text:
Michael Schwartz, MD
Robert H. Williams Endowed Chair in Medicine
Executive Director, UW Diabetes Institute
Director, Nutrition Obesity Research Center
Professor, Division of Metabolism and Endocrinology
Email Address: email@example.com
Division of Metabolism, Endocrinology and Nutrition Website: http://depts.washington.edu/metab/
Dr. Schwartz received his MD from Rush Medical College in 1983 and completed his residency in Medicine at UW in 1986. His fellowship training in Endocrinology and Metabolism, undertaken in the lab of Dr. Daniel Porte, Jr., at UW, was completed in 1990. In addition to clinical teaching and patient care responsibilities at Harborview Medical Center in Seattle, Dr. Schwartz currently holds two R01 grants and has been continuously funded by the NIH and other sources to study body weight regulatory systems, obesity and diabetes for over 20 years with >185 publications in this area. He serves as Director of the UW Medicine Diabetes and Obesity Center of Excellence, is a member of the American Society for Clinical Investigation and the Association of American Physicians, and serves on numerous editorial boards. He is the Director of the Nutrition Obesity Research Center (NORC) at UW, and is Principle Investigator on an NIH T32 Fellowship Training grant and two NIH R01 awards.
Dr. Schwartz's research focuses on hypothalamic and neuroendocrine control of energy balance and glucose metabolism and on CNS mechanisms involved in obesity, insulin resistance and diabetes.
Role of the Brain in the Pathogenesis of Obesity, Insulin Resistance and Type 2 Diabetes
A major focus of Dr. Schwartz's research program is to investigate the hypothesis that the brain plays an essential role to promote homeostasis of both energy balance and glucose metabolism in response to afferent input from adiposity- and nutrient-related signals. Accordingly, defects in this control system may play an important role in the link between obesity, insulin resistance and type 2 diabetes. The overarching hypothesis is that in times of plenty (i.e., ample fat stores and food availability), input to key brain areas from these afferent signals (e.g., insulin, leptin and long-chain free fatty acids) leads to inhibition of both energy intake and endogenous glucose production, while simultaneously increasing energy expenditure and mobilizing fat stores. The net effect is that when the brain senses that body energy content and nutrient availability are in sufficient supply, further increases of stored energy (in the form of fat) and circulating nutrients (e.g., glucose) are resisted. Conversely, a decrease in neuronal input from one or more of these afferent signals is proposed to alert the brain to a current or pending deficiency of stored energy or nutrient availability. In turn, the brain activates responses that promote positive energy balance (e.g., increased food intake and decreased energy expenditure) and raise circulating nutrient levels (i.e., increased hepatic glucose production). As body fat content and plasma glucose levels begin to increase, circulating concentrations of leptin, insulin and free fatty acids increase as well. The latter are sensed in the brain, favoring the return of food intake and glucose production to their original values. Should defects arise in either the secretion of or the CNS response to these signals, elevated levels of both body fat content and hepatic glucose production are expected consequences. Reduced secretion of, sensing of, or responsiveness to afferent hormonal or nutrient-related signals can therefore be predicted to set in motion a vicious cycle of weight gain and insulin resistance.
Since convergent signal transduction (e.g., via the insulin receptor substrate (IRS)-phosphatidylinositide 3-OH kinase (PI3K) signaling pathway) and termination (e.g., SOCS3) mechanisms mediate neuronal actions of insulin and leptin, defects within a single biochemical pathway can potentially cause resistance to the central actions of both hormones. This, in turn, can be predicted to induce hyperphagia, weight gain, hepatic insulin resistance and glucose intolerance. The feasibility of this concept is strengthened by evidence implicating impaired IRS-PI3K signal transduction in the insulin resistance of peripheral tissues in diabetic humans and animal models. When combined with a b-cell defect, a feed-forward mechanism is again set in motion whereby reduced insulin and leptin action in the brain and periphery initially favor weight gain and insulin resistance, progressing to glucose intolerance and ultimately, diabetes. Since functional resistance to both leptin and insulin is common among the obese, this hypothesis warrants careful consideration. This concept was recently introduced formally (Science 21: 375-9, 2005) and discussed in greater detail (Diabetes 54:1264-76, 2005) by the PI. To test this hypothesis, our lab is actively investigating the mechanism whereby hypothalamic actions of insulin and leptin regulate insulin sensitivity in peripheral tissues. The main goals are to identify the specific neuronal subsets that mediate these effects and the underlying intracellular signal transduction molecules involved, using adenoviral gene therapy and transgenic strategies in mouse and rat models.
Hypothalamic Inflammation and Energy Homeostasis
This research focus, developed collaboratively with Drs. Brent Wisse and Jay Heinecke, seeks to investigate mechanisms underlying hypothalamic inflammation and clarify how this response affects brain systems that govern energy balance. A key hypothesis is that changes in the function of microglia (the resident macrophage of the brain) contribute to the link between systemic inflammatory signals and the onset and maintenance of hypothalamic inflammation. Major goals of this project are to identify the cellular mechanisms that drive hypothalamic inflammation in response to both acute inflammatory stress and to obesity, and to determine the consequences of this response for the control of energy homeostasis and peripheral glucose metabolism.
Leptin Regulation of Peripheral Glucose Metabolism
In addition to the key role played by leptin in the control of food intake and body weight, growing evidence suggests that leptin action in the CNS is a critical determinant of insulin action in peripheral tissues. To investigate the physiological role of leptin in the control of glucose tolerance in insulin sensitivity, Drs. Schwartz and Morton are studying Koletsky (fak/fak) rats that develop severe obesity due to genetic absence of leptin receptors. To date, we have demonstrated a marked impairment of glucose tolerance in these animals that is substantially rescued by adenoviral gene therapy to introduce functional leptin receptors selectively into the hypothalamic arcuate nucleus (ARC, a key forebrain site of leptin action) of fak/fak rats. Moreover, these effects cannot be explained by reductions of food intake or body weight, but they are blocked by icv infusion of a PI3K inhibitor. Conversely, the use of adenoviral gene therapy to express a constitutively active mutant of Akt, a key enzyme downstream of PI3K, in the ARC recapitulated the ability of leptin receptor gene therapy to improve insulin sensitivity when directed to this brain area. Thus, leptin signaling via the IRS-PI3K pathway in ARC neurons appears to play a key role to regulate insulin action in peripheral tissues. Dr. Morton has taken on a leadership role in developing this area of study.
Support the Schwartz Lab Research
Representative Publications:
Thaler JP, Yi C-X, Schur EA, Guyenet SJ, Hwang BH, Dietrich MO, Zhao X, Sarruf SA, Izgur V, Maravilla KR, Nguyen HT, Fischer JD, Matsen ME, Wisse BE, Morton GJ, Horvath TL, Baskin DG, Tschöp MH, Schwartz MW. Obesity is associated with hypothalamic injury in rodent models and humans. J Clin Invest. 122:152-162, 2012. PMCID: PMC3248304.
Morton G, Matsen M, Bracy D, Meek T, Nguyen H, Stefanovski D, Bergman R, Wasserman DH, Schwartz MW. FGF19 action in the brain induces insulin-independent glucose lowering. J Clin Invest. 123:4799-4808, 2014. PMCID: PMC3809800.
Schwartz MW, Seeley RJ, Tschöp MH, Woods SC, Morton GJ, Myers MG, D'Alessio D. Cooperation between brain and islet in glucose homeostasis and diabetes. Nature. 503:59-66, 2013. PMCID: PMC3983910.
Morton GJ, Kaiyala KJ, Foster-Schubert KE, Cummings DE, Schwartz MW. Carbohydrate feeding dissociates the postprandial FGF19 response from circulating bile acid levels in humans. J Clin Endocrinol Metab. 99:E241-E245, 2014. PMCID: PMC3913810.
Berkseth KE, Guyenet SJ, Melhorn SJ, Lee D, Thaler JP, Schur EA, Schwartz MW. Hypothalamic gliosis associated with high fat diet feeding is reversible in mice: a combined immunohistochemical and magnetic resonance imaging study. Endocrinology. 155:2858-2567, 2014. PMC Journal – In Process.
Schwartz MW, Baskin DG. Leptin and the brain: then and now. J Clin Invest. 123:2344-2345, 2013. PMCID: PMC3668840.
Thaler JP, Guyenet SJ, Dorfman M, Wisse BE, Schwartz MW. Hypothalamic inflammation: Marker or mechanism of obesity pathogenesis? Diabetes. 62:2629-2634, 2013. PMCID: PMC3717869.
Morton GJ, Meek TH, Schwartz MW. Neurobiology of food intake in health and disease. Nat Rev Neurosci. 15:367-378, 2014. PMCID: PMC4076116.
Baura, G, Foster, D, Porte, D, Jr., Kahn, SE, Bergman, RN, Cobelli, C, Schwartz, MW. Saturable transport of insulin from plasma into the central nervous system of dogs in vivo: A mechanism for regulated insulin delivery to the brain. J Clin Invest. 92: 1824-1830, 1993.
Sipols AJ, Baskin DG, Schwartz MW. Effect of intracerebroventricular insulin infusion on diabetic hyperphagia and hypothalamic neuropeptide gene expression. Diabetes. 44:147-151, 1995.
Schwartz MW, Baskin DG, Bukowski TR, et al. Specificity of leptin action on elevated blood glucose levels and hypothalamic neuropeptide Y gene expression in ob/ob mice.Diabetes. 45:531-535, 1996.
Porte D Jr, Schwartz MW. Diabetes complications: Why is glucose potentially toxic?Science. 272:699-70, 1996.
Schwartz MW, Peskind E, Raskind M, Nicolson M, Moore J, Morawiecki A, Boyko EJ, Porte D Jr. Cerebrospinal Fluid leptin levels: Relationship to plasma levels and to adiposity in humans. Nature Medicine. 2:589-93, 1996.
Schwartz MW, Seeley RJ, Campfield LA, Burn P, Baskin DG. Identification of targets of leptin action in rat hypothalamus. J Clin Invest. 98:1101-1106, 1996.
Schwartz MW, Seeley RJ. Neuroendocrine aspects of Starvation and Weight Loss. New Eng J Med. 336:1802-1811, 1997.
Seeley RJ, Yagaloff KA, Fisher SL, Burn P, Thiele TE, van Dijk G, Baskin DG, Schwartz MW. Melanocortin receptors in leptin effects. Nature. 390:349, 1997.
Schwartz MW, Seeley RJ, Weigle DS, Woods SC, Campfield LA, Burn P, Baskin DG. Leptin increases proopimelanocortin (POMC) mRNA expression in the rostral arcuate nucleus.Diabetes. 46:2119-2123, 1997.
Baskin DG, Seeley RJ, Kuijper JL, Lok S, Weigle DS, Erickson JC, Palmiter RD, Schwartz MW. Increased expression of mRNA for the long form of the leptin receptor (OB-Rb) in the hypothalamus is associated with leptin hypersensitivity and fasting. Diabetes. 47:535-543, 1998.
Chavez M, Seeley RJ, Havel PJ, Friedman M, Woods SC, Schwartz MW. Effect of a high-fat diet on hypothalamic neuropeptide gene expression in streptozotocin diabetes. J Clin Invest. 102:340-346, 1998.
Hahn T, Breininger JF, Baskin DG, Schwartz MW. Coexpression of Agrp and NPY in fasting-activated hypothalamic neurons. Nature Neuroscience. 1:271-272, 1998.
