40 research outputs found

    Overexpression of the Gene Encoding Solanum lycopersicum Carotenoid Cleavage Dioxygenase 1A (SlCCD1A) Regulates Tomato Flavor Quality

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    SlCCD1A-OE lines of cherry tomato CI1005 and large-fruited tomato AC were selected to investigate the effect of SlCCD1A on tomato flavor quality. The transgenic plants were identified by real-time polymerase chain reaction (PCR), and the volatile components and major quality traits of the transgenic lines were determined. The results showed that SlCCD1A-OE mainly cleaved lycopene and β-carotene in tomato fruit, and increased the contents of 11 volatile isoprene compounds, including 6-methyl-5-heptene-2-one, compared with the wild type (WT). The total amount of these isoprene compounds was the highest in strain OE-3 from CI1005, which was 5.68 times of that in WT, and it increased 1.88 times in OE-8 from AC compared with WT, significantly enhancing the floral, fruity, and sweet aroma. The soluble solid content, total sugar content, and sugar/acid ratio in strain OE-3 from CI1005 increased to 6.2%, 37.34 mg/g, and 10.37, while the contents of total acid and vitamin C (VC) decreased to 0.36 mg/L and 42.10 mg/L, respectively. The soluble solid content, total sugar content, and sugar/acid ratio in strain OE-7 from AC increased to 4.77%, 20.03 mg/g, and 5.23, while the total acid and VC contents decreased to 0.38 mg/L and 37.10 mg/L, respectively, resulting in high-sweet and low-sour taste. The SlCCD1A gene is beneficial for enhancing the content and richness of carotenoid-derived volatiles in tomato fruit and increasing the contents of soluble solids and total sugars, thereby improving the flavor quality

    Incidence, risk factors and prognostic effect of imaging right ventricular involvement in patients with COVID-19: a dose–response analysis protocol for systematic review

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    Introduction Emerging evidence has shown that COVID-19 infection may result in right ventricular (RV) disturbance and be associated with adverse clinical outcomes. The aim of this meta-analysis is to summarise the incidence, risk factors and the prognostic effect of imaging RV involvement in adult patients with COVID-19.Methods A systematical search will be performed in PubMed, EMBase, ISI Knowledge via Web of Science and preprint databases (MedRxiv and BioRxiv) (until October 2021) to identify all cohort studies in adult patients with COVID-19. The primary outcome will be the incidence of RV involvement (dysfunction and/or dilation) assessed by echocardiography, CT or MRI. Secondary outcomes will include the risk factors for RV involvement and their association with all-cause mortality during hospitalisation. Additional outcomes will include the RV global or free wall longitudinal strain (RV-GLS or RV-FWLS), tricuspid annular plane systolic excursion (TAPSE), fractional area change (FAC) and RV diameter. Univariable or multivariable meta-regression and subgroup analyses will be performed for the study design and patient characteristics (especially acute or chronic pulmonary embolism and pulmonary hypertension). Sensitivity analyses will be used to assess the robustness of our results by removing each included study at one time to obtain and evaluate the remaining overall estimates of RV involvement incidence and related risk factors, association with all-cause mortality, and other RV parameters (RV-GLS or RV-FWLS, TAPSE, S’, FAC and RV diameter). Both linear and cubic spline regression models will be used to explore the dose–response relationship between different categories (>2) of RV involvement and the risk of mortality (OR or HR).Ethics and dissemination There was no need for ethics approval for the systematic review protocol according to the Institutional Review Board/Independent Ethics Committee of Fuwai Hospital. This meta-analysis will be disseminated through a peer-reviewed journal for publication.PROSPERO registration number CRD42021231689

    Reduced Right Frontal Fractional Anisotropy Correlated with Early Elevated Plasma LDL Levels in Obese Young Adults

