类叶升麻(毛茛科)自花传粉机制

毛茛科类叶升麻(Actaea asiatica)有2种开花方式, 一种与同属其它植物相同, 花萼片在开花早期脱落, 花药远离柱头; 而另一种较为特殊, 能使该植物进行自花授粉, 即在花开放前, 花萼从花托上脱离, 但萼片并不张开, 部分雄蕊的花丝伸长, 将花药推入萼片和柱头之间, 收缩的花萼片将开裂的花药压在宽大的柱头上, 进而完成自花授粉。套袋实验结果表明, 类叶升麻自发自交具有很高的结籽率, 不具有孤雌生殖和风媒传粉。繁育系统估测分析结果显示, 类叶升麻自交亲和,为兼性自交的繁育系统。     

RIP3 deficiency exacerbates inflammation in dextran sodium sulfate‐induced ulcerative colitis mice model

Ulcerative colitis (UC) is a chronic intestinal inflammatory disease. The receptor‐interacting protein kinase 3 (RIP3) was reported to be involved in many inflammatory disease. However, the mechanism of RIP3 in the pathogenesis of UC is still unclear. To investigate the effects and possible mechanism of RIP3 in UC pathogenesis, RIP3‐/‐ mice was used in dextran sulfate sodium (DSS)‐induced colitis model. It was found that by DSS‐induced colitis, RIP3‐/‐ mice showed significantly enhanced colitis symptoms, including increased weight loss, colon shortening, and colonic mucosa damage and severity, but decreased production of interleukin 6 and interleukin 1β. The results showed that RIP3 deficiency could not ameliorate but exacerbate the severity of colitis. On the mechanism, it was found that messenger RNA expressions of several repair‐associated cytokines including interleukin 6, interleukin 22, cyclooxygenase 2, epithelial growth factor receptor ligand Epiregulin and matrix metalloproteinase 10 were siginificant decreased in RIP3‐/‐ mice. Thus, RIP3‐/‐ mice exhibited an impaired tissue repair in response to DSS. In a conclusion, RIP3 deficiency exerted detrimental effects in DSS induced colitis partially because of the impaired repair‐associated cytokines expression.     

Design,synthesis, biological evaluation,and molecular modeling studies of chalcone-rivastigmine hybrids as cholinesterase inhibitors

A series of novel chalcone-rivastigmine hybrids were designed, synthesized, and tested in vitro for their ability to inhibit human acetylcholinesterase and butyrylcholinesterase. Most of the target compounds showed hBChE selective activity in the micro- and submicromolar ranges. The most potent compound 3 exhibited comparable IC₅₀ to the commercially available drug (rivastigmine). To better understand their structure activity relationships (SAR) and mechanisms of enzyme-inhibitor interactions, kinetic and molecular modeling studies including molecular docking and molecular dynamics (MD) simulations were carried out. Furthermore, compound 3 blocks the formation of reactive oxygen species (ROS) in SH-SY5Y cells and shows the required druggability and low cytotoxicity, suggesting this hybrid is a promising multifunctional drug candidate for Alzheimer’s disease (AD) treatment.     

Porcine Cloned Embryos Reconstructed with the Cell Nuclei of Tetraploid M-phase Fibroblast Cells Can Restore Normal Diploidy at the Blastocyst Stage

The cell cycle of donor cells as a major factor that affects cloning efficiency remains debatable. G2/M phase cells as a donor can successfully produce cloned animals, but a minimal amount is known regarding nuclear remodeling events. In this study, porcine fetal fibroblasts (PFFs) were carefully synchronized at G1 or M phase as donor cells. Most of the cloned embryos reconstructed from PFFs at G1 (G1-embryos) or M (M-embryos) phase formed a pronucleus-like nucleus (PN) within 6-h post fusion (hpf), but the M-embryos formed PN earlier than the G1-embryos did. Moreover, 77.4% of the M-embryos formed two PNs, whereas the G1-embryos formed a single PN. The rate of extrusion of polar body-like structures by the M-embryos was significantly lower than that extruded by the G1-embryos (26.3% vs. 37.1%, P?相似文献   

