Saline–alkali stress is a severely adverse abiotic stress limiting plant growth. Malus halliana Koehne is an apple rootstock that is tolerant to saline–alkali stress. To understand the molecular mechanisms underlying the tolerance of M. halliana to saline–alkali stress, an integrated metabolomic and proteomic approach was used to analyze the plant pathways involved in the stress response of the plant and its regulatory mechanisms. A total of 179 differentially expressed proteins (DEPs) and 140 differentially expressed metabolites (DEMs) were identified. We found that two metabolite-related enzymes (PPD and PAO) were associated with senescence and involved in porphyrin and chlorophyll metabolism; six photosynthesis proteins (PSAH2, PSAK, PSBO2, PSBP1, and PSBQ2) were significantly upregulated, especially PSBO2, and could act as regulators of photosystem II (PSII) repair. Sucrose, acting as a signaling molecule, directly mediated the accumulation of D-phenylalanine, tryptophan, and alkaloid (vindoline and ecgonine) and the expression of proteins related to aspartate and glutamate (ASP3, ASN1, NIT4, and GLN1−1). These responses play a central role in maintaining osmotic balance and removing reactive oxygen species (ROS). In addition, sucrose signaling induced flavonoid biosynthesis by activating the expression of CYP75B1 to regulate the homeostasis of ROS and promoted auxin signaling by activating the expression of T31B5_170 to enhance the resistance of M. halliana to saline–alkali stress. The decrease in peroxidase superfamily protein (PER) and ALDH2C4 during lignin synthesis further triggered a plant saline–alkali response. Overall, this study provides an important starting point for improving saline–alkali tolerance in M. halliana via genetic engineering.

Background and Purpose Although diabetes mellitus is an established independent risk factor for ischemic stroke, the association between fasting blood glucose and intracerebral hemorrhage is limited and inconsistent. The objectives of the current study was to examine the potential impact of long-term fasting blood glucose concentration on subsequent risk of intracerebral hemorrhage. Methods This prospective study included 96,110 participants of the Kailuan study, living in Kailuan community, Tangshan city, China, who were free of cardiovascular diseases and cancer at baseline(2006).Fasting blood glucose concentration was measured in 2006, 2008, 2010, and 2012. Updated cumulative average fasting blood glucose concentration was used as primary exposure of the current study. Incident intracerebral hemorrhage from 2006 to 2015 was confirmed by review of medical records. Results During 817,531 person-years of follow-up, we identified 755 incident intracerebral hemorrhage cases. The nadir risk of intracerebral hemorrhage was observed at fasting blood glucose concentration of 5.3 mmol/L. The adjusted hazard ratios and their 95% confidence intervals (CIs) of intracerebral hemorrhage were 1.59(95% CI, 1.26–2.02) for diabetes or fasting blood glucose ≥7.00 mmol/L, 1.31(95%CI, 1.02–1.69) for impaired fasting glucose (fasting blood glucose 6.10–6.99 mmol/L), 0.98(95% CI: 0.78–1.22) for fasting blood glucose 5.60–6.09 mmol/L, and 2.04 (95%CI, 1.23–3.38) for hypoglycemia (fasting blood glucose <4.00 mmol/L), comparing with normal fasting blood glucose 4.00–5.59 mmol/L. The results persisted after excluding individuals who used hypoglycemic, aspirin, antihypertensive agents, or anticoagulants, and those with intracerebral hemorrhagic cases occurred in the first two years of follow-up. Conclusions In this large community-based cohort, low (<4.0 mmol/L) and high (≥6.1 mmol/L) fasting blood glucose concentrations were associated with higher risk of incident intracerebral hemorrhage, relative to fasting blood glucose concentrations of 4.00–6.09 mmol/L.

