PLA Formation Research Articles

Conformational isomerism of pyridoxal. Infrared matrix isolation and theoretical studies

A combined matrix isolation FTIR and theoretical DFT/B3LYP/6–311++G(2p,2d) study of pyridoxal was performed. The calculations resulted in five stable PLHB conformers stabilized by intramolecular OH⋯O bonding between phenolic OH and carbonyl CO groups and another thirteen conformers in which OH or/and aldehyde groups are rotated by 180° around CO or/and CC bonds leading, respectively, to formation of PLO, PLA and PLOA conformers. The analysis of the spectra of the as-deposited matrix indicated that two most stable PLHB1 and PLHB2 conformers with intramolecular hydrogen bond are present in the matrix. The exposure of the PL/Ar matrix to mercury lamp radiation (λ>345nm) induced conformational change of PLHB isomers to PLOA ones.

Platelet Abnormalities during Colonic Inflammation

Patients with inflammatory bowel disease are susceptible to microvascular thrombosis and thromboembolism. The increased incidence of thrombosis is accompanied by enhanced coagulation and abnormalities in platelet function. Clinical studies have revealed thrombocytosis, alterations in platelet activation, enhanced platelet-leukocyte interactions, and elevated plasma levels of prothrombotic cytokines. This study was directed toward determining whether the thrombocytosis, altered platelet functions, and enhanced platelet-leukocyte interactions observed in patients with inflammatory bowel disease can be recapitulated in the dextran sodium sulfate and T-cell transfer models of murine colonic inflammation. Flow cytometry was used to characterize platelet function in heparin-anticoagulated whole blood of control mice and in mice with colonic inflammation. Platelets were identified by characteristic light scattering and membrane expression of CD41. Thiazole orange labeling was used to differentiate between immature and mature platelets. Platelet activation was monitored using the expression of an activation epitope of GPIIb/IIIa integrin. The combination of CD41, CD45.2, Gr-1, F4/80, and isotype control antibodies was used to detect and quantify aggregates of leukocytes, neutrophils, and monocytes with platelets. Our results indicated that colonic inflammation is associated with thrombocytosis, leukocytosis, and the appearance of immature platelets. An increased number of circulating activated platelets was detected in colitic mice, along with the formation of aggregates of leukocytes (PLA), neutrophils (PNA), and monocytes (PMA) with platelets. Selectin blockade with fucoidin inhibited dextran sodium sulfate-induced PLA formation. The findings of this study indicate that many features of the altered platelet function detected in human inflammatory bowel disease can be reproduced in animal models of colonic inflammation.

Foraminiferal fauna and depositional environment of the Triassic Kang Pla Formation (Song Group) distributed in the Northwest of Phrae, Northern Thailand

Foraminiferal fauna and depositional environment of the Triassic Kang Pla Formation (Song Group) distributed in the Northwest of Phrae, Northern Thailand

Platelet‐white blood cell (WBC) interaction, WBC apoptosis, and procoagulant activity in stored red blood cells

Nonleukoreduced units of red blood cells (RBCs) contain activated platelets (PLTs) that interact with white blood cells (WBCs) and may promote inflammation and thrombosis in the recipient. The aim of this study was to characterize PLT-WBC interactions (PLT-WBC aggregates [PLAs]), WBC apoptosis, WBC death, and the development of procoagulant activity in RBCs during storage. RBCs were prepared from volunteer donor blood and stored. Samples were analyzed with flow cytometry between Days 1 and 15 to measure PLT-monocyte aggregate (PMA) and PLT-neutrophil aggregate (PNA) formation, WBC apoptosis (annexin V binding), and cell death (binding of 7-aminoactinomycin D). Procoagulant activity in the supernatant of four RBC preparations was assessed between Days 1 and 39 using a clotting assay with and without the addition of an inhibitory anti-tissue factor (TF) antibody, αTF-5. PLA formation was extensive and maximal on Day 3 of storage (PNA, 23 ± 13%; PMA, 93 ± 4%; n = 6). Apoptosis was progressive throughout storage, with 95 ± 4% of neutrophils and 73 ± 19% of monocytes binding annexin V on Day 15. Cell death became measurable after apoptosis. Procoagulant activity was observed in all RBCs but with varying temporal patterns. It was partially TF dependent and removed with high-speed centrifugation, suggestive of an association with microparticles. The activation of PLTs during the storage of RBCs induces PLA formation that precedes WBC apoptosis and death. Procoagulant activity, likely associated with microparticles derived from apoptotic WBCs, may contribute to adverse effects of stored, nonleukoreduced RBCs.

