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  1. Book: Gene therapy of autoimmune diseases

    Prud'homme, Gérald J.

    (Medical intelligence unit)

    2005  

    Author's details Gérald J. Prud'homme
    Series title Medical intelligence unit
    Keywords Autoimmune Diseases / therapy ; Gene Therapy / methods ; Genetic Vectors ; Gene Targeting ; Gene Transfer Techniques ; Vaccines, DNA ; Autoimmune diseases/Gene therapy
    Subject code 616.978042
    Language English
    Size 138 S. : Ill.
    Publisher Landes Bioscience u.a.
    Publishing place Georgetown, Tex. u.a.
    Publishing country United States
    Document type Book
    Note Includes bibliographical references and index
    HBZ-ID HT014712608
    ISBN 0-306-47991-5 ; 978-0-306-47991-5
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2006 A 2194 order for loan Magazin

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  2. Article ; Online: Pathobiology of the Klotho Antiaging Protein and Therapeutic Considerations.

    Prud'homme, Gérald J / Kurt, Mervé / Wang, Qinghua

    Frontiers in aging

    2022  Volume 3, Page(s) 931331

    Abstract: The α-Klotho protein (henceforth denoted Klotho) has antiaging properties, as first observed in mice homozygous for a ... ...

    Abstract The α-Klotho protein (henceforth denoted Klotho) has antiaging properties, as first observed in mice homozygous for a hypomorphic
    Language English
    Publishing date 2022-07-12
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 3076785-4
    ISSN 2673-6217 ; 2673-6217
    ISSN (online) 2673-6217
    ISSN 2673-6217
    DOI 10.3389/fragi.2022.931331
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  3. Article: Causal effects of non-alcoholic fatty liver disease on osteoporosis: a Mendelian randomization study.

    Zhou, Yue / Ni, Yunzhi / Wang, Zhihong / Prud'homme, Gerald J / Wang, Qinghua

    Frontiers in endocrinology

    2023  Volume 14, Page(s) 1283739

    Abstract: Background: Osteoporosis (OP) is a systemic skeletal disease characterized by compromised bone strength leading to an increased risk of fracture. There is an ongoing debate on whether non-alcoholic fatty liver disease (NAFLD) is an active contributor or ...

    Abstract Background: Osteoporosis (OP) is a systemic skeletal disease characterized by compromised bone strength leading to an increased risk of fracture. There is an ongoing debate on whether non-alcoholic fatty liver disease (NAFLD) is an active contributor or an innocent bystander in the pathogenesis of OP. The aim of this study was to assess the causal association between NAFLD and OP.
    Methods: We performed two-sample Mendelian randomization (MR) analyses to investigate the causal association between genetically predicted NAFLD [i.e., imaging-based liver fat content (LFC), chronically elevated serum alanine aminotransferase (cALT) and biopsy-confirmed NAFLD] and risk of OP. The inverse variant weighted method was performed as main analysis to obtain the causal estimates.
    Results: Imaging-based LFC and biopsy-confirmed NAFLD demonstrated a suggestive causal association with OP ([odds ratio (OR): 1.003, 95% CI: 1.001-1.004, P < 0.001; OR: 1.001, 95% CI: 1.000-1.002, P = 0.031]). The association between cALT and OP showed a similar direction, but was not statistically significant (OR: 1.001, 95% CI: 1.000-1.002, P = 0.079). Repeated analyses after exclusion of genes associated with confounding factors showed consistent results. Sensitivity analysis indicated low heterogeneity, high reliability and low pleiotropy of the causal estimates.
    Conclusion: The two-sample MR analyses suggest a causal association between genetically predicted NAFLD and OP.
    MeSH term(s) Humans ; Non-alcoholic Fatty Liver Disease/epidemiology ; Non-alcoholic Fatty Liver Disease/genetics ; Mendelian Randomization Analysis ; Reproducibility of Results ; Osteoporosis/etiology ; Osteoporosis/genetics
    Language English
    Publishing date 2023-12-12
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2023.1283739
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  4. Article: Systemic Klotho therapy protects against insulitis and enhances beta-cell mass in NOD mice

    Prud’homme, Gérald J / Glinka, Yelena / Kurt, Merve / Liu, Wenjuan / Wang, Qinghua

    Biochemical and biophysical research communications. 2020 May 07, v. 525, no. 3

    2020  

    Abstract: The levels of the anti-aging protein α-Klotho, in its soluble form (s-Klotho), are depressed in the circulation of patients with type 1 diabetes (T1D) or type 2 diabetes (T2D). Gene transfer experiments have suggested a protective role for β-cell ... ...

