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  1. Article ; Online: A New Deep-Learning Method for Human Activity Recognition.

    Vrskova, Roberta / Kamencay, Patrik / Hudec, Robert / Sykora, Peter

    Sensors (Basel, Switzerland)

    2023  Volume 23, Issue 5

    Abstract: Currently, three-dimensional convolutional neural networks (3DCNNs) are a popular approach in the field of human activity recognition. However, due to the variety of methods used for human activity recognition, we propose a new deep-learning model in ... ...

    Abstract Currently, three-dimensional convolutional neural networks (3DCNNs) are a popular approach in the field of human activity recognition. However, due to the variety of methods used for human activity recognition, we propose a new deep-learning model in this paper. The main objective of our work is to optimize the traditional 3DCNN and propose a new model that combines 3DCNN with Convolutional Long Short-Term Memory (ConvLSTM) layers. Our experimental results, which were obtained using the LoDVP Abnormal Activities dataset, UCF50 dataset, and MOD20 dataset, demonstrate the superiority of the 3DCNN + ConvLSTM combination for recognizing human activities. Furthermore, our proposed model is well-suited for real-time human activity recognition applications and can be further enhanced by incorporating additional sensor data. To provide a comprehensive comparison of our proposed 3DCNN + ConvLSTM architecture, we compared our experimental results on these datasets. We achieved a precision of 89.12% when using the LoDVP Abnormal Activities dataset. Meanwhile, the precision we obtained using the modified UCF50 dataset (UCF50mini) and MOD20 dataset was 83.89% and 87.76%, respectively. Overall, our work demonstrates that the combination of 3DCNN and ConvLSTM layers can improve the accuracy of human activity recognition tasks, and our proposed model shows promise for real-time applications.
    MeSH term(s) Humans ; Deep Learning ; Neural Networks, Computer ; Human Activities ; Memory, Long-Term ; Recognition, Psychology
    Language English
    Publishing date 2023-03-04
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2052857-7
    ISSN 1424-8220 ; 1424-8220
    ISSN (online) 1424-8220
    ISSN 1424-8220
    DOI 10.3390/s23052816
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: A New Approach for Abnormal Human Activities Recognition Based on ConvLSTM Architecture.

    Vrskova, Roberta / Hudec, Robert / Kamencay, Patrik / Sykora, Peter

    Sensors (Basel, Switzerland)

    2022  Volume 22, Issue 8

    Abstract: Recognizing various abnormal human activities from video is very challenging. This problem is also greatly influenced by the lack of datasets containing various abnormal human activities. The available datasets contain various human activities, but only ... ...

    Abstract Recognizing various abnormal human activities from video is very challenging. This problem is also greatly influenced by the lack of datasets containing various abnormal human activities. The available datasets contain various human activities, but only a few of them contain non-standard human behavior such as theft, harassment, etc. There are datasets such as KTH that focus on abnormal activities such as sudden behavioral changes, as well as on various changes in interpersonal interactions. The UCF-crime dataset contains categories such as fighting, abuse, explosions, robberies, etc. However, this dataset is very time consuming. The events in the videos occur in a few seconds. This may affect the overall results of the neural networks that are used to detect the incident. In this article, we create a dataset that deals with abnormal activities, containing categories such as Begging, Drunkenness, Fight, Harassment, Hijack, Knife Hazard, Normal Videos, Pollution, Property Damage, Robbery, and Terrorism. We use the created dataset for the training and testing of the ConvLSTM (convolutional long short-term memory) neural network, which we designed. However, we also test the created dataset using other architectures. We use ConvLSTM architectures and 3D Resnet50, 3D Resnet101, and 3D Resnet152. With the created dataset and the architecture we designed, we obtained an accuracy of classification of 96.19% and a precision of 96.50%.
    MeSH term(s) Human Activities ; Humans ; Memory, Long-Term ; Neural Networks, Computer ; Recognition, Psychology
    Language English
    Publishing date 2022-04-12
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2052857-7
    ISSN 1424-8220 ; 1424-8220
    ISSN (online) 1424-8220
    ISSN 1424-8220
    DOI 10.3390/s22082946
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The Council of Europe should not reaffirm the ban on germline genome editing in humans.

    Sykora, Peter / Caplan, Arthur

    EMBO reports

    2017  Volume 18, Issue 11, Page(s) 1871–1872

    MeSH term(s) CRISPR-Cas Systems ; Clustered Regularly Interspaced Short Palindromic Repeats ; Europe ; Gene Editing ; Germ Cells ; Humans
    Language English
    Publishing date 2017-10-06
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.15252/embr.201745246
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Germline gene therapy is compatible with human dignity.

