Analyze the extent to which the macroeconomic environment in the United States impacts the supply and demand of APPLE’s product or service and assess the effects of macroeconomic conditions on APPLE’s financial performance.
Specifically, the following critical elements must be addressed:
I. Overview: Provide an overview consisting of a brief description of the chosen company, your chosen product or service, and annual sales.
II. Macroeconomic Variables
For this section, you will utilize macroeconomic variables such as GDP growth, inflation, unemployment, and so on to relate trends in data to the supply and demand of your product or service. Include all calculations in an Excel file.
a) Select three macroeconomic variables in the United States that impact the supply and demand of your chosen product or service. Justify your selections.
b) Interpret the trends of the three selected macroeconomic variables for the past three years. Be sure to include gathered data. Based on the trends of the three macroeconomic variables, assess how they will impact the supply and demand of your chosen product or service.
III. Macroeconomic Policies
a) Describe the current monetary and fiscal policies in the United States. Consider including how these policies affect your company and its
products and services.
b) Predict how possible changes in monetary and/or fiscal policy may impact the supply and demand of your product or service.
IV. Macroeconomic Conditions and Company Performance
a) Describe the trends of two previously selected company performance variables (e.g., sales, stock pricing, net income) over the past three years.
Keep in mind these are the performance variables selected in the microeconomic analysis.
b) Analyze the relationship between the two company performance variables and the three selected macroeconomic variables for the past three
years using a correlation graph. Be sure to include the graph that represents the correlation.
c) Assess how the current monetary policy and fiscal policy in the United States may impact your chosen company’s financial performance in the
short term (six months to one year). Justify your respons
Isoniazid(INH) and rifampicin(RFP) are first-line antituberculosis drugs, co-therapy with INH and RFP is highly effective. However, the combination of these two drugs frequently cause liver injury or liver failure in humans. The risk of hepatotoxicity is considerably higher in patients receiving both RFP and INH than in those receiving either RFP or INH alone. Numerous studies have been conducted to investigate the mechanism of injury after isoniazid or rifampicin used in various animal models, however, the important mechanism for the combination of isoniazid and rifampicin in humans remains unclear. Here we investigated this combination induced hepatotoxicity using L-02 cells and mice. Introduction Tuberculosis remains a global public health problem whose effects have major impact in developing countries. World Health Organization estimates that there were 8.6 million new TB cases in 2012 and 1.3 million TB deaths. The currently recommended treatment for new cases of drug-susceptible TB is a six-month regimen of four first-line drugs: isoniazid, rifampicin, ethambutol and pyrazinamide. (Global tuberculosis report 2013). However, the combination of isoniazid(INH) and rifampicin(RFP) frequently cause liver injury or liver failure. The risk of hepatotoxicity is considerably higher in patients receiving the combination than in those receiving either RFP or INH alone. The mechanisms leading to liver failure in humans were poorly understood. Recently, a new mechanism ,independent of INH metabolism, is found in the RFP and INH co-therapy induced liver injury. Li et al. (Li, et al. 2013) found that co-therapy with RFP and INH targets porphyrin biosynthesis and results in hepatic protoporphyrin IX (PPIX) accumulation and liver injury . PPIX is an intermediate in porphyrin biasynthesis. Normally the concentrations of PPIX is very low in the liver. However, in some cases the concentration abnormally elevated in blood and liver, such as erythropoietic protoporphyria. High concentrations of PPIX in the liver are known to cause liver injury (Anstey and Hift 2007; Casanova-Gonzalez, et al. 2010). Using hPXR mice, Li et al. demonstrated that the accumulation of endogenous PPIX is through PXR-mediated transcriptional activations of aminolevulinic synthase-1(ALAS1) genes. ALAS1 is the rate-limiting enzyme of heme synthesis in the liver and is drug-responsive, providing heme for CYPs and other hemoproteinsis. Activation of PXR can upregulate ALAS1 expression in liver (Fraser, et al. 2003). RFP upregulate ALAs1 increasing heme-biosynthesis in the liver and overproducing PPIX through activating PXR signalling pathway. However, PPIX accumulation strongly suggests that ferrochelatase became a ratelimiting enzyme during INH-RFP treatment (Lyoumi, et al. 2013).>GET ANSWER