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  1. AU="Payaningal R. Somanath"
  2. AU=Das Ananya
  3. AU="Dave, Riya"
  4. AU=Kwon Okyu
  5. AU="Ortiz-López, Francisco Javier"
  6. AU="Churiwal, Mehal"
  7. AU="Nandi, Asoke K"
  8. AU="Fishchenko, I"
  9. AU="Yong, Ken-Tye"
  10. AU="Alexander, Regi T"
  11. AU=Weng Cheng-Hao
  12. AU="Christine Hamel"

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  1. Artikel ; Online: Distinct Mechanisms of Human Retinal Endothelial Barrier Modulation In Vitro by Mediators of Diabetes and Uveitis

    Madhuri Rudraraju / S. Priya Narayanan / Payaningal R. Somanath

    Life, Vol 12, Iss 33, p

    2022  Band 33

    Abstract: Ocular diseases such as diabetic retinopathy (DR) and uveitis are associated with injury to the blood–retinal barrier (BRB). Whereas high glucose (HG) and advanced glycation end products (AGE) contribute to DR, bacterial infections causing uveitis are ... ...

    Abstract Ocular diseases such as diabetic retinopathy (DR) and uveitis are associated with injury to the blood–retinal barrier (BRB). Whereas high glucose (HG) and advanced glycation end products (AGE) contribute to DR, bacterial infections causing uveitis are triggered by endotoxins such as lipopolysaccharide (LPS). It is unclear how HG, AGE, and LPS affect human retinal endothelial cell (HREC) junctions. Moreover, tumor necrosis factor-α (TNFα) is elevated in both DR and ocular infections. In the current study, we determined the direct effects of HG, AGE, TNFα, and LPS on the expression and intracellular distribution of claudin-5, VE-cadherin, and β-catenin in HRECs and how these mediators affect Akt and P38 MAP kinase that have been implicated in ocular pathologies. In our results, whereas HG, AGE, and TNFα activated both Akt and P38 MAPK, LPS treatment suppressed Akt but increased P38 MAPK phosphorylation. Furthermore, while treatment with AGE and HG increased cell-junction protein expression in HRECs, LPS elicited a paradoxical effect. By contrast, when HG treatment increased HREC-barrier resistance, AGE and LPS stimulation compromised it, and TNFα had no effect. Together, our results demonstrated the differential effects of the mediators of diabetes and infection on HREC-barrier modulation leading to BRB injury.
    Schlagwörter blood–brain barrier ; claudin-5 ; AGE ; TNFα ; hyperglycemia ; lipopolysaccharide ; Science ; Q
    Thema/Rubrik (Code) 630
    Sprache Englisch
    Erscheinungsdatum 2022-12-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Pharmacological Inhibition of Spermine Oxidase Suppresses Excitotoxicity Induced Neuroinflammation in Mouse Retina

    Moaddey Alfarhan / Fang Liu / Shengshuai Shan / Prahalathan Pichavaram / Payaningal R. Somanath / S. Priya Narayanan

    International Journal of Molecular Sciences, Vol 23, Iss 2133, p

    2022  Band 2133

    Abstract: Polyamine oxidation plays a major role in neurodegenerative diseases. Previous studies from our laboratory demonstrated that spermine oxidase (SMOX, a member of the polyamine oxidase family) inhibition using MDL 72527 reduced neurodegeneration in models ... ...

    Abstract Polyamine oxidation plays a major role in neurodegenerative diseases. Previous studies from our laboratory demonstrated that spermine oxidase (SMOX, a member of the polyamine oxidase family) inhibition using MDL 72527 reduced neurodegeneration in models of retinal excitotoxicity and diabetic retinopathy. However, the mechanisms behind the neuroprotection offered by SMOX inhibition are not completely studied. Utilizing the experimental model of retinal excitotoxicity, the present study determined the impact of SMOX blockade in retinal neuroinflammation. Our results demonstrated upregulation in the number of cells positive for Iba-1 (ionized calcium-binding adaptor molecule 1), CD (Cluster Differentiation) 68, and CD16/32 in excitotoxicity-induced retinas, while MDL 72527 treatment reduced these changes, along with increases in the number of cells positive for Arginase1 and CD206. When retinal excitotoxicity upregulated several pro-inflammatory genes, MDL 72527 treatment reduced many of them and increased anti-inflammatory genes. Furthermore, SMOX inhibition upregulated antioxidant signaling (indicated by elevated Nrf2 and HO-1 levels) and reduced protein-conjugated acrolein in excitotoxic retinas. In vitro studies using C8-B4 cells showed changes in cellular morphology and increased reactive oxygen species formation in response to acrolein (a product of SMOX activity) treatment. Overall, our findings indicate that the inhibition SMOX pathway reduced neuroinflammation and upregulated antioxidant signaling in the retina.
    Schlagwörter neuroinflammation ; polyamine oxidation ; spermine oxidase ; acrolein ; microglia ; oxidative damage ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 572
    Sprache Englisch
    Erscheinungsdatum 2022-02-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Stimulation of Angiotensin II Type 2 Receptor Modulates Pro-Inflammatory Response in Microglia and Macrophages

