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Characterizing threading dislocations (TDs) in gallium nitride (GaN) semiconductors is crucial for ensuring the reliability of semiconductor devices. The current research addresses this issue by combining two techniques using a scanning electron microscope, namely electron channeling contrast imaging (ECCI) and high-resolution electron backscattered diffraction (HR-EBSD). It is a comparative study of these techniques to underscore how they perform in the evaluation of TD densities in GaN epitaxial layers. Experiments reveal that the dislocation line vectors mostly deviate from the growth direction of the film, i.e., ∦ [0001], followed by edge-type dislocations (dislocation lines || [0001]) with insignificant screw character. Furthermore, TDs from the dislocation clusters are characterized as edge- and (edge + mixed)-type TDs. By combining ECCI counting of dislocations and HR-EBSD description of geometrically necessary dislocation density type, it is possible to measure the total TD density and provide the proportion of pure (edge and screw) and mixed TDs. It has also been observed from the analyses of residual elastic strain fields and lattice rotations that it is not possible to identify individual dislocations for the spatial resolution of 50 nm in HR-EBSD. Nevertheless, ECCI and HR-EBSD can be complementarily used to count and characterize the TDs., Competing Interests: Conflict of Interest: The authors declare that they have no competing interest., (© The Author(s) 2025. Published by Oxford University Press on behalf of the Microscopy Society of America. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Reunion Island is a French department located in the southwestern Indian Ocean, with distinct trends in drug use, drug diversion and intoxication compared with metropolitan France (e.g. the misuse of drugs - clonazepam and trihexyphenidyl - combined with cannabis or cocaine, which is not observed in metropolitan France). The authors report a case of atypical intoxication in a 16-year-old female who consumed cannabis in conjunction with an unusual powdered mixture containing psychotropic substances. The intoxication led to confusion, hallucinations, sinus tachycardia and hospitalization. A comprehensive high-resolution mass spectrometry and liquid-chromatography mass spectrometry analysis of her plasma, her urine and a powder found in her possession revealed the presence of the same 5 medicines: citalopram/escitalopram, paroxetine, sertraline, venlafaxine and trihexyphenidyl. This case underscores the intricate interactions between psychoactive substances that are never prescribed together in clinical settings, along with the issue of diverted prescription drugs like trihexyphenidyl. It also emphasizes the potential circulation and use of crushed mixtures of medication for recreational purpose. Fortunately, powder analysis provided crucial insight to understand the intoxication., (© The Author(s) 2025. Published by Oxford University Press. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site–for further information please contact journals.permissions@oup.com.)

Glioblastoma is one of the most treatment-resistant and lethal cancers, with a subset of self-renewing brain tumour stem cells (BTSCs), driving therapy resistance and relapse. Here, we report that mubritinib effectively impairs BTSC stemness and growth. Mechanistically, bioenergetic assays and rescue experiments showed that mubritinib targets complex I of the electron transport chain, thereby impairing BTSC self-renewal and proliferation. Gene expression profiling and Western blot analysis revealed that mubritinib disrupts the AMPK/p27 Kip1 pathway, leading to cell-cycle impairment. By employing in vivo pharmacokinetic assays, we established that mubritinib crosses the blood-brain barrier. Using preclinical patient-derived and syngeneic models, we demonstrated that mubritinib delays glioblastoma progression and extends animal survival. Moreover, combining mubritinib with radiotherapy or chemotherapy offers survival advantage to animals. Notably, we showed that mubritinib alleviates hypoxia, thereby enhancing ROS generation, DNA damage, and apoptosis in tumours when combined with radiotherapy. Encouragingly, toxicological and behavioural studies revealed that mubritinib is well tolerated and spares normal cells. Our findings underscore the promising therapeutic potential of mubritinib, warranting its further exploration in clinic for glioblastoma therapy., Competing Interests: Disclosure and competing interests statement. The authors declare no competing interests., (© 2025. The Author(s).)

