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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