    Abdulkarim Alshammari / Yohan Han / Timothy W. Jones / Bindu Pillai / Duo Zhang / Adviye Ergul / Payaningal R. Somanath / Susan C. Fagan

    Life, Vol 13, Iss 1274, p

    Therapeutic Implications for the Treatment of Stroke

    2023  Band 1274

    Abstract: Background: Sustained microglial activation contributes to the development of post-stroke cognitive impairment (PSCI). Compound 21 (C21), an angiotensin II type 2 receptor agonist, has shown some neurovascular protection after stroke. This study aimed to ...

    Abstract Background: Sustained microglial activation contributes to the development of post-stroke cognitive impairment (PSCI). Compound 21 (C21), an angiotensin II type 2 receptor agonist, has shown some neurovascular protection after stroke. This study aimed to investigate the direct anti-inflammatory effects of C21 on macrophages, as well as brain innate immune cells. Methods: Murine microglial cell line (C8-B4) and RAW 264.7 macrophages were exposed to lipopolysaccharide (LPS) and co-treated with C21. Pro-inflammatory mediators were assessed via RT-qPCR and ELISA. Cellular reactive oxygen species (ROS) were evaluated via CellROXGreen staining, and nitrate production was assessed using Griess assay. Results: C21 suppressed LPS-induced inflammation and ROS generation in both cells. In microglia, C21 blunted LPS-induced mRNA expression of IL-1β, IL-12b, COX-1, iNOS, and IL-6. A similar pattern was observed in macrophages, where C21 suppressed LPS-induced IL-1β, TNF-α, and CXCL1 expression. These anti-inflammatory effects in microglia and macrophages were associated with increased neuroprotective gene expression, including GDNF and BDNF, in a dose-dependent manner. Conclusions: Our findings suggest a protective effect of C21 against the inflammatory response, in both macrophages and microglia, via suppression of the release of pro-inflammatory cytokines/chemokines and the generation of ROS while stimulating the production of neurotrophic factors.
    Schlagwörter stroke ; neuroinflammatory response ; Compound 21 ; renin–angiotensin system ; BDNF ; GDNF ; Science ; Q
    Thema/Rubrik (Code) 610 ; 616
    Sprache Englisch
    Erscheinungsdatum 2023-05-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Claudin-17 Deficiency in Mice Results in Kidney Injury Due to Electrolyte Imbalance and Oxidative Stress

    Mir S. Adil / Varun Parvathagiri / Arti Verma / Fang Liu / Madhuri Rudraraju / S. Priya Narayanan / Payaningal R. Somanath

    Cells, Vol 11, Iss 1782, p

    2022  Band 1782

    Abstract: The multi-gene claudin ( CLDN ) family of tight junction proteins have isoform-specific roles in blood–tissue barrier regulation. CLDN17 , a putative anion pore-forming CLDN based on its structural characterization, is assumed to regulate anion balance ... ...

    Abstract The multi-gene claudin ( CLDN ) family of tight junction proteins have isoform-specific roles in blood–tissue barrier regulation. CLDN17 , a putative anion pore-forming CLDN based on its structural characterization, is assumed to regulate anion balance across the blood-tissue barriers. However, our knowledge about CLDN17 in physiology and pathology is limited. The current study investigated how Cldn17 deficiency in mice affects blood electrolytes and kidney structure. Cldn17 −/− mice revealed no breeding abnormalities, but the newborn pups exhibited delayed growth. Adult Cldn17 −/− mice displayed electrolyte imbalance, oxidative stress, and injury to the kidneys. Ingenuity pathway analysis followed by RNA-sequencing revealed hyperactivation of signaling pathways and downregulation of SOD1 expression in kidneys associated with inflammation and reactive oxygen species generation, demonstrating the importance of Cldn17 in the maintenance of electrolytes and reactive oxygen species across the blood-tissue barrier.
    Schlagwörter CLDN17 ; kidney injury ; plasma electrolytes ; reactive oxygen species ; inflammation ; Biology (General) ; QH301-705.5
    Sprache Englisch
    Erscheinungsdatum 2022-05-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: The Roles of CCN1/CYR61 in Pulmonary Diseases

