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Article ; Online: Autologous transplantation of green tea epigallocatechin-3-gallate pretreated adipose-derived stem cells increases cardiac regenerative capability through C-X-C motif chemokine receptor 4 expression in the treatment of rats with diabetic cardiomyopathy.

Chen, Tung-Sheng / Kuo, Wei-Wen / Huang, Chih-Yang

2024

Abstract: Cardiomyopathy is one of complications related to diabetes. Stem cell transplantation shows potential in diabetic cardiomyopathy treatment. Epigallocatechin-3-gallate (EGCG) is one of the major components found in green tea. Although stem cell ... ...

Abstract	Cardiomyopathy is one of complications related to diabetes. Stem cell transplantation shows potential in diabetic cardiomyopathy treatment. Epigallocatechin-3-gallate (EGCG) is one of the major components found in green tea. Although stem cell transplantation and green tea EGCG supplementation show therapeutic effects on cardiomyopathy, the detailed cellular mechanisms in stem cell transplantation coupled with EGCG treatment remain unclear. This study investigates whether adipose-derived stem cells (ADSC) pretreated with EGCG show better protective effect on diabetic cardiomyopathy than ADSC without EGCG pretreatment. A cell model indicated that ADSC pretreated with EGCG increased cell functions including colony formation, migration and survival markers. All of these functions are blocked by small interfering C-X-C motif chemokine receptor 4 (siCXCR4) administration. These findings suggest that ADSC pretreatment with EGCG increases cell functions through CXCR4 expression. A diabetic animal model was designed to verify the above findings, including Sham, DM (diabetic rats), DM+ADSC (DM rats receiving autologous transplantation of ADSC) and DM+E-ADSC (DM rats receiving EGCG pretreated ADSC). Compared to the Sham, we found that all of pathophysiological signalings were activated in the DM group, including functional changes (decrease in ejection fraction and fractional shortening), structural changes (disarray and fibrosis) and molecular changes (increases in apoptotic, fibrotic, hypertrophic markers and decreases in survival and longevity markers). E-ADSC (DM+E-ADSC) transplantation shows significant improvement in the above pathophysiological signalings greater than ADSC (DM+ADSC). Therefore, ADSC pretreated with EGCG may contribute to clinical applications for diabetic patients with cardiomyopathy.
Language	English
Publishing date	2024-03-07
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2088228-2
ISSN	1881-7122 ; 1341-1357 ; 0007-5124
ISSN (online)	1881-7122
ISSN	1341-1357 ; 0007-5124
DOI	10.1538/expanim.23-0109
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Zs.B 1653: Show issues

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Article ; Online: Diallyl trisulfide (DATS) protects cardiac cells against advanced glycation end-product-induced apoptosis by enhancing FoxO3A-dependent upregulation of miRNA-210.

Lin, Kuan-Ho / Ng, Shang-Chuan / Lu, Shang-Yeh / Lin, Yueh-Min / Lin, Shu-Hui / Su, Tzu-Cheng / Huang, Chih-Yang / Kuo, Wei-Wen

The Journal of nutritional biochemistry

2024 Volume 125, Page(s) 109567

Abstract: Diabetic cardiomyopathy is a common complication of diabetes, resulting in cardiac hypertrophy and heart failure associated with excessive reactive oxygen species and mitochondria-mediated apoptosis generation. Mitogen-activated protein kinase-c-Jun N- ... ...

