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An intricate understanding of the fundamental β→α phase transformation upon the presence of metastable ω phase is vital for tailoring the multiphase microstructures of titanium and titanium alloys for various specific applications. To approach this, the structures and energetics of heterophase interfaces among α, β, and ω in titanium were thoroughly investigated, using the combination of high-resolution transmission electron microscopy and first-principles density functional theory calculations. The results strongly suggest that metastable ω does not necessarily act as the precursor of α but can reduce the energy barrier for α nucleation in β. The ω/β interfaces acts as favorable nucleation sites for α which, once forms, tends to grow favorably into the β matrix. These findings validate the ω-assisted α nucleation mechanism, and adequately rationalize many TEM observations on titanium alloys. [ABSTRACT FROM AUTHOR]

[Display omitted] • Crack tip stored energy density captures short fatigue crack growth rates across samples with strongly differing texture. • Elastic anisotropy and yield stress mismatch at grain boundaries in HCP Zircaloy-4 drive short crack growth rate fluctuations. • Crack path tortuosity in HCP single crystals is linked with the cyclic development of a shear back stress. Rates of fatigue crack growth in Zircaloy-4 are highly microstructurally sensitive and dependent upon texture. Crystal plasticity finite element modelling with the eXtended Finite Element Method and a stored energy density fracture criterion are used to simulate crack propagation in single crystals and polycrystalline microstructures for comparison with experimental crack growth rate data. Results demonstrate that growth rate fluctuations at microstructural features are driven primarily by elastic anisotropy and yield stress mismatch. Additionally, reduced rate of growth in soft hexagonal close packed grains (relative to the remote loading direction) can be linked with crack path tortuosity, which is shown to be controlled by the cyclic development of an in-plane shear back stress. Most importantly, stored energy density is shown to accurately capture major microstructure-driven differences in crack growth rate. Comparison of simulated fatigue crack growth rates with experimental data enables estimation of the critical stored energy density for crack propagation in Zircaloy-4 to be 250 J/m2. [ABSTRACT FROM AUTHOR]

Microstructurally short fatigue crack growth in blocky alpha Zircaloy-4 is experimentally investigated in cyclic three-point bend testing. The short crack propagation is sensitive to the local microstructure with respect to grain crystallographic orientation and grain boundaries. Polycrystals with predominant c-axis texture aligned out-of-plane and normal to loading give alternating crack paths along prismatic planes. Samples with c-axis texture aligned in plane and normal to loading typically show straight paths along prismatic planes, sometimes tortuous paths, but always crystallographic. Prismatic -direction crack growth rate is low compared to that for prismatic -direction growth for given loading. Hence the crystallographic plane within which cracks grow is important for determining overall growth rate. For tortuous cracks, with the predominant c-axis texture in plane and normal to loading, crack growth occurs along basal, prismatic and pyramidal planes, deflecting from one slip plane to another during transgranular propagation. Image 1 • Microstructurally short crack in blocky alpha Zircaloy-4 was found to grow along crystallographic planes. • Surface short crack growth were observed in prism planes along both Burgers vector and Non-Burgers vector directions. • Prismatic -direction crack growth rate is low compared to that for prismatic -direction growth. [ABSTRACT FROM AUTHOR]

• A new analytical model for microstructure-sensitive crack growth rate is developed, combining the latest physical understanding of short crack growth behaviour with the efficiency of classical fracture mechanics. • A stored energy fracture criterion is shown to capture microstructure-sensitivity of crack growth rates. Full-field implementation of the model is achieved using a new crystallographic criterion for crack path, showing strong agreement with experiment. • The potential for the model to be extended to make predictions in the Paris regime is also demonstrated in this paper. Short fatigue crack growth in engineering alloys is among the most prominent challenges in mechanics of materials. Owing to its microstructural sensitivity, advanced and computationally expensive numerical methods are required to solve for crack growth rate. A novel mechanistic analytical model is presented, which adopts a stored energy density fracture criterion. Full-field implementation of the model in polycrystalline materials is achieved using a crystallographic crack-path prediction method based on a local stress intensity factor term. The model is applied to a range of Zircaloy-4 microstructures and demonstrates strong agreement with experimental rates and crack paths. Growth rate fluctuations across individual grains and substantial texture sensitivity are captured using the model. More broadly, this work demonstrates the benefits of mechanistic analytical modelling over conventional fracture mechanics and recent numerical approaches for accurate material performance predictions and design. Additionally, it offers a significant computer processing time reduction compared with state-of-the-art numerical methods. [Display omitted] [ABSTRACT FROM AUTHOR]

Objective There is no previous reports available on stent-assisted coiling of ruptured multiple intracranial aneurysms using single Low-Profile Visualized Intraluminal Support (LVIS) in one stage. In the present study, we investigated the efficacy and feasibility of using single LVIS to bridge multiple intracranial aneurysms in one stage. Methods From April 2014 to August 2016, 24 patients treated with single LVIS to bridge 2 aneurysms in one stage were reviewed. The aneurysm morphology, clinical outcome, angiographic results, progressive occlusion, recurrence, and procedure-related complications were analyzed retrospectively. Results In the present study, middle term clinical outcome showed that 9 patients were had a modified Rankin Scale (mRS) score of 0, 11 patients had mRS 1, and 4 patients had mRS 2. A total of 20 patients (83.3%) achieved a good outcome, 4 patients (16.7%) had poor outcomes, and 7 of 18 patients (38.9%) displayed improved clinical neurologic status in long-term follow-up. Immediate angiographic results postprocedure showed Raymond Scale (RS) I in 33 aneurysms (68.8%), RS II in 11 aneurysms (22.9%), and RS III in 4 aneurysms (8.3%). The angiographic follow-up results showed RS I in 41 aneurysms (85.4%), RS II in 5 aneurysms (10.4%), and RS III in 2 aneurysms (4.2%). Of 15 incomplete occlusion aneurysms postprocedure, 10 aneurysms (66.7%) achieved to progressed occlusion on follow-up imaging, and no recanalization or mortality occurred in this group. Conclusions Single LVIS bridging wide-neck ruptured multiple intracranial aneurysms was effective and feasible in one stage. However, the procedure-related complications should be emphasized and long-term follow-up requires further evaluation. Highlights • No previous data have shown assisted coiling of ruptured multiple intracranial aneurysms using a single stent in one stage. • We investigated the efficacy and feasibility of using single LVIS to bridge MIAs in one stage. • Single LVIS bridging wide-neck ruptured MIAs is effective and feasible in one stage. [ABSTRACT FROM AUTHOR]

