of the patients in addition to the treatments they were receiving?

In the 1980’s, an epidemic of bovine spongiform encephalopathy, or mad cow disease, swept through cattle herds in the United Kingdom. Scientists and veterinarians were troubled and had a difficult time managing the disease because it spread from one animal to another, and behaved differently than other diseases in the past. 

When infectious material from affected animals was treated with high levels of radiation, for example, the material remained infectious. All known bacteria or viruses that carry disease would have been killed by such a treatment. Additionally, some animals developed the disease without first being exposed to sick animals. Perhaps most frustratingly, among those animals that are exposed before becoming sick, it can take many years after exposure for illness to appear.

There quickly emerged two distinct explanations for the disease. 

Scientist 1:

Mad cow disease is unlike any disease we have handled before. It is increasingly clear that the best explanation for the disease’s dynamics involve proteins, called the protein-only hypothesis. These protein molecules are likely causative of the disease, and they lack any DNA or RNA. It is damage to these DNA or RNA molecules that kills bacteria or viruses when exposed to high levels of radiation. The most important observations that made scientists consider a unique, protein-only model for this disease involved its resistance to radiation. Remarkably, this would be the first example of an infectious agent copying itself without DNA or RNA to mediate the process.

Moreover, some animals develop the disease spontaneously, without physically being infected by another animal. This suggests that internal disorder among protein molecules is a potential route to developing disease, and may be accelerated by exposure to other sick animals.

In fact, this is consistent with the proposed mechanism. It is likely that proteins fold incorrectly, and then influence proteins around them to take on this errant conformation. Some proteins may fold incorrectly by chance, which explains spontaneous disease development. It also explains the long course of disease, as it takes many years for enough proteins to fold incorrectly and result in observable disease.

Scientist 2:

The suggestion that mad cow disease is caused exclusively by protein, in the absence of DNA or RNA, is such a dramatic departure from accepted biological processes that it warrants careful scrutiny. Additionally, other more conventional explanations should be thoroughly investigated before coming to such a conclusion.

Some scientists have shown that very small particles resembling viruses are visible in infectious material under powerful microscopes. Additionally, these viruses are consistent in size and shape with known, highly radiation-resistant viruses called polyomaviruses. It takes much higher-than-typical doses of radiation to cause enough DNA damage to inactivate these viruses.

The observation that mad cow disease occurs spontaneously in some animals is also explained by the viral explanation. Many viruses exist in animals and humans for years, undetected and not causing any observable disease. Sickness or stress can make these viruses reactivate, offering the illusion of spontaneous illness. All of these observations are consistent with the viral hypothesis.

Scientist 1 includes the information about the long duration between likely infection and the development of symptoms most specifically to:

In the 1980’s, an epidemic of bovine spongiform encephalopathy, or mad cow disease, swept through cattle herds in the United Kingdom. Scientists and veterinarians were troubled and had a difficult time managing the disease because it spread from one animal to another, and behaved differently than other diseases in the past. 

When infectious material from affected animals was treated with high levels of radiation, for example, the material remained infectious. All known bacteria or viruses that carry disease would have been killed by such a treatment. Additionally, some animals developed the disease without first being exposed to sick animals. Perhaps most frustratingly, among those animals that are exposed before becoming sick, it can take many years after exposure for illness to appear.

There quickly emerged two distinct explanations for the disease. 

Scientist 1:

Mad cow disease is unlike any disease we have handled before. It is increasingly clear that the best explanation for the disease’s dynamics involve proteins, called the protein-only hypothesis. These protein molecules are likely causative of the disease, and they lack any DNA or RNA. It is damage to these DNA or RNA molecules that kills bacteria or viruses when exposed to high levels of radiation. The most important observations that made scientists consider a unique, protein-only model for this disease involved its resistance to radiation. Remarkably, this would be the first example of an infectious agent copying itself without DNA or RNA to mediate the process.

Moreover, some animals develop the disease spontaneously, without physically being infected by another animal. This suggests that internal disorder among protein molecules is a potential route to developing disease, and may be accelerated by exposure to other sick animals.