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    <div><p>Objective</p><p>To investigate the underlying physiological mechanisms of the structural differences in gray matter (GM) and white matter (WM) associated with obesity in young Chinese adults.</p><p>Materials and Methods</p><p>A total of 49 right-handed obese or overweight (n = 22, mean age 31.72±8.04 years) and normal weight (n = 27, mean age 29.04±7.32 years) Han Chinese individuals were recruited. All participants underwent voxel-based morphometry analysis of T1-weighted MRI and tract-based spatial statistics analysis of diffusion tensor imaging. Partial correlation analysis was performed between the physiological data obtained and the abnormal structural alterations.</p><p>Results</p><p>In the OO group, GM atrophy occurred in the left prefrontal cortex, bilateral cingulate gyrus, and the right temporal lobe, while enlargement was observed in the bilateral putamen. WM atrophy was observed predominantly in the regions that regulate food intake, such as the bilateral basal ganglia, the right amygdala, and the left insula. The OO group exhibited lower fractional anisotropy (FA) in bilateral frontal corticospinal tracts and the right brainstem. Significant negative correlations were observed between FA values of those three clusters and BMI, and waist circumference, while the volume of bilateral putamen positively correlated with both BMI and waist circumference. High plasma LDL levels were correlated with low FA values in the right frontal corticospinal tract. Interestingly, the negative correlation was limited to male participants.</p><p>Conclusions</p><p>Obesity-related alterations of GM and WM volumes were observed predominantly in food reward circuit, which may motivate abnormal dietary intake. Further, early elevated plasma LDL might contribute to low right frontal FA values of male adults, which requires further demonstration by larger-scale and longitudinal studies.</p></div

    Alteration of WM volume in the OO group compared with the NW group.

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    <p>Red represents regions with significantly reduced WM volume in the OO group (<i>P</i><0.05, FDR corrected). WM: white matter; OO: obese or overweight; NW: normal weight.</p

    Correlation analysis between plasma LDL levels and FA values extracted from the right frontal corticospinal tract (<i>P</i><0.05).

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    <p>FA values of the right frontal corticospinal tract and plasma LDL levels were significantly correlated in the OO group, rather than the NW group. FA values among male participants showed significant negative correlation with plasma LDL levels. OO: obese or overweight; NW: normal weight; FA: fractional anisotropy; LDL: low-density lipoprotein.</p

    Demographic and physiological characteristics of participants.

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    <p>NW: normal weight; OO: obese or overweight; HADS: hospital anxiety and depression scale; BMI: body mass index; LDL: low-density lipoprotein; HDL: high-density lipoprotein.</p><p>Demographic and physiological characteristics of participants.</p

    Placental Growth Factor Promotes Metastases of Non-Small Cell Lung Cancer Through MMP9

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    Background/Aims: Neovascularization and invasion coordinate cancer metastases in non-small cell lung cancer (NSCLC). However, the underlying molecular mechanisms are poorly understood. Recently, a substantial role of placental growth factor (PLGF) in cancer cell invasion has been acknowledged in several types of cancer, whereas a possible involvement of PLGF in the metastases of NSCLC has not been studied. Methods: Here, we analyzed the levels of PLGF and matrix metalloproteinase 9 (MMP9) in NSCLC specimens. We modified either PLGF or MMP9 levels in a NSCLC cell line A549, and examined the effects on the levels of MMP9 and PLGF. The cell invasiveness was quantified in a transwell cell migration assay. Pathway inhibitors were applied to determine the molecular mechanisms underlying the control of MMP9 by PLGF. Results: We found that PLGF and MMP9 levels both significantly increased in the NSCLC specimens and were strongly correlated. Overexpression of PLGF in NSCLC cells increased the levels of MMP9 and cell invasiveness, while inhibition of PLGF in NSCLC cells decreased the levels of MMP9 and cell invasiveness. However, modification of MMP9 levels in NSCLC cells did not alter the levels of PLGF. These data suggest that PLGF may regulate MMP9 in NSCLC cells, but not vice versa. Moreover, inhibition of MMP9 in PLGF-overexpressing NSCLC cells abolished the effects of PLGF on cell invasiveness, suggesting that PLGF increases cell invasion via MMP9. Furthermore, suppression of MAPK-p38, but not suppression of either MAPK-p42/p44, or PI3k, or JNK signaling, substantially abolished the effect of PLGF on MMP9, suggesting that PLGF may activate MMP9 via MAPK-p38 signaling pathway. Conclusion: PLGF-stimulated cancer invasion may be mediated through its effects on MMP9 activation in NSCLC cells

    Differences in FA between the OO group and the NW group using both TBSS analysis (Figure 3a) and VBA method (Figure 3b).

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    <p>(<b>3a</b>) Green represents mean FA skeleton of all participants, while red represents regions with significantly decreased FA in the OO group (<i>P</i><0.05, corrected for multiple comparisons). (<b>3b</b>) Red represents regions with significantly decreased FA in the OO group (<i>P</i><0.05, FDR corrected). OO: obese or overweight; NW: normal weight; FA: fractional anisotropy; TBSS: tract-based spatial statistics; VBA: voxel-based analysis.</p
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