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On May 28, 2004, F-Secure reported that the Korgo network worm a worm that spreads without user intervention using the Sasser vulnerability in Windows was spreading and sending bank usernames and passwords to the mothership. It also sent back everything infected users typed into a form, which would include credit card numbers, passwords, and so on. Korgo is a nice, slow little worm, and many systems were already patched because of the effects of Sasser. Still, it s working away across the Net and is now up to variant U (having already gone through A, B, C, and so on). 4, talks about cross-platform spyware and what a really aggressive worst-case worm can do. Real phishing schemes are often more complicated than the ones just shown, however. For example, multiple phishing emails sometimes for different spoofed institutions can point to the same website. The phisher can use redirects to send someone between various websites before landing at the final server. That way, if any one server is taken down, the phishers can route around it. Here s a complicated scam, a little more realistic than the simple schemes I just showed you. Although we don t know for sure whether email and spyware scams are perpetrated by the same or different groups, it wouldn t surprise me if they both came from the same source.



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This large hypothalamic area surrounds the ventromedial nucleus itself, receives projections from the ARC NPY and melanocortin neurones and has direct connections with the PVN and DMH. VMH efferents activate sympathetic outputs, including those that stimulate energy expenditure and gut motility. The VMH contains neurones expressing high levels of LepRb. Leptin depolarizes and increases the ring rate of VMH neurones that express steroidogenic factor-1 (SF-1), while transgenic deletion of LepRb on these neurones leads to excessive weight gain (Dhillon et al., 2006). Other VMH neurones express CCK-2 receptors (whose physiological role is unclear) and brain-derived neurotrophic factor (BDNF), an eating-inhibitory peptide; transgenic knockdown of BDNF expression increases eating and body weight (Xu et al., 2003). Finally, VMH glucose-excited neurones may be involved in sensing falls in plasma glucose and initiating appropriate neuroendocrine responses to hypoglycaemia.





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Analogously, for q = 2, we obtain a special form of equivariant algorithm useful if all source signals have non-symmetric distribution, [283, 321] as W(l + 1) = W(l) + (l) I ygT (y) W(l), (8.38)

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[7] H. Yaghoobi, Scalable OFDMA physical layer in IEEE 802.16 WirelessMAN, Intel Technology Journal, vol. 8, issue 3, 2004.

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Obesity has long been linked with various diseases and with premature death. Associations are well recognized with type 2 diabetes, hypertension, dyslipidaemia and vascular disease commonly grouped together as the metabolic syndrome and with osteoarthritis, sleep apnoea and the polycystic ovarian syndrome (PCOS). Obesity has also been implicated as a risk factor for many other diseases, including several malignancies and chronic renal failure (see Table 9.1). Wolf and Colditz (1998) and James et al. (2004) have estimated the proportion of total risk of developing several major diseases that can be attributed to obesity. There are some discrepancies between the two reports, probably due to differences in the study populations and sampling periods (Wolf and Colditz used only American data from the 1988 and 1994 National Health Interview Survey). Overall, however, obesity appears to contribute about 60% of the total risk for type 2 diabetes, up to 40% of that for hypertension and endometrial carcinoma, 20 30% of the risk for coronary heart disease, stroke, osteoarthritis and gall-bladder disease, and about 10% for carcinoma of the breast and colon (Figure 9.1). The relationship between risk and BMI varies considerably among these diseases, with the risk for type 2 diabetes rising particularly sharply as BMI increases above the normal range (Figure 9.2, and Figure 9.9 on page 226). This chapter reviews the key epidemiological evidence linking obesity to its main comorbidities and premature death, and touches on some of the possible aetiological mechanisms. We shall also discuss the predictive value of the various measures of obesity, and how risk is modulated by factors such as gender, ethnic origin, physical tness and smoking. Detailed accounts of the pathophysiology, clinical features and management of the major comorbidities can be found elsewhere in this book, namely type 2 diabetes

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