Stable-isotope resolved metabolomics (SIRM) is a powerful approach for characterizing metabolic states in cells and organisms. By incorporating isotopes, such as 13 C, into substrates, researchers can trace reaction rates across specific metabolic pathways. Integrating metabolomics data with gene expression profiles further enriches the analysis, as we demonstrated in our prior study on glioblastoma metabolic symbiosis. However, the bioinformatics tools for analyzing tracer metabolomics data have been limited. In this protocol, we encourage the researchers to use SIRM and transcriptomics data and to perform the downstream analysis using our software tool DIMet. Indeed, DIMet is the first comprehensive tool designed for the differential analysis of tracer metabolomics data, alongside its integration with transcriptomics data. DIMet facilitates the analysis of stable-isotope labeling and metabolic abundances, offering a streamlined approach to infer metabolic changes without requiring complex flux analysis. Its pathway-based "metabologram" visualizations effectively integrate metabolomics and transcriptomics data, offering a versatile platform capable of analyzing corrected tracer datasets across diverse systems, organisms, and isotopes. We provide detailed steps for sample preparation and data analysis using DIMet through its intuitive, web-based Galaxy interface. To showcase DIMet's capabilities, we analyzed LDHA/B knockout glioblastoma cell lines compared to controls. Accessible to all researchers through Galaxy, DIMet is free, user-friendly, and open source, making it a valuable resource for advancing metabolic research. Key features • Glioblastoma tumor spheroids in vitro replicate tumors' three-dimensional structure and natural nutrient, metabolite, and gas gradients, providing a more realistic model of tumor biology. • Joint analysis of tracer metabolomics and transcriptomics datasets provides deeper insights into the metabolic states of cells. • DIMet is a web-based tool for differential analysis and seamless integration of metabolomics and transcriptomics data, making it accessible and user-friendly. • DIMet enables researchers to infer metabolic changes, offering intuitive and visually appealing "metabologram" outputs, surpassing conventional visual representations commonly used in the field., Competing Interests: Competing interestsThere are no conflicts of interest or competing interests., (©Copyright : © 2025 The Authors; This is an open access article under the CC BY-NC license.)

Mounting evidence is identifying human cytomegalovirus (HCMV) as a potential oncogenic virus. HCMV has been detected in glioblastoma multiforme (GB). Herewith, we present the first experimental evidence for the generation of CMV-Elicited Glioblastoma Cells (CEGBCs) possessing glioblastoma-like traits that lead to the formation of glioblastoma in orthotopically xenografted mice. In addition to the already reported oncogenic HCMV-DB strain, we isolated three HCMV clinical strains from GB tissues that transformed HAs toward CEGBCs and generated spheroids from CEGBCs that resulted in the appearance of glioblastoma-like tumors in xenografted mice. These tumors were nestin-positive mostly in the invasive part surrounded by GFAP-positive reactive astrocytes. The glioblastoma immunohistochemistry phenotype was confirmed by EGFR and cMet gene amplification in the tumor parallel to the detection of HCMV IE and UL69 genes and proteins. Our results fit with an HCMV-induced glioblastoma model of oncogenesis in vivo which will open the door to new therapeutic approaches and assess the anti-HCMV treatment as well as immunotherapy in fighting GB which is characterized by poor prognosis., (© 2024. The Author(s).)

Motivation: Many diseases, such as cancer, are characterized by an alteration of cellular metabolism allowing cells to adapt to changes in the microenvironment. Stable isotope-resolved metabolomics (SIRM) and downstream data analyses are widely used techniques for unraveling cells' metabolic activity to understand the altered functioning of metabolic pathways in the diseased state. While a number of bioinformatic solutions exist for the differential analysis of SIRM data, there is currently no available resource providing a comprehensive toolbox., Results: In this work, we present DIMet, a one-stop comprehensive tool for differential analysis of targeted tracer data. DIMet accepts metabolite total abundances, isotopologue contributions, and isotopic mean enrichment, and supports differential comparison (pairwise and multi-group), time-series analyses, and labeling profile comparison. Moreover, it integrates transcriptomics and targeted metabolomics data through network-based metabolograms. We illustrate the use of DIMet in real SIRM datasets obtained from Glioblastoma P3 cell-line samples. DIMet is open-source, and is readily available for routine downstream analysis of isotope-labeled targeted metabolomics data, as it can be used both in the command line interface or as a complete toolkit in the public Galaxy Europe and Workfow4Metabolomics web platforms., Availability and Implementation: DIMet is freely available at https://github.com/cbib/DIMet, and through https://usegalaxy.eu and https://workflow4metabolomics.usegalaxy.fr. All the datasets are available at Zenodo https://zenodo.org/records/10925786., (© The Author(s) 2024. Published by Oxford University Press.)