Abstract	Diabetic cardiomyopathy is a common complication of diabetes, resulting in cardiac hypertrophy and heart failure associated with excessive reactive oxygen species and mitochondria-mediated apoptosis generation. Mitogen-activated protein kinase-c-Jun N-terminal kinase (MAPK-JNK), regulated by microRNA (miR)-210, affects mitochondrial function and is activated by advanced glycation end-products (AGE) in cardiac cells. Diallyl trisulfide (DATS), an antioxidant in garlic oil, inhibits stress-induced cardiac apoptosis. This study examined whether DATS enhances miR-210 expression to attenuate cardiac apoptosis. We investigated the DATS-mediated attenuation mechanism of AGE-enhanced cardiac apoptosis by modulating miR-210 and its upstream transcriptional regulator, FoxO3a. We found FoxO3a binding sites in the miR-210 promoter region. Our results indicated that DATS treatment inhibited AGE-induced JNK activation, phosphoprotein c-Jun nuclear transactivation, and cardiac apoptosis and reversed the AGE-induced reduction in cardiac miR-210 levels. The luciferase activity after DATS treatment was significantly lower than that of the control and was reversed following AGE treatment. We also showed that FoxO3a, upregulated by DATS treatment, may bind to the miR-210 promoter to enhance its expression and downregulates JNK expression to attenuate AGE-induced cardiac apoptosis. Oral administration of DATS enhanced FoxO3a expression in the heart and reduced diabetes-induced heart apoptosis. Our findings indicate that DATS mediates AGE-induced cardiac cell apoptosis attenuation by promoting FoxO3a nuclear transactivation to enhance miR-210 expression and regulate JNK activation. Our results suggest that DATS can be used as a cardioprotective agent, and miR-210 is a critical regulator in inhibiting diabetic cardiomyopathy.
MeSH term(s)	Humans ; Up-Regulation ; Diabetic Cardiomyopathies/prevention & control ; Glycation End Products, Advanced ; Maillard Reaction ; Sulfides/pharmacology ; Apoptosis ; Cell Line, Tumor ; Mitogen-Activated Protein Kinase Kinases ; MicroRNAs/genetics ; Allyl Compounds
Chemical Substances	diallyl trisulfide (0ZO1U5A3XX) ; Glycation End Products, Advanced ; Sulfides ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; MicroRNAs ; MIRN210 microRNA, human ; Allyl Compounds
Language	English
Publishing date	2024-01-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	1014929-6
ISSN	1873-4847 ; 0955-2863
ISSN (online)	1873-4847
ISSN	0955-2863
DOI	10.1016/j.jnutbio.2024.109567
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Zs.A 2838: Show issues

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Article ; Online: Reversion of glucocorticoid-induced senescence and collagen synthesis decrease by LY294002 is mediated through p38 in skin.

Le, Quoc-Vu / Wen, Su-Ying / Chen, Chih-Jung / Huang, Chih-Yang / Kuo, Wei-Wen

International journal of biological sciences

2022 Volume 18, Issue 16, Page(s) 6102–6113

Abstract: Glucocorticoids (GCs) are the most common treatment for inflammatory skin disorders; however, they show several adverse side effects, including atrophy and collagen decrease following chronic treatment. In particular, transcription factors and p38 ... ...

Abstract	Glucocorticoids (GCs) are the most common treatment for inflammatory skin disorders; however, they show several adverse side effects, including atrophy and collagen decrease following chronic treatment. In particular, transcription factors and p38 signaling for collagen synthesis have been shown to be suppressed by the active glucocorticoid receptor (GR). LY294002 (LY), a phosphoinositide 3-kinase (PI3K) inhibitor, has been reported to protect keratinocytes in epidermis against GC-induced hypoplasia; however, its protective effect in dermis remains unclear. Furthermore, clobetasol propionate (CP) is the most used commercial synthetic GC, yet studies on how CP causes side effects in dermal fibroblasts are limited. In this study, dermal atrophy was modeled using CP in human dermal fibroblasts (HDFs) and C57BL/6 mice. CP treatment significantly upregulated FK506 binding protein 5 (FKBP51), an atrophy marker (2.4 ± 0.25 and 3.3 ± 0.3 fold in
MeSH term(s)	Mice ; Humans ; Animals ; Glucocorticoids ; Phosphatidylinositol 3-Kinases ; Mice, Inbred C57BL ; Receptors, Glucocorticoid ; Phosphoinositide-3 Kinase Inhibitors ; Atrophy
Chemical Substances	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (31M2U1DVID) ; Glucocorticoids ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Receptors, Glucocorticoid ; Phosphoinositide-3 Kinase Inhibitors
Language	English
Publishing date	2022-10-18
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2179208-2
ISSN	1449-2288 ; 1449-2288
ISSN (online)	1449-2288
ISSN	1449-2288
DOI	10.7150/ijbs.73915
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Article ; Online: 9-POHSA prevents NF-kB activation and ameliorates LPS-induced inflammation in rat hepatocytes.

