Identification of QTLs associated with heat tolerance at the heading and flowering stage in rice (Oryza sativa L.)

Li, Mao-mao,Li, Xia,Yu, Li-qin,Wu, Jin-wen,Li, Hui,Liu, Jin,Ma, Xiao-ding,Jo, Su-min,Park, Dong-Soo,Song, Youchun,Shin, Dongjin,Han, Long-zhi Springer-Verlag 2018 Euphytica Vol.214 No.4

Copigmentation effects and thermal degradation kinetics of purple sweet potato anthocyanins with metal ions and sugars

Xiao-Ding Li,Jie Li,Meng Wang,Hong Jiang 한국응용생명화학회 2016 Applied Biological Chemistry (Appl Biol Chem) Vol.59 No.1

he copigmentation effects of purple sweet potato anthocyanins (PSPAs) with metal ions and sugars were investigated in model solutions at pH 4. The thermal stability of PSPAs was also explored in the presence of sugars and 5-hydroxymethylfurfural (5-HMF). Copigmentation are characterized by hyperchromic effect and bathochromic shift. The hyperchromic effect of Fe3+ reached 25.15 % even at a very low concentration 0.005 mol L−1, while the values of the other metal ions at 0.05 mol L−1 were ranked in the following ascending order: K+ < Ca2+ < Mg2+ < Zn2+ < Cu2+ < Fe2+ < Al3+. The bathochromic shift was not observed in all sugar reaction solutions; glucose showed the highest values of hyperchromic effect at the concentration range 150–300 g L−1, followed by fructose and sucrose; konjac glucomannan showed the highest effect even at a much lower concentration among the macromolecular sugars. Especially, the konjac glucomannan exhibited a much better color enhancement than glucose. Small molecular sugars accelerated the thermal degradation of PSPAs, whereas macromolecular sugars showed a protective effect particularly at high temperatures. Moreover, 5-HMF resulted in the deterioration of the thermal stability of PSPAs and was suggested to be an important labile factor for copigmented PSPA solutions.

Phylogeny and molecular evolution of the DMC1 gene within the StH genome species in Triticeae (Poaceae)

Xiao-Li Wang,Xing Fan,Jian Zeng,Li-Na Sha,Hai-Qin Zhang,Hou-Yang Kang,Rui-Wu Yang,Li Zhang,Chun-Bang Ding,Yong-Hong Zhou 한국유전학회 2012 Genes & Genomics Vol.34 No.3

To estimate the phylogeny and molecular evolution of a single-copy nuclear disrupted meiotic cDNA (DMC1) gene within the StH genome species, two DMC1 homoeologous sequences were isolated from nearly all the sampled StH genome species and were analyzed with those from seven diploid taxa representing the St and H genomes in Triticeae. Sequence diversity patterns and genealogical analysis suggested that (1) there is a close relationship among North American StH genome species;(2) the DMC1 gene sequences of the StH genome species from North America and Eurasia are evolutionarily distinct;(3) the StH genome polyploids have higher levels of sequence diversity in the St genome homoeolog than the H genome homoeolog;(4) the DMC1 sequence may evolve faster in the polyploid species than in the diploids; (5) high dN and dN/dS values in the St genome within polyploid species could be caused by low selective constraints or AT-biased mutation pressure. Our result provides some insight on evolutionary dynamics of duplicate DMC1 gene, the polyploidization events and phylogeny of the StH genome species.

Cinnamaldehyde Derivatives Inhibit Coxsackievirus B3-Induced Viral Myocarditis

Li, Xiao-Qiang,Liu, Xiao-Xiao,Wang, Xue-Ying,Xie, Yan-Hua,Yang, Qian,Liu, Xin-Xin,Ding, Yuan-Yuan,Cao, Wei,Wang, Si-Wang The Korean Society of Applied Pharmacology 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.3

The chemical property of cinnamaldehyde is unstable in vivo, although early experiments have shown its obvious therapeutic effects on viral myocarditis (VMC). To overcome this problem, we used cinnamaldehyde as a leading compound to synthesize derivatives. Five derivatives of cinnamaldehyde were synthesized: 4-methylcinnamaldehyde (1), 4-chlorocinnamaldehyde (2), 4-methoxycinnamaldehyde (3), ${\alpha}$-bromo-4-methylcinnamaldehyde (4), and ${\alpha}$-bromo-4-chlorocinnamaldehyde (5). Neonatal rat cardiomyocytes and HeLa cells infected by coxsackievirus B3 (CVB3) were used to evaluate their antiviral and cytotoxic effects. In vivo BALB/c mice were infected with CVB3 for establishing VMC models. Among the derivatives, compound 4 and 5 inhibited the CVB3 in HeLa cells with the half-maximal inhibitory concentrations values of $11.38{\pm}2.22{\mu}M$ and $2.12{\pm}0.37{\mu}M$, respectively. The 50% toxic concentrations of compound 4 and 5-treated cells were 39-fold and 87-fold higher than in the cinnamaldehyde group. Compound 4 and 5 effectively reduced the viral titers and cardiac pathological changes in a dose-dependent manner. In addition, compound 4 and 5 significantly inhibited the secretion, mRNA and protein expressions of inflammatory cytokines TNF-${\alpha}$, IL-$1{\beta}$ and IL-6 in CVB3-infected cardiomyocytes, indicating that brominated cinnamaldehyde not only improved the anti-vital activities for VMC, but also had potent anti-inflammatory effects in cardiomyocytes induced by CVB3.

