Rapid Regeneration Offsets Losses from Warming-Induced Tree Mortality in an Aspen-Dominated Broad-Leaved Forest in Northern China

Worldwide tree mortality as induced by climate change presents a challenge to forest managers. To successfully manage vulnerable forests requires the capacity of regeneration to compensate for losses from tree mortality. We observed rapid regeneration and the growth release of young trees after warming-induced mortality in a David aspen-dominated (Populus davidiana) broad-leaved forest in Inner Mongolia, China, as based on individual tree measurements taken in 2012 and 2015 from a 6-ha permanent plot. Warming and drought stress killed large trees 10–15 m tall with a total number of 2881 trees during 2011–2012, and also thinned the upper crowns. David aspen recruitment increased 2 times during 2012–2015 and resulted in a high transition probability of David aspen replacing the same or other species, whereas the recruitment of Mongolian oak (Quercus mongolica) was much lower: it decreased from 2012 to 2015, indicating that rapid regeneration represented a regrowth phase for David aspen, and not succession to Mongolian oak. Further, we found that the recruitment density increased with canopy openness, thus implying that warming-induced mortality enhanced regeneration. Our results suggest that David aspen has a high regrowth ability to offset individual losses from warming-induced mortality. This important insight has implications for managing this vulnerable forest in the semi-arid region of northern China

Epoxidized isosorbide-based esters with long alkyl chains as efficient and enhanced thermal stability and migration resistance PVC plasticizers

The development of a bio-based plasticizer with good plasticizing performance, migration resistance, and thermal stability for polyvinyl chloride (PVC) is still a notable challenge due to the trade-off between molecular weight and compatibility. Herein, epoxidized isosorbide-based esters featuring multiple epoxy groups were prepared via the esterification of isosorbide with various aliphatic acids with C-18 alkyl chains (oleic acid, linoleic acid, and linolenic acid) followed by epoxidation. The resulting epoxidized isosorbide-based esters were utilized as PVC resin plasticizers, and the overall performance of these plasticized PVC specimens was investigated in detail. Moreover, the esterification reaction was optimized and 1-propylsulfonic-3-methylimidazolium hydrogensulfate ionic liquid was selected as the catalyst. After the reaction was complete, the ionic liquid and product were in separate phases, enabling facile catalyst recycling in a simple, convenient, and environmentally friendly process. The most superior plasticizing effect was achieved by epoxidized isosorbide linolenate (EGLA-ISB). In comparison to the PVC samples plasticized with dioctyl terephthalate (DOTP), those plasticized with EGLA-ISB demonstrated a 15-fold increase in thermal stability during isothermal testing (a PVC/50EGLA-ISB film had a low weight loss of approximately 1.5% after heating at 200 °C for 120 min). Furthermore, the initial thermal decomposition temperature of the PVC plasticized by EGLA-ISB increased by almost 40 °C (up to 306.9 °C) compared to pure PVC, and a higher elongation at break (387%) was also observed. The excellent performance of the PVC plasticized by EGLA-ISB was attributed to the C-18 alkyl chains and multiple epoxy groups of EGLA-ISB, which improved its PVC compatibility, enhanced the thermal stability of the PVC

Design, Synthesis, and Antitumor Activity of Olmutinib Derivatives Containing Acrylamide Moiety

Two series of olmutinib derivatives containing an acrylamide moiety were designed and synthesized, and their IC50 values against cancer cell lines (A549, H1975, NCI-H460, LO2, and MCF-7) were evaluated. Most of the compounds exhibited moderate cytotoxic activity against the five cancer cell lines. The most promising compound, H10, showed not only excellent activity against EGFR kinase but also positive biological activity against PI3K kinase. The structure–activity relationship (SAR) suggested that the introduction of dimethylamine scaffolds with smaller spatial structures was more favorable for antitumor activity. Additionally, the substitution of different acrylamide side chains had different effects on the activity of compounds. Generally, compounds H7 and H10 were confirmed as promising antitumor agents

Synthesis and Biological Evaluation of Novel 8-Morpholinoimidazo[1,2-a]pyrazine Derivatives Bearing Phenylpyridine/Phenylpyrimidine-Carboxamides