    Abstract The levels of the anti-aging protein α-Klotho, in its soluble form (s-Klotho), are depressed in the circulation of patients with type 1 diabetes (T1D) or type 2 diabetes (T2D). Gene transfer experiments have suggested a protective role for β-cell specific expression of α-Klotho in murine models of T1D and T1D, but these approaches are not easily translatable to clinical therapy. It is unknown whether systemic s-Klotho protein treatment ameliorates disease in T1D, which is characterized by autoimmune destruction of β cells. We previously reported from in vitro experiments with β cells that s-Klotho increases insulin secretion, reduces cells death and promotes β-cell replication. Here, we investigated s-Klotho protein therapy in NOD mice, which have autoimmune T1D. We observed that diabetic NOD mice have significantly lower plasma levels of s-Klotho, compared to their non-diabetic counterparts. To examine in vivo effects of Klotho, we treated NOD mice with s-Klotho protein, or with a Klotho blocking antibody. Systemic treatment with s-Klotho ameliorated diabetes; notably increasing β-cell replication and total β-cell mass. Klotho expression was increased locally in the islets. s-Klotho also markedly reduced immune-cell infiltration of islets (insulitis). In contrast, administration of the Klotho antibody was detrimental, and aggravated the loss of β-cell mass. Thus, s-Klotho has protective effects in this model of T1D, and this appears to depend on a combination of increased β-cell replication and reduced insulitis. These findings suggest that s-Klotho might be effective as a new therapeutic agent for T1D.
    Keywords antibodies ; death ; gene transfer ; insulin secretion ; insulin-dependent diabetes mellitus ; mice ; noninsulin-dependent diabetes mellitus ; protective effect ; research ; therapeutics
    Language English
    Dates of publication 2020-0507
    Size p. 693-698.
    Publishing place Elsevier Inc.
    Document type Article
    Note NAL-AP-2-clean
    ZDB-ID 205723-2
    ISSN 0006-291X ; 0006-291X
    ISSN (online) 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2020.02.123
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

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  5. Article ; Online: Pharmacokinetic and pharmacodynamic studies of supaglutide in rats and monkeys.

    Liao, Yijing / Ma, Anran / Wang, Zhihong / Zhou, Yue / Liu, Lin / Zhang, Na / Zhang, Li / Prud'homme, Gerald J / Wang, Qinghua

    European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences

    2022  Volume 175, Page(s) 106218

    Abstract: We demonstrated recently that supaglutide, a novel GLP-1 mimetic generated by recombinant fusion protein techniques, exerted hypoglycemic effects in type 2 diabetes db/db mice and spontaneous diabetic monkeys. In this study, we investigated the ... ...

    Abstract We demonstrated recently that supaglutide, a novel GLP-1 mimetic generated by recombinant fusion protein techniques, exerted hypoglycemic effects in type 2 diabetes db/db mice and spontaneous diabetic monkeys. In this study, we investigated the pharmacokinetics and pharmacodynamics of supaglutide by single subcutaneous and intravenous injection(s) in rats and rhesus monkeys, as well as fourconsecutive subcutaneous injections in monkeys.We found the half-life (t1/2) of supaglutide was 39.7 h and 35.8 h at dosing 0.1 mg/kg upon subcutaneous or intravenous administration respectively, in rhesus monkeys. The plasma supaglutide peaked at 8-10 h, while the plasma drug exposure levels increased with the increase of dose, showing approximately a linear pharmacokinetic characteristic. The elimination kinetics (Ke) were found to be similar between subcutaneous (∼0.025 in rats and ∼0.018 in monkeys) and intravenous administration (0.021 in rats and 0.020 in monkeys), whereas the bioavailability was found to be 31.1% in rats and 63.9% in monkeys. In monkeys, a single dose injection of supaglutide markedly decreased the random blood glucose levels that reaching the maxima effects in 14-16 h, gradually recovered and returned to the baseline level approximately after 72 h.
    MeSH term(s) Animals ; Diabetes Mellitus, Type 2/drug therapy ; Hypoglycemic Agents/therapeutic use ; Injections, Intravenous ; Macaca fascicularis ; Macaca mulatta ; Mice ; Rats ; Rats, Sprague-Dawley
    Chemical Substances Hypoglycemic Agents
    Language English
    Publishing date 2022-05-23
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1154366-8
    ISSN 1879-0720 ; 0928-0987
    ISSN (online) 1879-0720
    ISSN 0928-0987
    DOI 10.1016/j.ejps.2022.106218
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    Zs.A 3705: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  6. Article ; Online: GABAergic regulation of pancreatic islet cells: Physiology and antidiabetic effects.

