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  1. AU=Tee Jie Kai
  2. AU=Bongaerts Dion AU=Bongaerts Dion
  3. AU=Assari Shervin
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  6. AU=Khosravi Fatemeh
  7. AU="Sandramara Sasso"
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  9. AU="Kristie Bloom"
  10. AU="Oliveira, Cláudia Regina G C M de"
  11. AU="Giuseppe Di Capua"
  12. AU=Leng Shuguang
  13. AU="Ahmed Y. Abdelbadee"
  14. AU=Berthold F
  15. AU="Virginia M.Y. Lee"
  16. AU="López-Lago, Ana M"
  17. AU="Barkley, Russell A"
  18. AU="Gahwai, Dharmendra"
  19. AU="Nardelli, S."
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  1. Artikel ; Online: An Evaluation of the In Vitro Roles and Mechanisms of Silibinin in Reducing Pyrazinamide- and Isoniazid-Induced Hepatocellular Damage.

    Goh, Zhang-He / Tee, Jie Kai / Ho, Han Kiat

    International journal of molecular sciences

    2020  Band 21, Heft 10

    Abstract: Tuberculosis remains a significant infectious lung disease that affects millions of patients worldwide. Despite numerous existing drug regimens for tuberculosis, drug-induced liver injury is a major challenge that limits the effectiveness of these ... ...

    Abstract Tuberculosis remains a significant infectious lung disease that affects millions of patients worldwide. Despite numerous existing drug regimens for tuberculosis, drug-induced liver injury is a major challenge that limits the effectiveness of these therapeutics. Two drugs that form the backbone of the commonly administered quadruple antitubercular regimen, that is, pyrazinamide (PZA) and isoniazid (INH), are associated with such hepatotoxicity. Yet, we lack safe and effective alternatives to the antitubercular regimen. Consequently, current research largely focuses on exploiting the hepatoprotective effect of nutraceutical compounds as complementary therapy. Silibinin, a herbal product widely believed to protect against various liver diseases, potentially provides a useful solution given its hepatoprotective mechanisms. In our study, we identified silibinin's role in mitigating PZA- and INH-induced hepatotoxicity and elucidated a deeper mechanistic understanding of silibinin's hepatoprotective ability. Silibinin preserved the viability of human foetal hepatocyte line LO2 when co-administered with 80 mM INH and decreased apoptosis induced by a combination of 40 mM INH and 10 mM PZA by reducing oxidative damage to mitochondria, proteins, and lipids. Taken together, this proof-of-concept forms the rational basis for the further investigation of silibinin's hepatoprotective effect in subsequent preclinical studies and clinical trials.
    Mesh-Begriff(e) Antitubercular Agents/toxicity ; Apoptosis ; Cell Line ; Chemical and Drug Induced Liver Injury/etiology ; Chemical and Drug Induced Liver Injury/prevention & control ; Hepatocytes/drug effects ; Hepatocytes/metabolism ; Humans ; Isoniazid/toxicity ; Oxidative Stress ; Protective Agents/pharmacology ; Protein Carbonylation ; Pyrazinamide/toxicity ; Silybin/pharmacology
    Chemische Substanzen Antitubercular Agents ; Protective Agents ; Pyrazinamide (2KNI5N06TI) ; Silybin (4RKY41TBTF) ; Isoniazid (V83O1VOZ8L)
    Sprache Englisch
    Erscheinungsdatum 2020-05-25
    Erscheinungsland Switzerland
    Dokumenttyp 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/ijms21103714
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  2. Artikel ; Online: An Evaluation of the In Vitro Roles and Mechanisms of Silibinin in Reducing Pyrazinamide- and Isoniazid-Induced Hepatocellular Damage

    Zhang-He Goh / Jie Kai Tee / Han Kiat Ho

    International Journal of Molecular Sciences, Vol 21, Iss 3714, p

    2020  Band 3714

    Abstract: Tuberculosis remains a significant infectious lung disease that affects millions of patients worldwide. Despite numerous existing drug regimens for tuberculosis, drug-induced liver injury is a major challenge that limits the effectiveness of these ... ...

