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1HGD'RODWNKDK0'3K' 0DMLG+DMLIDUDML3K' +RPD\XQ'RODWNKDK3K' 3URELRWLFVLQ*HVWDWLRQDO'LDEHWHV0HOOLWXV

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(IIHFWRI3URELRWLFVRQJOXFRVHPHWDEROLVPZHLJKWFKDQJHV DQGLQIODPPDWRU\DQGR[LGDWLYHVWUHVVLQGLFHVLQZRPHQ ZLWKJHVWDWLRQDOGLDEHWHVPHOOLWXV 1HGD'RODWNKDK0DMLG+DMLIDUDML+RPD\XQ'RODWNKDK ABSTRACT Background: In recent decades, unhealthy diets during pregnancy have lead to excessive weight gain and changes of the intestinal metabolic and microbial balance. The recent and unexpected increases in the prevalence of gestational diabetes mellitus and intermediate results of dietary interventions, some may be due to inattention or failure of modification of the new and inappropriate composition of the intestinal microbiota that is often seen in the second half of pregnancy, especially in overweight and obese women. The aim of this study was to evaluate the effect of known probiotics on weight changes and indicies of glucose metabolism, inflammation and oxidative stress in pregnant women with gestational diabetes and to evaluate its efficacy in the treatment of these patients. Materials and methods: A total of 64 pregnant women, singleton primigravida, at their 24-28 weeks of pregnancy synchronous to the diagnosis of GDM were recruited in this randomized double-blind controlled clinical trial and were randomly assigned to receive either probiotic supplements (n=32) or placebo (n=32) for 8 weeks after matching sequentially according to the pre-gestational body mass indices and fasting plasma glucose former to the intervention. Each probiotic capsule consisted of of four bacterial strains (4 biocap > 4*109 CFU) in standard freeze-dried culture included Lactobacillus acidophilus LA- 5, Bifidobacterium BB-12, Streptococcus Thermophilus STY-31, and Lactobacillus delbrueckii bulgaricus LBY-27; produce by CHR HANSEN. To obtain detailed information about the dietary intakes of study participants, three 3-day dietary records completed at the beginning, throughout and the end of the stXG\3DUWLFLSDQWV¶ZHLJKWV were assessed at baseline and in 2-week intervals during the study. The biochemical indices were measured at the beginning and end of the study. Homeostatic model assessment of insulin resistance (HOMA-IR) and Quantitative insulin sensitivity check index ;Yh/24 h

Odds ratio 3.28 2.66 1.91 4.07 10.38 10.88 3.87 3.43 1.88 4.11

95% CI 2.53-4.60 1.93-3.67 1.46-2.50 1.63-10.16 6.15-16.56 6.16-19.18 2.64-5.67 1.87-6.27 1.45-2.43 2.37-7.10

Macrosomia is the result of accelerated growth of the fetus due to maternal hyperglycemia (Lindsay, 2009). Increasing need for cesarean occurs through embryos macrosomia. Hyperglycemia also stimulates hyperplasia and hypertrophy of the fetus beta cells, leading to increased insulin secretion and high levels of insulin in the blood. High insulin and glucose can

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increase the rate of placental metabolism and stimulate peripheral hematopoiesis and neonatal polycythemia (Hay, 2012, Hatfield et al., 2011). After birth, excessive insulin accumulation can lead to a decrease in blood glucose and the irreversible damage of the brain cells (Hatfield et al., 2011). As a result of abnormal glucose metabolism, blood and urine glucose concentrations increase glucose and result in increasing the susceptibility to urinary tract infections (Wei et al., 2014). In addition to the unpleasant consequences of diabetes during pregnancy, the incidence of the disease in the 5 years after delivery increases the risk of type 2 diabetes by 18-50% (Kaufmann et al., 1995, Kim et al., 2002). Studies have also shown that gestational diabetes increases the risk of hypertension and dyslipidemia and, therefore, arteriosclerosis and heart disease in long term (Khaw et al., 2004, Gynecologists, 2002, Seely and Solomon, 2003). Women with gestational diabetes have a high risk of developing diabetes in their later pregnancies (Kim et al., 2002). Some studies estimate that in about 30-70% of the cases, the disease will occur in subsequent pregnancies (MacNeill et al., 2001, Moses et al., 1997). Also, studies on the long-term effects of maternal metabolism disorders on the fetus have shown that the children from mothers with gestational diabetes mellitus are prone to impaired glucose tolerance (IGT) and obesity (Hillier et al. 2007, Dabelea, 2007). 1-4-7 Control and treatment of gestational diabetes Different points of view in the treatment of gestational diabetes are due to the lack of a same standard to define glucose intolerance during pregnancy (Agarwal et al., 2005). For this reason, a number of studies in this field have had different outcomes and led to the confusion in efficacy of safe GDM treatment. According to review studies in this field, nutritional interventions along with accurate monitoring of blood glucose levels are considered as the primary treatment option, and drug therapy begins when controlling blood glucose levels fail with dietary changes (Poolsup et al., 2014). The standard drug for insulin dependent diabetic patients requiring medication is insulin. However, since Langer et al. (Langer et al., 2000) compared the use of insulin and glibenclamide in these patients, oral medications have been increasingly considered as alternative

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treatments, several descriptive studies and clinical trials have examined the use of oral medications, primarily glibenclamide and metformin (Lain et al., 2009). Blood sugar levels should be measured four times a day: fasting after waking up and one hour after eating at each major meal (Marion). Recent recommendations for blood sugar target patients with fasting blood sugar less than 96 mg / dl, sugar one hour after meals below 140 mg / dl and less than 120 mg / d 2 hours after meals (Metzger et al., 2007). The basis of work is dependent on proper nutrition (Jovanovic-Peterson and Peterson, 1992). Calorie allocation is based on ideal body weight. The recommendations are 30 kcal/kg body weight in women with normal body mass index, 24 kcal/kg in overweight women and 15-12 kcal/kg body weight in obese women. The recommended daily energy intake from macronutrients is 33-40% complex carbohydrates, 35-40% fat and 20% protein (Marion). Insulin requirements are needed in patients with gestational diabetes mellitus whose blood sugar does not change with diet (Crowther et al., 2005). There is no consensus on the timing of insulin therapy, but there are more conservative guidelines to reduce macrosomia and related risks in fetus (Marion, Aronovitz and Metzger, 2006). The oral hypoglycemic drug has been considered due to easy use and cost, and this has led to increased use of hypoglycemic drugs in pregnancy, particularly metformin and gliboride (Kalra et al., 2015). According to Rowan et al., 2008, who compared insulin and metformin in women with gestational diabetes mellitus, metformin is a safe option for the treatment of the disease and has a higher acceptance in patients. 1-4-8 Gestational diabetes and inflammation

The pre-inflammatory cytokines likely play a central role in exacerbating insulin resistance (Sell et al., 2006, Hotamisligil et al., 1993). The adipose tissue and skeletal muscle of pregnant women synthesize and secrete several inflammatory mediators (Lappas, 2014, Bari et al., 2014) that have been exacerbated in women with gestational diabetes mellitus (Bari et al., 2014, Basu et al., 2011) and its association with fat mass in the fetus (Radaelli et al., 2006, Krauss et al., 2002). Gestational diabetes mellitus seems to occur due to increased secretion of inflammatory cytokines from maternal tissues, which accelerates insulin resistance (Radaelli et al., 2003).

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1-4-8-1 TNF-Į TNF-Įis one of the molecules responsible for insulin resistance during pregnancy. It has been suggested that TNF-ĮLVDSUHGLFWRURILQVXOLQUHVLVWDQFHLQKXPDQSUHJQDQF\.LUZDQHWDO At the end of pregnancy, TNF-Į KDV D UHYHUVH Uelationship with insulin sensitivity. The normalization of TNF-ĮVLJQDOLQJUHVXOWVLQLPSURYHGLQVXOLQVHQVLWLYLW\8\VDOHWDO

Figure 1-2 Obesity, pregnancy and gestational diabetes mellitus (Abell et al., 2015)

1-4-8-2 CRP Recent studies have focused on CRP more than other inflammatory markers. CRP is a protein synthesized by the liver and then secreted in the bloodstream. CRP is a component of the immune system and one of the acute phase proteins increased in systemic inflammation. Studies have shown that higher levels of CRP in circulation are associated with a higher risk of type 2 diabetes, myocardial infarction, stroke, and peripheral blood vessel disease (Di Cianni et al., 2007). Circulating levels of CRP have a strong correlation with various lipid profiles including body mass index, waist circumference, waist circumference to hip ratio, body fat mass and body mass index measured by bioelectric impedance (Festa et al., 2001). 1-4-8-3 IL-6 This pleiotropic cytokine has a major influence on the immune and non-immune regulation processes in most cells and tissues outside the immune system (Kamimura et al., 2003) and its function in inflammatory response is consistent with CRP. That is, IL-6 induces CRP production from the liver by activating Janus Kinases. This cytokine stimulates a wide range of cellular, ϯϳ

physiological and immune responses. This cytokine is also associated with diabetes mellitus (Kristiansen and Mandrup-Poulsen, 2005, Pradhan et al., 2001). 1-4-9 Gestational diabetes and oxidative stress

In gestational diabetes, metabolism and glucose tolerance are altered, and the basic pathophysiological mechanisms of these changes are still not fully understood. However, all of these changes are associated with stress-free oxidation (Ceriello and Motz, 2004). Reduction of the ability to compensate for stress in women with gestational diabetes mellitus is associated with increased insulin resistance and a decrease in insulin sensitivity index (Zhu et al., 2015). Stress oxidative reactions increase in pregnant women with gestational diabetes mellitus and fetuses. Also, there are changes in the antioxidant defense mechanisms (Lappas et al., 2011). Growth factors, cytokines, matrix metaloproteins and apoptosis play an important role in the structure and performance of the fetus. Free radicals of oxygen result in inflammation, disturbances in the regulation of metaloproteins and apoptosis.

Figure 1-3: Relationship between pathologic oxidative stress and unwanted side effects in mother and metabolic planning in child (Figueroa and Agil, 2011)

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1-4-9-1 Oxidative stress Oxidative stress occurs due to imbalance between creation and neutralization of free radicals (Halliwell, 2001). The oxidative stress term in biologic systemswas first introduced by Sies with similar words like oxidant stress and peroxidant stress (Sies, 2000). Sies defined the oxidative stress as an imbalance in the proxidant/antioxidant, which is towards oxidants that results in damage. The effect of these toxic molecules on cellular actions (leading to FHOOGHDWK LVJHQHUDOO\UHIHUUHGWRDV³R[LGDWLYHVWUHVV7KHVHIUHHUDGLFDOVDUHKLJKO\DFWLYHDQG unstable and have electrons not paired on the outer electron layer. These radicals react with various cellular components, such as DNA, proteins, lipids, fatty acids, and carbonyls (Halliwell, 2001, Sies, 1985, Organization, 1985). The radicals from oxygen and reactive oxygen species (ROS) are the most important ones in living systems. High concentrations of ROSs are important intermediates for the destruction of cellular structures, nucleic acids, lipids, and proteins. Changes in genetic material due to oxidative damage, are the first stage of mutagenesis, carcinogenesis, and aging. ROS not only causes DNA damage but also damages in cellular components such as fatty acid residues, PUFA and phospholipids that are susceptible to oxidation, and Malone di-aldehyde (MDA) is produced as the most important lipid peroxidation product that has carcinogenic and mutagenic properties (Sies, 1991). , Gerschman et al., 1954). Antioxidants can have an external source, such as diet, or endogenous one, that are produced inside the body cells. Enzymatic antioxidants could detoxify superoxide. So that the superoxide is first converted to H2O2 and then reduced to produce water. Superoxide dismutase enzymes catalyze the first stage and remove the various peroxidases of H2O2. The glutathione system, including glutathione, glutathione reductase (GR), glutathione peroxidase (GPx) and glutathione S-transferase (GST), controls the formation of superoxide. Glutathione peroxidase catalyzes H2O2 catalysis and organic hydro-peroxides (Lappas et al., 2011). 1-4-9-2 Oxidative stress assessment Regarding the fact that reactive oxygen species lead to reduction of antioxidants, one of the strategies to evaluate the oxidative stress is to measure the total antioxidant capacity (TAC) ϯϵ

through non-enzymatic antioxidants such as vitamin E, vitamin C, or enzymatic antigens such as glutathione peroxidase, catalase and superoxide dismutase, and in most cases, the products created by oxidative degradation of lipids, proteins and DNA are estimated. However, since antioxidant enzymes may be expressed in an oxidative stress state, single antioxidant measurements do not show antioxidant defense, in general. Measuring oxidative degradation products is a more accurate assessment of the oxidative stress state. Oxidative lipids are conjugated, Malone dialdehyde, and isoprostanes. Oxidation products of proteins include carbonyls and nitrotyrosin residues. The amount of oxidated DNA is also determined by measuring 8-hydroxydesoxiguanosine. The most prudent evaluation of free radical synthesis is the use of methods that directly detect superoxide or other free radicals. However, the above techniques are complex and require special tools. The other strategy is to determine the ratio of the amount of reduced and oxidized forms of ascorbic acid and aminothiols. Generally, a method that provides only reliable information on the amount of oxidative stress, and a combination of different methods is used for this purpose (Poston and Raijmakers, 2004). 1-4-10 Gestational diabetes and obesity

Obesity plays a major role in the pathogenesis of several medical disorders, including metabolic and cardiovascular diseases (Lavie et al., 2009). Several researchers have shown that obesity is a chronic mild inflammation (Lemieux et al., 2001, Saijo et al., 2004, Pannacciulli et al., 2001, Park et al., 2005). Inflammation itself may be the cause of obesity-related disorders. Inflammatory cytokines such as CRP are associated with obesity and subsequently associated with an increased risk of insulin resistance, diabetes mellitus, hypertension, and dyslipidemia (Mokdad et al., 2003, Festa et al., 2002, Harris et al. 2000, Wilson et al. al., 2002, Mathieu et al., 2010, Rocha and Libby, 2009). Pre-pregnancy BMI has a significant effect on gestational diabetes mellitus. Compared to women with normal BMI, the ratio of a woman weighing less than normal to gestational diabetes mellitus (0.69-0.82: confidence interval of 95%) is 0.75. The ratio of woman with overweight, moderate obesity and severe obesity for gestational diabetes mellitus were (1.77-2.19: confidence interval of 95%) 1.97, (2.34-3.87%: confidence interval of 95%), 3.01 and (4.27-2.17: confidence interval of 95%) 5.55, respectively (Torloni et al., 2009).

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According to Endo et al., insulin sensitivity in obese women with no glucose tolerance disorder is lower than women with normal weight and insulin sensitivity in pregnant women with gestational diabetes mellitus decreases with increasing gestational age (Endo et al., 2006). Another parameter that is as important as pre-pregnancy BMI is weight gain during pregnancy. In women with overweight in the first trimester of pregnancy, the risk of developing gestational diabetes mellitus increases (Chu et al., 2007, Hedderson et al., 2010). The weight gain guidelines during pregnancy were published by the Institute of Medicine in 2009. These guidelines are designed based on the body mass index before pregnancy. In women with normal body mass index, the purpose is to weight gain of (12-25 kg) Ib (25-35), and in women with a lower body mass index (12-18 kg) Ib 28-40 during pregnancy. In overweight patients, the target weight gain is (6. 8-11.4 kg) Ib 15-25 and in obese women (9-5 kg) Ib 11-20 (Rasmussen et al., 2009). 1-4-11 Probiotics

In recent years, it has been shown that the optimum balance in the number of gastrointestinal microbes depends on nutrition and health. The main microorganisms affecting the preservation of this balance are lactobacilli and bifidobacteria (Tamime, 2005). Factors affecting intestinal microorganisms (such as stress and diet) will have adverse effects on the human health by breaking down the optimal microbial balance. The use of nutrients containing beneficial microorganisms, called probiotics, is a valuable contribution to the survival and maintenance of indigenous germs and the microbial balance and, as a result, has many benefits to human health. In recent years, probiotic bacteria have been incorporated into dietary supplements with a large number of foods (Kooshki and Khosravi, 2008). The term probiotic is derived from the Greek word probious meaning "resuscitative" and the opposite is the word antilife (Shen et al., 2013). This term was first used by Lilly and Stillwell in 1965 to explain "secretions by a microorganism that stimulates the growth of another microorganism," and thus the oppositeterm is antibiotic. Parker was the first one to use the term "probiotic" in the concept that is used today. He defined probiotics as "organisms and substances that affect the microbial balance of the intestine." In 1989, Fuller, in an effort to improve Parker's definition, introduced the definition: a nutritional supplement of living microbes that improves the

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microbial balance of the intestine, and has beneficial effects on the host (human or animal) (Kooshki and Khosravi, 2008). The definition below is the closest one of probiotics by Havenaar et al.: "A product containing live and specific microorganisms in a sufficient number that changes the microbial flora through deployment in a part of the host body, thereby causing beneficial effects on the host health "(Shen et al., 2013). 1-4-12 History of Probiotics

Although the term "probiotic" has been introduced as a food supplement since 1974, the history of food supplementsuse containing live microbes dates back to thousands of years ago. Probably fermented milk was the first food containing live microorganisms. Also, evidence of wall paintings dating back to 2500 BC shows that the Sumerians were accustomed toferment milk (Kooshki and Khosravi, 2008). The human interest in using probiotics for health dates back to 1908, when Russian Machinov said that humans should use fermented milk with lactobacillus to prolong their lives (Kooshki and Khosravi, 2008). He said the health and longevity of the Bulgarians are due to the high consumption of fermented milk called Yahourt. In 1908, he outlined the theory of "life without aging and continuing life". An important principle of this theory is the replacement of bacteria producing lactic acid instead of toxin-producing bacteria, which is commonly found in the middle age in the intestine. Mechnikov stated that due to acid lactic production of acid lactic-producing bacteria in sour milk, the anaerobic growth of toxic bacteria and fungi in the intestines becomes impossible. London Douglas, in a book titled "Bacillus for Long Life," published in 1911, re-examined the relationship between fermented milk and long life, as well as a complete overview of the bacteriology of fermented milk (Aggarwal et al., 2013). After World War II, interest in research on indigenous bacteria was reasserted. During 1960s, attention was drawn to the use of live bacterial supplements to counteract the use of antibiotics and avoid their side effects in the livestock. It has been shown that the administration of specific antibiotics to experimental animals protects them longer than others from being infected with

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Salmonella typhimurium, Shigella flexneri and Vibrio cholera (Walker and Lawley, 2013). Researchers at the France Pasteur Institute isolated Bifidobacter from the intestines of infants, and found that this bacterium is a major component of the intestinal microbes in the early days of life. They believed that eating bifidobacter in infants with diarrhea can treat the disease by replacing pathogenic bacteria with this bacterium as the dominant intestinal microorganism. Sprati introduced probiotics as a stimulant of microbial growth in 1971. Finally, in 1989, probiotics were defined as dietary supplements including living microbes that improved the intestinal microbial balance positively on their host (Kooshki and Khosravi, 2008). 1.4.13 Health Effects of Probiotics The total genome of the intestinal microbial population encodes 3/3 million unrelated genes that are 150 times larger than the entire human genome. This genetic enrichment enables the intestinal microbiota to possess many active metabolic functions that cannot be sustained by the human genome (Shen et al., 2013). The intestinal microbial population consists of about 200 predominant bacterial species and up to 1000 rare species, and is therefore similar to a multi-cell organ that shares with the host and provides its own metabolic function to the intestine, which the intestine itself cannot produce and supply (Ley et al., 2008). These functions include the metabolism of xenobiotic compounds, amino acids and carbohydrates (Turnbaugh et al., 2009a, Gill et al., 2006, Kurokawa et al., 2007). The intestinal microbial population is a dynamic organ in other organs of the human body, because cellular composition and gene transcriptional network change rapidly in response to dietary changes (Turnbaugh et al., 2009b, Hildebrandt et al., 2009, Sonnenburg et al. , 2005, Turnbaugh et al., 2008, Walker et al., 2011). Probiotics, by modulating the micro flora of the intestine, have a great health effect on the gastrointestinal tract and are effective in the prevention and treatment of many gastrointestinal diseases including diarrhea, constipation, inflammatory bowel disease, irritable bowel syndrome, gastric ulcer, lactose intolerance and colon cancer (Harish and Varghese, 2006, Picard et al., 2005). There is also growing evidence of intestinal microbial effects out of the digestive tract. Medical studies in the past decade have been associated with intestinal microbial population with metabolic disorders, particularly diabetes and obesity. The microbial environment of the intestine plays a role in the planning and control of many physiological actions, including epithelial evolution, ϰϯ

circulation, and intrinsic and adaptive intestinal mechanisms, although not fully understood (Mackie et al., 1999, Dethlefsen et al., 2006). A new hypothesis suggests that intestinal microbial environment is involved in regulating energy homeostasis. Therefore, in the presence of a vulnerable environment, the intestinal microbial population can disrupt the homeostasis of the energy and result in metabolic disorders (Moreno-Indias et al., 2014). Probiotics have antimicrobial activity and stimulate and modify the immune system activity and thus help the treatment of allergies and urinary tract infections. Probiotics have beneficial effects in increasing the access and absorption of micronutrients and lowering cholesterol and blood pressure (Goldin and Gorbach, 2008, Kaur et al., 2009).

Figure 1-4 Health Effects of Probiotics (School, 2010)

1-4-14 Functional mechanism

The effects of probiotics through their role in normalizing the intestinal microbiota, immunosuppression and maintenance of the intestinal barrierfunction are applied. The three main mechanisms to explain the function of probiotics have been proposed. The first mechanism is the suppression of pathogenic bacteria through competition to bind to the intestine surface and nutrients, as well as the production of antibacterial compounds such as AMPs, anti-microbial peptide human-ȕ-defensin 2, bacteriocines, and lactic acid and acetic acid. The second mechanism is the change in the activity of microbial enzymes. Fatty acids with short chain and bacteriocines decrease the activity of unwanted bacterial enzymes by decreasing the acidity of the intestine and stool. The third mechanism is the stimulation of host immune system by increasing the level of antibodies (eg, immunoglobulin A) and the activity of leukocytes and macrophages. Probiotics

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also increase the function of the intestinal mucus barrier and reduce the invasion of pathogenic microbial products (Peterson and Artis, 2014, Firouzi et al., 2013).

