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RISS 인기검색어
- 검색키워드
- 저자 : Yonghua He (검색결과 3 건)
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Yan Li,Yonghua Li,Pan Yang,Hua’ao Zhang,Dan He 한국원예학회 2017 Horticulture, Environment, and Biotechnology Vol.58 No.4
The objective of this study was to evaluate the relationship between cold hardiness and phospholipid andfatty acid content in leaves and roots of chrysanthemum, and to explore cold resistance mechanisms of chrysanthemumin order to provide a theoretical basis for selecting and breeding a new cold-resistant cultivar. We analyzed thephospholipid and fatty acid components in leaves and roots of 10 autumn chrysanthemum cultivars including sixearly-flowering cultivars and four late-flowering cultivars. We determined the content of phosphatidyl ethanolamine(PE), phosphatidyl choline (PC), phosphatidyl serine (PS), phosphatidyl glycerol (PG), myristic acid (C14:0), palmiticacid (C16:0), stearic acid (C18:0), docosanoic acid (C22:0), oleic acid (C18:1), linoleic acid (C18:2), and linolenic acid(C18:3) in leaves and roots of chrysanthemum seedlings grown at 16C and 5C. The cultivars had different responsesto low temperature that included changes in the cell membrane composition in leaves and roots. The main phospholipidin leaves and roots of chrysanthemum was PE, and the main saturated fatty acid was palmitic acid. Amongunsaturated fatty acids, linolenic acid was found in leaves, whereas oleic acid and linoleic acid were present in theroots. Based on the unsaturated fatty acid content and the ratio of unsaturated to saturated fatty acids in leaves, theearly-flowering cultivars ‘Tan Xiang Shi Zi’ and ‘Tong Que Chun Shen’ and the late-flowering cultivars ‘Guan DongXin Xia’ and ‘Yun Long Feng Wu’ were classified as strongly cold tolerant, while the early-flowering cultivar ‘JinFeng Ling’ and the late-flowering cultivar ‘Mo Bao’ were weakly cold tolerant.
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Xiaoyang Zhang,Yonghua He,Quanhui Lin,Lili Huang,Qunwei Zhang,Youqiong Xu 대한독성 유전단백체 학회 2020 Molecular & cellular toxicology Vol.16 No.1
Background Cooking oil fumes (COFs) are composed of particulate matter, polycyclic aromatic hydrocarbons, volatile organic compounds, aldehydes, and ketones, and are currently a global health concern. Some agents in COFs are mutagenic and carcinogenic. However, only a few reports have addressed the hazardous effects of COF exposure on the female reproductive system. In this study, we explored the effects of subchronic exposure to COFs on female gonads in vivo and the possible involvement of the G-protein-coupled receptor 30 signaling pathway. Methods COFs were generated by heating commercially available canola oil in an iron pot. Adult female Wistar rats at 2 months of age were exposed to COFs at 32 mg/m3 for 0, 0.5, 1, 2, or 4 h/day for 56 days. The estrous cycle in rats was studied twice at 7:00 a.m. and 7:00 p.m. on the 43rd treatment day until the current estrous cycle was complete. The rat body weight was measured before the experiment and at day 56 post-exposure. At the end of the experiment, rat blood was collected for gonadal hormone assay, and ovaries were collected for histology and mRNA isolation. The mRNA levels of GPR30, EGFR, STAT3, and ERK were determined by quantitative RT-PCR. Results At a concentration of 32.21 ± 5.11 mg/m3, COF exposure extended the estrous cycle in rats, and ovary coefficient decreased. COFs showed various effects on the sex hormone levels and follicles, depending on its exposure level. Exposure to COFs led to the changes in mRNA levels of the G-protein-coupled receptor 30 (GPR30), epidermal growth factor receptor (EGFR), signal transducer and activator of transcription 3 (STAT3), and extracellular signal-regulated kinase (ERK). Conclusion This study indicated that cooking oil fume exposure disrupted the estrous cycle, sex hormone patterns, and follicle development in female rats in a dose-dependent manner. These adverse effects of cooking oil fumes on female reproductive health were correlated with the G-protein-coupled receptor 30-mediated signaling pathway.
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Couso, Inmaculada,Pé,rez-Pé,rez, Marí,a Esther,Martí,nez-Force, Enrique,Kim, Hee-Sik,He, Yonghua,Umen, James G,Crespo, José,L Oxford University Press 2018 Journal of experimental botany Vol.69 No.6
<▼1><P>Inhibition of autophagic flux prevented the synthesis of triacylglycerols, formation of lipid bodies, and degradation of ribosomal proteins RPS6 and RPL37 in nitrogen- or phosphate-starved <I>Chlamydomonas</I> cells.</P></▼1><▼2><P><B>Abstract</B></P><P>Autophagy is an intracellular catabolic process that allows cells to recycle unneeded or damaged material to maintain cellular homeostasis. This highly dynamic process is characterized by the formation of double-membrane vesicles called autophagosomes, which engulf and deliver the cargo to the vacuole. Flow of material through the autophagy pathway and its degradation in the vacuole is known as autophagic flux, and reflects the autophagic degradation activity. A number of assays have been developed to determine autophagic flux in yeasts, mammals, and plants, but it has not been examined yet in algae. Here we analyzed autophagic flux in the model green alga <I>Chlamydomonas reinhardtii</I>. By monitoring specific autophagy markers such as ATG8 lipidation and using immunofluorescence and electron microscopy techniques, we show that concanamycin A, a vacuolar ATPase inhibitor, blocks autophagic flux in <I>Chlamydomonas</I>. Our results revealed that vacuolar lytic function is needed for the synthesis of triacylglycerols and the formation of lipid bodies in nitrogen- or phosphate-starved cells. Moreover, we found that concanamycin A treatment prevented the degradation of ribosomal proteins RPS6 and RPL37 under nitrogen or phosphate deprivation. These results indicate that autophagy might play an important role in the regulation of lipid metabolism and the recycling of ribosomal proteins under nutrient limitation in <I>Chlamydomonas</I>.</P></▼2>
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