A single-layer spatial power splitter-combiner structure is packaged in gap waveguide technology. The measured metal-only back-to-back structure features an average insertion loss less than 2.3 dB and a return loss larger than 10 to 20 dB over the entire 75-110 GHz W-band. The design procedure is outlined and the measured and simulated results are shown to be in good agreement. The structure can be used as a stand-alone power splitter and/or combiner (single-mode, all-excited in-phase channels), a quasi-optical beamformer to excite an array of slot antennas in the top ground plane by ridge gap waveguides, or as a back-to-back RF component in grid amplifier designs.

We showed that the rat Na(+)/P(i) cotransporter-1 (RNaPi-1) gene was regulated by insulin and glucose in rat hepatocytes. The aim of this work was to elucidate signaling pathways of insulin-mediated metabolic regulation of the RNaPi-1 gene in H4IIE cells. Insulin increased RNaPi-1 mRNA abundance in the presence of glucose and decreased RNaPi-1 mRNA in the absence of glucose, clearly establishing an involvement of metabolic signals for insulin-induced upregulation of the RNaPi-1 gene. Pyruvate and insulin increased RNaPi-1 expression but downregulated L-pyruvate kinase, indicating the existence of gene-specific metabolic signals. Although fructose, glycerol, and lactate could support insulin-induced upregulation of the RNaPi-1 gene, compounds entering metabolism beyond pyruvate oxidation, such as acetate and citrate, could not, suggesting that RNaPi-1-specific metabolic signals are generated at or above pyruvate oxidation. Wortmannin, LY-294002, and rapamycin abolished the insulin effect on the RNaPi-1 gene, whereas expression of dominant negative Asn(17) Ras and mitogen-activating protein kinase (MAPK) kinase (MEK) inhibitor PD-98059 exhibited no effect. Thus we herein propose that metabolic regulation of RNaPi-1 expression by insulin is mediated through the phosphatidylinositol 3-kinase/p70 ribosomal S6 kinase pathways, but not the Ras/MAPK pathway.

This study summarizes the importance of melatonin in different plants and fungi. In this review, we discussed the biosynthetic pathway of melatonin, its metabolites, and its oxidative reduction. Melatonin is a molecule derived from tryptophan, with pleiotropic activity. It is present in nearly every organism. Its synthetic course depends on the organism in which it resides. The tryptophan to the melatonin pathway, for example, varies in plants and animals. It is thought that the synthetic mechanism for melatonin was inherited in eukaryotes from bacteria caused by endosymbiosis. Nevertheless, the synthetic pathways of melatonin in microorganisms are unknown. The metabolism of melatonin is exceptionally complex with these enzymatic processes developed out of cytochrome C. As well as the enzymatic degradation, melatonin is metabolized by interactive pseudoenzymes and free radicals processes.

DNA methylation is a well-known epigenetic modification that is essential for gene regulation and genome stability. Anomalies in plant development can result from aberrant DNA methylation patterns. DNA methylation is much more important in plants with more complicated genomes when it comes to growth and abiotic stress tolerance. Dynamic regulation via de novo methylation, maintenance of methylation, and active demethylation, which are catalysed by diverse enzymes that are targeted by different regulatory mechanisms, results in a unique DNA methylation state. We explain DNA methylation in plants, including methylating and demethylating enzymes and regulatory changes, as well as the coordination of methylation and demethylation activities by a mechanism known as the methylstat. We also explain the roles of DNA methylation in regulating transposon silencing, gene expression, and chromosome interactions, as well as the intervention of DNA methylation in plant responses to biotic and abiotic stresses.