Figure 1-5. Functional physiological barrier of the intestine (Brown et al., 2013)

The role of gut microbes in regulating host body weight and homeostasis of energy was revealed in animal studies. Undoubtedly, the results of studies published by Backhed and colleagues in 2004 and 2007 are of great importance in discovering the probable relationship between gastrointestinal microbes and overweight and obesity (Backhed et al., 2004, Backhed et al., 2007). The researchers showed that, compared with sterile (non-gastro-enteric) mice, normal mice, in contrast to their dietary intake, had a higher 40 percent body fat. Microbial exposure to sterile mice and their conversion to normal mice resulted in an increase of 60% in body fat only in two weeks and without supplementary food intake. The researchers have revealed that parallel with increased body fat, insulin resistance, hypertrophy of fatty cells, and increased leptin and blood glucose occur in normal mice. Interestingly, sterile mice did not suffer from overweight and obesity, even when consumed by Western diets. The researchers described the two main mechanisms to justify these observations as "energy recovery" and "metabolic changes dependent on LPL." Increasing the population of Firmicutes and decreasing the ratio of Bacteroidetes found in obese mice may be associated with the presence of enzyme-encoding genes that break down hostresistant digestible polysaccharides and produce short chain fatty acids and mono saccharides and convert these short fatty acids into triglycerides in the liver (Figure 1-1). Human beings lack essential enzymes for the digestion of many types of plant polysaccharides, such as cellulose, xilane, starch, and inulin (Salyers et al., 1981). Non-activated carbohydrates can be fermented by ϰϱ

intestinal microbes to generate energy and produce short-chain fatty acids (SCFA). These short chain fatty acids can be attached to two receptors bonded to G protein (GPR41 and GPR43) in the gut epithelial cells and activate them. The activation of these receptors induce the secretion of the peptide YY (PYY), which suppresses intestinal motility and delays the movement of substances within the intestine. Through this mechanism, intestinal microbiota plays a role in increasing nutrient intake and participating in metabolic disturbances. It has also been shown that intestinal microbiota reduces the production of fasting-induced adipose factor (FIAF) from intestinal cells, which inhibits lipoprotein lipase activity (LPL) and increases the storage of triglycerides from hepatic origin (Backhed et al. 2007).

Figure 1-6. Intestinal microbiota function is required for the digestion of a number of polysaccharides (Moreno-Indias et al., 2014).

Initial studies using 16S rRNA gene sequencing techniques reported that the intestinal microbiota of obese American and mice (ob / ob) are compatible with microbial control of nonobese, based on the larger ratio of Firmicutes strains compared with the Bacteroidetes class. In addition, the microbiota of obese samples has a lower bacterial variation than non-obese one. n addition, the change in the contribution of Firmicutes and Bacteroidetes to the obese mice ;ob/ob) and under high-fat diet was not related to the intestinal microbial energy extraction

capacity, suggesting that the incidence of Firmicutes and Bacteroidetes and the F/B ratio GRHVQ¶W alter the microbiota energy extraction potential. Accordingly, the change in the contribution of Firmicutes and Bacteroidetes to host weight (gaining weight or weight loss) affects mechanisms independent of energy extraction (Cani et al., 2009b).

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Germ Free mouse colonization through naturally-breed microbiota induces the onset of sodium/glucose transporter-1 (SGLT1) in the small intestine and increases the capillary density in the small intestinal villus epithelium (Shen et al., 2013). Animal studies have shown that indigenous bacteria in humans can be used as probiotics in the treatment. Yin and colleagues examined the effects of four different Bifidobacterium species isolated from healthy human stools on obesity induced by high-fat diet. Compared with single fat diet rats, one species reduced body weight, one species increased body weight and two species had no significant effects on body weight suggesting that the anti-obesity effects of Bifidobacterium are speciesspecific. Interestingly, all four species have been able to significantly reduce serumand liver levels of triglyceride (Yin et al., 2010). 1.4.15 Mechanisms of balance and storage of host energy by intestinal microbiota Increasing energy extraction from diet: Evidence from mice and humans In conventional mice, serum levels of glycolysis-derived metabolites and TCA cycle (such as, for example, pyruvic acid, citric acid, fumaric acid, and malic acid) are higher than germ free mice, hence it seems that the host has access and higher levels of metabolism in the presence of intestinal bacteria (Shen et al ., 2013). The role of bacterial fermentation in the host energy harvesting Adjustment of host energy consumption and metabolism with SCFAs Regulation of intestinal peptides secretion with SCFAs The role of 2 and -3G protein-coupled Free Fatty Acid Receptors (FFARs) Control of appetite through interactions of microbiota and Toll like receptor5 (TLR5) TLRs are the pattern-recognition receptors (PRRs) of innate immune system that identify microbial invariant motifs (PAMPS) on bacteria, viruses, and fungi (Kumar et al., 2011). TLR5 specifically detects bacterial flagelin and has a high incidence in the intestinal mucosa of mice. Detection of extracellular flagelin induces NF-kB-mediated transcriptional host genes and strengthens the cell survival against inflammation (Shen et al., 2013). ϰϳ

The observations suggest that the intestinal microbiota regulates the host food intake and insulin resistance, and this adjustment to the TLR5 is highly dependent on the effect of the intestinal microbial composition. Metabolic control by inhibiting AMP-activated protein kinase (AMPK) AMPK is an enzyme expressed in liver and, brain and skeletal muscle and functions as cellular energy sensor and metabolic regulator. When the AMP: ATP or NAD: NADH ratio increases in response to metabolic stress, such as exercise and glucose deprivation, AMPK is activated by phosphorylation. Activation of AMPK increases cellular energy levels by stimulating catabolic pathways (such as glucose transport and fat oxidation) and inhibiting anabolic pathways (such as fatty acid, protein, and glycogen synthesis) and, to a lesser extent, by controlling the mammalian Target of Rapamycin (mTOR). Partly by reducing AMPK activity and fatty acid oxidation in peripheral tissues, Intestinal microbiota makes the host susceptible to obesity and insulin resistance (Kahn et al., 2006).

Adjustment of fatty acid withdrawal by inhibiting fasting-induced adipose factor (Fiaf/Angptl4):

Fiaf is a protein secreted by the adipose tissue, liver and intestine, and inhibits lipoprotein lipase. This protein can be regulated indirectly by protein catabolism against obesity (Backhed et al., 2004). Intestinal microbiota increases host susceptibility to excessive intake by inhibiting the occurrence of Fiaf (Backhed et al., 2007).

Adjustment in the transcriptional stage of liver-made fat via SREBP-1c and ChREBP

A comparison of Germ-Free with conventional mice shows that intestinal microbiota of the normal mouse increases the synthesis of liver triglyceride and changes the levels of various liver triglyceride components (Backhed et al., 2004). Synthesis of elevated triglyceride coincides with upward regulation of acetyl-coA-carboxylase (AC1) fatty genes and fatty acid synthase (Fas). Both Acc1 and Fas are targets for the transcription factors of Sterol Response Element Binding Protein 1c (SREBP-1c) and Carbohydrate Response Element Binding Protein (ChREBP), which are two

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vital transcription factors to make fat by liver cells in response to insulin and glucose (Backhed et al. , 2004). Metabolic disorders are characterized by low grade inflammation in which the role of the innate and acquired immune systems is important (Shoelson et al., 2006, Hotamisligil, 2006, Pickup and Crook, 1998, Caspar-Bauguil et al., 2005, Feuerer et al., 2009, Weisberg et al., 2003, Winer et al., 2009). Before the onset of obesity and diabetes, the origin of the inflammatory factors is unknown. According to various studies, increased plasma lipopolysaccharide concentrations due to high fat diet are known to be responsible for the onset of metabolic diseases, since continuous and slow subcutaneous infusion of the bacterial lipopolysaccharides have led to most types of metabolic diseases (Tremaroli and Backhed, 2012). First, it was hypothesized that lipopolysaccharides (LPS), which is an inflammatory component of the cell wall in gram-negative bacteria, has a causative role in the incidence of mild inflammation in response to high-fat diet (Cani et al., 2007a). Although the causes of increased bacterial LPS plasma concentrations due to high fat diet have not been determined, the levels are closely related to intestinal microbiota alterations, which increase the Gram-positive to Gramnegativeratio due to high-fat diet. On the other hand, dietary fiber that reduces the effect of high fat diet on the occurrence of metabolic diseases leads to a positive ratio of gram-negative to grampositive bacteria and plasma endotoxemia toward normal (Cani et al., 2009b). The lipopolysaccharides are absorbed by the intestine during the synthesis of chylomicrons (Harris et al., 2002, Ghoshal et al., 2009) and then transfected with other lipoproteins (Rensen et al., 1997), and then into target tissues such as liver (Kumwenda et al. al., 2002) or blood vessels (Westerterp et al., 2007) and result in inflammation (metabolic bacteremia). In the case of other bacterial components, there is still no hypothesis. The passing of gram negative bacteria through the intestine membrane occurs before the onset of diabetes. The 16S rRNA gene in the blood is likely to be a new biomarker at risk for diabetes (Amar et al., 2011b).

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1-4-16 Mechanisms for regulating the activity of bowel barrier and metabolic endotoxemia/ bacteremia: host interaction/microbiota

Figure 1-7 The response of the intestinal epithelium to the diet and bacteria (Guzman et al., 2013)

Mechanisms to maintain the function of the intestinal duct and prevention of bacterial transmission GLP-2 Intestinotrophic proglucagon- derived peptide (GLP)-2 is a peptide produced by intestinal L cells, which promotes intestinal growth and intestinal duct function through insulin-like growth -1 and b-cateninpathways. The effects of Bifidobacterium probiotic on the intestinal duct have been linked to the increase in GLP-2 production, while enhancing the integrity of tight intestinal bonds (increasing the mRNA of ZO-1 binding and occluding proteins) and reducing intestinal permeability (Cani et al., 2009b). 2-TLR TLR-2 is a PRR associated with cell membranes that identifies multiple microbial molecules including peptidoglycan of cell membrane, lipothichoic acid and lipoprotein from gram negative bacteria and lipo-arabinomanan from mycobacteria (Kawai and Akira, 2005).

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TLR-2 maintains the integrity of the intestinal epithelium barrier at the frontline host defense. The TLR-2 signaling activates the anti-apoptotic pathway PI3K / AKT. Therefore, TLR-2 protects the intestinal epithelial cells from stress-induced apoptosis (Shen et al., 2013). MyD88 MyD88 is required to maintain tight joints and function of the TLR-2 mediated intestinal duct response to inflammation and stress (Shen et al., 2013). MyD88-dependent up-regulation of host endogenous antimicrobial compounds is essential for controlling permeability of the intestinal barrier by resident and pathogenic bacteria. MyD88 is an important intermediate for hostmicrobiota interaction which maintains metabolic health (Larsson et al., 2012). NLRC2 (NOD2) NLRC2 is an important microbial sensor in the intestinal barrier, which recognizes the moral di peptide (MDP), which is a vital peptidoglycan component of all bacterial cell walls. NLRC2 maintains microbial population structure and inhibits the colonization of opportunistic microbes in the ileum by modulating cell-mediated immunity (Rehman et al., 2011). Humans carrying Nod2 frameshift (SNP13) mutants have a significant increase in Bacteroidetes and Firmicutes, and Nod2 multiple polymorphisms have a higher risk for inflammatory bowel disease.

Figure 1-8. The innate immune function of the intestinal epithelium plays a key role in maintaining intestinal hemostasis.

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Signaling

Host signaling mechanisms leading to bacterial alteration and its role in obesity

CD14/TLR4 Lipopolysaccharides induce cellular inflammatory responses by activating CD14 / TLR4 / MD2 signaling complexes. Therefore, the detection of Lipopolysaccharides via CD14 / TLR4 directly plays a role in metabolic bacteremia/endotoxemia induced by high fat diet and obesity (McGettrick and O'Neill, 2010). NLRC1(NOD1) NLRC1, a cytosolicPRR, detects bacterial cell wallPGNs. These PGNs are predominantly present in the germ cell wall of the Gram-negative bacteria. NLRC1 mediates the activation of NF-kB independent from MyD88 through interference with the homophilic effect of the RIP2 adapter, a protein kinase containing a caspase recruitment domain that interacts directly with the IkB kinase complex. A hypothesis has been suggested that these two pathways synergically stimulate the full inflammatory response in response to bacteria (Amar et al., 2011a). Endocannabinoid signaling The endocannabinoid system consists of an anadamide (AEA) and 2-arachidonylglycerol (2AG) and their receptors (CB1 and CB2), and enzymes decomposing them (fatty acid amide hydrolase [FAAH] and monacylglycerol lipase [MGL]) The endocannabinoid system regulates many physiological processes, including appetite and intestinal motility (Di Marzo et al., 2001). 1-4-17. Sterile Inflammation: Fatty Acids as PRR Ligands

PRRs are also activated by molecules with non-microbial origin (sterilized inflammation), particularly dietary fats. TLRs (TLR-2 and 4) and NLRCs could be activated by saturated fatty acids and controlled by omega-3 fatty acids (Davis et al., 2009). The activation of TLRs 2 and 4 directly contributes to the spread of inflammation associated with obesity and insulin resistance, which suggests that

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inflammation induced by free fatty acids can exacerbate metabolic endotoxemia or have synergistic effects (Shen et al., 2013).

Figure 1-9 Schematic representation of the metabolic endotoxemia pathway in inducing insulin resistance and obesity

The exact mechanism of probiotic effect on serum insulin levels and insulin resistance is unknown. Probiotics use glucose as a primary source of energy, and their effects on serum insulin levels are likely to interfere with effects on blood glucose levels. Probiotics may also decrease glucose uptake by altering the intestinal environment (Shen et al., 2013), gene expression and intestinal permeability (Awney, 2011). Probiotics may also affect the signaling pathway for insulin secretion. Reducing the activity of Jun N-terminal kinase (a TNF regulated kinase that increases insulin resistance) and reducing the binding activity of DNA to the NF-ț%and have been suggested as other mechanisms to improve insulin resistance by probiotics (Amar et al. 2011a). Also, the results of various studies indicate that some probiotic species have antioxidant activities (Carroll et al., 2007, de Moreno de LeBlanc et al., 2008), and therefore, could be effective in reducing oxidative-stress through several mechanisms. The proposed mechanisms in relation to the effect of probiotics on oxidative-stress are: expression of antioxidant enzymes, immune system stimulation and reduction of inflammation, and therefore, reduction of the antioxidant activity of cytokines, inhibition of various pathogens, reduction of inflammation and oxidative-stress activity, ϱϯ

enhancement of antioxidant-derived micronutrient intake and reduction of the lipids associated with oxidative-stress (Kullisaar et al., 2003, Mikelsaar and Zilmer, 2009, Songisepp et al., 2005, Uskova and Kravchenko, 2009). Studies have shown that Lactobacillus fermentum and Streptococcus thermophilus are capable of producing superoxide dismutase enzyme (Carroll et al., 2007; Kullisaar et al., 2002). Lactobacillus lactis also produces catalase enzyme (de Moreno de LeBlanc et al., 2008). The results of two recent studies show that probiotic bacteria of Lactobacillus acidophilus, Lactobacillus casei, Lactobacillus salivarius and Bifidobacterium bifidum increase glutathione synthesis and systemic glutathione (Lutgendorff et al., 2008; Lutgendorff et al., 2009). Exopolysaccharides are other important molecules produced by some probiotics that could be effective in reducing oxidative-stress. These are long-branch polysaccharides that contain glucose units such as galactose, glucose and rhamnose and have antioxidant properties and trap free radicals (Kodali and Sen, 2008). In addition to the production of antioxidants, probiotics also have metal chelating activity, which inhibits the production of free radicals. The results of the study show that Streptococcus thermophilus and Bifidobacterium lungum have the highest ability to chelate Fe2 + and Cu2 + ions (Lin and Yen, 1999).

Figure 1-10 Therapeutic strategies to challenge intestinal microbes. The discovery of the role of the intestinal microbial population in controlling metabolic diseases has led to various therapeutic strategies such as probiotics, prebiotics and immune modulation.

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1-4-18. Probiotics and gestational diabetes mellitus Several studies have shown that probiotics can reduce the incidence of gestational diabetes. No side effects have been observed in mothers and children who have taken probiotics during pregnancy. There was no significant difference in pre- and post-natal growth in the studied groups. This suggests that probiotics are safe and cost-effective means of preventing gestational diabetes mellitus. 1-4-19. Microbiota intestinal modulation for prevention and treatment Theoretically, mechanisms for regulating intestinal microbial could be conducted through lifestyle changes such as diet studies with exercise, surgery, or the use of drugs or grafts from healthy donors. -

Diet

Changing dietary composition is an important factor in determining the intestinal microbial population diversity. Western-style diets are associated with an increase in the frequency of Bacteroides compared with dietary polysaccharides (Yatsunenko et al., 2012, De Filippo et al., 2010). At the class level, studies on the effect of high-fat diets in mouse models have shown a decrease in the ratio of Bacteroides to Firmicutes (Turnbaugh et al., 2008, Turnbaugh et al., 2009b, Hildebrandt et al., 2009, Murphy et al. 2010), although human studies were not consistent with the results (Duncan et al., 2007, Ley et al., 2006, Arumugam et al., 2011). Clearly, the composition and functional capabilities of human intestinal microbiota adapt quickly to the change in the content of macronutrient diets (Cotillard et al., 2013, David et al., 2014). Recent studies in human and rabbit have shown that long-term dietary patterns can significantly alter the metabolic capacity of the intestinal microbiota (Koeth et al., 2014; Wang et al., 2011b, Koeth et al., 2013). -

Prebiotics

The term "prebiotic" refers to the components of the diet (mainly non-activated albumin), which selectively stimulate the growth and activity of a limited number of species and microbial classes (Roberfroid, 2007). Studies have shown that intestinal microbiota can be modulated by administering inulin fructans with a predominant effect on bifidobacteria and to some extent on ϱϱ

lactobacillus species (Meyer and Stasse-Wolthuis, 2009). In some human and animal studies, it has been shown that prebiotics decrease energy intake and body weight by changing the composition of microbiota (Cani et al., 2009a, Parnell and Reimer, 2009) and simultaneously reduce insulin resistance and hyperglycemia ( Sasaki et al., 2013, Everard et al., 2011, Neyrinck et al., 2011). These effects appear to be due to increased secretion of the intestinal hormones from GLP-1, GLP-2 and Pyy (Cani et al., 2009b, Cani et al., 2009a, Parnell and Reimer, 2009, Everard et al., 2011, Parnell and Reimer, 2012), reducing the appetite-inducing peptide and ghrelin (Parnell and Reimer, 2009, Parnell and Reimer, 2012, Cani et al., 2005) and endotoxemia reduction by enhancing the function of the mucous membrane and reducing the level of inflammatory markers (Cani et al., 2007b , Neyrinck et al., 2011, Cani et al., 2009b, Everard et al., 2013). The direct effect on the production of short-chain fatty acids (butyrate) is another potential mechanism of prebiotics which have a beneficial effect on host physiology (Morrison et al., 2006, Kleessen et al., 2001). - Probiotics Over the past decade, the therapeutic effects of probiotics in metabolic disturbances have been very much studied and although they have been fundamentally performed in mouse models, and have promising results. Several studies of obesity and diabetes in mouse models have shown the promotion of metabolic profiles following administration of different species of lactobacillus and bifidobacter (Hsieh et al., 2013; Yadav et al., 2008; Park et al., 2014, Bejar et al., 2013, Kang et al., 2013, Kang et al., 2010, Kim et al., 2013, Zhang et al. 2014, Plaza-Diaz et al., 2014, Reichold et al., 2014). Most human trials have shown beneficial effects of probiotics on the metabolic profile, and few have revealed beneficial effects on cardio-metabolic health (Andreasen et al., 2010, Asemi et al., 2011, Asemi et al., 2012a, Asemi et al , 2012b, Asemi et al., 2013b, Ejtahed et al., 2012, Luoto et al., 2012, Moroti et al., 2012, Mazloom et al., 2013a, Ataie-Jafari et al., 2009, de Roos et al., 1999, Kadooka et al., 2013). - Physical activity There is an increasing evidence of the effect of moderating the physical activity on the intestinal microbial population, although found essentially in animal models. It has been shown that physical activity affected the composition and diversity of intestinal microbial population in healthy rats (Queipo-Ortuno et al., 2013, Matsumoto et al., 2008), as well as obese mice models (Evans et al.,

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2014, Petriz et al, 2014) and high blood pressure (Petriz et al., 2014), which results suggested the independence of these effects from the diet (Evans et al., 2014, Petriz et al., 2014, Kang et al., 2014). Thenumber and design of human studies are limited, and there is only one study on changes in the diversity and structure of the bacteria family and species in athletes (Clarke et al., 2014). -

Antibiotics

Prescribing antimicrobials including broad-spectrum antibiotics has been suggested as a potential contributor to epidemic obesity and the reduction of intestinal microbial enrichment in the Western world. This hypothesis is supported by epidemiological studies with a small, but large volume, which has been shown to increase the likelihood of overweight at age 7 following antibiotic use in the neonate (Ajslev et al., 2011, Trasande et al., 2013). A recent study has shown that even administration of parenteral antibiotics may increase the risk of childhood obesity by influencing the microbial population of the intestine (Mueller et al., 2015). Although the risk of overweight children in mothers who have normal BMI before pregnancy increases with antibiotic therapy early in life, this risk decreases in overweight and obese mothers (Ajslev et al., 2011). In addition, interventional studies have shown an increase in body mass index in adults following an antibiotic treatment, especially the eradication of Helicobacter pylori in patients with gastric ulcer (Francois et al., 2011, Thuny et al., 2010). Although recent studies have shown short- and longterm effects of antibiotics (Jernberg et al., 2007) on the diversity or structure of the intestinal microbiota, further studies of the potential role of antibiotics in human metabolic diseases are needed. - Bariatric surgery Surgical interventions for weight loss, generally referred to bariatric surgery, have recently become the most effective treatment for obesity. Recent interventions suggest that most of the long-term health benefits of this surgery are likely to be partly due to changes in the intestinal microbial population (Hansen et al., 2015). Studies on the relationship between sex and specific bacterial species and metabolic and inflammatory variables (Graessler et al., 2013, Furet et al., 2010) and changes in the expression of the white fat tissue protein (Kong et al., 2013), and pointed to the probable role of intestinal microbial population as modulating beneficial metabolic effects of Bariatric surgery.

