The Biological Effects Of Polyp

In the United States, colorectal cancer affecting both men and women ranks high as a deadly cancer to individuals older than 50 years old. It was estimated in 2011 that 135,260 people diagnosed with colorectal cancer and 51,783 deaths. With an improved preventative measure of an early detection of precancerous lesions such as polyps, the prevalence of colorectal cancer and deaths will be decreased. There are several risk factors known to increase an individuals’ possibility of developing this disease. Most malignant neoplasms develop from adenomatous polyps if left untreated. The inactivation of APC gene caused the acceleration of the cell progression. Classical familial adenomatous polyposis (FAP) and attenuated familial adenomatous polyposis (AFAP) both inherited disorder that was caused by the APC gene mutation that resulted in the development of premalignant lesion and became invasive adenocarcinoma.

Huang, J., & Hornyak, T. (2015, January 7). Polycomb group proteins – epigenetic repressors with emerging roles in melanocytes and melanoma [Video file]. Retrieved from

For years people have been looking for a cure for the devastating disease of cancer. Cancer is the third highest killer in the US with over 2,500,000 victims per year. Oncologists and scientists around the country are researching all forms of cancer in an effort to understand, treat, and ultimately defeat this disease. Already there have been numerous advances in the field, such as chemotherapy and gene therapy. One advance has been the use of a cell process known as apoptosis. By harnessing this normal cell process, scientists hope to have found an effective way to combat cancer.

Annexing V FITIC/PI was used to detect for the involvement of apoptosis based upon externalization of phospholipid phosphatidylserine (PS) and permeabilization of nuclear membrane for staining with PI. PS is a biomarker of early apoptotic stage, Annexin V has specific and high affinity for the anionic PS, when PS is exposed on cell surface Annexing V binds to it. PS indicates intermediate stages of apoptosis. Caspases-3 activation, nuclear fragmentation and mitochondrial membrane flux preceded PS translocation [46]. From Fig.5 sonicated pectin induced dose apoptosis and reduced proportion of viable cells. The 400W sonicated pectin was more potent apoptosis inducer than 200W sonicated pectin. control cells had 89.29% viable cells 3.14% early apoptotic cells and 6.50% late apoptosis, 400W sonicated pectin at 0.1 and 0.5mg/ml induced significant reduction in viable cells to 70.90%, early apoptotic cells were 4.84% and late apoptosis 14.94% in the cells as shown in Fig.5b, on the other hand, 0.5mg/ml led to 50.79% viable cells, 22.65 %early apoptotic cells and 19.56% late apoptotic cells as shown in Fig.

Polypharmacy refers to the effects of taking multiple medications, usually 5 or more, concurrently to manage coexisting health problems, such as diabetes and hypertension. Polypharmacy is a common problem among the elderly population. “During a survey conducted on patients aging, between 62 and 85 years old, at least one prescription medication was used by 87 percent” (Rochon, 2016, page 1). “Five or more prescription medications were used by 36 percent, and 38 percent used over the counter medications” (Rochon, 2016, page 1.) This paper is going to talk about the different effects polypharmacy can have on the patient’s body and ways in which the nurse and other healthcare providers can assist in helping patients reduce the risk associated

Organ size regulation has continued to remain elusive. Recently, the Hippo pathway has been proposed to be involved in organ size regulation. The Hippo pathway regulates the size of organs through controlling cell number. A major downstream effector of the Hippo pathway is the transcription coactivator Yes-associated protein (YAP). YAP is responsible for upregulating genes that promote cell proliferation and downregulating genes that promote cell apoptosis. Elongated upregulation of YAP leads to hyperplasia and tumor formation. YAP is inhibited by Lats 1/2 through phosphorylation of serine 127. When serine 127 becomes phosphorylated YAP binds to

Now, let us discuss the diagnosis more in depth. A polyp of the colon is a growth of the inner lining of the colon, this growth protrudes into the colon tube. Polyps aren’t cancerous, however, some types of cancers can start in polyps. Polyps are quite common, approximately 30% of people over the age of 60 have one, or more. Genetic factors and environment play a major part in the development of a polyp, such as tobacco use, obesity and eating a high-fat diet.

Randomized patients, whose colonoscopy revealed the presences of adenomatous polyps, viewed a power point presentation that documented the precancerous nature of adenomatous polyps and associated an increased risk with immediate family members. Additionally, a randomized portion of the adenomatous positive population received a one page personalized letter reinforcing the information contained in the Computer Based Education Program (CBEP). Furthermore, each patient received a follow-up telephone survey to quantify how well they absorbed the information concerning adenomatous polyps. Access the full study @ https://rtips.cancer.gov/rtips/programDetails.do?programId=1472737 .