Situmorang, Jiro Hasegawa / Chen, Ming-Cheng / Kuo, Wei-Wen / Lin, Shinn-Zong / Shih, Cheng-Yen / Lin, Pi-Yu / Loh, Ching-Hui / Huang, Chih-Yang

Lipids

2023 Volume 58, Issue 5, Page(s) 241–249

Abstract: Liver inflammation has become increasingly prevalent in recent years, leading to the development of diseases like hepatitis, alcoholic liver disease, and fatty liver disease. One factor that has been linked to liver inflammation is increased levels of ... ...

Abstract	Liver inflammation has become increasingly prevalent in recent years, leading to the development of diseases like hepatitis, alcoholic liver disease, and fatty liver disease. One factor that has been linked to liver inflammation is increased levels of lipopolysaccharides (LPS), which can be caused by poor diets and sedentary lifestyles that contribute to liver inflammation. There is promising research on a new class of lipids called fatty acid esters of hydroxy fatty acids (FAHFAs), which have been shown to potentiate insulin release and exert an anti-inflammatory effect. Specifically, one type of FAHFA called 9-POHSA (palmitoleic acid ester of 9-hydroxy stearic acid) has been studied for its potential to attenuate inflammation-related indexes induced by LPS in hepatocytes, which play a critical role in the progression of liver inflammation. This study found that following LPS treatment, tumor necrosis factor- α, interleukin-6, and connective tissue growth factor (CTGF) were upregulated and increased cell migration, but 9-POHSA pre-treatment attenuated the upregulation of these markers and prevented cell migration induced by LPS. Using flowcytometry analysis, intracellular reactive oxygen species (ROS) was found to be responsible for CTGF upregulation. In addition, the effects of 9-POHSA were likely associated with its inhibition of the activation of the NF-kB. These results suggest that 9-POHSA has potential as a therapy for liver inflammation and fibrosis by attenuating inflammation-related indexes induced by LPS in hepatocytes. This study provides important insight into the mechanisms of liver inflammation and the potential for new treatments to address liver diseases.
MeSH term(s)	Animals ; Rats ; Lipopolysaccharides/toxicity ; NF-kappa B ; Inflammation/chemically induced ; Inflammation/drug therapy ; Cell Movement ; Fatty Acids ; Hepatocytes ; Hydroxy Acids
Chemical Substances	Lipopolysaccharides ; NF-kappa B ; Fatty Acids ; Hydroxy Acids
Language	English
Publishing date	2023-08-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	241539-2
ISSN	1558-9307 ; 0024-4201
ISSN (online)	1558-9307
ISSN	0024-4201
DOI	10.1002/lipd.12380
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Zs.A 645: Show issues

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Article ; Online: The involvement of Aurora-A and p53 in oxaliplatin-resistant colon cancer cells.

Chen, Mei-Chih / Yang, Bing-Ze / Kuo, Wei-Wen / Wu, Shih-Hsin / Wang, Tso-Fu / Yeh, Yu-Lan / Chen, Ming-Cheng / Huang, Chih-Yang

Journal of cellular biochemistry

2023 Volume 124, Issue 4, Page(s) 619–632

Abstract: Resistance to chemotherapy is the deadlock in cancer treatment. In this study, we used wild-type LOVO ( ... ...