Schwartz MW, Erickson JC, Baskin DG, Palmiter RD. Effect of fasting and leptin deficiency on hypothalamic neuropeptide Y gene transcription in vivo revealed by expression of a lacZ reporter gene. Endocrinology. 139:2629-2635, 1998.
Sindelar DK, Havel PJ, Seeley RJ, Wilkinson, CW, Woods SC and Schwartz MW. Low plasma leptin levels contribute to diabetic hyperphagia. Diabetes. 48:1275-1280, 1999.
Woods SC, Seeley RJ, Porte D Jr, Schwartz MW. Signals that regulate food intake and energy homeostasis. Science. 280:1378-1383, 1998.
Baskin DG, Breininger JF, Schwartz MW. Leptin receptor mRNA identifies a subpopulation of neuropeptide Y neurons activated by fasting in rat hypothalamus. Diabetes. 48:828-833, 1999.
Schwartz MW. Mahogany adds color to the evolving story of body weight regulation.Nature Med. 5:374-375, 1999.
Schwartz MW, Kahn SE. Insulin resistance and obesity. Nature. 402:860-861, 1999.
Mystkowski P, Seeley RJ. Hahn TM, Baskin DG, Havel PJ, Matsumoto AM, Wilkinson CW, Peacock-Kinzig K, Blake K, and Schwartz MW. Hypothalamicmelanocortin concentrating hormone and estrogen-induced weight loss. J Neuroscience. 20:8637-8642, 2000.
Schwartz MW, Woods SC, Seeley RJ, Porte D Jr., and Baskin DG. Central nervous system control of food intake. Nature. 404:661-671, 2000.
Havel PJ, Hahn T, Sindelar DK, Baskin DG, Dallman MF, Weigle, DS, and Schwartz MW. Effects of streptozotocin diabetes and insulin treatment onthe hypothalamic melanocortin system and muscle uncoupling protein 3 expression in rats. Diabetes. 49:244-252, 2000.
Kaiyala KJ, Prigeon RL, Kahn SE, Woods SC, and Schwartz MW. Obesity induced by a high-fat diet is associated with reduced brain transport in dogs. Diabetes. 49:1525-1533, 2000.
McMinn JE, Sidelar DK, Havel PJ, Schwartz MW. Leptin deficiency induced by fasting impairs the satiety response to cholecystokinin. Endocrinology. 141:4442-4447, 2000.
Cummings DE and Schwartz MW. Melanocortins and body weight regulation: A tale of two receptors. Nature Genetics. 26:8-9, 2000.
Schwartz MW. Staying slim with insulin in mind. Science. 2089:266-267, 2000.
Wisse BE, Frayo RS, Schwartz MW, Cummings DE. Reversal of cancer anorexia by blockade of central melanocortin receptors in rats. Endocrinology. 142:3292-3301, 2001.
Niswender KD, Morton GJ, Stearns WH, Rhodes CJ, Myers MG, Schwartz MW. Key enzyme in leptin-induced anorexia. Nature. 413:794-795, 2001.
Schwartz MW. Progress in the search for neuronal mechanisms coupling type 2 diabetes to obesity. J Clin Invest. 108:963-964, 2001.
Wisse BE, Schwartz MW. Role of melanocortins in control of obesity. Lancet. 358:857-859, 2001.
Sindelar DK, Mystkowski P, Marsh DJ, Palmiter RD, and Schwartz MW. Attenuation of diabetic hyperphagia in neuropeptide Y-deficient mice. Diabetes. 51:778-783, 2002.
Barsh GS, Schwartz MW. Genetic approaches to studying energy balance: Perception and integration. Nature Reviews Genetics. 3:589-600, 2002.
Schwartz MW, Morton GJ. Keeping hunger at bay. Nature. 418:595-596, 2002.
Schwartz MW, Gelling R. Rats lighten up with MCH antagonist. Nature Medicine. 8:779-780, 2002.
Schwartz MW, Woods SC, Seeley RJ, Barsh GS, Baskin DG and Leibel RL. Is the energy homeostasis system inherently biased towards weight gain? Diabetes. 52:232-238, 2003.
Cummings DE, Schwartz MW. Genetics and Pathophysiology of Human Obesity. Annu Rev Med. 54:453-471 2003.
Niswender, K. D., Morrison C. D, Clegg, D.J., Olson R., Baskin, D.G., Myers, M.G. Jr,. Seeley, R.J., Schwartz MW. Insulin activation of phosphatidylinositol 3-kinase in the hypothalamic arcuate nucleus: a key mediator of insulin-induced anorexia. Diabetes.52:227-231, 2003.
Bates SH, Stearns WH, Schubert M, Tso AWK, Wang Y, Banks AS, Dundon T, Lavery HJ, Haq AK, Maratos-Flier E, Neel BG, Schwartz MW, and Myers MG Jr.Leptin receptor-STAT3 signaling is required for leptin regulation of energy balance but not reproduction. Nature.421:856-859, 2003.
Morton GJ, Niswender KD, Rhodes CJ, Myers MG, Jr., Blevins JE, Baskin DG, Schwartz MW. Arcuate nucleus-specific leptin receptor gene therapy attenuates the obesity phenotype of Koletsky (fak/fak) rats. Endocrinology. 144:2016-2024, 2003.
Wisse BE, Schwartz MW. The skinny on neurotrophins. Nature Neuroscience. 6:655-656, 2003.
Sindelar DK, St. Marie L, Maura GI, Palmiter RD, McMinn JE and Schwartz MW. Neuropeptide Y is required for hyperphagic feeding in response to neuroglucopenia.Endocrinology. 145(7):3363-8, 2004.
Gelling RW, Overduin J, Morrison CD, Morton GJ, R. Frayo S, Cummings DE and Schwartz MW. Effect of uncontrolled diabetes on plasma ghrelin concentrations and ghrelin-induced feeding. Endocrinology. 145:4575-4582, 2004.
Schwartz MW, Niswender K: Adiposity signaling and biological defense against weight gain: Absence of protection or central hormone resistance? J Clin Endocrinol Metab.89:5889-5897, 2004.
Schwartz MW, Porte D Jr. Diabetes, Obesity and the Brain. Science. 307:375-379, 2005.
Morton GJ, Blevins JE, Williams DL, Niswender KD, Gelling RW, Rhodes CJ, Baskin DG, Schwartz MW. Leptin action in the forebrain regulates the hindbrain response to satiety signals. J Clin Invest. 115:703-710, 2005.
Porte D Jr., Baskin DG, Schwartz MW. Insulin signaling in the central nervous system: a critical role in metabolic homeostasis and disease from c. elegans to man. Diabetes.54:1264-1276, 2005.
Williams D, Schwartz MW. The melanocortin system as a central integrator of direct and indirect controls of food intake. Am J Physiol Regul Integr Comp Physiol. 289:R2-3, 2005.
Williams D, Schwartz MW. Out of synch: Clock mutation causes obesity in mice. Cell Metab. 1:355-356, 2005.
Morrison CD, Morton GJ, Niswender KD, Gelling RW and Schwartz MW. Leptin inhibits hypothalamic Npy and Agrp gene expression via a mechanism thatrequires phosphotidylinositol 3-OH kinase signaling. Am J Physiol Endocrinol Metab. 289:E1051-1057, 2005.
Kim F, Tyselling K, Rice J, Gallis B, Haji L, Giachelli CM, Raines EW, Corson MA, Schwartz MW. Activation of IKKbeta by glucose is necessary and sufficient to impair insulin signaling and nitric oxide production in endothelial cells. J Mol Cell Cardiol. 39:327-334, 2005.
Morton, GJ, Gelling, RN, Niswender KD, Morrison CD, Rhodes CJ, Schwartz MW. Leptin regulates insulin sensitivity via phosphatidylinositol-3-OH kinase signaling in mediobasal hypothalamic neurons. Cell Metab. 2:411-420, 2005.
Schwartz MW, Porte D Jr. Diabetes, obesity, and the brain. Science. 307:375-379, 2005.
Gelling RW, Morton GJ, Niswender KD, Morrison CD, Myers M, Rhodes CJ, Schwartz MW. Insulin action in the brain contributes to glucose lowering during insulin treatment of diabetes. Cell Metab. 3:67-73, 2006.
Schwartz MW. Central Nervous System Regulation of Food Intake. Obesity. 1:1S-8S, 2006.
Pardini AW, Nguyen HT, Figlewicz DP, Basking DG, Williams DL, Schwartz MW. Distribution of Insulin Receptor Substrate-2 in Brain Areas Involved in Energy Homeostasis.Brain Res. 1112:169-178, 2006.
Morton GJ, Cummings DE, Baskin DG, Barsh GS, Schwartz MW. Central nervous system control of food intake and body weight. Nature. 443:289-295, 2006.
Weydt P, Pineda VV, Torrence AE, Libby RT, Satterfield TF, Lazarowski ER, Gilbert ML, Morton GJ, Bammler TK, Strand AD, Cui L, Beyer RP, Easley CN, Smith AC, Krainc D, Luquet S, Sweet IR, Schwartz MW, La Spada AR. Thermoregulatory and metabolic defects in Huntington's disease transgenic mice implicate PGC-1a in Huntington's disease neurodegeneration. Cell Metab. 4:349-362, 2006.
Williams DL, Baskin DG, Schwartz MW. Leptin regulation of the anorexic response to glucagon-like Peptide-1 receptor stimulation. Diabetes. 55:3387-3393, 2006.
Kim F, Pham M, Luttrell I, Bannerman DD, Tupper J, Thaler JP, Hawn TR, Raines EW, Schwartz MW. Toll like receptor-4 mediates vascular inflammation and insulin resistance in diet-induced obesity. Circulation Research. 100:1589-1596, 2007.
Wisse BE, Ogimoto K, Tang J, Harris MK Jr, Raines EW, Schwartz MW. Evidence that LPS-induced anorexia depends upon central, rather thanperipheral, inflammatory signals.Endocrinology. 148:5230-5237, 2007.
Wisse BE, Kim F, Schwartz MW. Physiology. An integrative view of obesity. Science.318:928-929, 2007.
Williams DL, Schwartz MW, Bastian LS, Blevins JE, Baskin DG. Immunocytochemistry and Laser Capture Microdissection for Real-time Quantitative PCR Identify Hindbrain Neurons Activated by Interaction Between Leptin and Cholecystokinin. J Histochem Cytochem.56:285-293, 2008.
Gelling RW, Yan W, Fitzgerald SM, Lim PO, Al-Noori S, Pardini A, Morton GJ, Ogimoto K, Schwartz MW, Dempsey PJ. Deficiency of TNF-alpha Converting Enzyme (TACE/ADAM17) Causes a Lean, Hyper metabolic Phenotype in Mice. Endocrinology. 149:6053-6064, 2008.
Kim F, Pham M, Maloney E, Rizzo N, Morton GJ, Wisse BE, Kirk EA, Chait A, Schwartz MW. Vascular Inflammation, Insulin Resistance and Reduced Nitric Oxide Production Precede the Onset of Peripheral Insulin Resistance. Atheroscler Thromb Vasc Biol. 28:1982-1988, 2008.
Sarruf DA, Yu F, Nguyen H, Williams DL, Printz RL, Niswender KD, Schwartz MW. Expression of PPARg in key neuronal subsets regulating glucose metabolism and energy homeostasis. Endocrinology. 150:707-712, 2009.
Williams DL, Baskin DG, Schwartz MW. Evidence that intestinal GLP-1 plays a physiological role in satiety. Endocrinology. 150:1680-1687, 2009. PMCID: PMC2659282.
Posey K, Clegg DJ, Printz RL, Byun J, Morton GJ, Vivekanandan-Giri A, Pennathur S, Baskin DG, Heinecke JW, Woods SC, Schwartz MW, Niswender KD. Hypothalamic proinflammatory lipid accumulation, inflammation, and insulin resistance in rats fed a high-fat diet. Am J Physiol Endocrinol Metab. 296:E1003-1012, 2009. PMCID: PMC2681305.
Blevins JE, Morton GJ, Williams DJ, Caldwell DW, Bastian LS, Wisse BE, Schwartz MW, and Baskin DG. Forebrain melanocortin signaling enhances the hindbrain satiety response to CCK-8. Am J Physiol Regul Integr Comp Physiol. 296:R476-484, 2009.
Sweet IR, Gilbert M, Maloney E, Hockenbery DM, Schwartz MW, and Kim F. Endothelial inflammation induced by excess glucose is associated with cytosolic glucose-6-phosphate but not increased mitochondrial respiration. Diabetologia. 52:921-931, 2009. PMCID: PMC2741088.
Schur E, Kleinhans N, Goldberg J, Buchwald D, Schwartz MW, Maravilla K. Activation in brain energy regulation and reward centers by food cues varies with choice of visual stimulus. Int J Obes (Lond). 33:653-661, 2009. PMCID: PMC2697279.
Pamir N, McMillen TS, Kaiyala K, Schwartz MW, Leboeuf, R. Receptors for tumor necrosis factor-alpha play a protective role against obesity and alter adipose tissue macrophage status. Endocrinology. 150:4124-4134, 2009. PMCID: PMC2736076.
Maloney E, Sweet IR, Hockenbery DM, Pham M, Rizzo NO, Tateya, S Handa P, Schwartz MW, and Kim F. Activation of NF-ΚB by Palmitate in Endothelial Cells: A Key Role for NADPH Oxidase-Derived Superoxide in Response to TLR4 Activation. Arterioscler Thromb Vasc Biol. 29:1370-1375, 2009. PMCID: PMC2775080.
German J, Kim F, Schwartz GJ, Havel PJ, Rhodes CJ, Schwartz MW, Morton GJ. Hypothalamic Leptin signaling regulates hepatic insulin sensitivity via a neurocircuit involving the vagus nerve. Endocrinology. 150:4502-4511, 2009. PMCID: PMC2754686.
Williams DL, Baskin DG, Schwartz MW. Hindbrain leptin receptor stimulation enhances the anorexic response to cholecystokinin. Am J Physiol Regul Integr Comp Physiol.297:R1238-1246, 2009. PMCID: PMC2777775.
