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pan, z.

Publications and source records attributed to pan, z..

3 recordsLinked to original sources

Potassium stimulates fruit sugar accumulation by increasing carbon flow in Citrus

Soluble sugar is a key factor of flavor quality in citrus. Potassium (K) is known as a quality element, which plays key roles in improving sugar accumulation and fruit quality, but the mechanisms are largely unknown. This study aims to elucidate how K improves sugar accumulation by regulating carbon flow between source and sink in Newhall navel orange (Citrus sinensis). The results demonstrated that appropriate K concentration improved fruit quality and sugar accumulations in citrus, and 1.5% of K concentration in pulp was the optimal concentration for fruit quality. K increased strength of sink and source, as supported by the increased fruit growth rate, gene expressions related to sugar metabolism and sugar transport in fruit, and photosynthesis, gene expressions of sugar metabolism in leaf, respectively, which contributed to increasing sugars accumulation. Further study indicated that K improved carbon flow from source to sink by boosting symplastic and apoplastic loading of phloem, as supported by the increased CF signal intensities, plasmodesmata densities, and the expressions of CsSUT1 and CsSUT2 in leaf at early and mid stages of fruit development, finally increasing sugar accumulation in fruit. Conclusively, K stimulates fruit sugar accumulation by increasing carbon flow in Newhall navel orange. HighlightK application stimulated carbon flow between source and sink through symplastic and apoplastic loading, which were supported by the structural characteristics of phloem and the expression of CsSUTs and CsSWEETs, ultimately promoting sugar accumulation in Citrus sinensis.

plant biology↗

Distinct Microstructural Heterogeneities Underpin Specific Micromechanical Properties in Human ACL Femoral and Tibial Entheses

The anterior cruciate ligament (ACL) is anchored to the femur and tibia by a specialized interface tissue called the enthesis, which transfers forces in multiple directions and magnitudes without accruing fatigue damage during loading cycles over a lifetime. However, the precise structural and mechanical characteristics of the ACL femoral enthesis (FE) and tibial enthesis (TE) and their intricate interplay are unknown. In this study, we identified two ultrathin-graded mineralization regions in the FE ([~]21 m) and TE ([~]14 m), both of which exhibited distinct biomolecular compositions and mineral assembly patterns. FE interface exhibited progressively maturing hydroxyapatites (HAps), whereas minerals at the TE interface region changed from an amorphous phase (ACP) to HAps with increasing crystallinity. The LC-MS/MS results revealed that MGP protein uniquely enriched at the TE interface may be favorable for stabilizing ACP, while CLEC11A enriched at the FE interface could facilitate osteogenesis of the interface. The finite element analysis results indicated that the FE model was more resistant to shearing, while the TE model facilitated tensile resistance. It suggested that the great discrepancy in biomolecular expression and the corresponding mineral assembling heterogeneities together contributed to the superior mechanical properties of both the FE and TE models. These findings provide new perspectives regarding the management of ACL injury and the development of high-performance interface materials.

bioengineering↗

Nrf2 mediated ER-phagy protects against oxidative damage in intervertebral disc degeneration

Intervertebral disc degeneration (IDD) increases the risk of low back pain (LBP). Oxidative stress may induce cellular damage and contribute to various diseases including IDD. Endoplasmic reticulum autophagy (ER-phagy) is a specific type of autophagy, its role in oxidative stress induced damage as well as in IDD is unknown. This study explores the role of ER-phagy in oxidative damage in intervertebral disc nucleus pulposus cells (NPCs), as well as the Nrf2/FAM134B axis in ER-phagy regulation and IDD therapy. We found ER-phagy was decreased in NPCs during oxidative stress; while FAM134B may promote ER-phagy and alleviate oxidative stress induced ER-stress and apoptosis. In addition, the nuclear transcription factor Nrf2 may promote the expression of FAM134B as well as ER-phagy, and suppress ER-stress and apoptosis in NPCs. Furthermore, overexpression of FAM134B and Nrf2 could effectively attenuate the progression of IDD in rats in vivo. These results suggest Nrf2/FAM134B mediated ER-phagy may combat oxidative damage in cells; meanwhile, ER-phagy as well as Nrf2 could be potential therapeutic targets for IDD. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=114 SRC="FIGDIR/small/469451v1_ufig1.gif" ALT="Figure 1"> View larger version (44K): org.highwire.dtl.DTLVardef@188b390org.highwire.dtl.DTLVardef@1c4e4f6org.highwire.dtl.DTLVardef@193fe77org.highwire.dtl.DTLVardef@12770e2_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