Herein we designed and synthesized three series of novel 8-morpholinoimidazo[1,2-a]pyrazine derivatives bearing phenylpyridine/phenylpyrimidine-carboxamides (compounds 12a–g, 13a–g and 14a–g). All the compounds were evaluated for their IC50 values against three cancer cell lines (A549, PC-3 and MCF-7). Most of the target compounds exhibited moderate cytotoxicity against the three cancer cell lines. Two selected compounds 14b, 14c were further tested for their activity against PI3Kα kinase, and the results indicated that compound 14c showed inhibitory activity against PI3Kα kinase with an IC50 value of 1.25 μM. Structure-activity relationships (SARs) and pharmacological results indicated that the replacement of the thiopyranopyrimidine with an imidazopyrazine was beneficial for the activity and the position of aryl group has a significant influence to the activity of these compounds. The compounds 13a–g in which an aryl group substituted at the C-4 position of the pyridine ring were more active than 12a–g substituted at the C-5 position. Moreover, the cytotoxicity of compounds 14a–g bearing phenylpyrimidine-carboxamides was better than that of the compounds 12a–g, 13a–g bearing phenylpyridine-carboxamides. Furthermore, the substituents on the benzene ring also had a significant impact on the cytotoxicity and the pharmacological results showed that electron donating groups were beneficial to the cytotoxicity

Synthesis and Structure–Activity Relationships of 4-Morpholino-7,8-Dihydro-5H-Thiopyrano[4,3-d]pyrimidine Derivatives Bearing Pyrazoline Scaffold

Phosphatidylinositol 3-kinase/Protein kinase B/Mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway is abnormally active in the growth and proliferation of cancer cells. The inhibition of PI3K kinase can effectively block the conduction of signaling pathways and is an ideal target for drug design. In this paper; two series of 4-morpholino-7,8-dihydro-5H-thiopyrano[4,3-d]pyrimidine derivatives bearing pyrazoline moiety (7a–l; 8a–l) were synthesized; and their cytotoxicity in vitro were evaluated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method against four human cancer cell lines including A549; PC-3; MCF-7; and HepG2 cell lines. The activity of the most promising compound 8d against PI3Kα kinase was further evaluated. The results indicated that most of the target compounds showed moderate to excellent cytotoxicity and the most promising compound 8d showed excellent cytotoxicity against four cancer cell lines with half maximal inhibitory concentration (IC50) values of 6.02–10.27 μM. In addition; the compound 8d was found to have a moderate inhibitory activity in the PI3Kα enzyme assay. What’s more; the compounds of which the substituents of benzene ring at the C-4 position are electron-withdrawing groups such as substituents (Cl; F; Br) have better activity than the compounds containing the electron donating groups (OCH3; H). However; the exact action mechanism is not quite clear right now. Further study will be carried out to identify the exact target in near future

Design, synthesis and biological evaluation of novel 4-anlinoquinazoline derivatives as EGFR inhibitors with the potential to inhibit the gefitinib-resistant nonsmall cell lung cancers

A series of quinazoline derivatives with benzylidene hydrazine carboxamide were designed and synthesised as EGFR inhibitors. Most compounds exhibited exceptional anti-proliferative activity against A549, HepG2, MCF-7 and H1975 cells. Furthermore, six compounds demonstrated excellent inhibition activity against EGFRWT with the IC50 value both less than 2 nM. Among the six compounds, 44 exhibited the strongest activity (0.4 nM) and potently inhibited EGFRL858R/T790M (0.1 μM). Excitingly, the most potent compound 14 showed excellent enzyme inhibitory activity with 6.3 nM and 8.4 nM for both EGFRWT and EGFRT790M/L858R. The result of AO single staining and Annexin V/PI staining showed that the compound 14 and 44 could induce remarkable apoptosis of A549 cells. The compound 14 arrested the cell cycle at the S phase and compound 44 arrested the cell cycle at the G0 phase in A549 cells. These preliminary results demonstrate that compound 14 and 44 may be promising lead compound-targeting EGFR