    Yin Zhu / Sultan Almuntashiri / Yohan Han / Xiaoyun Wang / Payaningal R. Somanath / Duo Zhang

    International Journal of Molecular Sciences, Vol 21, Iss 7810, p

    2020  Band 7810

    Abstract: CCN1 (cysteine-rich 61, connective tissue growth factor, and nephroblastoma-1), previously named CYR61 (cysteine-rich angiogenic inducer 61) belongs to the CCN family of matricellular proteins. CCN1 plays critical roles in the regulation of proliferation, ...

    Abstract CCN1 (cysteine-rich 61, connective tissue growth factor, and nephroblastoma-1), previously named CYR61 (cysteine-rich angiogenic inducer 61) belongs to the CCN family of matricellular proteins. CCN1 plays critical roles in the regulation of proliferation, differentiation, apoptosis, angiogenesis, and fibrosis. Recent studies have extensively characterized the important physiological and pathological roles of CCN1 in various tissues and organs. In this review, we summarize both basic and clinical aspects of CCN1 in pulmonary diseases, including acute lung injury (ALI), chronic obstructive pulmonary disease (COPD), lung fibrosis, pulmonary arterial hypertension (PAH), lung infection, and lung cancer. We also emphasize the important challenges for future investigations to better understand the CCN1 and its role in physiology and pathology, as well as the questions that need to be addressed for the therapeutic development of CCN1 antagonists in various lung diseases.
    Schlagwörter lung injury ; COPD ; bronchopulmonary dysplasia ; fibrosis ; pulmonary hypertension ; lung infection ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2020-10-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: Liposomes Targeting P21 Activated Kinase-1 (PAK-1) and Selective for Secretory Phospholipase A 2 (sPLA 2 ) Decrease Cell Viability and Induce Apoptosis in Metastatic Triple-Negative Breast Cancer Cells

    Wided Najahi-Missaoui / Nhat D. Quach / Payaningal R. Somanath / Brian S. Cummings

    International Journal of Molecular Sciences, Vol 21, Iss 9396, p

    2020  Band 9396

    Abstract: P21 activated kinases (or group I PAKs) are serine/threonine kinases whose expression is altered in prostate and breast cancers. PAK-1 activity is inhibited by the small molecule “Inhibitor targeting PAK-1 activation-3” (IPA-3), which has selectivity for ...

    Abstract P21 activated kinases (or group I PAKs) are serine/threonine kinases whose expression is altered in prostate and breast cancers. PAK-1 activity is inhibited by the small molecule “Inhibitor targeting PAK-1 activation-3” (IPA-3), which has selectivity for PAK-1 but is metabolically unstable. Secretory Group IIA phospholipase A 2 (sPLA 2 ) expression correlates to increased metastasis and decreased survival in many cancers. We previously designed novel liposomal formulations targeting both PAK-1 and sPLA 2, called Secretory Phospholipase Responsive liposomes or SPRL-IPA-3, and demonstrated their ability to alter prostate cancer growth. The efficacy of SPRL against other types of cancers is not well understood. We addressed this limitation by determining the ability of SPRL to induce cell death in a diverse panel of cells representing different stages of breast cancer, including the invasive but non-metastatic MCF-7 cells, and metastatic triple-negative breast cancer (TNBC) cells such as MDA-MB-231, MDA-MB-468, and MDA-MB-435. We investigated the role of sPLA 2 in the disposition of these liposomes by comparing the efficacy of SPRL-IPA-3 to IPA-3 encapsulated in sterically stabilized liposomes (SSL-IPA-3), a formulation shown to be less sensitive to sPLA 2 . Both SSL-IPA-3 and SPRL-IPA-3 induced time- and dose-dependent decreases in MTT staining in all cell lines tested, but SPRL-IPA-3-induced effects in metastatic TNBC cell lines were superior over SSL-IPA-3. The reduction in MTT staining induced by SPRL-IPA-3 correlated to the expression of Group IIA sPLA 2 . sPLA 2 expression also correlated to increased induction of apoptosis in TNBC cell lines by SPRL-IPA-3. These data suggest that SPRL-IPA-3 is selective for metastatic TNBC cells and that the efficacy of SPRL-IPA-3 is mediated, in part, by the expression of Group IIA sPLA 2 .
    Schlagwörter triple-negative breast cancer ; SSL-IPA-3 ; SPRL-IPA-3 ; cell toxicity ; cell death ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2020-12-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel ; Online: Club Cell Secreted Protein CC16

