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Artykuły w czasopismach na temat „WISP3”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

Kutz, Wendy E., Yaoqin Gong, and Matthew L. Warman. "WISP3, the Gene Responsible for the Human Skeletal Disease Progressive Pseudorheumatoid Dysplasia, Is Not Essential for Skeletal Function in Mice." Molecular and Cellular Biology 25, no. 1 (2005): 414–21. http://dx.doi.org/10.1128/mcb.25.1.414-421.2005.

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ABSTRACT In humans, loss-of-function mutations in WISP3 cause the autosomal recessive skeletal disease progressive pseudorheumatoid dysplasia (PPD) (Online Mendelian Inheritance in Man database number 208230). WISP3 encodes Wnt1-inducible signaling protein 3, a cysteine-rich, multidomain, secreted protein, whose paralogous CCN (connective tissue growth factor/cysteine-rich protein 61/nephroblastoma overexpressed) family members have been implicated in diverse biologic processes including skeletal, vascular, and neural development. To understand the role of WISP3 in the skeleton, we targeted th

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2

Pojskic, Lejla, Ismet Gavrankapetanovic, Naida Lojo-Kadric, Rifat Hadziselimovic, and Kasim Bajrovic. "A genotyping assay for missense mutation in WISP3 gene associated with childhood onset pseudorheumatoid arthropathy." Journal of Health Sciences 5, no. 2 (2015): 59–64. http://dx.doi.org/10.17532/jhsci.2015.241.

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Introduction: Progressive pseudorheumatoid dysplasia (PPD) is an autosomal recessive genetic disorder reported to be caused by gene alterations of the Wnt1-inducible signaling pathway protein 3 corresponding gene (WISP3) located on chromosome position 6q22. Up to date, there is only a handful of WISP3 mutations identified in Europe, whereas most mutations are identified in Asia and Middle East. According to our knowledge, this is the first report of genetic dissection of WISP3 associated with spondyloepiphyseal dysplasia tarda from Bosnia and Herzegovina. Based on clinical examination findings

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3

Wu, Qunfeng, Marda Jorgensen, Joanna Song, Junmei Zhou, Chen Liu, and Liya Pi. "Members of the Cyr61/CTGF/NOV Protein Family: Emerging Players in Hepatic Progenitor Cell Activation and Intrahepatic Cholangiocarcinoma." Gastroenterology Research and Practice 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/2313850.

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Hepatic stem/progenitor cells (HPC) reside quiescently in normal biliary trees and are activated in the form of ductular reactions during severe liver damage when the replicative ability of hepatocytes is inhibited. HPC niches are full of profibrotic stimuli favoring scarring and hepatocarcinogenesis. The Cyr61/CTGF/NOV (CCN) protein family consists of six members, CCN1/CYR61, CCN2/CTGF, CCN3/NOV, CCN4/WISP1, CCN5/WISP2, and CCN6/WISP3, which function as extracellular signaling modulators to mediate cell-matrix interaction during angiogenesis, wound healing, fibrosis, and tumorigenesis. This s

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4

Repudi, S. R., M. Patra, and M. Sen. "WISP3-IGF1 interaction regulates chondrocyte hypertrophy." Journal of Cell Science 126, no. 7 (2013): 1650–58. http://dx.doi.org/10.1242/jcs.119859.

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5

Leask, Andrew. "CCN6 (WISP3): a new anti-cancer therapy?" Journal of Cell Communication and Signaling 4, no. 4 (2010): 199–200. http://dx.doi.org/10.1007/s12079-010-0106-y.

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6

Yi, Yang, Jun Ma, Lu Jianrao, Hangqing Wang, and Yingdan Zhao. "WISP3 prevents fibroblast–myofibroblast transdifferentiation in NRK-49F cells." Biomedicine & Pharmacotherapy 99 (March 2018): 306–12. http://dx.doi.org/10.1016/j.biopha.2018.01.005.

