We present the first-ever commercially available microcontroller families built with innovative split-gate based NOR flash memory that uses silicon nanocrystals as the storage medium. The 32-bit mixed-signal low-power Kinetis microcontroller families have nanocrystal based flash memories (referred to as TFS for `Thin Film Storage') with a wide range of array sizes from 32KB to 1MB. In addition, the unique capability of TFS has enabled inclusion of fully configurable embedded EEPROM functionality called `FlexMemory', which also manages wear leveling for high endurance. The TFS memory has been optimized to deliver read access time of <;30ns, fast source-side injection programming (10-20μs), fast tunnel erase into the gate (1-20ms), robust high temperature data retention before and after cycling, endurance of at least 10K cycles for flash and effective endurance up to 10M cycles in the EEPROM mode. In addition, the microcontroller core, analog and flash modules have been developed to deliver performance, reliability, and low-power operations across a temperature range of -40C to 105C and full operation down to 1.7V from a single power supply.

In this paper, we present the first-ever commercially available embedded Microcontrollers built on 90nm-node with silicon nanocrystal memories that has intrinsic capability of exceeding 500K program/erase cycles. We also show that the cycling performance across temperature (-40C to 125C) is very well behaved even while maintaining high performance that meets or exceeds the requirements of consumer, industrial, and automotive markets. In specific EEPROM implementation, such high endurance is capable of delivering in excess of 200M data updates. In addition, we also demonstrate that the nanocrystal flash memory is highly scalable to the next generation nodes and the scaling can be accomplished without degradation of program/erase speed, endurance and reliability.

beta-BaB2O4 Is a remarkable non-linear optical material for its large second harmonic generation coefficients and wide transparent range Glass ceramics as a kind of functional materials was recently paled more attention because large size products can be more easil obtained and their properties can be compared with those of corresponding single crystals. In this paper beta-BaB2O4 glass ceramics was prepared by melting BaCO3 and H3BO3 and following heat treatment the bulk samples. DTA XRD and FTIR were used to Investigate the phase separation and crystallization process of beta -BaB2O4 second harmonic generation of glass beta-BaB2O4 glass ceramics were studied.

This study examined the role of plasma adenosine in the modulation of platelet-activating factor (PAF) activity on platelet aggregation and serotonin (5-HT) release in human platelet-rich plasma (PRP). In addition, the effects of methylxanthines (e.g. theophylline and caffeine) were studied on PAF-induced platelet aggregation in PRP isolated from blood samples from healthy subjects. Also, PAF-induced platelet aggregation was examined in PRP samples of patients receiving theophylline treatment. These studies demonstrate that plasma adenosine levels (0.1 to 0.3 mu M) play a key role in negative modulation of PAF activity on platelet aggregation and 5-HT release. After depletion of plasma adenosine, the platelet-aggregating activity of PAF was increased greatly (> 10-fold). PAF at concentrations of 0.1 to 12 mu M caused no 5-HT release in PRP containing normal amounts of adenosine (blood collected in the presence of 2'-deoxycoformycin and dilazep), whereas PAF at 0.1 mu M caused 5-HT release (45%) in adenosine-depleted PRP, demonstrating that plasma adenosine is much more inhibitory of 5-HT release than platelet aggregation. The adenosine antagonists theophylline (50 mu M), caffeine (50 mu M) and a xanthine derivative, 3,7-dimethyl-1-propargylxanthine (DMPX, 10 mu M) (a more specific adenosine A(2) receptor antagonist), potentiated PAF activity on platelet aggregation in PRP samples containing adenosine. Also, patients receiving theophylline treatments showed significantly greater platelet aggregation induced by PAF in their PRP samples. PAF induced a rapid increase (80% in 15 sec) in intracellular Ca2+ mobilization, which was strongly inhibited by adenosine (IC50, 0.3 mu M). Our studies suggest that agents that can increase plasma adenosine levels (e.g. inhibitors of adenosine uptake and adenosine metabolism) or methylxanthines may be useful in altering (inhibiting or enhancing, respectively) PAF actions on platelets and other tissues.

