ERAS did not increase 30-day complications compared with CRAS after RC. ERAS may be better than CRAS in terms of bowel movement, tolerance of fluid and regular diet, and ambulation.

The plant growth retardant mepiquat chloride (MC) has been extensively used to produce compact plant canopies and increase yield in cotton (Gossypium hirsutum L.). Previous studies showed that MC reduced plant height and internode length by inhibiting GA biosynthesis and cell elongation. However, whether there are other molecular mechanisms underlying MC-induced growth retardation has remained largely unknown. In the present study, we conducted histological, transcriptomic, and phytohormone analyses of the second elongating internodes of cotton seedlings treated with MC. Histological analysis revealed that the MC shortened the internodes through suppressing both cell division and cell elongation. Consistent with the observed phenotype, many genes related to cell growth were significantly downregulated by MC. Transcriptome profiling showed that the expression of genes related not only to GA, but also to auxin, brassinosteroid (BR), and ethylene metabolism and signaling was remarkably suppressed, whereas that of genes related to cytokinin (CK) and abscisic acid (ABA) metabolism was induced by MC. Consistent with the expression pattern, significant decrease of endogenous GA, auxin, and BR content, but an increase in CK content was observed after MC treatment. Most of these hormone related genes displayed opposite regulation pattern by exogenous GA 3 treatment compared to MC; simultaneous application of MC and GA 3 could alleviate the genes expression changes induced by MC treatment, indicating MC does not directly affect other plant hormones, but through the inhibition of the GA biosynthesis. In addition, the expression of genes related to secondary metabolism and many transcription factors (TFs) were differentially regulated by MC. In summary, we confirmed the important role of GA in MC-induced growth inhibition of cotton, and further found that other hormones were also involved in this process in a GA-dependent manner. This study provides novel insights into the molecular mechanism underlying the MC-mediated inhibition of internode elongation in cotton seedlings.

BackgroundThe purpose of the study was to investigate the association between radiomic features based on contrast‐enhanced multidetector computed tomography (CT) and the Ki‐67 proliferation index (PI) in patients with lung cancer.MethodsOne hundred and ten patients with lung cancer confirmed by surgical histology were retrospectively included. Radiomic features were extracted from preoperative contrast‐enhanced chest multidetector CT images for each tumor using open‐source three‐dimensional Slicer software. Statistical analysis was performed to determine significant radiomic features serving as image predictors of Ki‐67 status in lung cancer and to investigate the relationship between these features and Ki‐67 PI.ResultsHigher Ki‐67 expression was more common in men (P = 0.02) and patients with a smoking history (P = 0.01). Twelve radiomic features were significantly associated with Ki‐67 status. Multivariate logistic regression analysis identified inverse variance, minor axis, and elongation as independent predictors of Ki‐67 PI. There was a positive correlation between inverse variance, minor axis, elongation (P = 0.00, P = 0.02, and P = 0.14, respectively) and Ki‐67 PI. The area under the curve to identify high Ki‐67 status for inverse variance was 0.77 with a cutoff value of 0.47, which was significantly higher than for minor axis and elongation (P = 0.02 and P = 0.03, respectively).ConclusionRadiomic features based on contrast CT images, including inverse variance, minor axis, and elongation, can serve as noninvasive predictors of Ki‐67 status in patients with lung cancer. Inverse variance could be superior to the other radiomic features to identify high Ki‐67 status.

Background: Isocitrate dehydrogenase 1/2 (IDH1/2), BAP1, ARID1A and PBRM1 have been reported as the most frequent mutant genes in intrahepatic cholangiocarcinoma (ICC), and their relationships with clinicopathological features and prognosis were researched in this study. Methods: We collected clinical data of 130 ICC patients from January 2012 to December 2017. The IDH1/2 mutation and loss of BAP1, ARID1A and PBRM1 expressions were detected by DNA sequencing or immunohistochemical methods, and histological subtype of ICCs was determined by hematoxylin-eosin, Alcian blue and S100P staining. Results: IDH1/2 mutation was related to decreased preoperative serum total bilirubin (P = 0.039), ferritin (P = 0.000) and higher histological differentiation (P = 0.024), and was associated with prolonged disease-free survival (P = 0.009) and a trend toward increased overall survival (P = 0.126) in small duct type of ICCs. Immunohistochemical staining results of MsMab-1 were generally consistent with DNA sequencing for IDH1/2 mutant in ICCs (κ = 0.691). Only BAP1 expression loss was correlated to prolonged disease-free survival (P = 0.031) and overall survival (P = 0.041) in large duct type of ICCs. Conclusions: IDH1/2 mutation is a favorable predictor and may be related to iron metabolism in small duct type of ICCs. Furthermore, we suggest that the detection of IDH1/2 mutation is indispensable to determine targeted therapy in small duct type ICCs, while it is not necessary in large duct of ICCs. MsMab-1 is a relatively effective multi-specific antibody against IDH1/2 mutant in ICCs. BAP1 expression loss was correlated with improved prognosis only in large duct type ICCs.

No abstract

No abstract

Summary Fibrosis, or the accumulation of extracellular matrix, is a common feature of many chronic diseases. To interrogate core molecular pathways underlying fibrosis, we cross-examine human primary cells from various tissues treated with TGF-β, as well as kidney and liver fibrosis models. Transcriptome analyses reveal that genes involved in fatty acid oxidation are significantly perturbed. Furthermore, mitochondrial dysfunction and acylcarnitine accumulation are found in fibrotic tissues. Substantial downregulation of the PGC1α gene is evident in both in vitro and in vivo fibrosis models, suggesting a common node of metabolic signature for tissue fibrosis. In order to identify suppressors of fibrosis, we carry out a compound library phenotypic screen and identify AMPK and PPAR as highly enriched targets. We further show that pharmacological treatment of MK-8722 (AMPK activator) and MK-4074 (ACC inhibitor) reduce fibrosis in vivo . Altogether, our work demonstrate that metabolic defect is integral to TGF-β signaling and fibrosis.

Abstract. Cell cycle-related kinase (CCRK) is a novel protein kinase homologous to both cyclin-dependent kinase 7 (Cdk7) and Cak1p groups of CDK-activating kinase (CAK). CCRK activates Cdk2, which controls the cell-cycle progression by phosphorylating a threonine residue conserved in Cdk2. Previous studies have indicated that the CCRK protein levels were elevated by more than 1.5-fold in tumor tissue, and that the overexpression of CCRK is associated with poor prognosis of the patients. Moreover, recent studies have shown that CCRK is involved in the Wnt signaling pathway associated with the genesis and evolution of cancer. This review aims to systematically present the information currently available on CCRK obtained from in vitro and in vivo studies and highlight its significance to tumorigenesis.