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7

Cui, Rong-Rong, Jiao Huang, Lu Yi, et al. "WISP3 suppresses insulin-like growth factor signaling in human chondrocytes." Molecular and Cellular Endocrinology 279, no. 1-2 (2007): 1–8. http://dx.doi.org/10.1016/j.mce.2007.08.007.

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8

Bhavani, Gandham SriLakshmi, Hitesh Shah, Ashwin B. Dalal, et al. "Novel and recurrent mutations in WISP3 and an atypical phenotype." American Journal of Medical Genetics Part A 167, no. 10 (2015): 2481–84. http://dx.doi.org/10.1002/ajmg.a.37164.

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9

Mahadevan, S., B. Navaneethan, N. Gopalakrishnapillai Syamala, M. Mamadapur, R. S, and T. Tn. "AB0779 CAN INFLAMMATION COEXIST IN PATIENTS WITH PROGRESSIVE PSEUDORHEUMATOID DYSPLASIA?" Annals of the Rheumatic Diseases 80, Suppl 1 (2021): 1415.4–1416. http://dx.doi.org/10.1136/annrheumdis-2021-eular.3480.

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Background:Progressive pseudorheumatoid dysplasia(PPRD) is considered as a degenerative genetic bone disorder. It is caused by loss of function mutation in WNT-1 inducible signaling pathway protein-3(WISP-3)1. WISP-3 gene function is required for the normal function of cartilage and skeletal development. The patients are normal at birth and start developing symptoms around 3-6 years of age2. The disease is characterised by stiffness, pain, deformity due to enlargement of the ends of short and long bones. Often, such patients are misdiagnosed as Juvenile idiopathic arthritis(JIA). In general, P

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10

Ulutaş, Alptekin, Dragiša Stanujkić, Darjan Karabašević, Gabrijela Popović, and Srđan Novaković. "Pallet truck selection with MEREC and WISP-S methods." Strategic Management, no. 00 (2022): 13. http://dx.doi.org/10.5937/straman2200013u.

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Background: The article presents an MCDM model based on the MEREC and WISPS methods for pallet truck selection. Purpose: The main purpose of the study was to apply a new MCDM model for pallet truck selection in the textile workshop. Study design/methodology/approach: This article presents a simplified adoption of the Simple Weighted Sum Product (WISP) method, the Simplified WISP (WISP-S) method. The proposed method has fewer computation steps than the regular WISP method. In addition, this study proposes a new hybrid MCDM model in the literature by combining the MEREC method and the WISPS meth

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11

Kleer, Celina G., Yanhong Zhang, Quintin Pan, et al. "WISP3 is a novel tumor suppressor gene of inflammatory breast cancer." Oncogene 21, no. 20 (2002): 3172–80. http://dx.doi.org/10.1038/sj.onc.1205462.

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12

Tran, Mai N., and Celina G. Kleer. "Matricellular CCN6 (WISP3) protein: a tumor suppressor for mammary metaplastic carcinomas." Journal of Cell Communication and Signaling 12, no. 1 (2018): 13–19. http://dx.doi.org/10.1007/s12079-018-0451-9.

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13

Hashimoto, Yasunobu. "Effect of Wnt signaling protein (Wisp2/CCN5) on angiogenesis and invasion in prostate cancer." Journal of Clinical Oncology 30, no. 5_suppl (2012): 227. http://dx.doi.org/10.1200/jco.2012.30.5_suppl.227.

