A 173-point genetic linkage map of cucumber (Cucumis sativus L.), consisting of 116 SRAPs, 33 RAPDs, 11 SSRs, 9 SCARs, 3 ISSRs, and 1 STS, was constructed using 130 F 2 progeny derived from a narrow cross between line S94 (Northern China open-field type) and line S06 (greenhouse European type). The seven linkage groups spanned 1016 cM with a mean marker interval of 5.9 cM. Using the F 2 population and its F 3 derived families, a total of 38 QTLs were detected on five linkage groups with an LOD threshold of 3.0 for nine fruit-related traits: fruit weight, length, and diameter, fruit flesh thickness, seed-cavity diameter, fruit-stalk length, fruit pedicel length, length/diameter and length/stalk ratio. Of the identified QTLs, fsl4.3 for fruit-stalk length explained the largest portion of phenotypic variation (r 2 ¼ 30%). Several QTLs were detected in the same linkage region in different generations and different seasons. Additionally, several QTLs for various fruit traits were mapped to the same or neighbouring marker intervals, suggesting they are possible character associations for controlling cucumber fruit development.

Coronary heart disease is a disease characterized by coronary artery atherosclerosis lesions caused by vascular cavity stenosis, occlusion, myocardial ischemia, hypoxia or necrosis. Previous studies have demonstrated that decoy receptor-3 (DCR-3) can act as a pleiotropic immunomodulation for enhancing angiogenesis, which may be associated with the progression of coronary heart disease. In the present study, ELISA assay was used to investigate the plasma concentration level of DCR-3 in patients with coronary heart disease. The mRNA and protein level of DCR-3 in myocardial cells were determined by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. The role and molecular mechanism of DCR-3 was also evaluated in myocardial cells in mice with coronary heart disease. The role of small interfering RNA that targeted phosphoinositide 3-kinase (PI3K) in DCR-3 mediated apoptosis was confirmed by terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling and immunofluorescence. C57BL/6 mice with coronary heart disease were used to evaluate the efficacy of DCR-3 on inflammation and apoptosis. The data indicated that plasma concentration level of DCR-3 was downregulated in mice with coronary heart disease and that DCR-3 administration improved symptoms of coronary heart disease and prolonged survival of mice with coronary heart disease. In addition, it was demonstrated that DCR-3 treatment suppressed the inflammatory response and apoptosis of myocardial cells. Circulating DCR-3 concentration levels may be identified as a predictor of coronary heart disease and prognosis of coronary heart disease. Notably, it was also demonstrated that DCR-3 inhibited inflammatory factor expression levels by regulation of the PI3K/protein kinase B (AKT) signaling pathway. Taken together, these results indicate that increasing circulating DCR-3 plasma concentration is associated with degree of coronary heart disease, suggesting that DCR-3 may be a promising drug for the treatment of coronary heart disease via regulating inflammation and apoptosis through the PI3K/AKT signaling pathway.

Background: TNF-like cytokine 1A (TL1A) is a subgroup of the tumor necrosis factor superfamily that exerts pleiotropic effects on cell proliferation, inflammation, activation, and differentiation of immune cells. The purpose of the current study is to investigate the clinical significance of TL1A expression in coronary and peripheral blood of patients with acute coronary syndrome (ACS) to determine if TL1A levels can serve as an accurate prognostic indicator. Methods: A total of 141 patients undergoing coronary angiography were divided into 4 groups: Control (n = 35), Unstable Angina (UA) (n = 35), acute non-ST segment elevation myocardial infarction (NSTEMI) (n = 37), and acute ST segment elevation myocardial infarction (STEMI) (n = 34). The levels of TL1A, MPO, hs-CRP, and IL-10 were detected in coronary and peripheral blood using enzyme linked immunosorbent assay (ELISA), and the MACE incidence rates were compared during 26.3 months of follow-up. Results: TL1A levels were not significantly different between the UA group and control group. In the UA group, TL1A levels were not significantly different between coronary blood and peripheral blood. However, TL1A levels were higher in the STEMI and NSTEMI groups than in the control group ( P < .05). Moreover, TL1A levels in the coronary blood of the STEMI and NSTEMI groups were higher than in the peripheral blood ( P < .05). The expression of TL1A in the coronary blood was the highest in the STEMI group. In addition, TL1A level in the coronary blood was highly correlated with levels in the peripheral blood (correlation coefficient: 0.899, P < .001). The hs-CRP and MPO levels in the coronary and peripheral blood of all the UA, NSTEMI, and STEMI groups were higher than the control group. Plasma IL-10 levels in all the UA, NSTEMI and STEMI groups were lower than those in the control group. Plasma TL1A level was positively correlated with the cTnI level, degree of coronary thrombus burden, occurrence of slow coronary flow / no coronary reflow and MACE, but negatively correlated with the IL-10 level or non-correlated with the Syntax score. Conclusion: Plasma TL1A concentration levels can be used as a predictor of inflammatory response and prognosis in patients with ACS. Trial Registration: ClinicalTrials.gov, number: NCT02430025; Unique Protocol ID: FJPH20150101; Brief Title: Fujian Province Cardiovascular Diseases Study (FJCVD)