Its role in the inhibition of caspase 12 activation was also analyzed. Development of apoptotic changes, including DNA fragmentation and cleavage of poly (adenosine diphosphate-ribose) polymerase (PARP), as well as activation of caspase-3 and -7, occurred followed by morphological changes of ER stress. Inhibition of TG-induced markers of ER stress; reduction of calcium efflux, induction of Bip/GRP78, and caspase-12 activation; and subsequently inhibition of effector caspases and apoptosis activation was mediated by TUDCA(Xie et al.,2002).Lo AC et

Polyps are small growths on the lining of the bowel. They don't need to be cancerous. Removal of them is called a polypectomy and is done by putting a wire through the instrument and severing the polyp at the base with a small, painless electric current. If these are removed early enough they don't become cancerous so this procedure is a way of protecting against colon cancer. Usually after a couple of days patients can begin to follow a normal routine.

Cytotoxin associated gene A contains a stored pattern at the C- terminus known as the conserved repeat responsible for phosphorylation independent activity (CRPIA) [34]. This motif interacts with β-catenin-E-cadherin complex [35-37], hepatocyte growth factor receptor (MET)[38, 39], phospholipase C gamma (PLC-γ)[40], and partitioning-defective 1b/microtubule affinity-regulating kinase 2 (PAR1b/MARK2) [41-43] [44, 45] It has also been associated with JAK/STAT3 [31]. These interactions lead to cellular responses that promote inflammation, uncontrolled replication, disruption of neighboring cells communication, loss of cell function, loss of cell shape and loss of cell structure [34]. Unphospoporylated Cytotoxin associated gene A also affects zonula occludens 1 (ZO-1) which are proteins essential for epithelial tight junction by dislocating it from its cellular location [46] [47]. It also interrupts the junctional adhesion molecule A (JAM-A), producing dysfunctional construction of cell junctions [48].A variety of studies suggest that Cytotoxin associated gene A interact with PAR1b/MARK2, a crucial regulator of cell function and structure. Cytotoxin associated gene A disrupts its activity by affecting the alignment of microtubule arrangement, in this way causing a loss of cell polarity [49] [22] [47]. PAR1b binds to the CM or CagA multimerization of CagA that is involve in the CagA dimerization [50]

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

Procaspases are precursors that exist in the cytoplasm, they become activated when a Fas protein or death receptor is activated by Fas ligand. Once activated the inhibitor Ced-9, which acts as a brake for apoptosis, is overridden and inactive proteins Ced-4 and Ced-3 become active and trigger proteases and nucleases the cut up the DNA and release vesicles that contain digestive enzymes. Some cells do not have Fas protein receptors and therefore cannot be triggered by external forces to undergo apoptosis, this can cause cancer because the cell cannot receive death signaling molecules when the body recognizes potentially harmful mutations. Although chromosomes have the potential to produce an enzyme called telomerase, which attaches a T and G loop to the 3’ end of the DNA while RNA polymerase Ⅱ transcribes the 451 nucleotides to complete the newly formed telomere protective cap. Unfortunately, the gene that codes for telomerase is now considered a pseudogene meaning it no longer contains the full DNA nucleotide set necessary for the transcription of telomerase. Telomerase is not present in human cells except for “cancerous cells, male germ cells, activated lymphocytes and certain types of stem cell populations” (Cong, 2002) So far most ageing researchers have concluded that the shortening of telomeres is the major cause of ageing, but others believe that there are

The mechanisms of apoptosis in PV may be based on the PV IgG-triggered activation of signalling pathways, such as the epidermal growth factor receptor activation-dependent intracellular signalling (extracellular signal-regulated kinase) pathway, and the apoptosis (FasR) pathway. However, understanding the mechanisms of apoptosis is pivotal for the development of more specific therapies.[31]

Given the vital role of caspase activation in apoptotic cell death, blocking their function is a useful approach to find out whether apoptosis has a causal effect in triggering compensatory proliferation. In various species tissue regeneration was impaired if cell death was blocked with pan-caspase or effector caspase inhibitors (Fan and Bergmann 2008; Li et al. 2010; Ryoo and Bergmann 2012; Tseng et al. 2007). This approach has also been shown to ameliorate loss of neuronal cells and function after traumatic brain injury and retinal detachment (Hisatomi et al. 2001; Zacks et al. 2003). Following this approach we found that the pan-caspase inhibitor reduced the number of cleaved CASP3+ cells in cultured retina explants, but not the overall