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Background Studies regarding whether light to moderate alcohol consumption is associated with a lower risk of cardiovascular diseases (CVD) have generated mixed results. Further, few studies have examined the potential impact of alcohol consumption on diverse disease outcomes simultaneously. We aimed to prospectively study the dose-response association between alcohol consumption and risk of CVD, cancer, and mortality. Methods This study included 83,732 adult Chinese participants, free of CVD and cancer at baseline. Participants were categorized into 6 groups based on self-report alcohol consumption: 0, 1–25, 26–150, 151–350, 351–750, and > 750 g alcohol/wk. Incident cases of CVD, cancers, and mortality were confirmed by medical records. Hazard ratios (HRs) for the composite risk of these three outcomes, and each individual outcome, were calculated using Cox proportional hazard model. Results During a median follow-up of 10.0 years, there were 6411 incident cases of CVD, 2947 cancers and 6646 deaths. We observed a J-shaped relation between alcohol intake and risk of CVD, cancer, and mortality, with the lowest risk at 25 g/wk., which is equivalent to ~ 2 servings/wk. Compared to consuming 1–25 g/wk., the adjusted HR for composite outcomes was 1.38 (95% confidence interval (CI):1.29–1.49) for non-drinker, 1.15 (95% CI: 1.04–1.27) for 26–150 g/wk., 1.22 (95% CI: 1.10–1.34) for 151–350 g/wk., 1.33 (95% CI: 1.21–1.46) for 351–750 g/wk., and 1.57 (95% CI: 1.30–1.90) for > 750 g/wk., after adjusting for age, sex, lifestyle, social economic status, and medication use. Conclusions Light alcohol consumption at ~ 25 g/wk was associated with lower risk of CVD, cancer, and mortality than none or higher consumption in Chinese adults.

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The disease symptoms recognized as ‘Anthracnose’ are caused by Colletotrichum spp. and lead to large-scale strawberry (Fragaria×ananassa Duchesne) losses worldwide in terms of both quality and production. Little is known regarding the mechanisms underlying the genetic variations in the strawberry–Colletotrichum spp. interaction. In this work, Colletotrichum gloeosporioides (C. gloeosporioides) infection was characterized in two varieties exhibiting different susceptibilities, and the involvement of salicylic acid (SA) was examined. Light microscopic observation showed that C. gloeosporioides conidia germinated earlier and faster on the leaf surface of the susceptible cultivar compared with the less-susceptible cultivar. Several PR genes were differentially expressed, with higher-amplitude changes observed in the less-susceptible cultivar. The less-susceptible cultivar contained a higher level of basal SA, and the SA levels increased rapidly upon infection, followed by a sharp decrease before the necrotrophic phase. External SA pretreatment reduced susceptibility and elevated the internal SA levels in both varieties, which were sharply reduced in the susceptible cultivar upon inoculation. The less-susceptible cultivar also displayed a more sensitive and marked increase in the transcripts of NB-LRR genes to C. gloeosporioides, and SA pretreatment differentially induced transcript accumulation in the two varieties during infection. Furthermore, SA directly inhibited the germination of C. gloeosporioides conidia; NB-LRR transcript accumulation in response to SA pretreatment was both dose- and cultivar-dependent. The results demonstrate that the less-susceptible cultivar showed reduced conidia germination. The contribution of SA might involve microbial isolate-specific sensitivity to SA, cultivar/tissue-specific SA homeostasis and signaling, and the sensitivity of R genes and the related defense network to SA and pathogens.

Background: Sedentary time was associated with myocardial infarction (MI) and metabolic diseases in previous studies. Purpose: To investigate whether sedentary time measured before disease onset was associated with all-cause mortality among MI survivors and whether the sedentary time-mortality association was mediated by physical activity status and metabolic phenotypes. Methods: In this prospective community-based cohort including 101,510 Chinese adults, we used sedentary time, evaluated at 2006 (baseline), to predict further all-cause mortality among individuals who then developed new onset MI from 2006 to December 2013 (n ¼ 989). The post-MI mortality was ascertained after the first non-fatal MI until December 2014. We assessed the mediating effects of physical inactivity and metabolic factors on the sedentary timemortality association. Results: During 7 years follow up, 180 deaths occurred among these participants with incident MI. Prolonged sedentary time was associated with a higher risk of mortality among MI survivors. The adjusted hazard ratio (HR) of mortality for sedentary time 4-8 hours/day versus <4 hours/day, was 1.62 (95% confidence interval (CI) 1.14-2.31). A high amount of sedentary time (>4 hours/day) and inactive physical activity had an increased risk of all-cause mortality (HR: 2.74, 95% CI 1.34-5.60), relative to those with sedentary time 4 hours/day and moderate/vigorous physical activity. Physical inactivity and metabolic factors mediated a small proportion (9.2 % for all) of the total association between sedentary time and post-MI mortality. Conclusion: High sedentary time was significantly associated with all-cause mortality among MI survivors, independent of physical activity status and metabolic abnormalities.

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