Optimum inhibition of human erythrocyte purine nucleoside phosphorylase by 9-(phosphonoalkyl)hypoxanthines required an alkyl chain of five carbons or longer. Appropriate modifications of either the base or phosphonate side chain resulted in increased inhibitory activity.

As industrialization has taken a great place in our world and also the competitiveness among industry is increasing day by day, so every industry is in a way of manufacturing products of high quality at low cost with a priority of delivering product to customers in stipulated time span. Every industry uses a system to manufacture the product. Therefore, industry needs a manufacturing system which is capable to produce the high quality product in the minimum input. This can be achieved by keeping the manufacturing system productivity high. Hence Productivity measurement is essential to measure the performance of the manufacturing system. In this present work we are developing the methodology to measure the productivity of manufacturing systems Therefore, we are proposing a mathematical model for productivity measurement of manufacturing system such as dedicated system, cellular system and flexible manufacturing system which are capable of producing mass and batch type product. Further the productivity is considered as one of the significant factor for performance measurement of manufacturing systems. The present work include the development of model for the measurement of productivity for the three manufacturing system followed by the case study for the application of the proposed model.

Adenosine (Ado, 10 μM) was metabolized in whole blood within 1 min, primarily to hypoxanthine and ATP. The concentration of Ado, the activities of adenosine deaminase (ADA) and Ado kinase, the K m values for Ado with ADA and Ado kinase, and the substrate inhibition of Ado kinase are factors that govern the Ado metabolism between deamination and phosphorylation. If ADA activity was blocked by 2′-deoxycoformycin (dCF, 5 μM), a tight-binding inhibitor of ADA, most of the Ado (96%) was incorporated into adenine nucleotides, whereas if Ado kinase activity was blocked with 5-iodotubercidin (10 μM), Ado was mainly (95%) metabolized into hypoxanthine. A high phosphate concentration (25 mM) caused marked increases in the formation of IMP. The nucleoside transport inhibitors dilazep (1 μM), dipyridamole (10 μM) and nitrobenzylthioinosine (NBMPR, 1 μM) strongly blocked cellular Ado metabolism. In the presence of nucleoside transport inhibitors, Ado which slowly enters the cell was metabolized principally by Ado kinase rather than ADA. Dilazep, NBMPR and dipyridamole were more effective in blocking Ado uptake and metabolism by erythrocytes suspended in a protein-free medium than by cells suspended in plasma.

Clinical, pharmacologic, and immunologic effects of 2'-deoxycoformycin (dCF) were evaluated in 15 patients with advanced malignancies. Toxicity was less severe with a low dose (4 mg/m2) of dCF, but this dose still resulted in suppression of cellular adenosine deaminase activity, skin test reactivity, and lymphocyte responses to mitogens. Improvement in cutaneous T cell lymphoma plaques was seen after dCF. Further investigations of antitumor efficacy with the use of this low dosage schedule should continue in patients with hematologic neoplasms, and additional preliminary studies of the combination of an adenosine deaminase inhibitor with an adenosine analog should also be considered.

Adenosine (Ado, 10 μM) was metabolized in whole blood within 1 min, primarily to hypoxanthine and ATP. The concentration of Ado, the activities of adenosine deaminase (ADA) and Ado kinase, the Km values for Ado with ADA and Ado kinase, and the substrate inhibition of Ado kinase are factors that govern the Ado metabolism between deamination and phosphorylation. If ADA activity was blocked by 2′-deoxycoformycin (dCF, 5 μM), a tight-binding inhibitor of ADA, most of the Ado (96%) was incorporated into adenine nucleotides, whereas if Ado kinase activity was blocked with 5-iodotubercidin (10 μM), Ado was mainly (95%) metabolized into hypoxanthine. A high phosphate concentration (25 mM) caused marked increases in the formation of IMP. The nucleoside transport inhibitors dilazep (1 μM), dipyridamole (10 μM) and nitrobenzylthioinosine (NBMPR, 1 μM) strongly blocked cellular Ado metabolism. In the presence of nucleoside transport inhibitors, Ado which slowly enters the cell was metabolized principally by Ado kinase rather than ADA. Dilazep, NBMPR and dipyridamole were more effective in blocking Ado uptake and metabolism by erythrocytes suspended in a protein-free medium than by cells suspended in plasma.