Thaler JP, Choi SJ, Sajan MP, Ogimoto K, Nguyen HT, Matsen M, Benoit SC, Wisse BE, Farese RV, Schwartz MW. Atypical protein kinase C activity in the hypothalamus is required for lipopolysaccharide-mediated sickness responses. Endocrinology. 150:5362-5372, 2009. PMCID: PMC2795721.
Enns LC, Morton JF, Mangalindan RS, McKnight GS, Schwartz MW, Kaeberlein MR, Kennedy BK, Rabinovitch PS, Ladiges WC. Attenuation of age-related metabolic dysfunction in mice with a targeted disruption of the Cb subunit of protein kinase A.Journal of Gerontology: Biological Sciences. 64:1221-1231, 2009. PMCID: PMC2773816.
Chiu HK, Qian K, Ogimoto K, Morton GJ, Wisse BE, Agrawal N, MacDonald T, Schwartz, MW, Dichek HL. Mice lacking hepatic lipase are lean and protected against diet-induced obesity and hepatic steatosis. Endocrinology. 151:993-1001, 2010. PMCID: PMC2840680.
Rizzo NO, Maloney E, Pham M, Luttrell I, Wessell H, Tateya S, Daum G, Handa P, Schwartz MW, and Kim F. Reduced Nitric Oxide/cGMP Signaling Contributes to Vascular Inflammation and Insulin Resistance Induced by High Fat Feeding. Atherosclerosis, Thrombosis and Vascular Biology. 30:758-765, 2010. PMCID: PMC2865555.
Sarruf DA, Thaler JP, Morton GJ, German J, Fischer JD, Ogimoto K, and Schwartz MW. FGF21 Action in the Brain Increases Energy Expenditure and Insulin Sensitivity in Obese Rats. Diabetes. 59:1817-1824, 2010. PMCID: PMC2889784.
Kaiyala KJ, Morton GJ, Leroux BG, Ogimoto K, Wisse BE and Schwartz MW. Identification of body fat mass as a major determinant of metabolic rate in mice. Diabetes. 59:1657-1666, 2010. PMCID: PMC2889765.
Oh-I S, Thaler JP, Ogimoto K, Wisse BE, Morton GJ, and Schwartz MW. Central administration of Interleukin-4 exacerbates hypothalamic inflammation and weight gain during hig-fat feeding. Am J Physiology. 299:E47-53, 2010. PMCID: PMC2904047.
Choi SJ, Kim F, Schwartz MW and Wisse BE. Cultured hypothalamic neurons are resistant to inflammation and insulin resistance induced by saturated fatty acids. Am J Physiology. 298:E1122-1130, 2010. PMCID: PMC2886534.
German J, Wisse BE, Thaler JP, Oh-I S, Sarruf DA, Ogimoto K, Kaiyala K, Fischer JD, Matsen ME, Taborsky GJ, Schwartz MW, and Morton GJ. Leptin deficiency causes insulin resistance induced by uncontrolled diabetes. Diabetes. 59:1626-1634, 2010. PMCID: PMC2889761.
Ellacott KL, Morton GJ, Woods SC, Tso P, and Schwartz MW. Assessment of feeding behavior in laboratory mice. Cell Metab. 12:10-17, 2010. PMCID: PMC2916675.
Baskin DG, Kim F, Gelling RW, Russell BJ, Schwartz MW, Morton GJ, Simhan HN, Moralejo DH, and Blevins JE. A new oxytocin-saporin cytotoxin for lesioning oxytocin-receptive neurons in the rat hindbrain. Endocrinology. 151:4207-4213, 2010. PMCID: PMC2940497
Koch C, Augustine R, Steger J, Ganjam G, Benzler J, Pracht C, Lowe C, Schwartz M, Peter S, Anderson G, Grattan D, Tups A. Leptin rapidly improves glucose homeostasis in obese mice by increasing hypothalamic insulin sensitivity. J Neurosci. 30:16180-16187, 2010.
German J, Thaler JP, Wisse BE, Oh-I S, Sarruf DA, Matsen ME, Fischer JD, Taborsky GJ, Schwartz MW, and Morton GJ. Leptin activates a novel CNS mechanism for insulin-independent normalization of severe diabetic hyperglycemia. Endocrinology. 152:394-404, 2011. PMCID: PMC3037161.
Morton GJ, Kaiyala K, Fischer JD, Ogimoto K, Schwartz MW, Wisse BE. Identification of a physiological role for leptin in the regulation of ambulatory activity and wheel running in mice. Am J Physiol Endocrinol Metab. 300:E392-401, 2011. PMCID: PMC3043625.
Lu M, Sarruf D, Talukdar S, Sharma S, Li P, Bandyopadhyay G, Nalbandian S, Fan W, Gayen JR, Mahata SK, Webster N, Schwartz M, Olefsky JM. Brain peroxisome proliferator-activated receptor gamma promotes obesity and is required for the full insulin-sensitizing effect of thiazolidinediones. Nat Med. 17:618-622, 2011. PMCID: PMC3380629.
Choi SJ, Yablonka-Reuveni Z, Kaiyala KJ, Ogimoto K, Schwartz MW, Wisse BE. Increased energy expenditure and leptin sensitivity account for low fat mass in myostatin-deficient mice. AM J Physiol Endocrinol Metab. 300:E1031-1037, 2011. PMCID: PMC3118591.
Diano S, Liu Z-W, Jeong JK, Dietrich MO, Ruan H-B, Kim E, Suyama S, Kelly K, Gyengesi E, Arbiser JL, Belsham DD, Sarruf DA, Schwartz MW, Bennett AM, Shanabrough M, Mobbs CV, Yang X, Gao X-B, Horvath TL. Peroxisome proliferation-related control of reactive oxygen species sets melanocortin tone and feeding in diet-induced obesity. Nat Med. 17:1121-1127, 2011. PMCID: PMC3388795.
Tateya S, Rizzo NO, Handa P, Cheng AM, Morgan-Stevenson V, Daum G, Clowes AW, Morton GJ, Schwartz MW, Kim F. Endothelial nitric oxide/cGMP/vasodilator-stimulated phosphoprotein signaling attenuates kupffer cell activation and hepatic insulin resistance induced by high-fat feeding. Diabetes. 60:2792-2801, 2011. PMCID: PMC3198085.
Handa P, Tateya S, Rizzo NO, Cheng AM, Morgan-Stevenson V, Han CY, Clowes AW, Daum G, O'Brien KD, Schwartz MW, Chait A, Kim F. Reduced vascular nitric oxide-cGMP signaling contributes to adipose tissue inflammation during high-fat feeding. Arterioscler Thromb Vasc Biol. 31:2827-2837, 2011. PMCID: PMC3342311.
Morton GJ, Thatcher BS, Reidelberger RD, Ogimoto K, Wolden-Hanson TW, Baskin DG, Schwartz MW, Blevins JE. Peripheral oxytocin suppresses food intake and causes weight loss in diet-induced obese rats. Am J Physiol Endocrinol Metab. 302:E134-E144, 2012. PMCID: PMC3328087.
Thaler JP, Yi C-X, Schur EA, Guyenet SJ, Hwang BH, Dietrich MO, Zhao X, Sarruf SA, Izgur V, Maravilla KR, Nguyen HT, Fischer JD, Matsen ME, Wisse BE, Morton GJ, Horvath TL, Baskin DG, Tschöp MH, Schwartz MW. Obesity is associated with hypothalamic injury in rodent models and humans. J Clin Invest. 122:152-162, 2012. PMCID: PMC3248304.
Buchner DA, Geisinger JM, Glazebrook PA, Morgan MG, Spiezio SH, Kaiyala KJ, Schwartz MW, Sakurai T, Furley AJ, Kunze DL, Croniger CM, Nadeau JH. The juxtaparanodal proteins Cntnap2 and Tag1 regulate diet-induced obesity. Mammalian Genome. 23:431-432, 2012.
Mehta S, Melhorn SJ, Smeraglio A, Tyagi V, Grabowski T, Schwartz MW, Schur EA. Regional brain response to visual food cues is a marker of satiety that predicts food choice. Am J Clin Nutr. 96:989-999, 2012. PMCID: PMC3471210.
Benzler J, Ganjam GK, Kruger M, Pinkenburg O, Kutsche M, Stohr S, Steger J, Koch CE, Olkrug R, Schwartz MW, Shepherd PR, Grattan DR, Tups A. Hypothalamic glycogen-synthase-kinase 3β has a central role in the regulation of food intake and glucose metabolism. Biochem J. 447:175-184, 2012. PMCID: PMC3679888.
Meek T, Wisse B, Thaler J, Guyenet S, Matsen M, Fischer J, Taborsky Jr. G, Schwartz M, Morton G. BDNF action in the brain attenuates diabetic hyperglycemia via insulin-independent inhibition of hepatic glucose production. Diabetes.62:1512-1518, 2013. PMCID: PMC3636618.
Guyenet S, Matsen M, Morton M, Kaiyala K, Schwartz M. Rapid glutamate release in the mediobasal hypothalamus accompanies feeding and is exaggerated by an obesogenic food. Molecular Metabolism. 2:116-122, 2013. PMCID: PMC3817387.
Matsen ME, Thaler JP, Wisse BE, Guyenet SJ, Meek TH, Ogimoto K, Cubelo A, Fischer JD, Kaiyala KJ, Schwartz MW and Morton GJ. In uncontrolled diabetes, thyroid hormone and sympathetic activators induce thermogenesis without increasing glucose uptake in brown adipose tissue. Am J Physiol Endocrinol Metab. 304:E734-E746, 2013. PMCID: PMC3625754.
Lu M, Sarruf DA, Li P, Osborn O, Sanchez-Alavez M, Talukdar S, Chen A, Bandyopadhyay G, Xu J, Morinaga H, Dines K, Watkins S, Kaiyala K, Schwartz MW, Olefsky JM. Neuronal Sirt1 Deficiency Increases Insulin Sensitivity in Both Brain and Peripheral Tissues. J Biol Chem. 288:10722-10735, 2013. PMCID: PMC3624452.
Guyenet SJ, Nguyen NT, Hwang BH, Schwartz MW, Baskin DG, Thaler JP. High-fat diet feeding causes rapid, non-apoptotic cleavage of caspase-3 in astrocytes. Brain Res. 1512:97-105, 2013. PMCID: PMC3684737.
Lee D, Thaler JP, Berkseth KE, Melhorn SJ, Schwartz MW, Schur EA. Longer T2 relaxation time is a marker of hypothalamic gliosis in mice with diet-induced obesity. Am J Physiol Endocrinol Metab. 304:E1245-E1250, 2013. PMCID: PMC3680680.
Morton G, Matsen M, Bracy D, Meek T, Nguyen H, Stefanovski D, Bergman R, Wasserman DH, Schwartz MW. FGF19 action in the brain induces insulin-independent glucose lowering. J Clin Invest. 123:4799-4808, 2014. PMCID: PMC3809800.
Schwartz MW, Seeley RJ, Tschöp MH, Woods SC, Morton GJ, Myers MG, D'Alessio D. Cooperation between brain and islet in glucose homeostasis and diabetes. Nature. 503:59-66, 2013. PMCID: PMC3983910.
Berkseth K, Schur E, Schwartz M. A Role for Natriuretic Peptides in the Central Control of Energy Balance? Diabetes. 62:1379-1381, 2013. PMCID: PMC3636633.
Schwartz MW, Baskin DG. Leptin and the brain: then and now. J Clin Invest. 123:2344-2345, 2013. PMCID: PMC3668840.
Thaler JP, Guyenet SJ, Dorfman M, Wisse BE, Schwartz MW. Hypothalamic inflammation: Marker or mechanism of obesity pathogenesis? Diabetes. 62:2629-2634, 2013. PMCID: PMC3717869.
Gao Y, Ottaway N, Schriever SC, Legutko B, García-Cáceres C, de la Fuente E, Mergen C, Bour S, Thaler JP, Seeley RJ, Filosa J, Stern JE, Perez-Tilve D, Schwartz MW, Tschöp MH, Yi CX. Hormones and diet, but not body weight, control hypothalamic microglial activity. Glia. 62:17-25, 2014.
Morton GJ, Kaiyala KJ, Foster-Schubert KE, Cummings DE, Schwartz MW. Carbohydrate feeding dissociates the postprandial FGF19 response from circulating bile acid levels in humans. J Clin Endocrinol Metab. 99:E241-E245, 2014. PMCID: PMC3913810.
Morton GJ, Meek TH, Schwartz MW. Neurobiology of food intake in health and disease. Nat Rev Neurosci. 15:367-378, 2014. PMCID: PMC4076116.
Schwartz MW, Tschop M, Zeltser LM. A mother's influence on metabolic disorders. Nat Med. 20:244-145, 2014.
Rojas JM, Schwartz MW. Conrol of hepatic glucose metabolism by islet and brain. Diabetes Obes Metab. In press, 2014.
Berkseth KE, Guyenet SJ, Melhorn SJ, Lee D, Thaler JP, Schur EA, Schwartz MW. Hypothalamic gliosis associated with high fat diet feeding is reversible in mice: a combined immunohistochemical and magnetic resonance imaging study. Endocrinology. 155:2858-2567, 2014. PMC Journal – In Process.
Ho JM, Anekonda AV, Thompson BW, Zhu M, Curry RW, Hwang BH, Morton GJ, Schwartz MW, Baskin DG, Appleyard SM, Blevins JE. Hindbrain oxytocin receptors contribute to the effects of circulating oxytocin on food intake in male rats. Endocrinology. 155:2845-2857, 2014. PMC Journal – In Process.
Laeger T, Henagan TM, Albarado DC, Redman LM, Bray GA, Noland RC, Munzberg H, Gettys TW, Schwartz MW, Morrison CD. FGF21 is an endocrine signal of protein restriction. J Clin Invest. In press, 2014. PMC Journal – In Process.
Spiezio S, Amon L, McMillen T, Vick C, Houston B, Caldwell M, Ogimoto K, Morton G, Kirk E, Schwartz M, Nadeau J, LeBoeuf R. Genetic determinants of atherosclerosis, obesity and energy balance in consomic mice. Mammalian Genome. In press, 2014.
Current Collaborations:
Within the Diabetes and Obesity Center of Excellence and its Affiliated Members
Denis Baskin, PhD
Ernie Blevins, PhD
Renee LeBoeuf, PhD
Jay Heinecke, MD
Steven Kahn, MB, ChB
Francis Kim, MD
Greg Morton, PhD
Joshua Thaler, MD, PhD
Brent Wisse, MD
Vincenzo Cirulli, MD
Lab Members:
Jarrad Scarlett, MD, PhD
Jennifer Rojas, PhD
Kenjiro Muta, PhD
Hong Nguyen
Kayoko Ogimoto, PhD
Miles Matsen
Nick Acharya
Vincent Damian
Jarrell Nelson
Loan Nguyen
Trista Harvey
Kevin Velasco
Jenny Brown
Chelsea Kasper


