Germination of aged oat seeds associated with changes in antioxidant enzyme activity and storage compounds mobilization.

Germination of aged seeds may be associated with specific metabolic changes. The objective of this study was to examine physiological and metabolic alterations before and after germination of control and aged oat (Avena sativa) seeds. The activity of antioxidant enzymes and the level of storage compounds were measured in the embryo and endosperm at 0, 4, 16, and 32 h of imbibition for control seeds and 0, 4, 16, 32, and 60 h of imbibition for medium vigor seeds after artificially accelerated aging; metabolomic changes were determined in embryos at 16 and 32 h of seed imbibition. In aged oat seeds, superoxide dismutase activity and catalase activity increased in the late imbibition stage. The content of soluble sugars decreased significantly in the later stages of imbibition, while the content of proteins increased in 32 h of seed imbibition eventually producing mannitol and proline. The mobilization of fat in deteriorated seeds was mainly through the sphingolipid metabolic pathway generated by cell growth-promoting dihydrosphingosine-1-phosphate. Ascorbic acid, avenanthramide and proline levels increased significantly at 60 h of imbibition, playing an important role in the germination of aged oat seeds.

Melatonin inhibiting the survival of human gastric cancer cells under ER stress involving autophagy and Ras-Raf-MAPK signalling.

Melatonin exhibits antitumour activities in the treatment of many human cancers. In the present study, we aimed to improve the therapeutic potential of melatonin in gastric cancer. Our results confirmed that melatonin dose-dependently suppressed the proliferation and necrosis, and increased G0/G1 phase arrest, apoptosis, autophagy and endoplasmic reticulum (ER) stress. The Ras-Raf-MAPK signalling pathway was activated in cells after melatonin treatment. RNA-seq was performed and GSEA analysis further confirmed that many down-regulated genes in melatonin-treated cells were associated with proliferation. However, GSEA analysis also indicated that many pathways related to metastasis were increased after melatonin treatment. Subsequently, combinatorial treatment was conducted to further investigate the therapeutic outcomes of melatonin. A combination of melatonin and thapsigargin increased the apoptotic rate and G0/G1 cell cycle arrest when compared to treatment with melatonin alone. Melatonin in combination with thapsigargin triggered the increased expression of Bip, LC3-II, phospho-Erk1/2 and phospho-p38 MAPK. In addition, STF-083010, an IRE1a inhibitor, further exacerbated the decrease in survival rate induced by combinatorial treatment with melatonin and thapsigargin. Collectively, melatonin was effective in gastric cancer treatment by modifying ER stress.

47,XY,+der(X)t(X;18)(p11.4;p11.22): A Unique Aneuploidy Associated with Klinefelter Syndrome due to an Extra Derivative X Chromosome Inherited Maternally.

A derivative X chromosome formed by translocation involving an X chromosome and a chromosome 18 in a Klinefelter syndrome (KS) patient with a 47,XXY karyotype has not been reported before. In this study, we present the clinical and molecular cytogenetic characteristics. The patient presented with small testes and azoospermia. G-banding analysis identified the karyotype as 47,XY,del(X)(p?11.4). Array CGH detected a 10.36-Mb duplication of chromosome region 18p11.22p11.32 (14,316-10,377,516) and a 111.18-Mb duplication of chromosome region Xp11.4q28 (61,931, 689-155,111,583), in addition to the normal chromosome 18 and an X chromosome. FISH results further revealed the extra 18p located at the end of the short arm of a deleted X chromosome, forming a derivative X chromosome. Finally, we identified the karyotype of the patient as 47,XY,+der(X)t(X;18)(p11.4;p11.22). The derivative X chromosome was maternally inherited. To our knowledge, this rare karyotype has not yet been reported in the literature. The present study may suggest a novel karyotype associated with KS.