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- Transplantation Since the successful transplantation of fecal microbiota to treat recurrent clostridium difficile enterocolitis (van Nood et al., 2013, Youngster et al., 2014), fecal transplantation as a moderator of cardimetabolic disorders has been considered a lot. A study on 18 men with insulin resistance showed that after 6 weeks of microbiota infusion from non-obese donors, insulin sensitivity improved along with increased bacterial diversity (Vrieze et al., 2012).

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Chapter 2 Review of Previous Studies

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2-1. An overview of the experimental studies on the metabolic effects of probiotics

A study by Yadav et al. in 2005 aimed at assessing the effect of dahi supplementation, a fermentation product containing Lactobacillus lactis with a dose of approximately 67 106* cfu / g was induced by high fructose diet on glucose tolerance test and glycosylated hemoglobin, insulin, triglyceride and fatty acid levels in the mouse model. Serum glucose, glycosylated hemoglobin and insulin levels were significantly lower in dahi-fed group than in control animals. These results indicate that hyperglycemia and the progression of diabetes through a high fructose diet are likely to be preventable or delayed by probiotics. Accordingly, the researcher concludes that a dahi-supplemented diet is likely to prevent insulin resistance/type 2 diabetes induced by a fructose-rich diet (Yadav et al., 2006). The results of this study are published in the Journal of Bioscience, Biotechnology, and Biochemistry, No. 70. In another study by Yadav et al., 2007, the effect of dahi, a low-fat probiotic containing Lactobacillus acidophilus and Lactobacillus casei on the risk factors for type 2 diabetes mellitus was investigated. Based on the results, fermented milk delayed the onset of glucose intolerance, hyperglycemia and hyper-insulinemia, and reduced dyslipidemia and oxidative-stress, and the risk of diabetes and its complications in these mice. These observations indicate that dahi may prevent or delay the induction of high fructose-induced hyperglycemia in diabetic rats (Yadav et al., 2007). The results of this study were published in an article in the Nutrition journal No. 23. In a study by Harisa et al. on diabetes induced by streptozocin in rats, published in the 2009 issue of Australian Basic and Applied Sciences (Harisa et al., 2009), treatment with Lactobacillus acidophilus significantly reduced the level of fasting blood glucose , glycosylatedhemoglobin, triglyceride and malondialdehyde and increased the antioxidant activity of aryl esterase in these rats (P ͕͘EKZZ'͕'͘Θs͕͘s͘;ĞĚƐ͘Ϳ ,ĂŶĚďŽŽŬŽŶƚŚĞ ƚŽǆŝĐŽůŽŐǇŽĨŵĞƚĂůƐ͘EĞǁzŽƌŬ͗ůƐĞǀŝĞƌ͘ >>͕^͕͘:͘͘Θd͕,͘:͘ϮϬϭϱ͘/ŶĨůĂŵŵĂƚŽƌǇĂŶĚKƚŚĞƌŝŽŵĂƌŬĞƌƐ͗ZŽůĞ ŝŶWĂƚŚŽƉŚǇƐŝŽůŽŐǇĂŶĚWƌĞĚŝĐƚŝŽŶŽĨ'ĞƐƚĂƚŝŽŶĂůŝĂďĞƚĞƐDĞůůŝƚƵƐ͘/Ŷƚ:DŽů^Đŝ͕ϭϲ͕ϭϯϰϰϮͲϳϯ͘ hͲ>^͕E͘D͕͘>,D͕͘'͕͘>ͲĂĐƚŽďĂĐŝůůƵƐĂĐŝĚŽƉŚŝůƵƐŽŵďŝŶĞĚǁŝƚŚEĂƚƵƌĂůŶƚŝŽǆŝĚĂŶƚƐDŝƚŝŐĂƚĞƐŽǆŽƌƵďŝĐŝŶͲ /ŶĚƵĐĞĚĂƌĚŝŽŵǇŽƉĂƚŚǇŝŶZĂƚƐ͘:DĞĚ&ŽŽĚ͘ 'Zt>͕D͘D͕͘,dd͕'͘^͕͘WhEEK^͕:͘Θ͕:͕͘^tD/͕'͘Θs͕d͕͘͘EZÊ͕͘^͕͘'DKZ'͕D͕͘^KZEÊ͕d͘/͘Θ:^^͕d͘ϮϬϭϭ͘ŚŝůĚŚŽŽĚŽǀĞƌǁĞŝŐŚƚ ĂĨƚĞƌĞƐƚĂďůŝƐŚŵĞŶƚŽĨƚŚĞŐƵƚŵŝĐƌŽďŝŽƚĂ͗ƚŚĞƌŽůĞŽĨĚĞůŝǀĞƌǇŵŽĚĞ͕ƉƌĞͲƉƌĞŐŶĂŶĐǇǁĞŝŐŚƚĂŶĚ ĞĂƌůǇĂĚŵŝŶŝƐƚƌĂƚŝŽŶŽĨĂŶƚŝďŝŽƚŝĐƐ͘/Ŷƚ:KďĞƐ;>ŽŶĚͿ͕ϯϱ͕ϱϮϮͲϵ͘ >/͕͘ͲZ͕͘͘Ddt>>z͕͘D͕͘D,DKh͕͘,͘Θdd/͕,͘&͘zĞĂƌ͘ĨĨĞĐƚŽĨĨĞĞĚŝŶŐƉƌŽďŝŽƚŝĐƐŽŶƌĂƚƐ͛ ŝŵŵƵŶŝƚǇĂŶĚŚĞĂůƚŚĐŽŶĚŝƚŝŽŶƐĚƵƌŝŶŐƉƌĞŐŶĂŶĐǇ͘/Ŷ͗&ŽŽĚEƵƚƌ^Đŝ͕ϮϬϭϭ͘ϵϲͲϭϬϰ͘ >/WKhZ͕ ͕͘ ,KDzKhE/ͲZ͕ ͕͘ s',&ͲD,ZEz͕ ͕͘ ^,Z/&͕ ^͘ >E͕^͘:͘ϮϬϭϱ͘dŚĞWŽƚĞŶƚŝĂůŽĨWƌŽďŝŽƚŝĐƐƚŽWƌĞǀĞŶƚůŽƐƚƌŝĚŝƵŵĚŝĨĨŝĐŝůĞ/ŶĨĞĐƚŝŽŶ͘/ŶĨĞĐƚ͘ŝƐ͘ůŝŶ͘EŽƌƚŚ ŵ͕͘Ϯϵ͕ϭϯϱͲϭϰϰ͘ >K͕ D͘ ^͕͘ ^/K͕ ^͕͘ >Ͳ^>,͕ z͕͘ >Ͳ',Z/͕ E͘ D͕͘ >W/͕ d͕͘ >,d/EE͕ ^͕͘ Kht,E͕ ͕͘ >E'>>͕ W͕͘ ZhdKEE͕ E͕͘ Ê^KEdd/͕ W͘ :͘ Θ hZ>/E͕ Z͘ ϮϬϭϭĂ͘ /ŶƚĞƐƚŝŶĂů ŵƵĐŽƐĂů ĂĚŚĞƌĞŶĐĞ ĂŶĚ ƚƌĂŶƐůŽĐĂƚŝŽŶ ŽĨ ĐŽŵŵĞŶƐĂůďĂĐƚĞƌŝĂĂƚƚŚĞĞĂƌůǇŽŶƐĞƚŽĨƚǇƉĞϮĚŝĂďĞƚĞƐ͗ŵŽůĞĐƵůĂƌŵĞĐŚĂŶŝƐŵƐĂŶĚƉƌŽďŝŽƚŝĐ ƚƌĞĂƚŵĞŶƚ͘DKDŽůDĞĚ͕ϯ͕ϱϱϵͲϳϮ͘ DZ͕:͕͘^Z/EK͕D͕͘>E'͕͕͘,K͕͕͘/KsKE/͕:͕͘DKEKd͕^͕͘>W'͕W͕͘KWW͕͕͘DZ/dd͕ :͕͘ Kh,͕ K͕͘ WZ͕ >͕͘ KhZdEz͕ D͕͘ DZZ͕ D͕͘ KWW͕ W͕͘ >Ed/Z/͕ K͕͘ KZ͕ :͕͘ ,Z>^͕D͕͘>/E͕Z͘ϮϬϭϭď͘/ŶǀŽůǀĞŵĞŶƚŽĨƚŝƐƐƵĞďĂĐƚĞƌŝĂŝŶƚŚĞŽŶƐĞƚŽĨ ĚŝĂďĞƚĞƐŝŶŚƵŵĂŶƐ͗ĞǀŝĚĞŶĐĞĨŽƌĂĐŽŶĐĞƉƚ͘ŝĂďĞƚŽůŽŐŝĂ͕ϱϰ͕ϯϬϱϱͲϲϭ͘ DZdd/͕͕͘/EhE/K͕D͕͘WKDW/͕͕͘Z/DKE/͕^͕͘ZK^^/͕D͘ΘKZKE/͕͘ϮϬϭϯ͘ŶƚŝŽǆŝĚĂŶƚ ƉƌŽƉĞƌƚŝĞƐ ŽĨ ƉŽƚĞŶƚŝĂůůǇ ƉƌŽďŝŽƚŝĐ ďĂĐƚĞƌŝĂ͗ ŝŶ ǀŝƚƌŽ ĂŶĚ ŝŶ ǀŝǀŽ ĂĐƚŝǀŝƚŝĞƐ͘ ƉƉů DŝĐƌŽďŝŽů ŝŽƚĞĐŚŶŽů͕ϵϳ͕ϴϬϵͲϭϳ͘ EE,Z:͕ D͕͘ ^/sÊZÊ͕E͕͘WZÊͲ^>Z͕E͕ ^͕͘ hZ>d/Z͕͕͘>W^>/Z͕͕͘zD͕d͕͘DE͕͘Z͕͘&ZEE^͕'͘Z͕͘ dW͕ :͕͘ Zh>^͕ d͕͘ ddK͕ :͘ D͕͘ Zd>E͕ D͕͘ KZZh>͕ E͕͘ ^>>^͕ &͕͘ &ZEE͕ >͕͘ 'hd/Z͕>͕͘,EÊ͕d͕͘,ddKZ/͕D͕͘,z^,/͕d͕͘ZD͕D͕͘sE͕ &͕͘ DE/,E,͕ ͕͘ E/>Ê͕ ,͘ ͕͘ E/>Ê͕ d͕͘ WKE^͕ E͕͘ WKh>/E͕ :͕͘ Y/E͕ :͕͘ ^/,Z/dͲWKEdE͕ d͕͘ d/D^͕ ^͕͘ dKZZEd^͕ ͕͘ h'Zd͕ ͕͘ KdE>͕ ͘ '͕͘ tE'͕ :͕͘ 'hZEZ͕&͕͘WZÊ͕K͕͘sK^͕t͘D͕͘ZhE/E͕D͕͘Zd/'hEs͕ &͕͘ >Kdd/Z͕ ,͘ D͕͘ >D/͕ D͕͘ Z,Kd͕ ͕͘ Z͕ ͕͘ ,Zshy͕ ͕͘ h>dZKE͕ ͕͘ >KZD͕ ͕͘ EZ/͕ '͕͘ ZszE͕ Z͕͘ &KZ^dEZ͕ /'͕:͕͘:Dd͕͕͘:h^d͕͕͘KD/EZ/͕Z͕͘ DΖZ/E/͕ ͕͘ Dh>>Z͕ :͕͘ KKZ͕ Z͕͘ WZ>͕ :͕͘ ZEh>d͕ W͕͘ Z^/'EK͕ D͕͘ Ê,͕ E͕͘ ^hE't͕ ^͕͘ dKZZ:KE͕ ͕͘ dhZEZ͕ ZKhZ͕'͕͘t/^Ê,͕:͕͘,Z>/,͕^͘͘ΘKZ,͕ ͘ ϮϬϭϮĂ͘ĨĨĞĐƚŽĨĚĂŝůǇĐŽŶƐƵŵƉƚŝŽŶŽĨƉƌŽďŝŽƚŝĐǇŽŐƵƌƚŽŶŽǆŝĚĂƚŝǀĞƐƚƌĞƐƐŝŶƉƌĞŐŶĂŶƚǁŽŵĞŶ͗ ĂƌĂŶĚŽŵŝǌĞĚĐŽŶƚƌŽůůĞĚĐůŝŶŝĐĂůƚƌŝĂů͘ŶŶEƵƚƌDĞƚĂď͕ϲϬ͕ϲϮͲϴ͘ ^D/͕ ͕͘ /,͕ ^͘ ͕͘ ^,>,͕ ͘ ϮϬϭϯĂ͘ ĨĨĞĐƚƐ ŽĨ ƐǇŶďŝŽƚŝĐĨŽŽĚĐŽŶƐƵŵƉƚŝŽŶŽŶŵĞƚĂďŽůŝĐƐƚĂƚƵƐŽĨĚŝĂďĞƚŝĐƉĂƚŝĞŶƚƐ͗ĚŽƵďůĞͲďůŝŶĚƌĂŶĚŽŵŝǌĞĚ ĐƌŽƐƐͲŽǀĞƌĐŽŶƚƌŽůůĞĚĐůŝŶŝĐĂůƚƌŝĂů͘ůŝŶEƵƚƌ͘ ^D/͕ ͕͘ ^D/D/͕D͕͘ d^/͕ ͕͘ d>/E͕W͕͘ Z͕ ͕͘ ,zZ,͕͘ Θ ^D/>>,͕ ͘ ϮϬϭϮď͘ĨĨĞĐƚŽĨĚĂŝůǇĐŽŶƐƵŵƉƚŝŽŶŽĨƉƌŽďŝŽƚŝĐǇŽŐŚƵƌƚŽŶůŝƉŝĚƉƌŽĨŝůĞƐŝŶƉƌĞŐŶĂŶƚǁŽŵĞŶ͗Ă ƌĂŶĚŽŵŝǌĞĚĐŽŶƚƌŽůůĞĚĐůŝŶŝĐĂůƚƌŝĂů͘:DĂƚĞƌŶ&ĞƚĂůEĞŽŶĂƚĂůDĞĚ͕Ϯϱ͕ϭϱϱϮͲϲ͘ ^D/͕͕͘^D/D/͕D͕͘d^^/͕͕͘E',//Z͕D͕͘Z,/D/&KZKh^,E/͕͕͘>,͕͘ϮϬϭϯď͘ĨĨĞĐƚŽĨĚĂŝůǇĐŽŶƐƵŵƉƚŝŽŶŽĨƉƌŽďŝŽƚŝĐǇŽŐŚƵƌƚŽŶŝŶƐƵůŝŶƌĞƐŝƐƚĂŶĐĞ ŝŶƉƌĞŐŶĂŶƚǁŽŵĞŶ͗ĂƌĂŶĚŽŵŝǌĞĚĐŽŶƚƌŽůůĞĚƚƌŝĂů͘Ƶƌ:ůŝŶEƵƚƌ͕ϲϳ͕ϳϭͲϰ͘ ^D/͕͕͘^D/D/͕D͕͘d^^/͕͕͘E',//͕Z͘D͕͘Z,/D/͕&͕͘͘>,͕ ͘ ϮϬϭϯĐ͘ ĨĨĞĐƚ ŽĨ ĚĂŝůǇ ĐŽŶƐƵŵƉƚŝŽŶ ŽĨ ƉƌŽďŝŽƚŝĐ ǇŽŐŚƵƌƚ ŽŶ ŝŶƐƵůŝŶ ƌĞƐŝƐƚĂŶĐĞ ŝŶ ƉƌĞŐŶĂŶƚ ǁŽŵĞŶ͗ĂƌĂŶĚŽŵŝǌĞĚĐŽŶƚƌŽůůĞĚƚƌŝĂů͘Ƶƌ͘:͘ůŝŶ͘EƵƚƌ͕͘ϲϳ͕ϳϭͲϳϰ͘ ^D/͕͕͘Z͕͕͘^,>,͕͘ϮϬϭϯĚ͘ĨĨĞĐƚŽĨŵƵůƚŝƐƉĞĐŝĞƐƉƌŽďŝŽƚŝĐ ƐƵƉƉůĞŵĞŶƚƐŽŶŵĞƚĂďŽůŝĐƉƌŽĨŝůĞƐ͕ŚƐͲZW͕ĂŶĚŽǆŝĚĂƚŝǀĞƐƚƌĞƐƐŝŶƉĂƚŝĞŶƚƐǁŝƚŚƚǇƉĞϮĚŝĂďĞƚĞƐ͘ ŶŶEƵƚƌDĞƚĂď͕ϲϯ͕ϭͲϵ͘ ^',Z/Ͳ:&Z/͕D͘Θ^',/ͲZ'E/͕,͘ϮϬϭϰ͘ZĂŶĚŽŵŝǌĂƚŝŽŶ͗dĞĐŚŶŝƋƵĞƐĂŶĚ^ŽĨƚǁĂƌĞͲ ĂŝĚĞĚ/ŵƉůĞŵĞŶƚĂƚŝŽŶŝŶDĞĚŝĐĂů^ƚƵĚŝĞƐ͘:ŽƵƌŶĂůŽĨůŝŶŝĐĂůZĞƐĞĂƌĐŚΘ'ŽǀĞƌŶĂŶĐĞ͕ϯ͘ ϭϱϳ

