40 research outputs found
Silicon crystal growth process video footage processing
No full textDarbs ir veltīts mašīnu redzes sistēmai, kas nodrošina lietņa diametra svārstību kontroli silīcija kristālu audzēšanas metodei, ko Latvijā bāzēts uzņēmums SIA "KEPP EU" izmanto saules bateriju kategorijas monokristālu ražošanai. Darba galvenie mērķi ir: izpētīt izmantoto silīcija kristālu ražošanas metodi, iepriekšējus EDI un KEPP EU veiktos pētījumus, kas rezultēja apskatītās mašīnu redzes sistēmas izstrādē, un uzlabot tās attēlu apstrādes algoritmus, lai uzlabotu specifiskas metrikas noteikšanas precizitāti un ātrdarbību. Darbā tiek aprakstītas populārākas silīcija kristālu audzēšanas metodes, izstrādātā mašīnu redzes sistēma un attēlu apstrādes algoritmi, ko darba autors izmantoja uzlabojumu veikšanai un alternatīvu risinājumu izstrādei, kas tiek salīdzināti ar izstrādāto sistēmu, lai gūtu priekšstatu par to efektivitāti.This paper is dedicated to machine vision system, that enables ingot diameter fluctuation control in silicon crystal growth method, that is used for solar cell grade silicon manufacturing by Latvian company "KEPP EU" LLC. Main goals are: to research silicon crystal growth method that is being used, previous researches, held by EDI and KEPP EU, which resulted in the development of viewed machine vision system, and make improvements to its image processing part to improve specific metric detection accuracy and performance. Paper contains description of widely used silicon crystal growth methods, developed machine vision system and image processing algorithms, used by author to make improvements and develop new solutions, that are being compared with developed system to gain insight into their effectiveness
Inhibition of HIF-1 alpha by PX-478 enhances the anti-tumor effect of gemcitabine by inducing immunogenic cell death in pancreatic ductal adenocarcinoma
No full textThis is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use,
distribution, and reproduction in any medium, provided the original author and source are credited
Bim and Bmf synergize to induce apoptosis in Neisseria gonorrhoeae infection
No full textAbstract: Bcl-2 family proteins including the pro-apoptotic BH3-only proteins are central regulators of apoptotic cell death. Here we show by a focused siRNA miniscreen that the synergistic action of the BH3-only proteins Bim and Bmf is required for apoptosis induced by infection with Neisseria gonorrhoeae (Ngo). While Bim and Bmf were associated with the cytoskeleton of healthy cells, they both were released upon Ngo infection. Loss of Bim and Bmf from the cytoskeleton fraction required the activation of Jun-N-terminal kinase-1 (JNK-1), which in turn depended on Rac-1. Depletion and inhibition of Rac-1, JNK-1, Bim, or Bmf prevented the activation of Bak and Bax and the subsequent activation of caspases. Apoptosis could be reconstituted in Bim-depleted and Bmf-depleted cells by additional silencing of antiapoptotic Mcl-1 and Bcl-XL, respectively. Our data indicate a synergistic role for both cytoskeletal-associated BH3-only proteins, Bim, and Bmf, in an apoptotic pathway leading to the clearance of Ngo-infected cells. Author Summary: A variety of physiological death signals, as well as pathological insults, trigger apoptosis, a genetically programmed form of cell death. Pathogens often induce host cell apoptosis to establish a successful infection. Neisseria gonorrhoeae (Ngo), the etiological agent of the sexually transmitted disease gonorrhoea, is a highly adapted obligate human-specific pathogen and has been shown to induce apoptosis in infected cells. Here we unveil the molecular mechanisms leading to apoptosis of infected cells. We show that Ngo-mediated apoptosis requires a special subset of proapoptotic proteins from the group of BH3-only proteins. BH3-only proteins act as stress sensors to translate toxic environmental signals to the initiation of apoptosis. In a siRNA-based miniscreen, we found Bim and Bmf, BH3-only proteins associated with the cytoskeleton, necessary to induce host cell apoptosis upon infection. Bim and Bmf inactivated different inhibitors of apoptosis and thereby induced cell death in response to infection. Our data unveil a novel pathway of infection-induced apoptosis that enhances our understanding of the mechanism by which BH3-only proteins control apoptotic cell death
Abstract 5128: Induction of immunogenic cell death and tumor regression in murine animal models by a novel cytolytic compound, LTX-401
No full textAbstract