    Wang, Qinghua / Ren, Liwei / Wan, Yun / Prud'homme, Gerald J

    Journal of cellular physiology

    2019  Volume 234, Issue 9, Page(s) 14432–14444

    Abstract: Diabetes occurs when pancreatic β-cell death exceeds β-cell growth, which leads to loss of β-cell mass. An effective therapy must have two actions: promotion of β-cell replication and suppression of β-cell death. Previous studies have established an ... ...

    Abstract Diabetes occurs when pancreatic β-cell death exceeds β-cell growth, which leads to loss of β-cell mass. An effective therapy must have two actions: promotion of β-cell replication and suppression of β-cell death. Previous studies have established an important role for γ-aminobutyric acid (GABA) in islet-cell hormone homeostasis, as well as the maintenance of the β-cell mass. GABA exerts paracrine actions on α cells in suppressing glucagon secretion, and it has autocrine actions on β cells that increase insulin secretion. Multiple studies have shown that GABA increases the mitotic rate of β cells. In mice, following β-cell depletion with streptozotocin, GABA therapy can restore the β-cell mass. Enhanced β-cell replication appears to depend on growth and survival pathways involving Akt activation. Some studies have also suggested that it induces transdifferentiation of α cells into β cells, but this has been disputed and requires further investigation. In addition to proliferative effects, GABA protects β cells against injury and markedly reduces their apoptosis under a variety of conditions. The antiapoptotic effects depend at least in part on the enhancement of sirtuin-1 and Klotho activity, which both inhibit activation of the NF-κB inflammatory pathway. Importantly, in xenotransplanted human islets, GABA therapy stimulates β-cell replication and insulin secretion. Thus, the intraislet GABAergic system is a target for the amelioration of diabetes therapy, including β-cell survival and regeneration. GABA (or GABAergic drugs) can be combined with other antidiabetic drugs for greater effect.
    Language English
    Publishing date 2019-01-28
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 3116-1
    ISSN 1097-4652 ; 0021-9541
    ISSN (online) 1097-4652
    ISSN 0021-9541
    DOI 10.1002/jcp.28214
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  7. Article ; Online: Systemic Klotho therapy protects against insulitis and enhances beta-cell mass in NOD mice.

    Prud'homme, Gérald J / Glinka, Yelena / Kurt, Merve / Liu, Wenjuan / Wang, Qinghua

    Biochemical and biophysical research communications

    2020  Volume 525, Issue 3, Page(s) 693–698

    Abstract: The levels of the anti-aging protein α-Klotho, in its soluble form (s-Klotho), are depressed in the circulation of patients with type 1 diabetes (T1D) or type 2 diabetes (T2D). Gene transfer experiments have suggested a protective role for β-cell ... ...

    Abstract The levels of the anti-aging protein α-Klotho, in its soluble form (s-Klotho), are depressed in the circulation of patients with type 1 diabetes (T1D) or type 2 diabetes (T2D). Gene transfer experiments have suggested a protective role for β-cell specific expression of α-Klotho in murine models of T1D and T1D, but these approaches are not easily translatable to clinical therapy. It is unknown whether systemic s-Klotho protein treatment ameliorates disease in T1D, which is characterized by autoimmune destruction of β cells. We previously reported from in vitro experiments with β cells that s-Klotho increases insulin secretion, reduces cells death and promotes β-cell replication. Here, we investigated s-Klotho protein therapy in NOD mice, which have autoimmune T1D. We observed that diabetic NOD mice have significantly lower plasma levels of s-Klotho, compared to their non-diabetic counterparts. To examine in vivo effects of Klotho, we treated NOD mice with s-Klotho protein, or with a Klotho blocking antibody. Systemic treatment with s-Klotho ameliorated diabetes; notably increasing β-cell replication and total β-cell mass. Klotho expression was increased locally in the islets. s-Klotho also markedly reduced immune-cell infiltration of islets (insulitis). In contrast, administration of the Klotho antibody was detrimental, and aggravated the loss of β-cell mass. Thus, s-Klotho has protective effects in this model of T1D, and this appears to depend on a combination of increased β-cell replication and reduced insulitis. These findings suggest that s-Klotho might be effective as a new therapeutic agent for T1D.
    MeSH term(s) Animals ; Cell Proliferation ; Female ; Glucuronidase/blood ; Glucuronidase/therapeutic use ; Humans ; Insulin-Secreting Cells/pathology ; Mice, Inbred NOD ; Organ Size
    Chemical Substances Glucuronidase (EC 3.2.1.31) ; klotho protein (EC 3.2.1.31)
    Language English
    Publishing date 2020-03-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2020.02.123
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    Zs.A 116: Show issues Location:
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  8. Article ; Online: Cancer stem cells and novel targets for antitumor strategies.

