Volume and mass of coarse woody debris (> 20 cm diameter) in an old-growth forest on the Cumberland Plateau in southeastern Kentucky averaged 66.3 m3/ha and 21.8 Mg/ha, respectively. Coarse woody debris was patchily distributed among 80 sample plots (0.04 ha each), with 10 plots containing 39% of the total mass. Coarse woody debris mass was inversely, although not strongly, related to plot basal area. While 23 species contributed to the accumulation of coarse woody debris, five accounted for 72% of the total mass. These included Quercusprinus L. (25% of the total), Fagusgrandifolia L. (16%), Quercusalba L. (12%), Castaneadentata (Marsh.) Borkh. (11%), and Quercusvelutina Lam. (9%). The few studies of coarse woody debris in old-growth deciduous forests of North America suggest a regional pattern of accumulation correlated with temperature. In warmer regions, old-growth deciduous forests accumulate a mass in the range of 22–32 Mg/ha, while in cooler ecosystems, coarse woody debris ranges from 34 to 49 Mg/ha.

Phytochrome-interacting factors (PIFs) regulate an array of developmental responses ranging from seed germination to vegetational architecture in Arabidopsis. However, information regarding the functions of the PIF family in monocots has not been widely reported. Here, we investigate the roles of OsPIL15, a member of the rice (Oryza sativa L. cv. Nipponbare) PIF family, in regulating seedling growth. OsPIL15 encodes a basic helix-loop-helix factor localized in the nucleus. OsPIL15-OX seedlings exhibit an exaggerated shorter aboveground part and undeveloped root system relative to wild-type seedlings, suggesting that OsPIL15 represses seedling growth in the dark. Microarray analysis combined with gene ontology analysis revealed that OsPIL15 represses a set of genes involved in auxin pathways and cell wall organization or biogenesis. Given the important roles of the auxin pathway and cell wall properties in controlling plant growth, we speculate that OsPIL15 represses seedling growth likely by regulating the auxin pathway and suppressing cell wall organization in etiolated rice seedlings. Additionally, exposure to red light or far-red light relieved growth retardation and promoted seedling elongation in the OsPIL15-OX lines, despite higher levels of OsPIL15 transcripts under red light and far-red light than in the dark. These results suggest that light regulation of OsPIL15 expression is probably involved in photomorphogenesis in rice.

No abstract

Long non‐coding RNA (lncRNA) plays important roles in tumour progression. Accumulating studies demonstrated that lncRNA colon cancer‐associated transcript 2 (CCAT2) acted as an oncogene in many tumours. However, the role of CCAT2 in the development of osteosarcoma has not been elucidated. In our study, we indicated that CCAT2 expression was up‐regulated in osteosarcoma tissues and cell lines (SOSP‐9607, MG‐63, U2OS and SAOS‐2). In addition, osteosarcoma cases with higher CCAT2 expression had a poorer disease‐free survival and shorter the overall survival time compared to those with lower expression. Overexpression of CCAT2 promoted osteosarcoma cell proliferation, invasion and cell cycle. Furthermore, ectopic expression of CCAT2 increased the expression of mesenchymal markers N‐cadherin, vimentin and snail and reduced the expression of N‐cadherin marker E‐cadherin. CCAT2 overexpression promoted the LATS2 and c‐Myc expression in osteosarcoma cell. These data indicated that CCAT2 served as an oncogene in osteosarcoma and promoted osteosarcoma cell proliferation, cell cycle and invasion.

No abstract

Long noncoding RNA (lncRNA) Linc00511 is a novel lncRNA, and it was reported to play important roles in the progression and carcinogenesis of several tumors. However, the expression and biological roles of Linc00511 in osteosarcoma were still unknown. In this research, we showed that the expression of Linc00511 was upregulated in osteosarcoma samples and cell lines. Ectopic expression of Linc00511 promoted osteosarcoma cell growth, colony formation, and migration. Moreover, overexpression of Linc00511 enhanced the epithelial‐mesenchymal transition progression in osteosarcoma cell. In addition, we showed that elevated expression of Linc00511 suppressed microRNA‐765 (miR‐765) expression and promoted apurinic/apyrimidinic endonuclease 1 (APE1) expression in osteosarcoma cell. The expression of miR‐765 was downregulated in osteosarcoma cells and samples and was negatively related to Linc00511 expression in osteosarcoma tissues. Ectopic expression of miR‐765 inhibited osteosarcoma cell growth and migration. Furthermore, we showed that Linc00511 overexpression promoted MG‐63 cells proliferation, colony formation, and migration via downregulation of miR‐765. These results suggested that Linc00511 played as an oncogene in the development of osteosarcoma.

Osteosarcoma is the most common type of malignant bone tumor, often affecting adolescents and children. MicroRNAs (miRNAs) are a group of small, non-protein coding, endogenous RNAs that play critical roles in osteosarcoma tumorigenesis. In our study, we demonstrated that miR-448 expression was downregulated in osteosarcoma tissues and cell lines. Overexpression of miR-448 suppressed osteosarcoma cell proliferation, colony formation and migration. Moreover, we found that EPHA7 was a direct target gene of miR-448 in osteosarcoma cells. We further demonstrated that the EPHA7 expression level was upregulated in osteosarcoma tissues. Interestingly, the expression level of EPHA7 was inversely correlated with the expression level of miR-448 in osteosarcoma tissues. In addition, elevated expression of miR-448 suppressed osteosarcoma cell proliferation and invasion through targeting EPHA7. Taken together, these findings suggest that miR-448 functioned as a tumor suppressor gene in the development of osteosarcoma through targeting EPHA7.

Patients with acute myocardial infarction (AMI) complicated by heart failure with preserved ejection fraction (HFpEF) are likely to have more adverse cardiovascular events and higher mortality. The purpose of this study was to examine the predictors and outcomes in AMI patients complicated by HFpEF.We examined the demographics, clinical data, and clinical outcomes in 405 consecutive subjects who firstly presented with AMI after undergoing emergency percutaneous coronary intervention from January 2013 to June 2016.Three hundred twenty patients and eighty-five patients were classified into the nonheart failure (non-HF) group and HFpEF group, respectively. Patients with HFpEF had higher prevalence of prior hypertension, had higher levels of biomarkers, and had a larger left atrial diameter with a nondilated left ventricle were more likely to develop multivessel disease-vessels and had infarction-related artery located in left anterior descending artery than patients without HF. Moreover, patients with HFpEF had a higher probability of developing the in-hospital incident cardiovascular complications and death than non-HF patients.Two routine biomarkers, levels of hypersensitive C-reactive protein and N-terminal-pro brain natriuretic peptide, and number of diseased-vessels were independent predictors for in-hospital HFpEF incidence in AMI patients with preserved LVEF. AMI patients with HFpEF had a higher probability of in-hospital cardiovascular outcomes and mortality.