116 research outputs found

    Potential of tropical maize populations for improving an elite maize hybrid

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    Identifying exotic maize (Zea mays L) populations possessing favorable new alleles lacking in local elite hybrids is an important strategy for improving maize hybrids. Selection of an appropriate breeding method will increase the chance of successfully transferring these favorable new alleles into elite inbred lines of local hybrids. The objec¬tives of this study were to: (i) evaluate 14 maize populations from CIMMYT and identify those containing favorable alleles for grain yield, ear length, ear diameter, kernel length, plant height, and ear height that are lacking in a local super hybrid [Jidan261 (W9706 × Ji853)], and to (ii) determine which inbred parent should be improved. These re¬sults showed that the populations Pob43, Pob501, and La Posta had positive and significant numbers of favorable alleles not found in hybrid W9706 × Ji853 that could be used for simultaneous improvement of its grain yield, ear length, and kernel length, and that population QPM-Y was also a good donor for improvement of ear diameter and kernel length in the hybrid. Based on allele frequencies in the two inbred lines and the donor population, when the populations Pob43, La Posta, Pob501, and QPM-Y were used as donors, inbred line W9706 would be improved by selfing the F1 of the cross W9706 × donor population. These results suggested that CIMMYT germplasm has potential to improve temperate elite hybrids. The relationship between GCA and SCA from a previous study and the parameters obtained from the Dudley method are discussed. The results showed that the values of Lplμ’ esti¬mates obtained by applying the Dudley method had the same trend as GCA effects for grain yield but a less clear trend for ear length, while the trends in the relationship value were reversed for SCA between these populations and Lancaster-derived lines

    Voluntary agreements to achieve energy efficiency, a comparison between China and The Netherlands

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    China has gained experience with voluntary agreements. In this paper the experiences in China will be analysed and compared to the factors contributing to the success of this model in the Netherlands. Are voluntary agreements an alternative for the Chinese command and control system? We distinguish different types of voluntary agreements and compare those in China and the Netherlands on a number of dimensions. The hypothesis is tested that voluntary agreements are more effective in achieving pollution control than the traditional command and control approach. It is found that indeed most voluntary agreements score good in China as well as in the Netherlands on a number of chosen indicators. Voluntary agreements are effective in achieving ambitious energy saving targets in a flexible and cost-effective way. Voluntary agreements have the function to mobilise support for energy saving, which is not easily mobilised through the traditional command-and-control approaches. There are however some important differences between the functioning of the system in China and in the Netherlands, where a more bottom-up approach is common. The Netherlands has a tradition of stakeholders' involvement and experience over a longer time of monitoring the effectiveness of the project and adjusting them if necessary

    TLR3 Regulated Poly I:C-Induced Neutrophil Extracellular Traps and Acute Lung Injury Partly Through p38 MAP Kinase

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    Acute lung injury (ALI) is the leading cause of morbidity and mortality in critically ill patients. Neutrophil extracellular traps (NETs) have been well documented in the ALI model of bacterial infection. In the present study, we demonstrated that poly I:C could induce pulmonary NETs. Upon poly I:C intratracheal inoculation, neutrophil infiltration in the bronchoalveolar lavage fluid (BALF) was significantly increased. Furthermore, the inflammatory cytokines IL-1β, IL-6, and TNF-α in the lung were also significantly elevated. Neutrophil depletion abolished NETs and decreased both neutrophil infiltration and IL-1β in the lung. As expected, DNase I, an inhibitor of MPO and NADPH, decreased pulmonary inflammation and NETs. Blocking of the poly I:C receptor TLR3 reduced lung inflammation and NETs. The MAPK kinase inhibitor p38 diminished the formation of NETs and restored the expression of the tight junction protein claudin-5 in the mouse lung when challenged with poly I:C. In summary, poly I:C induced the formation of pulmonary NETs and ALI, which may be associated with the activation of p38 MAPK and the decreased expression of claudin-5

    Oral Administration of Alkylglycerols Differentially Modulates High-Fat Diet-Induced Obesity and Insulin Resistance in Mice

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    Alkylglycerols (AKGs) from shark liver oil (SLO) were demonstrated to have strong potency to stimulate immune response. However, no study has been conducted on the effects of AKGs on diet-induced obesity and metabolic inflammatory disorder. The purpose of the present study was to investigate the effect of two AKGs isoforms on obesity and insulin resistance in mice fed high-fat (HF) diet. Forty-eight C57BL/6 mice were divided into normal, HF, HF+20 mg/kg selachyl alcohol (SA), HF+200 mg/kg SA, HF+20 mg/kg batyl alcohol (BA), and HF+200 mg/kg BA groups. Body weight, fasting glucose, lipids, insulin and leptin levels, serum IL-1β, and TNF-α levels were compared among different groups. Our results showed that high-dose SA decreased body weight, serum triglyceride, cholesterol, fasting glucose level, insulin level, and serum leptin level of the HF fed mice, while high-dose BA increased fasting insulin level of the HF fed mice. Pretreatment of primary adipocytes with 10 μM SA or BA differentially modulates LPS-mediated MAPK and NF-κB signaling. Our study demonstrated that oral administration of AKGs has differential effects on HF-induced obesity and metabolic inflammatory disorder in mice

    Genetic characterization and linkage disequilibrium mapping of resistance to gray leaf spot in maize (Zea mays L.)