The posttranslational modification of proteins critically influences many biological processes and is a key mechanism that regulates the function of the RNA-binding protein Hu antigen R (HuR), a hub in liver cancer. Here, we show that HuR is SUMOylated in the tumor sections of patients with hepatocellular carcinoma in contrast to the surrounding tissue, as well as in human cell line and mouse models of the disease. SUMOylation of HuR promotes major cancer hallmarks, namely proliferation and invasion, whereas the absence of HuR SUMOylation results in a senescent phenotype with dysfunctional mitochondria and endoplasmic reticulum. Mechanistically, SUMOylation induces a structural rearrangement of the RNA recognition motifs that modulates HuR binding affinity to its target RNAs, further modifying the transcriptomic profile toward hepatic tumor progression. Overall, SUMOylation constitutes a mechanism of HuR regulation that could be potentially exploited as a therapeutic strategy for liver cancer., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)

Glioblastoma (GB), the most malignant subtype of diffuse glioma, is highly aggressive, invasive and vascularized. Its median survival is still short even with maximum standard care. There is a need to identify potential new molecules and mechanisms, that are involved in the interactions of GB cells with the tumor microenvironment (TME), for therapeutic intervention. Thrombospondin-1 (TSP1) is a multi-faceted matricellular protein which plays a significant role in development, physiology and pathology including cancer. Recent studies have pinpoint an important role of TSP1 in GB development which will be summarized and discussed herein. We will discuss studies, mainly from preclinical research, which should lead to a deeper understanding of TSP1's role in GB development. We will also discuss some issues with regard to the use of this knowledge for the clinic., Competing Interests: Declaration of Competing Interest There is no conflict of interest to declare., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Organoids are unique tools to mimic how tumors evolve in a 3D environment. Here, we present a protocol to embed spheroids invading a 3D matrix into a paraffin mold. We describe steps for preparing spheroids, collagen and agarose inclusion, and paraffinization. We then detail procedures for sectioning, staining, and visualization. This protocol allows histological identification of markers expressed in cells escaping the tumor. For complete details on the use and execution of this protocol, please refer to Guyon et al. (2022). 1 ., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.)

The transfer of intact mitochondria between heterogeneous cell types has been confirmed in various settings, including cancer. However, the functional implications of mitochondria transfer on tumor biology are poorly understood. Here we show that mitochondria transfer is a prevalent phenomenon in glioblastoma (GBM), the most frequent and malignant primary brain tumor. We identified horizontal mitochondria transfer from astrocytes as a mechanism that enhances tumorigenesis in GBM. This transfer is dependent on network-forming intercellular connections between GBM cells and astrocytes, which are facilitated by growth-associated protein 43 (GAP43), a protein involved in neuron axon regeneration and astrocyte reactivity. The acquisition of astrocyte mitochondria drives an increase in mitochondrial respiration and upregulation of metabolic pathways linked to proliferation and tumorigenicity. Functionally, uptake of astrocyte mitochondria promotes cell cycle progression to proliferative G2/M phases and enhances self-renewal and tumorigenicity of GBM. Collectively, our findings reveal a host-tumor interaction that drives proliferation and self-renewal of cancer cells, providing opportunities for therapeutic development., (© 2023. The Author(s).)

Lactate is a central metabolite in brain physiology but also contributes to tumor development. Glioblastoma (GB) is the most common and malignant primary brain tumor in adults, recognized by angiogenic and invasive growth, in addition to its altered metabolism. We show herein that lactate fuels GB anaplerosis by replenishing the tricarboxylic acid (TCA) cycle in absence of glucose. Lactate dehydrogenases (LDHA and LDHB), which we found spatially expressed in GB tissues, catalyze the interconversion of pyruvate and lactate. However, ablation of both LDH isoforms, but not only one, led to a reduction in tumor growth and an increase in mouse survival. Comparative transcriptomics and metabolomics revealed metabolic rewiring involving high oxidative phosphorylation (OXPHOS) in the LDHA/B KO group which sensitized tumors to cranial irradiation, thus improving mouse survival. When mice were treated with the antiepileptic drug stiripentol, which targets LDH activity, tumor growth decreased. Our findings unveil the complex metabolic network in which both LDHA and LDHB are integrated and show that the combined inhibition of LDHA and LDHB strongly sensitizes GB to therapy., (© 2022 The Authors. Published under the terms of the CC BY 4.0 license.)

