A Computational Complexity Theory in Membrane Computing

In this paper, a computational complexity theory within the framework of Membrane Computing is introduced. Polynomial complexity classes associated with di erent models of cell-like and tissue-like membrane systems are de ned and the most relevant results obtained so far are presented. Many attractive characterizations of P 6= NP conjecture within the framework of a bio-inspired and non-conventional computing model are deduced.Ministerio de Educación y Ciencia TIN2006-13425Junta de Andalucía P08–TIC-0420

Experiments on the Reliability of Stochastic Spiking Neural P Systems

In the area of membrane computing, time-freeness has been defined as the ability for a timed membrane system to produce always the same result, independently of the execution times associated to the rules. In this paper, we use a similar idea in the framework of spiking neural P systems, a model inspired by the structure and the functioning of neural cells. In particular, we introduce stochastic spiking neural P systems where the time of firing for an enabled spiking rule is probabilistically chosen and we investigate when, and how, these probabilities can influence the ability of the systems to simulate, in a reliable way, universal machines, such as register machines. This is the preliminary version of a paper that was published in Natural Computing, 7, 4, 2008. The original publication is available at http://www.springerlink.co

Effect of growth hormone-release inhibiting hormone on hormones stimulating exocrine pancreatic secretion.

The nature and extent of growth hormone-release inhibiting hormone (GH-RIH, somatostatin)-induced inhibition of pancreatic secretion of bicarbonate and protein, an index of enzyme secretion, were studied by administration of exogenous secretin or cholecystokinin (CCK) and of a number of stimulants for endogenous release of these hormones in fasted pancreatic fistula dogs with and without an infusion of GH-RIH. The results of this study show that GH-RIH inhibits the pancreatic fluid and bicarbonate secretion induced by duodenal acidification and exogenous secretion. The kinetic analysis shows that the interaction between GH-RIH and secretin affecting pancreatic bicarbonate secretion possesses the characteristics of competitive inhibition. GH-RIH does not change the pancreatic protein response to exogenous CCK, but profoundly inhibits pancreatic response to a variety of the endogenous stimulants of CCK release, including duodenal perfusion of sodium oleate, amino acid mixture, or feeding of a peptone meal. We conclude that GH-RIH is a very potent inhibitor of the endogenous release of CCK from the intestinal mucosa and inhibits competitively the action of secretin but not CCK on the exocrine pancreatic secretion

Aberrant repair of etheno-DNA adducts in leukocytes and colon tissue of colon cancer patients

International audienceTo assess the role of lipid peroxidation-induced DNA damage and repair in colon carcinogenesis, the excision rates and levels of 1,N-6-etheno-2'-deoxyadenosine (epsilon dA), 3,N-4-etheno-2'-deoxycytidine (epsilon dC), and 1,N-2-etheno-2'-deoxyguanosine (1,N-2-epsilon dG) were analyzed in polymorphic blood leukocytes (PBL) and resected colon tissues of 54 colorectal carcinoma (CRC) patients and PBL of 56 healthy individuals. In PBL the excision rates of 1,N-6-ethenoadenine (epsilon Ade) and 3,N-4-ethenocytosine (epsilon Cyt), measured by the nicking of oligodeoxynucleotide duplexes with single lesions, and unexpectedly also the levels of epsilon dA and 1,N-2-epsilon dG, measured by LC/MS/MS, were lower in CRC patients than in controls. In contrast the mRNA levels of repair enzymes, alkylpurine- and thymine-DNA glycosylases and abasic site endonuclease (APE1), were higher in PBL of CRC patients than in those of controls, as measured by QPCR. In the target colon tissues epsilon Ade and epsilon Cyt excision rates were higher, whereas the epsilon dA and epsilon dC levels in DNA, measured by P-32-postlabeling, were lower in tumor than in adjacent colon tissue, although a higher mRNA level was observed only for APE1. This suggests that during the onset of carcinogenesis, etheno adduct repair in the colon seems to be under a complex transcriptional and posttranscriptional control, whereby deregulation may act as a driving force for malignancy