Phage Display Essay

Alzheimer 's disease (AD) was discovered by a German doctor Alois Alzheimer in 1906 when he found amyloid plaques and neurofibrillary tangles in the autopsy of a woman who died of an unknown mental disease. The extracellular amyloid plaque deposits, composed of insoluble amyloid-Beta peptide were hypothesized to be the main etiological factor. “The most important abnormality is an excess of Amyloid-beta peptides brought about through either overproduction or failure in degradation.” (Uzun, Kozumplik, & Folnegović-Smalc, 2011) Later, it was discovered that intracellular neurofibrillary tangles composed of hyper-phosphorylated, helically-paired tau

The overall goal is to either discover a new novel phage that has not yet been discovered, or provide new research on an already discovered phage. The isolation of the phage takes several steps under the streak protocol that is present in materials and methods section of this report.

The titer of recombinant phage was determined with the number of plaques on the E.coli K plates and the titer of total phage progeny was determined with the number of plaque on the E.coli B plates.

After decades of paper based medical records, a new type of record keeping has surfaced - the Electronic Health Record (EHR). EHR is an electronic or digital format concept of an individual’s past and present medical history. It is the principle storage place for data and information about the health care services provided to an individual patient. It is maintained by a provider over time and capable of being shared across different healthcare settings by network-connected information systems. Such records may include key administrative and clinical data relevant to that persons care under a particular provider. Examples of such records may include: demographics, physician notes, problems or injuries, medications and allergies, vital

Titer of the Bacterial virus, the Measurement of the Recombination and the Reversion Rate, and the Gene Map Distance (Phage Recombination)

The main objectives of this experiment included making dilutions of solutions, plating phage or bacteria, and determining the number of bacterial viruses or phage in a suspension. It was also conducted to demonstrate that two different mutants of phage T4 can exchange genetic material to give rise to wild-type phage. The experiment was used to distinguish mutants from wild-type by their host specificity. The recombination in bacteriophage was performed to determine the concentration of unadsorbed phage from the U series plates, total concentration from B series, and concentration of

Even today, after so much study, Alzheimer’s is not fully understood. However, researchers do agree that this degenerative disease is caused by the gradual buildup of fibrous protein compounds in the brain, which are known in the scientific world as amyloids. These amyloids in the brain area act like plaque and as a result of their presence, the normal brain functioning is disrupted.

Alzheimer’s disease is named after Dr. Alois Alzheimer who first discovered deviations from normal tissues of healthy individuals in the brain tissue of a lady in 1906. The woman, who showed symptoms of erratic behavior, loss of memory, and problems with communication, died of a then unfamiliar mental disorder. This led Dr. Alzheimer to investigate the cause of her unusual death. He assessed the brain of the woman and found that there were many anomalous masses (amyloid plaques) and intertwined bundles of fiber (neurofibrillary tangles). Scientists today have pinpointed the qualities of Alzheimer’s to be a) tangles in the brain (neurofibrillary tangles), b) plaque in the brain (amyloid plaques), and c) loss of connections among nerve cells.

Genetic transformation occurs when genes are inserted into another gene to change the organism’s trait (Weedman2016). In this experiment, we proceeded to transform the E. coli bacteria with a gene that contained green fluorescent protein. The green fluorescent protein is used in experiments because it beams a green color under a UV light (Chalfie2008). Typically, it is used to mark the expression of genes, which is why it serves as the symbol for all gene expressions (Tsien1998). In the experiment, we will be using pGLO as the organisms that will transmit the disease, otherwise known as a vector. The pGLO in the experiment

5. List the four most commonly used styles of citation and demonstrate how to correctly

Under normal condition tau binds to microtubules, stabilizing neuronal structure and integrity. Hyperphosphorylation of tau is assumed to be the cause of the formation of paired helical filaments - neurofibrillary tangles (NFT). The principle components of the senile plaques are neurofibrillary tangles in the cell bodies, neuropil threads, and neurites as well as extracellular A-beta amyloid. These lesions are surrounded by microglial and astrocytes. The brain regions affected by Alzheimer’s disease also contain neuritic or senile plaques in which extracellular deposits of amyloid are surrounded by dystrophic axons as well as the process of astrocytes and microglia. The principle constituent of amyloid is a 4kDa peptide called A-beta amyloid. A-beta amyloid is cleaved from a larger precursor protein called amyloid precursor protein. Similar abnormalities occur in transgenic mice with mutant APP and in individuals with Alzheimer’s

Cognitive impairment associated with Alzheimer’s disease occurs when synapses, which transmit information from one neuron to another, become interrupted and communication ceases (7). The result is death of the nerve cell within the brain, also referred to as synaptic failure (6). Synaptic failure takes place when amyloid plaque and neurofibrillary tangles develop (7). Amyloid plaque develops from amyloid beta proteins, which are released by enzymes from the amyloid precursor protein that is located on the surface of the neuron (7). The amyloid beta proteins are normally cleared within the body once they are released however, in

“Alzheimer’s Disease (AD) is a type of dementia, which is affecting the population that develops in the brain and can lead to problems with memory, thinking and behavior”. The Amyloid Hypothesis claims that the build up of the beta-amyloid in the brain is a cause in the development of Alzheimer disease in patients. This plaque of the beta-amyloid and its cascade of events can be linked to the deterioration and negative effects of cognitive function of the brain over time. The beta-amyloid is described to be a “sticky” protein located in the brain therefore plaques or build up of the amyloid is common. These plaques in turn can block the brain cells from communicating with each other. Which then activates an immune system, that leads to inflammation

There is a large supply of amyloid plaques in the cells of people with Alzheimer’s disease. Amyloid plaques are clustered pieces of protein that build up between nerve cells. They speed up the production of beta amyloid, which are polypeptides of about thirty-six to forty-three amino acids long (emedicinehealth, 2014; Stanford Medicine, 2013). Amyloid precursor proteins (APP), when split into specific pieces, are producers of beta amyloid. They are found in tissues and organs, such as the brain. Amyloid precursor proteins pass through a fatty membrane on the outside of a cell. This allows them to extend from the

We used a EWAS approach for modeling a PHE as a complex network of interdependent determinants by inferring associations between multiple and diverse factors and the incidence of microcephaly attributed to ZVI in Brazil municipalities during the first semester of 2016. Figure 1 summarizes the steps of the modeling process we describe in this section.