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    AbstractGray leaf spot (GLS), caused by Cercospora zeae-maydis, is an important foliar disease of maize (Zea mays L.) worldwide, resistance to which is controlled by multiple quantitative trait loci (QTL). To gain insights into the genetic architecture underlying the resistance to this disease, an association mapping population consisting of 161 inbred lines was evaluated for resistance to GLS in a plant pathology nursery at Shenyang in 2010 and 2011. Subsequently, a genome-wide association study, using 41,101 single-nucleotide polymorphisms (SNPs), identified 51 SNPs significantly (P<0.001) associated with GLS resistance, which could be converted into 31 QTL. In addition, three candidate genes related to plant defense were identified, including nucleotide-binding-site/leucine-rich repeat, receptor-like kinase genes similar to those involved in basal defense. Two genic SNPs, PZE-103142893 and PZE-109119001, associated with GLS resistance in chromosome bins 3.07 and 9.07, can be used for marker-assisted selection (MAS) of GLS resistance. These results provide an important resource for developing molecular markers closely linked with the target trait, enhancing breeding efficiency

    Measuring urban resilience to climate change in three chinese cities

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    Building an urban resilience index results in developing an increasingly popular tool for monitoring progress towards climate-proof cities. This paper develops an urban resilience index in the context of urban China, which helps planners and policy-makers

    Vitamin D and IL-10 Deficiency in Preterm Neonates With Bronchopulmonary Dysplasia

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    Introduction: Vitamin D deficiency and inflammation are involved with bronchopulmonary dysplasia (BPD) in preterm neonates; however, the clinical evidence still remains scarce. We hypothesized that vitamin D and inflammatory cytokines may be risk factors for BPD in infants.Methods: Preterm infants born between 28 and 31 weeks' gestation were recruited between January 2016 and 2017. Blood samples were all collected at corresponding time points. Vitamin D was measured using an automatic biochemical analyzer, and inflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-10) were measured using ELISA.Results: The baseline characteristics for preterm infants without BPD (non-BPD control, n = 20) or with BPD (n = 19) were similar. In the blood samples collected 24-h post birth, vitamin D was significantly reduced in the BPD neonates (non-BPD vs. BPD, 28.96 ± 3.404 vs. 17.99 ± 2.233 nmol/l, p = 0.0134). Inflammatory cytokines TNF-α, IL-1β, and IL-6 were comparable in both groups. The anti-inflammatory cytokine IL-10, however, was significantly decreased in 24-h blood samples from BPD preterm infants (non-BPD vs. BPD, 44.61 ± 10.48 vs. 11.64 ± 2.351 pg/ml, p = 0.0054). In the BPD infants with mild or moderate disease, vitamin D deficiency was quite similar. IL-10 deficiency, however, was more aggravated in the BPD infants with moderate disease. No changes in Vitamin D or cytokines (TNF-α, IL-1β, IL-6, and IL-10) were observed for blood samples collected 2 or 4 weeks after birth.Conclusion: In our pilot study, Vitamin D and IL-10 levels at 24-h of life were risk factors for the development of BPD in very preterm infants

    CXCR2 is essential for cerebral endothelial activation and leukocyte recruitment during neuroinflammation

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    Chemokines and chemokine receptors cooperate to promote immune cell recruitment to the central nervous system (CNS). In this study, we investigated the roles of CXCR2 and CXCL1 in leukocyte recruitment to the CNS using a murine model of neuroinflammation. Wild-type (WT), CXCL1−/−, and CXCR2−/− mice each received an intracerebroventricular (i.c.v.) injection of lipopolysaccharide (LPS). Esterase staining and intravital microscopy were performed to examine neutrophil recruitment to the brain. To assess endothelial activation in these mice, the expression of adhesion molecules was measured via quantitative real-time polymerase chain reaction (PCR) and Western blotting. To identify the cellular source of functional CXCR2, chimeric mice were generated by transferring bone marrow cells between the WT and CXCR2−/− mice. Expression levels of the chemokines CXCL1, CXCL2, and CXCL5 were significantly increased in the brain following the i.c.v. injection of LPS. CXCR2 or CXCL1 deficiency blocked neutrophil infiltration and leukocyte recruitment in the cerebral microvessels. In the CXCR2−/− and CXCL1−/− mice, the cerebral endothelial expression of adhesion molecules such as P-selectin and VCAM-1 was dramatically reduced. Furthermore, the bone marrow transfer experiments demonstrated that CXCR2 expression on CNS-residing cells is essential for cerebral endothelial activation and leukocyte recruitment. Compared with microglia, cultured astrocytes secreted a much higher level of CXCL1 in vitro. Astrocyte culture conditioned medium significantly increased the expression of VCAM-1 and ICAM-1 in cerebral endothelial cells in a CXCR2-dependent manner. Additionally, CXCR2 messenger RNA (mRNA) expression in cerebral endothelial cells but not in microglia or astrocytes was increased following tumor necrosis factor-α (TNF-α) stimulation. The intravenous injection of the CXCR2 antagonist SB225002 significantly inhibited endothelial activation and leukocyte recruitment to cerebral microvessels. CXCL1 secreted by astrocytes and endothelial CXCR2 play essential roles in cerebral endothelial activation and subsequent leukocyte recruitment during neuroinflammation.https://doi.org/10.1186/s12974-015-0316-
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