Neuronal apoptosis is a crucial pathological process in early brain injury after subarachnoid hemorrhage (SAH). The effective therapeutic strategies to ameliorate neuronal apoptosis are still absent. We intended to determine whether intranasal administration of exogenous Netrin-1 (NTN-1) could attenuate neuronal apoptosis after experimental SAH, specifically via activating DCC-dependent APPL-1/AKT signaling cascade. Two hundred twenty-five male Sprague-Dawley rats were subjected to the endovascular perforation model of SAH. Recombinant human NTN-1 (rNTN-1) was administered intranasally. NTN-1 small interfering RNA (siRNA), APPL-1 siRNA, and AKT inhibitor MK2206 were administered through intracerebroventricular (i.c.v.) injection. SAH grade, neurological score, neuronal apoptosis assessed by cleaved caspase-3 (CC-3) expression and Fluoro-Jade C (FJC) staining, double immunofluorescence staining, and Western blot were examined. Our results revealed that endogenous NTN-1 level was increased after SAH. Administration of rNTN-1 improved neurological outcomes at 24 h and 72 h after SAH, while knockdown of endogenous NTN-1 worsened neurological impairments. Furthermore, exogenous rNTN-1 treatment promoted APPL-1 activation, increased phosphorylated-AKT and Bcl-2 expression, as well as decreased apoptotic marker CC-3 expression and the number of FJC-positive neurons, thereby alleviated neuronal apoptosis. Conversely, APPL-1 siRNA and MK2206 abolished the anti-apoptotic effect of exogenous rNTN-1 at 24 h after SAH. Collectively, intranasal administration of exogenous rNTN-1 attenuated neuronal apoptosis and improved neurological function in SAH rats, at least in apart via activating DCC/APPL-1/AKT signaling pathway. [ABSTRACT FROM AUTHOR]

A biomedical β titanium alloy (Ti–7Nb–10Mo) was designed and prepared by vacuum arc self-consumable melting. The ingot was forged and rolled to plates, followed by quenching and aging. Age-hardening behavior, microstructure evolution and its influence on mechanical properties of the alloy during aging were investigated, using X-ray diffraction, transmission electron microscopy, tensile and hardness measurements. The electrochemical behavior of the alloy was investigated in Ringer's solution. The microstructure of solution-treated (ST) alloy consists of the supersaturated solid solution β phase and the ω ath formed during athermal process. The ST alloy exhibits Young's modulus of 80 GPa, tensile strength of 774 MPa and elongation of 20%. The precipitation sequences during isothermal aging at different temperatures were determined as β + ω ath → β + ω iso (144 h) at T aging = 350–400 °C, β + ω ath → β + ω iso + α → β + α at T aging = 500 °C, and β + ω ath → β + α at T aging = 600–650 °C, where ω iso forms during isothermal process. The mechanical properties of the alloy can be tailored easily through controlling the phase transition during aging. Comparing with the conventional Ti-6Al-4 V alloy, the Ti–7Nb–10Mo alloy is more resistant to corrosion in Ringer's solution. Results show that the Ti–7Nb–10Mo alloy is promising for biomedical applications. [ABSTRACT FROM AUTHOR]

The poor prognosis of glioblastoma requires new innovative treatment strategies. We and others have shown that targeting tumor as well as angiogenesis in glioblastoma are effective therapeutic strategies. In line with these efforts, this work reveals that Quinacrine, an antimalarial drug, is a dual inhibitor of angiogenesis and glioblastoma. Using multiple glioblastoma cell lines, we found that Quinacrine inhibited proliferation and induced apoptosis in these cells, and acted in synergy with Temozolomide. Quinacrine potently inhibited tubular structure formations of glioblastoma microvascular endothelial cell (GMVEC) isolated from glioblastoma patients, especially for early stage tubular structure formation. Although Quinacrine induces apoptosis in GMVEC, the anti-angiogenic activity of Quinacrine is independent of its pro-apoptotic activity in GMVECs. Quinacrine inhibits glioblastoma angiogenesis and growth in vivo , and acts synergistically with Temozolomide in inhibiting glioblastoma growth in mice. Mechanistically, we found that Quinacrine acts on glioblastoma through inducing oxidative stress, impairing mitochondrial function and activating AMP-activated protein kinase (AMPK). Our work is the first to demonstrate the anti-angiogenic activity of Quinacrine. Our findings highlight Quinacrine as an attractive candidate to support treatment of glioblastoma. • Quinacrine has anti-glioblastoma activity. • Quinacrine is a novel angiogenesis inhibitor in vitro and in vivo. • The combination of quinacrine and temozolomide is synergistic. • Quinacrine acts on glioblastoma and angiogenesis via multiple mechanisms. [ABSTRACT FROM AUTHOR]