In fact, this is consistent with the proposed mechanism. It is likely that proteins fold incorrectly, and then influence proteins around them to take on this errant conformation. Some proteins may fold incorrectly by chance, which explains spontaneous disease development. It also explains the long course of disease, as it takes many years for enough proteins to fold incorrectly and result in observable disease.

Scientist 2:

The suggestion that mad cow disease is caused exclusively by protein, in the absence of DNA or RNA, is such a dramatic departure from accepted biological processes that it warrants careful scrutiny. Additionally, other more conventional explanations should be thoroughly investigated before coming to such a conclusion.

Some scientists have shown that very small particles resembling viruses are visible in infectious material under powerful microscopes. Additionally, these viruses are consistent in size and shape with known, highly radiation-resistant viruses called polyomaviruses. It takes much higher-than-typical doses of radiation to cause enough DNA damage to inactivate these viruses.

The observation that mad cow disease occurs spontaneously in some animals is also explained by the viral explanation. Many viruses exist in animals and humans for years, undetected and not causing any observable disease. Sickness or stress can make these viruses reactivate, offering the illusion of spontaneous illness. All of these observations are consistent with the viral hypothesis.

Which of the following would most directly refute the protein-only hypothesis?

I. It is found that more animals than previously thought develop the disease spontaneously, without exposure to infected material

II. Another disease is found to be caused by a protein lacking any DNA or RNA

III. Treatment with an enzyme that breaks down DNA and RNA makes infectious material non-infectious

In the 1980’s, an epidemic of bovine spongiform encephalopathy, or mad cow disease, swept through cattle herds in the United Kingdom. Scientists and veterinarians were troubled and had a difficult time managing the disease because it spread from one animal to another, and behaved differently than other diseases in the past. 

When infectious material from affected animals was treated with high levels of radiation, for example, the material remained infectious. All known bacteria or viruses that carry disease would have been killed by such a treatment. Additionally, some animals developed the disease without first being exposed to sick animals. Perhaps most frustratingly, among those animals that are exposed before becoming sick, it can take many years after exposure for illness to appear.

There quickly emerged two distinct explanations for the disease. 

Scientist 1:

Mad cow disease is unlike any disease we have handled before. It is increasingly clear that the best explanation for the disease’s dynamics involve proteins, called the protein-only hypothesis. These protein molecules are likely causative of the disease, and they lack any DNA or RNA. It is damage to these DNA or RNA molecules that kills bacteria or viruses when exposed to high levels of radiation. The most important observations that made scientists consider a unique, protein-only model for this disease involved its resistance to radiation. Remarkably, this would be the first example of an infectious agent copying itself without DNA or RNA to mediate the process.

Moreover, some animals develop the disease spontaneously, without physically being infected by another animal. This suggests that internal disorder among protein molecules is a potential route to developing disease, and may be accelerated by exposure to other sick animals.

In fact, this is consistent with the proposed mechanism. It is likely that proteins fold incorrectly, and then influence proteins around them to take on this errant conformation. Some proteins may fold incorrectly by chance, which explains spontaneous disease development. It also explains the long course of disease, as it takes many years for enough proteins to fold incorrectly and result in observable disease.

Scientist 2:

The suggestion that mad cow disease is caused exclusively by protein, in the absence of DNA or RNA, is such a dramatic departure from accepted biological processes that it warrants careful scrutiny. Additionally, other more conventional explanations should be thoroughly investigated before coming to such a conclusion.

Some scientists have shown that very small particles resembling viruses are visible in infectious material under powerful microscopes. Additionally, these viruses are consistent in size and shape with known, highly radiation-resistant viruses called polyomaviruses. It takes much higher-than-typical doses of radiation to cause enough DNA damage to inactivate these viruses.

The observation that mad cow disease occurs spontaneously in some animals is also explained by the viral explanation. Many viruses exist in animals and humans for years, undetected and not causing any observable disease. Sickness or stress can make these viruses reactivate, offering the illusion of spontaneous illness. All of these observations are consistent with the viral hypothesis.

Which of the following facts is an implicit assumption in the argument of Scientist 1?