    Abstract Tuberculosis remains a significant infectious lung disease that affects millions of patients worldwide. Despite numerous existing drug regimens for tuberculosis, drug-induced liver injury is a major challenge that limits the effectiveness of these therapeutics. Two drugs that form the backbone of the commonly administered quadruple antitubercular regimen, that is, pyrazinamide (PZA) and isoniazid (INH), are associated with such hepatotoxicity. Yet, we lack safe and effective alternatives to the antitubercular regimen. Consequently, current research largely focuses on exploiting the hepatoprotective effect of nutraceutical compounds as complementary therapy. Silibinin, a herbal product widely believed to protect against various liver diseases, potentially provides a useful solution given its hepatoprotective mechanisms. In our study, we identified silibinin’s role in mitigating PZA- and INH-induced hepatotoxicity and elucidated a deeper mechanistic understanding of silibinin’s hepatoprotective ability. Silibinin preserved the viability of human foetal hepatocyte line LO2 when co-administered with 80 mM INH and decreased apoptosis induced by a combination of 40 mM INH and 10 mM PZA by reducing oxidative damage to mitochondria, proteins, and lipids. Taken together, this proof-of-concept forms the rational basis for the further investigation of silibinin’s hepatoprotective effect in subsequent preclinical studies and clinical trials.
    Schlagwörter drug-induced liver injury (DILI) ; silibinin ; oxidative stress ; tuberculosis ; pyrazinamide ; isoniazid ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2020-05-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Engineering tumoral vascular leakiness with gold nanoparticles.

    Setyawati, Magdiel Inggrid / Wang, Qin / Ni, Nengyi / Tee, Jie Kai / Ariga, Katsuhiko / Ke, Pu Chun / Ho, Han Kiat / Wang, Yucai / Leong, David Tai

    Nature communications

    2023  Band 14, Heft 1, Seite(n) 4269

    Abstract: Delivering cancer therapeutics to tumors necessitates their escape from the surrounding blood vessels. Tumor vasculatures are not always sufficiently leaky. Herein, we engineer therapeutically competent leakage of therapeutics from tumor vasculature with ...

    Abstract Delivering cancer therapeutics to tumors necessitates their escape from the surrounding blood vessels. Tumor vasculatures are not always sufficiently leaky. Herein, we engineer therapeutically competent leakage of therapeutics from tumor vasculature with gold nanoparticles capable of inducing endothelial leakiness (NanoEL). These NanoEL gold nanoparticles activated the loss of endothelial adherens junctions without any perceivable toxicity to the endothelial cells. Microscopically, through real time live animal intravital imaging, we show that NanoEL particles induced leakiness in the tumor vessels walls and improved infiltration into the interstitial space within the tumor. In both primary tumor and secondary micrometastases animal models, we show that pretreatment of tumor vasculature with NanoEL particles before therapeutics administration could completely regress the cancer. Engineering tumoral vasculature leakiness represents a new paradigm in our approach towards increasing tumoral accessibility of anti-cancer therapeutics instead of further increasing their anti-cancer lethality.
    Mesh-Begriff(e) Animals ; Endothelial Cells/pathology ; Gold ; Metal Nanoparticles/therapeutic use ; Nanoparticles ; Endothelium/pathology ; Neoplasms/pathology ; Neoplasms, Vascular Tissue
    Chemische Substanzen Gold (7440-57-5)
    Sprache Englisch
    Erscheinungsdatum 2023-07-17
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-40015-4
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Effects of inorganic nanoparticles on liver fibrosis: Optimizing a double-edged sword for therapeutics.

    Tee, Jie Kai / Peng, Fei / Ho, Han Kiat

    Biochemical pharmacology

    2018  Band 160, Seite(n) 24–33

    Abstract: Liver fibrosis is a condition of sustained wound healing in response to chronic liver injury caused by various factors such as viral, cholestatic and inflammatory diseases. Despite significant advances in the understanding of the mechanistic details of ... ...