Abstract	Resistance to chemotherapy is the deadlock in cancer treatment. In this study, we used wild-type LOVO (LOVO
MeSH term(s)	Humans ; Oxaliplatin/pharmacology ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Cell Line, Tumor ; Colonic Neoplasms/drug therapy ; Colonic Neoplasms/genetics ; Colonic Neoplasms/metabolism ; Drug Resistance, Neoplasm
Chemical Substances	Oxaliplatin (04ZR38536J) ; Antineoplastic Agents ; Tumor Suppressor Protein p53
Language	English
Publishing date	2023-03-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.30394
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Zs.A 1114: Show issues

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Article ; Online: Doxorubicin induced ROS-dependent HIF1α activation mediates blockage of IGF1R survival signaling by IGFBP3 promotes cardiac apoptosis.

Wen, Su-Ying / Ali, Ayaz / Huang, I-Chieh / Liu, Jian-Sheng / Chen, Po-Yuan / Padma Viswanadha, Vijaya / Huang, Chih-Yang / Kuo, Wei-Wen

Aging

2023 Volume 15, Issue 1, Page(s) 164–178

Abstract: Doxorubicin (Dox) causes the generation of intracellular reactive oxygen species (ROS) and inactivates insulin-like growth factor 1 (IGF1) signaling, leading to cardiomyocyte apoptosis. IGF-binding protein 3 (IGFBP3) is the most abundant circulating IGF1 ...

Abstract	Doxorubicin (Dox) causes the generation of intracellular reactive oxygen species (ROS) and inactivates insulin-like growth factor 1 (IGF1) signaling, leading to cardiomyocyte apoptosis. IGF-binding protein 3 (IGFBP3) is the most abundant circulating IGF1 carrier protein with high affinity, which has been reported to mediate ROS-induced apoptosis. Hypoxia-inducible factor 1α (HIF1A), an upstream protein of IGFBP3 is regulated by prolyl hydroxylase domain (PHD) through hydroxylation. In this study, we investigated the role of IGFBP3, HIF1A, and PHD in Dox-induced cardiac apoptosis.Cells challenged with 1 μM Dox for 24 h increased ROS generation, augmented intracellular and secreted IGFBP3 levels, and reduced IGF1 signaling. Further, we showed that Dox enhanced the extracellular association of IGF1 with IGFBP3. Moreover, echocardiography parameters, especially ejection fraction (EF) and fractional shortening (FS) were significantly reduced in ventricle tissue of Dox challenged rats. Notably, siRNA approach against IGFBP3 or an anti-IGFBP3 antibody rescued Dox-induced cardiac apoptosis, mitochondrial ROS, and the decrease in the IGF1 signaling activity. Furthermore, silencing HIF1A either using siRNA or inhibitor downregulated intracellular IGFBP3, rescued apoptosis, mitochondrial generation, and reduction in IGF1 signaling. Finally, western blot data revealed that ROS scavenger reversed Dox-induced cardiac apoptosis, increased levels of HIF1A and secreted IGFBP3, and decreased IGF1 survival signaling and PHD expression.These findings suggest that Dox-induced ROS generation suppressed PHD, which might stabilize nuclear HIF1A protein, leading to increased IGFBP3 expression and secretion. This in turn results in enhanced extracellular association of the latter with IGF1 and blocks IGF1 pro-survival signaling and may result in inducing cardiac apoptosis.
MeSH term(s)	Animals ; Rats ; Apoptosis ; Doxorubicin/pharmacology ; Insulin-Like Growth Factor Binding Protein 3/genetics ; Insulin-Like Growth Factor Binding Protein 3/metabolism ; Myocytes, Cardiac/metabolism ; Reactive Oxygen Species/metabolism ; RNA, Small Interfering/metabolism
Chemical Substances	Doxorubicin (80168379AG) ; Insulin-Like Growth Factor Binding Protein 3 ; Reactive Oxygen Species ; RNA, Small Interfering ; Hif1a protein, rat ; Igf1r protein, rat
Language	English
Publishing date	2023-01-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.204466
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Article ; Online: Activation of PI3K/Akt mediates the protective effect of diallyl trisulfide on doxorubicin induced cardiac apoptosis.

