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Article ; Online: Modeling Fibrosis in Three-Dimensional Organoids Reveals New Epithelial Restraints on Fibroblasts.

Chanda, Diptiman / Thannickal, Victor J

American journal of respiratory cell and molecular biology

2019 Volume 61, Issue 5, Page(s) 556–557

MeSH term(s)	Bone Morphogenetic Proteins ; Fibroblasts ; Fibrosis ; Humans ; Lung ; Organoids
Chemical Substances	Bone Morphogenetic Proteins
Language	English
Publishing date	2019-06-24
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2019-0153ED
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Article ; Online: Integrated bioinformatics analysis identifies established and novel TGFβ1-regulated genes modulated by anti-fibrotic drugs.

Wilson, Ava C / Chiles, Joe / Ashish, Shah / Chanda, Diptiman / Kumar, Preeti L / Mobley, James A / Neptune, Enid R / Thannickal, Victor J / McDonald, Merry-Lynn N

Scientific reports

2022 Volume 12, Issue 1, Page(s) 3080

Abstract: Fibrosis is a leading cause of morbidity and mortality worldwide. Although fibrosis may involve different organ systems, transforming growth factor-β (TGFβ) has been established as a master regulator of fibrosis across organs. Pirfenidone and Nintedanib ... ...

Abstract	Fibrosis is a leading cause of morbidity and mortality worldwide. Although fibrosis may involve different organ systems, transforming growth factor-β (TGFβ) has been established as a master regulator of fibrosis across organs. Pirfenidone and Nintedanib are the only currently-approved drugs to treat fibrosis, specifically idiopathic pulmonary fibrosis, but their mechanisms of action remain poorly understood. To identify novel drug targets and uncover potential mechanisms by which these drugs attenuate fibrosis, we performed an integrative 'omics analysis of transcriptomic and proteomic responses to TGFβ1-stimulated lung fibroblasts. Significant findings were annotated as associated with pirfenidone and nintedanib treatment in silico via Coremine. Integrative 'omics identified a co-expressed transcriptomic and proteomic module significantly correlated with TGFβ1 treatment that was enriched (FDR-p = 0.04) with genes associated with pirfenidone and nintedanib treatment. While a subset of genes in this module have been implicated in fibrogenesis, several novel TGFβ1 signaling targets were identified. Specifically, four genes (BASP1, HSD17B6, CDH11, and TNS1) have been associated with pirfenidone, while five genes (CLINT1, CADM1, MTDH, SYDE1, and MCTS1) have been associated with nintedanib, and MYDGF has been implicated with treatment using both drugs. Using the Clue Drug Repurposing Hub, succinic acid was highlighted as a metabolite regulated by the protein encoded by HSD17B6. This study provides new insights into the anti-fibrotic actions of pirfenidone and nintedanib and identifies novel targets for future mechanistic studies.
MeSH term(s)	Adaptor Proteins, Vesicular Transport/genetics ; Adaptor Proteins, Vesicular Transport/metabolism ; Antifibrotic Agents/pharmacology ; Antifibrotic Agents/therapeutic use ; Cadherins/genetics ; Cadherins/metabolism ; Cell Adhesion Molecule-1/genetics ; Cell Adhesion Molecule-1/metabolism ; Computational Biology/methods ; Extracellular Matrix Proteins/physiology ; Female ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/genetics ; Humans ; Idiopathic Pulmonary Fibrosis/drug therapy ; Idiopathic Pulmonary Fibrosis/genetics ; Idiopathic Pulmonary Fibrosis/pathology ; Indoles/pharmacology ; Indoles/therapeutic use ; Interleukins/genetics ; Interleukins/metabolism ; Male ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Pyridones/pharmacology ; Pyridones/therapeutic use ; Racemases and Epimerases/genetics ; Racemases and Epimerases/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Tensins/genetics ; Tensins/metabolism ; Transforming Growth Factor beta/physiology
Chemical Substances	Adaptor Proteins, Vesicular Transport ; Antifibrotic Agents ; BASP1 protein, human ; CADM1 protein, human ; CLINT1 protein, human ; Cadherins ; Cell Adhesion Molecule-1 ; Extracellular Matrix Proteins ; Indoles ; Interleukins ; MYDGF protein, human ; Membrane Proteins ; Nerve Tissue Proteins ; Pyridones ; Repressor Proteins ; TNS1 protein, human ; Tensins ; Transforming Growth Factor beta ; betaIG-H3 protein (148710-76-3) ; osteoblast cadherin (156621-71-5) ; pirfenidone (D7NLD2JX7U) ; HSD17B6 protein, human (EC 5.1.-) ; Racemases and Epimerases (EC 5.1.-) ; nintedanib (G6HRD2P839)
Language	English
Publishing date	2022-02-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-07151-1
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Article: Fgf10 Signaling in Lung Development, Homeostasis, Disease, and Repair After Injury.