^^K/d/KE͕ ͘ ͘ ϭϵϴϬ͘ tŽƌŬƐŚŽƉͲŽŶĨĞƌĞŶĐĞ ŽŶ ŐĞƐƚĂƚŝŽŶĂů ĚŝĂďĞƚĞƐ͗^ƵŵŵĂƌǇ ĂŶĚ ƌĞĐŽŵŵĞŶĚĂƚŝŽŶƐ͘ŝĂďĞƚĞƐĂƌĞ ϯ͕ϰϵϵͲϱϬϭ͘ ^^K/d/KE͕ ͘ ͘ ϮϬϬϭ͘ DĞĚŝĐĂů EƵƚƌŝƚŝŽŶ dŚĞƌĂƉǇ͕ ǀŝĚĞŶĐĞͲĂƐĞĚ 'ƵŝĚĞƐ ĨŽƌ WƌĂĐƚŝĐĞ͗ EƵƚƌŝƚŝŽŶ WƌĂĐƚŝĐĞ'ƵŝĚĞůŝŶĞƐĨŽƌ'ĞƐƚĂƚŝŽŶĂůŝĂďĞƚĞƐDĞůůŝƚƵƐ;ZKDͿ ŚŝĐĂŐŽ͕/>͘ ^^K/d/KE͕͘͘ϮϬϭϭĂ͘ŝĂŐŶŽƐŝƐĂŶĚĐůĂƐƐŝĨŝĐĂƚŝŽŶŽĨĚŝĂďĞƚĞƐŵĞůůŝƚƵƐ ŝĂďĞƚĞƐĂƌĞ͕ϯϰ^ƵƉƉůϭ͕^ϲϮͲϲϵ͘ ^^K/d/KE͕͘͘ϮϬϭϭď͘^ƚĂŶĚĂƌĚƐŽĨŵĞĚŝĐĂůĐĂƌĞŝŶĚŝĂďĞƚĞƐͲͲϮϬϭϭ͘ŝĂďĞƚĞƐĂƌĞ͘ϮϬϭϭͬϬϭͬϭϰĞĚ͘ ^^K/d/KE͕͘͘ϮϬϭϯ͘^ƚĂŶĚĂƌĚƐŽĨŵĞĚŝĐĂůĐĂƌĞŝŶĚŝĂďĞƚĞƐͲͲϮϬϭϯ͘ϮϬϭϯͬϬϭͬϬϰĞĚ͗͘ŝĂďĞƚĞƐĂƌĞ ^^K/d/KE͕͘͘ϮϬϭϰ͘^ƚĂŶĚĂƌĚƐŽĨŵĞĚŝĐĂůĐĂƌĞŝŶĚŝĂďĞƚĞƐͲͲϮϬϭϰ͘ϮϬϭϯͬϭϮͬϮϭĞĚ͗͘ŝĂďĞƚĞƐĂƌĞ͘ d/Ͳ:&Z/͕͕͘>Z/:E/͕͕͘>s/D:͕,͘Θd,͕&͘ϮϬϬϵ͘ŚŽůĞƐƚĞƌŽůͲůŽǁĞƌŝŶŐĞĨĨĞĐƚŽĨƉƌŽďŝŽƚŝĐ ǇŽŐƵƌƚŝŶĐŽŵƉĂƌŝƐŽŶǁŝƚŚŽƌĚŝŶĂƌǇǇŽŐƵƌƚŝŶŵŝůĚůǇƚŽŵŽĚĞƌĂƚĞůǇŚǇƉĞƌĐŚŽůĞƐƚĞƌŽůĞŵŝĐƐƵďũĞĐƚƐ͘ ŶŶEƵƚƌDĞƚĂď͕ϱϰ͕ϮϮͲϳ͘ d^,,^,KZ/,͕&͘ϮϬϬϲ͘&ƌĞƋƵĞŶĐǇŽĨŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐĂŶĚŝƚƐƌĞůĂƚĞĚĨĂĐƚŽƌƐŝŶƉƌĞŐŶĂŶƚ ǁŽŵĞŶĂƚƚĞŶĚĞĚƚŽdĞŚƌĂŶhŶŝǀĞƌƐŝƚǇŽĨDĞĚŝĐĂů^ĐŝĞŶĐĞƐŽďƐƚĞƚƌŝĐƐĂŶĚŐǇŶĞĐŽůŽŐǇĐůŝŶŝĐƐϮϬϬϬͲ ϮϬϬϭ͘:ZĂĨƐĂŶũĂŶhŶŝǀDĞĚ^ĐŝĞŶ͕ϱ͕ϭϳϱͲϴϬ͘ d'K͕:͘D͕͘'Z/^^͕K͕͘z^^Kh&Kh͕͕͘,/,D/͕͕͘ZDE͕͕͘DKhd/ZKh͕͕͕͘ 'Z/^^͕͕͘:Z/͕D͕͘dͲzE͕Z͕͘Zz^ͲDhEK͕͕͘DZd/EͲZh͕E͕͘KZd'Ͳ'KE>͕͕͘s/>ͲZZ^K͕͘ Θ^d/>>KͲDKZ͕͘ϮϬϭϰ͘ZŝƐŬĨĂĐƚŽƌƐĂƐƐŽĐŝĂƚĞĚǁŝƚŚƚŚĞŶĞĞĚƚŽƵƐĞŝŶƐƵůŝŶƚŚĞƌĂƉǇŝŶǁŽŵĞŶ ǁŝƚŚŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐŵĞůůŝƚƵƐ͘KďƐƚĞƚ'ǇŶĞĐŽů͕ϭϮϯ^ƵƉƉůϭ͕ϭϯϲ^͘ /͕z͕͘h^dhEZ͕/͕͘Ͳ^K,Dz͕͘Θ/͕D͘ϮϬϭϬ͘dǇƉĞϮ ĚŝĂďĞƚĞƐŵĞůůŝƚƵƐĂŶĚŝŶĨůĂŵŵĂƚŝŽŶ͗WƌŽƐƉĞĐƚƐĨŽƌďŝŽŵĂƌŬĞƌƐŽĨƌŝƐŬĂŶĚŶƵƚƌŝƚŝŽŶĂůŝŶƚĞƌǀĞŶƚŝŽŶ͘ ŝĂďĞƚĞƐDĞƚĂď^ǇŶĚƌKďĞƐ͕ϯ͕ϭϳϯͲϴϲ͘ ͕͘D/,>Ê͕E ^/>sD/'>/KZE͕>͘ϮϬϭϰ͘ĞŶĞĨŝĐŝĂůĞĨĨĞĐƚƐŽĨ>ĂĐƚŽďĂĐŝůůƵƐƉůĂŶƚĂƌƵŵŽŶŐůǇĐĞŵŝĂĂŶĚ ŚŽŵŽĐǇƐƚĞŝŶĞůĞǀĞůƐŝŶƉŽƐƚŵĞŶŽƉĂƵƐĂůǁŽŵĞŶǁŝƚŚŵĞƚĂďŽůŝĐƐǇŶĚƌŽŵĞ͘EƵƚƌŝƚŝŽŶ͕ϯϬ͕ϵϯϵͲϰϮ͘ ZZdd͕,͘>͕͘>>tz͕>͕͕͘͘>͘^͘Θ>>tz͕>͘>K͕D͕͘^/E',͕z͕>͕͘d>EK͕W͘D͘Θ,h'h>ͲDKhKE͕^͘ϮϬϭϭ͘WƌĞŐƌĂǀŝĚŽďĞƐŝƚǇĂƐƐŽĐŝĂƚĞƐ ǁŝƚŚŝŶĐƌĞĂƐĞĚŵĂƚĞƌŶĂůĞŶĚŽƚŽǆĞŵŝĂĂŶĚŵĞƚĂďŽůŝĐŝŶĨůĂŵŵĂƚŝŽŶ͘ KďĞƐŝƚǇ;^ŝůǀĞƌ^ƉƌŝŶŐͿ͕ϭϵ͕ ϰϳϲͲϴϮ͘ hDEE͕,͘Θ'h>/͕:͘ϭϵϵϰ͘dŚĞĂĐƵƚĞƉŚĂƐĞƌĞƐƉŽŶƐĞ͘/ŵŵƵŶŽůdŽĚĂǇ͕ϭϱ͕ϳϰͲϴϬ͘ zE^͕:͘t͘ϭϵϵϭ͘ZŽůĞŽĨŽǆŝĚĂƚŝǀĞƐƚƌĞƐƐŝŶĚĞǀĞůŽƉŵĞŶƚŽĨĐŽŵƉůŝĐĂƚŝŽŶƐŝŶĚŝĂďĞƚĞƐ͘ŝĂďĞƚĞƐ͕ϰϬ͕ ϰϬϱͲϭϮ͘ zE^͕:͘t͘Θd,KZW͕^͘Z͘ϭϵϵϵ͘ZŽůĞŽĨŽǆŝĚĂƚŝǀĞƐƚƌĞƐƐŝŶĚŝĂďĞƚŝĐĐŽŵƉůŝĐĂƚŝŽŶƐ͗ĂŶĞǁƉĞƌƐƉĞĐƚŝǀĞ ŽŶĂŶŽůĚƉĂƌĂĚŝŐŵ͘ŝĂďĞƚĞƐ͕ϰϴ͕ϭͲϵ͘ :Z͕ t͕͘ ,DE͕ ,͕ Z͘ Θ ,KhzĂĐƚŽďĂĐŝůůƵƐ ƉůĂŶƚĂƌƵŵ dEϲϮϳ ƐŝŐŶŝĨŝĐĂŶƚůǇƌĞĚƵĐĞƐĐŽŵƉůŝĐĂƚŝŽŶƐŽĨĂůůŽǆĂŶͲŝŶĚƵĐĞĚĚŝĂďĞƚĞƐŝŶƌĂƚƐ͘ŶĂĞƌŽďĞ͕Ϯϰ͕ϰͲϭϭ͘ >>Dz͕ >͕͘ ^^͕ :͘ W͕͘ ,/E'KZE/͕ ͘ ͘ Θ t/>>/D^͕ ͘ ϮϬϬϵ͘ dǇƉĞ Ϯ ĚŝĂďĞƚĞƐ ŵĞůůŝƚƵƐ ĂĨƚĞƌ ŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐ͗ĂƐǇƐƚĞŵĂƚŝĐƌĞǀŝĞǁĂŶĚŵĞƚĂͲĂŶĂůǇƐŝƐ͘>ĂŶĐĞƚ͕ϯϳϯ͕ϭϳϳϯͲϵ͘ EͲ,ZKh^,͕ ͕͘ zK's͕ z͘ Θ ,K͕ D͘ ϮϬϬϰ͘ ƉŝĚĞŵŝŽůŽŐǇ ŽĨ ŐĞƐƚĂƚŝŽŶĂů ĚŝĂďĞƚĞƐ ŵĞůůŝƚƵƐ ĂŶĚ ŝƚƐ ĂƐƐŽĐŝĂƚŝŽŶǁŝƚŚdǇƉĞϮĚŝĂďĞƚĞƐ͘ŝĂďĞƚDĞĚ͕Ϯϭ͕ϭϬϯͲϭϯ͘ ZdKE/͕͘'͕͘hZŝƉƉŝŶĐŽƚƚ tŝůůŝĂŵƐΘtŝŬŝŶƐ͘

ϭϱϵ

/>E͕W͘:͕͘^DKKs͕s͕͘/͕͕͘D/,/>/͕&͕͘D^^KZ/K͕D͘ΘW'EK͕ '͘ϮϬϬϭ͘ŝĞƚĂƌǇĨĂƚĂŶĚŐĞƐƚĂƚŝŽŶĂůŚǇƉĞƌŐůǇĐĂĞŵŝĂ͘ŝĂďĞƚŽůŽŐŝĂ͕ϰϰ͕ϵϳϮͲϴ͘ KZ͕&͘͘E͘ϭϵϵϬ͘EƵƚƌŝƚŝŽŶƵƌŝŶŐWƌĞŐŶĂŶĐǇ͘WĂƌƚϭ͗tĞŝŐŚƚ'ĂŝŶ͘WĂƌƚϮ͗EƵƚƌŝĞŶƚ^ƵƉƉůĞŵĞŶƚƐ͘ tĂƐŚŝŶŐƚŽŶ͕͗/ŶƐƚŝƚƵƚĞŽĨDĞĚŝĐŝŶĞ͕EĂƚŝŽŶĂůĐĂĚĞŵǇŽĨ^ĐŝĞŶĐĞƐ͘ K>:͕'͕͘Z'͕:͕͘W/,>Z͕Z͘Θ/Ê,͕'͘ϮϬϬϲĂ͘WƌĞǀĂůĞŶĐĞ͕ƐĞǀĞƌŝƚǇĂŶĚƉƌĞĚŝĐƚŽƌƐŽĨ,KDͲ ĞƐƚŝŵĂƚĞĚŝŶƐƵůŝŶƌĞƐŝƐƚĂŶĐĞŝŶĚŝĂďĞƚŝĐĂŶĚŶŽŶĚŝĂďĞƚŝĐƉĂƚŝĞŶƚƐǁŝƚŚĞŶĚͲƐƚĂŐĞƌĞŶĂůĚŝƐĞĂƐĞ͘ :͘EĞƉŚƌŽů͕͘ϭϵ͕ϲϬϳͲϲϭϮ͘ K>:͕'͕͘Z'͕:͕͘W/,>Z͕Z͘Θ/Ê,͕'͘ϮϬϬϲď͘WƌĞǀĂůĞŶĐĞ͕ƐĞǀĞƌŝƚǇĂŶĚƉƌĞĚŝĐƚŽƌƐŽĨ,KDͲ ĞƐƚŝŵĂƚĞĚŝŶƐƵůŝŶƌĞƐŝƐƚĂŶĐĞŝŶĚŝĂďĞƚŝĐĂŶĚŶŽŶĚŝĂďĞƚŝĐƉĂƚŝĞŶƚƐǁŝƚŚĞŶĚͲƐƚĂŐĞƌĞŶĂůĚŝƐĞĂƐĞ͘: EĞƉŚƌŽů͕ϭϵ͕ϲϬϳͲϭϮ͘ K'Ê͕͘^͕͘͘&>KZE͕͘͘Z͕͘WZ/E͕E͕͘Zhd/͕Z͕͘͘EsZZKͲZKZ/'h͕d͕͘/^/'͕:͘E͘Θ K>/s/Z͕D͘E͘ϮϬϭϭ͘ZdZd͗WƌŽďŝŽƚŝĐƐŝŶƚĂŬĞĂŶĚŵĞƚĂďŽůŝĐƐǇŶĚƌŽŵĞ͗ƉƌŽƉŽƐĂů͘dƌĞŶĚƐ ŝŶ&ŽŽĚ^ĐŝĞŶĐĞΘdĞĐŚŶŽůŽŐǇ͕ϮϮ͕ϰϱϳͲϰϲϰ͘ K,DZ͕͘D͕͘>͕ ͕͘ /Kd͕ '͕͘ > Zh͕ '͕͘ >,Z/͕ ͕͘ h'Z/͕ >͕͘ hW^͕ :͘ >͕͘ DZdh͕ W͕͘ ZDW>͕ W͕͘ DKz^͕ ͕͘ ^>,͕ ͕͘ > 'hZE͕ D͘ ͘ Θ '>D/,͕ :͘ W͘ ϮϬϭϯ͘ ^ĂĐĐŚĂƌŽŵǇĐĞƐ ďŽƵůĂƌĚŝŝĚŽĞƐŶŽƚƉƌĞǀĞŶƚƌĞůĂƉƐĞŽĨƌŽŚŶΖƐĚŝƐĞĂƐĞ͘ůŝŶ'ĂƐƚƌŽĞŶƚĞƌŽů,ĞƉĂƚŽů͕ϭϭ͕ϵϴϮͲϳ͘ ZE^,͕͕͘^,h͕͕͘,/Z,͕&͕͘^dE'>͕'͘/͘ΘZ͕͕͘Dz,Z͕Z͕͘,h'E͕D͕͘Dz͕s͕͘D'Eh^͕W͕͘:K^^KE͕͘Θ D>dZ͕,͘D͘ϮϬϭϭ͘/ŶƚĂŬĞŽĨƉƌŽďŝŽƚŝĐĨŽŽĚĂŶĚƌŝƐŬŽĨƉƌĞĞĐůĂŵƉƐŝĂŝŶƉƌŝŵŝƉĂƌŽƵƐǁŽŵĞŶ͗ ƚŚĞEŽƌǁĞŐŝĂŶDŽƚŚĞƌĂŶĚŚŝůĚŽŚŽƌƚ^ƚƵĚǇ͘ŵ:ƉŝĚĞŵŝŽů͕ϭϳϰ͕ϴϬϳͲϭϱ͘ Zz͕'͘͘ϮϬϬϲ͘tĞŝŐŚƚŽŶƚƌŽů͗ƐƐĞƐƐŵĞŶƚĂŶĚDĂŶĂŐĞŵĞŶƚ͕ŵĞƌŝĐĂŶŽůůĞŐĞŽĨKďƐƚĞƚƌŝĐŝĂŶƐĂŶĚ 'ǇŶĞĐŽůŽŐŝƐƚƐ͘ ZKtE͕͘D͕͘^ZE'E/͕D͘Θ&/E>z͕͘͘ϮϬϭϯ͘dŚĞƌŽůĞŽĨƚŚĞŝŵŵƵŶĞƐǇƐƚĞŵŝŶŐŽǀĞƌŶŝŶŐŚŽƐƚͲ ŵŝĐƌŽďĞŝŶƚĞƌĂĐƚŝŽŶƐŝŶƚŚĞŝŶƚĞƐƚŝŶĞ͘EĂƚ/ŵŵƵŶŽů͕ϭϰ͕ϲϲϬͲϳ͘ Zh^dDE͕>͕͘͘>E'Z͕K͕͘/D^KE͕͕͘^ZW>>/͕^͘Θ>KhD͕ ͕͘ Kh^/E͕ ͕͘ ^h>W/͕ d͕͘ ,DKEd/E͕ ͕͘ &ZZ/Z^͕ :͕͘ dEd/͕ :͘ &͕͘ '/^KE͕ '͘ Z͕͘ ^d/>>͕ >͕͘ >EE͕ E͘ D͕͘ >^^/͕ D͘ ͘ Θ hZ>/E͕Z͘ϮϬϬϳĂ͘DĞƚĂďŽůŝĐĞŶĚŽƚŽǆĞŵŝĂŝŶŝƚŝĂƚĞƐŽďĞƐŝƚǇĂŶĚŝŶƐƵůŝŶƌĞƐŝƐƚĂŶĐĞ͘ŝĂďĞƚĞƐ͕ϱϲ͕ ϭϳϲϭͲϳϮ͘

ϭϲϬ

E/͕W͘͘Θ>EE͕E͘D͘ϮϬϬϵ͘dŚĞƌŽůĞŽĨƚŚĞŐƵƚŵŝĐƌŽďŝŽƚĂŝŶĞŶĞƌŐǇŵĞƚĂďŽůŝƐŵĂŶĚŵĞƚĂďŽůŝĐ ĚŝƐĞĂƐĞ͘ƵƌƌWŚĂƌŵĞƐ͕ϭϱ͕ϭϱϰϲͲϱϴ͘ E/͕W͘͘Θ>EE͕E͘D͘ϮϬϭϭ͘dŚĞŐƵƚŵŝĐƌŽďŝŽŵĞĂƐƚŚĞƌĂƉĞƵƚŝĐƚĂƌŐĞƚ͘ WŚĂƌŵĂĐŽůdŚĞƌ͕ϭϯϬ͕ ϮϬϮͲϭϮ͘ E/͕W͕͘͘>KhZd͕͕͘th>&͕͘D͕͘^K,d͕&͘D͕͘W,//E͕͕͕͘d͕͘'h/Kd͕z͕͘sZZ͕͕͘ZKdd/Z͕K͕͘'hZd^͕>͕͘E^>/E͕ ͕͘EzZ/EDZd͕͘D͕͘Dh/K>/͕'͘'͘Θ>EE͕E͘D͘ϮϬϬϵď͘ŚĂŶŐĞƐŝŶŐƵƚ ŵŝĐƌŽďŝŽƚĂ ĐŽŶƚƌŽů ŝŶĨůĂŵŵĂƚŝŽŶ ŝŶ ŽďĞƐĞ ŵŝĐĞ ƚŚƌŽƵŐŚ Ă ŵĞĐŚĂŶŝƐŵ ŝŶǀŽůǀŝŶŐ '>WͲϮͲĚƌŝǀĞŶ ŝŵƉƌŽǀĞŵĞŶƚŽĨŐƵƚƉĞƌŵĞĂďŝůŝƚǇ͘'Ƶƚ͕ϱϴ͕ϭϬϵϭͲϭϬϯ͘ WZKs͕D͕͘,^/͕ /͘ D͕͘ EZh^͕ :͘ D͕͘ ZhEKͲZE͕ :͘ D͕͘ E,DDZ͕ d͘ Z͕͘ ,^Ê͕ ,͘ D͘ Θ d,Z'/>>͕ ͘ ^͘ ϮϬϬϳ͘ ŶƚŝͲŝŶĨůĂŵŵĂƚŽƌǇ ƉƌŽƉĞƌƚŝĞƐ ŽĨ >ĂĐƚŽďĂĐŝůůƵƐ ŐĂƐƐĞƌŝ ĞǆƉƌĞƐƐŝŶŐ ŵĂŶŐĂŶĞƐĞƐƵƉĞƌŽǆŝĚĞĚŝƐŵƵƚĂƐĞƵƐŝŶŐƚŚĞŝŶƚĞƌůĞƵŬŝŶϭϬͲĚĞĨŝĐŝĞŶƚŵŽƵƐĞŵŽĚĞůŽĨĐŽůŝƚŝƐ͘ŵ: WŚǇƐŝŽů'ĂƐƚƌŽŝŶƚĞƐƚ>ŝǀĞƌWŚǇƐŝŽů͕Ϯϵϯ͕'ϳϮϵͲϯϴ͘ ^WZͲh'h/>͕^͕͘Kh^/E͕͕͘'>/E/Z͕͕͘^'&ZK͕͕͘E/>/E>͕>͘ Θ WE/h͕ >͘ ϮϬϬϱ͘ ĚŝƉŽƐĞ ƚŝƐƐƵĞƐ ĂƐ ĂŶ ĂŶĐĞƐƚƌĂů ŝŵŵƵŶĞ ŽƌŐĂŶ͗ ƐŝƚĞͲƐƉĞĐŝĨŝĐ ĐŚĂŶŐĞ ŝŶ ŽďĞƐŝƚǇ͘&^>Ğƚƚ͕ϱϳϵ͕ϯϰϴϳͲϵϮ͘ d>EK͕ W͘ D͕͘ &ZZ>>͕ z͕ >͕͘ DE/E͕ W͕͘ DKhKE͕ ^͘ ,͘ Θ D/E/͕^͘͘ϮϬϬϵ͘WĞƌŝŶĂƚĂůƌŝƐŬĨĂĐƚŽƌƐĨŽƌĐŚŝůĚŚŽŽĚŽďĞƐŝƚǇĂŶĚŵĞƚĂďŽůŝĐĚǇƐƌĞŐƵůĂƚŝŽŶ͘ŵ: ůŝŶEƵƚƌ͕ϵϬ͕ϭϯϬϯͲϭϯ͘ d>EK͕ W͘ D͕͘ ,h^dKE͕ >͕͘ D/E/͕ ^͘ ͘ Θ ,E͕ ^͘ ͘ ϭϵϵϵ͘ >ŽŶŐŝƚƵĚŝŶĂů ĐŚĂŶŐĞƐ ŝŶ ŐůƵĐŽƐĞ ŵĞƚĂďŽůŝƐŵ ĚƵƌŝŶŐ ƉƌĞŐŶĂŶĐǇ ŝŶŽďĞƐĞ ǁŽŵĞŶ ǁŝƚŚŶŽƌŵĂů ŐůƵĐŽƐĞ ƚŽůĞƌĂŶĐĞĂŶĚ ŐĞƐƚĂƚŝŽŶĂů ĚŝĂďĞƚĞƐŵĞůůŝƚƵƐ͘ŵ:KďƐƚĞƚ'ǇŶĞĐŽů͕ϭϴϬ͕ϵϬϯͲϭϲ͘ d>EK͕ W͘ D͕͘ >͕ d͘ K͘ ϮϬϬϱ͘ KǆŝĚĂƚŝǀĞ ƐƚƌĞƐƐ͗ ĐŚĂŶŐĞƐ ŝŶ ƉƌĞŐŶĂŶĐǇ ĂŶĚ ǁŝƚŚ ŐĞƐƚĂƚŝŽŶĂů ĚŝĂďĞƚĞƐ ŵĞůůŝƚƵƐ͘ƵƌƌŝĂďZĞƉ͕ϱ͕ϮϴϮͲϴ͘ ,E͕y͕͘^,K>>͕d͘K͕͘>^>͕:͘Θ^d/E͕d͘W͘ϮϬϭϬ͘ŝĨĨĞƌĞŶĐĞƐŝŶŵĂƚĞƌŶĂůĐŝƌĐƵůĂƚŝŶŐ ĨĂƚƚǇĂĐŝĚĐŽŵƉŽƐŝƚŝŽŶĂŶĚĚŝĞƚĂƌǇĨĂƚŝŶƚĂŬĞŝŶǁŽŵĞŶǁŝƚŚŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐŵĞůůŝƚƵƐŽƌŵŝůĚ ŐĞƐƚĂƚŝŽŶĂůŚǇƉĞƌŐůǇĐĞŵŝĂ͘ŝĂďĞƚĞƐĂƌĞ͕ϯϯ͕ϮϬϰϵͲϱϰ͘ ,E͕͕͘tdE͕Z͘D͕͘^dZD͕͘K͕͘h,EE͕d͘͘Θy/E'͕͘,͘ϮϬϭϰ͘,ŝŐŚĐĂůŽƌŝĞŝŶƚĂŬĞŝƐ ĂƐƐŽĐŝĂƚĞĚ ǁŝƚŚ ǁŽƌƐĞŶŝŶŐ ŝŶƐƵůŝŶ ƌĞƐŝƐƚĂŶĐĞ ĂŶĚ ďĞƚĂͲĐĞůů ĨƵŶĐƚŝŽŶ ŝŶ ,ŝƐƉĂŶŝĐ ǁŽŵĞŶ ĂĨƚĞƌ ŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐŵĞůůŝƚƵƐ͘ŝĂďĞƚĞƐĂƌĞ͕ϯϳ͕ϯϮϵϰͲϯϬϬ͘ ,/E͕:͘ϮϬϬϱ͘WƌŽƐƉĞĐƚƐĨŽƌďĞŶĞĨŝĐŝĂůŚĞĂůƚŚŽƵƚĐŽŵĞƐĨƌŽŵŝŶƚĞƐƚŝŶĂůŵŝĐƌŽĨůŽƌĂ͘ƐŝĂWĂĐ͘:͘ůŝŶ͘EƵƚƌ͕ ϭϰ͕ϲϰͲϲϱ͘ ,K͕͘Z͕͘͘ΘD͘D͘Θ>^Z͕D͘:͘;ĞĚƐ͘ͿDŝĐƌŽďŝĂůĐŽůŽŐǇŝŶ^ƚĂƚĞƐŽĨ,ĞĂůƚŚĂŶĚŝƐĞĂƐĞ͗tŽƌŬƐŚŽƉ^ƵŵŵĂƌǇ EĂƚŝŽŶĂůĐĂĚĞŵŝĐWƌĞƐƐ;EWͿ͘ ,Kt͕^͘Ͳ͘Θ>/h͕:͘ͲW͘ϮϬϬϰ͘ĞƐŝŐŶĂŶĚĂŶĂůǇƐŝƐŽĨĐůŝŶŝĐůƚƌŝĂůƐEĞǁ:ĞƌƐĞǇ͕:ŽŚŶtŝůĞǇΘ^ŽŶƐ͕/ŶĐ͘ ,ZKh^K^͕'͘W͘ϭϵϵϱ͘dŚĞŚǇƉŽƚŚĂůĂŵŝĐͲƉŝƚƵŝƚĂƌǇͲĂĚƌĞŶĂůĂǆŝƐĂŶĚŝŵŵƵŶĞͲŵĞĚŝĂƚĞĚŝŶĨůĂŵŵĂƚŝŽŶ͘E ŶŐů:DĞĚ͕ϯϯϮ͕ϭϯϱϭͲϲϮ͘ ,h͕^͘z͕͘>>',E͕t͘D͕͘h͕:͕͘E'>E͕>͘:͘Θ/d͕W͘D͘ϮϬϬϳ͘ DĂƚĞƌŶĂůŽďĞƐŝƚǇĂŶĚƌŝƐŬŽĨŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐŵĞůůŝƚƵƐ͘ŝĂďĞƚĞƐĂƌĞ͕ϯϬ͕ϮϬϳϬͲϲ͘ >Z>/sE͕ K͕͘ >hz͕ ͘ :͕͘ ,hDW,Zz^͕ D͕͘ ,K'E͕ ͕͘ ,z^͕ W͕͘ KΖZ/>>z͕D͕͘:&&Zz͕/͕͘͘tKKͲDZd/E͕Z͕͘sz͕͕͘^,E,E͕&͘ΘKddZ͕W͘͘ϮϬϭϰ͘ǆĞƌĐŝƐĞĂŶĚĂƐƐŽĐŝĂƚĞĚ ĚŝĞƚĂƌǇĞǆƚƌĞŵĞƐŝŵƉĂĐƚŽŶŐƵƚŵŝĐƌŽďŝĂůĚŝǀĞƌƐŝƚǇ͘'Ƶƚ͕ϲϯ͕ϭϵϭϯͲϮϬ͘ Edd/E'/h^͕^͘Θ>D͕D͘ϮϬϬϮ͘dƌĞŶĚƐŝŶƐŵŽŬŝŶŐĂŶĚŽǀĞƌǁĞŝŐŚƚĚƵƌŝŶŐƉƌĞŐŶĂŶĐǇ͗ƉƌĞǀĂůĞŶĐĞ͕ ƌŝƐŬƐŽĨƉƌĞŐŶĂŶĐǇĐŽŵƉůŝĐĂƚŝŽŶƐ͕ĂŶĚĂĚǀĞƌƐĞƉƌĞŐŶĂŶĐǇŽƵƚĐŽŵĞƐ͘^ĞŵŝŶWĞƌŝŶĂƚŽů͕Ϯϲ͕ϮϴϲͲϵϱ͘ Edd/E'/h^͕^͕͘s/>>DKZ͕͕͘:K,E^^KE͕^͕͘^ddKEDz͕͘>K͕ Z͕͘ s/d>͕ '͕͘ >K KK͕ >͘ Θ EKsK͕ ^͘ ϮϬϬϲ͘ /ŶĐƌĞĂƐĞĚ ůĞǀĞůƐ ŽĨ ͲƌĞĂĐƚŝǀĞ ƉƌŽƚĞŝŶ ĂŶĚ ĨŝďƌŝŶŽŐĞŶ ŝŶĨůƵĞŶĐĞ ƚŚĞ ƌŝƐŬ ŽĨ ǀĂƐĐƵůĂƌ ĞǀĞŶƚƐ ŝŶ ƉĂƚŝĞŶƚƐǁŝƚŚE/D͘/Ŷƚ:ĂƌĚŝŽů͕ϭϬϲ͕ϭϲͲϮϬ͘ Kd/>>Z͕ ͕͘ >ZKE͕E͕͘'Kh'/^͕^͕͘Z/>͕^͕͘ddK͕:͘D͕͘ZEh>d͕W͕͘ KZ͕:͕͘hDEd͕/,͕^͘͘ϮϬϭϯ͘ŝĞƚĂƌǇŝŶƚĞƌǀĞŶƚŝŽŶŝŵƉĂĐƚŽŶŐƵƚ ŵŝĐƌŽďŝĂůŐĞŶĞƌŝĐŚŶĞƐƐ͘EĂƚƵƌĞ͕ϱϬϬ͕ϱϴϱͲϴ͘ Kh',>E͕D͘d͕͘sZsZd͕W͘W͕͘WZD>͕D͕͘'KZ'/Kh͕,͘D͘ΘZ/͕'͘͘ϮϬϬϰ͘ůƚĞƌĞĚƉůĂĐĞŶƚĂů ŽǆŝĚĂƚŝǀĞƐƚƌĞƐƐƐƚĂƚƵƐŝŶŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐŵĞůůŝƚƵƐ͘WůĂĐĞŶƚĂ͕Ϯϱ͕ϳϴͲϴϰ͘ Z>z͕^͘:͕͘DdZEE͕W͘'͕͘>Z͕:͕͘͘DK^^͕:͘Z͕͘DW,͕͘:͕͘:&&Z/^͕t͘^͘ΘZK/E^KE͕:͘^͘ϮϬϬϱ͘ĨĨĞĐƚ ŽĨƚƌĞĂƚŵĞŶƚŽĨŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐŵĞůůŝƚƵƐŽŶƉƌĞŐŶĂŶĐǇŽƵƚĐŽŵĞƐ͘EŶŐů:DĞĚ͕ϯϱϮ͕ϮϰϳϳͲ ϴϲ͘ ZhD͕ d͘ >͕͘ K'E͕ >͕͘ t^d͕ E͘ ͕͘ s,/͕͕͘Ê>>ͲZ'KE͕:͕͘͘>͕͘/^,K&&͕/E͕͘^͕͘sZD͕z͕͘&/^,,͕D͕͘͘//E'Z͕^͕͘͘hddKE͕Z͘:͘ΘdhZEh',͕ W͘:͘ϮϬϭϰ͘ŝĞƚƌĂƉŝĚůǇĂŶĚƌĞƉƌŽĚƵĐŝďůǇĂůƚĞƌƐƚŚĞŚƵŵĂŶŐƵƚŵŝĐƌŽďŝŽŵĞ͘EĂƚƵƌĞ͕ϱϬϱ͕ϱϱϵͲϲϯ͘ s/^͕:͕͘͘'>Z͕E͘^͕:͘Θ^WhZ>KϭĂĚŝƉŽĐǇƚĞƐ͘,ŽƌŵDĞƚĂďZĞƐ͕ϰϭ͕ϱϮϯͲϯϬ͘ &/>/WWK͕͕͘s>/Z/͕͕͘/WK>͕D͕͘ZDKdd/͕D͕͘WKh>>d͕:͕͘͘D^^Zd͕^͕͘K>>/E/͕^͕͘ W/Z/E/͕ '͘ Θ >/KEdd/͕ W͘ ϮϬϭϬ͘ /ŵƉĂĐƚ ŽĨ ĚŝĞƚ ŝŶ ƐŚĂƉŝŶŐ ŐƵƚ ŵŝĐƌŽďŝŽƚĂ ƌĞǀĞĂůĞĚ ďǇ Ă ĐŽŵƉĂƌĂƚŝǀĞƐƚƵĚǇŝŶĐŚŝůĚƌĞŶĨƌŽŵƵƌŽƉĞĂŶĚƌƵƌĂůĨƌŝĐĂ͘WƌŽĐEĂƚůĐĂĚ^Đŝh^͕ϭϬϳ͕ϭϰϲϵϭͲ ϲ͘ DKZEK>>E͕͕͘>>E͕:͘'͕͘WZ/'KE͕'͕͘D/zK^,/͕͕͘>E'>>͕W͕͘sK͕s͘Θ ^^D͕ &͘ ϮϬϬϴ͘ KƌĂů ĂĚŵŝŶŝƐƚƌĂƚŝŽŶ ŽĨ Ă ĐĂƚĂůĂƐĞͲƉƌŽĚƵĐŝŶŐ >ĂĐƚŽĐŽĐĐƵƐ ůĂĐƚŝƐ ĐĂŶ ƉƌĞǀĞŶƚ Ă ĐŚĞŵŝĐĂůůǇŝŶĚƵĐĞĚĐŽůŽŶĐĂŶĐĞƌŝŶŵŝĐĞ͘:DĞĚDŝĐƌŽďŝŽů͕ϱϳ͕ϭϬϬͲϱ͘ ϭϲϯ