Wen, Su-Ying / Ng, Shang-Chuan / Ho, Wen-Kun / Huang, Han-Zhe / Huang, Chih-Yang / Kuo, Wei-Wen

Current research in toxicology

2023 Volume 5, Page(s) 100136

Abstract: Diallyl trisulfide (DATS), an organosulfide compound derived from garlic, is renowned for its potent antioxidant properties, particularly in countering the generation of reactive oxygen species (ROS). It has also gained recognition as a potential agent ... ...

Abstract	Diallyl trisulfide (DATS), an organosulfide compound derived from garlic, is renowned for its potent antioxidant properties, particularly in countering the generation of reactive oxygen species (ROS). It has also gained recognition as a potential agent for preventing heart-related conditions. Doxorubicin (Dox), a commonly used chemotherapeutic drug, is known to induce severe cardiac complications by promoting ROS production. Therefore, it was imperative to investigate whether DATS possesses cardioprotective capabilities against Dox-induced cardiac apoptosis and elucidate the underlying mechanisms. In this study, we observed that the intracellular ROS levels and cardiac apoptosis were heightened in H9c2 cells exposed to Dox (1 μM). However, treatment with 10 μM DATS effectively mitigated the Dox-induced ROS generation and apoptotic signaling, concurrently activating the PI3K/Akt pathway. Notably, the anti-apoptotic effects of DATS were attenuated when PI3K siRNA and the LY294002 PI3K inhibitor were employed. Furthermore, the TUNEL assay results demonstrated a significant reduction in Dox-induced apoptosis with DATS treatment. In summary, our findings indicate that DATS can activate the PI3K/Akt pathway, reducing ROS production in cardiac cells exposed to Dox, and subsequently rescue cardiac cells from apoptosis.
Language	English
Publishing date	2023-11-11
Publishing country	Netherlands
Document type	Journal Article
ISSN	2666-027X
ISSN (online)	2666-027X
DOI	10.1016/j.crtox.2023.100136
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Article ; Online: Paeoniflorin found in Paeonia lactiflora root extract inhibits melanogenesis by regulating melanin-related signal transduction in B16F10 cells.

Wen, Su-Ying / Wu, Ya-Shian / Liu, Hsun / Ng, Shang-Chuan / Padma, Viswanadha Vijaya / Huang, Chih-Yang / Kuo, Wei-Wen

Journal of cosmetic dermatology

2023 Volume 22, Issue 10, Page(s) 2824–2830

Abstract: Background: Skin pigmentation is modulated by various processes, with melanogenesis playing a key role. Melanin is synthesized by the catalysis of melanogenesis-related enzymes, such as tyrosinase and tyrosine-related proteins TRP-1 and TRP-2. ... ...

Abstract	Background: Skin pigmentation is modulated by various processes, with melanogenesis playing a key role. Melanin is synthesized by the catalysis of melanogenesis-related enzymes, such as tyrosinase and tyrosine-related proteins TRP-1 and TRP-2. Paeoniflorin is the main bioactive component of Paeonia suffruticosa Andr., Paeonia lactiflora., or Paeonia veitchii Lynch and has been used for centuries for its anti-inflammatory, anti-oxidant, and anti-carcinogenic properties. Aims & methods: In this study, melanin biosynthesis in mouse melanoma (B16F10) cells was induced using α-melanocyte-stimulating hormone (α-MSH), and then cells were co-treated with paeoniflorin to evaluate its potential anti-melanogenic effect. Results: α-MSH stimulation increased melanin content, tyrosinase activity, and melanogenesis-related markers in a dose-dependent manner. However, treatment with paeoniflorin reversed α-MSH-induced upregulation of melanin content and tyrosinase activity. Furthermore, paeoniflorin inhibited cAMP response element-binding protein activation and TRP-1, TRP-2, and microphthalmia-associated transcription factor protein expression in α-MSH-stimulated B16F10 cells. Conclusion: Overall, these findings show the potential of paeoniflorin as a depigmenting agent for cosmetic products.
MeSH term(s)	Animals ; Mice ; Melanins ; Monophenol Monooxygenase ; Paeonia ; alpha-MSH/pharmacology ; alpha-MSH/metabolism ; Signal Transduction ; Antioxidants/pharmacology
Chemical Substances	Melanins ; Monophenol Monooxygenase (EC 1.14.18.1) ; peoniflorin (21AIQ4EV64) ; alpha-MSH (581-05-5) ; Antioxidants
Language	English
Publishing date	2023-06-08
Publishing country	England
Document type	Journal Article
ZDB-ID	2280551-5
ISSN	1473-2165 ; 1473-2130
ISSN (online)	1473-2165
ISSN	1473-2130
DOI	10.1111/jocd.15789
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Zs.A 6539: Show issues