    Abstract Liver fibrosis is a condition of sustained wound healing in response to chronic liver injury caused by various factors such as viral, cholestatic and inflammatory diseases. Despite significant advances in the understanding of the mechanistic details of fibrosis, therapeutic intervention with the use of anti-fibrotic drugs achieved only marginal efficacy. Among which, pharmacokinetics profile of agents leading to off-targeting and suboptimal distribution are the principal limiting factors. Concurrently, inorganic nanoparticles (NPs) have gained significant recognition in biomedicine, owning to their unique physicochemical properties. Since NPs are known to accumulate in well vascularised organs, the intuitive therapeutic targeting of the liver using engineered NPs seems to be a plausible approach in treating liver fibrosis. However, the application of inorganic NPs also raised concerns of its potential long-term impact to humans. Current literatures have reported both negative risks as well as surprising benefits, thus sparking off a needful discussion about the feasibility of using inorganic NPs in treating liver fibrosis. Inorganic NPs entrapped in the liver may pose health risks, particularly due to their non-biodegradability and potential toxicity when accumulated in undesirable concentrations. This highlighted the need to assess the health risk of using inorganic NPs, and also to establish a framework to evaluate the conditions when the beneficial effects of these NPs would outweigh potential risks. Hence, this review takes a balanced approach on assessing the mechanistic details behind inorganic NP-induced biochemical perturbations, which could either alleviate or worsen liver fibrosis. Consequently, it attempts to chart out possibilities for future directions through optimizing therapeutic outcomes by design.
    Mesh-Begriff(e) Animals ; Drug Carriers/adverse effects ; Drug Carriers/pharmacokinetics ; Drug Delivery Systems/adverse effects ; Drug Delivery Systems/methods ; Humans ; Liver/drug effects ; Liver Cirrhosis/drug therapy ; Nanoparticles/adverse effects ; Nanoparticles/therapeutic use ; Tissue Distribution
    Chemische Substanzen Drug Carriers
    Sprache Englisch
    Erscheinungsdatum 2018-12-06
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/j.bcp.2018.12.003
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Angiopoietin-1 accelerates restoration of endothelial cell barrier integrity from nanoparticle-induced leakiness.

    Tee, Jie Kai / Setyawati, Magdiel Inggrid / Peng, Fei / Leong, David Tai / Ho, Han Kiat

    Nanotoxicology

    2019  Band 13, Heft 5, Seite(n) 682–700

    Abstract: Nanoparticles (NPs) have been widely used in biomedical field for therapeutic treatments, drug carriers, and bio-imaging agent. Recent studies have highlighted the possibility of utilizing inorganic NPs in inducing endothelial leakiness through ... ...

    Abstract Nanoparticles (NPs) have been widely used in biomedical field for therapeutic treatments, drug carriers, and bio-imaging agent. Recent studies have highlighted the possibility of utilizing inorganic NPs in inducing endothelial leakiness through endothelial remodeling to promote drug transport across the barrier. However, an uncontrolled and persistent leakiness could lead to promiscuous transport of molecules and cells across the barrier, highlighting the pressing need to control the timely recovery from endothelial cell leakiness. Herein, we show that angiopoietin-1 (Ang1) could promote recovery of human microvascular endothelial cells (HMVECs) from titanium dioxide nanoparticle (TiO
    Mesh-Begriff(e) Angiopoietin-1/genetics ; Angiopoietin-1/metabolism ; Animals ; Capillary Permeability/drug effects ; Cell Culture Techniques ; Cell Line, Tumor ; Cell Movement/drug effects ; Cells, Cultured ; Endothelial Cells/drug effects ; Humans ; Microvessels/cytology ; Microvessels/drug effects ; Nanoparticles/toxicity ; Receptor, TIE-2/metabolism ; Titanium/toxicity
    Chemische Substanzen ANGPT1 protein, human ; Angiopoietin-1 ; titanium dioxide (15FIX9V2JP) ; Titanium (D1JT611TNE) ; Receptor, TIE-2 (EC 2.7.10.1)
    Sprache Englisch
    Erscheinungsdatum 2019-02-19
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2237988-5
    ISSN 1743-5404 ; 1743-5390
    ISSN (online) 1743-5404
    ISSN 1743-5390
    DOI 10.1080/17435390.2019.1571646
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel: Magnesium Isoglycyrrhizinate Ameliorates Fibrosis and Disrupts TGF-β-Mediated SMAD Pathway in Activated Hepatic Stellate Cell Line LX2.