JCAD deficiency attenuates activation of hepatic stellate cells and cholestatic fibrosis

Li Xie,Hui Chen,Li Zhang,Yue Ma,Yuan Zhou,Yong-Yu Yang,Chang Liu,Yu-Li Wang,Ya-Jun Yan,Jia Ding,Xiao Teng,Qiang Yang,Xiu-Ping Liu,Jian Wu 대한간학회 2024 Clinical and Molecular Hepatology(대한간학회지) Vol.30 No.2

Background/Aims: Cholestatic liver diseases including primary biliary cholangitis (PBC) are associated with active hepatic fibrogenesis, which ultimately progresses to cirrhosis. Activated hepatic stellate cells (HSCs) are the main fibrogenic effectors in response to cholangiocyte damage. JCAD regulates cell proliferation and malignant transformation in nonalcoholic steatoheaptitis-associated hepatocellular carcinoma (NASH-HCC). However, its participation in cholestatic fibrosis has not been explored yet. Methods: Serial sections of liver tissue of PBC patients were stained with immunofluorescence. Hepatic fibrosis was induced by bile duct ligation (BDL) in wild-type (WT), global JCAD knockout mice (JCAD-KO) and HSC-specific JCAD knockout mice (HSC-JCAD-KO), and evaluated by histopathology and biochemical tests. In situ-activated HSCs isolated from BDL mice were used to determine effects of JCAD on HSC activation. Results: In consistence with staining of liver sections from PBC patients, immunofluorescent staining revealed that JCAD expression was identified in smooth muscle α-actin (α-SMA)-positive fibroblast-like cells and was significantly up-regulated in WT mice with BDL. JCAD deficiency remarkably ameliorated BDL-induced hepatic injury and fibrosis, as documented by liver hydroxyproline content, when compared to WT mice with BDL. Histopathologically, collagen deposition was dramatically reduced in both JCAD-KO and HSC-JCAD-KO mice compared to WT mice, as visualized by Trichrome staining and semi-quantitative scores. Moreover, JCAD deprivation significantly attenuated in situ HSC activation and reduced expression of fibrotic genes after BDL. Conclusions: JCAD deficiency effectively suppressed hepatic fibrosis induced by BDL in mice, and the underlying mechanisms are largely through suppressed Hippo-YAP signaling activity in HSCs.

MTHFR C677T Polymorphism and Ovarian Cancer Risk: A Meta-analysis

Ding, Xiao-Ping,Feng, Li,Ma, Li Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.8

Background: Many studies have investigated possible association between the methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism and ovarian cancer risk, but the impact is still unclear owing to the obvious inconsistencies. This study was performed to quantify the strength of the association with a metaanalysis. Methods: We searched the PubMed, Embase, and CNKI databases for studies relating the association between MTHFR C677T polymorphism and ovarian cancer risk and estimated summary odds ratios (ORs) with confidence intervals (CIs) for assessment. Results: Finally, eight studies with a total of 3,379 ovarian cancer cases and 4,078 controls were included into this meta-analysis. Overall the showed that MTHFR C677T polymorphism was not associated with ovarian cancer risk under all genetic models ($OR_{T\;versus\;C}$ = 1.03, 95%CI 0.90-1.18; $OR_{TT\;versus\;CC}$ = 1.08, 95%CI 0.79-1.47; $OR_{TT\;versus\;TC+CC}$ = 1.05, 95%CI 0.80-1.37; $OR_{TT+TC\;versus\;CC}$ = 1.05, 95%CI 0.86-1.21). Meta-analyses of studies with confirmation of HWE also showed no significant association. Subgroup analyses by ethnicity showed there was no significant association in the Caucasians but MTHFR C677T polymorphic variant T contributed to increased risk of ovarian cancer in East Asians. No evidence of publication bias was observed. Conclusion: Meta-analyses of available data show that MTHFR C677T polymorphism is not associated with ovarian cancer risk in Caucasians, but the MTHFR polymorphic variant T may contribute to increased risk in East Asians.

