5 research outputs found
Entrance analysis of turbulent flow in an array of heated rectangular blocks
A numerical study is conducted to investigate the entrance behavior of turbulent flow over arrays of rectangular heated blocks. The problem formulation is three dimensional and the solution domain includes both the developing and fully-developed regions of the array. The blocks are deployed along the lower wall of a parallel-plate duct in an attempt to simulate the cooling passages of electronics equipments. The standard k-ε turbulence model was applied to the developing region of the flow at high Reynolds numbers, while a modified Lam-Bremhorst turbulence model was considered at low-Reynolds numbers. The computations are performed for two conventional thermal boundary conditions, namely constant heat flux and constant wall temperature. Reynolds numbers ranged from 102 to 105, with Prandtl number being equal to 0.7. The array geometry was identified with H/L = 1/8, S/L = 1/8, B/L = 1/2 and the entrance length, I/L = 1/2, 2 and 6. To evaluate the accuracy of the turbulence models, numerical solutions were compared with experiment
AR-UROLO - Augmented Reality System fuer die Urologie Abschlussbericht
SIGLEAvailable from TIB Hannover: F04B116 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekBundesministerium fuer Bildung und Forschung, Berlin (Germany)DEGerman
A single N6-methyladenosine site regulates lncRNA HOTAIR function in breast cancer cells.
N6-methyladenosine (m6A) modification of RNA regulates normal and cancer biology, but knowledge of its function on long noncoding RNAs (lncRNAs) remains limited. Here, we reveal that m6A regulates the breast cancer-associated human lncRNA HOTAIR. Mapping m6A in breast cancer cell lines, we identify multiple m6A sites on HOTAIR, with 1 single consistently methylated site (A783) that is critical for HOTAIR-driven proliferation and invasion of triple-negative breast cancer (TNBC) cells. Methylated A783 interacts with the m6A "reader" YTHDC1, promoting chromatin association of HOTAIR, proliferation and invasion of TNBC cells, and gene repression. A783U mutant HOTAIR induces a unique antitumor gene expression profile and displays loss-of-function and antimorph behaviors by impairing and, in some cases, causing opposite gene expression changes induced by wild-type (WT) HOTAIR. Our work demonstrates how modification of 1 base in an lncRNA can elicit a distinct gene regulation mechanism and drive cancer-associated phenotypes