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[PMID]: 29524899
[Au] Autor:Barbosa APM; Méndez-Fernandez P; Dias PS; Santos MCO; Taniguchi S; Montone RC
[Ad] Address:Laboratório de Química Orgânica Marinha, Instituto Oceanográfico, Universidade de São Paulo, São Paulo, SP 05508-120, Brazil.
[Ti] Title:Transplacental transfer of persistent organic pollutants in La Plata dolphins (Pontoporia blainvillei; Cetartiodactyla, Pontoporiidae).
[So] Source:Sci Total Environ;631-632:239-245, 2018 Mar 07.
[Is] ISSN:1879-1026
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Persistent organic pollutants (POPs) accumulate in the fat tissue of living organisms and are found in relatively high concentrations in animals at the top of the food chain, such as dolphins. The ability of these compounds to interact with the endocrine system of marine mammals constitutes a risk for the reproduction and conservation of species. The La Plata dolphin, Pontoporia blainvillei, is exclusive to the southwestern Atlantic Ocean and is classified on the IUCN red list as a vulnerable species. Blubber, liver, kidney and muscle samples from four P. blainvillei mother-fetus pairs were analyzed to evaluate the transfer of POPs to fetal tissues through the placenta. The presence of POPs in fetal tissues indicates the maternal transfer of compounds. In the pregnant females, blubber was the tissue with POP highest concentration, followed by the liver, kidneys and muscles. In the fetuses, POP accumulation mainly occurred in the blubber followed by the muscles, liver and kidneys. Polychlorinated biphenyls (PCBs) and dichlorodiphenyltrichloroethane (DDTs) were found in all tissues analyzed and had the highest concentrations among all compounds. The main PCB congeners in the fetal samples had five to seven chlorine atoms. The only polybrominated diphenyl ether (PBDE) in the fetal samples was 47 and was found only in blubber. The main DDT metabolite in the fetuses was p,p'-DDE. POP transfer via the placenta occurs in the first months of gestation and increases with fetal development, according to fetus/mother (F/M) ratio: HCB>DDT>PCB>PBDE>Mirex, which may follow the order of the octanol/water partition coefficient (K ) values.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524898
[Au] Autor:McGrew AK; O'Hara TM; Stricker CA; Salman MD; Van Bonn W; Gulland FMD; Whiting A; Ballweber LR
[Ad] Address:Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO, USA. Electronic address: ashley.mcgrew@colostate.edu.
[Ti] Title:Ecotoxicoparasitology of the gastrointestinal tracts of pinnipeds: the effect of parasites on the potential bioavailability of total mercury (THg).
[So] Source:Sci Total Environ;631-632:233-238, 2018 Mar 07.
[Is] ISSN:1879-1026
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Acanthocephalans, cestodes, and some species of nematodes acquire nutrients from the lumen contents in the gastrointestinal (GI) tract of their definitive host. These parasites are exposed to toxicants, such as mercury (Hg), through passive or active feeding mechanisms; therefore, the focus of this study was to determine if there is an effect of parasites on the dietary availability of total mercury (THg) within piscivorous pinniped hosts. THg concentrations ([THg]) in selected host tissues, parasites, and GI lumen contents from 22 California sea lions (Zalophus californianus), 15 ringed seals (Phoca hispida), and 4 spotted seals (Phoca largha) were determined. Among all pinnipeds, [THg] in acanthocephalans of the large intestine were significantly higher than concentrations in other samples (host lumen contents, other parasites and host intestinal wall), irrespective of location within the host GI tract. δ N values of parasites depended both on parasite group and location within the GI tract. δ N values were consistently higher in parasites inhabiting the large intestine, compared to elsewhere in the GI tract, for both sea lions and seals. δ C values in parasites did not differ significantly from host GI tissues. Based on both [THg] and stable isotope values, parasites are likely affecting the Hg bioavailability within the GI lumen contents and host tissues, and toxicant-parasite interactions appear to depend on both parasitic taxon as well as their location within the host intestine.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524886
[Au] Autor:Shan Z; An N; Qin J; Yang J; Sun H; Yang W
[Ad] Address:Clinical Laboratory, Children's Hospital Affiliated to Zhengzhou University, Henan Children's Hospital, Zhengzhou Children's Hospital, Zhengzhou City, Henan Province, China.
[Ti] Title:Long non-coding RNA Linc00675 suppresses cell proliferation and metastasis in colorectal cancer via acting on miR-942 and Wnt/ß-catenin signaling.