    Tee, Jie Kai / Peng, Fei / Tan, Yeong Lan / Yu, Bo / Ho, Han Kiat

    Frontiers in pharmacology

    2018  Band 9, Seite(n) 1018

    Abstract: Liver fibrosis is a histological change often attributed to the activation of hepatic stellate cells (HSCs) and the excessive formation of scar tissues in the liver. Advanced stages of the disease frequently lead to cirrhosis. Magnesium ... ...

    Abstract Liver fibrosis is a histological change often attributed to the activation of hepatic stellate cells (HSCs) and the excessive formation of scar tissues in the liver. Advanced stages of the disease frequently lead to cirrhosis. Magnesium isoglycyrrhizinate (MgIG) has been accepted as a hepatoprotective drug with the potential of alleviating inflammatory conditions and thus promote liver recovery from viral- or drug-induced injury. While MgIG has been empirically integrated into the clinics to treat some liver diseases, its anti-fibrotic effect and the associated mechanisms remain poorly characterized. Herein, we demonstrated that 1 mg/ml MgIG attenuated the production of αSMA and collagen-1 in activated HSCs using TGF-β1-induced human HSCs LX2 as the fibrotic cell model. We found that MgIG exerts an inhibitory effect on the TGF-β-SMAD signaling pathway by arresting the binding of downstream transcription factors SMAD2/3 and SMAD4. Furthermore, MgIG was shown to suppress proliferation and induce senescence of activated LX2 cells. Protein expression of p27 and enzymatic activity of senescence-associated β-galactosidase were elevated upon exposure to MgIG. In addition, we observed that exposure of activated LX2 cells to MgIG reduces TGF-β-induced apoptosis. Interestingly, a lower toxicity profile was observed when human fetal hepatocytes LO2 were exposed to the same concentration and duration of the drug, suggesting the specificity of MgIG effect toward activated HSCs. Overall, hepatoprotective concentrations of MgIG is shown to exert a direct effect on liver fibrosis through inhibiting TGF-β-signaling, in which SMAD2/3 pathway could be one of the mechanisms responsible for the fibrotic response, thereby restoring the surviving cells toward a more quiescent phenotype. This provides critical mechanistic insights to support an otherwise empirical therapy.
    Sprache Englisch
    Erscheinungsdatum 2018-09-25
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2018.01018
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Titanium Dioxide Nanoparticles Enhance Leakiness and Drug Permeability in Primary Human Hepatic Sinusoidal Endothelial Cells.

    Tee, Jie Kai / Ng, Li Yang / Koh, Hannah Yun / Leong, David Tai / Ho, Han Kiat

    International journal of molecular sciences

    2018  Band 20, Heft 1

    Abstract: Liver sinusoidal endothelial cells (LSECs) represent the permeable interface that segregates the blood compartment from the hepatic cells, regulating hepatic vascular tone and portal pressure amidst changes in the blood flow. In the presence of ... ...

