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Roughness surfaces likely present on high-speed flight vehicles due to ablation can greatly impact the laminar-turbulent transition process. In this work, effects of a randomly distributed roughness patch with roughness Reynolds number R e k k = 474 on the stability and transition in a Mach 6.5 boundary-layer flow over a flat plate have been investigated via stability analyses and direct numerical simulation (DNS). The roughness patch induces several streamwise streaks downstream. The streaks slightly stabilize the Mack mode instability, yet sustain strongly unstable shear-layer modes, achieving a significantly larger integrated growth rate than the smooth case. The most amplified shear-layer mode extracts energy primarily through the spanwise velocity gradient and develops nonlinearly into hairpin vortices residing on the strongest low-speed streak. The hairpin vortices eventually contaminate the whole flowfield, leading to a fully turbulent state. We further assess the influences of wall-temperature ratio and the roughness geometry on the flowfield and the pertaining instability characteristics. The results reveal that the high wall-temperature ratio weakens the streak amplitudes and shear-layer instabilities; while randomly distributed roughness tends to induce larger-amplitude streaks than the regular counterpart with the same R e k k , the flowfield of the former one can even be more stable than the latter. We find that the spanwise gradient of streamwise velocity should also be considered along with the streak amplitude in determining the strength of shear-layer instabilities. [ABSTRACT FROM AUTHOR]

Nonmodal linear stability analysis results are presented for hypersonic flow over a cone at 6° angle of attack complementing earlier modal stability analysis. Based on the parallel flow assumption, singular value decomposition is applied to obtain the optimal linear combination of global crossflow modes. The optimal disturbance exhibits significant transient growth in the initial short distance and progressively follows the path of the most unstable mode downstream. The largest transient energy gain is observed for disturbances at around 40 kHz close to the most amplified modal frequency and tends to increase with the Reynolds number. The optimal disturbance initially exhibits two amplitude peaks in the azimuthal direction, one lying in the leeward region where the unstable crossflow modes reside and the other in the windward region where the adjoint modes exist. As the optimal disturbance travels downstream, the second amplitude peak rapidly shifts toward the leeward side and reaches the optimal energy gain when it eventually merges with the first amplitude peak. The evolution process of the optimal disturbance indicates that the optimal disturbance might have exploited the locally crossflow instability through traveling from the windward side to the leeward side. [ABSTRACT FROM AUTHOR]

Tetrahymena telomerase holoenzyme subunits p75, p45 and p19 form a subcomplex (7-4-1) peripheral to the catalytic core. We report structures of p45 and p19 and reveal them as the Stn1 and Ten1 subunits of the CST complex, which stimulates telomerase complementary-strand synthesis. 7-4-1 binds telomeric single-stranded DNA, and mutant p19 overexpression causes telomere 3'-overhang elongation. We propose that telomerase-tethered Tetrahymena CST coordinates telomere G-strand and C-strand synthesis.

Identifying new targets for overcoming radioresistance is crucial for improving the efficacy of lung cancer radiotherapy, given that tumor cell resistance is a leading cause of treatment failure. Recent research has spotlighted the significance of Musashi2 (MSI2) in cancer biology. In this study, we first demonstrated that MSI2 plays a key function in regulating the radiosensitivity of lung cancer. The expression of MSI2 is negatively correlated with overall survival in cancer patients, and the knockdown of MSI2 inhibits tumorigenesis and increases radiosensitivity of lung cancer cells. Cellular radiosensitivity, which is closely linked to DNA damage, is influenced by MSI2 interaction with ataxia telangiectasia mutated and Rad3‐related kinase (ATR) and checkpoint kinase 1 (CHK1) post‐irradiation; moreover, knockdown of MSI2 inhibits the ATR‐mediated DNA damage response pathway. RNA‐binding motif protein 17 (RBM17), which is implicated in DNA damage repair, exhibits increased interaction with MSI2 post‐irradiation. We found that knockdown of RBM17 disrupted the interaction between MSI2 and ATR post‐irradiation and increased the radiosensitivity of lung cancer cells. Furthermore, we revealed the potential mechanism of MSI2 recruitment into the nucleus with the assistance of RBM17 to activate ATR to promote radioresistance. This study provides novel insights into the potential application of MSI2 as a new target in lung cancer radiotherapy. [ABSTRACT FROM AUTHOR]