FLRT3 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

A point mutation is one where only one nucleotide is changed and a missense mutation is when the amino acid changes due to the base(s) mutated. FGFR3 consists of 19 exons, with the mutation occuring in exon 10 (1, 16). Furthermore, the mutated base is 1138, where the base can undergo two possible mutations. G(guanine)→A(adenine) transition accounts for 98% of all cases of ACH while the G→C(cytosine) transversion mutation occurs in 1% of cases (6). Both of these mutations result in the amino acid arginine being substituted for glycine at codon 380 which is in the transmembrane of FGFR3 (1, 4, 17) (See Figure 1). The FGFR3 mutation is a gain-of function mutation due to the resulting activation of receptors, which is opposite the normal inhibitory effect the FGFR3 has on the receptors, which upon activation, negatively regulate bone growth (4, 6). Thus, FGFR3 has been found to become hyperactivated when mutated and undergo ligand-independent dimerization (1, 11, 18).

What is its melting point? 1,405 K: 1,132 C: 2,070 F. boiling point? 4,404 K: 4,131 C: 7,468 F

First, we need to plug in the variables into the numbers from the information to create our first equation for the system. 3j (glasses of orange juice) + 5p (5 pancakes) = 7.60. Now, plug in the variables into the numbers from the information for the second equation for the system. j ( a glass of orange juice) + 2p ( 2 pancakes) = 2.90.

Ionic compounds are soluble in water to a certain point depending on the compound. The level of solubility changes among different compounds. Some ionic compounds can completely dissolve in water and appear to be a homogeneous mixture. Although, some ionic compounds dissolve very little, and could be considered insoluble, since it does not dissolve fully. Depending on the compound, the level of solubility can be high or low. However, ionic compounds could dissolve to a certain degree. If the solution appears to be a heterogeneous mixture, many may assume through visual representation that it may be insoluble. As stated previously, the smallest amount of solubility should be considered. To confirm whether or not the substance is soluble, observe the efficiency when conducting electricity. Due to practical reasons, the slightest solubility could be considered insoluble by people.

A) Describe in your own words, in as much detail as you can, the anaerobic metabolism of glucose to pyruvate. B) Draw this pathway (by hand), indicating all substrates, enzymes, cofactors and products. (You do not need to include reaction mechanisms.)

The Panasonic Lumix DMC TS30 comes with a resolution of 16.10 Megapixels with a Sensor size of 1/2.33 inch. The Lens flaunts a 4.00x zoom (25-100mm eq) quality, enabling distant object to appear closer through the lens. With an ISO of 100-1600 and a Shutter speed of 60 (minimum) and 1/1300 (maximum), the Panasonic Camera comes with the dimensions of 4.1 x 2.3 x 0.8 in.(104 x 58 x 20 mm). the Camera weighs about 5.1 oz ((144 g)includes batteries).

We made a table to help us figure out how to find the pattern. In Table 1.2, the first column you see the number of cuts. The second column is the most pieces possible, and the last column is the differences we got between the upper bound of the cut before and the cut we were on. For example, we got four pieces for two cuts and seven pieces for three cuts, this means that between two cuts and three cuts there was a difference of three pieces. We noticed that the difference was also equal to the number of cuts.

Fig. 12 CXL10-/- mice are relatively protected against FFC-induced liver injury and inflammation. WT & CXCL10-/- mice were fed either chow or FFC-diet for 20 weeks. (A) Plasma alanine aminotransferase (ALT) levels were measured. (C) Total RNA was extracted from liver tissue and mRNA expression of surface macrophage marker cluster of differentiation (CD)68 was evaluated by real-time qPCR. (D) Assessment of macrophage infiltration in fixed liver tissue was done by immunohistochemistry using macrophage galactose-specific lectin (Mac-2) antibody. Bar columns represent mean ± S.E.M. *** P < .001, * P < .05 compared to WT chow-fed mice.

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.

This laboratory experiment was conducted to examine the effects of a non-ionic surfactant known as Triton X-100 on the viability of a ciliated unicellular eukaryote, Tetrahymena thermophila. Due to T. thermophila being a ciliated unicellular microorganism, with a very short doubling time through binary fission it excels at being an alternative model organism utilized in the field of toxicology (Orias et al., 2011). These advantages along with its direct applicability to the toxicant without any further preparation allow T. thermophila to be an ideal choice for this time constrained experiment when compared to other possible test organisms available.

Subjects: Subjects who participated in this lab were colleagues enrolled in HL031, aged (range 19 -26 years) males (n=5) and females (n=7).

Resistance to apoptosis will be assayed via western blot for Thyroid, FTC cells with mutations, and PTC with mutations treated and not treated with siFLRT3 knockouts with antibodies specific for caspase-3 , actin and FLRT3. The appearance of caspase-3 indicates DNA damage and subsequent apoptosis, since caspase is a DNA repairing protein that is cleaved when cells undergo apoptosis. Additionally, resistance to apoptosis will be calculated using a TUNEL-assay protocol [4] for FTC cells harboring mutations, and PTC cells containing mutations treated and not treated with siFLRT3 and infrared radiation. TUNEL assays quantify apoptosis by using TdT enzymes to bind to the 3’ end of DNA in order to gauge the amount of DNA fragmentation, a marker of apoptosis. We will evaluate FLRT3’s impact on motility for FTC cell lines with / mutations by testing for metastasis over various time intervals. Metastasis in vivo experiments will be performed by injecting immunodeficient mice in the tail with PTC cells containing either or / mutations and checking for metastasis to the lymph nodes at various time intervals[5]. PTC cells with / / mutations will be generated by performing a mouse knock out by isolating embryonic stem cells from / containing white mouse blastocysts and subsequently introducing ∆flrt3::neoR containing plasmids with homologous primers attached into the cells

FLCN expression is conserved throughout the eukaryotic system and is known to have binding partners, folliculin interacting proteins (FNIP) 1 and 2. FNIP1/2 interacts with AMP-activated protein kinase (AMPK), a direct energy sensor and negative regulator of mTOR, suggesting FLCN’s role in AMPK and TOR signaling. Moreover, mammalian cells with reduced expression of FLCN resulted in concomitant reduction of TORC1 activity, strengthening FLCN’s probable role in TOR signaling.

Specific aims: EGFR and c-Met are receptor tyrosine kinases (RTKs), and tyrosine kinase inhibitors (TKIs) against these receptors have been initially effective when prescribed to patients in combination with traditional chemotherapy or radiation. However, the overall efficacy of TKIs is limited due to the development of resistance as seen through clinical trials in NSCLC. Epithelial Mesenchymal Transition (EMT) is a process by which epithelial cells undergo phenotypic and morphological changes to acquire mesenchymal characteristics including increased motility and invasiveness. Currently, the role of EMT in TKI drug resistance is poorly understood. EMT results in loss of tight junction proteins such as E-cadherin and upregulation of transcriptional repressors of these proteins such as ZEB1. Recently, protein arginine methyl transferase 1 (PRMT1) has been shown to be an important regulator of EMT, cancer cell migration and metastasis. However, the role of PRMT1 in TKI resistance is not known. In this study, we propose to evaluate the role of EMT proteins in TKI resistance using H2170 and H358 cell lines (wild type EGFR) that were made resistant to an EGFR inhibitor, erlotinib and a c-Met inhibitor, SU11274 and a combination of both. H3255 cell line (with L858R EGFR mutation), and H1975 cell line with L858R and T790M EGFR mutations which we have made resistant to erlotinib will also be used. Our recent in vitro studies indicate that TKI resistance may be due to the activation