Cell Cycle Progression Analysis Of T. Bucei Procyclic Cells

In conclusion, parasitic hairworms cause grasshoppers’ deaths by controlling their central nervous systems. Also, biologists have discovered that the parasites control the central nervous systems by injecting the hosts with a cocktail of chemicals. Scientists have used this information to learn more about the relationship between parasites and hosts. Because of these findings, the development of new medical treatments may be possible. Not only do hairworms illustrate this behavior, other living creatures do

For my parasite I picked Ophiocordyceps unilateralis or the zombie ant fungus. This fungus infects tree dwelling carpenter ants in tropical rainforests and forces them to do its biding. The parasitic fungus spreads itself around by releasing spores into the air like most fungi. The catch is that to be able to mature itself to the point of passing along its offspring it has to sacrifice an ant. Once an ant has become infected it behaves very bizarrely. The fungus forces the ant to crawl out to the end of a leaf and then it begins to shake violently. This causes the ant to fall to the forest floor where it begins to look for a nearby plant. Once it has found a suitable plant, usually one around 10cm from the ground, it climbs out onto a leaf

In part 2 of the experiment we are inducing RNAi through the process of feeding. To do so, a black pen is used to label the bottom of an OP50 seeded plate with the date and “wild type”. Another OP50 seeded plate is labeled with the date and “dpy-13”. A black pen is then used to label the bottom of the plate seeded with dpy-13 RNAi feeding strain with the date and “wild type”. Five L4-stage worms from the plate of wild type worms are then picked and moved to the OP50 seeded plate labeled “wild type”. Any eggs or young larvae that may have been accidentally transferred are to be picked off of the plate and then flamed in a Bunsen burner. The same method is used to move five L4 wild type worms to the plate seeded with the dpy-13 RNAi feeding strain, and once again to move five L4 dpy-13 worms to the OP50 seeded plate labeled “dpy-13”. These plates are then incubated upside down at 20˚C.

To make the specimen compatible with both forms of advanced microscopy, they sufficiently prepared samples by coupling the specimen with a fluorescence that was also conductive. This technique was accomplished with the FlouroNanogold label, which contains gold nanoparticles covalently bonded to a fluorescence label. That way, the LM worked as well as the EM for the same set of kinetochores that were being studied. The Hec1 protein was stained in this case because this protein naturally delineates the structures to be studied.

Firstly, eggs were collected from the eyes of Scomberomorus niphonius and disinfected in 1% sodium sulfite solution for 3 min, and subsequently in 3% Lysol brand disinfectant for 5 min. The disinfected eggs were then transferred to sterile vials to clone. Secondly, third stage larvae of Lucilia sericata were selected to be placed in 3.5% formalin for 5 min, 2% hydrogen peroxide solution for 3 min, and then 5% dilute hydrochloric acid solution for 5 min. After the two-step disinfection, the larvae remined vigorous. A hundred randomly selected larvae were proven to be aseptic by bacterial culture test.

This experiment can be enhanced in many ways. The amount of alcohol used as treatments could be lessened to measure the viability of A. salina more accurately. The amount of cysts in each Petri dish was not consistent because there

Karnovsky’s fixative is made of gluteraldehyde, paraformaldehyde, and phosphate buffer. This fixative is considered the best one used in this class, so the best results were expected when using Karnovsky’s fixative. Gluteraldehyde functions similarly to formaldehyde in that it cross-links effectively. However, this molecule is larger than that of formaldehyde, so it is not possible to use in paraffin embedding, because the large wax molecules would be unable to penetrate the tissue after fixation. The largest disadvantage of this exceptional fixative is the higher cost, both of the materials required for fixation, and for the required plastic embedding rather than paraffin. On the other hand, the benefits of using Karnovsky’s fixative often outweigh the increased cost. The cytological preservation of tissue using this fixative is incredible, and allows for great visualization of structures under the microscope (Hopwood, 1967). This fixative can be used for electron microscopy due to this feature, and offers stunning results using less powerful microscopes as well. A further disadvantage of this fixative and embedding process is that the stains we are able to use are more limited as well.

The host adaptive immune response produces an inflammatory reaction to the death or dying parasites. The subsequent release of parasite molecules and inflammatory mediators results an irreversible lymphatics dysfunction. (Figueredo-Silva et al., 2002; Nutman, 2013). The lymphatic dysfunction predispose a suitable environment for secondary bacterial or fungal infection, initiate inflammatory reaction in the skin and subcutaneous tissue, and enhance progression of lymphedema and precipitate the development of elephantiasis (Nutman, 2013)

[98, 99]. The detrimental effects of ROS become more pronounced with age due to the limits of cellular antioxidant defense systems.

Most of these disease-causing eukaryotic microorganisms depend on other organisms for nourishment. Different parasites have different hosts. The parasites obtain nutrients from their hosts whole causing damage to the tissues and overall nutrition of the host. These parasites have distinct features that enable them to survive in the bodies of their hosts.

In a eukaryotic host cell, DNA is packaged into chromatin found in the nucleus that regulates the access of enzymes to the genome. Within the chromatin structure there are histone protein components that help package the DNA. The histone subunits have tails that are modification targets by enzymes that alter the construction of the chromatin.10 There are also many accessory proteins that recognize and bind to these parts of the histone to further alter their function.10 Thus, they create an opportunity for bacterial invaders to come in and set in motion pathogenesis.

Protozoans hemoflagellates of the genus trypanosome become infected, which is the root cause of Sleeping Sickness (8). There are many species of trypanosome, however only T. b. gambiense and T. b. rhodesiense are the causes of sleeping sickness. When the trypanosome gets infected the antibodies, IgM and IgG, start to get produced by the immune system, which leads to a decrease of parasitemia (7). However, some of the trypanosomes have a new surface coat that is resistant to the antibodies, so they keep proliferating and the immune system isn’t able to eliminate the parasite (7).

Another potential variable that enormously improves the rise of new pathogens is the multiplication of new strains of the pathogens. Diverse strains of parasites act distinctively including their affectability to medications and this is the reason the medication safe strains of Plasmodium has prompted to the spread and increment pervasiveness of intestinal sickness. Various parasites have created distinctive strains with different possibilities including those that can make them make due in cruel situations and fast multiplication and down direction of host safe reactions.

While in the Leishmanial stage in the host it uses the white blood cells to hide its self. At the site of infection The While blood cells eat the parasite, trying to clean the host. While inside the white blood cells cell body, the Leishmania releases a chemical that tells the hosts other immune defenses that everything at the site of infection is under control. This chemical extends the life of the white blood cell from 6-8 hours to 2-3 days in order to wait for the macrophages to arrive which could take up to 3 days. Macrophages are known as the wondering cell, meaning it can go different places in the body. This is how the parasite can move while in the Leishmanial form. The life expectancy of the macrophages is much longer of the white blood cells giving the parasite time to reproduce. Once at the site of infection the macrophages eat the white blood cells that have the parasite inside thinking that they are dying and need a place to be destroyed and be recycled. After the macrophage eats the parasite unknowingly, the parasite starts to reproduce and once the cell is full it will burst releasing the parasite in to the body looking to start this process again (“Lesihmania ” n.db).

their hardest to contain the parasite to where it now exists. The range of a