This introductory report deals with some of the ingredients of the data exchange process. Current vendor interactive graphics CAD/CAM systems (Applicon, Calma, Computervision, CD-2000, ANVIL-4000, etc.) are discussed from a generic point of view. Also discussed is the data format given in the Initial Graphics Exchange Specification, which is intended to be a standardized format for the communication of data between interactive graphics CAD/CAM systems. 12 refs., 7 figs.

Adenosine (Ado, 10 - 50 μM), a potent inhibitor of ADP-induced human platelet aggregation in platelet-rich plasma (PRP), does not inhibit aggregation in whole blood. However, the Ado analogs, 2-fluoroadenosine, 2-chloroadenosine and 5′-N-ethylcarboxamidoadenosine (NECA) which are resistant to deamination (2-fluoroadenosine) or deamination and phosphorylation (2-chloroadenosine and NECA), inhibit aggregation in whole blood with IC50 values of 12 μM, 2.3 μM and 0.26 μM, respectively. The inhibitory effect of NECA (200 nM) is potentiated by the platelet cAMP phosphodiesterase (PDE) inhibitor RA 233 (5 μM). Inhibition of the erythrocytic nucleoside transport system by dilazep (1 μM) or dipyridamole (10 pM), or blockade of Ado metabolism by 2'-deoxycoformycin (5 μM) plus 5-iodotubercidin (10 μM), evokes the antiaggregatory action of Ado in whole blood (IC50 = 2 μM). RA 233 (5 μM) potentiates Ado-mediated inhibition about 10-fold when nucleoside transport or Ado metabolism is blocked. Ado (10 μM or 200 nM) is rapidly metabolized within 1 min in whole blood. When nucleoside transport is inhibited by dilazep or dipyridamole, or when Ado metabolism is blocked by 2′-deoxycoformycin and 5-iodotubercidin, 50 - 60 % of the Ado remains in the plasma after 5 min. These results show that the failure of Ado to inhibit platelet aggregation in whole blood results from its rapid uptake and metabolism by erythrocytes. More importantly, these data emphasize the key role of nucleoside transport inhibition in the antiplatelet actions of dipyridamole and dilazep. In addition, superior therapeutic results may be obtained from the combination of blockade of the nucleoside transport system with inhibition of platelet cAMP PDE.

5′-Deoxy-5′-halogenated adenosines are alternative substrates for 5′-deoxy-5′-methylthioadenosine phosphorylase (MTAPase), an enzyme responsible for the metabolism of 5′-deoxy-5′-methylthioadenosine (MTA), a by-product of polyamine biosynthesis. The relative reactivity of these nucleosides with MTAPase from HL-60 human promyelocytic leukemia cells is MTA > 5′-deoxy-5′-fluoroadenosine (5′-FlAdo) > 5′-chloro-5′-deoxyadenosine (5′-ClAdo) > 5′-bromo-5′-deoxyadenosine (5′-BrAdo) > 5′-deoxy-5′-iodoadenosine (5′-IAdo). In MTAPase-containing cells, the adenine released from the 5′-halogenated adenosine was incorporated into adenine nucleotide pools; cleavage by (MTAPase appeared to be the rate-limiting step in this process. 5′-BrAdo and 5′-IAdo were growth inhibitors (Spec 50 values < 10 μM) of MTAPase-containing cell lines HL-60 human promyelocytic leukemia and the L5178Y murine lymphoblastic leukemia but were much less active (Spec)(In50) values > 65 μM) against MTAPase-deficient cell lines (the CCRF-CEM human T cell leukemia and the L1210 murine leukemia). The full cytotoxidty of these compounds, therefore, appeared to be related to their phosphorolysis by MTAPase. Indirect evidence suggests that 5-halogenated ribose-1 -phosphate derivatives of 5′-BrAdo or 5′-IAdo produced by the MTAPase reaction were the active metabolites of these 5′-halogenated adenosines.