Cell motility is critical for tumor malignancy. Metabolism being an obligatory step in shaping cell behavior, we looked for metabolic weaknesses shared by motile cells across the diverse genetic contexts of patients' glioblastoma. Computational analyses of single-cell transcriptomes from thirty patients' tumors isolated cells with high motile potential and highlighted their metabolic specificities. These cells were characterized by enhanced mitochondrial load and oxidative stress coupled with mobilization of the cysteine metabolism enzyme 3-Mercaptopyruvate sulfurtransferase (MPST). Functional assays with patients' tumor-derived cells and -tissue organoids, and genetic and pharmacological manipulations confirmed that the cells depend on enhanced ROS production and MPST activity for their motility. MPST action involved protection of protein cysteine residues from damaging hyperoxidation. Its knockdown translated in reduced tumor burden, and a robust increase in mice survival. Starting from cell-by-cell analyses of the patients' tumors, our work unravels metabolic dependencies of cell malignancy maintained across heterogeneous genomic landscapes., (© 2022. The Author(s).)

High-N Ni-free stainless steels are used for their excellent mechanical properties combined with their high corrosion resistance, especially for biomedical applications. Even though it is well-known that secondary hardening during annealing after cold working has been observed in many materials, this phenomenon was not reported for these materials, one of the best known being Biodur108©, although numerous efforts have been made to increase its hardness. In this work, thermomechanical treatments at low temperature of cold-deformed Biodur108© were conducted to increase the hardness. Hardness as high as 830 Hv was obtained. For this material, the annealing of a deformed sample at intermediate temperature leads to a secondary hardening phenomenon. The mechanisms responsible for this secondary hardening were analyzed. It was found that for deformed samples, annealing at 575 °C leads to the formation of small Cr 2 N precipitates along grain boundaries and sub-grain boundaries, and simultaneously with a new body-centered cubic (BCC) phase that possesses a super structure. The newly formed phases have sub-micrometric grain sizes.

Nirmatrelvir/ritonavir association has been authorized for conditional use in the treatment of COVID-19, especially in solid-organ transplant recipients who did not respond to vaccine and are still at high risk of severe disease. This combination remains at risk of drug interactions with immunosuppressants, so monitoring drug levels seems necessary. After a simple protein precipitation of plasma sample, analytes were analyzed using an ultrahigh performance liquid chromatography system coupled with tandem mass spectrometry in a positive ionization mode. Validation procedures were based on the guidelines on bioanalytical methods issued by the European Medicine Agency. The analysis time was 4 min per run. The calibration curves were linear over the range from 10 to 1000 ng/mL for ritonavir and 40 to 4000 ng/mL for nirmatrelvir, with coefficients of correlation above 0.99 for all analytes. Intra-/interday imprecisions were below 10%. The analytical method also meets criteria of matrix effect, carryover, dilution integrity, and stability. In the context of a SARS-CoV-2 infection in a renal transplant recipient, we present a case of tacrolimus overdose with serious adverse events despite discontinuation of nirmatrelvir and ritonavir. The patient had still effective concentrations of nirmatrelvir and tacrolimus 4 days after drug discontinuation. This method was successfully applied for therapeutic drug monitoring in clinical practice.

Radiosensitization of glioblastoma is a major ambition to increase the survival of this incurable cancer. The 5-aminolevulinic acid (5-ALA) is metabolized by the heme biosynthesis pathway. 5-ALA overload leads to the accumulation of the intermediate fluorescent metabolite protoporphyrin IX (PpIX) with a radiosensitization potential, never tested in a relevant model of glioblastoma. We used a patient-derived tumor cell line grafted orthotopically to create a brain tumor model. We evaluated tumor growth and tumor burden after different regimens of encephalic multifractionated radiation therapy with or without 5-ALA. A fractionation scheme of 5 × 2 Gy three times a week resulted in intermediate survival [48-62 days] compared to 0 Gy (15-24 days), 3 × 2 Gy (41-47 days) and, 5 × 3 Gy (73-83 days). Survival was correlated to tumor growth. Tumor growth and survival were similar after 5 × 2 Gy irradiations, regardless of 5-ALA treatment (RT group (53-67 days), RT+5-ALA group (40-74 days), HR = 1.57, p = 0.24). Spheroid growth and survival were diminished by radiotherapy in vitro, unchanged by 5-ALA pre-treatment, confirming the in vivo results. The analysis of two additional stem-like patient-derived cell lines confirmed the absence of radiosensitization by 5-ALA. Our study shows for the first time that in a preclinical tumor model relevant to human glioblastoma, treated as in clinical routine, 5-ALA administration, although leading to important accumulation of PpIX, does not potentiate radiotherapy.