[So] Source:Biomed Pharmacother;101:769-776, 2018 Mar 07.
[Is] ISSN:1950-6007
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Substantial evidence has demonstrated the involvement of long non-coding RNAs (lncRNAs) in the development and progression of colorectal cancer (CRC) via their regulation on cancer cell proliferation, apoptosis, invasion and metastasis pathways. The current study aimed to understand the role of lncRNA Linc00675 in the progression and metastasis of CRC and to identify the potential lncRNA-miRNA interactions and signaling pathways underlying the mechanisms of action of Linc00675 in CRC. Our data firstly demonstrated the down-regulation of Linc00675 in both CRC cells and clinical CRC tissues. Expression of Linc00675 was also relatively low in metastatic tumors and advanced tumors. Further studies also showed that overexpression of Linc00675 inhibited the proliferation, invasion and migration of CRC cells. In addition, our data also revealed the negative regulation of miR-942 by Linc00675 and the relatively higher expression of miR-942 in clinical CRC tissues. More importantly, the inhibitory effect of Linc00675 on proliferation, invasion and migration of HCT116 cells was also significantly attenuated in the presence of miR-942 mimic, suggesting that down-regulation of miR-942 represented one of the mechanisms by which Linc00675 inhibited the proliferation and metastasis of CRC. Furthermore, we also demonstrated the inhibition of Wnt/ß-catenin signaling in the Linc00675/miR-942 regulated pathway in CRC cells. Taken together, our findings suggested Linc00675 as a potential molecular marker and target for the diagnosis and treatment of CRC and enhanced the current understanding on the mechanisms of action of Linc00675 in CRC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524885
[Au] Autor:Chen Q; Wu S; Wu Y; Chen L; Pang Q
[Ad] Address:Department of Orthopaedics Surgery, Ningbo No. 2 Hospital, Ningbo 315010, Zhejiang, People's Republic of China.
[Ti] Title:MiR-149 suppresses the inflammatory response of chondrocytes in osteoarthritis by down-regulating the activation of TAK1/NF-κB.
[So] Source:Biomed Pharmacother;101:763-768, 2018 Mar 07.
[Is] ISSN:1950-6007
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:BACKGROUND: Osteoarthritis (OA) is a degenerative joint disease that with the complication of disability, while inflammation is the important response of OA. MiR-149 was down-regulated in the OA tissues, while the potential mechanism of miR-149 in OA is unclear. METHODS: A total of 20 OA patients and 20 healthy persons were enrolled in the present study. Real-time PCR was used to detect miR-149 and the mRNA expression of TAK1, western blot was used to detect the protein expression of TAK1. Luciferase reporter assay was performed to identify the targeting relationship between miR-149 and TAK1. Elisa assay was used to identify the level of several pro-inflammatory cytokines. RESULTS: MiR-149 was down-regulated in both OA tissues and IL-1ß-induced chondrocytes, while the expression of TAK1 was opposite. TAK1 was the target gene miR-149 targets TAK1 to regulate its expression. Human normal chondrocytes subjected to IL-1ß significantly promoted the inflammatory response, and also accelerated the activation of NF-κB signaling pathway, while alternatively si-TAK1, miR-149 mimic or PDTC reversed the effects of IL-1ß. Cells transfected with miR-149 inhibitor promotes the level of inflammation cytokines, as well as the activation of NF-κB, while cells co-transfected with si-TAK1 and miR-149 inhibitor abolishes the effects of miR-149 inhibitor. CONCLUSION: MiR-149 targets TAK1 to regulate the pathogenesis of OA, among which TAK1/NF-κB signaling acted as an important pathway in the inflammatory response that induced by IL-1ß.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 927739 MEDLINE  
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[PMID]: 29524745
[Au] Autor:Camuri IJ; Costa AB; Ito AS; Pazin WM
[Ad] Address:Department of Physics, Faculty of Philosophy, Sciences and Letters of Ribeirão Preto, University of São Paulo (USP), Ribeirão Preto, SP, Brazil.
[Ti] Title:Optical absorption and fluorescence spectroscopy studies of Artepillin C, the major component of green propolis.
[So] Source:Spectrochim Acta A Mol Biomol Spectrosc;198:71-77, 2018 Feb 23.