    Abstract Liver sinusoidal endothelial cells (LSECs) represent the permeable interface that segregates the blood compartment from the hepatic cells, regulating hepatic vascular tone and portal pressure amidst changes in the blood flow. In the presence of pathological conditions, phenotypic changes in LSECs contribute to the progression of chronic liver diseases, including the loss of endothelial permeability. Therefore, modulating LSECs offers a possible way to restore sinusoidal permeability and thereby improve hepatic recovery. Herein, we showed that titanium dioxide nanoparticles (TiO₂ NPs) could induce transient leakiness in primary human hepatic sinusoidal endothelial cells (HHSECs). Interestingly, HHSECs exposed to these NPs exhibited reduced protein kinase B (Akt) phosphorylation, an important protein kinase which regulates cell attachment. Using a 3D co-culture system, we demonstrated that TiO₂ NPs diminished the attachment of HHSECs onto normal human hepatic cell LO2. To further illustrate the significance of leakiness in liver sinusoids, we showed that NP-induced leakiness promoted Sunitinib transport across the HHSEC layer, resulting in increased drug uptake and efficacy. Hence, TiO₂ NPs have the potential to modulate endothelial permeability within the specialized sinusoidal endothelium, especially during events of fibrosis and occlusion. This study highlighted the possible use of inorganic NPs as a novel strategy to promote drug delivery targeting the diseased liver.
    Mesh-Begriff(e) Cell Communication ; Cell Survival/drug effects ; Cells, Cultured ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Hepatocytes/drug effects ; Hepatocytes/metabolism ; Humans ; Liver/cytology ; Liver/drug effects ; Liver/pathology ; Nanoparticles/chemistry ; Oxidative Stress/drug effects ; Permeability ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/drug effects ; Titanium/chemistry ; Titanium/pharmacology
    Chemische Substanzen titanium dioxide (15FIX9V2JP) ; Titanium (D1JT611TNE) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2018-12-21
    Erscheinungsland Switzerland
    Dokumenttyp 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/ijms20010035
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Nanoparticles promote in vivo breast cancer cell intravasation and extravasation by inducing endothelial leakiness.

    Peng, Fei / Setyawati, Magdiel Inggrid / Tee, Jie Kai / Ding, Xianguang / Wang, Jinping / Nga, Min En / Ho, Han Kiat / Leong, David Tai

    Nature nanotechnology

    2019  Band 14, Heft 3, Seite(n) 279–286

    Abstract: While most cancer nanomedicine is designed to eliminate cancer, the nanomaterial per se can lead to the formation of micrometre-sized gaps in the blood vessel endothelial walls. Nanomaterials-induced endothelial leakiness (NanoEL) might favour ... ...

    Abstract While most cancer nanomedicine is designed to eliminate cancer, the nanomaterial per se can lead to the formation of micrometre-sized gaps in the blood vessel endothelial walls. Nanomaterials-induced endothelial leakiness (NanoEL) might favour intravasation of surviving cancer cells into the surrounding vasculature and subsequently extravasation, accelerating metastasis. Here, we show that nanoparticles induce endothelial leakiness through disruption of the VE-cadherin-VE-cadherin homophilic interactions at the adherens junction. We show that intravenously injected titanium dioxide, silica and gold nanoparticles significantly accelerate both intravasation and extravasation of breast cancer cells in animal models, increasing the extent of existing metastasis and promoting the appearance of new metastatic sites. Our results add to the understanding of the behaviour of nanoparticles in complex biological systems. The potential for NanoEL needs to be taken into consideration when designing future nanomedicines, especially nanomedicine to treat cancer.
    Mesh-Begriff(e) Animals ; Blood Vessels/pathology ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Endothelial Cells/pathology ; Extravasation of Diagnostic and Therapeutic Materials/pathology ; Female ; Humans ; Metal Nanoparticles/chemistry ; Mice ; Neoplasm Metastasis ; Neoplastic Cells, Circulating/pathology ; Permeability ; Titanium/chemistry
    Chemische Substanzen titanium dioxide (15FIX9V2JP) ; Titanium (D1JT611TNE)
    Sprache Englisch
    Erscheinungsdatum 2019-01-28
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2254964-X
    ISSN 1748-3395 ; 1748-3387
    ISSN (online) 1748-3395
    ISSN 1748-3387
    DOI 10.1038/s41565-018-0356-z
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Nanoparticles' interactions with vasculature in diseases.

    Tee, Jie Kai / Yip, Li Xian / Tan, Eveline Sheau / Santitewagun, Supawan / Prasath, Arun / Ke, Pu Chun / Ho, Han Kiat / Leong, David Tai

    Chemical Society reviews

    2019  Band 48, Heft 21, Seite(n) 5381–5407

    Abstract: The ever-growing use of inorganic nanoparticles (NPs) in biomedicine provides an exciting approach to develop novel imaging and drug delivery systems, owing to the ease with which these NPs can be functionalized to cater to various applications. In ... ...