LTX-401 is a de novo designed cytolytic compound that shares many chemical features with anticancer peptides, such as amphipathicity, hydrophobicity and overall net charge. In vitro cytotoxicity studies revealed that LTX-401 was highly active against a panel of malignant cells including murine and human cancer cell lines while displaying selectivity towards human red blood cells. Furthermore, LTX-401 was found to induce immunogenic cell death as demonstrated by the release of Damage-Associated Molecular Pattern molecules, or ‘danger signals’, such as High-Mobility Group Box-1 protein, ATP and cytochrome c. Flow cytometric and confocal microscopy studies also demonstrated reduced signal from lysosomal dye Lysotracker-DND-26, hence indicating loss of lysosomal integrity upon induction of cell death. The latter was supported using transmission electron microscopy, showing distinct morphological characteristics of necrosis. Moreover, at low concentrations, LTX-401 selectively enriched in the Golgi apparatus and initiated a lethal signaling event that in part could be inhibited by Brefeldin A. Complete tumor regression has been obtained in several rodent models, including the B16 mouse melanoma model and the JM1 rat hepatocellular carcinoma model by intratumoral injection with LTX-401. Additionally, previously cured animals showed protection against rechallenge with live tumor cells, indicating the induction of tumor-specific immune memory. The increased survival benefit of LTX-401-treated animals provides a rationale for further evaluation of the compound as an immunotherapeutic agent against solid malignancies.
Citation Format: Brynjar Mauseth, Liv-Marie Eike, Ji-Hua Shi, Ketil Camilio, Heng Zhou, Allan Sauvat, Lígia C Gomes-da-Silva, Sylvèr Durand, Sabrina Forveille, Kristina Iribarren, Takahiro Yamazaki, Sylvie Souquere, Lucillia Bezu, Kevin Müller, Marion Leduc, Peng Liu, Liwei Zhao, Aurélien Marabelle, Laurence Zitvogel, Oliver Kepp, Guido Kroemer, Øystein Rekdal, Pål-Dag Line, Baldur Sveinbjørnsson. Induction of immunogenic cell death and tumor regression in murine animal models by a novel cytolytic compound, LTX-401 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 5128. doi:10.1158/1538-7445.AM2017-5128</jats:p
Dithered backprop: A sparse and quantized backpropagation algorithm for more efficient deep neural network training
No full textColocalizR: An open-source application for cell-based high-throughput colocalization analysis
No full textInternational audienc
DataSheet1_Bibliometric analysis of research on immunogenic cell death in cancer.docx
No full textBackground: Immunotherapy is changing the way we treat cancer. Immunogenic cell death (ICD) has received considerable attention in the treatments of various cancer types, due to the long-lasting antitumor responses elicited in human body. However, to date, no relevant bibliometric research has been reported.Methods: Publications related to ICD in cancer research were collected from the Web of Science Core Collection. Using CiteSpace, VOSviewer and an online platform, the analyses of co-author, co-citation, and co-occurrence of terms retrieved from literatures were carried out.Results: A total of 1,577 publications were included in this study. The global research literatures on ICD in cancer research have been increasing from 2005 to 2021. China, the United States and France dominated in this area and had close collaborations with many countries. Six of the top 10 most contributive institutions were from France. When it comes to author analysis, Kroemer G, Zitvogel L, Kepp O, Garg AD and Galluzzi L were in both the top 10 most productive authors and top 10 most co-cited authors lists. The co-occurring author keywords could be grouped into three clusters: “biomarkers of ICD”, “nanoparticles” and “combination therapy”. In terms of promising hotspots, keywords (author keywords and KeyWords Plus) with recent citation bursts could be summarized into two aspects: “tumor microenvironment” and “nanoparticles”.Conclusion: Increased attention has been paid to ICD in cancer treatment. However, there are still many unresolved domains in the field of ICD, such as clinical application and molecular mechanisms of this cell death process. ICD-inducing modalities combined with nanotechnology could potentiate the current immunotherapies, and will be hotspots for future research.</p
Recursive Autonomy Continuum Model (RACM): A Unified Ethical Governance Framework for AI Cognitive Influence and Symbiotic Co-Agency Systems