[Is] ISSN:1873-3557
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The bioactivity of propolis against several pathogens is well established, leading to the extensive consumption of that bee product to prevent diseases. Brazilian green propolis, collected by the species Apis mellifera, is one of the most consumed in the world. The chemical composition of green propolis is complex and it has been shown that it displays antioxidant, antimicrobial, anti-inflammatory and antitumor activities, especially due to the high content of Artepillin C. The molecule is a derivative of cinnamic acid with two prenylated groups, responsible for the improvement of the affinity of the compound for lipophilic environment. A carboxylic group (COOH) is also present in the molecule, making it a pH-sensitive compound and the pH-dependent structure of Artepillin C, may modulate its biological activity related to interactions with the cellular membrane of organisms and tissues. Molecular properties of Artepillin C on aqueous solution were examined by optical absorption, steady state and time-resolved fluorescence spectroscopies. Acid-base titration based on the spectral position of the near UV absorption band, resulted in the pKa value of 4.65 for the carboxylic group in Artepillin C. In acidic pH, below the pKa value, an absorption band raised around 350nm at Artepillin C concentration above 50µM, due to aggregation of the molecule. In neutral pH, with excitation at 310nm, Artepillin C presents dual emission at 400 and 450nm. In pH close to the pKa, the optical spectra show contribution from both protonated and deprotonated species. A three-exponential function was necessary to fit the intensity decays at the different pHs, dominated by a very short lifetime component, around 0.060ns. The fast decay resulted in emission before fluorescence depolarization, and in values of fluorescence anisotropy higher than could be expected for monomeric forms of the compound. The results give fundamental knowledge about the protonation-deprotonation state of the molecule, that may be relevant in processes mediated by biological membranes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 927739 MEDLINE  
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[PMID]: 29524675
[Au] Autor:Hu Y; Ran J; Zheng Z; Jin Z; Chen X; Yin Z; Tang C; Chen Y; Huang J; Le H; Yan R; Zhu T; Wang J; Lin J; Xu K; Zhou Y; Zhang W; Cai Y; Dominique P; Chin Heng B; Chen W; Shen W; Ouyang HW
[Ad] Address:Dr. Li Dak Sum & Yip Yio Chin Center for Stem Cell and Regenerative Medicine, Zhejiang University, Zhejiang, 310000, China; Key Laboratory of Tissue Engineering and Regenerative Medicine of Zhejiang Province, School of Medicine, Zhejiang University, China; Department of Sports Medicine, School o
[Ti] Title:Exogenous stromal derived factor-1 releasing silk scaffold combined with intra-articular injection of progenitor cells promotes Bone-Ligament-Bone regeneration.
[So] Source:Acta Biomater;, 2018 Mar 07.
[Is] ISSN:1878-7568
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Anterior cruciate ligament (ACL) is one of the most difficult tissues to heal once injured. Ligament regeneration and tendon-bone junction healing are two major goals of ACL reconstruction. This study aimed to investigate the synergistic therapeutic effects of Stromal cell-derived factor 1(SDF-1)-releasing collagen-silk (CSF) scaffold combined with intra-articular injection of ligament-derived stem/progenitor cells (LSPCs) for ACL regeneration and the amelioration in the long-term complication of osteoarthritis (OA). The stem cell recruitment ability of CSF scaffold and the multipotency, particularly the tendon forming ability of LSPCs from rabbits were characterized in vitro, while the synergistic effect of the CSF scaffold and LSPCs for ACL regeneration and OA amelioration were investigated in vivo at 1, 3, and 6 months with a rabbit ACL reconstruction model. The CSF scaffold was used as a substitute for the ACL, and LSPCs were injected into the joint cavity after 7 days of the ACL reconstruction. CSF scaffold displayed a controlled release pattern for the encapsulated protein for up to 7 days with an increased stiffness in the mechanical property. LSPCs, which exhibited highly I Collagen and CXCR4 expression, were attracted by SDF-1 and successfully relocated into the CSF scaffold at 1 month in vivo. At 3 and 6 months post-treatment, the CSF scaffold combined with LSPCs (CSFL group) enhanced the regeneration of ACL tissue, and promoted bone tunnel healing. Furthermore, the OA progression was impeded efficiently. Our findings here provided a new strategy that using stem cell recruiting CSF scaffold with tissue-specific stem cells, could be a promising solution for ACL regeneration. SIGNIFICANCE: In this study, we developed a silk scaffold with increased stiffness and SDF-1 controlled release capacity for ligament repair. This advanced scaffold transplantation combined with intra-articular injection of LSPCs (which was isolated from rabbit ligament for the first time in this study) promoted the regeneration of both the tendinous and bone tunnel portion of ACL. This therapeutic strategy also ameliorated cartilage degeneration and reduced the severity of arthrofibrosis. Hence, combining LSPCs injection with SDF-1-releasing silk scaffold is demonstrated as a therapeutic strategy for ACL regeneration and OA treatment in the clinic.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 927739 MEDLINE  
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[PMID]: 29524672
[Au] Autor:Ma B; Han J; Zhang S; Liu F; Wang S; Duan J; Sang Y; Jiang H; Li D; Ge S; Yu J; Liu H
[Ad] Address:State Key Laboratory of Crystal Materials, Shandong University, Jinan, Shandong, 250100, China.