Yuan, Tingting / Volckaert, Thomas / Chanda, Diptiman / Thannickal, Victor J / De Langhe, Stijn P

Frontiers in genetics

2018 Volume 9, Page(s) 418

Abstract: The lung is morphologically structured into a complex tree-like network with branched airways ending distally in a large number of alveoli for efficient oxygen exchange. At the cellular level, the adult lung consists of at least 40-60 different cell ... ...

Abstract	The lung is morphologically structured into a complex tree-like network with branched airways ending distally in a large number of alveoli for efficient oxygen exchange. At the cellular level, the adult lung consists of at least 40-60 different cell types which can be broadly classified into epithelial, endothelial, mesenchymal, and immune cells. Fibroblast growth factor 10 (Fgf10) located in the lung mesenchyme is essential to regulate epithelial proliferation and lineage commitment during embryonic development and post-natal life, and to drive epithelial regeneration after injury. The cells that express
Language	English
Publishing date	2018-09-25
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2018.00418
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Article: Effects of Cellular Methylation on Transgene Expression and Site-Specific Integration of Adeno-Associated Virus.

Chanda, Diptiman / Hensel, Jonathan A / Higgs, Jerome T / Grover, Rajat / Kaza, Niroop / Ponnazhagan, Selvarangan

Genes

2017 Volume 8, Issue 9

Abstract: DNA methylation is a major epigenetic event that affects not only cellular gene expression but that also has the potential to influence bacterial and viral DNA in their host-dependent functions. Adeno-associated virus (AAV) genome contains a high degree ... ...

Abstract	DNA methylation is a major epigenetic event that affects not only cellular gene expression but that also has the potential to influence bacterial and viral DNA in their host-dependent functions. Adeno-associated virus (AAV) genome contains a high degree of CpG sequences capable of methylation in its terminal repeat sequences, which are the sole elements retained in AAV-based vectors used in gene therapy. The present study determined the influence of methylation status of the host cell on wild type (wt) AAV integration and recombinant (r) AAV transgene expression in HeLa cells. Results of the study indicated that hypo-methylation significantly enhanced both wtAAV chromosomal integration and transgene expression of rAAV. A direct influence of methylation on AAV integration was further confirmed by methylating the AAVS1 integration sites prior to viral infection with DNA trans-complementation assay. These results signify the importance of epigenetic status of target cells as one of the key factors in long-term transgene expression in AAV gene therapy.
Language	English
Publishing date	2017-09-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes8090232
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Article ; Online: Restoration of SIRT3 gene expression by airway delivery resolves age-associated persistent lung fibrosis in mice.