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ϭϲϱ

s'͕͘ΘDKZ>^Ͳ'KE>͕:͘͘ϮϬϭϭ͘/ŶĨůĂŵŵĂƚŝŽŶ͕ŽǆŝĚĂƚŝǀĞƐƚƌĞƐƐ͕ĂŶĚŽďĞƐŝƚǇ͘/Ŷƚ:DŽů ^Đŝ͕ϭϮ͕ϯϭϭϳͲϯϮ͘ &^d͕ ͕͘ Ζ'K^d/EK͕ Z͕͘ :Z͕͘ dZz͕ Z͘ W͘ Θ ,&&EZ͕ ^͘ D͘ ϮϬϬϮ͘ ůĞǀĂƚĞĚ ůĞǀĞůƐ ŽĨ ĂĐƵƚĞͲƉŚĂƐĞ ƉƌŽƚĞŝŶƐĂŶĚƉůĂƐŵŝŶŽŐĞŶĂĐƚŝǀĂƚŽƌŝŶŚŝďŝƚŽƌͲϭƉƌĞĚŝĐƚƚŚĞĚĞǀĞůŽƉŵĞŶƚŽĨƚǇƉĞϮĚŝĂďĞƚĞƐ͗ƚŚĞ ŝŶƐƵůŝŶƌĞƐŝƐƚĂŶĐĞĂƚŚĞƌŽƐĐůĞƌŽƐŝƐƐƚƵĚǇ͘ŝĂďĞƚĞƐ͕ϱϭ͕ϭϭϯϭͲϳ͘ &^d͕͕͘Ζ'K^d/EK͕Z͕͘:Z͕͘t/>>/D^͕>dd͕ ͕͘ E͕ ͕͘ tKE'͕ :͕͘ EzZ͕ ͕͘ >͕ :͕͘ 'K>&/E͕ ͘ ͕͘ EK/^d͕͕͘^,K>^KE͕^͘ΘDd,/^͕͘ϮϬϬϵ͘>ĞĂŶ͕ďƵƚŶŽƚŽďĞƐĞ͕ĨĂƚŝƐĞŶƌŝĐŚĞĚĨŽƌĂƵŶŝƋƵĞ ƉŽƉƵůĂƚŝŽŶŽĨƌĞŐƵůĂƚŽƌǇdĐĞůůƐƚŚĂƚĂĨĨĞĐƚŵĞƚĂďŽůŝĐƉĂƌĂŵĞƚĞƌƐ͘EĂƚDĞĚ͕ϭϱ͕ϵϯϬͲϵ͘ &/'hZK͕͘Θ'/>͕͘ϮϬϭϭ͘ŚĂŶŐĞƐŝŶWůĂƐŵĂƐKǆŝĚĂƚŝǀĞ^ƚƌĞƐƐĂŶĚŶƚŝŽǆŝĚĂŶƚĐƚŝǀŝƚǇ͕DĞĂƐƵƌĞĚ ǁŝƚŚDĞůĂƚŽŶŝŶ>ĞǀĞůƐ͕ĂŶĚŝƚƐZĞůĂƚŝŽŶƐŚŝƉƚŽEĞǁďŽƌŶƐĨƌŽŵKďĞƐĞĂŶĚŝĂďĞƚŝĐWƌĞŐŶĂŶĐŝĞƐ͘ :ŽƵƌŶĂůŽĨŝĂďĞƚĞƐΘDĞƚĂďŽůŝƐŵ͕Ɛϰ͕ϬϬϮ͘ &/ZKh/͕^͕͘Z͕ D͘ /͘ Θ >/D͕ &͘ ͘ ϮϬϬϳ͘ ĚŝƉŽƐĞ ƚŝƐƐƵĞ ĂƐ ĂŶ ĞŶĚŽĐƌŝŶĞŽƌŐĂŶ͗ĨƌŽŵƚŚĞŽƌǇƚŽƉƌĂĐƚŝĐĞ͘:WĞĚŝĂƚƌ;ZŝŽ:Ϳ͕ϴϯ͕^ϭϵϮͲϮϬϯ͘ &ZEK/^͕&͕͘ZKWZ͕:͕͘:K^W,͕E͕͘W/͕͕͘,,͕͕͘^,dKE͕͘ ϭϵϴϱ͘'ĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐŵĞůůŝƚƵƐ͘,ĞƚĞƌŽŐĞŶĞŝƚǇŽĨŵĂƚĞƌŶĂůĂŐĞ͕ǁĞŝŐŚƚ͕ŝŶƐƵůŝŶƐĞĐƌĞƚŝŽŶ͕,> ĂŶƚŝŐĞŶƐ͕ĂŶĚŝƐůĞƚĐĞůůĂŶƚŝďŽĚŝĞƐĂŶĚƚŚĞŝŵƉĂĐƚŽĨŵĂƚĞƌŶĂůŵĞƚĂďŽůŝƐŵŽŶƉĂŶĐƌĞĂƚŝĐͲĐĞůůĂŶĚ ƐŽŵĂƚŝĐĚĞǀĞůŽƉŵĞŶƚŝŶƚŚĞŽĨĨƐƉƌŝŶŐ͘ŝĂďĞƚĞƐ͕ϯϰ^ƵƉƉůϮ͕ϭͲϳ͘ &ZE͕E͘ϭϵϴϱ͘^ƵŵŵĂƌǇĂŶĚƌĞĐŽŵŵĞŶĚĂƚŝŽŶƐŽĨƚŚĞ^ĞĐŽŶĚ/ŶƚĞƌŶĂƚŝŽŶĂůtŽƌŬƐŚŽƉͲŽŶĨĞƌĞŶĐĞ ŽŶ'ĞƐƚĂƚŝŽŶĂůŝĂďĞƚĞƐ ŝĂďĞƚĞƐ͕ϯϰ;^ƵƉƉůϮͿ͗^ϭϮϯʹϲ͘ &Z/^͕͕͘͘DKZ'E͕d͕͘͘͘dW͕:͕͘WK/dKh͕͕͘^sEd͕͕͘Kh/>>Kd͕:͘>͕͘DZ/d͕͕͘KZd,/Z͕'͕͘ KZ͕:͕͘,E'Z͕͕͘Z/>͕^͘Θ>DEd͕͘ϮϬϭϮ͘/ŶƚĂŬĞ͗dŚĞEƵƚƌŝĞŶƚƐĂŶĚdŚĞŝƌDĞƚĂďŽůŝƐŵ͘/Ŷ͗>yKWKh>K^͕z͘;ĞĚ͘Ϳ͕͘Ez͕^͘t͕͘tzZ͕W͘Θ&EE͕t͘K͘ϭϵϱϰ͘KǆǇŐĞŶƉŽŝƐŽŶŝŶŐĂŶĚǆͲ ŝƌƌĂĚŝĂƚŝŽŶ͗ĂŵĞĐŚĂŶŝƐŵŝŶĐŽŵŵŽŶ͘^ĐŝĞŶĐĞ͕ϭϭϵ͕ϲϮϯͲϲ͘ ',&&ZWKhZ͕D͕͘,KK^,zZZ͕͘Θ>/Z^͕ t͘ Θ ŝƉŝĚZĞƐ͕ϱϬ͕ϵϬͲϳ͘ '/>>͕ ^͘ Z͕͘ WKW͕ D͕͘ Kz͕ Z͘ d͕͘ ͕ ͘ ^͕͘ 'KZKE͕ :͘ /͕͘ Z>DE͕͕͘͘&Z^ZͲ>/''dd͕͘D͘ΘE>^KE͕͕ Z͘ :͕͘ >ZÊ͕ E͕͘ :'Z͕ ͘ Θ D/,>Ê͕ ͘ϮϬϬϴ͘ůŝŶŝĐĂůŝŶĚŝĐĂƚŝŽŶƐĨŽƌƉƌŽďŝŽƚŝĐƐ͗ĂŶŽǀĞƌǀŝĞǁ͘ůŝŶ/ŶĨĞĐƚŝƐ͕ϰϲ ^ƵƉƉůϮ͕^ϵϲͲϭϬϬ͖ĚŝƐĐƵƐƐŝŽŶ^ϭϰϰͲϱϭ͘ 'KDZE'K͕>͘&͕͘ZZdd͕,͘>͕͘>>tz͕>͘>,͕/͕͘s/KYh͕:͕͘,hDE^͕͕͘^hZd͕͕͘>>͕D͕͘ '/DEͲWZ͕ '͘ Θ DhZ//K͕ ͘ ϮϬϬϳ͘ /ŶĐƌĞĂƐĞĚ ĐŚŽůĞƐƚĞƌŽů ŝŶƚĂŬĞ ŝŶ ǁŽŵĞŶ ǁŝƚŚ ŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐŵĞůůŝƚƵƐ͘ŝĂďĞƚĞƐDĞƚĂď͕ϯϯ͕ϮϱͲϵ͘ 'Z^^>Z͕:͕͘Y/E͕z͕͘,KE'͕,͕͘,E'͕:͕͘>//E/K͕:͕͘tKE'͕D͘>͕͘yh͕͕͘,sDKhE/ZͲWdZ͕s͕͘>K,DEE͕d͕͘tK>&͕d͘ΘKZE^d/E͕ ^͘ Z͘ ϮϬϭϯ͘ DĞƚĂŐĞŶŽŵŝĐ ƐĞƋƵĞŶĐŝŶŐ ŽĨƚŚĞ ŚƵŵĂŶ ŐƵƚ ŵŝĐƌŽďŝŽŵĞ ďĞĨŽƌĞĂŶĚ ĂĨƚĞƌ ďĂƌŝĂƚƌŝĐ ƐƵƌŐĞƌǇ ŝŶ ŽďĞƐĞ ƉĂƚŝĞŶƚƐ ǁŝƚŚ ƚǇƉĞ Ϯ ĚŝĂďĞƚĞƐ͗ ĐŽƌƌĞůĂƚŝŽŶ ǁŝƚŚ ŝŶĨůĂŵŵĂƚŽƌǇ ĂŶĚ ŵĞƚĂďŽůŝĐ ƉĂƌĂŵĞƚĞƌƐ͘WŚĂƌŵĂĐŽŐĞŶŽŵŝĐƐ:͕ϭϯ͕ϱϭϰͲϮϮ͘ 'ZE,Kh^͕^͘t͘Θ'/^^Z͕^͘ϭϵϱϵ͘KŶŵĞƚŚŽĚƐŝŶƚŚĞĂŶĂůǇƐŝƐŽĨƉƌŽĨŝůĞĚĂƚĂ͘WƐǇĐŚŽŵĞƚƌŝŬĂ͕Ϯϰ͕ ϵϱͲϭϭϮ͘ 'Z/EZ͕d͘Θ/h͕y͘D͕͘,E'͕Y͘y͕͘^,E͕͕͘d/E͕&͘t͕͘,E'͕,͕͘^hE͕͘,͕͘,E'͕,͘W͘Θ,E͕t͘ ϮϬϭϭ͘ /ŶĨůƵĞŶĐĞ ŽĨ ĐŽŶƐƵŵƉƚŝŽŶ ŽĨ ƉƌŽďŝŽƚŝĐƐ ŽŶ ƚŚĞ ƉůĂƐŵĂ ůŝƉŝĚ ƉƌŽĨŝůĞ͗ Ă ŵĞƚĂͲĂŶĂůǇƐŝƐ ŽĨ ƌĂŶĚŽŵŝƐĞĚĐŽŶƚƌŽůůĞĚƚƌŝĂůƐ͘EƵƚƌDĞƚĂďĂƌĚŝŽǀĂƐĐŝƐ͕Ϯϭ͕ϴϰϰͲϱϬ͘ 'hDE͕ :͘ Z͕͘ KE>/E͕ s͘ ^͘ Θ :K/E͕ ͘ ϮϬϭϯ͘ ŝĞƚ͕ DŝĐƌŽďŝŽŵĞ͕ ĂŶĚ ƚŚĞ /ŶƚĞƐƚŝŶĂů ƉŝƚŚĞůŝƵŵ͗ Ŷ ƐƐĞŶƚŝĂůdƌŝƵŵǀŝƌĂƚĞ͍ŝŽDĞĚZĞƐĞĂƌĐŚ/ŶƚĞƌŶĂƚŝŽŶĂů͕ϮϬϭϯ͕ϭϮ͘ 'zEK>K'/^d^͕͘͘K͘K͘͘ϮϬϬϮ͘K'ƉƌĂĐƚŝĐĞďƵůůĞƚŝŶ͘ŝĂŐŶŽƐŝƐĂŶĚŵĂŶĂŐĞŵĞŶƚŽĨƉƌĞĞĐůĂŵƉƐŝĂ ĂŶĚĞĐůĂŵƉƐŝĂ͘ϮϬϬϮͬϬϳͬϬϰĞĚ͗͘/Ŷƚ:'ǇŶĂĞĐŽůKďƐƚĞƚ

