Bcr Defect

Dr. Sia’s father was a chemical engineer and worked at Dow Chemical company for his entire career. He modeled a scientific approach to problems throughout Dr. Sia’s childhood and instilled in her a enthusiasm for science and technology. While she attended Michigan State University, she worked as a technical assistant for Dr. Wendy Champness in the Department of Microbiology and continued that position for a year after graduation. Interacting with Dr. Champness led Dr. Sia to believe that she wanted to become a college professor and researcher. Dr. Champness was instrumental in her decision to attend graduate school. Dr. David Figurski was her graduate school mentor and was a fantastic role model, and helped Dr. Sia to learn to become a very successful independent researcher. It is standard in her field to have several years of postdoctoral experience with a different mentor, so after she obtained her PhD, Dr. Sia went to work in the laboratory of Dr. Tom Petes in the Biology Department in

Besides testing all of the substances, the experimentation would help build a better understanding of how and why it is that the bacterium Salmonella converts back into its wild-type, and how it is that amino acids carry out this job.

As shown in the figure above, it is evident that V.natriegens grew faster when the Brain Heart Infusion (BHI) broth contained 250mM NaCl. The # of bacterial cells at each time point was measured following the equation given in the “How to generate a bacterial growth curve” supplemental material posted on D2L. (2) The data was then recorded in the table listed above. A growth curve graph was constructed using the data above which illustrated the differences between each of the different BHI mixtures. The graph was then used to determine the generation time of V.natriegens for each different environmental condition. In order to calculate the generation time (g) the mean growth rate (k) must be calculated. The formula to do this is posted in the supplemental material “How to generate a bacterial growth curve” on D2L. The k value calculated for each condition goes as follows:

It will also highlight how successfully integrated plasmids can affect the cell and what proteins are produced by the DNA, and how easy it is to change the genetics of cell and the future generations of that cell. The experiment also demonstrates how natural selection would work in a lab environment, and how the addition of a gene or a mutation can protect an organism from adverse conditions in the environment. This lab also illustrates the change in DNA in a visual sense. Molecular genetics is a very small scale science that cannot be seen by the human eye, however by illuminating the bacteria with the GFP it will produce the very small process can be clearly seen before and after the genetic splicing. The bacteria will produce quickly and the successful bacteria will be clearly seen by the human eye, even after generations upon generations of bacteria.

Severe Combine Immunodeficiency(SCID) is a disease that infects infants within the first few months of life. Some of these infections can be life threatening. The cause of SCID is usually a defect in the T- & B-lymphocyte systems. SCID is known as the “Bubble Boy Disease”. According to the article The SCID Homepage, “SCID became widely known during the 1970’s and 80’s, when the world learned of David Vetter, a boy with X-linked SCID, who lived for 12 years in a plastic, germ-free bubble.” There are multiple versions of SCID, but the most common form is caused by the X-chromosome. Because this disease only affects the X-chromosome, it can affect male infants.

SCID is caused by genetic defects. These defects are either inherited from the parents or result from a new mutation formed in a

Before explaining her work in the lab, Miller informed us with a primer about the three main players in an immune response: B-Cells, T-Cells and

For my experiment, I will be exploring the question of what is the ontogeny, or origination and development, of IgM memory cells that exist within a mouse. In regards to ontogeny, a more distinct question that can be asked is what B-cell subset are the memory cells developed from, whether it is marginal-zone, follicular, or B-1 cells within the organism. My hypothesis is that the B-1 B-cells give rise to the IgM memory population in mice infected with E. muris, a population that is independent of T-cell help and activation.

An attempt to cure an animal was made through bone marrow transplant, the horse died after a year. Similar to the "bubble boy" disease in humans, a foal that is born with the mutation causing SCID lacks both T and B appropriate cell function, their antigen receptors are dysfunctional, its natural killer cells, despite being a part of the innate immune response, may be affected, as they are also descendants of the common lymphoid progenitor. Without these receptors, the lymphocytes do not differentiate, with all components of the adaptive immunity affected, the sick individuals are in a state of immunodeficiency: their immune systems are incapable of fighting infectious diseases. This explains why affected animals die because of multisystemic infections, a consequence of SCID: without any functional B cells, no antibodies are produced, they can’t perform their usual roles of neutralization, opsonization and complement activation. They also can’t be activated by T cells. T cells, on the other hand, are unable to kill infected cells, activate macrophages and B

The mother and the father must have the defective gene in order for the child to inherit the gene. Most of the time the parents do not realize they are carriers.

Today, scientists have figured out that ADA-SCID is potentially caused by mutations in at least fifteen different genes-- and there is a possibility that there is more that has not been researched yet.

In order to observe the different effects of antibiotics and antimicrobials on different bacterial cultures, we utilized the Kirby-Bauer method. With four different bacterial species and two plates for each, one to test antibiotics and the other to test antimicrobials, we created lawns on each plate with the respective bacteria. Before creating the lawns, one must label each plate to indicate the sample, the method, and the types of antibiotics or antimicrobials used. To create a lawn, one sterilizes an inoculating loop with an open flame, allows it to cool, dips it into the sample, and then proceeds to create a dense zig-zag pattern that covers the area of the plate in one direction. Then the plate is rotated 45 degrees and the process is repeated. Finally the plate is rotated 45 degrees once more and the process is repeated again. The creation of a

The adaptive immune system consists of primary cells known as lymphocytes, which are specialized white blood cells manufactured in both bone marrow and the thymus gland. The lymphatic system is the storage unit of the lymphocytes until they are needed to fight pathogens. The major classes of lymphocytes, B cells and T cells manage antibody-mediated immunity and cell-mediate immunity, respectively. T cells respond to antigens on a cells’ membrane binding to infected macrophage triggering several reactions simultaneously. Including, the reproduction of more T cells with the specific receptor necessary to destroy the pathogens (Pinel, 2014).

This arm of adaptive immune response is mediated by antibodies secreted by B cells. B cells originate from hematopoietic stem cells in the liver during fetal development and from bone marrow after birth. In order to be able to recognize a huge number of different antigen, antibodies must be so rich in diversity. Instead of having separate gene for each different immunoglobulin, diversity of the antibody repertoire is generated from a limited number of inherited sequences that undergo alteration including recombination and mutation.

Diseases caused by infectious agents has had a negative effect on human culture and biology. Infectious diseases have devastated human populations all around the world from past to present. As a result of this, humans have learned to adapt to the infectious agents through the evolution of genetics. This paper will primarily focus on the production of sickle cell hemoglobin and malaria. The purpose of this essay is to analyze the research on how human genes can evolve to better survive their environment.