Neural Network Viscosity Models for Multi-Component Liquid Mixtures

An artificial neural network has been developed for the prediction of the kinematic viscosity of ternary, quaternary, and quinary systems. The systems investigated consisted of the following components: Heptane, Octane, Toluene, Cyclohexane, and Ethylbenzene at atmospheric pressure and temperatures of 293.15, 298.15, 308.15, and 313.15 K. The developed model was based on a three-layer neural network with six neurons in the hidden layer and a back propagation learning algorithm. The neural network was trained with binary systems consisting of 440 data sets and using mole fractions combined with temperature as the input. A comparison of the experimental values and the results predicted from the neural network revealed a satisfactory correlation, with the overall absolute average deviation (AAD) for the ternary, quaternary, and quinary systems of 0.8646%, 1.1298%, and 4.3611%, respectively. The results were further compared to the generalized McAllister model as an alternative empirical model. The neural network produced better results than the generalized McAllister model. The new approach established in this work helps reduce the amount of experimental work required in order to determine most of the parameters needed for other models and illustrates the potential of using a neural network method to estimate the kinematic viscosity of many other mixtures

Early diagnosis of pancreatic cancer: neutrophil gelatinase-associated lipocalin as a marker of pancreatic intraepithelial neoplasia

Pancreatic cancer is a highly lethal malignancy with a dismal 5-year survival of less than 5%. The scarcity of early biomarkers has considerably hindered our ability to launch preventive measures for this malignancy in a timely manner. Neutrophil gelatinase-associated lipocalin (NGAL), a 24-kDa glycoprotein, was reported to be upregulated nearly 27-fold in pancreatic cancer cells compared to normal ductal cells in a microarray analysis. Given the need for biomarkers in the early diagnosis of pancreatic cancer, we investigated the expression of NGAL in tissues with the objective of examining if NGAL immunostaining could be used to identify foci of pancreatic intraepithelial neoplasia, premalignant lesions preceding invasive cancer. To examine a possible correlation between NGAL expression and the degree of differentiation, we also analysed NGAL levels in pancreatic cancer cell lines with varying grades of differentiation. Although NGAL expression was strongly upregulated in pancreatic cancer, and moderately in pancreatitis, only a weak expression could be detected in the healthy pancreas. The average composite score for adenocarcinoma (4.26±2.44) was significantly higher than that for the normal pancreas (1.0) or pancreatitis (1.0) (P<0.0001). Further, although both well- and moderately differentiated pancreatic cancer were positive for NGAL, poorly differentiated adenocarcinoma was uniformly negative. Importantly, NGAL expression was detected as early as the PanIN-1 stage, suggesting that it could be a marker of the earliest premalignant changes in the pancreas. Further, we examined NGAL levels in serum samples. Serum NGAL levels were above the cutoff for healthy individuals in 94% of pancreatic cancer and 62.5% each of acute and chronic pancreatitis samples. However, the difference between NGAL levels in pancreatitis and pancreatic cancer was not significant. A ROC curve analysis revealed that ELISA for NGAL is fairly accurate in distinguishing pancreatic cancer from non-cancer cases (area under curve=0.75). In conclusion, NGAL is highly expressed in early dysplastic lesions in the pancreas, suggesting a possible role as an early diagnostic marker for pancreatic cancer. Further, serum NGAL measurement could be investigated as a possible biomarker in pancreatitis and pancreatic adenocarcinoma

Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases

The production of peroxide and superoxide is an inevitable consequence of aerobic metabolism, and while these particular "reactive oxygen species" (ROSs) can exhibit a number of biological effects, they are not of themselves excessively reactive and thus they are not especially damaging at physiological concentrations. However, their reactions with poorly liganded iron species can lead to the catalytic production of the very reactive and dangerous hydroxyl radical, which is exceptionally damaging, and a major cause of chronic inflammation. We review the considerable and wide-ranging evidence for the involvement of this combination of (su)peroxide and poorly liganded iron in a large number of physiological and indeed pathological processes and inflammatory disorders, especially those involving the progressive degradation of cellular and organismal performance. These diseases share a great many similarities and thus might be considered to have a common cause (i.e. iron-catalysed free radical and especially hydroxyl radical generation). The studies reviewed include those focused on a series of cardiovascular, metabolic and neurological diseases, where iron can be found at the sites of plaques and lesions, as well as studies showing the significance of iron to aging and longevity. The effective chelation of iron by natural or synthetic ligands is thus of major physiological (and potentially therapeutic) importance. As systems properties, we need to recognise that physiological observables have multiple molecular causes, and studying them in isolation leads to inconsistent patterns of apparent causality when it is the simultaneous combination of multiple factors that is responsible. This explains, for instance, the decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference

Ischemic Cerebrovascular Disease: Risk Factors and Outcome Predictors with special reference to the role of leukocytes and inflammatory mediators

Ischemic cerebrovascular disease (CVD) is usually a consequence of atherosclerosis and is the commonest cause of stroke. The identification of risk factors and outcome predictors and the initiation of preventive measures constitute the cornerstone of efforts to reduce the risk of stroke and improve outcome. The trend for long-term outcome after stroke and the predictors of this outcome were evaluated in the light of data accumulated during the first four years after the founding of the Malmö Stroke Registry in 1989. Early predictors of ischemic CVD were studied in middle-aged, apparently healthy individuals, from the Malmö Prevention Project cohort. Since leukocytes are believed to play important parts regarding the risk and outcome of ischemic CVD, their possible involvement was the focus of special interest in this study. Although stroke incidence remained unchanged during the first four years of the Malmö stroke registry (1989-92), there was a trend toward a decline in the long-term recurrence and mortality rates following stroke. The long-term outcome predictors were evaluated. The age-standardized recurrence-free survival rate differs significantly between different residential areas in the city. In middle-aged, apparently healthy individuals, apart from traditional risk factors, a history of calf pain while walking (OR 1.9; p=0.002), a high serum uric acid level (OR 1.2; p<0.05) were found to be significant predictors of future ischemic CVD. In subjects with asymptomatic atherosclerosis (n=156), plasma levels of leukocyte activation markers neutrophil protease 4 (NP4), neutrophil gelatinase associated lipocalin (NGAL), tumor necrosis factor a (TNFa) and soluble TNF receptor-1 (sTNFR-1) were related to atherosclerosis risk factors (age, blood pressure, history of hypertension, and smoking). Patients with acute ischemic CVD (n=120) manifested higher plasma levels of NP4, NGAL and sTNFR-1 than did controls. During 4-year follow-up of patients with ischemic CVD (n=144) plasma levels of leukocyte activation markers at the time of acute cerebral ischemia, NGAL (OR 3.6; p<0.05) and sTNFR-1 (OR 2.0; p<0.01), were independent predictors of cardiovascular mortality. In conclusion, despite the observed trend of improving long-term outcome following stroke, the burden of this disease is still high. The observed variation of the long-term stroke free survival rate between different residential areas of the same city might be due to intra-urban differences in risk factor exposure or might indicate the importance of sociodemographic factors vis-à-vis long-term prognosis after stroke. Apart from traditional factors predicting ischemic CVD, the routine use of a simple questionnaire on calf pain while walking, and determination of the serum uric acid level might help in identifying those at high risk of ischemic CVD. Leukocyte activation seems to be an important factor both in atherosclerosis and ischemic CVD, and regarding outcome after ischemic CVD. The plasma levels of leukocyte activation markers might be useful in risk assessment, and possible targets for therapeutic medical intervention

Leukocyte activation detected by increased plasma levels of inflammatory mediators in patients with ischemic cerebrovascular diseases

Background and Purpose: Leukocytes have been implicated in the development of ischemia atherosclerotic vascular disease. In a prospective study we investigated whether the plasma concentration of inflammatory mediator, ie, proteases and cytokine, as markers for systemic leukocyte activation, are increased in patient with acute ischemic cerebrovascular diseases. Methods: Using enzyme-linked immunosorbent assays, we measured the plasma level of neutrophil gelatinase-associated lipocalin (NGAL), neutrophil proteinase 4 (NP4), tumor necrosis factor-α (TNF)m and soluble TNF receptor protein-1 p55 (sTNFR-1) in 120 patients with acute ischemic cerebrovascular insult (72 with and 48 stroke and 48 with transient ischemic attack (TIAl) and in 35 age-and sex-matched healthy subject. Results: Compared with the control group, plasma NGAL levels were higher in the stroke group (P<.0001) and the TIA group (P<.01); plasma NP4 levels were higher in the stroke group (P<.0001) and the TIA group (P<.01); and plasma sTNFR-1 levels wee higher in the stroke group (P<.04). There was significant correlation between the plasma levels of fibrinogen and those of both sTNFR-1 (r=.32; P=32; P=.005) and NGAL 9r=.40; P=.0001) and between the erythrocyte sedimentation rate and the plasma levels of both sTNFR-1 (r=.35; P=.001) and NGAL (r=.34;P=.002). Conclusions: Our study demonstrated that marker for systemic leukocyte activation, ie, plasma levels of cytokine and protease, were higher in patients with acute ischemic cerebrovascular disease than in healthy control subject. Activated leukocytes and leukocytic mediator may have an important role in acute cerebrovascular ischemia and it consequences