Glioblastoma (GB) are the most frequent brain cancers. Aggressive growth and limited treatment options induce a median survival of 12-15 months. In addition to highly proliferative and invasive properties, GB cells show cancer-associated metabolic characteristics such as increased aerobic glycolysis. Pyruvate dehydrogenase (PDH) is a key enzyme complex at the crossroads between lactic fermentation and oxidative pathways, finely regulated by PDH kinases (PDHKs). PDHKs are often overexpressed in cancer cells to facilitate high glycolytic flux. We hypothesized that targeting PDHKs, by disturbing cancer metabolic homeostasis, would alter GB progression and render cells vulnerable to additional cancer treatment. Using patient databases, distinct expression patterns of PDHK1 and PDHK2 in GB tissues were obvious. To disturb protumoral glycolysis, we modulated PDH activity through the genetic or pharmacological inhibition of PDHK in patient-derived stem-like spheroids. Striking effects of PDHKs inhibition using dichloroacetate were observed in vitro on cell morphology and metabolism, resulting in increased intracellular ROS levels and decreased proliferation and invasion. In vivo findings confirmed a reduction in tumor size and better survival of mice implanted with PDHK1 and PDHK2 knockout cells. Adding a radiotherapeutic protocol further resulted in a reduction in tumor size and improved mouse survival in our model.

Background: Microtubes (MTs), cytoplasmic extensions of glioma cells, are important cell communication structures promoting invasion and treatment resistance through network formation. MTs are abundant in chemoresistant gliomas, in particular, glioblastomas (GBMs), while they are uncommon in chemosensitive IDH-mutant and 1p/19q co-deleted oligodendrogliomas. The aim of this study was to identify potential signaling pathways involved in MT formation., Methods: Bioinformatics analysis of TCGA was performed to analyze differences between GBM and oligodendroglioma. Patient-derived GBM stem cell lines were used to investigate MT formation under transforming growth factor-beta (TGF-β) stimulation and inhibition in vitro and in vivo in an orthotopic xenograft model. RNA sequencing and proteomics were performed to detect commonalities and differences between GBM cell lines stimulated with TGF-β., Results: Analysis of TCGA data showed that the TGF-β pathway is highly activated in GBMs compared to oligodendroglial tumors. We demonstrated that TGF-β1 stimulation of GBM cell lines promotes enhanced MT formation and communication via calcium signaling. Inhibition of the TGF-β pathway significantly reduced MT formation and its associated invasion in vitro and in vivo. Downstream of TGF-β, we identified thrombospondin 1 (TSP1) as a potential mediator of MT formation in GBM through SMAD activation. TSP1 was upregulated upon TGF-β stimulation and enhanced MT formation, which was inhibited by TSP1 shRNAs in vitro and in vivo., Conclusion: TGF-β and its downstream mediator TSP1 are important mediators of the MT network in GBM and blocking this pathway could potentially help to break the complex MT-driven invasion/resistance network., (© The Author(s) 2021. Published by Oxford University Press on behalf of the Society for Neuro-Oncology.)

Stroke is the leading cause of neurological disability in people over 40 years of age and the fourth leading cause of death in Argentina. In the last ten years, the indexed publications related to the treatment of ischemic stroke were more numerous than those of hemorrhagic stroke. The objective of this material is to provide local and updated recommendations for the management of patients with spontaneous intracerebral hemorrhage during hospitalization. For the writing of this manuscript, diferent specialists were convened to form working groups. Ten central topics expressed as epidemiology, initial care, imaging, blood pressure treatment, reversal of antithrombotics, indication for surgery, seizure prophylaxis, prognosis, prevention of complications and resumption of antithrombotics were raised. For each topic, the most frequent questions of daily practice were raised through PICO questions. After a systematic review of the literature, recommendations were generated, evaluated using the GRADE system and agreed between authors and patients.

Glioblastoma is among the most common tumor of the central nervous system in adults. Overall survival has not significantly improved over the last decade, even with optimizing standard therapeutic care including extent of resection and radio- and chemotherapy. In this article, we review features of the brain vasculature found in healthy cerebral tissue and in glioblastoma. Brain vessels are of various sizes and composed of several vascular cell types. Non-vascular cells such as astrocytes or microglia also interact with the vasculature and play important roles. We also discuss in vitro engineered artificial blood vessels which may represent useful models for better understanding the tumor-vessel interaction. Finally, we summarize results from clinical trials with anti-angiogenic therapy alone or in combination, and discuss the value of these approaches for targeting glioblastoma., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Guyon, Chapouly, Andrique, Bikfalvi and Daubon.)