    Sultan Almuntashiri / Yin Zhu / Yohan Han / Xiaoyun Wang / Payaningal R. Somanath / Duo Zhang

    Journal of Clinical Medicine, Vol 9, Iss 4039, p

    Potential Applications in Prognosis and Therapy for Pulmonary Diseases

    2020  Band 4039

    Abstract: Club cell secretory protein (CC16) is encoded by the SCGB1A1 gene. It is also known as CC10, secretoglobin, or uteroglobin. CC16 is a 16 kDa homodimeric protein secreted primarily by the non-ciliated bronchial epithelial cells, which can be detected in ... ...

    Abstract Club cell secretory protein (CC16) is encoded by the SCGB1A1 gene. It is also known as CC10, secretoglobin, or uteroglobin. CC16 is a 16 kDa homodimeric protein secreted primarily by the non-ciliated bronchial epithelial cells, which can be detected in the airways, circulation, sputum, nasal fluid, and urine. The biological activities of CC16 and its pathways have not been completely understood, but many studies suggest that CC16 has anti-inflammatory and anti-oxidative effects. The human CC16 gene is located on chromosome 11, p12-q13, where several regulatory genes of allergy and inflammation exist. Studies reveal that factors such as gender, age, obesity, renal function, diurnal variation, and exercise regulate CC16 levels in circulation. Current findings indicate CC16 not only may reflect the pathogenesis of pulmonary diseases, but also could serve as a potential biomarker in several lung diseases and a promising treatment for chronic obstructive pulmonary disease (COPD). In this review, we summarize our current understanding of CC16 in pulmonary diseases.
    Schlagwörter Clara cell ; SCGB1A1 ; lung injury ; COPD ; bronchopulmonary dysplasia ; sarcoidosis ; Medicine ; R
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2020-12-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  8. Artikel ; Online: Inhibition of glypican-1 expression induces an activated fibroblast phenotype in a human bone marrow-derived stromal cell-line

    Sukhneeraj P. Kaur / Arti Verma / Hee. K. Lee / Lillie M. Barnett / Payaningal R. Somanath / Brian S. Cummings

    Scientific Reports, Vol 11, Iss 1, Pp 1-

    2021  Band 14

    Abstract: Abstract Cancer-associated fibroblasts (CAFs) are the most abundant stromal cell type in the tumor microenvironment. CAFs orchestrate tumor-stromal interactions, and contribute to cancer cell growth, metastasis, extracellular matrix (ECM) remodeling, ... ...

    Abstract Abstract Cancer-associated fibroblasts (CAFs) are the most abundant stromal cell type in the tumor microenvironment. CAFs orchestrate tumor-stromal interactions, and contribute to cancer cell growth, metastasis, extracellular matrix (ECM) remodeling, angiogenesis, immunomodulation, and chemoresistance. However, CAFs have not been successfully targeted for the treatment of cancer. The current study elucidates the significance of glypican-1 (GPC-1), a heparan sulfate proteoglycan, in regulating the activation of human bone marrow-derived stromal cells (BSCs) of fibroblast lineage (HS-5). GPC-1 inhibition changed HS-5 cellular and nuclear morphology, and increased cell migration and contractility. GPC-1 inhibition also increased pro-inflammatory signaling and CAF marker expression. GPC-1 induced an activated fibroblast phenotype when HS-5 cells were exposed to prostate cancer cell conditioned media (CCM). Further, treatment of human bone-derived prostate cancer cells (PC-3) with CCM from HS-5 cells exhibiting GPC-1 loss increased prostate cancer cell aggressiveness. Finally, GPC-1 was expressed in mouse tibia bone cells and present during bone loss induced by mouse prostate cancer cells in a murine prostate cancer bone model. These data demonstrate that GPC-1 partially regulates the intrinsic and extrinsic phenotype of human BSCs and transformation into activated fibroblasts, identify novel functions of GPC-1, and suggest that GPC-1 expression in BSCs exerts inhibitory paracrine effects on the prostate cancer cells. This supports the hypothesis that GPC-1 may be a novel pharmacological target for developing anti-CAF therapeutics to control cancer.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2021-04-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  9. Artikel ; Online: Elevated Intracranial Pressure in Cryptococcal Meningoencephalitis