Microstructure evolution and effect on deuterium retention in oxide dispersion strengthened tungsten during He⁺ irradiation

Ding, Xiao-Yu,Xu, Qiu,Zhu, Xiao-yong,Luo, Lai-Ma,Huang, Jian-Jun,Yu, Bin,Gao, Xiang,Li, Jian-Gang,Wu, Yu-Cheng Korean Nuclear Society 2020 Nuclear Engineering and Technology Vol.52 No.12

Oxide dispersion-strengthened materials W-1wt%Pr₂O₃ and W-1wt%La₂O₃ were synthesized by wet chemical method and spark plasma sintering. The field emission scanning electron microscopy (FE-SEM) analysis, XRD and Vickers microhardness measurements were conducted to characterize the samples. The irradiations were carried out with a 5 keV helium ion beam to fluences up to 5.0 × 10²¹ ions/m² under 600 ℃ using the low-energy ion irradiation system. Transmission electron microscopy (TEM) study was performed to investigate the microstructural evolution in W-1wt%Pr₂O₃ and W-1wt%La₂O₃. At 1.0 × 10²⁰ He⁺/m², the average loops size of the W-1wt%Pr₂O₃ was 4.3 nm, much lower than W-1wt% La₂O₃ of 8.5 nm. However, helium bubbles were not observed throughout in both doped W materials. The effects of pre-irradiation with 1.0 × 10²¹ He⁺/m² on trapping of injected deuterium in doped W was studied by thermal desorption spectrometry (TDS) technique using quadrupole mass spectrometer. Compared with the samples without He⁺ pre-irradiation, deuterium (D) retention of doped W materials increased after He⁺ irradiation, whose retention was unsaturated at the damage level of 1.0 × 10²²D₂⁺/m². The present results implied that irradiation effect of He⁺ ions must be taken into account to evaluate the deuterium retention in fusion material applications.

Cinnamaldehyde Derivatives Inhibit Coxsackievirus B3-Induced Viral Myocarditis

( Xiao-qiang Li ),( Xiao-xiao Liu ),( Xue-ying Wang ),( Yan-hua Xie ),( Qian Yang ),( Xin-xin Liu ),( Yuan-yuan Ding ),( Wei Cao ),( Si-wang Wang ) 한국응용약물학회 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.3

The chemical property of cinnamaldehyde is unstable in vivo, although early experiments have shown its obvious therapeutic effects on viral myocarditis (VMC). To overcome this problem, we used cinnamaldehyde as a leading compound to synthesize derivatives. Five derivatives of cinnamaldehyde were synthesized: 4-methylcinnamaldehyde (1), 4-chlorocinnamaldehyde (2), 4-methoxycinnamaldehyde (3), α-bromo-4-methylcinnamaldehyde (4), and α-bromo-4-chlorocinnamaldehyde (5). Neonatal rat cardiomyocytes and HeLa cells infected by coxsackievirus B3 (CVB3) were used to evaluate their antiviral and cytotoxic effects. In vivo BALB/c mice were infected with CVB3 for establishing VMC models. Among the derivatives, compound 4 and 5 inhibited the CVB3 in HeLa cells with the half-maximal inhibitory concentrations values of 11.38 ± 2.22 μM and 2.12 ± 0.37 μM, respectively. The 50% toxic concentrations of compound 4 and 5-treated cells were 39-fold and 87-fold higher than in the cinnamaldehyde group. Compound 4 and 5 effectively reduced the viral titers and cardiac pathological changes in a dose-dependent manner. In addition, compound 4 and 5 significantly inhibited the secretion, mRNA and protein expressions of inflammatory cytokines TNF-α, IL-1β and IL-6 in CVB3-infected cardiomyocytes, indicating that brominated cinnamaldehyde not only improved the anti-vital activities for VMC, but also had potent anti-inflammatory effects in cardiomyocytes induced by CVB3.

