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In this chapter, a model for portfolio selection under fixed and/or proportional transaction costs together with non-negativity and integer constraints was presented and empirically studied on basis of DAX data. The major results from this study are that the presence of transaction costs might lead to significantly different results than for a perfect market and that the types of costs the investor occurs have different effects. Also, the optimal solution under transaction costs can not always be derived from the solution for frictionless markets.

Introducing transaction costs might have severe effects on the optimal portfolio structure. Even low fixed costs can lead to a substantial reduction in the number of different assets that ought to be included in a portfolio; the same is true for proportional costs or compound cost schemes. In due course, the asset weights might differ substantially. An investor facing transaction costs might therefore even have distinct advantages from individual stock selection over investing into a market fund — provided she does not simply try to replicate its weights but includes the relevant costs and additional constraints into the optimization process. Unlike claimed for a perfect market situation, in real world it might therefore be reasonable to hold a portfolio that deviates from the market portfolio even when all investors have homogeneous expectations. Another conclusion from these results is that investors might have advantages when they can invest in funds that are not just tracking the market portfolio, but also anticipate their clients’ transaction costs.

An interactive network comprised of neuropeptide Y (NPY) and cohorts is obligatory in the hypothalamic integration of appetite and energy expenditure on a minute-to-minute basis. High or low abundance of NPY and cognate receptors dysregulates the homeostatic milieu engendering hyperphagia, decreased energy expenditure, obesity and attendant metabolic syndrome cluster of dyslipidemia, glucose intolerance, insulin resistance and hyperinsulinemia, risk factors for type II diabetes and cardiovascular diseases. Increasing the supply of the endogenous repressor hormone leptin locally in the hypothalamus with the aid of leptin gene therapy, blocked age-related and dietary obesities, and the sequential development of dyslipidemia, hyperglycemia, and insulin resistance. Thus, sustained repression of NPY signaling with increased leptin selectively in the hypothalamus can avert environmental obesity and the risks of metabolic diseases.

An interactive network comprised of neuropeptide Y (NPY) and cohorts is obligatory in the hypothalamic integration of appetite and energy expenditure on a minute-to-minute basis. High or low abundance of NPY and cognate receptors dysregulates the homeostatic milieu engendering hyperphagia, decreased energy expenditure, obesity and attendant metabolic syndrome cluster of dyslipidemia, glucose intolerance, insulin resistance and hyperinsulinemia, risk factors for type II diabetes and cardiovascular diseases. Increasing the supply of the endogenous repressor hormone leptin locally in the hypothalamus with the aid of leptin gene therapy, blocked age-related and dietary obesities, and the sequential development of dyslipidemia, hyperglycemia, and insulin resistance. Thus, sustained repression of NPY signaling with increased leptin selectively in the hypothalamus can avert environmental obesity and the risks of metabolic diseases.

Reverse transcription polymerase chain reaction (RT-PCR) studies identified the mRNA coding for the Y and Y receptors in human mammary artery/vein and saphenous vein biopsies. Y receptors are expressed in vascular smooth muscles and potentiate the contractile action of sympathetic co-transmitters, adenosine triphosphate (ATP) and noradrenaline (NA); BIBP 3226, a competitive Y receptor antagonist, blocked the neuropeptide Y (NPY)-induced modulation. The Y receptor is expressed in sympathetic nerves terminals and modulates the pool of sympathetic co-transmitters released at the neuroeffector junction. NPY plays a dual role as a modulator of sympathetic co-transmission; it facilitates vascular smooth muscle reactivity and modulates the presynaptic release of ATP and NA. Sympathetic reflexes regulate human vascular resistance, where NPY plays a modulator role of paramount importance following increased sympathetic discharges, such as stress and vascular disease.

There is not doubt today that NPY does play a role in regulating cytosolic and nuclear Ca in heart cells including ventricular cardiomyocytes and EECs. The recent work in the literature including ours, agree that the major effect of NPY in both ventricular cardiomyocytes and EECs is mediated primarily by the activation of the Y and Y receptors. However, other NPY receptors may also contribute to the peptide’s effect on cardiomyocytes and EECs such as the Y receptors. The mechanisms by which these effects take place could be via indirect activation of the voltage dependent resting R-type Ca channels. One important aspect that should be mentioned is that EECs could be an important source of NPY which may highly contribute to both circulating NPY as well as locally released NPY. Furthermore, the presence of different types of NPY receptors in the nuclear membranes may suggest that these receptors may also contribute to the modulation of nuclear function and more particularly to the regulation of nucleoplasmic Ca metabolism which is known to modulate nuclear function and transport. It is very likely that overactivation of different NPY receptors in both cardiomyocytes and EECs and more particularly the Y and Y receptors could be implicated in hypertrophy and cardiac heart failure. We are quite sure that future work in the field of NPY and cardiac function will help us to better understand the implication of this peptide in cardiac physiopathology.