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227 Background: The Wnt-Induced Signaling Protein-2 (Wisp-2 /CCN5) is a secreted protein implicated in modification of extracellular matrix, invasion, and angiogenesis. The regulation of Wisp-2 and its function in CaP is poorly explored although it is highly expressed in advanced CaP cells. We discovered recently that a pro-inflammatory chemokine, Interleukin-8 (IL-8) strongly modulates Wisp2 expression in CaP cells. Since IL-8 is a major effecter of inflammatory pathway, we investigated the physiological consequence of Wisp-2 modulation in CaP cells. We hypothesised that Wisp-2 is a down-stre

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14

Hashimoto, Yasunobu, Rajendra Singh, and Bal L. Lokeshwar. "Effect of Wnt-1 induced signaling protein-2 (Wisp-2/CCN5) on angiogenesis and invasion in prostate cancer." Journal of Clinical Oncology 31, no. 6_suppl (2013): 164. http://dx.doi.org/10.1200/jco.2013.31.6_suppl.164.

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164 Background: The Wnt-Induced Signaling Protein-2 (Wisp-2/CCN5) is a secreted protein implicated in modification of extracellular matrix, invasion, and angiogenesis. The regulation of Wisp-2 and its function in CaP is poorly explored although it is highly expressed in advanced CaP cells. We discovered recently that a pro-inflammatory chemokine, Interleukin-8 (IL-8) strongly modulates Wisp2 expression in CaP cells. Since chronic inflammation is thought to be significant in CaP metastasis and IL-8 is a major effecter of inflammatory pathway, we investigated the physiological consequence of Wis

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15

Hurvitz, Jennifer R., Wafaa M. Suwairi, Wim Van Hul, et al. "Mutations in the CCN gene family member WISP3 cause progressive pseudorheumatoid dysplasia." Nature Genetics 23, no. 1 (1999): 94–98. http://dx.doi.org/10.1038/12699.

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16

Sen, Malini, Yu-Ho Cheng, Mary B. Goldring, Martin K. Lotz, and Dennis A. Carson. "WISP3-dependent regulation of type II collagen and aggrecan production in chondrocytes." Arthritis & Rheumatism 50, no. 2 (2004): 488–97. http://dx.doi.org/10.1002/art.20005.

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17

Robotham, A. S. G., J. C. J. D’Silva, R. A. Windhorst, et al. "Dynamic Wisp Removal in JWST NIRCam Images." Publications of the Astronomical Society of the Pacific 135, no. 1050 (2023): 085003. http://dx.doi.org/10.1088/1538-3873/acea42.

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Abstract The James Webb Space Telescope (JWST) near-infrared camera has been found to exhibit serious wisp-like structures in four of its eight short-wavelength detectors. The exact structure and strength of these wisps is highly variable with the position and orientation of JWST, so the use of static templates is non-optimal. Here we investigate a dynamic strategy to mitigate these wisps using long-wavelength reference images. Based on a suite of experiments where we embed a worst-case scenario median-stacked wisp into wisp-free images, we define suitable parameters for our wisp removal strat

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18

Chowdhury, Md Faizul Islam, Shamima Sharmin Shova, Afia Zahin Monami, Rajibul Alam, and M. Ekhlasur Rahman. "Progressive pseudo-rheumatoid dysplasia -a rare genetic disorder: Case Report." Anwer Khan Modern Medical College Journal 13, no. 1 (2021): 52–55. http://dx.doi.org/10.3329/akmmcj.v13i1.64730.

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Progressive pseudorheumatoid dysplasia (PPRD), also known as spondyloepiphyseal dysplasia tarda with progressive arthropathy (SEDT-PA), is an autosomal recessive disorder, resulting from mutations in the WNT1-inducible signaling pathway protein 3 (WISP3) gene involving the axial skeleton as well as small peripheral joints. Because of rarity here we present a case of 14-year-old boy, 1st issue of consanguineous parents who was presented with pain & gradual development of contracture in 3rd distal interphalangeal joint of right hand when he was 4-year-old, then gradual involvement of other i

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19

Yu, Xiaofu, Ruoying Mao, Wei Feng, et al. "WISP3 suppresses ESCC progression by inhibiting the IGF-2-IGF1R-AKT signaling cascade." Experimental Cell Research 409, no. 1 (2021): 112871. http://dx.doi.org/10.1016/j.yexcr.2021.112871.