Rehan, Mohammad / Kurundkar, Deepali / Kurundkar, Ashish R / Logsdon, Naomi J / Smith, Samuel R / Chanda, Diptiman / Bernard, Karen / Sanders, Yan Y / Deshane, Jessy S / Dsouza, Kevin G / Rangarajan, Sunad / Zmijewski, Jaroslaw W / Thannickal, Victor J

Nature aging

2021 Volume 1, Issue 2, Page(s) 205–217

Abstract: Aging is a risk factor for progressive fibrotic disorders involving diverse organ systems, including the lung. Idiopathic pulmonary fibrosis, an age-associated degenerative lung disorder, is characterized by persistence of apoptosis-resistant ... ...

Abstract	Aging is a risk factor for progressive fibrotic disorders involving diverse organ systems, including the lung. Idiopathic pulmonary fibrosis, an age-associated degenerative lung disorder, is characterized by persistence of apoptosis-resistant myofibroblasts. In this report, we demonstrate that sirtuin-3 (SIRT3), a mitochondrial deacetylase, is downregulated in lungs of IPF human subjects and in mice subjected to lung injury. Over-expression of the SIRT3 cDNA via airway delivery restored capacity for fibrosis resolution in aged mice, in association with activation of the forkhead box transcription factor, FoxO3a, in fibroblasts, upregulation of pro-apoptotic members of the Bcl-2 family, and recovery of apoptosis susceptibility. While transforming growth factor-β1 reduced levels of SIRT3 and FoxO3a in lung fibroblasts, cell non-autonomous effects involving macrophage secreted products were necessary for SIRT3-mediated activation of FoxO3a. Together, these findings reveal a novel role of SIRT3 in pro-resolution macrophage functions that restore susceptibility to apoptosis in fibroblasts
MeSH term(s)	Humans ; Animals ; Mice ; Sirtuin 3/genetics ; Lung/metabolism ; Fibrosis ; Idiopathic Pulmonary Fibrosis/metabolism ; Gene Expression
Chemical Substances	Sirtuin 3 (EC 3.5.1.-) ; SIRT3 protein, human (EC 3.5.1.-)
Language	English
Publishing date	2021-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ISSN	2662-8465
ISSN (online)	2662-8465
DOI	10.1038/s43587-021-00027-5
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Article: Small Extracellular Vesicle Signaling and Mitochondrial Transfer Reprograms T Helper Cell Function in Human Asthma.

Hough, Kenneth P / Trevor, Jennifer L / Chacko, Balu K / Strenkowski, John G / Wang, Yong / Goliwas, Kayla F / Bone, Nathaniel B / Kim, Young-Il / Holmes, Renita / Vang, Shia / Pritchard, Alexandra / Chin, Jay / Bodduluri, Sandeep / Antony, Veena B / Tousif, Sultan / Athar, Mohammad S / Chanda, Diptiman / Mitra, Kasturi / Zmijewski, Jaroslaw /

Zhang, Jianhua / Duncan, Steven R / Thannickal, Victor J / Gabrielsson, Susanne / Darley-Usmar, Victor M / Deshane, Jessy S

bioRxiv : the preprint server for biology

2024

Abstract: Rationale: Asthma is a chronic inflammatory disease of the airways that involves crosstalk between myeloid-derived regulatory cells (MDRCs) and CD4+ T cells. Although small extracellular vesicles (sEVs) are known to mediate cell-cell communication, the ... ...