    Sykora, Peter / Caplan, Arthur

    EMBO reports

    2017  Volume 18, Issue 12, Page(s) 2086

    MeSH term(s) Genetic Therapy ; Human Rights ; Humans ; Personhood
    Language English
    Publishing date 2017-11-15
    Publishing country England
    Document type Letter ; Comment
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.15252/embr.201745378
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Skin Immuno-CometChip in 3D vs. 2D Cultures to Screen Topical Toxins and Skin-Specific Cytochrome Inducers

    Rosenthal, Dean S. / Kuo, Li-Wei / Seagrave, Sarah L. / Soni, Vikas / Islam, Nusrat / Minsky, Geetanjali / Dussan-Cuellar, Lucia / Ell, Brian / Simbulan-Rosenthal, Cynthia M. / Sykora, Peter

    Genes (Basel). 2023 Mar. 02, v. 14, no. 3

    2023  

    Abstract: The targets of topical genotoxic agents are basal and stem cells of the skin. These cells may misrepair DNA lesions, resulting in deleterious mutations of tumor suppressors or oncogenes. However, the genotoxicity of many compounds has not as yet been ... ...

    Abstract The targets of topical genotoxic agents are basal and stem cells of the skin. These cells may misrepair DNA lesions, resulting in deleterious mutations of tumor suppressors or oncogenes. However, the genotoxicity of many compounds has not as yet been determined and needs to be tested using a relevant skin model. To this end, we designed a new high-throughput assay for the detection of agents that create DNA damage in epidermal stem and basal cells and used it to test known DNA-damaging agents. We utilized either 2D epidermal cells or 3D skin equivalents and topically exposed them to different compounds. The Skin Immuno-CometChip assay uses arrays of microwells formed in a collagen/agarose mixture to capture single basal cells in each microwell by virtue of collagen binding to α2β1 integrin, which is present only on basal and stem cells. The presence of β1 integrin was verified by immunofluorescent labeling cells that were then subjected to an electrical field, allowing for the migration of nicked DNA out of the nucleoid in alkali, with the resulting DNA comets stained and imaged. Furthermore, using improved comet detection software allowed for the automated and rapid quantification of DNA damage. Our study indicates that we can accurately predict genotoxicity by using 3D skin cultures, as well as keratinocytes grown in 2D monolayers.
    Keywords DNA ; DNA damage ; agarose ; automation ; collagen ; computer software ; electric field ; genotoxicity ; integrins ; keratinocytes ; models ; mutagens ; neoplasms ; oncogenes
    Language English
    Dates of publication 2023-0302
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article ; Online
    ZDB-ID 2527218-4
    ISSN 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes14030630
    Database NAL-Catalogue (AGRICOLA)

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  6. Article: TRIP12 governs DNA Polymerase β involvement in DNA damage response and repair.

    Inanc, Burcu / Fang, Qingming / Andrews, Joel F / Zeng, Xuemei / Clark, Jennifer / Li, Jianfeng / Dey, Nupur B / Ibrahim, Md / Sykora, Peter / Yu, Zhongxun / Braganza, Andrea / Verheij, Marcel / Jonkers, Jos / Yates, Nathan A / Vens, Conchita / Sobol, Robert W

    bioRxiv : the preprint server for biology

    2024  

    Abstract: The multitude of DNA lesion types, and the nuclear dynamic context in which they occur, present a challenge for genome integrity maintenance as this requires the engagement of different DNA repair pathways. Specific 'repair controllers' that facilitate ... ...

    Abstract The multitude of DNA lesion types, and the nuclear dynamic context in which they occur, present a challenge for genome integrity maintenance as this requires the engagement of different DNA repair pathways. Specific 'repair controllers' that facilitate DNA repair pathway crosstalk between double strand break (DSB) repair and base excision repair (BER), and regulate BER protein trafficking at lesion sites, have yet to be identified. We find that DNA polymerase β (Polβ), crucial for BER, is ubiquitylated in a BER complex-dependent manner by TRIP12, an E3 ligase that partners with UBR5 and restrains DSB repair signaling. Here we find that, TRIP12, but not UBR5, controls cellular levels and chromatin loading of Polβ. Required for Polβ foci formation, TRIP12 regulates Polβ involvement after DNA damage. Notably, excessive TRIP12-mediated shuttling of Polβ affects DSB formation and radiation sensitivity, underscoring its precedence for BER. We conclude that the herein discovered trafficking function at the nexus of DNA repair signaling pathways, towards Polβ-directed BER, optimizes DNA repair pathway choice at complex lesion sites.
    Language English
    Publishing date 2024-04-10
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.04.08.588474
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Skin Immuno-CometChip in 3D vs. 2D Cultures to Screen Topical Toxins and Skin-Specific Cytochrome Inducers.