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20

Huang, Wei, Emily E. Martin, Boris Burman, Maria E. Gonzalez, and Celina G. Kleer. "The matricellular protein CCN6 (WISP3) decreases Notch1 and suppresses breast cancer initiating cells." Oncotarget 7, no. 18 (2016): 25180–93. http://dx.doi.org/10.18632/oncotarget.7734.

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21

Kleer, Celina G., Yanhong Zhang, and Sofia D. Merajver. "CCN6 (WISP3) as a New Regulator of the Epithelial Phenotype in Breast Cancer." Cells Tissues Organs 185, no. 1-3 (2007): 95–99. http://dx.doi.org/10.1159/000101308.

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22

Nakamura, Yukio, Yajun Cui, Carol Fernando, Wendy E. Kutz, and Matthew L. Warman. "Normal growth and development in mice over-expressing the CCN family member WISP3." Journal of Cell Communication and Signaling 3, no. 2 (2009): 105–13. http://dx.doi.org/10.1007/s12079-009-0040-z.

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23

Luo, Haiyang, Changhe Shi, Chengyuan Mao, et al. "A novel compound WISP3 mutation in a Chinese family with progressive pseudorheumatoid dysplasia." Gene 564, no. 1 (2015): 35–38. http://dx.doi.org/10.1016/j.gene.2015.03.029.

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24

Tanaka, Shinji, Keishi Sugimachi, Shin-Ichiro Maehara, Mitsuo Shimada, and Yoshihiko Maehara. "A loss of function mutation in WISP3 derived from microsatellite unstable gastric carcinoma." Gastroenterology 125, no. 5 (2003): 1563–64. http://dx.doi.org/10.1016/j.gastro.2003.04.013.

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25

Patel, Chandreshkumar, Anas M. Khanshour, David Wilkes, et al. "Novel homozygous variant in WISP3 in a family with unrecognized progressive pseudorheumatoid dysplasia." Clinical Case Reports 8, no. 8 (2020): 1452–57. http://dx.doi.org/10.1002/ccr3.2884.

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26

Miller, Dustyn S., and Malini Sen. "Potential role of WISP3 (CCN6) in regulating the accumulation of reactive oxygen species." Biochemical and Biophysical Research Communications 355, no. 1 (2007): 156–61. http://dx.doi.org/10.1016/j.bbrc.2007.01.114.

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Outrequin, Antoine, Julie Manon, Amaury Paulmier, Dan Putineanu, Pierre-Louis Docquier, and Olivier Cornu. "Multiple Joint Replacements for Progressive Pseudorheumatoid Dysplasia: A Case Report." Journal of Orthopaedic Case Reports 14, no. 4 (2024): 18–23. http://dx.doi.org/10.13107/jocr.2024.v14.i04.4344.

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Introduction: Progressive pseudorheumatoid dysplasia is a rare autosomal recessive disorder caused by a mutation in the Wnt1-inducible signaling protein 3 gene, with few cases reported. Case Report: We discuss the case of a 19-year-old Caucasian male patient with polyarticular involvement, including shoulders, elbows, wrists, hands, spine, hips, knees, and notably the ankles. Despite a well-conducted medical treatment, due to the rapid progression of his condition, the patient underwent bilateral total hip and knee arthroplasties, as well as left ankle replacement. Conclusion: This case report

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28

Schütze, Norbert, Rita Schenk, Jörg Fiedler, Thomas Mattes, Franz Jakob, and Rolf E. Brenner. "CYR61/CCN1 and WISP3/CCN6 are chemoattractive ligands for human multipotent mesenchymal stroma cells." BMC Cell Biology 8, no. 1 (2007): 45. http://dx.doi.org/10.1186/1471-2121-8-45.

