Novel schmitt trigger based on lahbda diode

A new circuit to realise a Schmitt trigger has been conceived. This circuit, which is based on the well known lambda diode, is suitable for integration using CMOS technology. It requires only three devices and is probably simpler than any other conventional Schmitt trigger circuit.

Novel CMOS Schmitt trigger

A novel CMOS Schmitt trigger using only four MOS transistors is discussed. This circuit, which works on the principle of load-coupled regenerative feedback, can be implemented using conventional CMOS technology with only one extra fabrication step. It can be implemented even more easily in CMOS/SOS (silicon-on-sapphire) integrated circuits. The hysteresis of this Schmitt trigger can be controlled by a proper choice of the transistor geometries.

A ternary Schmitt trigger

A new ternary circuit, namely, a ternary Schmitt trigger, is presented. This novel circuit which is based on the well-known lambda diode, is suitable for integration using CMOS technology. The circuit has been simulated using the SPICE 2G Program. The results of the simulation are presented. The circuit offers a high degree of design flexibility. This circuit is expected to be a very useful functional block in the processing of ternary and pseudoternary signals.

Research note A novel BIMOS Schmitt trigger

A new Schmitt trigger circuit based on the lambda bipolar transistor is presented. This circuit which exhibits a hysteresis in its transfer characteristic seems to use a smaller chip area than many of the circuits proposed so far.

Intracellular Pathogen Sensor NOD2 Programs Macrophages to Trigger Notch1 Activation

Intracellular pathogen sensor, NOD2, has been implicated in regulation of wide range of anti-inflammatory responses critical during development of a diverse array of inflammatory diseases; however, underlying molecular details are still imprecisely understood. In this study, we demonstrate that NOD2 programs macrophages to trigger Notch1 signaling. Signaling perturbations or genetic approaches suggest signaling integration through cross-talk between Notch1-PI3K during the NOD2-triggered expression of a multitude of immunological parameters including COX-2/PGE(2) and IL-10. NOD2 stimulation enhanced active recruitment of CSL/RBP-Jk on the COX-2 promoter in vivo. Intriguingly, nitric oxide assumes critical importance in NOD2-mediated activation of Notch1 signaling as iNOS(-/-) macrophages exhibited compromised ability to execute NOD2-triggered Notch1 signaling responses. Correlative evidence demonstrates that this mechanism operates in vivo in brain and splenocytes derived from wild type, but not from iNOS(-/-) mice. Importantly, NOD2-driven activation of the Notch1-PI3K signaling axis contributes to its capacity to impart survival of macrophages against TNF-alpha or IFN-gamma-mediated apoptosis and resolution of inflammation. Current investigation identifies Notch1-PI3K as signaling cohorts involved in the NOD2-triggered expression of a battery of genes associated with anti-inflammatory functions. These findings serve as a paradigm to understand the pathogenesis of NOD2-associated inflammatory diseases and clearly pave a way toward development of novel therapeutics.

Time delay to firing of a triggered vacuum gap with barium titanate in trigger gap

The time delay to the firing of a triggered vacuum gap (t.v.g.) containing barium titanate in the trigger gap is investigated as a function of the main gap voltage, main gap length, trigger pulse duration, trigger current and trigger voltage. The time delay decreases steadily with increasing trigger current and trigger voltage until it reaches saturation. The effect of varying the main gap length and voltage on the time delay is not strong. Before `conditioning�¿ the t.v.g. two groups of time delays, long (>100�¿s) and short (<10�¿s), are simultaneously observed when a large number of trials are conducted. After conditioning, only the group of short time delays are present. This is attributed to the marked reduction of the resistance of the trigger gap across the surface of the solid dielectric resulting directly from the conditioning effect.

NDK Interacts with FtsZ and Converts GDP to GTP to Trigger FtsZ Polymerisation - A Novel Role for NDK

Introduction Nucleoside diphosphate kinase (NDK), conserved across bacteria to humans, synthesises NTP from NDP and ATP. The eukaryotic homologue, the NDPK, uses ATP to phosphorylate the tubulin-bound GDP to GTP for tubulin polymerisation. The bacterial cytokinetic protein FtsZ, which is the tubulin homologue, also uses GTP for polymerisation. Therefore, we examined whether NDK can interact with FtsZ to convert FtsZ-bound GDP and/or free GDP to GTP to trigger FtsZ polymerisation. Methods Recombinant and native NDK and FtsZ proteins of Mycobacterium smegmatis and Mycobacterium tuberculosis were used as the experimental samples. FtsZ polymersation was monitored using 90 degrees light scattering and FtsZ polymer pelleting assays. The gamma 32P-GTP synthesised by NDK from GDP and gamma 32P-ATP was detected using thin layer chromatography and quantitated using phosphorimager. The FtsZ bound P-32-GTP was quantitated using phosphorimager, after UV-crosslinking, followed by SDS-PAGE. The NDK-FtsZ interaction was determined using Ni2+-NTA-pulldown assay and co-immunoprecipitation of the recombinant and native proteins in vitro and ex vivo, respectively. Results NDK triggered instantaneous polymerisation of GDP-precharged recombinant FtsZ in the presence of ATP, similar to the polymerisation of recombinant FtsZ (not GDP-precharged) upon the direct addition of GTP. Similarly, NDK triggered polymerisation of recombinant FtsZ (not GDP-precharged) in the presence of free GDP and ATP as well. Mutant NDK, partially deficient in GTP synthesis from ATP and GDP, triggered low level of polymerisation of MsFtsZ, but not of MtFtsZ. As characteristic of NDK's NTP substrate non-specificity, it used CTP, TTP, and UTP also to convert GDP to GTP, to trigger FtsZ polymerisation. The NDK of one mycobacterial species could trigger the polymerisation of the FtsZ of another mycobacterial species. Both the recombinant and the native NDK and FtsZ showed interaction with each other in vitro and ex vivo, alluding to the possibility of direct phosphorylation of FtsZ-bound GDP by NDK. Conclusion Irrespective of the bacterial species, NDK interacts with FtsZ in vitro and ex vivo and, through the synthesis of GTP from FtsZ-bound GDP and/or free GDP, and ATP (CTP/TTP/UTP), triggers FtsZ polymerisation. The possible biological context of this novel activity of NDK is presented.