Further, hCG treatment after JNK inhibition failed to correct the luteal defect and promote P4 output. Similar to hCG, LH treatment improved luteal function as well and this action of LH was associated with JNK activation in the luteal GCs. These findings could be important from the perspective of corpus luteum biology and luteal phase in human because we for the first time identify a critical role for JNK signaling pathway downstream LH receptor activation by hCG/LH in luteal granulosa cells. © The Author(s) 2020. Published by Oxford University Press on behalf of Society for the Study of Reproduction.Gray matter networks (GMn) provide essential information on the intrinsic organization of the brain and appear to be disrupted in Alzheimer's disease (AD). Apolipoprotein E (APOE)-ε4 represents the major genetic risk factor for AD, yet the association between APOE-ε4 and GMn has remained unexplored. Here, we determine the impact of APOE-ε4 on GMn in a large sample of cognitively unimpaired individuals, which was enriched for the genetic risk of AD. We used independent component analysis to retrieve sources of structural covariance and analyzed APOE group differences within and between networks. Analyses were repeated in a subsample of amyloid-negative subjects. Compared with noncarriers and heterozygotes, APOE-ε4 homozygotes showed increased covariance in one network including primarily right-lateralized, parietal, inferior frontal, as well as inferior and middle temporal regions, which mirrored the formerly described AD-signature. This result was confirmed in a subsample of amyloid-negative individuals. APOE-ε4 carriers showed reduced covariance between two networks encompassing frontal and temporal regions, which constitute preferential target of amyloid deposition. Our data indicate that, in asymptomatic individuals, APOE-ε4 shapes the cerebral organization in a way that recapitulates focal morphometric alterations observed in AD patients, even in absence of amyloid pathology. This suggests that structural vulnerability in neuronal networks associated with APOE-ε4 may be an early event in AD pathogenesis, possibly upstream of amyloid deposition. © The Author(s) 2020. Published by Oxford University Press.The acquisition of fear memories involves plasticity of the thalamic and cortical pathways to the lateral amygdala (LA). In turn, the maintenance of synaptic plasticity requires the interplay between input-specific synaptic tags and the allocation of plasticity-related proteins. Based on this interplay, weakly activated synapses can express long-lasting forms of synaptic plasticity by cooperating with strongly activated synapses. Increasing the number of activated synapses can shift cooperation to competition.  https://www.selleckchem.com/products/l-glutamic-acid-monosodium-salt.html  Synaptic cooperation and competition can determine whether two events, separated in time, are associated or whether a particular event is selected for storage. The rules that determine whether synapses cooperate or compete are unknown. We found that synaptic cooperation and competition, in the LA, are determined by the temporal sequence of cortical and thalamic stimulation and that the strength of the synaptic tag is modulated by the endocannabinoid signaling. This modulation is particularly effective in thalamic synapses, supporting a critical role of endocannabinoids in restricting thalamic plasticity. Also, we found that the availability of synaptic proteins is activity-dependent, shifting competition to cooperation. Our data present the first evidence that presynaptic modulation of synaptic activation, by the cannabinoid signaling, functions as a temporal gating mechanism limiting synaptic cooperation and competition. © The Author(s) 2020. Published by Oxford University Press. All rights reserved. For permissions, please e-mail journals.permission@oup.com.A HPLC-DAD method was established for the simultaneous determination of eight components in Leonuri Herba from different habitats, as well as providing methodological reference for quality control of Leonuri Herba. In this study, absolute ethanol extracts of the medicinal material were considered as the sample solutions to be analyzed. Agilent ZORBAX SB-C18 column (250 mm × 4.6 mm, 5 μm) was used for determination maintained at the temperature of 30°C. Gradient elution was performed with a mobile phase of methanol (B)-0.1% phosphoric acid solution (A) at the flow rate of 1.0 mL·min-1. The analysis was carried out at the wavelength of 225, 280 and 320 nm. The measured eight components showed good linear relationships within their own concentration range. Average recoveries ranged from 98.83 to 100.36% with RSDs of 1.14~1.97%. The proposed method was found to be simple, accurate and reproducible, which provided an effective quantitative analytical method for quality control of Leonuri Herba from different habitats. © The Author(s) 2020. Published by Oxford University Press. All rights reserved. For permissions, please email journals.permissions@oup.com.Tartary buckwheat shell is an important by-product of Tartary buckwheat production. Previous studies shown that Tartary buckwheat shells are rich in flavonoids, which are responsible for their antioxidant properties. Due to lack of advanced separation technologies, the purification for Tartary buckwheat shell is still in the laboratory scale, and could not realize the industrialization production. According to the results of static adsorption experiment, AB-8 resin was selected for Tartary buckwheat shell flavonoids (TBSF) adsorption. The adsorption isotherm, resin adsorption thermodynamic and dynamic adsorption parameters were studied. And the adsorption of AB-8 resin for TBSF was determined as an endothermic process. Results of preparative chromatography experiment showed that TBSF could be efficiently purified by AB-8 resin. And the optimal parameters were feed concentration 25 mg/mL, desorption flow rate 2.5 mL/min. Under these conditions, the TBSF were separated effectively. Results of liquid chromatograroducts purification. © The Author(s) 2020. Published by Oxford University Press. All rights reserved. For permissions, please email journals.permissions@oup.com.