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Sun, Jing, Weibo Xia, Shuli He, et al. "Novel and Recurrent Mutations of WISP3 in Two Chinese Families with Progressive Pseudorheumatoid Dysplasia." PLoS ONE 7, no. 6 (2012): e38643. http://dx.doi.org/10.1371/journal.pone.0038643.

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Lee, Ju Hwa, Youn Jin Choi, Eun Mi Je, Ho Shik Kim, Nam Jin Yoo, and Sug Hyung Lee. "Frameshift mutation of WISP3 gene and its regional heterogeneity in gastric and colorectal cancers." Human Pathology 50 (April 2016): 146–52. http://dx.doi.org/10.1016/j.humpath.2015.12.009.

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Song, Dandan, Liang Wang, Ke Su, Huanhuan Wu та Junli Li. "WISP1 aggravates cell metastatic potential by abrogating TGF-β-Smad2/3-dependent epithelial-to-mesenchymal transition in laryngeal squamous cell carcinoma". Experimental Biology and Medicine 246, № 11 (2021): 1244–52. http://dx.doi.org/10.1177/1535370221992703.

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Laryngeal squamous cell cancer (LSCC) is a common carcinoma with high morbidity and mortality. Metastasis constitutes the major cause of death and poor prognosis among patients with LSCC. Recent evidence confirms critical function of Wnt1-inducible signaling protein 1 (WISP1) in several cancers. However, its contribution in LSCC metastasis remains unclear. Specimens of tumor tissues and adjacent normal mucosa were collected from patients with LSCC. The mRNA and protein levels were determined using quantitative real-time PCR and Western blot, respectively. RNA interference was applied to silenc

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32

Babenko, L. I. "ON THE MANUFACTURE TECHNIQUE OF PSEUDO-TWISTED WISPS OF THE PECTORAL FROM THE TOVSTA MOHYLA BARROW." Archaeology and Early History of Ukraine 42, no. 1 (2022): 19–32. http://dx.doi.org/10.37445/adiu.2022.01.01.

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The pectoral from the Tovsta Mohyla is an astonishing artifact which gathered different technical ways of Hellenic jewelry art. During this jewelry, which is composed of more than 160 details, a few dozens of different technical operations had been used. Till that time the less understood thing is a complex of ways that have been used by a craftsman during manufacturing of four pseudo-twisted hollow wisps, that framed figured pectoral friezes. None of the proposed reconstructions doesn’t give clear understanding on the most important elements of the technologic process of manufacture of the wi

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33

Nakamura, Yukio, Gilbert Weidinger, Jennifer O. Liang, et al. "The CCN family member Wisp3, mutant in progressive pseudorheumatoid dysplasia, modulates BMP and Wnt signaling." Journal of Clinical Investigation 117, no. 10 (2007): 3075–86. http://dx.doi.org/10.1172/jci32001.

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34

Liu, Limin, Nan Li, Zhen Zhao, Wei Li, and Weibo Xia. "Novel WISP3 mutations causing spondyloepiphyseal dysplasia tarda with progressive arthropathy in two unrelated Chinese families." Joint Bone Spine 82, no. 2 (2015): 125–28. http://dx.doi.org/10.1016/j.jbspin.2014.10.005.

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35

Riaz, Maira, Zubair Khoso, Versha Rani Rai, Misbah Iqbal Hanif, Mohsina Noor Ibrahim, and Syed Jamal Raza. "A RARE SKELETAL DYSPLASIA-CLOSE MIMICKER OF JUVENILE IDIOPATHIC ARTHRITIS-PROGRESSIVE PSEUDORHEUMATOID DYSPLASIA." Journal of Ayub Medical College Abbottabad 34, no. 4(SUPPL 1) (2022): 1050–52. http://dx.doi.org/10.55519/jamc-04-s4-10897.

