Dual-Energy CT Iodine Concentration to Evaluate Postoperative Pancreatic Fistula after Pancreatoduodenectomy.

Background Pancreatic fibrosis and fatty infiltration are associated with postoperative pancreatic fistula (POPF), but accurate preoperative assessment remains a challenge. Iodine concentration (IC) and fat fraction derived from dual-energy CT (DECT) may reflect the amount of fibrosis and steatosis, potentially enabling the preoperative prediction of POPF. Purpose To identify multiphasic DECT-derived IC and fat fraction that improve the prediction of POPF risks compared with contrast-enhanced CT attenuation values and to evaluate the underlying histopathologic changes. Materials and Methods This retrospective study included patients who underwent pancreatoduodenectomy and DECT (including pancreatic parenchymal, portal venous, and delayed phase scanning) between January 2020 and December 2020. The relationships of the quantitative DECT-derived IC and fat fraction, along with CT attenuation values from enhanced images with POPF risk, were analyzed with logistic regression analysis. The predictive performance of the IC was compared with that of the CT values. The histopathologic underpinnings of IC were evaluated with multivariable linear regression analysis. Results A total of 107 patients (median age, 65 years; interquartile range, 57-70 years; 56 men) were included. Of these, 23 (21%) had POPF. The pancreatic parenchymal-to-portal venous phase IC ratio (adjusted odds ratio [OR], 13; 95% CI: 2, 162; P < .001) was an independent predictor of POPF occurrence. The accuracy of the pancreatic parenchymal-to-portal venous phase IC ratio in predicting POPF was higher than that of the CT value ratio in the same phases (78% vs 65%, P < .001). The pancreatic parenchymal-to-portal venous phase IC ratio was independently associated with pancreatic fibrosis (ß = -1.04; 95% CI: -0.44, -1.64; P = .001). Conclusion A higher pancreatic parenchymal-to-portal venous phase IC ratio was associated with less histologic fibrosis and greater risk of POPF. © RSNA, 2022 Online supplemental material is available for this article. See also the editorial by Lee and Yoon in this issue.

Small RNA deep sequencing identifies novel and salt-stress-regulated microRNAs from roots of Medicago sativa and Medicago truncatula.

Small 21- to 24-nucleotide (nt) ribonucleic acids (RNAs), notably the microRNA (miRNA), are emerging as a posttranscriptional regulation mechanism. Salt stress is one of the primary abiotic stresses that cause the crop losses worldwide. In saline lands, root growth and function of plant are determined by the action of environmental salt stress through specific genes that adapt root development to the restrictive condition. To elucidate the role of miRNAs in salt stress regulation in Medicago, we used a high-throughput sequencing approach to analyze four small RNA libraries from roots of Zhongmu-1 (Medicago sativa) and Jemalong A17 (Medicago truncatula), which were treated with 300 mM NaCl for 0 and 8 h. Each library generated about 20 million short sequences and contained predominantly small RNAs of 24-nt length, followed by 21-nt and 22-nt small RNAs. Using sequence analysis, we identified 385 conserved miRNAs from 96 families, along with 68 novel candidate miRNAs. Of all the 68 predicted novel miRNAs, 15 miRNAs were identified to have miRNA*. Statistical analysis on abundance of sequencing read revealed specific miRNA showing contrasting expression patterns between M. sativa and M. truncatula roots, as well as between roots treated for 0 and 8 h. The expression of 10 conserved and novel miRNAs was also quantified by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). The miRNA precursor and target genes were predicted by bioinformatics analysis. We concluded that the salt stress related conserved and novel miRNAs may have a large variety of target mRNAs, some of which might play key roles in salt stress regulation of Medicago.

MiR-128 inhibits tumor growth and angiogenesis by targeting p70S6K1.

MicroRNAs are a class of small noncoding RNAs that function as critical gene regulators through targeting mRNAs for translational repression or degradation. In this study, we showed that miR-128 expression levels were decreased in glioma, and identified p70S6K1 as a novel direct target of miR-128. Overexpression of miR-128 suppressed p70S6K1 and its downstream signaling molecules such as HIF-1 and VEGF expression, and attenuated cell proliferation, tumor growth and angiogenesis. Forced expression of p70S6K1 can partly rescue the inhibitory effect of miR-128 in the cells. Taken together, these findings will shed light to the role and mechanism of miR-128 in regulating glioma tumor angiogenesis via miR-128/p70S6K1 axis, and miR-128 may serve as a potential therapeutic target in glioma in the future.