    Rosenthal, Dean S / Kuo, Li-Wei / Seagrave, Sarah L / Soni, Vikas / Islam, Nusrat / Minsky, Geetanjali / Dussan-Cuellar, Lucia / Ell, Brian / Simbulan-Rosenthal, Cynthia M / Sykora, Peter

    Genes

    2023  Volume 14, Issue 3

    Abstract: The targets of topical genotoxic agents are basal and stem cells of the skin. These cells may misrepair DNA lesions, resulting in deleterious mutations of tumor suppressors or oncogenes. However, the genotoxicity of many compounds has not as yet been ... ...

    Abstract The targets of topical genotoxic agents are basal and stem cells of the skin. These cells may misrepair DNA lesions, resulting in deleterious mutations of tumor suppressors or oncogenes. However, the genotoxicity of many compounds has not as yet been determined and needs to be tested using a relevant skin model. To this end, we designed a new high-throughput assay for the detection of agents that create DNA damage in epidermal stem and basal cells and used it to test known DNA-damaging agents. We utilized either 2D epidermal cells or 3D skin equivalents and topically exposed them to different compounds. The Skin Immuno-CometChip assay uses arrays of microwells formed in a collagen/agarose mixture to capture single basal cells in each microwell by virtue of collagen binding to α2β1 integrin, which is present only on basal and stem cells. The presence of β1 integrin was verified by immunofluorescent labeling cells that were then subjected to an electrical field, allowing for the migration of nicked DNA out of the nucleoid in alkali, with the resulting DNA comets stained and imaged. Furthermore, using improved comet detection software allowed for the automated and rapid quantification of DNA damage. Our study indicates that we can accurately predict genotoxicity by using 3D skin cultures, as well as keratinocytes grown in 2D monolayers.
    MeSH term(s) Skin/metabolism ; Epidermis ; Keratinocytes ; Cytochromes/metabolism ; DNA/metabolism
    Chemical Substances Cytochromes ; DNA (9007-49-2)
    Language English
    Publishing date 2023-03-02
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2527218-4
    ISSN 2073-4425 ; 2073-4425
    ISSN (online) 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes14030630
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Slow mitochondrial repair of 5'-AMP renders mtDNA susceptible to damage in APTX deficient cells.

    Akbari, Mansour / Sykora, Peter / Bohr, Vilhelm A

    Scientific reports

    2015  Volume 5, Page(s) 12876

    Abstract: Aborted DNA ligation events in eukaryotic cells can generate 5'-adenylated (5'-AMP) DNA termini that can be removed from DNA by aprataxin (APTX). Mutations in APTX cause an inherited human disease syndrome characterized by early-onset progressive ataxia ... ...

    Abstract Aborted DNA ligation events in eukaryotic cells can generate 5'-adenylated (5'-AMP) DNA termini that can be removed from DNA by aprataxin (APTX). Mutations in APTX cause an inherited human disease syndrome characterized by early-onset progressive ataxia with ocular motor apraxia (AOA1). APTX is found in the nuclei and mitochondria of eukaryotic cells. Depletion of APTX causes mitochondrial dysfunction and renders the mitochondrial genome, but not the nuclear genome susceptible to damage. The biochemical processes that link APTX deficiency to mitochondrial dysfunction have not been well elucidated. Here, we monitored the repair of 5'-AMP DNA damage in nuclear and mitochondrial extracts from human APTX(+/+) and APTX(-/-) cells. The efficiency of repair of 5'-AMP DNA was much lower in mitochondrial than in nuclear protein extracts, and resulted in persistent DNA repair intermediates in APTX deficient cells. Moreover, the removal of 5'-AMP from DNA was significantly slower in the mitochondrial extracts from human cell lines and mouse tissues compared with their corresponding nuclear extracts. These results suggest that, contrary to nuclear DNA repair, mitochondrial DNA repair is not able to compensate for APTX deficiency resulting in the accumulation of mitochondrial DNA damage.
    MeSH term(s) Adenosine Monophosphate/metabolism ; Animals ; Brain/metabolism ; Cell Line ; DNA Damage ; DNA Repair ; DNA, Mitochondrial/genetics ; DNA, Mitochondrial/metabolism ; Databases, Factual ; Depsipeptides/deficiency ; Depsipeptides/genetics ; Humans ; Liver/metabolism ; Mice ; Mitochondria/genetics ; Mitochondria/metabolism
    Chemical Substances DNA, Mitochondrial ; Depsipeptides ; apratoxin A ; Adenosine Monophosphate (415SHH325A)
    Language English
    Publishing date 2015-08-10
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep12876
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Employing CRISPR-Cas9 to Generate CD133 Synthetic Lethal Melanoma Stem Cells.