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Progressive pseudorheumatoid dysplasia or spondyloepiphyseal dysplasia tarda is caused by a mutation in Wnt1 inducible signalling pathway protein 3 (WISP3) and passes in an autosomal recessive manner. Prevalence underestimated as one per million and most of the cases remain undiagnosed or treated as Juvenile Idiopathic Arthritis (JIA). Differentiation between JIA and PPRD is really challenging however, this case is genetically confirmed from our country. 7-year-old, short stature boy, with multiple joint swellings of hands and feet, initially suspected to have JIA and had been worked up and to

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Kleer, Celina G., Yanhong Zhang, Quintin Pant, and Sofia D. Merajver. "WISP3 (CCN6) Is a Secreted Tumor-Suppressor Protein that Modulates IGF Signaling in Inflammatory Breast Cancer." Neoplasia 6, no. 2 (2004): 179–85. http://dx.doi.org/10.1593/neo.03316.

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YU, YAFEN, MAN HU, XUESHA XING, et al. "Identification of a mutation in the WISP3 gene in three unrelated families with progressive pseudorheumatoid dysplasia." Molecular Medicine Reports 12, no. 1 (2012): 419–25. http://dx.doi.org/10.3892/mmr.2015.3430.

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Gao, Hong, Fen‐Fen Yin, Dong‐Xian Guan та ін. "Liver cancer: WISP3 suppresses hepatocellular carcinoma progression by negative regulation of β‐catenin/TCF/LEF signalling". Cell Proliferation 52, № 3 (2019): e12583. http://dx.doi.org/10.1111/cpr.12583.

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Yue, Hua, Zhen-Lin Zhang, and Jin-Wei He. "Identification of novel mutations in WISP3 gene in two unrelated Chinese families with progressive pseudorheumatoid dysplasia." Bone 44, no. 4 (2009): 547–54. http://dx.doi.org/10.1016/j.bone.2008.11.005.

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Hann, Steven, Laura Kvenvold, Brittney N. Newby, Minh Hong, and Matthew L. Warman. "A Wisp3 Cre-knockin Allele Produces Efficient Recombination in Spermatocytes during Early Prophase of Meiosis I." PLoS ONE 8, no. 9 (2013): e75116. http://dx.doi.org/10.1371/journal.pone.0075116.

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Chouery, Eliane, Sandra Corbani, Jaleleddine Dahmen, et al. "Progressive pseudorheumatoid dysplasia in North and West Africa: Clinical description in ten patients with mutations of WISP3." Egyptian Journal of Medical Human Genetics 18, no. 3 (2017): 299–303. http://dx.doi.org/10.1016/j.ejmhg.2016.11.004.

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Zhou, Hou-De, Yan-Hong Bu, Hui Xie, Yi-Qun Peng, Min Wan, and Er-Yuan Liao. "Cellular and molecular responses in progressive pseudorheumatoid dysplasia articular cartilage associated with compound heterozygous WISP3 gene mutation." Bone 43 (October 2008): S48. http://dx.doi.org/10.1016/j.bone.2008.08.030.

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Zhou, Hou-De, Yan-Hong Bu, Yi-Qun Peng, et al. "Cellular and molecular responses in progressive pseudorheumatoid dysplasia articular cartilage associated with compound heterozygous WISP3 gene mutation." Journal of Molecular Medicine 85, no. 9 (2007): 985–96. http://dx.doi.org/10.1007/s00109-007-0193-2.

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Paciejewska, Maja Maria, Marijke Maijenburg, Christian Gilissen, et al. "Differential Effects of Wnt Signaling on Proliferation and Hematopoietic Support of Adult and Fetal Bone Marrow-Derived MSCs." Blood 124, no. 21 (2014): 5137. http://dx.doi.org/10.1182/blood.v124.21.5137.5137.