    Abstract The ever-growing use of inorganic nanoparticles (NPs) in biomedicine provides an exciting approach to develop novel imaging and drug delivery systems, owing to the ease with which these NPs can be functionalized to cater to various applications. In cancer therapeutics, nanomedicine generally relies on the enhanced permeability and retention (EPR) effect observed in tumour vasculature to deliver anti-cancer drugs across the endothelium. However, such a phenomenon is dependent on the tumour microenvironment and is not consistently observed in all tumour types, thereby limiting drug transport to the tumour site. On the other hand, there is a rise in utilizing inorganic NPs to intentionally induce endothelial leakiness, creating a window of opportunity to control drug delivery across the endothelium. While this active targeting approach creates a similar phenomenon compared to the EPR effect arising from tumour tissues, its drug delivery applications extend beyond cancer therapeutics and into other vascular-related diseases. In this review, we summarize the current findings of the EPR effect and assess its limitations in the context of anti-cancer drug delivery systems. While the EPR effect offers a possible route for drug passage, we further explore alternative uses of NPs to create controllable endothelial leakiness within short exposures, a phenomenon we coined as nanomaterial-induced endothelial leakiness (NanoEL). Furthermore, we discuss the main mechanistic features of the NanoEL effect that make it unique from conventionally established endothelial leakiness in homeostatic and pathologic conditions, as well as examine its potential applicability in vascular-related diseases, particularly cancer. Therefore, this new paradigm changes the way inorganic NPs are currently being used for biomedical applications.
    Mesh-Begriff(e) Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Cell Proliferation/drug effects ; Drug Delivery Systems ; Humans ; Nanomedicine ; Nanoparticles/chemistry ; Neoplasms/blood supply ; Neoplasms/drug therapy ; Neoplasms/pathology ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/pathology
    Chemische Substanzen Antineoplastic Agents
    Sprache Englisch
    Erscheinungsdatum 2019-09-05
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review
    ZDB-ID 1472875-8
    ISSN 1460-4744 ; 0306-0012
    ISSN (online) 1460-4744
    ISSN 0306-0012
    DOI 10.1039/c9cs00309f
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: Inorganic Nanomaterials as Highly Efficient Inhibitors of Cellular Hepatic Fibrosis.

    Peng, Fei / Tee, Jie Kai / Setyawati, Magdiel Inggrid / Ding, Xianguang / Yeo, Hui Ling Angie / Tan, Yeong Lan / Leong, David Tai / Ho, Han Kiat

    ACS applied materials & interfaces

    2018  Band 10, Heft 38, Seite(n) 31938–31946

    Abstract: Chronic liver dysfunction usually begins with hepatic fibrosis. To date, no effective anti-fibrotic drugs have been approved for clinical use in humans. In the current work, titanium dioxide ( ... ...

    Abstract Chronic liver dysfunction usually begins with hepatic fibrosis. To date, no effective anti-fibrotic drugs have been approved for clinical use in humans. In the current work, titanium dioxide (TiO
    Mesh-Begriff(e) Actins/genetics ; Cell Line ; Collagen/genetics ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression/drug effects ; Hepatic Stellate Cells/drug effects ; Humans ; Liver Cirrhosis/drug therapy ; Nanostructures/chemistry ; Silicon Dioxide/chemistry ; Silicon Dioxide/pharmacology ; Titanium/chemistry ; Titanium/pharmacology
    Chemische Substanzen Actins ; titanium dioxide (15FIX9V2JP) ; Silicon Dioxide (7631-86-9) ; Collagen (9007-34-5) ; Titanium (D1JT611TNE)
    Sprache Englisch
    Erscheinungsdatum 2018-09-11
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 1944-8252
    ISSN (online) 1944-8252
    DOI 10.1021/acsami.8b10527
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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