ϭϲϳ

,',͕&͕͘>/t>>͕͘ϮϬϬϭ͘ZŽůĞŽĨĨƌĞĞƌĂĚŝĐĂůƐŝŶƚŚĞŶĞƵƌŽĚĞŐĞŶĞƌĂƚŝǀĞĚŝƐĞĂƐĞƐ͗ƚŚĞƌĂƉĞƵƚŝĐŝŵƉůŝĐĂƚŝŽŶƐĨŽƌ ĂŶƚŝŽǆŝĚĂŶƚƚƌĞĂƚŵĞŶƚ͘ƌƵŐƐŐŝŶŐ͕ϭϴ͕ϲϴϱͲϳϭϲ͘ ,EÊ͕d͘,͕͘'K>͕Z͘:͕͘,EÊ͕d͘ΘWZÊ͕K͘ϮϬϭϱ͘dŚĞŐƵƚŵŝĐƌŽďŝŽŵĞŝŶĐĂƌĚŝŽͲŵĞƚĂďŽůŝĐ ŚĞĂůƚŚ͘'ĞŶŽŵĞDĞĚ͕ϳ͕ϯϯ͘ ,Z/^͕ '͕͘ d,͕ ͕͘ />͕ ͘ Θ ^>D͕ D͘ ϮϬϬϵ͘ KƌĂů ĂĚŵŝŶŝƐƚƌĂƚŝŽŶ ŽĨ >ĂĐƚŽďĂĐŝůůƵƐ ĂĐŝĚŽƉŚŝůƵƐ ƌĞƐƚŽƌĞƐŶŝƚƌŝĐŽǆŝĚĞůĞǀĞůŝŶĚŝĂďĞƚŝĐƌĂƚƐ͘ƵƐƚ:ĂƐŝĐĂŶĚƉƉů^Đŝ͕ϯ͕ϮϵϲϯͲϵ͘ ,Z/^,͕͘ϭϵϵϭ͘^ĞŶƐŝƚŝǀĞ>/^ĨŽƌŝŶƚĞƌůĞƵŬŝŶͲϲ͗ ĚĞƚĞĐƚŝŽŶŽĨ/>ͲϲŝŶďŝŽůŽŐŝĐĂůĨůƵŝĚƐ͗ƐǇŶŽǀŝĂůĨůƵŝĚƐĂŶĚƐĞƌĂ͘:ŽƵƌŶĂůŽĨŝŵŵƵŶŽůŽŐŝĐĂůŵĞƚŚŽĚƐ͕ ϭϯϴ͕ϰϳͲϱϲ͘ ,ZZ/E'͕^͘:͕͘K͕͘Z/,ͲtZ^͕:͘t͕͘^dh͕͘D͕͘/EDE͕ZEd͕D͕͘͘,K&&DEE͕͕͘^,ZZ/>>ͲD/y͕^͕͘͘h',͕^͕͘͘,Dz͕D͕͘,E͕z͘z͕͘ Z/:E/͕ D͘ ϮϬϬϯ͘ ůŝŶŝĐĂů ĂŶĚ ůĂďŽƌĂƚŽƌǇ ĨŝŶĚŝŶŐƐ ŝŶ ŐůƵĐŽƐĞ ƚŽůĞƌĂŶĐĞ ĚƵƌŝŶŐ ƉƌĞŐŶĂŶĐǇ͘/ƌĂŶŝĂŶ:ŽƵƌŶĂůŽĨŝĂďĞƚĞƐĂŶĚ>ŝƉŝĚ͕Ϯ͕ϭϯϭͲϰϰ͘ ,KdD/^>/'/>͕'͘^͘ϮϬϬϲ͘/ŶĨůĂŵŵĂƚŝŽŶĂŶĚŵĞƚĂďŽůŝĐĚŝƐŽƌĚĞƌƐ͘EĂƚƵƌĞ͕ϰϰϰ͕ϴϲϬͲϳ͘ ,KdD/^>/'/>͕ '͘ ^͕͘ ZEZ͕ W͕͘ ZK͕ :͘ &͕͘ d͘ Θ ^W/'>DE͕ ͘ D͘ ϭϵϵϱ͘ /ŶĐƌĞĂƐĞĚ ĂĚŝƉŽƐĞƚŝƐƐƵĞĞǆƉƌĞƐƐŝŽŶŽĨƚƵŵŽƌŶĞĐƌŽƐŝƐĨĂĐƚŽƌͲĂůƉŚĂŝŶŚƵŵĂŶŽďĞƐŝƚǇĂŶĚŝŶƐƵůŝŶƌĞƐŝƐƚĂŶĐĞ͘ :ůŝŶ/ŶǀĞƐƚ͕ϵϱ͕ϮϰϬϵͲϭϱ͘ ,KdD/^>/'/>͕'͘^͕͘^,Z'/>>͕E͘^͘Θ^W/'>DE͕͘D͘ϭϵϵϯ͘ĚŝƉŽƐĞĞǆƉƌĞƐƐŝŽŶŽĨƚƵŵŽƌŶĞĐƌŽƐŝƐ ĨĂĐƚŽƌͲĂůƉŚĂ͗ĚŝƌĞĐƚƌŽůĞŝŶŽďĞƐŝƚǇͲůŝŶŬĞĚŝŶƐƵůŝŶƌĞƐŝƐƚĂŶĐĞ͘^ĐŝĞŶĐĞ͕Ϯϱϵ͕ϴϳͲϵϭ͘ ,Kh^^/h͕&͕͘͘sK'>Z͕:͘W͕͘sEDD͕:͕͘hy,/Ê^͕͘E͘ΘsEÊ/z͕^͘d͕͘D/EE͕^͘Θ/^K>hZ/͕͘ϮϬϬϴ͘ĂƌůǇĚŝĨĨĞƌĞŶĐĞƐŝŶĨĞĐĂůŵŝĐƌŽďŝŽƚĂ ĐŽŵƉŽƐŝƚŝŽŶŝŶĐŚŝůĚƌĞŶŵĂǇƉƌĞĚŝĐƚŽǀĞƌǁĞŝŐŚƚ͘ŵ:ůŝŶEƵƚƌ͕ϴϳ͕ϱϯϰͲϴ͘ Z͕ ͕͘ 'hWd͕ z͕͘ ^/E'>͕ Z͘ Θ Z͕ ^͘ ϮϬϭϱ͘ hƐĞ ŽĨ ŽƌĂů ĂŶƚŝͲĚŝĂďĞƚŝĐ ĂŐĞŶƚƐ ŝŶ ƉƌĞŐŶĂŶĐǇ͗ Ă ƉƌĂŐŵĂƚŝĐĂƉƉƌŽĂĐŚ͘Eŵ:DĞĚ^Đŝ͕ϳ͕ϲͲϭϮ͘ ͕͕͘͘'KD͕͕͘>Z͕ D͘ ͕͘ KKK>/͕E͕͘>WK>>͕͕͘^͕͕͘DZZ͕D͕͘s^^>>K͕ :͘ Θ ^sKEͲsEdhZ͕ ͘ ϮϬϭϰ͘ ZĞůĂƚŝŽŶ ŽĨ ƚŚĞ DĞĚŝƚĞƌƌĂŶĞĂŶ ĚŝĞƚ ǁŝƚŚ ƚŚĞ ŝŶĐŝĚĞŶĐĞ ŽĨ ŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐ͘Ƶƌ:ůŝŶEƵƚƌ͕ϲϴ͕ϴͲϭϯ͘

ϭϳϬ

^^KE͕&͘,͕͘dZDZK>/͕s͕͘EKKÊ͕ :͘ΘͲDKhKE͕^͕͘>WZY͕:͕͘,>>/Z͕:͕͘͘,h^dKEͲWZ^>z͕>͕͘&Z/DE͕ :͘ ͕͘ ,E͕ ^͘ ͘Θ d>EK͕W͘D͘ ϮϬϬϮ͘dE&ͲĂůƉŚĂ ŝƐ Ă ƉƌĞĚŝĐƚŽƌŽĨ ŝŶƐƵůŝŶ ƌĞƐŝƐƚĂŶĐĞ ŝŶ ŚƵŵĂŶƉƌĞŐŶĂŶĐǇ͘ŝĂďĞƚĞƐ͕ϱϭ͕ϮϮϬϳͲϭϯ͘ Ăď^Đŝ͕ Ϯϴ͕ϯϯϭͲϰϲ͘

ϭϳϭ

/͕s͘W͘ΘÊ͕Z͘ϮϬϬϴ͘ŶƚŝŽǆŝĚĂŶƚĂŶĚĨƌĞĞƌĂĚŝĐĂůƐĐĂǀĞŶŐŝŶŐĂĐƚŝǀŝƚŝĞƐŽĨĂŶĞǆŽƉŽůǇƐĂĐĐŚĂƌŝĚĞ ĨƌŽŵĂƉƌŽďŝŽƚŝĐďĂĐƚĞƌŝƵŵ͘ŝŽƚĞĐŚŶŽů:͕ϯ͕ϮϰϱͲϱϭ͘ s/^KE͕͘^͕͘h>>z͕D͘/͕>͕͘ ^D/d,͕:͕͘͘dE'͕t͘,͕͘/KEdK͕:͕͘͘>h^/^͕͘:͘Θ,E͕^͘>͘ϮϬϭϰ͘ŐĂŵŵĂͲƵƚǇƌŽďĞƚĂŝŶĞ ŝƐĂƉƌŽĂƚŚĞƌŽŐĞŶŝĐŝŶƚĞƌŵĞĚŝĂƚĞŝŶŐƵƚŵŝĐƌŽďŝĂůŵĞƚĂďŽůŝƐŵŽĨ>ͲĐĂƌŶŝƚŝŶĞƚŽdDK͘ĞůůDĞƚĂď͕ ϮϬ͕ϳϵϵͲϴϭϮ͘ /͕ >͕͘^D/d,͕:͕͘͘/KEdK͕:͕͘͘,E͕:͕͘>/͕,͕͘th͕'͕͘͘>t/^͕:͕͘͘tZZ/Z͕D͕͘ZKtE͕ :͘D͕͘/^Z͕d͕͘/>DZ͕D͕͘D/^Z͕D͕͘s/,>DD͕d͕͘EEh͕͘ Z/,͕:͕͘,h'h>ͲDKhKE͕^͘Θ:tZhD͕͘ϮϬϭϭ͘ dŚĞƌŽůĞŽĨŽǆŝĚĂƚŝǀĞƐƚƌĞƐƐŝŶƚŚĞƉĂƚŚŽƉŚǇƐŝŽůŽŐǇŽĨŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐŵĞůůŝƚƵƐ͘ŶƚŝŽǆŝĚZĞĚŽǆ ^ŝŐŶĂů͕ϭϱ͕ϯϬϲϭͲϭϬϬ͘ >Z/:E/͕͕͘,K^^/EͲE,͕͕͘Z/s/͕^͘t͕͘DhE/Z͕^͘Θs^^/',͕͘Z͘ϮϬϬϯ͘ŽƐƚĂŶĂůǇƐŝƐŽĨĚŝĨĨĞƌĞŶƚ ƐĐƌĞĞŶŝŶŐƐƚƌĂƚĞŐŝĞƐĨŽƌŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐŵĞůůŝƚƵƐ͘ŶĚŽĐƌWƌĂĐƚ͕ϵ͕ϱϬϰͲϵ͘ >ZÊ͕E͕͘sK'EÊ͕&͘Ž^KŶĞ͕ϱ͕ĞϵϬϴϱ͘ >Z^^KE͕͕͘dZDZK>/͕s͕͘>͕z͘^͕͘h͕͕͘͘,/>>KE͕͕͘zE͕,͕͘^D/ds/͕͘:͕͘D/>E/͕Z͘s͘ΘsEdhZ͕,͘K͘ϮϬϬϵ͘KďĞƐŝƚǇĂŶĚĐĂƌĚŝŽǀĂƐĐƵůĂƌĚŝƐĞĂƐĞ͗ƌŝƐŬĨĂĐƚŽƌ͕ƉĂƌĂĚŽǆ͕ ĂŶĚŝŵƉĂĐƚŽĨǁĞŝŐŚƚůŽƐƐ͘:ŵŽůůĂƌĚŝŽů͕ϱϯ͕ϭϵϮϱͲϯϮ͘ >DK/E͕K͕͘s/Z͕:͕͘s^dZ͕:͘D͕͘Zh^/hy͕͕͘hZE͕&͕͘ZEhh͕:͕͘'K>DE͕D͘Θ E,DKh͕:͘W͘ϭϵϵϰ͘/ŶƚĞƌůĞƵŬŝŶͲϲ͗ĂŶĞĂƌůǇŵĂƌŬĞƌŽĨďĂĐƚĞƌŝĂůŝŶĨĞĐƚŝŽŶŝŶĚĞĐŽŵƉĞŶƐĂƚĞĚ ĐŝƌƌŚŽƐŝƐ͘:,ĞƉĂƚŽů͕ϮϬ͕ϴϭϵͲϮϰ͘ >͕͘:͘Θ͕,͘z͕͘WZZKhyͲZK>^͕'͕͘K&&EZ͕&͕͘W,/>/WW͕:͘ΘsZDh>E͕͘ϭϵϴϴ͘/ŶĨůƵĞŶĐĞŽĨďůŽŽĚͲĐŽůůĞĐƚŝŶŐƐǇƐƚĞŵƐ ŽŶĐŽŶĐĞŶƚƌĂƚŝŽŶƐŽĨƚƵŵŽƌŶĞĐƌŽƐŝƐĨĂĐƚŽƌŝŶƐĞƌƵŵĂŶĚƉůĂƐŵĂ͘ůŝŶŚĞŵ͕ϯϰ͕ϮϯϳϯͲϰ͘ >t/^͕͕͘͘&hEͿ ĐŚŽůĞƐƚĞƌŽů ŝŶ ǇŽƵŶŐ ĂĚƵůƚ ǁŽŵĞŶ͘ dŚĞ Z/^ƚƵĚǇ͘ŽƌŽŶĂƌǇƌƚĞƌǇZŝƐŬĞǀĞůŽƉŵĞŶƚŝŶzŽƵŶŐĚƵůƚƐ͘ŵ:ƉŝĚĞŵŝŽů͕ϭϰϰ͕ϮϰϳͲϱϰ͘ >z͕Z͕͘͘'>͕D͘>͕͘ dh͕D͕͘͘z͕Z͕͘͘dhZEh',͕W͘:͕͘/E͕^͘Θ'KZKE͕:͘/͘ϮϬϬϲ͘DŝĐƌŽďŝĂůĞĐŽůŽŐǇ͗ŚƵŵĂŶŐƵƚŵŝĐƌŽďĞƐ ĂƐƐŽĐŝĂƚĞĚǁŝƚŚŽďĞƐŝƚǇ͘EĂƚƵƌĞ͕ϰϰϰ͕ϭϬϮϮͲϯ͘ >/͕͕͘zE'͕^͕͘>/E͕,͕͘,hE'͕:͕͘tdĂĐƚŽďĂĐŝůůƵƐĂĐŝĚŽƉŚŝůƵƐdϰϯϱϲ͘ŝŐŝƐ^Đŝ͕ϰϱ͕ϭϲϭϳͲϮϮ͘ >/E͕D͘z͘ΘzE͕͘>͘ϭϵϵϵ͘ŶƚŝŽǆŝĚĂƚŝǀĞĂďŝůŝƚǇŽĨůĂĐƚŝĐĂĐŝĚďĂĐƚĞƌŝĂ͘:ŐƌŝĐ&ŽŽĚŚĞŵ͕ϰϳ͕ϭϰϲϬͲϲ͘ >/E^z͕͕͘ZEEE͕>͕͘>z͕D͕͘͘D'h/Z͕K͕͘͘^D/d,͕d͕͘hZZE͕^͕͘K&&z͕D͕͘&K>z͕ D͕͘͘,dhE/͕D͕͘^,E,E͕&͘ΘDh>/&&͕&͘D͘ϮϬϭϱ͘/ŵƉĂĐƚŽĨƉƌŽďŝŽƚŝĐƐŝŶǁŽŵĞŶǁŝƚŚ ŐĞƐƚĂƚŝŽŶĂů ĚŝĂďĞƚĞƐ ŵĞůůŝƚƵƐ ŽŶ ŵĞƚĂďŽůŝĐ ŚĞĂůƚŚ͗ Ă ƌĂŶĚŽŵŝǌĞĚ ĐŽŶƚƌŽůůĞĚ ƚƌŝĂů͘ ŵ : KďƐƚĞƚ 'ǇŶĞĐŽů͘ >/E^z͕͕͘ZEEE͕>͘ΘDh>/&&͕&͘D͘ϮϬϭϰĂ͘ĐĐĞƉƚĂďŝůŝƚǇŽĨĂŶĚĐŽŵƉůŝĂŶĐĞǁŝƚŚĂƉƌŽďŝŽƚŝĐ ĐĂƉƐƵůĞŝŶƚĞƌǀĞŶƚŝŽŶŝŶƉƌĞŐŶĂŶĐǇ͘/Ŷƚ:'ǇŶĂĞĐŽůKďƐƚĞƚ͕ϭϮϱ͕ϮϳϵͲϴϬ͘ >/E^z͕͕͘>z͕D͕͘h>>/dKE͕D͕͘^D/d,͕d͕͘D'h/Z͕K͕͘͘^,E,E͕&͕͘ZEEE͕>͘Θ Dh>/&&͕&͘D͘ϮϬϭϰď͘WƌŽďŝŽƚŝĐƐŝŶŽďĞƐĞƉƌĞŐŶĂŶĐǇĚŽŶŽƚƌĞĚƵĐĞŵĂƚĞƌŶĂůĨĂƐƚŝŶŐŐůƵĐŽƐĞ͗ ĂĚŽƵďůĞͲďůŝŶĚ͕ƉůĂĐĞďŽͲĐŽŶƚƌŽůůĞĚ͕ƌĂŶĚŽŵŝǌĞĚƚƌŝĂů;WƌŽďŝŽƚŝĐƐŝŶWƌĞŐŶĂŶĐǇ^ƚƵĚǇͿ͘ ŵ:ůŝŶ EƵƚƌ͕ϵϵ͕ϭϰϯϮͲϵ͘ >/E^z͕͕͘t>^,͕͕͘͘ZEEE͕>͘ΘDh>/&&͕&͘D͘ϮϬϭϯ͘WƌŽďŝŽƚŝĐƐŝŶƉƌĞŐŶĂŶĐǇĂŶĚŵĂƚĞƌŶĂů ŽƵƚĐŽŵĞƐ͗ĂƐǇƐƚĞŵĂƚŝĐƌĞǀŝĞǁ͘:DĂƚĞƌŶ&ĞƚĂůEĞŽŶĂƚĂůDĞĚ͕Ϯϲ͕ϳϳϮͲϴ͘ >/E^z͕Z͘^͘ϮϬϬϵ͘'ĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐ͗ĐĂƵƐĞƐĂŶĚĐŽŶƐĞƋƵĞŶĐĞƐ͘ dŚĞƌŝƚŝƐŚ:ŽƵƌŶĂůŽĨŝĂďĞƚĞƐΘ sĂƐĐƵůĂƌŝƐĞĂƐĞ͕ϵ͕ϮϳͲϯϭ͘ >/^d͕E͘͘ϭϵϴϴ͘'ůƵĐŽƐĞƚŽůĞƌĂŶĐĞŝŶƉƌĞŐŶĂŶĐǇͲͲƚŚĞǁŚŽĂŶĚŚŽǁŽĨƚĞƐƚŝŶŐ͘>ĂŶĐĞƚ͕Ϯ͕ϭϭϳϯͲϰ͘ >hKdK͕ Z͕͘ >/KD/d/EE͕ hZ/͕ ͘ ϮϬϭϬĂ͘ dŚĞ ŝŵƉĂĐƚ ŽĨ ƉĞƌŝŶĂƚĂů ƉƌŽďŝŽƚŝĐ ŝŶƚĞƌǀĞŶƚŝŽŶ ŽŶ ƚŚĞ ĚĞǀĞůŽƉŵĞŶƚ ŽĨŽǀĞƌǁĞŝŐŚƚ ĂŶĚŽďĞƐŝƚǇ͗ ĨŽůůŽǁͲƵƉ ƐƚƵĚǇ ĨƌŽŵ ďŝƌƚŚ ƚŽϭϬ ǇĞĂƌƐ͘/Ŷƚ:KďĞƐ;>ŽŶĚͿ͕ϯϰ͕ϭϱϯϭͲϳ͘ >hKdK͕Z͕͘>/d/EE͕hZ/͕͘ϮϬϭϬď͘/ŵƉĂĐƚŽĨŵĂƚĞƌŶĂůƉƌŽďŝŽƚŝĐͲƐƵƉƉůĞŵĞŶƚĞĚ ĚŝĞƚĂƌǇĐŽƵŶƐĞůůŝŶŐŽŶƉƌĞŐŶĂŶĐǇŽƵƚĐŽŵĞĂŶĚƉƌĞŶĂƚĂůĂŶĚƉŽƐƚŶĂƚĂůŐƌŽǁƚŚ͗ĂĚŽƵďůĞͲďůŝŶĚ͕ ƉůĂĐĞďŽͲĐŽŶƚƌŽůůĞĚƐƚƵĚǇ͘ƌ:EƵƚƌ͕ϭϬϯ͕ϭϳϵϮͲϵ͘