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Article ; Online: PKC-δ-dependent mitochondrial ROS attenuation is involved as 9-OAHSA combats lipoapotosis in rat hepatocytes induced by palmitic acid and in Syrian hamsters induced by high-fat high-cholesterol high-fructose diet.

Loh, Ching-Hui / Kuo, Wei-Wen / Lin, Shinn-Zong / Shih, Cheng-Yen / Lin, Pi-Yu / Situmorang, Jiro Hasegawa / Huang, Chih-Yang

Toxicology and applied pharmacology

2023 Volume 470, Page(s) 116557

Abstract: Metabolic-associated fatty liver disease (MAFLD) is a global concern, often undetected until reaching an advanced stage. Palmitic acid (PA) is a type of fatty acid that increases and leads to liver apoptosis in MAFLD. However, there is currently no ... ...

Abstract	Metabolic-associated fatty liver disease (MAFLD) is a global concern, often undetected until reaching an advanced stage. Palmitic acid (PA) is a type of fatty acid that increases and leads to liver apoptosis in MAFLD. However, there is currently no approved therapy or compound for MAFLD. Recently, branched fatty acid esters of hydroxy fatty acids (FAHFAs), a group of bioactive lipids, have emerged as promising agents to treat associated metabolic diseases. This study utilizes one type of FAHFA, oleic acid ester of 9-hydroxystearic acid (9-OAHSA), to treat PA-induced lipoapoptosis in an in vitro MAFLD model using rat hepatocytes and a high-fat high-cholesterol high-fructose (HFHCHFruc) diet in Syrian hamsters. The results indicate that 9-OAHSA rescues hepatocytes from PA-induced apoptosis and attenuates lipoapoptosis and dyslipidemia in Syrian hamsters. Additionally, 9-OAHSA decreases the generation of mitochondrial reactive oxygen species (mito-ROS) and stabilizes the mitochondrial membrane potential in hepatocytes. The study also demonstrates that the effect of 9-OAHSA on mito-ROS generation is at least partially mediated by PKC-δ signaling. These findings suggest that 9-OAHSA shows promise as a therapy for MAFLD.
MeSH term(s)	Cricetinae ; Rats ; Animals ; Palmitic Acid/toxicity ; Reactive Oxygen Species/metabolism ; Mesocricetus ; Fructose/toxicity ; Hepatocytes ; Fatty Acids/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; Cholesterol/metabolism ; Diet, High-Fat/adverse effects
Chemical Substances	Palmitic Acid (2V16EO95H1) ; Reactive Oxygen Species ; Fructose (30237-26-4) ; Fatty Acids ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2023-05-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1016/j.taap.2023.116557
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Article ; Online: Corrigendum to "PKC-δ-dependent mitochondrial ROS attenuation is involved as 9-OAHSA combats lipoapotosis in rat hepatocytes induced by palmitic acid and in Syrian hamsters induced by high-fat high-cholesterol high-fructose diet" [Toxicology and Applied Pharmacology, 470, (2023), 116557].

Loh, Ching-Hui / Kuo, Wei-Wen / Lin, Shinn-Zong / Shih, Cheng-Yen / Lin, Pi-Yu / Situmorang, Jiro Hasegawa / Huang, Chih-Yang

Toxicology and applied pharmacology

2023 Volume 476, Page(s) 116658

Language	English
Publishing date	2023-08-19
Publishing country	United States
Document type	Published Erratum
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1016/j.taap.2023.116658
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