Brugge Lab Report

The mole is a convenient unit for analyzing chemical reactions. Avogadro’s number is equal to the mole. The mass of a mole of any compound or element is the mass in grams that corresponds to the molecular formula, also known as the atomic mass. In this experiment, you will observe the reaction of iron nails with a solution of copper (II) chloride and determine the number of moles involved in the reaction. You will determine the number of moles of copper produced in the reaction of iron and copper (II) chloride, determine the number of moles of iron used up in the reaction of iron and copper (II) chloride, determine the ratio of moles of iron to moles of copper, and determine the number of atoms and formula units involved in

Background: cancer has developed mechanisms to survive and resist drugs including methotrexate, a DHFR inhibitor

The oxidation number of an atom of any free element is ZERO. Means to say there is only one kind of atom present, no charge.

2. (5 pts) List and explain the names and affiliations of the various characters/stakeholders in this story – I’m looking for us to use the story to map out the complexities that are generally associated with solving public health puzzles – the stakeholders you list and explain here should apply to many of the cases we consider going forward.

The anti-apoptotic mutations related to cytochrome c are not the only mechanisms acquired by cells in the development of a tumor. Another important hallmark of cancer is the alteration of cellular metabolism, also known as the Warburg Effect, which demonstrates an increased rate of glycolysis despite the presence of oxygen in tumor cells (Hallmarks). Due to the unlimited and uncontrollable division by tumorigenic cells, the Warburg Effect confers growth advantages compared to non-proliferating cells because it promotes the uptake of glucose, it produces less reactive oxygen species (ROS), and it generates ATP more rapidly than oxidative phosphorylation, all of which are considered to facilitate rapid growth and survival (1).

2. When 2.00 g of NaOH were dissolved in 49.0 g water in a calorimeter at 24.0 ˚C, the temperature of the

Many doctors, physicians, researchers and biotech companies--including the revolutionary Seattle Genetics research facility--are now turning to antibody-assisted cancer treatments and precisely targeted cures instead of treating cancer with a cocktail of chemicals and radiation that generate risky side effects and damage the healthy tissue that patients need to recover. Cancers are among the most frightening and difficult-to-treat illnesses. Ranked as the leading cause of death and disability, cancer is actually an umbrella term that covers many different diseases. Each person faces a unique disease because cancers interact with the body's existing cells, so each case has a

The mean voltage of the battery terminals while connected to the identification resistors is presented in Figure ‎4 12. These samples have been pulled out from the voltage sensor of the PEB panel. The voltage decreased as expected from 12.53 to 12.5 during first 20 seconds of connection to the

There are many ways for cancer to get in the body, like exposure to uranium and oxidative stress. [8]. When the mechanisms of the body loose the protein Glutathione it leads to making oxygen free radical neutral. Two of the most important proteins in the body are glutathione (GSH) and superoxide dismutase (SOD). Glutathione (GSH) works as an antioxidant [9]. Also, glutathione (GSH) has an important job that removes toxic metals out of the body because glutathione (GSH) has a sulphydryl group. This group strongly binds with toxic metals, effectively [3]. When uranium enters the body, it will reduce glutathione (GSH). When there is a reduction of glutathione (GSH), it leads to an increase of the

Tumour cells contain many mutated and misregulated genes, some of which the tumour requires for its survival, growth or metastasis. Overexpressed proteins have previously made good drug targets, for example Trastuzumab targets Her2 in breast cancer and Gleevec targets BCR-ABL in CML. When studying a potential novel drug target, I would search the literature and online databases such as Oncomine to determine whether the gene is known to be misregulated or mutated in human cancers. I would be particularly interested in studies on the effects of tumourigenesis when the potential target has been overexpressed or knocked-down/out,

Genomic research has shown that the presence of certain gene alterations/mutations can reliably predict the likelihood of clinical benefit using agents that inhibit the expression of defective genes responsible for carcinogenesis or DNA repair. Relevant to this case, is the demonstration of an altered ATM gene that appears to predict the sensitivity to PARP inhibitors, such as olaparib. Clinical responses have demonstrated in at least one clinical trial. 1 Olaparib has been granted “Breakthrough Therapy” designation by the US Food and Drug Administration (FDA) for treatment of metastatic castration-resistant prostate cancer harboring an ATM gene mutation. Based on similar data, olaparib has already received FDA-approval for use in treating metastatic ovarian cancer in patients having a BRCA 1/2 mutation. The benefit of “Breakthrough Therapy” designation is to expedite development of

In the experiment, a ruler was dropped and a test subject reacted as fast as they could to catch it. The ruler was first dropped while they were concentrated and looking at the ruler. Then, it was dropped while the test subject was distracted by reading a paper out loud. When the ruler was dropped, the test subject caught it aThe reaction time of someone who is distracted will be slower than someone who is concentrated. nd recorded where their thumb and forefinger landed.

The ability of p53 to regulate metabolism is also associated with the ability to regulate cellular ROS levels. As previously mentioned, p53 can either remove damaged cells that have suffered sustained oxidative stress, or limit levels of ROS in order to lower oxidative stress and consequently, potential cell damage. Through the regulation of carbohydrate and lipid metabolism, p53 is able to influence the response to ROS accordingly. By driving the expression of TIGAR and promoting PPP activity, p53 can increase the production of NAPDH, which can be used to generate the cellular antioxidant GSH (Bensaad 2006). Moreover, at the expense of nucleotide synthesis, p53 can also promote GSH synthesis following serine starvation, thereby lowering ROS

preventing the repair of cancer cell and tumor growth.8 However, This drug is under initial stage

Unlike Gilead that has only one product in its Oncology line, Bristol-Myers Squibb presently have four different drugs namely: Erbitux –an epidermal growth factor receptor (EGFR) antagonist for the treatment of Head & Neck cancer and Colorectal cancer,(2) Opdivo (nivolumab) for the treatment of unresectable or metastic melanoma and lungs cancer, (3) Syrcel( dasatinb) for the treatment of newly diagnosed adult with Philadelphia chromosome –positive (ph+) chronic myeloid leukemia and (4) Yervoy (ipilimumob) for the treatment of melanoma a type of skin cancer that spread and as such cannot be remove by surgery. Like Seattle Genetics, the company products use either Antibody-drug Conjugate (ADC) though in a different version by linking potent cytotoxic to monoclonal antibodies targeted to specific tumor cells or immune-oncology, an innovative technology that unlocks the body own immune system to fight against cancerous cells. It also expanded its focus to Nolch inhibitor (used in blocking powerful pathway that promotes tumor cell survival for certain other types of cancer. (Bristol-Myer Squibb, 2014) Because the technology is similar but used differently, BMS would be considered a close competitor who currently has the advantage of having four targeted specific drugs and 12 other oncology and immune-oncology in various trial phases.