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The most common questions I get on this blog are about the master cleanse and weight loss so I thought I would take a minute and answer some of those today. If the master cleanse is something you would like to try I would encourage you to sign up for my free newsletter at the bottom of this post, when you do I'll email you a free guide for doing the master cleanse.
I was going through these blogs. Suddenly a question came in my mind…I want to try MC specifically for the weight loss..but one of the blogs says that it is temporary.we really need to work out to loose weight.is it a reality that the weight loss is temporary in this case as i am not fatty i just want to loose weight from hip and the waist line as i have developed flabs….so please help.
While you can lose a significant amount of weight on the master cleanse, and keep most of it off (you'll gain back some water weight) the real weight loss benefits come after you finish the master cleanse. Most people will find that they no longer consume as much food as they did prior to the master cleanse, and the food they do crave is usually much healthier.
Here's some more info on losing weight after the master cleanse
Next we have a reader who wants to accomplish the opposite. They want to know how to do the master cleanse without losing weight:
I am interested in the cleanse for removal of toxins and NOT for weight. loss. I have always been thin with a high metabolism. I don't want to lose wt. is the master cleanse still for me? I am worried about doing it for 10 days straight, not only for convenience factors but because my metabolism is unusual and i don't want to lose weight or wind up feeling faint, etc., especially when I'm working.
This is a good question that doesn't get talked about much. Here's a post I made that will help you do the master cleanse without losing too much weight