Abstract	Rationale: Asthma is a chronic inflammatory disease of the airways that involves crosstalk between myeloid-derived regulatory cells (MDRCs) and CD4+ T cells. Although small extracellular vesicles (sEVs) are known to mediate cell-cell communication, the role of sEV signaling via mitochondria in perpetuating asthmatic airway inflammation is unknown. Objectives: We investigated the effects of MDRC-derived exosomes on dysregulated T cell responses in asthmatics. Methods: Small extracellular vesicles isolated from bronchoalveolar lavage fluid or airway MDRCs of mild to moderate asthmatics or healthy controls were co-cultured with autologous peripheral and airway CD4+ T lymphocytes. sEV internalization, sEV-mediated transfer of mitochondria targeted GFP to T cells, sEV mitochondrial signaling, and subsequent activation, proliferation and polarization of CD4+ T lymphocytes to Th1, Th2 and Th17 subsets were assessed. Measurements and main results: Airway MDRC-derived sEVs from asthmatics mediated T cell receptor engagement and transfer of mitochondria that induced antigen-specific activation and polarization into Th17 and Th2 cells, drivers of chronic airway inflammation in asthma. CD4+ T cells internalized sEVs containing mitochondria predominantly by membrane fusion, and blocking mitochondrial oxidant signaling in MDRC-derived exosomes mitigated T cell activation. Reactive oxygen species-mediated signaling that elicited T cell activation in asthmatics was sEV-dependent. A Drp1-dependent mitochondrial fission in pro-inflammatory MDRCs promoted mitochondrial packaging within sEVs, which then co-localized with the polarized actin cytoskeleton and mitochondrial networks in the organized immune synapse of recipient T cells. Conclusions: Our studies indicate a previously unrecognized role for mitochondrial fission and exosomal mitochondrial transfer in dysregulated T cell activation and Th cell differentiation in asthma which could constitute a novel therapeutic target.
Language	English
Publishing date	2024-05-03
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.04.30.589227
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Article ; Online: Mitochondrial uncoupling protein-2 reprograms metabolism to induce oxidative stress and myofibroblast senescence in age-associated lung fibrosis.

Rangarajan, Sunad / Locy, Morgan L / Chanda, Diptiman / Kurundkar, Ashish / Kurundkar, Deepali / Larson-Casey, Jennifer L / Londono, Pilar / Bagchi, Rushita A / Deskin, Brian / Elajaili, Hanan / Nozik, Eva S / Deshane, Jessy S / Zmijewski, Jaroslaw W / Eickelberg, Oliver / Thannickal, Victor J

Aging cell

2022 Volume 21, Issue 9, Page(s) e13674

Abstract: Mitochondrial dysfunction has been associated with age-related diseases, including idiopathic pulmonary fibrosis (IPF). We provide evidence that implicates chronic elevation of the mitochondrial anion carrier protein, uncoupling protein-2 (UCP2), in ... ...

Abstract	Mitochondrial dysfunction has been associated with age-related diseases, including idiopathic pulmonary fibrosis (IPF). We provide evidence that implicates chronic elevation of the mitochondrial anion carrier protein, uncoupling protein-2 (UCP2), in increased generation of reactive oxygen species, altered redox state and cellular bioenergetics, impaired fatty acid oxidation, and induction of myofibroblast senescence. This pro-oxidant senescence reprogramming occurs in concert with conventional actions of UCP2 as an uncoupler of oxidative phosphorylation with dissipation of the mitochondrial membrane potential. UCP2 is highly expressed in human IPF lung myofibroblasts and in aged fibroblasts. In an aging murine model of lung fibrosis, the in vivo silencing of UCP2 induces fibrosis regression. These studies indicate a pro-fibrotic function of UCP2 in chronic lung disease and support its therapeutic targeting in age-related diseases associated with impaired tissue regeneration and organ fibrosis.
MeSH term(s)	Aged ; Animals ; Fibroblasts/metabolism ; Fibrosis ; Humans ; Idiopathic Pulmonary Fibrosis/metabolism ; Lung/metabolism ; Mice ; Myofibroblasts/metabolism ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Uncoupling Protein 2/genetics ; Uncoupling Protein 2/metabolism
Chemical Substances	Reactive Oxygen Species ; UCP2 protein, human ; Ucp2 protein, mouse ; Uncoupling Protein 2
Language	English
Publishing date	2022-08-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.13674
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Article ; Online: Developmental pathways in the pathogenesis of lung fibrosis.

