ACE16k: a 128x128 focal plane analog processor with digital I/O

This paper presents a new generation 128x128 Focal-Plane Analog Programmable Array Processor -FPAPAP, from a system level perspective. It has been manufactured in a 0.35 microm standard digital 1P-5M CMOS technology. It has been designed to achieve the high-speed and moderate-accuracy -8b- requirements of most real time -early-vision applications. External data interchange and control are completely digital. The chip contains close to four million transistors, 90% of them working in analog mode. It achieves peak computing values of 0.33TeraOPS while keeping power consumption at reasonable limits -82.5GOPS/W. Preliminary experimental results are also provided in the paper.     

Conformational preferences in diastereomeric(5S)-methyl-3-(o-aryl)-2,4-oxazolidinediones

The thermally interconvertible diastereomers of the (5S)-methyl-3-(o-aryl)-2,4-oxazolidinediones were synthesized and their conformers studied by (1)H NMR and HPLC. The barriers to rotation about the N-C(aryl) bond were found to be very much solvent dependent. For the o-fluoro oxazolidinedione, difference in barriers to rotation in deuterated methanol and deuterated chloroform amounted to 34 kJ/mol. ortho-Bromo substitution increased the barrier to rotation up to 100 kJ/mol in ethanol, which enabled the analytical separation of the diastereomers and observation of the thermodynamic enrichment of the S-P conformer by HPLC. In CDCl(3) by (1)H NMR, on the other hand, a barrier of only 89 kJ/mol was determined. The S-M and S-P conformers of the diastereomers of o-methyl, alpha-naphthyl and o-iodo derivatives have been assigned by NOESY experiments and the kinetic and thermodynamic constants for the interconversion between the S-M and S-P conformers were determined.     

The protective effect of lisinopril on membrane-bound enzymes in myocardial preservation

A number of studies have reported that oxidant stress reduces the activity of isolated Na(+)-K(+) ATPase and Ca(2+) ATPase which are known to affect the cell membrane integrity. The aim of the study is to determine whether the administration of lisinopril is able to protect the membrane-bound enzyme levels in isolated guinea pig hearts and also ascertain whether or not a relationship exists between oxygen free radicals and membrane bound Na(+)-K(+) ATPase and Ca(2+) ATPase. Forty guinea pig hearts were studied in an isolated Krebs-Henseleit solution-perfused Langendorff cardiac model. In all groups cardioplegic arrest was achieved by administering St. Thomas' Hospital cardioplegic solution (STHCS). Group 1 (control, n=10) received only STHCS. Group 2 (n=10) were arrested with lisinopril (l micromol l(-1)) added STHCS. Group 3 (n=10) were pretreated with oral lisinopril (0.2 mg kg(-1) twice a day) for 10 days and then arrested with STHCS. Group 4 were also pretreated with oral lisinopril (0.2 mg kg(-1) twice a day for 10 days), arrested with STHCS and reperfused with lisinopril added to Krebs-Henseleit solution (l micromol l(-1)). Hearts were subjected to normothermic global ischaemia for 90 min and then reperfused at 37 degrees C. Pretreatment and addition of lisinopril in the reperfusion buffer improved the levels of membrane-bound enzymes. When the treated groups were compared with control hearts, the best results were achieved in group 4. The Na(+)-K(+) and Ca(2+) ATPase levels increased from 466.38+/-5.99 to 560.12+/-18.02 and 884.69+/-9.13 to 1287.71+/-13.01 nmolPi mg(-1) protein h(-1) respectively (p<0.05). These results suggest that lisinopril protects the cell membrane integrity and lessens free radical-induced oxidant stress.     

Self-organization and competition in the immune response to cancer invasion: a phase-orientated computational model of oncogenesis

Motivation: Recent studies indicate that fractal dimensionscan uncover aspects of cellular dynamics prior to pathological manifestation. In this respect we are interested in buildinga computational model of oncogenesis able to generate patternswith the same fractal dimension spectrum as the in vivo tumor. Results: A new theoretical model incorporating a systemic viewof oncogenesis in a computational model was proposed. Thetumor growth is viewed as competition for resources betweenthe two self-organizing subsystems: the neoplastic and theimmune. Numerical simulations revealed that tumor escape canbe uncovered in some earlier stage of the immune-system–tumorinteraction using multifractal measures. The described computationalmodel is able to simulate also the case of immune, surgical,chemical and radiotherapeutical treatment, as well as theireffects. Availability: The software used is available on request fromthe authors. Contact: Sorinel Oprisan, University of New Orleans, Department of Psychology, New Orleans, LA 70148, USA. soprisan{at}uno.edu Received on July 6, 1999 ; revised on September 15, 1999 ; accepted on September 17, 1999     

Pancreatic secretory response to feeding in the calf: CCK-A receptors, but not CCK-B/gastrin receptors are involved

In bovine species, as in human, the pancreas predominantly expresses cholecystokinin-B (CCK-B)/gastrin receptors. However, the role of this receptor in the regulation of meal-stimulated pancreatic enzyme release has not been determined. In milk-fed calves, we previously described prandial patterns of exocrine pancreatic secretion and a long prefeeding phase was observed. The present study was aimed at determining both the role of external stimuli in the outset of the prefeeding phase and the implication of pancreatic CCK-A and CCK-B/gastrin receptors in the mediation of pancreatic response to feeding. The first objective was studied by suppressing external stimuli associated with food intake (unexpected meal) and the second by infusing highly specific and potent antagonists of CCK-A (SR 27897) and CCK-B/gastrin (PD 135158) receptors during the prandial period. When calves were given an unexpected meal, the long prefeeding increase in pancreatic secretion was absent. SR 27897 (but not PD 135158) inhibited the preprandial phase and greatly reduced postprandial pancreatic juice and enzyme outflows. The expectancy of a meal seemed to elicit an increased pancreatic response right before a meal and CCK-A receptors may mediate this information via neural pathways. The implication of CCK and CCK-A receptors in mediating the postfeeding pancreatic response was also demonstrated. The participation of CCK-B/gastrin receptors in this regulation was not demonstrated.