subset: commoncrawl


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The model's struggles are taking a toll on her family, but they're still keeping the faith — she has such a loving support system.
Lauren Scruggs' recovery after her horrific airplane accident has been well-documented, and now her loving mother is giving an update on the trials and tribulations on the family.
Lauren, 23, and her family are finally coming to terms with the extent of her injuries, her mother revealed on their CaringBridge blog.
"The last three weeks, we all have been running on adrenaline, and now some of the reality is hitting," she writes. "Now that the excitement of Christmas is over, we are continuing the marathon of recovery, constantly being reminded that this is not a sprint, but a MARATHON……..a long rode for Lauren, and us, as her family. We trust Jesus, but, being human, this is hard…..very very hard. Life stopped as we knew it, and changed overnight."
We're keeping the Scruggs family in our prayers through this tough time.
— William Earl
More Lauren Scruggs News:
- Lauren Scruggs' Community Raises $10,000 For Her Recovery
- Model Lauren Scruggs Christmas Miracle: Her Latest news 'Positive, Hungry And Cheery
- Lauren Scruggs Now Exercising Regularly & Dressing Herself
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Shudder when turning?
Ok I am new to this Jeep, only had it for a month and only driven it a few times. It is an 06 GC limited 5.7 with 40k on it. the problem is when I turn real sharp from a stop I notice a shudder coming from the rear. My wife says it is when turned in either direction. Is it the diff or a charictaristic of the awd system? Has anyone noticed this before?
Re: Shudder when turning?
Change the diff fluid and I bet your problem will be solved.
Re: Shudder when turning?
I would say it's because of the diff fluid, but more specifically the limited slip additive has broken down or is not there. Definitely change it and include the LSD additive and it should be gone.
Side question...does anybody have that feeling coming from the front as I'm turing in reverse only? I'm wondering if it's as simple as fluid or do I go thru the BS of taking it to the dealer (3 mo used car warranty)
Re: Shudder when turning?
Re: Shudder when turning?
I figured that it might be a fluid prob. I'll change it to see but just wanted to ask before I called the dealer to complain. :thumbsup:
Re: Shudder when turning?
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The following entry was written by Natalie Valdes, Class of 2013.
Transitioning to life in the city can be a big change. With Emerson's location in the heart of downtown Boston it's important to be aware of your surroundings at all times, but also know that Emerson takes every possible measure to keep its community safe on and around campus. Below is a breakdown of the systems in place to put you at ease:
- The Emerson Police Department has on office on campus that is staffed 24/7 by officers who are Massachusetts state-trained and -certified police officers.
- All buildings are monitored by Securitas officers who are employed by a national security company. You'll have to swipe your Emerson ID to get into any academic building.
- The Residence Halls are a 24 hour ID-tap system, and you can only gain access to the building you live in. If you don't live there, you'll have to be signed in and out by a student who does live there. Guests who are not Emerson College students must also be signed in and out and leave a valid ID at the front desk.
- Emerson is prepared for emergency communication through an emergency notification system called Blackboard Connect. All students must register their contact information and an emergency contact as well. In case of any emergency on campus or in Boston, they will call, text, and email everyone at once. Read more about emergency preparedness here.
- A taxi voucher system is provided through a local cab company called Town Taxi. Students can carry a voucher in the event they need a cab and are without cash or a credit card. The fare gets added to your tuition bill at the end of the semester. Some local cab companies also accept the Emerson ID as a form of payment, so you never have to feel like you can't get home safely.
- Another way to feel secure at any time is to request the walking safety escort service provided by ECPD. You can have an officer accompany you to any of Emerson's buildings as well as the T station or a nearby intersection.
- Blue light phones are installed in the Boston Common across the street from Emerson. They can be used to report a crime or emergency or to request immediate assistance.
With all these helpful services, it's still worth mentioning that being aware of your surroundings and traveling in groups is always smart. Making Emerson a safe place to call home for our faculty, staff, and students is an important consideration for our community.


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Can Outsourcing Save Sony?
Outsourcing isn't a word that executives in Japan like to toss around. Japan Inc. prefers to tie its fortunes to state-of-the-art factories that churn out chips, cars, and flat-screen TVs for the global market. But when Sony (SNE) Chief Executive Howard Stringer announced on Jan. 22 that he was considering drastic cost-cutting steps for the company's core electronics division, outsourcing topped his to-do list.
The shift marks a minor victory for Stringer. After more than three years at the helm, Stringer finally appears to be breaking the company's addiction to manufacturing, and to be channeling ever more resources into developing and designing products that users crave. To show he now really means business, the Welsh-born American CEO has said he will close five or six of the company's 57 plants globally and slash the company's budget for factories and chipmaking equipment by a third over the next fiscal year, ending March 2010. "There is no aspect of Sony that isn't being examined right now," Stringer told journalists in Tokyo last week. "We have to move very, very quickly and control our costs."
Sony will spend the next couple of months drawing up a detailed plan. But Stringer appears to have made up his mind about outsourcing one product: TVs. The TV division accounts for 10% of Sony's overall sales but hasn't made a profit since it launched the Bravia brand of flat-panel TVs in 2005. By the March 2008 fiscal yearend, the division's three-year losses had reached $2.3 billion. Goldman Sachs (GS) predicts the division could bleed another $1.1 billion this year.
An In-House Tradition
The shift toward outsourcing is the clearest sign yet that Stringer wants Sony to act more like Apple (AAPL) or Cisco (CSCO). They consistently earn fatter profit margins by designing their own products and leaving manufacturing to others, and have made serious inroads into portable music players and home entertainment systems, where Sony was once king. In contrast, Sony, like many Japanese tech manufacturers, still makes many of its own products in-house, a process known as vertical integration, which "tends to lead to higher overall costs because you need extra layers of management to coordinate all the activities," says Robert Kennedy, a professor at the University of Michigan's Ross School of Business and author of The Services Shift.
Sony's domestic factories account for half of overall sales. They provided a boost to earnings while the yen was weak and overseas demand strong. But recently, when the yen surged and the global economy faltered, Sony found itself badly exposed. The sudden reversal was partly to blame for Sony's grim earnings forecast this fiscal year—an expected $2.9 billion operating loss, its first in 14 years.
Before the global financial crisis wiped out consumer spending, Sony seemed confident the TV unit would soon be profitable. The company's LCD-TV sales had risen over the past three years, from a little over 1 million units to as many as 15 million expected this fiscal year. Last year, Sony was second in global LCD-TV sales, behind Korea's Samsung Electronics.
But the TV unit's problems are now confounding Stringer's efforts to fix what ails Japan's best-known tech brand. Sony officials say they are rushing to centralize TV development and design and consolidate production in Japan after closing one of two domestic plants.
"Before the electronics division can be healthy, TVs must be profitable," Ryoji Chubachi, who heads the electronics unit, said last week.
Keeping Secrets
What will Stringer's outsourcing strategy look like? So far, he isn't saying, but experts predict Sony will continue to make ultra-thin high-end TVs on its own. That's where the company can command a premium and earn higher margins. Keeping cutting-edge technology in-house also prevents innovations from being leaked to rivals.
For the small and midsize sets, however, Sony might hire one or more manufacturers in Taiwan or Hong Kong. Wistron, Qisda, AmTRAN Technology, TPV Technology, and Foxconn International, a subsidiary of Taiwan's Hon Hai Precision Industry, have all made LCD TVs for Sony in the past but only in small volumes—less than 8% of Sony's overall TV production last year, according to estimates from market researcher iSuppli. "You might want to keep the premium product, but the commodity product you don't need to be manufacturing yourself," says Macquarie Securities' David Gibson. "It's a simple principle of globalization."
In practice, though, it's anything but simple. To be sure, Sony already relies on contract manufacturers to make some of its point-and-shoot Cybershot digital cameras, Vaio laptops, and PlayStation video game consoles, but Sony's TV unit has always jealously protected its secrets, and outsourcing would mark a serious departure from traditional practice. Currently the company buys the specialized sheets of glass from its joint venture with Samsung and ships them to high-security plants in Asia, North and South America, and Europe for assembly. Most of its suppliers get design specifications for specific parts but know little about the entire assembly process.
Outsourcing doesn't work that way. It involves more collaboration and information-sharing. Gartner (IT) analyst Yuko Adachi says many U.S. companies begin discussions with contract manufacturers as early as the conceptual or design phase. "It's more of an alliance," she says. Many tech giants have tried to outsource manufacturing to tech companies in Asia, only to end up repeatedly sending teams of designers and engineers to help those companies get up to speed, says iSuppli analyst Adam Pick. Still, says Pick, "If managed properly, [outsourcing products] can be a phenomenal bonus."
But outsourcing alone isn't going to help Stringer, who has other priorities as well. For instance: wedding Sony's products to its vast library of movies, TV shows, and music. Last fall, Sony streamed the Hollywood blockbuster movie Hancock to Sony TVs connected to the Internet. At this year's Consumer Electronics Show in Las Vegas, the company showed off Net-linked TVs featuring software from Yahoo! (YHOO) that lets viewers check out content from popular Web pages. The key to success there, too, lies in making TVs more efficiently. "We have to find a way to embrace network services, to provide the kind of sustainable differentiation that will give us attractive margins," Stringer said. "In order to do that, we've obviously got to bring down the cost of our televisions."


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More Quality Time, More Savings At Your Favorite Resorts
Get more time to enjoy all of the great dining, shopping, and entertainment that the Grand Strand has to offer, while saving on your North Myrtle Beach vacation with our Weekly Condo Rates.
Weekly Condo Rates provide savings at 3 participating North Myrtle Beach resort locations by removing added costs for services such as daily housekeeping and others.
To book a Weekly Condo Rate at Bay Watch Resort, Atlantic Breeze Ocean Resort, or Harbourgate Marina Club in North Myrtle Beach, call 877.779.7376 or Book Online with a reservation of 7 nights or longer and select the "Weekly Condo Package" rate plan.
Please Note: In order to maximize the savings to our guests, Weekly Condo Rates do not include daily housekeeping service. Weekly Condo Rates feature a unique set of policies and fees that differ from our nightly rental policies. We recommend that you review our Weekly Rental Policies prior to making a reservation.
*Terms and Conditions
Valid on 7 night stays or longer. Savings are based on published rates and will vary based on resort, room type, time of booking, dates of travel, length of stay, and number of occupants. Offer includes only accommodations and specifically excludes travel costs and other expenses that may be incurred. Accommodations and travel times are subject to availability and confirmed on a first come, first served basis. Offer includes accommodations and specifically excludes travel costs and other expenses that may be incurred. Taxes, additional fees and charges may apply. Daily housekeeping service is not included with Weekly Condo Rates, but can be added for an additional fee. Promotional discounts and offers may not apply to all properties. Cannot be combined with any other offers, discounts or package rates and is valid on new reservations only. Other restrictions may apply. Offer void where prohibited by law. All prices are based in U.S. dollars (USD).
Weekly Condo Rates Are Available At These Resorts
Bay Watch Resort & Conference Center
Features & Amenities:
- Studios and 1, 2 and 3 Bedroom Suites available
- Premier oceanfront North Myrtle Beach location with beachfront access
- 18 water amenities on site including indoor and outdoor pools, lazy rivers, hot tubs and kiddie pools
- On-site dining including oceanfront restaurant, sports bar & grill, and seasonal beach bar
Added Benefits Available At This Resort:
Atlantic Breeze Ocean Resort
Features & Amenities:
- 2 and 3 Bedroom Suites available with fully equipped kitchens and glass paneled balconies
- Oceanfront North Myrtle Beach location with beachfront access
- Over 5 water amenities on-site including outdoor pool, lazy river, hot tubs, and seasonally enclosed 5th floor pool
- Oceanfront Fitness Center
Added Benefits Available At This Resort:
Harbourgate Marina Club
Resort Features & Amenities:
- 1, 2 & 3 Bedroom Suites Available
- Convenient Location On The Intracoastal Waterway In North Myrtle Beach
- Full Service Marina With Access To Water Sport Rentals, Cruises & Tours
- Outdoor Pool & Hot Tub Deck Overlooking The Waterway
- Business Center & Fitness Center
Added Benefits Available At This Resort:
Also, Look For These Added Benefits Available During Your Stay
Note: Not all benefits listed below may be applicable to all resorts and/or travel dates available in this promotion. Availability may vary.
Receive unlimited access to Wild Water & Wheels Water Park included with all summer stays.
All Oceana Resorts guests enjoy unlimited free round of golf at Lost Mine Miniature Golf before 7:00 PM.
Oceana guests pay no greens fee at select Myrtle Beach golf courses in summer and select months in winter.
Oceana guests receive special discounts at a multitude of the area's best shopping, dining, and attractions.
Receive a special discount on select services at The Awakening Spa when you stay with Oceana Resorts.
Families visiting during the summer can take part in fun activities including games, crafts, and special events.
Feel Confident In Your Vacation Investment
Secure your vacation investment! If your plans suddenly change, this optional protection plan will offer you peace of mind.