High-yield of biologically active recombinant human fibroblast growth factor-16 in E. coli and its mechanism of proliferation in NCL-H460 cells

Fibroblast growth factor-16 (FGF16) is a member of FGF9 subfamily, which plays key role in promoting mitosis and cell survival, and also involved in embryonic development, cell growth, tissue repair, morphogenesis, tumor growth, and invasion. However, the successful high-yield purification of recombinant human fibroblast growth factor-16 (rhFGF16) protein has not been reported. In addition, lung cancer is a major cause of cancer-related deaths, which threats people’s lives and its incidence has continued to rise. Learning pathways or proteins, which involved in lung tumor progression will contribute to the development of early diagnosis and targeted therapy. FGF16 promoted proliferation and invasion behavior of SKOV-3 ovarian cancer cells, whose function may be similar in lung cancer. The hFGF16 was cloned into pET-3d and expressed in Escherichia coli BL21 (DE3) pLysS. Finally, obtained two forms of FGF16 that exhibited remarkable biological activity and the purity is over 95%, meanwhile, the yield of soluble 130?mg/100?g and insoluble 240?mg/100?g. Experiments demonstrated FGF16 could promote proliferation of NCL-H460 cells by activating Akt, Erk1/2, and p38 MAPK signaling, whereas JNK had no significant effect. In total, this optimized expression strategy enables significant quantity and activity of rhFGF16, thereby meeting its further pharmacological and clinical usages.     

PCK1 expression is correlated with the plasma glucose level in the duck

Phosphoenolpyruvate carboxykinase 1 (soluble) (PCK1) is a key gene in gluconeogenesis and glyceroneogenesis. Although its functions have been extensively studied in mice, bats and humans, little is known in ducks. Here, PCK1 functions were studied using a duck domestication model and a 48‐h fasting experiment. We found PCK1 expression significantly decreased in two breeds of domestic ducks (Jinyun Pockmark ducks and Cherry Valley ducks) as compared with wild ducks (Anas platyrhynchos). Simultaneously, plasma levels of glucose, triglycerides and free fatty acid in domestic ducks were lower than in wild ducks. When compared with fed ducks, the plasma triglyceride level was observed to be significantly decreased, while the glucose and free fatty acid levels remained constant in 48‐h fasting ducks. The expression analysis of gluconeogenic genes revealed that fructose‐1,6‐bisphosphatase genes (FBP1 and FBP2) and the glucose‐6‐phosphatase gene (G6PC2) were not changed, whereas PCK1 was significantly upregulated. In addition, the reported regulators of PCK1, including forkhead box A2 (FOXA2) gene and orphan nuclear receptor NR4A family genes (NR4A1, NR4A2 and NR4A3), exhibited similar expression levels between 48‐h fasting ducks and fed ducks, suggesting that PCK1 is not regulated by these genes in the duck under fasting conditions. In conclusion, PCK1 expression may affect plasma levels of glucose, triglycerides and free fatty acid during the duck domestication process. This work demonstrates for the first time in duck that PCK1 is a key gene in maintaining plasma glucose homeostasis during fasting and that the upregulated expression of PCK1 may be responsible for constant plasma free fatty acid level by the glyceroneogenesis process.     

Reactive Oxygen Species: Potential Regulatory Molecules in Response to Hypomagnetic Field Exposure

Organisms, including humans, could be exposed to hypomagnetic fields (HMFs, intensity <5 μT), e.g. in some artificially shielded magnetic environments and during deep-space flights. Previous studies have demonstrated that HMF exposure could have negative effects on the central nervous system and embryonic development in many animals. However, the underlying mechanisms remain unknown. Studies have revealed that HMFs affect cellular reactive oxygen species (ROS) levels and thereby alter physiological and biological processes in organisms. ROS, the major component of highly active free radicals, which are ubiquitous in biological systems, were hypothesized to be the candidate signaling molecules that regulate diverse physiological processes in response to changes in magnetic fields. Here, we summarize the recent advances in the study of HMF-induced negative effects on the central nervous system and early embryonic development in animals, focusing on cellular ROS and their role in response to HMFs. Furthermore, we discuss the potential mechanism through which HMFs regulate ROS levels in cells. © 2020 Bioelectromagnetics Society