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Abstract Background The association between the number of food kinds and the risk of depression in adults was examined. Methods According to the inclusion and exclusion criteria, a total of 4593 adults were included in the study. The number of food kinds was collected via 24‒hour dietary recalls. Depression was assessed using the Patient Health Questionnaire‒9. Logistic regression and restricted cubic spline models were applied to assess the association between the number of food kinds and the risk of depression. Results This study included 4593 study participants, 451 of whom were diagnosed with depression. The revised advantage ratios (with corresponding confidence intervals) for the prevalence of depression among individuals in the fourth quartiles of the number of food kinds (Q4) in comparison to the lowest quartile (Q1) were determined to be 0.59 (0.36‒0.96), respectively. According to our subgroup analyses, the number of food kinds was negatively associated with the risk of depression in females, participants aged 18‒45 and 45‒65 years, and participants with a body mass index (BMI) of 25 to 24.9 kg/m2. According to our dose‒response analysis, the number of food kinds was linearly associated with the risk of depression (P for nonlinear=0.5896). Conclusion The risk of depression exhibited a linear and negative correlation with the number of food kinds. The results indicated that a diversified diet was an effective nonpharmacological approach that deserved further generalization.

The identification of stable quantitative trait locus (QTL) for yield-related traits and tightly linked molecular markers is important for improving wheat grain yield. In the present study, six yield-related traits in a recombinant inbred line (RIL) population derived from the Zhongmai 578/Jimai 22 cross were phenotyped in five environments. The parents and 262 RILs were genotyped using the wheat 50K single nucleotide polymorphism (SNP) array. A high-density genetic map was constructed with 1 501 non-redundant bin markers, spanning 2 384.95 cM. Fifty-three QTLs for six yield-related traits were mapped on chromosomes 1D (2), 2A (9), 2B (6), 2D, 3A (2), 3B (2), 4A (5), 4D, 5B (8), 5D (2), 7A (7), 7B (3) and 7D (5), which explained 2.7–25.5% of the phenotypic variances. Among the 53 QTLs, 23 were detected in at least three environments, including seven for thousand-kernel weight (TKW), four for kernel length (KL), four for kernel width (KW), three for average grain filling rate (GFR), one for kernel number per spike (KNS) and four for plant height (PH). The stable QTLs QKl.caas-2A.1, QKl.caas-7D, QKw.caas-7D, QGfr.caas-2B.1, QGfr.caas-4A, QGfr.caas-7A and QPh.caas-2A.1 are likely to be new loci. Six QTL-rich regions on 2A, 2B, 4A, 5B, 7A and 7D, showed pleiotropic effects on various yield traits. TaSus2-2B and WAPO-A1 are potential candidate genes for the pleiotropic regions on 2B and 7A, respectively. The pleiotropic QTL on 7D for TKW, KL, KW and PH was verified in a natural population. The results of this study enrich our knowledge of the genetic basis underlying yield-related traits and provide molecular markers for high-yield wheat breeding.

Stem lignin content (SLC) in common wheat (Triticum aestivum L.) contributes to lodging resistance. Caffeic acid 3-O-methyltransferase (COMT) is a key enzyme involved in lignin biosynthesis. Characterization of TaCOMT genes and development of gene-specific markers could enable marker-assisted selection in wheat breeding. In the present study, the full-length genomic DNA (gDNA) sequences of TaCOMT genes located on chromosomes 3A, 3B, and 3D were cloned by homologous cloning. Two allelic variants, TaCOMT-3Ba and TaCOMT-3Bb, were identified and differed by a 222-bp insertion/deletion (InDel) in the 3′-untranslated region (3′-UTR). A co-dominant gene-specific marker based on this InDel was developed and designated as TaCOMT-3BM. A total of 157 wheat cultivars and advanced lines grown in four environments were used to validate the associations between allelic patterns and SLC. The SLC of cultivars with TaCOMT-3Ba was significantly (P