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Nike to Release Michael Jordan's Air Jordan 9 'Barons' This Weekend
This weekend, Michael Jordan's Air Jordan 9 'Barons' will release to pay homage to his days in the minor leagues. The legendary basketball player fell in love with baseball as a kid and tried his hand at making it big on the diamond. Check out the shoes that commemorate his short lived baseball career.
The release date for the Air Jordan 9 'Barons' is April 5th at all Jordan Brand retailers.
The retro Air Jordan 9 feature a wolf grey and white dominated upper with the accent color of black to bring in a nice contrast. The wolf grey nubuck mudguard divides the black midsole and white quarter paneling. The inner lining is dressed in pinstripes while '45' is embroider on the heel instead of the traditional '23.'
MJ retired from basketball after his father was murdered and some believe baseball was his way of grieving. He later returned back to playing basketball to win three more championships. What are your thoughts on his upcoming retro Air Jordan release?


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ED Magedson – Founder
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Grantmaster ,deluxe Editionwww.grant master.com Las Vegas, Nevada U.S.A.
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The strong eat the weak for lunch.
At least that's true in the battle between small fish and birds with large beaks. But there's a point for all of us in that photo on top — a wood stork enjoying a late afternoon snack along an inlet near Vero Beach in Florida.
I've been down here for several days for our annual meetings with alumnae on both coasts, and we've had a wonderful time! I never tire of telling the stories of how Trinity has grown and flourished — once a small fish in a large and scary sea of big universities in Washington, Trinity today is strong and thriving with terrific students and faculty, and great ambition for the future.
Since our alumnae luncheons in Florida take place in towns on both sides of the state, I have spent some time driving from place to place, and along the way I occasionally stopped to see the abundant wildlife. Of course, my trusty long lens is always nearby (it's well worth the trouble to pack it, there's so much wildlife to see just about everywhere I look while driving around!)
Pelicans were much in the news last year as among the species gravely harmed in the BP oil spill in the Gulf of Mexico. Little was told at that time of the even larger threats to pelicans in the last century. Near Vero Beach is a habitat now known as Pelican Island National Wildlife Refuge.
This was actually the very first NWR in the United States, established with the leadership of Theodore Roosevelt who was a champion of conservation. When Roosevelt first visited Pelican Bay, the place teemed with the big birds and many other waterfowl. But hunting for bird feathers in the early part of the 20th Century decimated the population, and land development further destroyed the habitat.
But thanks to a concerted effort to restore the habitat and protect wildlife in Florida, pelicans, wood storks, and other waterfowl are making a small comeback.
Most birds spend their entire day looking for food, eating, or resting. The great blue heron, below, appeared to be resting in the shade of a large lilypad…
But there was a sudden pounce, followed by a triumphant emergence:
Nobody looked more surprised than the lunch entree…
Meanwhile, the wood stork, having snatched that fish away from the pelicans, finished her tasty snack and settled down for an afternoon in the sun.
Remember: Darwin was right!


text: All right so I had time to kill on Sunday. After being appalled at the crap in the Penguin store. I walked Through the glitzy marble store front of Sean John. Located on 5th Ave at 41st street across from the NY Public Library. The store's location seems  so wrong. Again, I am not the typical Sean John Target customer. 47 year old, not into the hip hop world at all. I was wearing a beaten up leather jacket and a black hat with a stingy brim. I was not once asked if I needed help. The quality of the merchandise was actaully pretty good. Both piece goods and construction. Good asian factories. The pricing was not terrible. Of course I was not fond of the styling or the logo that was on everything. There was one shirt in a 5X. I don't think I have ever made anything that big before. They even had a canvas front suit that was made in China for $600. It was a decent make. But I know the mark up must be obscene. LDP that suit could not cost them more then $90. I do have a bit of a prejudice against the Sean John line. I made sample garments for two fashion shows. BOth times they were late in paying me. They needed shirts made in three days. I delivered on time. Why couldn't they pay me as quickly. I also had some personal dealing with Mr. Diddy as well. He wore one shirt in the show that I made for him. His manners left something to be desired. Lets leave it at that. Carl www.cego.com


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Metallic Base/Clear Issue
I am shooting a fender and bumper cover using PPG Omni with metallic base (silver) and clear. The base laid down fine, and after the final coat I let it flash off for extra time (2 hrs at the recommended temp).
When I shot the clear, the first layer when down... second layer had a few runs. I thought no big deal, I'll wetsand that out later. So I proceeded to throw down the third and final layer, then let it cure for 2 days.
So today I went to knock the runs down with 1000, and after levelling the clear, I can clearly see where every one of the runs was, the metallic is reflecting differently. I did not break through the clear... it is almost like the basecoat was absorbed up into the clear coat or the base sagged after the second coat of clear. Is this even possible?
It is absolutely possible and you will need to shoot some color over the top and re-clear the whole thing to correct it properly.
The run in the clear coat was full of solvent and it soaked into the base.
What he said ^^^^^^^^^^, Stu
You avoid it by not getting runs. Letting the basecoat flash further is going to help, but not much. That run in the clear is FULL of solvent and it's going to lay there on the base and loosen it up. Just don't get the runs in the clear.
Okay, I will be extra careful with the clear this time.
Is this something that the new low VOC paints are more succeptible to? In the past I would always do a heavy final coat of clear to make sure there were no dry spots. Before this job, I have never had any issues with the base mixing up into the clear even if I had the occasional run. Previous experiences were with with tri-stage candy, so maybe the midcoat isolated the metallic?
I don't have any technical explanation but the way I see it is the more high solids products of today don't flash as fast so they are just laying there wet and soaking in. They also use things like acetone and oxhall (spelling?) as a solvent because they are heavy and don't go up into our atmosphere, thus "low VOC" (or NO VOC actually) and they just sit there in the film taking a long time to leave.
That's how my brain sees it anyway. :sweat:
I re-shot it, and was extra careful with the clear... the first 2 coats were basically dusted on, and the 3rd and 4th progressively wetter. Came out perfect.
I think you are right in that it has something to do with the new paint. This is PPG Omni MBX, which is essentially a 1K.... there is no hardener, only the base and reducer.
When I shot tri-stage and did other jobs in the past, I always used DBU or DBC with DX57 hardener, which when cured will not allow the base coat to "re-melt" as easily if there was extra solvent from runs in the clear.
A lot of guys put a bit of activator in their base coat to help control the metallic even though the base coat does not call for activator.
So this job never ends. We go the fender and bumper cover based and cleared, installed them on the car and went to cut and buff it today after sitting for 4 days.
I guess I had the buffer too fast and melted the paint where the fender meets the a-pillar. It went through the clear into the base.
I sanded it out, and then went to shoot base over top with an airbrush, but it keeps reacting and lifting along the feathered edge of the clear. Do I need to shoot a primer sealer across the holes where it broke through the clear?
Often if you spray the base dryer, use a fast reducer and let it flash good you can get away with it.
If it's a real small place you can get away with murder, you don't want to push this out too far though the adhesion can be poor because you aren't spraying wet enough for it to stick to the previous coat good.
But I have pushed this to the limit, I am talking "dusting" a little base over, NO WHERE NEAR coverage, I am talking something like "overspray" no where near a "coat". Just dust some, leave it for a while and come back and dust a little more, leave it. Build up a layer over the top of that sensitive area one dust after another until you have it covered. Then a "light coat" to distribute the metallic properly and to get it a "little" wet so it sticks around the edges. Let that flash a long time, depending on the shop temp, we could be talking hours. Then come back and clear over it.
This is a gamble, but you would be surprised how much you can get away with. Like I said, it's cheating and if you push it with too large of an area you are going to have trouble though.
But think about it, if the solvent in the base is what is causing this lifting, the and no solvent (paint) painted there it doesn't lift, there is a point of solvent you could apply there, a very tiny amount that won't lift it. So you do just that, apply that tiny amount. Then again, and again, and again until it's covered. Once it's covered it is often a barrier.
The best way is to sand that area out and get some primer down. But that too can lift it, and you have to spray the primer real dry too. Or use a water borne primer which will cover just about anything.
I will never use a non hardened basecoat again. The cost savings are not worth the headache if things don't lay down perfect.
Shot it last night with the hardener and it worked like a dream. I am sure there are some people who can shoot MBX day in and day out with no issues, but for me the hardener makes the stuff a lot easier to work with especially if it is metallic.
This job is finally done. Thanks to all for the advice.
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|Thread Tools
New to forum, just stopping by to say hello
Hello all, and let me say that your site is great. I have been reading lots of the posts made here in the interiors section as that is one thing that really intrigues me. I ordered one of the books that has been mentioned in here so I hope that it helps clear up some of my "Dumb Questions" LOL I am hoping to redo the interior of my 38 Chevy Sedan so maybe with all thses posts, ideas and what I read, it'll go okay. If not then I'll turn to a upholstery guy and let him do it, But I am after the pride of doing it myself, so with luck it'll turn out okay. I have done sheet metal work in the past on racecars, building everything from door panels, dashes in door slammers, to ****pits, interior and bodies for dirt cars. The forming of the panels I think I might can handle, it's the fabric work that imtimidates me. Any way, I'm rambling on. The last thing to say is that the stuff I have seen from hotrodup, Kristkustoms, is very nice, you guys keep up the good work! Have a great day, Red
Welcome, the 38 Chevy is a great car, much luck in your restoration. I for one look foward to sharing information with another fellow rodder.
Welcome to the best site on the web, Red!
Don't hesitate to post questions ... I'm like you, looking forward to doing the interior on my 54 Chevy pickup this summer -- I'm gonna kick it off by putting a pair of Lincoln power seats in. Then I'll know what my color scheme is gonna be and I'll start making panels.
The interior section is my favorite, so I'm looking forward to getting into as many cool posts as possible. I've learned everything I know here! I just bought my truck last year (Jan 2003) and I've gotten so much help here it's hard to believe!
I don't know how to do interiors either, but between all the cool info in those books you mentioned (you probably got them from one of my links here) and all the helpful info we get here, I'm convinced that I'm gonna do a beautiful job on my truck! And I'll bet you'll do the same on your 38 Chevy!
54 Chevy Pickup
|Recent Interior posts with photos
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Posted by Duncan Jones on February 25, 2009
I get this question all the time because, let's face it, it's a significant decision. For example, an Enterprise Agreement (EA) renewal for an enterprise with the main desktop suite on, say, 10,000 PCs could cost around $1,500,000 per year. So what do you get for this outlay? You've already purchased a perpetual license for the relevant Microsoft products via your original EA, so the renewal is merely an extension of the maintenance element, which Microsoft calls Software Assurance (SA). Like most terms in Microsoft licensing, SA looks like an industry standard concept, but has sufficient Microsoft-specific nuances that confuses customers. The key differences from most vendors' software maintenance offerings are that SA:
Posted by Site Administrator on February 10, 2009
SUN announced the Glassfish portfolio today and makes a significant move towards a commercial open source business model.