    Prud'homme, Gérald J

    Current pharmaceutical design

    2011  Volume 18, Issue 19, Page(s) 2838–2849

    Abstract: Cancer stem cells (CSCs) were identified in human leukemias in landmark studies of John Dick and his colleagues. Subsequently, similar cancer stem-like cells were identified in solid tumors of the breast, colon, brain and other sites. CSCs have distinct ... ...

    Abstract Cancer stem cells (CSCs) were identified in human leukemias in landmark studies of John Dick and his colleagues. Subsequently, similar cancer stem-like cells were identified in solid tumors of the breast, colon, brain and other sites. CSCs have distinct markers and are highly tumorigenic compared to other subsets. They can differentiate into all the cell phenotypes of the parental tumor. Other key features include activation of pluripotency genes (Oct4, Sox2, Nanog), self-renewal, formation of tumor spheres in low-adherence cultures, and multi-drug resistance. Clinically, drug resistance is probably the most important feature, because CSCs resist conventional cancer therapies and are likely to play a major role in cancer relapse. Based on their properties, several molecules have been targeted for therapy with drugs as follows. 1) The self-renewal pathways Wnt/β-catenin, Hedgehog and Notch. 2) The aryl hydrocarbon receptor (AHR), with tranilast and other AHR agonists. 3) Cytokines and inflammatory pathways (e.g., IL-6, IL-8, NF-κB). 4) TGF-β and epithelial- to-mesenchymal transition (EMT) pathways. 5) Homing molecules involved in metastasis; most notably CXCR4 or its ligand CXCL12. 6) Growth factors, their receptors and coreceptors (such as neuropilin-1), and signaling components (e.g., tyrosine kinases). 7) Cell-surface markers (CD44 and integrins). Several drugs have been identified by screening or other observations (salinomycin, metformin, tesmilifene, sulforaphane, curcumin, piperine and others). Some of these drugs are at preclinical or early clinical phases of development, and it remains to be seen how many will progress to clinical application. This review focuses on some promising new developments in anti-CSC drug therapy.
    MeSH term(s) Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Chemokines/metabolism ; Cytokines/metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplastic Stem Cells/drug effects ; Signal Transduction
    Chemical Substances Antineoplastic Agents ; Chemokines ; Cytokines ; Intercellular Signaling Peptides and Proteins
    Language English
    Publishing date 2011-08-04
    Publishing country United Arab Emirates
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1304236-1
    ISSN 1873-4286 ; 1381-6128
    ISSN (online) 1873-4286
    ISSN 1381-6128
    DOI 10.2174/138161212800626120
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    Zs.A 4714: Show issues Location:
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  9. Article ; Online: Combined effect of GABA and glucagon-like peptide-1 receptor agonist on cytokine-induced apoptosis in pancreatic β-cell line and isolated human islets.

    Son, Dong Ok / Liu, Wenjuan / Li, Xiaoming / Prud'homme, Gerald J / Wang, Qinghua

    Journal of diabetes

    2019  Volume 11, Issue 7, Page(s) 563–572

    Abstract: Background: Treatment with GABA or glucagon-like peptide-1 (GLP-1) can preserve pancreatic β-cell mass and prevent diabetes. Recently, we reported that the combination of GABA and sitagliptin (a dipeptidyl peptidase-4 inhibitor that increases endogenous ...

