As we ride the glucose molecule into the small intestine we see a curious rod shaped organism. Upon further inspection we notice that it has an outer membrane with lipopolysaccharide. We barely have time to contemplate what this means before we feel the pull of transport. We ride past the cell wall (outer membrane and peptidoglycan) and are pulled through a transporter and into the cytoplasmic membrane of the cell. We ride through the transporter’s hydrophilic center, down the concentration gradient and into the cytoplasm.

1. What type of protein is this transporter?

Membrane transport protein

2. What type of transport are we experiencing?

What is the relationship between Microvilli of gut, epithelium, glucose, circulatory system, capillary fenestrations, glucose/ATP/life. Major emphasis on RELATIONSHIP

why you think a solid understanding of Biology is important for our everyday lives.

• What is LTP?
• What are some of the presynaptic changes observed?
• What are some of the postsynaptic changes observed?
• How do the AMPA and NMDA glutamate receptors contribute to LTP?

Many ecologists view continual growth as impossible in the long run due to limits imposed by nonrenewable resources and the capacity of the biosphere to absorb wastes. Others argue that through the use of technology and social organization, we can manage to meet our needs and provide long-term (but not infinite) growth. WHAT DO YOU THINK ? Please provide a structured essay with your thoughts,

During starvation, the body adapts to ensure that cells have access to a variety of fuel sources. Select all of the biochemical pathways that are active during periods of prolonged starvation.

Choose All That Apply

A. Ketogenesis

B. Lipolysis

C. Proteolysis

D. Gluconeogenisis

E. Glycogenesis

F. Lipogenesis

1. How is race/ethnicity defined genetically and phenotypically? Is it even possible to define race/ethnicity by genetics?
2. How does it help or hinder health care when sickle cell is considered a disease of individuals of African-descent?

Even though Gram stain is not very specific, studies have found that it is as accurate as DNA-based methods for identifying the causative pathogen of most urinary tract infections. Why do you think this is the case?

Susan and Joe were worried. Their little boy, Daniel, had been having an awful lot of bacterial infections and he was barely a year old. It seemed that the antibiotics cleared up one bacterial respiratory infection only to have another follow shortly. The scary thing was that Daniel had just fought off a case of pneumonia caused by Pneumocystis carnii, a fungal infection that was usually found in people with HIV. Waiting for the test results of an HIV test for their little boy was one of the worst waits ever. Thank goodness it came back negative.

However, it seemed that their troubles were just beginning. After this last lung infection, the fungal one, and a negative HIV test, their doctor had ordered a number of other blood tests, including a genetic test that Susan didn’t fully understand. Apparently the doctor was worried about Daniel’s immune system functions. Susan had also met with a genetic counselor who collected a family history of any immune disorders. The details were vague, but Susan’s mother, Helen, knew that one of her three brothers had died young from an unexplained lung infection. Unfortunately, Grandma Ruth had passed away a few years ago, leaving them with numerous unanswered questions.

Susan and Joe had an appointment with their doctor that afternoon to go over the results. When they arrived Dr. Dresdner led them into an office where Ms. Henchey, the genetic counselor, waited. This can’t be good, thought Susan. The doctor began by explaining that they had analyzed Daniel’s blood and found that while he had normal levels of B cells and T cells, his antibody levels were anything but normal. The levels of IgG, IgA, and IgE were very low, almost undetectable, and Daniel had abnormally high levels of IgM and IgD. He went on to explain the nature of these different categories of immunoglobulins.

Ms. Henchey, the genetic counselor, explained that Daniel had a genetic mutation in the gene for the CD40 ligand.

How does a deficiency in CD40 ligand explain Daniel’s immunological deficiency?

1. ) Prior to 1900, the natural range of the moose, Alces alces, included all Canadian provinces except the island of Newfoundland. In 1904, two male and two female moose were transported from New Brunswick to Newfoundland, where they have founded a large population of 110,000 moose.

Describe and explain the expected evolutionary consequences due to genetic drift, shortly after the transport of the four moose, on (1) the New Brunswick population and (2) the Newfoundland moose population

Describe the mechanism of action of the drug ZAVESCA

Briefly describe the normal cell biology, the pathogenic state and how the drug alters the pathogenic state.

Come up with an experimental plan by which you can prove where in the cell the drug acts; what cellular functions it modulates, and the mechanism by which it works.

I KNOW THOSE ANSWERS BUT I NEED HOW TO SOLVE

Q1 ANSWER E(1487)

Q B

Q 1

What is the equilibrium constant for the reaction shown below?

glutathione + NADPH + H⁺ ↔ reduced glutathione + reduced glutathione + NADP⁺

In a paragraph, relate the following terms:  Metabolism, anabolism, catabolism, hydrolysis, condensation, endergonic, exergonic.  

Relate means group those terms together that belong together. For example, anabolism means to build up larger molecules. What process do we use to build up larger molecules and does that process store energy or release energy?