text:
I don't have tonnes to update you with, hence the lack of posts. I have asked Michael for a camera for Christmas, so hopefully soon there will be decent quality photos on my blog?!
I have been so busy these past couple of weeks as Mike has been studying and spent all of last week at his parents place doing assessments. I have always had the upmost respect for single parents but being alone over nights with a teething toddler (hello 15th and 16th teeth!) has been plain hard so my respect has risen even further!
We had a gorgeous birthday party for a little friend with baby farm animals and all sorts of fun this weekend. Cam had a blast despite me being late!
This time of year is always busy for everyone. We have only a couple of little things to get for Cameron for his Christmas and birthday presents (he is born on New Years Eve!) but we have so much coming up in these last 6 weeks of 2011!
I have been so busy (& loving it) with organising & finalising presents for everything coming up! We have Cam's best matey's b'day, my nephew's b'day & Australia Zoo, a big Christmas, Cam's birthday & party – all before the end of the year!! Not to mention my baby shower plans for February. It's all so much fun!!
This weekend I've been focussing on Cameron's birthday plans. I've finalised a guest list, menu, the favours and printed out & readied all the invitations, decorations, labels and what not.
His party won't be as big as last year (thank goodness, our poor little house & my pregnant self couldn't handle that!) but I'm so looking forward to Cam's birthday because he knows what a birthday is & will love it all! He talks about birthdays a fair bit now and likes to blow out candles and thinks all balloons mean it's someone's birthday.
I'm not yet into the spirit of Christmas, but I'm looking forward to that too. Cammy waves at Santa now and said he'd like to ask for "a plane" from Santa (I assume a toy – hah!). However, I'm not convinced he'll be into the whole sitting-on-a-strangers-lap or getting-a-photo thing… which I'm absolutely fine about!
Aside from the craziness, there has still been plenty of time for normality. We have read and re-read books (Cam is loving all things phonics as well as expanding on his animal loves – newest faves being lizards, ants, rhinos and hippos), and sung many songs (new faves are 'little Peter Rabbit' & 'galumph went the little green frog').
Anyway, I'll leave you with our fun from today – playing with ice 🙂


text:
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text:
Brazilian Reginaldo and Gaetano D'Agostino scored the goals to give Siena a semi-final, first leg victory although it may live to rue Emanuele Pesoli's late own goal.
Napoli may still be favourite to progress ahead of next month's second leg in Naples but Siena can be well pleased with their work.
The visitors played a full-strength side while the Serie A strugglers rested several first choice players.
And yet they had more determination and cohesion as they put one foot in the final and a possible glamour tie against one of the country's heavyweights.
Juventus won by the same score away to AC Milan in the first semi-final, first leg.


text:
Rihanna shocked by Chris Brown's public apology
Brown, 20, who pleaded guilty to attacking the 'Umbrella" singer in June and was sentenced to five years supervised probation and community service, was also ordered to stay away from her.
He did not give any details about the incident on the advice of his attorney, but earlier this month he released a two-minute video on TMZ.com expressing his "deepest regret" for his actions. But for Rihanna, the video has left her reeling, as it has led to more publicity about the fall-out.
"She"s in total shock. It was like he gave her another blow, albeit one of a different kind," the Daily Express quoted a source as having told Britain"s Now magazine.
"All she knows is that it"s in the news again and that"s the one thing she didn"t want. She"s been trying to put it behind her and move on as fast as possible. They spoke earlier last week and Chris made no mention of any public statement then. She wishes he"d given her at least a heads-up about it. But that"s Chris, always thinking of himself first and forgetting how this would impact on her," the source added.


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Wow! Great photos-thanks for sharing.
Camps Bay, with no designer sunglasses? DIOS MIO!!
Trip Start Jun 10, 2010
14Trip End Jun 25, 2010
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Where I stayed
The Bay Atlantic Guesthouse, Camps Bay, Cape Town, S.A.
The mountains all have names, signal hill, Lion's Head, Table Mountain and behind our beautiful Guesthouse, The 12 Apostles. The owner of the Bay Atlantic, Bernie took us to see firing of The Noon Gun. This is a Cape Town tradition which has been observed since 1919. A cannon is fired at noon every day and the Capetonians observe 2 minutes of silence in remembrance and thanks to those who served in wartime
We watched USA vs Algeria in a pub with a bunch of other Americans! Camps Bay was crawling with Brits and Portugese. We went to the V&A Waterfront where we found throngs of soccer fans, activities and the Fifa Store! Marcus was called to a stage to play his vuvuzela! See the video! Finally we went to a german beer hall in cape town with hundreds of other germans to watch the 3rd game. We had tickets to this game but chose to see Cape Town rather than travel more to Johannesburg for the game.