    Abstract Background: Treatment with GABA or glucagon-like peptide-1 (GLP-1) can preserve pancreatic β-cell mass and prevent diabetes. Recently, we reported that the combination of GABA and sitagliptin (a dipeptidyl peptidase-4 inhibitor that increases endogenous GLP-1) was more effective than either agent alone in reducing drug-induced β-cell damage and promoting β-cell regeneration in mice. However, in human islets, it remains unclear whether GABA and GLP-1 exert similar effects.
    Methods: To investigate GABA and GLP-1 interactions, human islets or INS-1 cells were treated with GABA and/or exendin-4, a GLP-1 receptor agonist (GLP-1RA) in clinical use, and incubated with a cytokine mixture for 24 hours. Cleaved caspase-3 and annexin V binding were measured by western blot and flow cytometry analysis, respectively, to investigate effects on cytokine-induced apoptosis.
    Results: Cytokine-induced apoptosis was reduced by either GABA or exendin-4 alone. This was markedly improved by combining GABA and exendin-4, resulting in a reversal of apoptosis. The combination notably increased Akt pathway signaling. Furthermore, sirtuin-1 (SIRT1) and α-Klotho, both reported to have protective effects on β-cells, were increased. Importantly, the combination ameliorated insulin secretion by human β-cells.
    Conclusions: The combination of GABA and a GLP-1RA exerted additive effects on β-cell survival and function, suggesting that this combination may be superior to either drug alone in the treatment of diabetes.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Cell Survival ; Cells, Cultured ; Cytokines/pharmacology ; Exenatide/pharmacology ; Female ; Glucagon-Like Peptide-1 Receptor/agonists ; Humans ; Hypoglycemic Agents/pharmacology ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/pathology ; Male ; Middle Aged ; Rats ; Signal Transduction ; gamma-Aminobutyric Acid/metabolism
    Chemical Substances Cytokines ; Glucagon-Like Peptide-1 Receptor ; Hypoglycemic Agents ; gamma-Aminobutyric Acid (56-12-2) ; Exenatide (9P1872D4OL)
    Language English
    Publishing date 2019-01-01
    Publishing country Australia
    Document type Journal Article
    ZDB-ID 2503337-2
    ISSN 1753-0407 ; 1753-0393
    ISSN (online) 1753-0407
    ISSN 1753-0393
    DOI 10.1111/1753-0407.12881
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    Zs.A 6791: Show issues Location:
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  10. Article ; Online: Combined therapy of GABA and sitagliptin prevents high-fat diet impairment of beta-cell function.

    Wang, Zhihong / Fan, Linling / Ni, Yunzhi / Wu, Di / Ma, Anran / Zhao, Ying / Li, Jia / Cui, Qiaoli / Zhou, Yue / Zhang, Li / Lou, Yan-Ru / Prud'homme, Gerald J / Wang, Qinghua

    Molecular and cellular endocrinology

    2022  Volume 559, Page(s) 111755

    Abstract: We recently demonstrated that combined therapy of GABA and sitagliptin promoted beta-cell proliferation, and decreased beta-cell apoptosis in a multiple low-dose streptozotocin (STZ)-induced beta-cell injury mouse model. In this study, we examined ... ...

    Abstract We recently demonstrated that combined therapy of GABA and sitagliptin promoted beta-cell proliferation, and decreased beta-cell apoptosis in a multiple low-dose streptozotocin (STZ)-induced beta-cell injury mouse model. In this study, we examined whether this combined therapy is effective in ameliorating the impairment of beta-cell function caused by high-fat diet (HFD) feeding in mice. Male C57BL/6J mice were fed normal chow diet, HFD, or HFD combined with GABA, sitagliptin, or both drugs. Oral drug daily administration was initiated one week before HFD and maintained for two weeks. After two weeks of intervention, we found that GABA or sitagliptin administration ameliorated the impairment of glucose tolerance induced by HFD. This was associated with improved insulin secretion in vivo. Notably, combined administration of GABA and sitagliptin significantly enhanced these effects as compared to each of the monotherapies. Combined GABA and sitagliptin was superior at increasing beta-cell mass, and associated Ki67
    MeSH term(s) Male ; Mice ; Animals ; Mice, Inbred C57BL ; Sitagliptin Phosphate/pharmacology ; Sitagliptin Phosphate/therapeutic use ; Diet, High-Fat/adverse effects ; Streptozocin ; Multiple Trauma ; gamma-Aminobutyric Acid/pharmacology
    Chemical Substances Sitagliptin Phosphate (TS63EW8X6F) ; Streptozocin (5W494URQ81) ; gamma-Aminobutyric Acid (56-12-2)
    Language English
    Publishing date 2022-08-29
    Publishing country Ireland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2022.111755
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