Maduro Cleaning is a small organization that provides cleaning services to both residential and commercial clients. As a small organization, the owner assigns crews of two, three, or four employees to jobs each morning but the owner does not have a good method of determining a reasonable amount of time that each cleaning should take. The owner decided to keep data on job times and crew sizes in the hopes of developing a productivity measure. In a 4-5 page paper, not including the cover and reference pages, calculate which of the crew sizes has the best productivity per worker, and explain your method. Evaluate your outcome and the possible reasons that would explain those results. Project what the productivity might be for a crew size of five and explain your reasoning.
elevated levels of uric acid above the saturation point for urate crystal formation is a major determinant of the disease. Purine catabolism leads to the formation of metabolic by-product, uric acid. In most mammals like higher primates, many birds and some reptiles, the urate oxidase (uricase) enzyme converts uric acid (relatively insoluble) to allantoin (highly soluble), leading to very low serum uric acid levels. A series of parallel mutations in the genes of uricase in the Miocene period results in the production of the dysfunctional form of uricase that leads to accumulation of relatively higher level of insoluble uric acid and subsequently the development of gouty arthritis (Liote and Ea 2006; Eggebeen 2007). Degradation of purines results in the endogenous production of uric acid that usually contributes about two-thirds of the body urate pool, the remainder being originated by dietry intake. Of the uric acid formed daily, about 70% is excreted through the kidney while the rest is eliminated into the biliary tract and then converted to allantoin by colonic bacterial uricase. Therefore, in the vast majority gouty patients, hyperuricaemia occurs from reduced efficiency of renal urate clearance (Laubscher et al. 2009; Terkeltaub 2010). Development of the acute and chronic inflammatory gout is facilitated with the deposition of monosodium urate (MSU) crystals in joints. while MSU crystals were first identified as the aetiological agent of gout in the eighteenth century and more recently as a ‘danger signal’ released from dying cells, little is known about the molecular mechanisms underlying MSU-induced inflammation (Martinon et al. 2006). For crystal formation n occurrence of gout, the ionic product of sodium and uric acid must be at or above the saturation level at which MSU crystals can form. Uric acid is a weak acid of pKa 5.75 and, it exists mainly in the ionized form as urate at physiological pH of 7.40. MSU has limited solubility under physiological conditions and the saturation level in plasma at a pH of 7.40 is 6.8 mg/dl (408 Âµmol/l) and when the plasma concentration exceeds this level, crystals may form in the joints and tissues (Terkeltaub 2010). MSU crystals preferentially form within cartilage and fibrous tissues, where they are relatively safer from contact with inflammatory mediators and may dwell for years without causing any defects. However, if ‘shed’ from these sites of origin into the joint space or bursa, they are highly phlogistic particles that are immediately phagocytosed by monocytes and macrophages, stimulating the NALP3 inflammasome, triggering the release of IL-1 and other cytokines and a subsequent infiltration of neutrophils. Here the white cells release a package of inflammatory mediator substances which, in addition to destroying the crystals, also damage the surrounding tissues (Martinon et al. 2006). This acute inflammation defines the symptoms of an acute flare such as pain, swelling and redness and is typically self-limiting. Continual deposition of large numbers of MSU crystals may also heading out the joint damage through mechanical effects on cartilage and bone (pressure erosion), and probably low-grade inflammation. However, these more chronic crystal-tissue interactions still remain elusive and in need of further investigations (VanItallie 2010). Systematic Lupus Erythematosus (SLE) Introduction Lupus is an autoimmune disease which leads to both acute and chronic inflammation of various tissues of the human body. Lupus can be classified into different form depending upon the target tissues and organ system. Defined as Type III hypersensitivity reaction, people with lupus produce abnormal antibodies in their blood that target tissues within their own body rather than foreign infectious agents. Because the antibodies and accompanying cells of inflammation can affect tissues anywhere in the body, lupus has the potential to affect a variety of areas such as heart, joints, skin, lungs, blood vessels, liver, kidneys, and nervous system. When internal organs are involved, the >GET ANSWER