Chanda, Diptiman / Otoupalova, Eva / Smith, Samuel R / Volckaert, Thomas / De Langhe, Stijn P / Thannickal, Victor J

Molecular aspects of medicine

2018 Volume 65, Page(s) 56–69

Abstract: Idiopathic pulmonary fibrosis (IPF) is a progressive and terminal lung disease with no known cure. IPF is a disease of aging, with median age of diagnosis over 65 years. Median survival is between 3 and 5 years after diagnosis. IPF is characterized ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is a progressive and terminal lung disease with no known cure. IPF is a disease of aging, with median age of diagnosis over 65 years. Median survival is between 3 and 5 years after diagnosis. IPF is characterized primarily by excessive deposition of extracellular matrix (ECM) proteins by activated lung fibroblasts and myofibroblasts, resulting in reduced gas exchange and impaired pulmonary function. Growing evidence supports the concept of a pro-fibrotic environment orchestrated by underlying factors such as genetic predisposition, chronic injury and aging, oxidative stress, and impaired regenerative responses may account for disease development and persistence. Currently, two FDA approved drugs have limited efficacy in the treatment of IPF. Many of the genes and gene networks associated with lung development are induced or activated in IPF. In this review, we analyze current knowledge in the field, gained from both basic and clinical research, to provide new insights into the disease process, and potential approaches to treatment of pulmonary fibrosis.
MeSH term(s)	Animals ; Biomarkers ; Cellular Microenvironment ; Disease Susceptibility ; Homeodomain Proteins/metabolism ; Humans ; Myofibroblasts/metabolism ; Pulmonary Fibrosis/etiology ; Pulmonary Fibrosis/metabolism ; Pulmonary Fibrosis/pathology ; Signal Transduction ; Stromal Cells ; Trans-Activators ; Transforming Growth Factor beta/metabolism
Chemical Substances	Biomarkers ; Homeodomain Proteins ; Trans-Activators ; Transforming Growth Factor beta ; pancreatic and duodenal homeobox 1 protein
Language	English
Publishing date	2018-08-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	197640-0
ISSN	1872-9452 ; 0098-2997
ISSN (online)	1872-9452
ISSN	0098-2997
DOI	10.1016/j.mam.2018.08.004
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Article ; Online: Mesenchymal stromal cell aging impairs the self-organizing capacity of lung alveolar epithelial stem cells.

Chanda, Diptiman / Rehan, Mohammad / Smith, Samuel R / Dsouza, Kevin G / Wang, Yong / Bernard, Karen / Kurundkar, Deepali / Memula, Vinayak / Kojima, Kyoko / Mobley, James A / Benavides, Gloria A / Darley-Usmar, Victor / Kim, Young-iL / Zmijewski, Jaroslaw W / Deshane, Jessy S / De Langhe, Stijn / Thannickal, Victor J

eLife

2021 Volume 10

Abstract: Multicellular organisms maintain structure and function of tissues/organs through emergent, self-organizing behavior. In this report, we demonstrate a critical role for lung mesenchymal stromal cell (L-MSC) aging in determining the capacity to form three- ...

Abstract	Multicellular organisms maintain structure and function of tissues/organs through emergent, self-organizing behavior. In this report, we demonstrate a critical role for lung mesenchymal stromal cell (L-MSC) aging in determining the capacity to form three-dimensional organoids or 'alveolospheres' with type 2 alveolar epithelial cells (AEC2s). In contrast to L-MSCs from aged mice, young L-MSCs support the efficient formation of alveolospheres when co-cultured with young or aged AEC2s. Aged L-MSCs demonstrated features of cellular senescence, altered bioenergetics, and a senescence-associated secretory profile (SASP). The reactive oxygen species generating enzyme, NADPH oxidase 4 (Nox4), was highly activated in aged L-MSCs and Nox4 downregulation was sufficient to, at least partially, reverse this age-related energy deficit, while restoring the self-organizing capacity of alveolospheres. Together, these data indicate a critical role for cellular bioenergetics and redox homeostasis in an organoid model of self-organization and support the concept of thermodynamic entropy in aging biology.
MeSH term(s)	Alveolar Epithelial Cells/metabolism ; Alveolar Epithelial Cells/physiology ; Animals ; Cells, Cultured ; Cellular Senescence/physiology ; Male ; Mesenchymal Stem Cells/metabolism ; Mesenchymal Stem Cells/physiology ; Mice ; NADPH Oxidase 4/genetics ; NADPH Oxidase 4/metabolism ; Organoids/cytology ; Organoids/metabolism ; Oxidative Stress
Chemical Substances	NADPH Oxidase 4 (EC 1.6.3.-) ; Nox4 protein, mouse (EC 1.6.3.-)
Language	English
Publishing date	2021-09-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.68049
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Article: Hormonal induction of ovulation stimulates atresia of antral follicles in a vespertilionid bat, Scotophilus heathi.