Background: It is well documented that sevoflurane postconditioning (SP) has a significant myocardial protection effect. However, the mechanisms underlying SP are still unclear. In the present study, we investigated the hypothesis that the Pim-1 kinase played a key role in SP-induced cardioprotection by regulating dynamics-related protein 1 (Drp1). Methods: A Langendorff model was used in this study. Seventy-two rats were randomly assigned into six groups as follows: CON group, ischemia reperfusion (I/R) group, SP group , SP+proto-oncogene serine/threonine-protein kinase 1 (Pim-1) inhibitor II group, SP+dimethylsufoxide group, and Pim-1 inhibitor II group (n = 12, each). Hemodynamic parameters and infarct size were measured to reflect the extent of myocardial I/R injury. The expressions of Pim-1, B-cell leukemia/lymphoma 2 (Bcl-2) and cytochrome C (Cyt C) in cytoplasm and mitochondria, the Drp1 in mitochondria, and the total Drp1 and p-Drp1ser637 were measured by Western blotting. In addition, transmission electron microscope was used to observe mitochondrial morphology. The experiment began in October 2014 and continued until July 2016. Results: SP improved myocardial I/R injury-induced hemodynamic parametric changes, cardiac function, and preserved mitochondrial phenotype and decreased myocardial infarct size (24.49 ± 1.72% in Sev group compared with 41.98 ± 4.37% in I/R group; P< 0.05). However, Pim-1 inhibitor II significantly (P < 0.05) abolished the protective effect of SP. Western blotting analysis demonstrated that, compared with I/R group, the expression of Pim-1 and Bcl-2 in cytoplasm and mitochondria as well as the total p-Drp1ser637 in Sev group (P < 0.05) were upregulated. Meanwhile, SP inhibited Drp1 compartmentalization to the mitochondria followed by a reduction in the release of Cyt C. Pretreatment with Pim-1 inhibitor II significantly (P < 0.05) abolished SP-induced Pim-1/p-Drp1ser637 signaling activation. Conclusions: These findings suggested that SP could attenuate myocardial ischemia-reperfusion injury by increasing the expression of the Pim-1 kinase. Upregulation of Pim-1 might phosphorylate Drp1 and prevent extensive mitochondrial fission through Drp1 cytosolic sequestration.

Background:. Sevoflurane preconditioning (SP) has been shown to invoke potent myocardial protection in animal studies and clinical trials. However, the mechanisms underlying SP are complex and not yet well understood. We investigated the hypothesis that the cardioprotection afforded by SP is mediated via the Wnt/glycogen synthase kinase 3β (GSK3β)/β-catenin signaling pathway. Methods:. Two models were established: A Langendorff perfused rat heart model and the H9C2 cell hypoxia/reoxygenation model. Both rats and H9C2 cells were randomly divided into 6 groups as follows: S group, ischemia-reperfusion (I/R) group, DMSO group, IWP group, SP group, and SP + IWP group. Hemodynamic parameters, lactate dehydrogenase (LDH) activity in coronary effluent and cell culture supernatant, and the infarct size were measured to evaluate myocardial ischemia-reperfusion injuries. To determine the activity of Wnt/GSK3β/β-catenin signaling pathway, the expressions of Wnt3a, phospho-GSK3β, and β-catenin were measured by Western blotting. Results:. SP improved cardiac function recovery, reduced infarct size (18 ± 2% in the SP group compared with 35 ± 4% in the I/R group; P < 0.05), decreased LDH activity in coronary effluent, and culture supernatant. IWP-2, an inhibitor of Wnt, abolished the cardioprotection by SP. In addition, Western blotting analysis demonstrated that the expressions of Wnt3a, phospho-GSK3β, and β-catenin significantly (P < 0.05) increased in the I/R group, compared with the S group; and compared to I/R group, SP significantly (P < 0.05) increased Wnt3a, phospho-GSK3β, and β-catenin expressions. Pretreatment with IWP-2 significantly (P < 0.05) abolished SP-induced Wnt/GSK3β/β-catenin signaling activation. Conclusions:. The results showed for the first time that cardioprotection afforded by SP may be mediated partly via the Wnt/GSK3β/β-catenin signaling pathway.