NPY is a mediator and a marker of chronic stress in humans, including extreme trauma and PTSD, but its actions are complex. In the periphery, as a sympathetic neurotransmitter, it exerts excitatory effects on the cardiovascular system and modulates immune responses. In contrast, in the central nervous system, NPY-ergic neurons are powerful inhibitory, -stress and anxiolytic system. In PTSD, stress-induced elevations of plasma NPY are associated with increases in cortisol, catecholamines and blood pressure, consistent with peptide’s actions in the cardiovascular system. However, plasma NPY levels, baseline, stress-induced, and/or post-stress are associated with behavioral performance under stress — suggesting that reduced activity of the central NPY system diminishes individual’s stress resilience. Many of the peripheral -stress and central -stress actions of NPY appears to be mediated by the same subtype of receptors, the Y1, which complicates the case of using Y1 antagonists for treatment of stress-related cardiovascular and immune symptoms, unless drugs which do not penetrate the blood-brain-barrier are used. Future studies should determine more precise mechanisms of NPY’s actions and type of receptors involved in psychological, behavioral, cardiovascular and immune consequences of chronic stress, particularly PTSD, where peptide’s role appears to be quite compelling.

The presence of NPY receptors on both endothelial and vascular smooth muscle cells indicates that blood-borne NPY as well as NPY stemming from surrounding nerves can affect contractile responses of cerebral vessels. In addition, endothelial cells may themselves be a source of NPY as well as a site of NPY metabolism. Understanding the roles of NPY in cerebrovascular regulation is complicated by multiple receptor subtypes, signalling pathways and cellular responses. Vasodilatory effects and vascular remodeling actions underscore the fact that NPY cannot just be classified as a potent vasoconstrictor. NPY is an important sympathetic transmitter, but it clearly acts via intracerebral nerves as well to regulate local CBF.

In this chapter, a model for portfolio selection under fixed and/or proportional transaction costs together with non-negativity and integer constraints was presented and empirically studied on basis of DAX data. The major results from this study are that the presence of transaction costs might lead to significantly different results than for a perfect market and that the types of costs the investor occurs have different effects. Also, the optimal solution under transaction costs can not always be derived from the solution for frictionless markets.

Introducing transaction costs might have severe effects on the optimal portfolio structure. Even low fixed costs can lead to a substantial reduction in the number of different assets that ought to be included in a portfolio; the same is true for proportional costs or compound cost schemes. In due course, the asset weights might differ substantially. An investor facing transaction costs might therefore even have distinct advantages from individual stock selection over investing into a market fund — provided she does not simply try to replicate its weights but includes the relevant costs and additional constraints into the optimization process. Unlike claimed for a perfect market situation, in real world it might therefore be reasonable to hold a portfolio that deviates from the market portfolio even when all investors have homogeneous expectations. Another conclusion from these results is that investors might have advantages when they can invest in funds that are not just tracking the market portfolio, but also anticipate their clients’ transaction costs.

The presence in the mammalian kidney of NPY and at least one of its receptor subtypes has been proven by several independent methodologies. Also, numerous studies using physiological and pharmacological approaches indicated that this peptide has the capacity to alter renal function. In particular, these studies suggest that NPY may exert renal vasoconstrictor and tubular actions that are species dependent, and may also influence renin secretion by the kidney. The question whether NPY plays an important role in the physiological regulation of renal hemodynamics and electrolyte excretion, remains largely unanswered at present. No major impairments in renal function have been reported in genetically models deficient in NPY or its Y receptor. Thus, additional studies are required to elucidate the role of NPY in the physiological and pathophysiological regulation of renal function.

The NPY system may well be one of the most interesting target systems for development of treatments for alcohol dependence as well as mood disorders such as depression and anxiety syndromes. NPY is an endogenous anxiolytic compound, functions as an antidepressant, and is effective in modifying alcohol intake in high drinking states. Through receptor subtype specific compounds, the NPY system offers an interesting and innovative future approach for treatment designs. Selective Y2 receptor antagonists and/or Y1 agonists that are peripherally available and effectively penetrate the CNS are possible candidates. In conclusion, the NPY system offers attractive targets for development of future treatments for depression, anxiety, and alcohol dependence.