text:
Read an Excerpt
"Mr. Reed, our facial recognition software has detected a match for the Barracuda in pit three near the dollar slots."
Nate smiled. Like a moth to a flame, Annie had walked right into his trap. He knew she couldn't pass up the chance to play at his poker tournament, even if it meant returning to the scene of the crime. As the owner and manager of the Desert Sapphire Hotel and Casino, it was easy to have Annie red-flagged by his security team. The moment she strolled back in to his casino he knew it.
"We have visual confirmation. She's on her way to the high-roller area." Gabriel Hansen, his chief of security, lifted his hand to his earpiece and listened intently for a moment before nodding in confirmation. "She's joined the Texas Hold'em game with Mr. Nakimori and Mr. Kline."
"Of course she has." Nate set aside his paperwork and made his way to the elevator. There was no time to waste. The Japanese businessman and the oil tycoon had credit lines in the millions, and they'd need every penny if he didn't get down there. They didn't call her the Barracuda for nothing.
"Do you need assistance with this, Mr. Reed?" Gabe was also his best friend, despite the formalities they used at work. Gabe knew what Annie's arrival meant. His offer to accompany him was less about work and more about helping his friend.
Nate sighed and straightened his navy silk tie. He suspected Gabe would relish handcuffing Annie and parading her through the casino so everyone would see. To be honest, he wouldn't mind that himself, but she'd never agree to his plan if he did. "No, I've got this handled."
A quick swipe of his identification card sent the elevator plummeting down the twenty-five floors from his suite to the main casino lobby. A soft chime announced his arrival, and the doors opened to the office corridors where casino operations took place.
The walk through the casino to the high-roller area wasn't long, but each step weighed more heavily on him than the last. Annie was here. In his casino. After three long years. He should be excited to finally confront her. To have his chance to exact his revenge and make her miserable. Or if not excited, perhaps smug. His plan was working just as he'd hoped it would. And yet he was none of those things.
His mouth was dry, his pulse racing in his throat. If he didn't know better, he might think he was nervous. Imagine that: Nathan Reed, millionaire casino owner, former most eligible bachelor in Las Vegas, nervous. It was a ridiculous idea. And yet Annie had always been his weakness.
Nate rounded the corner and spied the entrance to the high-roller lounge. Even across the casino floor, he could spot her. Her back was to him as she leaned over her cards, her legs crossed beneath the table. Her long raven hair spilled over the olive skin of her bare shoulders. Beside her Mr. Nakimori leaned back into his seat, throwing his cards down in disgust.
Nate stopped just behind Annie and placed a heavy hand on her shoulder. She didn't flinch. She'd been expecting him. Game on.
"Gentlemen," he said, flashing a confident smile at the other players at the table and extending a hand to each of them. "It's good to have you both back here at the Sapphire. Is everything going well for you this afternoon?"
Jackson Kline grinned wide and leaned back into his chair. "It was until this pretty little thing showed up. She's taken more of my money than my ex-wife."
Nate smiled and nodded. "Then I'm sure you gentlemen won't mind if I deprive you of her company."
"We're in the middle of a hand."
They were the first words she'd spoken to him since she disappeared. She didn't say "hello." Not even "I'm sorry" or "You're looking well." Just a complaint that he was interrupting her poker hand.
He leaned down and pressed his lips against the soft outer shell of her ear. The smell of her jasmine shampoo filled his lungs as he hovered near. The familiar scent was alluring and reminded him of the tangled sheets she left behind, but he wasn't going to fall prey to her this time. "We need to talk. Fold." The demand was simple and quiet, but powerful.
"Well, gentlemen-" Annie sighed "-I guess I'm done." She slid the cards across the table and reached up to gently extract Nate's hand from her shoulder. He complied, stepping back far enough to allow her to rise from her seat.
"Good afternoon," the men responded in their respective Southern and Japanese accents, although they both seemed visibly relieved to see her go.
Annie grasped her red leather handbag and strolled to the exit with Nate quick on her heels. He moved alongside her, scooping her elbow up with a firm hand and guiding her toward the elevator.
"Take your hands off me," she hissed through gritted teeth. She tugged against his grasp, but it was futile.
Nate couldn't contain a chuckle. "I will not. You and I both know what happened the last time I did that. If you'd prefer, I could have security escort you upstairs instead."
She came to a sudden stop, jerking Nate to turn back to her. Her azure-blue eyes were alight with anger. They penetrated him, a connection forming between them with a sudden snap of electricity. "You wouldn't dare," she said.
God, she was still beautiful. Nate felt the familiar pull in his gut, the heat flooding his groin. The sexual spark had always been there; it was what brought them together. It just couldn't keep them together. It pissed him off that he still reacted to her like this after everything she'd done.
"I wouldn't?" Nate retorted. Annie didn't know him at all. He leaned down, his face inches from hers. "You wanna call my bluff?" Nate didn't wait for an answer but quickly turned and tugged her behind him.
Annie silenced her protests and stopped resisting his pull. He didn't let go until they stepped off the elevator at his suite. She pulled away, turning left toward his office and dropping angrily onto the leather sofa.
"So?" she asked. "You've dragged me up here and cost me a five-thousand-dollar hand. What do you want?"
Nate avoided the couch, opting instead to lean against the large mahogany desk that had once been his grandfather's. He crossed his arms over his chest and took a deep breath. "I have a proposition for you, Barbara Ann."
Annie arched her eyebrow suspiciously at him, obviously not caring for his use of her given name. "You don't have anything I want, Nathan, or my lawyer would've asked for it already."
"That's not true. I can give you the one thing you've wanted for the last three years-a divorce."
Her blue gaze searched his face, probably looking for the catch. "You and your lawyer have been stonewalling the process for years. You've cost me a fortune in legal fees. And now you're just going to wrap it up in a bow and give it to me?"
"Not exactly." Nate smiled and turned to the bar to pour himself a scotch. He'd let her stew awhile and prolong the torture. She'd made him wait long enough. "Drink?" he offered with his glass held up, more out of politeness than a desire to be truly hospitable.
"You know I don't drink."
Nate stiffened. He'd forgotten. She hated the way alcohol made her feel out of control. It was amazing how the details could slip your mind when you were apart. What else had he forgotten? "A soda, then? Water?"
"No, I'm fine, thank you."
Nate dropped ice cubes into his own glass and nodded before pouring the golden liquid over it. "Very well." He took a sip, appreciating the warm sensation it lit in his stomach. It fueled his resolve and distracted him from the pangs of lust he was determined to ignore.
It was getting harder every minute he spent with her. There was something about Annie that made his blood sing. It was more than just her exotic beauty or her shrewd intelligence. He could still feel the silky slide of her ebony hair across his bare chest as she hovered over him. The musical sound of her laughter. All together it was an intoxicating combination. Just being around her again was enough to ignite the flames of his desire.
And then he would remember that she wanted a divorce. That she had left him in the night after less than two weeks of marriage without a word until he was served the papers.
He supposed he should be grateful that Annie had bothered to file for divorce. His mother hadn't gone to the trouble. She'd just disappeared and sent his father into a spiral of depression that nearly destroyed the Desert Sapphire and his grandfather's legacy with it. Nate was stronger than that. He'd rebuilt the hotel and helped transform the industry, even as she'd left him. He wasn't about to be broken by a woman.
Even one as breathtaking as Annie.
She watched him warily from her seat as he walked toward her and leisurely sipped his drink. "I know you haven't had a sudden change of heart. So what's going on?"
He certainly hadn't. Honestly, it pained him to finally give her what she wanted, but the tournament was more important. The organization that sponsored the most prestigious poker tournament in the industry had a long-standing agreement with another casino. To lure them to the Desert Sapphire, it had taken him three years and a few promises he needed Annie to help him keep.
"I am working on a side project of sorts during the tournament and you're just the right person for the job." He paused, sipping his scotch thoughtfully. "If I sign the papers and give you the divorce you want, you agree to help me."
"I don't understand. How could I possibly-" Nate cut her protest short with a wave of his hand. "I'm sure you've heard about the cheating problem the poker circuit is having. The rumors are getting fairly loud and the tournament sponsor's reputation is suffering for it. Everyone is anticipating they'll hit the tournament."
Annie sighed. "There's always rumors of cheating, but nothing ever comes of it. The people they catch are usually small potatoes compared to the amount of money exchanged in one of these events. What's the big deal?"
"Hosting the tournament is a huge draw for my hotel. As you well know, it's been held at the Tangiers for the last twenty years. Talking the organizers into moving it here had taken more than some nice negotiating. They wanted concrete guarantees that anyone cheating during the tournament would be caught and prosecuted, to send a message to the community."
"And why are they so confident that your team can do a better job than the Tangiers?"
"Because I have one of the best security systems in the business, with some of the most qualified staff you can hire. We go well beyond the typical measures most casinos employ."
"Seems like overkill to me. I hardly think you can stop cheating."
"This hotel was on the verge of going under when I took over from my father. He wasn't well at the time and people took advantage of the situation. Our biggest issue was people gaming the house, especially our own employees. I wouldn't tolerate that on my watch and invested in cutting-edge technology to stop it. Over the last five years, our estimated losses from cheating are down by eighty percent."
"Then why do you need me?" Annie crossed her arms defensively, pressing her breasts tight against the low V-cut of her sleeveless red silk top.
Just a quick glance at the soft curves of her femininity sent a sharp spike of need down his spine and forced him to turn away. "Because," he said, "I suspect this is a more elaborate and wellorganized operation than we're used to. More people are involved new faces with clean records. But we have to succeed. If we manage to bust this ring, I've got a guaranteed ten-year contract for the tournament. That's something my grandfather wouldn't have even hoped for."
"And what?" she prompted. "You think I know who's involved?"
"I think you probably have your suspicions. You've been active in the community for several years and have to have heard your share of stories." He lifted his gaze to meet hers. "I also think you could flush them out with the right motivation.''''
Annie leaped up from her seat, the nervous energy his proposal generated propelling her off the leather couch. "I'm not a snitch." There was no way she was going to ruin her reputation like that. Not for a divorce, not for the attentions of a charming, handsome man like Nate. Her honor was all she had in this business.
"If we do it right, no one will ever know that you are."
"And how's that? There are cameras everywhere. The odds are they have help on the inside, possibly even your own security guys and dealers. You don't think they'll notice us talking?"
"Nope. They won't."
He hadn't told her everything. Her game was poker, but Nate's game was chess. He was already three moves ahead of her. Annie hated being outmaneuvered. "Enlighten me."
His mouth curved up in a sly smile. "There are no cameras in here."
Annie looked around the office and down the dark corridor to his suite. She sincerely hoped not. They would've gotten an eyeful during their wedding night. "And no one will find it suspicious that I'm up in your suite? That I'm spending all my time with the casino boss?"
"Why shouldn't you spend time with your husband?"
Annie's blood turned to ice in her veins. If there was one thing she clung to, it was that no one knew about their mistake. Their marriage had been a secret she'd shared only with her sister, Tessa, and her mother. Yes, she and Nate would've told people eventually, but in the beginning they'd been far too wrapped up in one another to share the good news. Then it was over. "You don't think people will question that we're suddenly married? That we're together again after all this time apart?"
Nate shrugged. "We'll just tell the truth. We got married three years ago. It didn't work out. We separated. You came back for the tournament and we reconciled."
"That's not the truth."
"No, but the best lies have a good bit of truth in them. The paper trail will back up our story. And we won't give them any reason to doubt it." He smiled a wide, confident smile that started to melt her defenses away before she could think through his statement.
No reason to doubt they were married? "You you don't honestly expect us to ?" The air in the room suddenly seemed cooler, her skin contracting with goose bumps. Annie crossed her arms protectively over her chest and ran her hands over the bumpy flesh of her bare upper arms.
"No-" he laughed "-of course not. It will just be for show. You'll need to stay here in the suite with me. We'll eat together in public, be affectionate. You might have to suffer through a few of my kisses so any time we spend alone will be chalked up to romantic interludes. No one will suspect what we're really doing together."


text: Keeping in tune with their nostalgic influences, Japanese brand Beauty & Youth once again go to work at a pair of classic Vans sneakers. This time around, they utilize the Chukka Boot, implementing their own brand of design elements with buttery suede uppers, contrast piping, and contrast midsoles. Retail is set at ¥10,290 (Approx. $111 USD), with a release set at select United Arrows retail locations.


text:
This includes 1,794 single-aisle, 475 twin-aisle and 38 very large aircraft worth an estimated US$292 billion (216.7 billion euros). Globally, by 2032 some 29,230 new freighter and passenger aircraft will be required to satisfy future robust market demand.
With GDP growing above the world average, socioeconomic indicators forecast that Latin America's middle class will grow to represent more than half of the population by 2032. Between 2012 and 2020, Latin America's economy is expected to outperform the world average, largely thanks to Mexico and Brazil's consumer spending.
As a result, traffic growth in Latin America in the next 20 years is expected to outperform the world average of 4.7 percent with an annual growth rate of 5.2 percent.
A growing middle class and increased consumer spending have led to air transport becoming more accessible throughout Latin America in the past 10 years, increasing 14 percent in terms of total number of cities served. Still, while almost 100 percent of the 20 largest cities in North America and Europe connect passengers with at least one flight per day, only 40 percent of Latin America's top 20 cities do the same.
As a result, in the next 20 years, intra-regional and domestic traffic is expected to grow at a rate of 6.3 percent.
"Very large aircraft, such as the A380, not only help alleviate traffic congestion at busy airports, but they can assist Latin American airlines to compete with their foreign competitors," said Rafael Alonso, executive vice president of Airbus for Latin America and the Caribbean. "At the same time, the A380 addresses international air traffic requirements needed to serve long-haul flights to Europe."
Another prevalent trend in Latin America is the rise of low-cost carriers, which accounts for nearly 40 percent of the market share of total air traffic in the region, up from just 12 percent in 2003, with Mexico and Brazil representing nearly the entire market.
While many Latin American airlines have maintained a young fleet, the average aircraft age in Latin America could decrease further when Caribbean carriers start their renewal process.
"Aircraft in the Caribbean average about 17 years of age. That's more than seven years older than the Latin America and world average," Alonso said. "We've already started seeing some airlines in the Caribbean take advantage of current market opportunities and achieve greater operational benefits associated to newer generation aircraft. As more follow, the average aircraft age in the region will continue to drop."


text:
I have screwed up my user ID.
It will not take my password and when I get it to email my instructions
nothing shows up in my Hotmail inbox. Can you delete user ID
commando57 and let me re-register? I can supply the email address
associated with that user ID, but I would rather not post it.
Thank you.
How did you make this post, if it won't accept your password?
I was not clear.
I newly registered as hendrixhendrix and can get in fine, but I would like to get my old commando57 userID back that I must have screwed up somehow
trying to get back in after the upgrade. Your "supply an email address and we will send instructions to get back in" box, accepts my email address promising
to send instructions but have never arrived. Giving up on this I was requesting
that "commando57" userID be deleted so that I can RE-register as commando57. This is all. Thanks for reading this.
Ah, I get it now.
Our new board software allows us to merge two memberships into one. Does that sound like something that would be helpful to you here? If so, which membership would you like to keep as your "main" username?
Yes, that would be great!
Kill off mr hendrixhendrix and make me commando57 or merge me or whatever.
OK. PM me the password that you'd like to use for commando57.
I am running out of userID's
hendrix doesn't work
hendrix email doesn't work
commando57 doesn't work
second suggested commando57 email doesn't work
orig email for commando57 sent me, finally an email
saying my account had been locked out because
someone was trying to log in (me) I will be LT-1
here I guess.
I just double-checked this. I was able to login as you, as commando57, with the password you PM'd me (begins with "q").
The system is set up to lock people out after consecutive unsuccessful login attempts -- it's a security feature. Try again after a little while, I can re-PM you the password if necessary. I know it's frustrating.
I am back!!!!
It was fixed by killing off all
hotrodders.com cookies and
relogging on. Thanks for being
patient with me.
No problem -- glad it's taken care of. Keep an eye out for any quirks though, this is our first time using the new "merge user" function.
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