[Ti] Title:Hydroxyapatite Nanobelt/Polylactic Acid Janus Membrane with Osteoinduction/Barrier Dual Functions for Precise Bone Defect Repair.
[So] Source:Acta Biomater;, 2018 Mar 07.
[Is] ISSN:1878-7568
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Controllable osteoinduction maintained in the original defect area is the key to precise bone repair. To meet the requirement of precise bone regeneration, a hydroxyapatite (HAp) nanobelt/polylactic acid (PLA) (HAp/PLA) Janus membrane has been successfully prepared in this study by coating PLA on a paper-like HAp nanobelt film by a casting-pervaporation method. The Janus membrane possesses dual functions: excellent osteoinduction from the hydrophilic HAp nanobelt side and barrier function originating from the hydrophobic PLA film. The cell viability and osteogenic differentiation ability of human adipose-derived stem cells (hADSCs) on the Janus membrane were assessed. The in vitro experimental results prove that the HAp nanobelt side presents high cell viability and efficient osteoinduction without any growth factor and that the PLA side can prohibit cell attachment. The in vivo repair experiments on a rat mandible defect model prove that the PLA side can prevent postoperative adhesion between bone and adjacent soft tissues. Most importantly, the HAp side has a strong ability to promote defect repair and bone regeneration. Therefore, the HAp/PLA Janus membrane will have wide applications as a kind of tissue engineering material in precise bone repair because of its unique dual osteoinduction/barrier functions, biocompatibility, low cost, and its ability to be mass-produced. STATE OF SIGNIFICANCE: Precise bone defect repair to keeping tissue integrity and original outline shape is a very important issue for tissue engineering. Here, we have designed and prepared a novel HAp/PLA Janus membrane using a casting-pervaporation method to form a layer of PLA film on paper-like HAp nanobelt film. HAp nanobelt side of the Janus membrane can successfully promote osteogenic differentiation. PLA side of the Janus membrane exhibits good properties as a barrier for preventing the adhesion of cells in vitro. Mandible repair experiments in vivo have shown that the HAp/PLA Janus membrane can promote rat mandible repair on the HAp side and can successfully prevent postoperative adhesion on the PLA side at the same time. Therefore, the HAp/PLA Janus membrane with its osteoinduction/barrier dual functions can be applied to repair bone defect precisely.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  8 / 927739 MEDLINE  
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[PMID]: 29524631
[Au] Autor:Wang H; Sun W; Sun M; Fu Z; Zhou C; Wang C; Zuo D; Zhou Z; Wang G; Zhang T; Xu J; Chen J; Wang Z; Yin F; Duan Z; Hornicek FJ; Cai Z; Hua Y
[Ad] Address:Department of Orthopedics, Shanghai General Hospital, School of Medicine Shanghai Jiao Tong University, Shanghai, China; Shanghai Bone Tumor Institution, Shanghai, China; Department of Orthopedics, Yangpu Hospital, Tongji University, Shanghai, China.
[Ti] Title:HER4 promotes cell survival and chemoresistance in osteosarcoma via interaction with NDRG1.