    Abdulaziz H. Alanazi / Mir S. Adil / Xiaorong Lin / Daniel B. Chastain / Andrés F. Henao-Martínez / Carlos Franco-Paredes / Payaningal R. Somanath

    Pathogens, Vol 11, Iss 783, p

    Examining Old, New, and Promising Drug Therapies

    2022  Band 783

    Abstract: Despite the availability of effective antifungal therapy, cryptococcal meningoencephalitis (CM) remains associated with elevated mortality. The spectrum of symptoms associated with the central nervous system (CNS) cryptococcosis is directly caused by the ...

    Abstract Despite the availability of effective antifungal therapy, cryptococcal meningoencephalitis (CM) remains associated with elevated mortality. The spectrum of symptoms associated with the central nervous system (CNS) cryptococcosis is directly caused by the high fungal burden in the subarachnoid space and the peri-endothelial space of the CNS vasculature, which results in intracranial hypertension (ICH). Management of intracranial pressure (ICP) through aggressive drainage of cerebrospinal fluid by lumbar puncture is associated with increased survival. Unfortunately, these procedures are invasive and require specialized skills and supplies that are not readily available in resource-limited settings that carry the highest burden of CM. The institution of pharmacologic therapies to reduce the production or increase the resorption of cerebrospinal fluid would likely improve clinical outcomes associated with ICH in patients with CM. Here, we discuss the potential role of multiple pharmacologic drug classes such as diuretics, corticosteroids, and antiepileptic agents used to decrease ICP in various neurological conditions as potential future therapies for CM.
    Schlagwörter Cryptococcus neoformans ; meningitis ; intracranial pressure ; blood-brain-barrier ; edema ; Medicine ; R
    Sprache Englisch
    Erscheinungsdatum 2022-07-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  10. Artikel ; Online: Neuroprotective Effects of Fingolimod in a Cellular Model of Optic Neuritis

    Amritha A. Candadai / Fang Liu / Arti Verma / Mir S. Adil / Moaddey Alfarhan / Susan C. Fagan / Payaningal R. Somanath / S. Priya Narayanan

    Cells, Vol 10, Iss 2938, p

    2021  Band 2938

    Abstract: Visual dysfunction resulting from optic neuritis (ON) is one of the most common clinical manifestations of multiple sclerosis (MS), characterized by loss of retinal ganglion cells, thinning of the nerve fiber layer, and inflammation to the optic nerve. ... ...

    Abstract Visual dysfunction resulting from optic neuritis (ON) is one of the most common clinical manifestations of multiple sclerosis (MS), characterized by loss of retinal ganglion cells, thinning of the nerve fiber layer, and inflammation to the optic nerve. Current treatments available for ON or MS are only partially effective, specifically target the inflammatory phase, and have limited effects on long-term disability. Fingolimod (FTY) is an FDA-approved immunomodulatory agent for MS therapy. The objective of the current study was to evaluate the neuroprotective properties of FTY in the cellular model of ON-associated neuronal damage. R28 retinal neuronal cell damage was induced through treatment with tumor necrosis factor-α (TNFα). In our cell viability analysis, FTY treatment showed significantly reduced TNFα-induced neuronal death. Treatment with FTY attenuated the TNFα-induced changes in cell survival and cell stress signaling molecules. Furthermore, immunofluorescence studies performed using various markers indicated that FTY treatment protects the R28 cells against the TNFα-induced neurodegenerative changes by suppressing reactive oxygen species generation and promoting the expression of neuronal markers. In conclusion, our study suggests neuroprotective effects of FTY in an in vitro model of optic neuritis.
    Schlagwörter optic neuritis ; multiple sclerosis ; oxidative stress ; neuroprotection ; fingolimod ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2021-10-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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