ϭϳϰ

>hKdK͕Z͕͘>/d/EE͕hZ/͕͘ϮϬϭϮ͘/ŵƉĂĐƚŽĨŵĂƚĞƌŶĂůƉƌŽďŝŽƚŝĐͲƐƵƉƉůĞŵĞŶƚĞĚ ĚŝĞƚĂƌǇ ĐŽƵŶƐĞůŝŶŐ ĚƵƌŝŶŐ ƉƌĞŐŶĂŶĐǇ ŽŶ ĐŽůŽƐƚƌƵŵ ĂĚŝƉŽŶĞĐƚŝŶ ĐŽŶĐĞŶƚƌĂƚŝŽŶ͗ Ă ƉƌŽƐƉĞĐƚŝǀĞ͕ ƌĂŶĚŽŵŝǌĞĚ͕ƉůĂĐĞďŽͲĐŽŶƚƌŽůůĞĚƐƚƵĚǇ͘ĂƌůǇ,ƵŵĞǀ͕ϴϴ͕ϯϯϵͲϰϰ͘ >hd'EKZ&&͕ &͕͘ E/:D/:Z͕ Z͘ D͕͘ Ê^dZKD͕ W͘ ͕͘ dZh>^^KE͕ >͘ D͕͘ D'Eh^^KE͕ ͘W͕͘Z/:^^KE͕>͘D͕͘sED/EEE͕>͘W͕͘Z/:ŝǀĞƌWŚǇƐŝŽů͕Ϯϵϱ͕'ϭϭϭϭͲϮϭ͘ >z͕,͘^͕͘/͕y͘ϮϬϭϬ͘dŚĞĐŚĂŶŐĞƐŽĨǀŝƐĨĂƚŝŶŝŶƐĞƌƵŵĂŶĚŝƚƐ ĞǆƉƌĞƐƐŝŽŶŝŶĨĂƚĂŶĚƉůĂĐĞŶƚĂůƚŝƐƐƵĞŝŶƉƌĞŐŶĂŶƚǁŽŵĞŶǁŝƚŚŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐ͘ŝĂďĞƚĞƐZĞƐ ůŝŶWƌĂĐƚ͕ϵϬ͕ϲϬͲϱ͘ DKE>͕ D͘ :͘ Θ 'W/E^/^ ĨŽƌ ŵĞĂƐƵƌŝŶŐ ŝŶƐƵůŝŶ ŝŶ Ă ůĂƌŐĞ ŶƵŵďĞƌ ŽĨ ƌĞƐĞĂƌĐŚƐĂŵƉůĞƐ͘DĞƚĂďŽůŝƐŵ͕ϯϴ͕ϰϱϬͲϰϱϮ͘ D͕^͕͘K^͕>͕͘,D/>dKE͕͕͘͘ZD^KE͕͘͘ΘsEE,K&͕D͘ϮϬϬϭ͘ZĂƚĞƐĂŶĚƌŝƐŬĨĂĐƚŽƌƐ ĨŽƌƌĞĐƵƌƌĞŶĐĞŽĨŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐ͘ŝĂďĞƚĞƐĂƌĞ͕Ϯϰ͕ϲϱϵͲϲϮ͘ Dz͕͘D͕͘,z^͕d͘͘ΘdZz͕Z͘W͘ϭϵϵϳ͘sĂƌŝĂďŝůŝƚǇŝŶƚŚĞŵĞĂƐƵƌĞŵĞŶƚŽĨͲƌĞĂĐƚŝǀĞƉƌŽƚĞŝŶŝŶ ŚĞĂůƚŚǇƐƵďũĞĐƚƐ͗ŝŵƉůŝĐĂƚŝŽŶƐĨŽƌƌĞĨĞƌĞŶĐĞŝŶƚĞƌǀĂůƐĂŶĚĞƉŝĚĞŵŝŽůŽŐŝĐĂůĂƉƉůŝĐĂƚŝŽŶƐ͘ůŝŶŚĞŵ͕ ϰϯ͕ϱϮͲϴ͘ D>K>D͕ :͘ ϮϬϭϮ͘ dŚƌŽƵŐŚ ƚŚĞ ůŽŽŬŝŶŐ ŐůĂƐƐ͗ ŐĞƐƚĂƚŝŽŶĂů ĚŝĂďĞƚĞƐ ĂƐ Ă ƉƌĞĚŝĐƚŽƌ ŽĨ ŵĂƚĞƌŶĂů ĂŶĚ ŽĨĨƐƉƌŝŶŐůŽŶŐͲƚĞƌŵŚĞĂůƚŚ͘ŝĂďĞƚĞƐDĞƚĂďZĞƐZĞǀ͕Ϯϴ͕ϯϬϳͲϭϭ͘ D>>WW͕Z͘,͕͘ZK>/͕D͕͘͘^hZ/͕^͕͘K,/KE/͕D͕͘^/>s/͕^͕͘,/E/͕͘ΘWKDW/͕W͘ϮϬϭϭ͘ ĨĨĞĐƚŽĨĂƉƌŽďŝŽƚŝĐŝŶƚĂŬĞŽŶŽǆŝĚĂŶƚĂŶĚĂŶƚŝŽǆŝĚĂŶƚƉĂƌĂŵĞƚĞƌƐŝŶƉůĂƐŵĂŽĨĂƚŚůĞƚĞƐĚƵƌŝŶŐ ŝŶƚĞŶƐĞĞǆĞƌĐŝƐĞƚƌĂŝŶŝŶŐ͘ƵƌƌDŝĐƌŽďŝŽů͕ϲϮ͕ϭϲϴϵͲϵϲ͘ Dd,/h͕ W͕͘ >D/hy͕ /͘ Θ ^WZ^͕ :͘ W͘ ϮϬϭϬ͘ KďĞƐŝƚǇ͕ ŝŶĨůĂŵŵĂƚŝŽŶ͕ ĂŶĚ ĐĂƌĚŝŽǀĂƐĐƵůĂƌ ƌŝƐŬ͘ ůŝŶ WŚĂƌŵĂĐŽůdŚĞƌ͕ϴϳ͕ϰϬϳͲϭϲ͘ ϭϳϱ

Dd^hDKdK͕D͕͘/EKh͕Z͕͘d^hKKD͕͕͘zKh^&/E:͕͘Θ',DE^,͕D͘,͘ϮϬϭϯď͘ĨĨĞĐƚŽĨƉƌŽďŝŽƚŝĐƐŽŶůŝƉŝĚƉƌŽĨŝůĞ͕ ŐůǇĐĞŵŝĐĐŽŶƚƌŽů͕ŝŶƐƵůŝŶĂĐƚŝŽŶ͕ŽǆŝĚĂƚŝǀĞƐƚƌĞƐƐ͕ĂŶĚŝŶĨůĂŵŵĂƚŽƌǇŵĂƌŬĞƌƐŝŶƉĂƚŝĞŶƚƐǁŝƚŚƚǇƉĞ ϮĚŝĂďĞƚĞƐ͗ĂĐůŝŶŝĐĂůƚƌŝĂů͘/ƌĂŶ:DĞĚ^Đŝ͕͘ϯϴ͕ϯϴͲϰϯ͘ DhZz͕͕͘͘/^,KW͕:͘D͕͘t/>>/D^͕^͘D͕͘'Zz^KE͕͕͘͘^D/d,͕D͘^͕͘&Z/DE͕:͘͘Θ'ZKs͕ ͘ϮϬϬϵ͘DĂƚĞƌŶĂůŚŝŐŚͲĨĂƚĚŝĞƚƚƌŝŐŐĞƌƐůŝƉŽƚŽǆŝĐŝƚǇŝŶƚŚĞĨĞƚĂůůŝǀĞƌƐŽĨŶŽŶŚƵŵĂŶƉƌŝŵĂƚĞƐ͘: ůŝŶ/ŶǀĞƐƚ͕ϭϭϵ͕ϯϮϯͲϯϱ͘ D'ddZ/>͕>͘͘ϮϬϭϬ͘ZĞŐƵůĂƚŽƌƐŽĨd>ZϰƐŝŐŶĂůŝŶŐďǇĞŶĚŽƚŽǆŝŶƐ͘^ƵďĐĞůůŝŽĐŚĞŵ͕ϱϯ͕ ϭϱϯͲϳϭ͘ DEh',d͕͕͘͘tKKK/s͕͕͘hE'Z͕͕͘͘,E͕͘Z͕͘,K͕D͕͘ >Z͕:͘>͕͕͘͘Kd^͕:͘E͕͘Wdd/dd͕͘:͕͘^͕D͕͘ZDKh'KD͕&͕͘>/Ks//͕>͘ΘZKh>d͕͘ϮϬϭϮ͘ŽŵƉĂƌĂƚŝǀĞ ŵĞƚĂͲĂŶĂůǇƐŝƐŽĨƚŚĞĞĨĨĞĐƚŽĨ>ĂĐƚŽďĂĐŝůůƵƐƐƉĞĐŝĞƐŽŶǁĞŝŐŚƚŐĂŝŶŝŶŚƵŵĂŶƐĂŶĚĂŶŝŵĂůƐ͘DŝĐƌŽď WĂƚŚŽŐ͕ϱϯ͕ϭϬϬͲϴ͘ D/ED/͕:͕͘/K͕y͕͘ZK^>͕D͕͘͘,Zz͕:͘Z͘ΘZZz͕Z͘ ͕͘:Z͘ϮϬϭϯ͘/ŶƐƚŝƚƵƚĞŽĨŵĞĚŝĐŝŶĞϮϬϬϵŐĞƐƚĂƚŝŽŶĂůǁĞŝŐŚƚŐĂŝŶŐƵŝĚĞůŝŶĞŬŶŽǁůĞĚŐĞ͗ƐƵƌǀĞǇŽĨ ŽďƐƚĞƚƌŝĐƐͬŐǇŶĞĐŽůŽŐǇĂŶĚĨĂŵŝůǇŵĞĚŝĐŝŶĞƌĞƐŝĚĞŶƚƐŽĨƚŚĞhŶŝƚĞĚ^ƚĂƚĞƐ͘ŝƌƚŚ͕ϰϬ͕ϮϯϳͲϰϲ͘ DKKZ͕d͘Z͘ϮϬϭϬ͘&ĞƚĂůĞǆƉŽƐƵƌĞƚŽŐĞƐƚĂƚŝŽŶĂů ĚŝĂďĞƚĞƐĐŽŶƚƌŝďƵƚĞƐƚŽƐƵďƐĞƋƵĞŶƚĂĚƵůƚ ŵĞƚĂďŽůŝĐ ƐǇŶĚƌŽŵĞ͘ŵ͘:͘KďƐƚĞƚ͘'ǇŶĞĐŽů͕͘ϮϬϮ͕ϲϰϯͲϲϰϵ͘ DKZEKͲ/E/^͕/͕͘ZKE͕&͕͘d/E,KE^͕&͘:͘ΘYh/WKͲKZdhEK͕D͘/͘ϮϬϭϰ͘/ŵƉĂĐƚŽĨƚŚĞŐƵƚ ŵŝĐƌŽďŝŽƚĂŽŶƚŚĞĚĞǀĞůŽƉŵĞŶƚŽĨŽďĞƐŝƚǇĂŶĚƚǇƉĞϮĚŝĂďĞƚĞƐŵĞůůŝƚƵƐ͘&ƌŽŶƚDŝĐƌŽďŝŽů͕ϱ͕ϭϵϬ͘ DKZKd/͕͕͘^KhD'Z/͕>͘&͕͘ZEK^d͕D͕͘s>>/E/͕͘͘Θ^/s/Z/͕ŝƉŝĚƐ,ĞĂůƚŚŝƐ͕ϭϭ͕Ϯϵ͘ DKZZ/^KE͕ ͘ :͕͘ D>K͕ D͘ '͕͘ t/E͕ ͘ D͕͘ ,^^KhE͕͕͘WZZ͕&͘ΘZhE>͕͘ϮϬϭϱ͘WƌĞŶĂƚĂůĞǆƉŽƐƵƌĞƚŽĂŶƚŝďŝŽƚŝĐƐ͕ĐĞƐĂƌĞĂŶƐĞĐƚŝŽŶ ĂŶĚƌŝƐŬŽĨĐŚŝůĚŚŽŽĚŽďĞƐŝƚǇ͘/Ŷƚ:KďĞƐ;>ŽŶĚͿ͕ϯϵ͕ϲϲϱͲϳϬ͘ DhZW,z͕ ͘ &͕͘ KddZ͕ W͘ ͕͘ ,>z͕ ^͕͘ DZYh^͕ d͘ D͕͘ KΖ^h>>/sE͕ K͕͘ &Kh,z͕ &͕͘ >Z͕W͘t͕͘Yh/'>z͕͘D͕͘^dEdKE͕͕͘ZK^^͕W͘Z͕͘KΖK,Zdz͕Z͘D͘Θ^,E,E͕&͘ ϮϬϭϬ͘ ŽŵƉŽƐŝƚŝŽŶ ĂŶĚ ĞŶĞƌŐǇ ŚĂƌǀĞƐƚŝŶŐ ĐĂƉĂĐŝƚǇ ŽĨ ƚŚĞ ŐƵƚ ŵŝĐƌŽďŝŽƚĂ͗ ƌĞůĂƚŝŽŶƐŚŝƉ ƚŽ ĚŝĞƚ͕ ŽďĞƐŝƚǇĂŶĚƚŝŵĞŝŶŵŽƵƐĞŵŽĚĞůƐ͘'Ƶƚ͕ϱϵ͕ϭϲϯϱͲϰϮ͘ Dzdd͕>͘ϮϬϭϬ͘ZĞǀŝĞǁ͗ZĞĂĐƚŝǀĞŽǆǇŐĞŶĂŶĚŶŝƚƌŽŐĞŶƐƉĞĐŝĞƐĂŶĚĨƵŶĐƚŝŽŶĂůĂĚĂƉƚĂƚŝŽŶŽĨƚŚĞƉůĂĐĞŶƚĂ͘ WůĂĐĞŶƚĂ͕ϯϭ^ƵƉƉů͕^ϲϲͲϵ͘ E/WKhZ͕ /͕͘ ^KE͕KtE>Z͕͕͘ ^sE^^KE͕ h͘ Whh͕ D͘ ϮϬϬϳ͘ ĚŵŝŶŝƐƚƌĂƚŝŽŶ ŽĨ >ĂĐƚŽďĂĐŝůůƵƐ ĞǀŽŬĞƐ ĐŽŽƌĚŝŶĂƚĞĚ ĐŚĂŶŐĞƐŝŶƚŚĞŝŶƚĞƐƚŝŶĂůĞǆƉƌĞƐƐŝŽŶƉƌŽĨŝůĞŽĨŐĞŶĞƐƌĞŐƵůĂƚŝŶŐĞŶĞƌŐǇŚŽŵĞŽƐƚĂƐŝƐĂŶĚŝŵŵƵŶĞ ƉŚĞŶŽƚǇƉĞŝŶŵŝĐĞ͘ƌ:EƵƚƌ͕ϵϳ͕ϭϭϭϳͲϮϳ͘ Et'Z͕͕͘͘E͕:͕͘/E͕:͘Z͕͘Dh,>hZ͕D͘:͕͘^dsE^͕Z͕͘͘>/E͕>͘&͕͘,YY͕͘D͕͘^,,͕ ^͘,͕͘Z>KddK͕D͕͘^>Ed͕͕͘͘ZK,KE͕:͕͘'>>hW͕͕͘/>Z͕ D͘ ͘ Θ ^sd͘W͘ϮϬϬϵ͘ďƌĂŶĐŚĞĚͲĐŚĂŝŶĂŵŝŶŽĂĐŝĚͲƌĞůĂƚĞĚŵĞƚĂďŽůŝĐƐŝŐŶĂƚƵƌĞƚŚĂƚĚŝĨĨĞƌĞŶƚŝĂƚĞƐ ŽďĞƐĞĂŶĚůĞĂŶŚƵŵĂŶƐĂŶĚĐŽŶƚƌŝďƵƚĞƐƚŽŝŶƐƵůŝŶƌĞƐŝƐƚĂŶĐĞ͘ĞůůDĞƚĂď͕ϵ͕ϯϭϭͲϮϲ͘ EtDE͕͘:͘ΘWZ/͕͘W͘ϭϵϵϵ͘ZĞŶĂůĨƵŶĐƚŝŽŶĂŶĚŶŝƚƌŽŐĞŶŵĞƚĂďŽůŝƚĞƐ͘/Ŷ͗hZd/^͕͘Θ^,tKK͕ ͘;ĞĚƐ͘ͿdĞǆƚďŽŽŬŽĨůŝŶŝĐĂůŚĞŵŝƐƚƌǇ͘ϯƌĚĞĚ͘WŚŝůĂĚĞůƉŚŝĂ͗t͘^ĂƵŶĚĞƌƐŽŵƉĂŶǇ͘ EzZ/E͕d͕͘ZKE>>͕ z͘Θ>EE͕E͘D͘ϮϬϭϭ͘WƌĞďŝŽƚŝĐĞĨĨĞĐƚƐŽĨǁŚĞĂƚĂƌĂďŝŶŽǆǇůĂŶƌĞůĂƚĞĚƚŽƚŚĞŝŶĐƌĞĂƐĞŝŶ ďŝĨŝĚŽďĂĐƚĞƌŝĂ͕ZŽƐĞďƵƌŝĂ ĂŶĚ ĂĐƚĞƌŽŝĚĞƐͬWƌĞǀŽƚĞůůĂŝŶ ĚŝĞƚͲŝŶĚƵĐĞĚ ŽďĞƐĞ ŵŝĐĞ͘ W>Ž^ KŶĞ͕ϲ͕ ĞϮϬϵϰϰ͘ E'hzE͕d͘>͕͘s//ZͲ^/>s͕^͕͘>/^dKE͕͘ΘZ^͕:͘ϮϬϭϱ͘,ŽǁŝŶĨŽƌŵĂƚŝǀĞŝƐƚŚĞŵŽƵƐĞĨŽƌŚƵŵĂŶŐƵƚ ŵŝĐƌŽďŝŽƚĂƌĞƐĞĂƌĐŚ͍ŝƐDŽĚĞůDĞĐŚ͕ϴ͕ϭͲϭϲ͘ E/^͘KEE͕:͘d͕͘Ezz^^KEE͕͕͘&KyZK&d͕>E͕͕͘t/>/E'tKK͕͕͘dK/E͕:͘ D͕͘D^tEz͕͕͘KΖZKhZ>tz͕>͘>z͕D͕͘EEz͕D͕͘͘'&&Ez͕'͘ΘhEE͕&͘ϮϬϭϭ͘ƚůĂŶƚŝĐ ŝĂďĞƚĞƐŝŶWƌĞŐŶĂŶĐǇ;/WͿ͗ƚŚĞƉƌĞǀĂůĞŶĐĞĂŶĚŽƵƚĐŽŵĞƐŽĨŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐŵĞůůŝƚƵƐƵƐŝŶŐ ŶĞǁĚŝĂŐŶŽƐƚŝĐĐƌŝƚĞƌŝĂ͘ŝĂďĞƚŽůŽŐŝĂ͕ϱϰ͕ϭϲϳϬͲϱ͘ KΖ^h>>/sE͕ :͘ ͘ Θ D,E͕ ͘ D͘ ϭϵϲϰ͘ ƌŝƚĞƌŝĂ ĨŽƌ ƚŚĞ ŽƌĂů ŐůƵĐŽƐĞ ƚŽůĞƌĂŶĐĞ ƚĞƐƚ ŝŶ ƉƌĞŐŶĂŶĐǇ͘ ŝĂďĞƚĞƐ͕ϭϯ͕ϮϳϴͲϴϱ͘ KZ'E/d/KE͕t͘,͘ϭϵϴϱ͘ŝĂďĞƚĞƐŵĞůůŝƚƵƐ͘ZĞƉŽƌƚŽĨĂt,K^ƚƵĚǇ'ƌŽƵƉ͘ϭϵϴϱͬϬϭͬϬϭĞĚ͗͘tŽƌůĚ ,ĞĂůƚŚKƌŐĂŶdĞĐŚZĞƉ^Ğƌ KZ'E/d/KE͕͘t͘,͘ΘEd/KE^͕&͘͘͘K͘K͘d͘h͘ϮϬϬϯ͘ŝĞƚ͕ŶƵƚƌŝƚŝŽŶĂŶĚƚŚĞƉƌĞǀĞŶƚŝŽŶŽĨĐŚƌŽŶŝĐ ĚŝƐĞĂƐĞƐ͘tŽƌůĚ,ĞĂůƚŚKƌŐĂŶdĞĐŚZĞƉ^Ğƌ͕ϵϭϲ͕ŝͲǀŝŝŝ͕ϭͲϭϰϵ͕ďĂĐŬĐŽǀĞƌ͘ KsÊ͕ W͕͘ Z^Dh^Ê͕ ^͘ Θ ͕ h͘ ϮϬϭϭ͘ ĨĨĞĐƚ ŽĨ ƉƌĞƉƌĞŐŶĂŶĐǇ ŵĂƚĞƌŶĂů ŽǀĞƌǁĞŝŐŚƚ ĂŶĚ ŽďĞƐŝƚǇŽŶƉƌĞŐŶĂŶĐǇŽƵƚĐŽŵĞ͘KďƐƚĞƚ'ǇŶĞĐŽů͕ϭϭϴ͕ϯϬϱͲϭϮ͘ KsÊ͕W͘'͕͘:EÊ͕͘D͕͘DD͕W͕͘Z^Dh^Ê͕^͘Θ͕h͘^͘ϮϬϭϱ͘DĂƚĞƌŶĂůĂŶĚŶĞŽŶĂƚĂů ŽƵƚĐŽŵĞƐŝŶƉƌĞŐŶĂŶĐŝĞƐĐŽŵƉůŝĐĂƚĞĚďǇŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐ͘ĂŶĂƚŝŽŶͲǁŝĚĞƐƚƵĚǇ͘:DĂƚĞƌŶ&ĞƚĂů EĞŽŶĂƚĂůDĞĚ͕ϭͲϱ͘

