Genetically optimizing soybean nodulation improves yield and protein content.

Symbiotic nitrogen fixation in legume nodules requires substantial energy investment from host plants, and soybean (Glycine max (L.) supernodulation mutants show stunting and yield penalties due to overconsumption of carbon sources. We obtained soybean mutants differing in their nodulation ability, among which rhizobially induced cle1a/2a (ric1a/2a) has a moderate increase in nodule number, balanced carbon allocation, and enhanced carbon and nitrogen acquisition. In multi-year and multi-site field trials in China, two ric1a/2a lines had improved grain yield, protein content and sustained oil content, demonstrating that gene editing towards optimal nodulation improves soybean yield and quality.

Correlation of neck circumference, coronary calcification severity and cardiovascular events in Chinese elderly patients with acute coronary syndromes.

BACKGROUND AND AIMS: We aimed to investigate whether neck circumference (NC) can predict metabolic syndrome (MetS), coronary calcification and lesion, and major adverse cardiovascular events (MACEs). METHODS: A total of 867 patients with acute coronary syndrome (ACS) over 60 years old from the Second Hospital of Shandong University, who had undergone coronary computed tomography, were randomly selected for a retrospective analysis. The subjects were divided into male and female groups, NC quartile 1-4 groups (Q1-Q4 groups), non-multivessel coronary disease (non-MVCD) and multi-vessel coronary disease (MVCD) groups. RESULTS: After adjusting for potential confounders, NC was associated with risk factors promoting coronary artery disease (CAD) and coronary artery calcification score (CACS). The severity of CAD increased by 0.202 times and 0.372 times for each unit of NC in male and female groups, respectively. Compared with the lower CACS group, the risk of coronary calcification increased by 0.139 times, and MVCD increased 0.268 times, with each unit increase of NC. Except for all-cause death, there were significant differences between the Q1-Q4 groups in the prevalence of all primary endpoints, cardiogenic death, unexpected re-hospitalization of heart failure, ACS recurrence or unplanned revascularization, and non-fatal stroke (p log-rank <0.01). In view of the overall trend, with the increase of NC quartiles, the prevalence of MACEs gradually increased (all p < 0.01). CONCLUSIONS: NC is closely associated with MetS and its components, coronary calcification and lesion degree, and MACEs. NC could be used as surrogate of CACS to predict the coronary condition and prognosis of elderly patients with ACS.

MiR-489 inhibited the development of gastric cancer via regulating HDAC7 and PI3K/AKT pathway.

BACKGROUND: Mounting evidences have displayed that the dysregulation of miRNAs plays important roles in the pathogenesis of gastric cancer (GC). The purpose of this study was to explore the biological functions and potential mechanism of miR-489 in GC progression. METHODS: Quantitative real-time PCR (qRT-PCR) and western blot were performed to examine the mRNA expression and protein levels of miR-489 and HDAC7. The relationship between miR-489 and HDAC7 was analyzed by Spearman rank correlation. 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay and transwell assays were conducted for determining the effect of miR-489 and HDAC7 on GC cell viability, migration, and invasion. TargetScan and luciferase reporter assay were used to confirm the target gene of miR-489 in GC cells. RESULTS: The findings showed that miR-489 was dramatically decreased in GC tissues and GC cell lines (SGC-7901 and MKN45). Moreover, it was closely correlated with overall survival (OS) and progression-free survival (PFS) of GC patients. Downregulation of miR-489 significantly promoted GC cell proliferation, invasion, and migration. Additionally, HDAC7 was confirmed as the direct target of miR-489. Knockdown of HDAC7 exerted inhibited effect on GC progression and it markedly overturned miR-489 inhibitor-medicated effect on GC cells. More interestingly, via targeting HDAC7, miR-489 blocked the activation of PI3K/AKT pathway in GC cells. CONCLUSIONS: Correctively, miR-489 played as a tumor suppressor in GC cell growth by targeting HDAC7, and miR-489 might function as a novel biomarker for diagnosis or therapeutic targets of human GC.