[So] Source:Biochim Biophys Acta;, 2018 Mar 07.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Osteosarcoma (OS) is the most common primary malignant bone tumor in children and adolescents. The abilities of chemotherapy resistance are major roadblock in the successful treatment of OS. The clarification of mechanism regarding cell survival during OS chemotherapy are important. Here, we examined HER4 expression by immunohistochemistry in a large series of OS tissues, and found HER4 expression correlated with tumor characteristics and patient survival rates. HER4 knockdown by shRNA inhibited OS cell growth and tumorigenesis, and induced cell senescence and apoptosis in vitro and in vivo. We demonstrated that HER4 expression upregulated in the adverse conditions, such as serum starvation and sphere culture. Moreover, HER4 knockdown cells became more sensitive in stressful conditions such as loss of attachment, cytotoxic agents or nutrition insufficiency. Mechanism studies revealed that HER4 interacted with NDRG1, and NDRG1 overexpression could antagonize HER4 knockdown-mediated cell growth and apoptosis in stressed conditions. There was a positive correlation between HER4 and NDRG1 immunoreactivity in OS patients. Together, our present study shows that HER4 and/or NDRG might play a critical role for the cell survival and chemo-resistance of OS, and could be used as potential therapeutic targets in OS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 927739 MEDLINE  
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[PMID]: 29524628
[Au] Autor:Gabriel Enge T; Ecroyd H; Jolley DF; Yerbury JJ; Kalmar B; Dosseto A
[Ad] Address:Wollongong Isotope Geochronology Laboratory and School of Earth and Environmental Sciences, University of Wollongong, Australia. Electronic address: tge571@uowmail.edu.au.
[Ti] Title:Assessment of metal concentrations in the SOD1 mouse model of amyotrophic lateral sclerosis and its potential role in muscular denervation, with particular focus on muscle tissue.
[So] Source:Mol Cell Neurosci;, 2018 Mar 07.
[Is] ISSN:1095-9327
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Amyotrophic lateral sclerosis (ALS) is among the most common of the motor neuron diseases, and arguably the most devastating. During the course of this fatal neurodegenerative disorder, motor neurons undergo progressive degeneration. The currently best-understood animal models of ALS are based on the over-expression of mutant isoforms of Cu/Zn superoxide dismutase 1 (SOD1); these indicate that there is a perturbation in metal homeostasis with disease progression. Copper metabolism in particular is affected in the central nervous system (CNS) and muscle tissue. METHODS: This present study assessed previously published and newly gathered concentrations of transition metals (Cu, Zn, Fe and Se) in CNS (brain and spinal cord) and non-CNS (liver, intestine, heart and muscle) tissues from transgenic mice over-expressing the G93A mutant SOD1 isoform (SOD1 ), transgenic mice over-expressing wildtype SOD1 (SOD1 ) and non-transgenic controls. RESULTS: Cu accumulates in non-CNS tissues at pre-symptomatic stages in SOD1 tissues. This accumulation represents a potentially pathological feature that cannot solely be explained by the over-expression of mSOD1. As a result of the lack of Cu uptake into the CNS there may be a deficiency of Cu for the over-expressed mutant SOD1 in these tissues. Elevated Cu concentrations in muscle tissue also preceded the onset of symptoms and were found to be pathological and not be the result of SOD1 over-expression. CONCLUSIONS: It is hypothesized that the observed Cu accumulations may represent a pathologic feature of ALS, which may actively contribute to axonal retraction leading to muscular denervation, and possibly significantly contributing to disease pathology. Therefore, it is proposed that the toxic-gain-of-function and dying-back hypotheses to explain the molecular drivers of ALS may not be separate, individual processes; rather our data suggests that they are parallel processes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  10 / 927739 MEDLINE  
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[PMID]: 29524629
[Au] Autor:Craft CS; Broekelmann TJ; Mecham RP
[Ad] Address:Division of Bone and Mineral Research, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, United States.
[Ti] Title:Microfibril-associated glycoproteins MAGP-1 and MAGP-2 in disease.
[So] Source:Matrix Biol;, 2018 Mar 07.
[Is] ISSN:1569-1802
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Microfibril-associated glycoproteins 1 and 2 (MAGP-1, MAGP-2) are protein components of extracellular matrix microfibrils. These proteins interact with fibrillin, the core component of microfibrils, and impart unique biological properties that influence microfibril function in vertebrates. MAGPs bind active forms of TGFß and BMPs and are capable of modulating Notch signaling. Mutations in MAGP-1 or MAGP-2 have been linked to thoracic aneurysms and metabolic disease in humans. MAGP-2 has also been shown to be an important biomarker in several human cancers. Mice lacking MAGP-1 or MAGP-2 have defects in multiple organ systems, which reflects the widespread distribution of microfibrils in vertebrate tissues. This review summarizes our current understanding of the function of the MAGPs and their relationship to human disease.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher


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