ϭϳϴ

Kd͕D͕͘DZ'E͕D͕͘K/͕͕͘z/E͕͕͘Ê/^K'>h͕^͘z͕͘K>h͕͕͘z/>D͕D͘/͕͘^z>͕͕͘ /^/DZ͕͘ΘKD/Z͕/͘͘ϮϬϬϮ͘/ŶĐƌĞĂƐĞĚŽǆŝĚĂƚŝǀĞƐƚƌĞƐƐĂŶĚŚǇƉŽǌŝŶĐĞŵŝĂŝŶŵĂůĞŽďĞƐŝƚǇ͘ ůŝŶŝŽĐŚĞŵ͕ϯϱ͕ϲϮϳͲϯϭ͘ Kh'h͕h͕͘ /^/͕'͘ ϮϬϬϭ͘ͲƌĞĂĐƚŝǀĞƉƌŽƚĞŝŶŝƐŝŶĚĞƉĞŶĚĞŶƚůǇĂƐƐŽĐŝĂƚĞĚǁŝƚŚƚŽƚĂůďŽĚǇĨĂƚ͕ĐĞŶƚƌĂůĨĂƚ͕ĂŶĚŝŶƐƵůŝŶ ƌĞƐŝƐƚĂŶĐĞŝŶĂĚƵůƚǁŽŵĞŶ͘/Ŷƚ:KďĞƐZĞůĂƚDĞƚĂďŝƐŽƌĚ͕Ϯϱ͕ϭϰϭϲͲϮϬ͘ WWE/K>Kh͕͕͘͘t/>Z͕Z͘>͕͘DEK>'^͕^͘͘Θ,ZKh^K^͕'͘W͘ϭϵϵϴ͘dŚĞƉĂƚŚŽƉŚǇƐŝŽůŽŐŝĐ ƌŽůĞƐŽĨŝŶƚĞƌůĞƵŬŝŶͲϲŝŶŚƵŵĂŶĚŝƐĞĂƐĞ͘ŶŶ/ŶƚĞƌŶDĞĚ͕ϭϮϴ͕ϭϮϳͲϯϳ͘ WZ>͕:͘͘ΘZ/DZ͕Z͘͘ϮϬϬϵ͘tĞŝŐŚƚůŽƐƐĚƵƌŝŶŐŽůŝŐŽĨƌƵĐƚŽƐĞƐƵƉƉůĞŵĞŶƚĂƚŝŽŶŝƐĂƐƐŽĐŝĂƚĞĚǁŝƚŚ ĚĞĐƌĞĂƐĞĚŐŚƌĞůŝŶĂŶĚŝŶĐƌĞĂƐĞĚƉĞƉƚŝĚĞzzŝŶŽǀĞƌǁĞŝŐŚƚĂŶĚŽďĞƐĞĂĚƵůƚƐ͘ŵ:ůŝŶEƵƚƌ͕ϴϵ͕ ϭϳϱϭͲϵ͘ WZE>>͕:͘͘ΘZ/DZ͕Z͘͘ϮϬϭϮ͘WƌĞďŝŽƚŝĐĨŝďƌĞƐĚŽƐĞͲĚĞƉĞŶĚĞŶƚůǇŝŶĐƌĞĂƐĞƐĂƚŝĞƚǇŚŽƌŵŽŶĞƐĂŶĚ ĂůƚĞƌĂĐƚĞƌŽŝĚĞƚĞƐĂŶĚ&ŝƌŵŝĐƵƚĞƐŝŶůĞĂŶĂŶĚŽďĞƐĞ:Z͗>ͲĐƉƌĂƚƐ͘ƌ:EƵƚƌ͕ϭϬϳ͕ϲϬϭͲϭϯ͘ W^dKZ>>/͕>͕͘^>sK͕͕͘DZK͕:͘Z͕͘s,/͕D͘ΘW/ZZK͕d͘d͘ϮϬϭϯ͘ĞŶƚƌĂůƌŽůĞŽĨƚŚĞŐƵƚ ĞƉŝƚŚĞůŝĂů ďĂƌƌŝĞƌ ŝŶ ƚŚĞ ƉĂƚŚŽŐĞŶĞƐŝƐ ŽĨ ĐŚƌŽŶŝĐ ŝŶƚĞƐƚŝŶĂů ŝŶĨůĂŵŵĂƚŝŽŶ͗ ůĞƐƐŽŶƐ ůĞĂƌŶĞĚ ĨƌŽŵ ĂŶŝŵĂůŵŽĚĞůƐĂŶĚŚƵŵĂŶŐĞŶĞƚŝĐƐ͘&ƌŽŶƚ/ŵŵƵŶŽů͕ϰ͕ϮϴϬ͘ WE͕ :͘ ͘ Θ sZ^>Ks/͕ :͘ ϮϬϬϯ͘ >ĂĐƚŽďĂĐŝůůƵƐ ƌŚĂŵŶŽƐƵƐ '' ĚĞĐƌĞĂƐĞƐ dE&ͲĂůƉŚĂ ƉƌŽĚƵĐƚŝŽŶ ŝŶ ůŝƉŽƉŽůǇƐĂĐĐŚĂƌŝĚĞͲĂĐƚŝǀĂƚĞĚ ŵƵƌŝŶĞ ŵĂĐƌŽƉŚĂŐĞƐ ďǇ Ă ĐŽŶƚĂĐƚͲŝŶĚĞƉĞŶĚĞŶƚ ŵĞĐŚĂŶŝƐŵ͘ Ğůů DŝĐƌŽďŝŽů͕ϱ͕ϮϳϳͲϴϱ͘ WWz^͕D͘͘Θ,/Z^,&/>͕'͘D͘ϮϬϬϯ͘ͲƌĞĂĐƚŝǀĞƉƌŽƚĞŝŶ͗ĂĐƌŝƚŝĐĂůƵƉĚĂƚĞ͘:ůŝŶ/ŶǀĞƐƚ͕ϭϭϭ͕ϭϴϬϱͲϭϮ͘ WZE͕ >͕͘ ^/ZZ͕ ^͕͘ KD>͕ D͕͘ >ZͲs/>>K^>͕ &͕͘ />KE͕ ͕͘ E/dK͕ ͕͘ KE,͕ ͕͘ K>/sZ^͕D͕͘Zh>K͕͕͘yh^͕:͘Θ'>s͕:͘ϮϬϬϳ͘ĐŽŵƉĂƌĂƚŝǀĞƐƚƵĚǇŽĨƚŚĞƉƌĞǀĞŶƚĂƚŝǀĞ ĞĨĨĞĐƚƐ ĞǆĞƌƚĞĚ ďǇ ƚǁŽ ƉƌŽďŝŽƚŝĐƐ͕ >ĂĐƚŽďĂĐŝůůƵƐ ƌĞƵƚĞƌŝ ĂŶĚ >ĂĐƚŽďĂĐŝůůƵƐ ĨĞƌŵĞŶƚƵŵ͕ ŝŶ ƚŚĞ ƚƌŝŶŝƚƌŽďĞŶǌĞŶĞƐƵůĨŽŶŝĐĂĐŝĚŵŽĚĞůŽĨƌĂƚĐŽůŝƚŝƐ͘ƌ:EƵƚƌ͕ϵϳ͕ϵϲͲϭϬϯ͘ WdZ^KE͕>͘t͘ΘZd/^͕͘ϮϬϭϰ͘/ŶƚĞƐƚŝŶĂůĞƉŝƚŚĞůŝĂůĐĞůůƐ͗ƌĞŐƵůĂƚŽƌƐŽĨďĂƌƌŝĞƌĨƵŶĐƚŝŽŶĂŶĚŝŵŵƵŶĞ ŚŽŵĞŽƐƚĂƐŝƐ͘EĂƚZĞǀ/ŵŵƵŶŽů͕ϭϰ͕ϭϰϭͲϱϯ͘ WdZ/͕͕͘͘^dZK͕͘W͕͘>D/͕:͕͘͘'KD^͕͘W͕͘&ZEE^͕'͘Z͕͘/WW^͕>͘,͕͘Êd,>KZEd͕ ͕͘ /ͲDK>/E͕ &͕͘ ^Ͳ>Z͕ D͘ :͕͘ DWEͲDZd/E͕ >͕͘ DhEKͲYh͕^͕͘ZKDZK͕&͕͘'/>͕͘Θ&KEdE͕>͘ϮϬϭϰ͘ĨĨĞĐƚƐŽĨ>ĂĐƚŽďĂĐŝůůƵƐƉĂƌĂĐĂƐĞŝ ED/ͲϰϬϯϰ͕ŝĨŝĚŽďĂĐƚĞƌŝƵŵďƌĞǀĞED/ͲϰϬϯϱĂŶĚ>ĂĐƚŽďĂĐŝůůƵƐƌŚĂŵŶŽƐƵƐED/ͲϰϬϯϲŽŶ ŚĞƉĂƚŝĐƐƚĞĂƚŽƐŝƐŝŶƵĐŬĞƌƌĂƚƐ͘W>Ž^KŶĞ͕ϵ͕ĞϵϴϰϬϭ͘ WKK>^hW͕E͕͘^hŽ^KŶĞ͕ϵ͕ĞϵϮϰϴϱ͘ WK^dKE͕>͘ΘWd>͕E͘ϮϬϭϰ͘ŝĞƚĂƌǇƌĞĐŽŵŵĞŶĚĂƚŝŽŶƐĨŽƌŽďĞƐĞƉƌĞŐŶĂŶƚǁŽŵĞŶ͗ĐƵƌƌĞŶƚƋƵĞƐƚŝŽŶƐ ĂŶĚĐŽŶƚƌŽǀĞƌƐŝĞƐ͘ĐƚĂKďƐƚĞƚ'ǇŶĞĐŽů^ĐĂŶĚ͕ϵϯ͕ϭϬϴϭͲϰ͘ WK^dKE͕ >͘ Θ Z/:D,/͕͘tE'͕͘z͕͘^/E',͕͕͘t>/͕z͕͘/͕͕͘>/͕^͕͘,h͕:͕͘,E'͕&͕͘>/E'͕^͕͘,E'͕t͕͘'hE͕z͕͘^,E͕͕͘WE'͕z͕͘,E'͕ ͕͘:/͕͕͘th͕t͕͘Y/E͕z͕͘yh͕t͕͘>/͕:͕͘,E͕>͕͘>h͕͕͘th͕W͕͘/͕z͕͘^hE͕y͕͘>/͕͕͘dE'͕͕͘ ,KE'͕^͕͘>/͕y͕͘,E͕t͕͘yh͕Z͕͘tE'͕D͕͘&E'͕Y͕͘'KE'͕D͕͘zh͕:͕͘,E'͕z͕͘,E'͕ D͕͘,EÊ͕d͕͘Ê,͕'͕͘Z^͕:͕͘&>KEz͕'͕͘KD/͕D͕͘>,d>/Z͕͕͘ ZEh>d͕W͕͘WKE^͕E͕͘ddK͕:͘D͕͘,E'͕͕͘,E͕,͕͘zE'͕Z͕͘,E'͕t͕͘zE'͕,͕͘tE'͕ :͕͘ ,Z>/,͕ ^͘ ͕͘ E/>Ê͕ Z͕͘ WZÊ͕ K͘ Θ Ž^KŶĞ͕ϴ͕Ğϲϱϰϲϱ͘ Z//͕^͕͘^,>/͕d͕͘hsEͲ>Z͕:͕͘D/E/hD͕:͕͘,h^dKEͲWZ^>z͕>͕͘d>EK͕W͘Θ,h'h>Ͳ DKhKE͕^͘ϮϬϬϲ͘DĂƚĞƌŶĂůŝŶƚĞƌůĞƵŬŝŶͲϲ͗ŵĂƌŬĞƌŽĨĨĞƚĂůŐƌŽǁƚŚĂŶĚĂĚŝƉŽƐŝƚǇ͘ :^ŽĐ'ǇŶĞĐŽů /ŶǀĞƐƚŝŐ͕ϭϯ͕ϱϯͲϳ͘

ϭϴϬ

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:͘ ͕͘>h^/^͕͘:͘Θ,E͕^͘>͘ϮϬϭϭď͘'ƵƚĨůŽƌĂŵĞƚĂďŽůŝƐŵŽĨƉŚŽƐƉŚĂƚŝĚǇůĐŚŽůŝŶĞƉƌŽŵŽƚĞƐ ĐĂƌĚŝŽǀĂƐĐƵůĂƌĚŝƐĞĂƐĞ͘EĂƚƵƌĞ͕ϰϳϮ͕ϱϳͲϲϯ͘ t/͕:͕͘'K͕:͘Θ,E'͕:͘ϮϬϭϰ͘'ĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐŵĞůůŝƚƵƐĂŶĚŝŵƉĂŝƌĞĚŐůƵĐŽƐĞƚŽůĞƌĂŶĐĞƉƌĞŐŶĂŶƚ ǁŽŵĞŶ͘WĂŬ:DĞĚ^Đŝ͕ϯϬ͕ϭϮϬϯͲϴ͘ t/^Z'͕^͘W͕͘DEE͕͕͘^/͕D͕͘ZKÊhD͕D͕͘>/>͕Z͘>͘Θ&ZZEd͕͘t͕͘:Z͘ϮϬϬϯ͘ KďĞƐŝƚǇŝƐĂƐƐŽĐŝĂƚĞĚǁŝƚŚŵĂĐƌŽƉŚĂŐĞĂĐĐƵŵƵůĂƚŝŽŶŝŶĂĚŝƉŽƐĞƚŝƐƐƵĞ͘:ůŝŶ/ŶǀĞƐƚ͕ϭϭϮ͕ϭϳϵϲͲ ϴϬϴ͘ tE>E͕͘D͕͘dKZ>KE/͕D͘Z͕͘&>s/'E͕D͕͘dZh:/>>K͕:͕͘K͕D͕͘͘DWK^͕D͕͘͘hEE͕ ͘͘Θ^,D/d͕D͘/͘ϮϬϭϮ͘'ĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐĂŶĚƉƌĞŐŶĂŶĐǇŽƵƚĐŽŵĞƐͲͲĂƐǇƐƚĞŵĂƚŝĐƌĞǀŝĞǁ ŽĨ ƚŚĞ tŽƌůĚ ,ĞĂůƚŚ KƌŐĂŶŝǌĂƚŝŽŶ ;t,KͿ ĂŶĚ ƚŚĞ /ŶƚĞƌŶĂƚŝŽŶĂů ƐƐŽĐŝĂƚŝŽŶ ŽĨ ŝĂďĞƚĞƐ ŝŶ WƌĞŐŶĂŶĐǇ^ƚƵĚǇ'ƌŽƵƉƐ;/W^'ͿĚŝĂŐŶŽƐƚŝĐĐƌŝƚĞƌŝĂ͘DWƌĞŐŶĂŶĐǇŚŝůĚďŝƌƚŚ͕ϭϮ͕Ϯϯ͘ t^dZdZW͕D͕͘Z͕:͘&͕͘W/Z^͕E͘D͕͘sED/Z>K͕'͘:͕͘DEE͕Z͕͘ZKD/:E͕:͕͘͘,s͘ D͘ΘZEÊ͕W͘͘ϮϬϬϳ͘ƉŽůŝƉŽƉƌŽƚĞŝŶͲ/ŝƐĐƌƵĐŝĂůůǇŝŶǀŽůǀĞĚŝŶůŝƉŽƉŽůǇƐĂĐĐŚĂƌŝĚĞͲŝŶĚƵĐĞĚ ĂƚŚĞƌŽƐĐůĞƌŽƐŝƐĚĞǀĞůŽƉŵĞŶƚŝŶĂƉŽůŝƉŽƉƌŽƚĞŝŶͲŬŶŽĐŬŽƵƚŵŝĐĞ͘ŝƌĐƵůĂƚŝŽŶ͕ϭϭϲ͕ϮϭϳϯͲϴϭ͘ t/>>dd͕ t͘ ϭϵϵϴ͘ ϮϰͲŚŽƵƌ ĚŝĞƚĂƌǇ ƌĞĐĂůů ĂŶĚ ĨŽŽĚ ƌĞĐŽƌĚŵĞƚŚŽĚƐ͘ /Ŷ͗ hZ͕ D͘ ;ĞĚ͘Ϳ EƵƚƌŝƚŝŽŶĂů ƉŝĚĞŵŝŽůŽŐǇ͘ϮŶĚĞĚ͘EĞǁzŽƌŬ͗KǆĨŽƌĚhŶŝǀĞƌƐŝƚǇWƌĞƐƐ͘ t/>>dd͕t͕͘͘,Kt͕'͘Z͘Θ͘,͘ϭϵϵϳ͘ĚũƵƐƚŵĞŶƚĨŽƌƚŽƚĂůĞŶĞƌŐǇŝŶƚĂŬĞŝŶĞƉŝĚĞŵŝŽůŽŐŝĐ ƐƚƵĚŝĞƐ͘ŵ:ůŝŶEƵƚƌ͕ϲϱ͕ϭϮϮϬ^ͲϭϮϮϴ^͖ĚŝƐĐƵƐƐŝŽŶϭϮϮϵ^ͲϭϮϯϭ^͘ t/>^KE͕ W͘ t͕͘ Ζ'K^d/EK͕ Z͘ ͕͘ ^h>>/sE͕ >͕͘ WZ/^͕ ,͘ Θ ͕ t͘ ͘ ϮϬϬϮ͘ KǀĞƌǁĞŝŐŚƚ ĂŶĚ ŽďĞƐŝƚǇĂƐĚĞƚĞƌŵŝŶĂŶƚƐŽĨĐĂƌĚŝŽǀĂƐĐƵůĂƌƌŝƐŬ͗ƚŚĞ&ƌĂŵŝŶŐŚĂŵĞǆƉĞƌŝĞŶĐĞ͘ƌĐŚ/ŶƚĞƌŶDĞĚ͕ϭϲϮ͕ ϭϴϲϳͲϳϮ͘ t/EZ͕^͕͘,E͕z͕͘W>d^Z͕'͕͘dZhKE'͕͕͘d^h/͕,͕͘,ZD/͕:͕͘KZ&DE͕Z͕͘tE'͕z͕͘/>E^ĂĐƚŽĐŽĐĐƵƐůĂĐƚŝƐŽŶƚŚĞƉƌŽŐƌĞƐƐŝŽŶŽĨ ĚŝĂďĞƚĞƐŝŶĚƵĐĞĚďǇĂŚŝŐŚͲĨƌƵĐƚŽƐĞĚŝĞƚŝŶƌĂƚƐ͘ŝŽƐĐŝŝŽƚĞĐŚŶŽůŝŽĐŚĞŵ͕ϳϬ͕ϭϮϱϱͲϴ͘ zs͕ ,͕͘ :/E͕ ^͘ Θ ^/E,͕ W͘ Z͘ ϮϬϬϳ͘ ŶƚŝĚŝĂďĞƚŝĐ ĞĨĨĞĐƚ ŽĨ ƉƌŽďŝŽƚŝĐ ĚĂŚŝ ĐŽŶƚĂŝŶŝŶŐ >ĂĐƚŽďĂĐŝůůƵƐ ĂĐŝĚŽƉŚŝůƵƐĂŶĚ>ĂĐƚŽďĂĐŝůůƵƐĐĂƐĞŝŝŶŚŝŐŚĨƌƵĐƚŽƐĞĨĞĚƌĂƚƐ͘EƵƚƌŝƚŝŽŶ͕Ϯϯ͕ϲϮͲϴ͘ zs͕,͕͘:/E͕^͘Θ^/E,͕W͘Z͘ϮϬϬϴĂ͘dŚĞĞĨĨĞĐƚŽĨƉƌŽďŝŽƚŝĐĚĂŚŝĐŽŶƚĂŝŶŝŶŐ>ĂĐƚŽďĂĐŝůůƵƐĂĐŝĚŽƉŚŝůƵƐ ĂŶĚ>ĂĐƚŽďĂĐŝůůƵƐĐĂƐĞŝŽŶŐĂƐƚƌŽƉĂƚŚŝĐĐŽŶƐĞƋƵĞŶĐĞƐŝŶĚŝĂďĞƚŝĐƌĂƚƐ͘:DĞĚ&ŽŽĚ͕ϭϭ͕ϲϮͲϴ͘ zs͕,͕͘:/E͕^͘Θ^/E,͕W͘Z͘ϮϬϬϴď͘KƌĂůĂĚŵŝŶŝƐƚƌĂƚŝŽŶŽĨĚĂŚŝĐŽŶƚĂŝŶŝŶŐƉƌŽďŝŽƚŝĐ>ĂĐƚŽďĂĐŝůůƵƐ ĂĐŝĚŽƉŚŝůƵƐĂŶĚ>ĂĐƚŽďĂĐŝůůƵƐĐĂƐĞŝĚĞůĂǇĞĚƚŚĞƉƌŽŐƌĞƐƐŝŽŶŽĨƐƚƌĞƉƚŽǌŽƚŽĐŝŶͲŝŶĚƵĐĞĚĚŝĂďĞƚĞƐŝŶ ƌĂƚƐ͘:ĂŝƌǇZĞƐ͕ϳϱ͕ϭϴϵͲϵϱ͘ zs͕,͕͘>͕:͘,͕͘>>Kz͕:͕͘t>dZ͕W͘ΘZE͕^͘'͘ϮϬϭϯ͘ĞŶĞĨŝĐŝĂůŵĞƚĂďŽůŝĐĞĨĨĞĐƚƐŽĨĂƉƌŽďŝŽƚŝĐ ǀŝĂďƵƚǇƌĂƚĞͲŝŶĚƵĐĞĚ'>WͲϭŚŽƌŵŽŶĞƐĞĐƌĞƚŝŽŶ͘:ŝŽůŚĞŵ͕Ϯϴϴ͕ϮϱϬϴϴͲϵϳ͘ zE'͕,͕͘t/͕z͕͘'K͕y͕͘yh͕y͕͘&E͕>͕͘,͕:͕͘,h͕z͕͘>/h͕y͕͘,E͕y͕͘zE'͕͘Θ,E'͕͘ϮϬϬϵ͘ZŝƐŬ ĨĂĐƚŽƌƐ ĨŽƌ ŐĞƐƚĂƚŝŽŶĂů ĚŝĂďĞƚĞƐ ŵĞůůŝƚƵƐ ŝŶ ŚŝŶĞƐĞ ǁŽŵĞŶ͗ Ă ƉƌŽƐƉĞĐƚŝǀĞ ƐƚƵĚǇ ŽĨ ϭϲ͕Ϯϴϲ ƉƌĞŐŶĂŶƚǁŽŵĞŶŝŶŚŝŶĂ͘ŝĂďĞƚDĞĚ͕Ϯϲ͕ϭϬϵϵͲϭϬϰ͘ zE'͕ ^͕͘ >/͕ t͕͘ ,>>/^͕ :͘ Z͕͘ Z/͕ '͕͘ >K͕ D͘ '͕͘ KEdZZ^͕ D͕͘ D'Z/^͕ D͕͘ ,/>'K͕ '͕͘ >^ÊK͕ Z͘ E͕͘ EK͕͘ ,E'͕ :͕͘ >/͕ z͕͘ ,͕ Y͕͘ >/͕ ,͕͘ 'hK͕ y͕͘ 'hK͕ :͘ Θ ,E'͕ ,͘ ϮϬϭϰ͘ WƌŽďŝŽƚŝĐ >ĂĐƚŽďĂĐŝůůƵƐ ĐĂƐĞŝ ŚĂŶŐ ĂŵĞůŝŽƌĂƚĞƐ ŚŝŐŚͲĨƌƵĐƚŽƐĞͲŝŶĚƵĐĞĚ ŝŵƉĂŝƌĞĚ ŐůƵĐŽƐĞ ƚŽůĞƌĂŶĐĞ ŝŶ ŚǇƉĞƌŝŶƐƵůŝŶĞŵŝĂƌĂƚƐ͘Ƶƌ:EƵƚƌ͕ϱϯ͕ϮϮϭͲϯϮ͘ ,h͕͕͘zE'͕,͕͘'E'͕Y͕͘D͕Y͕͘>KE'͕z͕͘,Kh͕͘Θ,E͕D͘ϮϬϭϱ͘ƐƐŽĐŝĂƚŝŽŶŽĨŽǆŝĚĂƚŝǀĞƐƚƌĞƐƐ ďŝŽŵĂƌŬĞƌƐǁŝƚŚŐĞƐƚĂƚŝŽŶĂůĚŝĂďĞƚĞƐŵĞůůŝƚƵƐŝŶƉƌĞŐŶĂŶƚǁŽŵĞŶ͗ĂĐĂƐĞͲĐŽŶƚƌŽůƐƚƵĚǇ͘W>Ž^KŶĞ͕ ϭϬ͕ĞϬϭϮϲϰϵϬ͘

ϭϴϴ

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