Nitiric oxide (NO) and eicosanoids function as crucial immune mediators in insects. This study focuses on cross-talkbetween two immune mediators in term of humoral immune response in Spodoptera exigua. Up-regulation of eight differentanti-microbial peptides (AMP) was observed against bacterial challenge. In contrast, injection of E. coli along with L-NAMEsignificantly down regulation the AMP production whereas D-NAME was not effective. The injection of E. coli withdexamethasone or SNAP also decreased AMP production whereas arachidonic acid (AA) compensated the dexamethasoneeffects. RNA inerferece against SeNOS showed the down-regulation of defensin mRNA level, whereas dsNOS injectionswith AA reversed the gene regulation.

We have constructed a wide-field photometric survey system called as the Korea Microlensing Telescope Network (KMTNet) in 2015. It consists of three 1.6 m optical telescopes equipped with mosaic CCD cameras. Four 9k CCDs were installed on the focal plane of each telescope. In this paper, we present the crosstalk analysis of the KMTNet mosaic CCD images. The crosstalk victims caused by bright sources were visible at eight sub-images obtained through different readout ports of each CCD. The crosstalk coefficients were estimated to be several tens of 10-4 in maximum, differing from sub-image to sub-image, and the non-linearity effect certainly appeared at the victims made from saturated sources. We developed software functions to correct the crosstalk effect of the KMTNet CCD images. The software functions showed satisfying results to remove clearly most of the crosstalk victims and have been implemented in the KMTNet image processing pipeline since 2015 September.

Uniform brightness is very crucial for LCD panels, which should be made in during manufacturing. Usually some compensating algorithms are applied to recover the brightness deviation that occurs in actual panels. Although such remedying tools are used, it is very hard to prevent horizontal or vertical crosstalks that represent the brightness level difference in horizontal or vertical direction. This research applied transformability Taguchi dynamic characteristics and “nominal is best” static characteristic simultaneously to design the compensating circuit optimally that may reduce the crosstalks and make uniform brightness level.

Substantia gelatinosa (SG) neurons receive synaptic inputs from primary afferent Aδ- and C-fibers, where nociceptive information is integrated and modulated by numerous neurotransmitters or neuromodulators. A number of studies were dedicated to the molecular mechanism underlying the modulation of excitability or synaptic plasticity in SG neurons and revealed that second messengers, such as cAMP and cGMP, play an important role. Recently, cAMP and cGMP were shown to downregulate each other in heart muscle cells. However, involvement of the crosstalk between cAMP and cGMP in neurons is yet to be addressed. Therefore, we investigated whether interaction between cAMP and cGMP modulates synaptic plasticity in SG neurons using slice patchclamp recording from rats. Synaptic activity was measured by excitatory post-synaptic currents (EPSCs) elicited by stimulation onto dorsal root entry zone. Application of 1 mM of 8- bromoadenosine 3,5-cyclic monophosphate (8-Br-cAMP) or 8-bromoguanosine 3,5-cyclic monophosphate (8-Br-cGMP) for 15 minutes increased EPSCs, which were maintained for 30 minutes. However, simultaneous application of 8-BrcAMP and 8-Br-cGMP failed to increase EPSCs, which suggested antagonistic cross-talk between two second messengers. Application of 3-isobutyl-1-methylxanthine (IBMX) that prevents degradation of cAMP and cGMP by blocking phosphodiesterase (PDE) increased EPSCs. Co-application of cAMP/cGMP along with IBMX induced additional increase in EPSCs. These results suggest that second messengers, cAMP and cGMP, might contribute to development of chronic pain through the mutual regulation of the signal transduction.

Autophagy means “self-eating” and it is a major catabolic pathway within cells. A basal level of autophagy is required for survival of cells or organisms, but prolonged activation of autophagy may have an adverse effect. In mammalian systems, autophagy is stimulated by nutrient starvation or deprivation of growth factors. Ovariectomy on day 4 of pregnancy in mice to deprive blastocysts of estrogen induces “dormancy” in blastocysts and delay the process of implantation until estrogen is given. Dormant blastocysts maintain a state of low metabolism in utero and survive for many days without initiating implantation under the unfavorable condition of estrogen deficiency. We tested the hypothesis if an autophagic response is operative in dormant blastocysts for prolonged survival in utero during the delayed implantation. We observed that autophagy is highly activated in dormant blastocysts. Interestingly, autophagic activation is more prominent in trophectoderm than in inner cell mass. Activation of blastocysts by estrogen supplementation induces formation of multivesicular bodies and exosomes in the trophectoderm. Dormant blastocysts with longer period of autophagic activation show compromised development after implantation. Thus, autophagy may be a critical cellular mechanism to provide energy source during extended survival of dormant blastocysts. However, prolonged activation of autophagy may compromise developmental outcome of blastocysts with irreparable cellular damage.

Seed germination and the establishment of young seedlings are critical phases in the plant’s life cycle. To control these processes, plants have evolved diverse hormonal signaling networks in which brassinosteroids (BRs) attenuate abscisic acid (ABA) responses; however, the underlying regulatory mechanism remains elusive. Here, we reveal that epigenetic silencing of the ABA signaling regulator ABI3 via the BR-related transcription factor BES1 is essential for the inhibitory effect of BRs on ABA signaling during early seedling development. BR-activated BES1 forms a transcriptional repressor complex with TPL via its EAR motif that recruits the histone deacetylase HDA19. This facilitates the histone H3-mediated deacetylation of ABI3 chromatin, leading to the suppression of ABI3 and its downstream target ABI5, which results in reduced ABA sensitivity. We propose that the BR-activated BES1-TPL-HDA19 repressor complex controls epigenetic silencing of ABI3 and thereby suppresses the ABA response during early seedling development.