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Abstract Human adult bone marrow-derived mesenchymal stromal cells MSC (ABMSC) are increasingly applied in the clinic to decrease graft versus host disease and to enhance hematopoietic recovery. Fetal bone marrow-derived MSC (FBMSC) display similar immune suppressive and regenerative capacities as adult MSC, and have been transplanted into patients. The proliferation capacity of FBMSC, however, is much larger than that of ABMSC. The aim of our studies is to understand the molecular mechanism of proliferation and hematopoietic support by MSC to optimize the expansion of functional MSC for clini

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45

Lorenzatti, G., W. Huang, A. Pal, A. M. Cabanillas, and C. G. Kleer. "CCN6 (WISP3) decreases ZEB1-mediated EMT and invasion by attenuation of IGF-1 receptor signaling in breast cancer." Journal of Cell Science 124, no. 10 (2011): 1752–58. http://dx.doi.org/10.1242/jcs.084194.

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Huang, Wei, Maria E. Gonzalez, Kathy A. Toy, Mousumi Banerjee, and Celina G. Kleer. "Blockade of CCN6 (WISP3) Activates Growth Factor–Independent Survival and Resistance to Anoikis in Human Mammary Epithelial Cells." Cancer Research 70, no. 8 (2010): 3340–50. http://dx.doi.org/10.1158/0008-5472.can-09-4225.

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47

Jiang, Nan, Yu Wang, Zhiqiang Yu, et al. "WISP3 (CCN6) Regulates Milk Protein Synthesis and Cell Growth Through mTOR Signaling in Dairy Cow Mammary Epithelial Cells." DNA and Cell Biology 34, no. 8 (2015): 524–33. http://dx.doi.org/10.1089/dna.2015.2829.

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Barcus, Craig E., and Gregory D. Longmore. "Collagen Linearization within Tumors." Cancer Research 81, no. 22 (2021): 5611–12. http://dx.doi.org/10.1158/0008-5472.can-21-2939.

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Abstract It is now well appreciated that the tumor microenvironment (TME) surrounding primary tumors impacts tumor growth, progression (invasion and migration), and response to therapy. Broadly speaking, the TME is composed of cells (immune cells, activated fibroblasts, adipocytes, endothelial cells), acellular extracellular matrix (ECM), and cytokines or growth factors, some of which are bound or tethered to the ECM proteins. All these compartments undergo significant changes during tumor development and progression. Changes to the ECM, in particular, can dramatically influence cancer biology

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Stinebring, D. R., K. M. Becker, J. E. Espinoza Goodman, et al. "A (new) Phenomenon in Pulsar Dynamic Spectra." International Astronomical Union Colloquium 177 (2000): 559–60. http://dx.doi.org/10.1017/s0252921100060619.

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AbstractSeveral studies in the last decade have explored dramatic instances of refractive fringing in dynamic spectra. We draw attention to a subtler but more widespread refractive effect: wisp-like structures extending (either linearly or with curvature) outward from the origin in the secondary spectrum plane. We have employed a simple pinhole screen simulation to investigate this phenomenon. It appears that the presence of one or more wisps in a secondary spectrum indicates a clump of scattering material that is significantly offset from the optical axis. Unlike the dramatic fringing events

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Batsali, Aristea, Charalampos Pontikoglou, Emmanuel Agrafiotis, et al. "Emerging Roles of Wisp-1 and SFRP4 in Proliferation and Differentiation Potential of Wharton's Jelly Mesenchymal Stem/Stromal Cells." Blood 124, no. 21 (2014): 4375. http://dx.doi.org/10.1182/blood.v124.21.4375.4375.

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Abstract We have previously shown (Batsali A et al., Blood 2013:122, 1212) that ex vivo expanded human mesenchymal stem/stromal cells (MSCs) derived from the Wharton's jelly (WJ) of the umbilical cord exhibit increased proliferative capacity and reduced potential to differentiate in vitro to adipocytes and osteocytes, compared to bone marrow (BM) derived-MSCs. Provided that the WNT-pathways are involved in proliferation and differentiation of BM-MSCs, we assumed that the aforementioned findings might be attributed, at least in part, to aberrant WNT-signaling in WJ-MSCs. In support of this hypo

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