Chanda, Diptiman / Abhilasha / Krishna, Amitabh

Zoology (Jena, Germany)

2006 Volume 109, Issue 3, Page(s) 208–216

Abstract: Scotophilus heathi is a seasonally monoestrous subtropical vespertilionid bat found at Varanasi, India. Although the antral follicles remain present in the ovaries of S. heathi from November till March, ovulation is delayed in this species until early ... ...

Abstract	Scotophilus heathi is a seasonally monoestrous subtropical vespertilionid bat found at Varanasi, India. Although the antral follicles remain present in the ovaries of S. heathi from November till March, ovulation is delayed in this species until early March. In order to understand the mechanism of ovulation suppression during this period of delayed ovulation, the effects of human chorionic gonadotropin (hCG), pregnant mare's serum gonadotropin (PMSG), follicle stimulating hormone (FSH) and gonadotropin releasing hormone agonist (GnRH agonist) on ovarian morphology and steroid concentration were investigated. Hormonal treatments were given as a single i.p. dose 24 h after capture. The bats were sacrificed 48 h after the injection. Treatment with hCG, PMSG, FSH and GnRH agonist failed to induce ovulation in S. heathi, although these hormones produced a high degree of ovarian stimulation. The administration of hCG and PMSG induced ovarian enlargement, intense hyperemia, marked changes in the interstitial cells (ICs), development of several antral follicles and a varying degree of abnormalities in the oocytes of most of the antral follicles. In the bats treated with hCG, PMSG and GnRH agonist, androstenedione concentration increased significantly to extraordinarily high levels, whereas estradiol concentration decreased. Administration of FSH caused regression of ICs and pyknosis of granulosa cells in the majority of antral follicles. FSH did not enhance androstenedione concentration. The results of the present study suggest that the failure of hormonal treatments to induce ovulation during the period of delayed ovulation might be due to a seasonal desensitization of ovarian follicles in S. heathi. The hormonal treatment instead stimulated the ICs to produce a high level of androstenedione resulting in atretic changes of the antral follicles.
MeSH term(s)	Animals ; Chiroptera/physiology ; Chorionic Gonadotropin/pharmacology ; Female ; Follicle Stimulating Hormone/pharmacology ; Follicular Atresia/drug effects ; Follicular Atresia/physiology ; Gonadotropin-Releasing Hormone/agonists ; Gonadotropins, Equine/pharmacology ; India ; Oocytes/drug effects ; Ovary/cytology ; Ovary/drug effects ; Ovary/physiology ; Ovulation Induction/methods ; Radioimmunoassay ; Theca Cells/drug effects ; Theca Cells/metabolism
Chemical Substances	Chorionic Gonadotropin ; Gonadotropins, Equine ; Gonadotropin-Releasing Hormone (33515-09-2) ; Follicle Stimulating Hormone (9002-68-0)
Language	English
Publishing date	2006
Publishing country	Germany
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1191401-4
ISSN	1873-2720 ; 0944-2006
ISSN (online)	1873-2720
ISSN	0944-2006
DOI	10.1016/j.zool.2006.02.001
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