Glioblastomas (GBMs), grade IV malignant gliomas, are one of the deadliest types of human cancer because of their aggressive characteristics. Despite significant advances in the genetics of these tumors, how GBM cells invade the healthy brain parenchyma is not well understood. Notably, it has been shown that GBM cells invade the peritumoral space via different routes; the main interest of this paper is the route along white matter tracts (WMTs). The interactions of tumor cells with the peritumoral nervous cell components are not well characterized. Herein, a method has been described that evaluates the impact of neurons on GBM cell invasion. This paper presents an advanced co-culture in vitro assay that mimics WMT invasion by analyzing the migration of GBM stem-like cells on neurons. The behavior of GBM cells in the presence of neurons is monitored by using an automated tracking procedure with open-source and free-access software. This method is useful for many applications, in particular, for functional and mechanistic studies as well as for analyzing the effects of pharmacological agents that can block GBM cell migration on neurons.

Two-dimensional (2D) cell cultures do not mimic in vivo tumor growth satisfactorily. Therefore, three-dimensional (3D) culture spheroid models were developed. These models may be particularly important in the field of neuro-oncology. Indeed, brain tumors have the tendency to invade the healthy brain environment. We describe herein an ideal 3D glioblastoma spheroid-based assay that we developed to study tumor invasion. We provide all technical details and analytical tools to successfully perform this assay.

Background: Glioblastomas are heterogeneous tumors composed of a necrotic and tumor core and an invasive periphery., Methods: Here, we performed a proteomics analysis of laser-capture micro-dissected glioblastoma core and invasive areas of patient-derived xenografts., Results: Bioinformatics analysis identified enriched proteins in central and invasive tumor areas. Novel markers of invasion were identified, the genes proteolipid protein 1 (PLP1) and Dynamin-1 (DNM1), which were subsequently validated in tumors and by functional assays., Conclusions: In summary, our results identify new networks and molecules that may play an important role in glioblastoma development and may constitute potential novel therapeutic targets., (© The Author(s) 2019. Published by Oxford University Press, the Society for Neuro-Oncology and the European Association of Neuro-Oncology.)

In this paper, we report the successful combination of macroscopic uniaxial tensile testing of bulk specimen combined with In situ dislocation-scale observations of the evolution of deformation microstructures during loading at several stress states. The dislocation-scale observations were performed by Accurate Electron Channeling Contrast Imaging in order to follow the defects evolution and their interactions with grain boundaries for several regions of interest during macroscopic loading. With this novel in situ procedure, the slip systems governing the deformation in polycrystalline bulk β-Ti21S are tracked during the macroscopic uniaxial tensile test. For instance, curved slip lines that are associated with "pencil glide" phenomenon and tangled dislocation networks are evidenced.

In this work, plastic deformation was locally introduced at room temperature by nanoindentation on a γ-TiAl-based alloy. Comprehensive analyses of microstructures were performed before and after deformation. In particular, the Burgers vectors, the line directions, and the mechanical twinning systems were studied via accurate electron channeling contrast imaging. Accommodation of the deformation are reported and a scenario is proposed. All features help to explain the poor ductility of the TiAl-based alloys at room temperature.

A new setup for automatic 3D EBSD data collection in static mode has been developed using a conventional FIB-SEM system. This setup requires no stage or sample movements between the FIB milling and EBSD mapping. Its capabilities were tested experimentally on a coherent twin boundary of an INCONEL sample. Our result demonstrates that this static setup holds many advantages in terms of data throughput and quality as compared with other ones requiring stage/sample movements. The most important advantages are the better slice alignment and an improved orientation precision in 3D space, both being prerequisite for a reliable grain boundary characterization., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Conventional orientation mapping in a scanning electron microscope (SEM) is a valuable technique for characterizing crystalline materials, but its application to ultrafine or nano-grain materials is limited by its spatial resolution. The resolution can be increased by collecting transmission diffraction patterns in SEM. In previous works, such patterns were collected using off-axis detectors in nearly vertical position. To avoid some drawbacks of such arrangement, a new configuration was devised in which the scintillator is located underneath the thin foil on the optical axis of the microscope, and the light is reflected towards the camera by a mirror. This simple configuration gives intense patterns even at very low probe currents, and can be potentially used for collecting maps of relatively high spatial resolution. Example maps reveal details with dimensions of about 5nm. Because of its resolution and geometric simplicity, the proposed configuration will open new opportunities in SEM-based characterization of nanocrystalline materials., (Copyright © 2015 Elsevier B.V. All rights reserved.)