    Simbulan-Rosenthal, Cynthia M / Haribabu, Yogameenakshi / Vakili, Sahar / Kuo, Li-Wei / Clark, Havens / Dougherty, Ryan / Alobaidi, Ryyan / Carney, Bonnie / Sykora, Peter / Rosenthal, Dean S

    International journal of molecular sciences

    2022  Volume 23, Issue 4

    Abstract: Malignant melanoma is a lethal skin cancer containing melanoma-initiating cells (MIC) implicated in tumorigenesis, invasion, and drug resistance, and is characterized by the elevated expression of stem cell markers, including CD133. The siRNA knockdown ... ...

    Abstract Malignant melanoma is a lethal skin cancer containing melanoma-initiating cells (MIC) implicated in tumorigenesis, invasion, and drug resistance, and is characterized by the elevated expression of stem cell markers, including CD133. The siRNA knockdown of CD133 enhances apoptosis induced by the MEK inhibitor trametinib in melanoma cells. This study investigates the underlying mechanisms of CD133's anti-apoptotic activity in patient-derived BAKP and POT cells, harboring difficult-to-treat NRAS
    MeSH term(s) Apoptosis/genetics ; CRISPR-Cas Systems/genetics ; Caspases/metabolism ; Cell Line, Tumor ; Humans ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/pathology ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; RNA, Small Interfering/pharmacology ; Skin Neoplasms ; Stem Cells/metabolism ; bcl-2-Associated X Protein/metabolism ; Melanoma, Cutaneous Malignant
    Chemical Substances Poly(ADP-ribose) Polymerase Inhibitors ; Proto-Oncogene Proteins c-bcl-2 ; RNA, Small Interfering ; bcl-2-Associated X Protein ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Caspases (EC 3.4.22.-)
    Language English
    Publishing date 2022-02-20
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23042333
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: The impact of base excision DNA repair in age-related neurodegenerative diseases.

    Leandro, Giovana S / Sykora, Peter / Bohr, Vilhelm A

    Mutation research

    2015  Volume 776, Page(s) 31–39

    Abstract: The aging process and several age-related neurodegenerative disorders have been linked to elevated levels of DNA damage induced by ROS and deficiency in DNA repair mechanisms. DNA damage induced by ROS is a byproduct of cellular respiration and ... ...

    Abstract The aging process and several age-related neurodegenerative disorders have been linked to elevated levels of DNA damage induced by ROS and deficiency in DNA repair mechanisms. DNA damage induced by ROS is a byproduct of cellular respiration and accumulation of damage over time, is a fundamental aspect of a main theory of aging. Mitochondria have a pivotal role in generating cellular oxidative stress, and mitochondrial dysfunction has been associated with several diseases. DNA base excision repair is considered the major pathway for repair of oxidized bases in DNA both in the nuclei and in mitochondria, and in neurons this mechanism is particularly important because non-diving cells have limited back-up DNA repair mechanisms. An association between elevated oxidative stress and a decrease in BER is strongly related to the aging process and has special relevance in age-related neurodegenerative diseases. Here, we review the role of DNA repair in aging, focusing on the implications of the DNA base excision repair pathways and how alterations in expression of these DNA repair proteins are related to the aging process and to age-related neurodegenerative diseases.
    MeSH term(s) Aging/genetics ; Aging/metabolism ; Aging/pathology ; Animals ; DNA Repair ; DNA, Mitochondrial/genetics ; DNA, Mitochondrial/metabolism ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondria/pathology ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Oxidative Stress ; Reactive Oxygen Species/metabolism
    Chemical Substances DNA, Mitochondrial ; Reactive Oxygen Species
    Language English
    Publishing date 2015-01-04
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 206607-5
    ISSN 1873-135X ; 1383-5718 ; 0027-5107 ; 0165-1110 ; 0165-1161 ; 0165-7992 ; 0921-8777 ; 0165-1218 ; 1383-5726 ; 0167-8817 ; 0921-8734 ; 1383-5742
    ISSN (online) 1873-135X
    ISSN 1383-5718 ; 0027-5107 ; 0165-1110 ; 0165-1161 ; 0165-7992 ; 0921-8777 ; 0165-1218 ; 1383-5726 ; 0167-8817 ; 0921-8734 ; 1383-5742
    DOI 10.1016/j.mrfmmm.2014.12.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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