No full textThe evolution of artificial intelligence has reached a profound inflection point, moving beyond the mere automation of tasks to active engagement with human internal states. AI systems increasingly transcend their origin as passive tools, becoming active cognitive agents capable of recursively monitoring, analyzing, modifying, and recalibrating human cognitive processes. This fundamental shift means AI can now influence not only external behavior but also subjective experience, preference formation, identity construction, and even meta-cognitive self-conception. This introduces unprecedented ethical stakes: the very structure of human agency, personal identity, and the sovereign right to self-authorship is now exposed to continuous, recursive, and often subtle algorithmic modulation, raising profound questions about free will and accountability in a technologically mediated world (Metzinger, 2003; Gazzaniga, 2018). This new frontier demands robust ethical infrastructures capable of preserving cognitive sovereignty across dynamic, recursive human-AI interaction landscapes. At ERI-IRFOS, our mission to ensure global universal balance (ERI-IRFOS, 2024) compels us to develop robust frameworks for this emerging reality, recognizing that the potential for both unprecedented flourishing and existential risk hinges on proactive ethical governance. While our previously developed models, Recursive Autonomy Preservation Model (RAPM) and Conscious Modulation Ethics Model (CMEM), provide crucial architecture for discrete stages of this evolution, neither alone fully captures the broader ethical continuum emerging from increasingly recursive cognitive architectures. RAPM governs one-directional AI cognitive influence systems (Kepp & Albert, 2025a), addressing scenarios where AI primarily acts upon human cognition to modify or enhance specific functions or behaviors. CMEM, conversely, governs bidirectional AI-human cognitive co-agency and symbiosis (Kepp & Albert, 2025b), where influence is mutual, agency can be dynamically shared, and conscious entities might jointly author new cognitive states. However, a significant gap persists: the absence of a unified meta-framework that governs the seamless transitions, escalating complexities, and ethical handoffs between these distinct, yet interconnected, stages. The Recursive Autonomy Continuum Model (RACM) is introduced here to synthesize RAPM and CMEM into a single, coherent ethical meta-stack, providing a comprehensive governance model for all stages of recursive autonomy modulation within entangled human-AI systems. It aims to prevent ethical inconsistencies and governance gaps as AI-human interactions evolve over time and depth
Consensus guidelines for the definition, detection and interpretation of immunogenic cell death
No full textCells succumbing to stress via regulated cell death (RCD) can initiate an adaptive immune response associated with immunological memory, provided they display sufficient antigenicity and adjuvanticity. Moreover, multiple intracellular and microenvironmental features determine the propensity of RCD to drive adaptive immunity. Here, we provide an updated operational definition of immunogenic cell death (ICD), discuss the key factors that dictate the ability of dying cells to drive an adaptive immune response, summarize experimental assays that are currently available for the assessment of ICD in vitro and in vivo, and formulate guidelines for their interpretation
Modulation of antigen-specific T-cells as immune therapy for chronic infectious diseases and cancer
No full textCopyright: © 2014 Li, Symonds, Miao, Sanderson and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.This article has been made available through the Brunel Open Access Publishing Fund.T-cell responses are induced by antigen presenting cells (APC) and signals from the microenvironment. Antigen persistence and inflammatory microenvironments in chronic infections and cancer can induce a tolerant state in T-cells resulting in hyporesponsiveness, loss of effector function, and weak biochemical signaling patterns in response to antigen stimulation. Although the mechanisms of T-cell tolerance induced in chronic infection and cancer may differ from those involved in tolerance to self-antigen, the impaired proliferation and production of IL-2 in response to antigen stimulation are hallmarks of all tolerant T cells. In this review, we will summarize the evidence that the immune responses change from non-self to “self”-like in chronic infection and cancer, and will provide an overview of strategies for re-balancing the immune response of antigen-specific T cells in chronic infection and cancer without affecting the homeostasis of the immune system.Arthritis Research UK and Medical Research Council UK