An Improved Algorithm for the Construction of Decision Diagrams by Rearranging and Partitioning the Input Cube Set

Decision diagrams (DDs) are a data structure that allows compact representation of discrete functions. The efficient construction of DDs in terms of space and time is often considered problem. A particular problem is that during the construction of a DD, a large number of temporary nodes are created. We address this problem in the case when the functions are specified in the PLA format. A common practice is to construct a DD by recursively processing all the cubes in PLA specification. The DD representing a subfunction defined by a single cube is merged with the DD for the subfunction defined by all the previously processed cubes. We proposed a method of reordering and partitioning the set of cubes in PLA specification that results in the reduction of both space and time complexities of the construction of DDs. First, we arrange cubes by their suffices. Then we partition the set of cubes, construct DDs for the subfunctions representing each partition separately, and merge them into a final DD. The reordering and partitioning ensures that these intermediary decision diagrams never exceed a certain size which is controlled by the size of the partitions. In this way, the number of operations on the nodes during the merging decision diagrams is reduced. This reduction results in a decrease both in the number of temporary nodes and construction time. The proposed method is used for the construction of DDs for the set of standard benchmark functions. The experiments show that the total number of created nodes is reduced on average by 34.65 percent, while the construction time is decreased by 48.6 percent.

Using ordered binary decision diagrams to factorize multi-level logic

A novel approach that employs ordered binary decision diagrams (OBDDs) is contributed to factorize multi-level logic functions by requiring as few literals as possible. A logic function with PLA format is represented as an OBDD form first. A heuristic decision method of variable ordering, called theorder lookahead method, is derived for the construction of OBDDs. This method is based on the constant cofactor and the number of erasable logic terms for each input variable. The total execution time of the OBDD construction by the above ordering decisions is very fast for some MCNC benchmarks. With the above OBDDs, we introduce a simple yet effective graph manipulation, calledEXT, to obtain a minimal number of literals in the Boolean function. This greedyEXT algorithm consists mainly of two phases. The first phase, calledgraph analysis, identifies the similarities between nodes on the same level in the OBDD. The second phase, calledtree analysis, utilizes the above features to extract the common parts of the nodes. TheEXT procedure runs from the bottom level up to the top level of the OBDD. The computational complexity depends on the number of nodes in the OBDD. The results of simulations show thatEXT has a very fast CPU execution time and a competitive literal ratio with other methods for some MCNC benchmarks.EXT will produce the smallest literal number, especially for structured or symmetric circuits.

Levels and localization of group II phospholipase A 2 and annexin I in interleukin- and dexamethasone-treated rat mesangial cells: evidence against annexin mediation of the dexamethasone-induced inhibition of group II phospholipases A 2

The mechanism by which glucocorticosteroids inhibit the synthesis and secretion of pro-inflammatory arachidonate metabolites is still controversial. Initially it was postulated that glucocorticoids can induce the formation of PLA 2 inhibitory proteins termed annexins. We have previously shown that the cytokine-induced 14 kDa PLA 2 activity and the synthesis of prostaglandin E 2 in rat mesangial cells is dose-dependently blocked by pretreatment of the cells with dexamethasone (Schalkwijk et al. (1991) Biochem. Biophys. Res. Commun. 180, 46–52). Concurrently, the synthesis of 14 kDa group II PLA 2 is suppressed. The regulation of PLA 2 activity is complex and may well involve superimposable mechanisms. Thus, although the decrease in PLA 2 protein levels could in itself explain the dexamethasone-induced decrease in PLA 2 activity, a contribution of the glucocorticoid-induced anti-phospholipase A 2 protein annexin cannot be ruled out a priori. To investigate this possibility we analyzed the level of annexin I by Western blotting and immunostaining in mesangial cells treated with interleukin-1β and/or dexamethasone. Under conditions where 14 kDa group II PLA 2 activity and protein levels were dramatically affected by interleukin-1 and dexamethasone, the level of annexin I in the cells remained constant. Dexamethasone also did not induce the secretion of annexin I. In addition, no evidence for dexamethasone-induced translocation of annexin I from the cytosol to membranes, thereby possibly sequestering the substrates for PLA 2, was obtained. Immunofluorescence studies localized the cytokine-induced PLA 2 to the Golgi area and punctate structures in the cytoplasm. We have also studied the subcellular localization of annexin I in rat mesangial cells using confocal microscopy. These studies located annexin I mainly in the cytoplasma and the nucleus. We conclude from these experiments that the dexamethasone-induced inhibition of 14 kDa group II PLA 2 in rat mesangial cells is not mediated by annexin I and is solely due to the suppression of PLA 2 gene expression.

Automatic generation of PLA from ASM charts

A state machine design entry tool has been designed and integrated into the Silvar-Lisco SL2000 CAD system. Using ASM techniques, it allows the generation of both state table and PLA format files suitable for input to ESPRESSO. It also supports both manual and automatic state assignments. An example is given to show the operation of the tool.