Relationship between porcine miR-20a and its putative target low-density lipoprotein receptor based on dual luciferase reporter gene assays

Yueyun Ding,Shujiao Zhu,Chaodong Wu,Li Qian,DengTao Li,Li Wang,Yuanlang Wang,Wei Zhang,Min Yang,Jian Ding,Xudong Wu,Xiao-Dong Zhang,Yafei Gao,Zongjun Yin 아세아·태평양축산학회 2019 Animal Bioscience Vol.32 No.7

Objective: Mutations in low-density lipoprotein receptor (LDLR), which encodes a critical protein for cholesterol homeostasis and lipid metabolism in mammals, are involved in cardiometabolic diseases, such as familial hypercholesterolemia in pigs. Whereas microRNAs (miRNAs) can control LDLR regulation, their involvement in circulating cholesterol and lipid levels with respect to cardiometabolic diseases in pigs is unclear. We aimed to identify and analyze LDLR as a potential target gene of SSC-miR-20a. Methods: Bioinformatic analysis predicted that porcine LDLR is a target of SSC-miR-20a. Wild-type and mutant LDLR 3′-untranslated region (UTR) fragments were generated by polymerase chain reaction (PCR) and cloned into the pGL3-Control vector to construct pGL3 Control LDLR wild-3′-UTR and pGL3 Control LDLR mutant-3′-UTR recombinant plasmids, respectively. An miR-20a expression plasmid was constructed by inserting the porcine pre-miR-20a-coding sequence between the HindIII and BamHI sites in pMR-mCherry, and constructs were confirmed by sequencing. HEK293T cells were co-transfected with the miR-20a expression or pMR-mCherry control plasmids and constructs harboring the corresponding 3′-UTR, and relative luciferase activity was determined. The relative expression levels of miR-20a and LDLR mRNA and their correlation in terms of expression levels in porcine liver tissue were analyzed using reverse-transcription quantitative PCR. Results: Gel electrophoresis and sequencing showed that target gene fragments were successfully cloned, and the three recombinant vectors were successfully constructed. Compared to pMR-mCherry, the miR-20a expression vector significantly inhibited wild-type LDLR-3′-UTR-driven (p<0.01), but not mutant LDLR-3′-UTR-driven (p>0.05), luciferase reporter activity. Further, miR-20a and LDLR were expressed at relatively high levels in porcine liver tissues. Pearson correlation analysis revealed that porcine liver miR-20a and LDLR levels were significantly negatively correlated (r = –0.656, p<0.05). Conclusion: LDLR is a potential target of miR-20a, which might directly bind the LDLR 3′-UTR to post-transcriptionally inhibit expression. These results have implications in understanding the pathogenesis and progression of porcine cardiovascular diseases.

Involvement of ER–calreticulin–Ca²⁺ signaling in the regulation of porcine oocyte meiotic maturation and maternal gene expression

Zhang, Ding-Xiao,Li, Xiao-Ping,Sun, Shao-Chen,Shen, Xing-Hui,Cui, Xiang-Shun,Kim, Nam-Hyung Wiley Subscription Services, Inc., A Wiley Company 2010 Molecular reproduction and development Vol.77 No.5

<P>Calcium is one of the most ubiquitous signaling molecules, and controls a wide variety of cellular processes. It is mainly stored in the endoplasmic reticulum (ER), bound to lumenal proteins. Calreticulin is the major Ca<SUP>2+</SUP>-binding chaperone in oocytes, and is integral to numerous cellular functions. To better understand the role of the ER– calreticulin–Ca<SUP>2+</SUP> pathway in oocyte maturation and early embryogenesis, we characterized the porcine calreticulin gene and investigated its expression profile during oocyte maturation and early embryonic development. Calreticulin was widely expressed in pig tissues and its transcripts were downregulated during maturation, especially at 44 hr, and were undetectable at the blastocyst stage. We also investigated the effect of increased cytosolic Ca<SUP>2+</SUP> induced by the Ca<SUP>2+</SUP>-ATPase inhibitor, cyclopiazonic acid (CPA), on pig oocyte maturation and maternal gene expression. CPA at 10 µM did not inhibit germinal vesicle breakdown, but did result in the arrest of 38.6% oocytes at or before the MI stage. In addition, expression of the maternal genes C-mos, BMP15, GDF9, and Cyclin B1 was significantly increased in CPA-treated MII oocytes compared with control groups. These data were supported by the results of poly(A)-test PCR, which revealed that the cyclin B1 short isoform (CB-S), GDF9, and C-mos underwent more intensive polyadenylation modification in CPA-treated oocytes than control oocytes, suggesting that polyadenylation may influence Ca<SUP>2+</SUP>-modulated changes in gene expression. Furthermore, CPA treatment decreased the percentage of four-cell parthenotes that developed into blastocysts, suggesting the need for functional SR/ER Ca<SUP>2+</SUP>-ATPase pumps or Ca<SUP>2+</SUP> signals during early embryo development after zygotic genome activation. Together, these data indicate that ER–calreticulin-associated Ca<SUP>2+</SUP> homeostasis plays a role in oocyte and embryo development, and that alterations in maternal gene expression may contribute to the underlying molecular mechanism, at least partially, via polyadenylation. Mol. Reprod. Dev. 77: 462–471, 2010. © 2010 Wiley-Liss, Inc.</P>