EXPERIMENTAL PROTOCOL:

This exercise will engage students in examining uptake of green fluorescent-tagged bacteria by macrophage cells and unveil the endocytic mechanism used by them. Half of the class will assess bacterial endocytosis by macrophages at different time points, while the other half of the class will test the impact of a endocytosis-altering compound on bacterial uptake.

THIS TABLE OF CONTEXT BELOW IS THE GRAPH INFO ON ALL THE DATA COLECTED FROM THE STUDENTS. 1/2 STUDENTS USED THE CONTROL THE Latrunculin WITH THE E COLI. OTHER 1/2 CLASS DID IT WITHOUT THE CONTROL (MACROPAGES WITH E COLI.). IN STEP 9 EACH GROUP WAS ASSIGNED A DIFFERT TIME OF INCUBATION RANGING FROM 0,15,30 MIN.

1. Summarize your interpretation of the findings.

2.  Include a statement about the future scientific directions suggested by your findings from the experiment (suggest future experiments using as base the results obtained in the lab)

4. Creat a graph with data given. A STANDARD DEVIATION AND AVERAGE graph.

Respond to the following:

An acquired immune response necessitates exposure to an antigen. This initial exposure does not always elicit a leukocyte attack but does program central memory and effector memory T-cell. The innate system is responsible for triggering an adaptive response; the reduction of antigens terminates the immune response. As the infection is eliminated, the quantity of antigens begins to decline. This creates competition between lymphocytes and reduction of new lymphocyte differentiation. Expression of inhibitory signals like CTLA-4, PD-1, and KLRG-1 also occur, along with a reduction in cellular ATP. The cells involved in the adaptive immune response that are not wasted or die, become new memory cells. For some pathogens, innate or humoral immunity is insufficient for defense. This is the case with Bordetella pertussis, which requires a strong T-cell response, to provide immunity. B. pertussis causes whooping cough which can be lethal is allowed to progress, or reinfection occurs. An innate response is initiated and last about 7 days, then a short latent period, followed by acquired response around day 10. The acquired response last until the infection is cleared. The infection by B. pertussis produces a response by Th1, Th2 and Th17 cells. The antigens on B. pertussis, activate signal chains of TNF-α, IFN-γ, IL-5 and IL-13 cytokines (2). T-cell antibodies respond to Filamentous hemagglutinin (FHA), pertussis toxin (PT) and pertactin (PRN) from the B. pertussis bacteria or as components of a vaccine. Vaccines that contain all three components have a higher success rate of immunization. Some vaccines contain B. pertussis fimbriae (FIM) as an antigen. Acquired immune response to B. pertussis is primarily from CCR7+CD45RA−T and CCR7+CD45RA− cells during early childhood (2). A difficulty in illuminating the respiratory track of B. pertussis arises from a type III secretion system (2). Bacterial mechanism serves to produces an anti-inflammatory state in the host leading bacterial proliferation. This protein that the bacteria scan inject directly into the cytosol of tissue cells or most commonly responding leukocytes. It is thought that type III secretion systems disrupt the differing leukocytes ability to attach, T-cell recruitment and cytotoxicity (1). The toxicity and lethality of B. pertussis, arises from the potential to overwhelmed the immune system with type III secretion systems injected cells. It is also thought that B. pertussis immunity is not lifelong and depends on the type of exposure. B. pertussis is vaccinated for children and adults withe the dTap vaccine. It is recommended to be given at 2,4,6,15 months, 4 and 12 years. Pregnant women and healthcare workers are recommended to receive additional vaccinations as well as individuals over 65(3). Natural exposure to B. pertussis elevates the T-cell response more efficiently than synthetic boosters.

Respond to the following:

Acquired immune responses are capable of controlling an infection, however, the acquired immune response is controlled itself through different mechanisms. It is primarily activated by a threshold level of antigen that is produced through the defensive action of the innate immune system. Pathogens and antigens interact and cause dendritic cells to activate to become antigen-presenting cells. Then, the antigens are transported to the lymphoid organs by the antigen-presenting cells. After several days, antigen-specific T cells and B cells locate the foreign antigen, and ultimately differentiate into armed effector cells. These cells either leave the lymphoid organ to go to the sites of infection or stay within the organ to promote humoral immunity. The path the effector cells take is dependent on the differentiation of CD4 T cells. There are two different subsets of CD4 T cells, Th1 and Th2. The function of Th1 is to activate macrophages, while Th2 works to activate B cells, especially during the primary response. Both of these CD4 T cell subset are capable of regulating each other, which is essential done by the cytokines of each respective T cell type. Ultimately, the effector cells remove the pathogens to control the infection (1). Once an infection is effectively under control, it is critical to remove the effector cells to allow for the restoration of the tissue. The immune system has mechanisms in which it is capable of removing these cells. When effector cells are no longer needed, they undergo apoptosis. The function of effector cells is to remove the stimulus that activated them, but when that stimulus is gone, the effector cells no longer have anything to remove except for themselves, which occurs through apoptosis. Apoptosis causes cells to die, and they are subsequently removed through macrophages. They are capable of identifying the dying cells through the composition of their membrane, specifically the lipid phosphatidylserine. In a normal cell, the lipid is found on the inner portion of the plasma membrane. However, when a cell undergoes apoptosis, it redistributes to the outer surface which allows for easy recognition by phagocytes. While some effector cells are removed, some are retained to allow for formation of memory T-cell and B-cells (1). The acquired protective immune response is critical in providing protection against pathogens. It is acquired through effector T cells or antibodies that are generated when exposed to the pathogen, as described above. This can be done by initial infection or through vaccination that allows for immunological memory. The specific pathogen involved influences the type of effector T cell or antibody that provides protection. For example, the polio inactivated vaccine utilizes preexisting antibodies (IgA) to neutralize the virus and prevent its spread of infection (1). These antibodies are known as IgA, and are produced within the gut mucosa. In order to activate the mucosal immune response, antigens are transported across the epithelium through the use of microfold (M cells). They are then presented to effector B lymphocytes that result in stimulated B cells to migrate to distant mucosal cites. This ultimately leads to the production of IgA that neutralizes the antigen. The neutralization of these substances prevents it from binding to receptors within the tissue. Therefore, the neutralized antibody-antigen complex formed is ultimately removed and destroyed by macrophages (2).

Briefly describe the cytoskeletal structure and biological function of motile cilia why do we need to study the bending properties of single cilia?

Did lead poisoning bring down ancient Rome?

Some researchers have questioned whether lead poisoning contributed to the downfall of the Roman Empire. There are several published papers explaining the potential evidence and their importance.

You need to search different resources and discuss if this could be true or not? And why?

Assume you are studying some species of flower that comes in three different colors: red, pink, and white. You know that color is determined by a single locus with two alleles with incomplete dominance. You count 124 red flowers, 62 pink flowers, and 30 white flowers. What are the allele frequencies and is the population in Hardy-Weinberg equilibrium? Calculate the chi squared test statistic and p-value.

What is the Hardy-Weinberg principle for a gene with two alleles in a tetraploid?

Should researchers or the family “play God” and try to correct the neuronal cells that are affected in Spinal Muscular Atrophy? Discuss your views on this potential stem cell therapy and discuss the ethical questions that you think need to be considered when developing new DNA based medical treatments.

Describe how animals produce energy in aerobic and anaerobic conditions.

Is acid rain a problem for plant species and crops today? How are plants impacted by acid rain? Do a web-search and include the name of at least one specific crop in your answer. Your answer should be at least 10 sentences long. As always, include references to information sources used.

Has anyone ever watched this video and can critique it?

Protein synthesis: an epic on the cellular level

https://www.youtube.com/watch?v=u9dhO0iCLww

There are often several receptor subtypes for one neurotransmitter, like acetylcholine, which are distributed in different parts of the nervous system. Why might it be useful to have different receptor subtypes in specific areas? What clinical implications would it have?

Suppose the following genotypes are in a 1:1:1:1 ratio. TTDD, TtDD, ttDD, TdDd If there are a total of 160 individuals, how many of them have the genotype TdDD?

1. In a nutshell, what are the major steps performed during next generation sequencing of DNA? How do these steps differ in the Illumina platform as compared to the Roche 454 platform?

2. In a nutshell, describe the major steps performed during DNA sequencing by the Pacific Biosciences, as well as the Oxford Nanopore Sequencing Technologies.

3. In a nutshell, describe the major advantages and disadvantages of each DNA sequencing platform.

Which of the amino acids neurotransmitters would be responsible for producing an action potential and which would most likely be released to prevent an action potential from occurring? Can you think of a time when it might be helpful to have a neurotransmitter that, when it binds to the post-synaptic cell, it inhibits an action potential?