Why Is the Periodic Table Color Coded

Most periodic tables are color-coded. You can get black and white or uncolored tables, but mainly these are used when you cant print color or need just the most basic facts about the periodic table and the elements. Why Color Code? Colored tables are important because they give you an extra dimension of information. A typical periodic table is colored according to element groups, which are elements that share chemical and physical properties. Some element groups are easily identified as columns on the periodic table, but as you move across the table, the trends arent so clear-cut. The metalloids and nonmetals, for example, dont fall neatly into the same column. Color coding helps identify similar elements such as these at a glance. Periodic tables can use color to identify other element characteristics. For example, an electronegativity periodic table color codes the elements based on how electronegative they are. The valence periodic table uses color to identify the most common valence state for each element. The element abundance periodic table shows the relative amounts of each element. How Are Colors Chosen? There is no standard set of colors used to identify element groups or other properties. Colors are selected based on how well the text shows up against them, but mostly its a matter of personal preference. You can find periodic tables in a variety of color schemes.

The Relationship Between Porcine And Human Cysticercosis

Some of the other risk factors are linked to both porcine and human cysticercosis. According to Bhutta et al (2012) ,Garrett et al (2015) and Assana et al (2010), low level hygiene environment such as dirty contaminated soil and lack of latrine may rise opportunities to access Taeniid ova because dirty soil can increase the possibility of exposure to taeniid ova for both human and pig and taeniid ova can flow to water resource like wells in rainy season. Certainly, according to many of these articles including WHO, the installment of a large number of latrines can control the risk factor because it can prevent the contamination(WHO 2015), However, there is the article reporting that public(community) latrine can bring weaker effect and all†¦show more content†¦Interestingly, more than 10 members decreased the risk in the result. Although Mwape infer this is because such large size family cannot consume pork frequently due to the costs, a stronger evidence would be necessary to prove this. Therefore,a more large-scale observation such as cohort study is highly recommendable to identify the necessity of latrines in the future. Each of the resources examines other risk factors why such transmission situation between pig and human occur from various points of view in detail. Carabin et al(2015) and Edia-Asukeet al(2014) maintain that the older people, the higher infection rate it is. They infer that the frequency of the exposure is related to the infection. Interestingly, the change point analysis which determine the number of people with active infections (cysticercosis)increases from at 30 years old in Zambia. This result is quite younger than the result in Ecuador under the same analysis (Mwape et al, 2015). This result could imply that sub-saharan Africa is at higher risk for T. solium infection than Latin America. As an interesting site as a possible risk factor, slaughterhouse situations are referred in some articles. For example, in Nigeria, there is an existing abattoir law to do proper management. However, various problem is identified from the actual situations. Especially, unregistered and private home pig slaughter slabs may cause more

Peroxisome Proliferators for PPAR Nuclear Receptor - myassignmenthelp

Question: Discuss about thePeroxisome Proliferators for PPAR Nuclear Receptor. Answer: The PPAR nuclear receptor subfamilyis composed of PPAR, also known as PPAR, along with PPAR and PPAR. These receptors regulate transcription by binding to segments of DNA containing 2 repeats of AGGTCA sequence separated by 1 nucleotide in promoter region. PPAR is expressed in the skeletal muscles, adipose tissue (brown), liver, heart and intestinal mucosa. PPAR and PPAR are ubiquitously expressed in liver, kidneys, intestine, adipose tissue in abdomen and skeletal muscles. PPAR is most widely studied and generally expressed in the white and brown adipose tissues, spleen, liver, and the large intestine (Lagan et al. 2016). These transcription factors are ligand activated. On interacting with their synthetic or natural agonists (Thiazolidinediones), they translocate inside the nucleus and heterodimerize with a receptor for retinoid acid, NR2B or RNR. Dietary fatty acids, principally polyunsaturated fatty acids activate the receptors, which control various metabolic activities like glu cose and lipid metabolism (Monsalve et al. 2013). They also regulate energy balance in the body. They are responsible for controlling the expression of genes in type II diabetes, obesity, metabolic syndromes and dyslipidemia. PPAR is activated in the adipocytes and induces fat cell apoptosis in visceral and subcutaneous deposits. It also leads to pre-adipocyte cells differentiation into mature fat cells in subcutaneous fat deposits of human beings. It is associated with upregulation of triglyceride storage and lipogenesis genes. The PPAR shows maximum expression in metabolic tissues and is currently not a target for any drug or therapeutic study (Reilly and Lee 2008). References Lagan, A.S., Vitale, S.G., Nigro, A., Sofo, V., Salmeri, F.M., Rossetti, P., Rapisarda, A.M.C., La Vignera, S., Condorelli, R.A., Rizzo, G. and Buscema, M., 2016. Pleiotropic actions of Peroxisome Proliferator-Activated Receptors (PPARs) in dysregulated metabolic homeostasis, inflammation and cancer: current evidence and future perspectives.International journal of molecular sciences,17(7), p.999. Monsalve, F.A., Pyarasani, R.D., Delgado-Lopez, F. and Moore-Carrasco, R., 2013. Peroxisome proliferator-activated receptor targets for the treatment of metabolic diseases.Mediators of inflammation,2013. Reilly, S.M. and Lee, C.H., 2008. PPAR as a therapeutic target in metabolic disease.FEBS letters,582(1), pp.26-31.