Database : MEDLINE
Search on : pathologic and processes [Words]
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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

  2 / 10863 MEDLINE  
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[PMID]: 29438717
[Au] Autor:Zhang L; Zhang YJ; Chen J; Huang XL; Fang GS; Yang LJ; Duan Y; Wang J
[Ad] Address:Medical Genetics Center, Anhui Medical College, Hefei, China.
[Ti] Title:The association of HLA-B27 and Klebsiella pneumoniae in ankylosing spondylitis: A systematic review.
[So] Source:Microb Pathog;117:49-54, 2018 Feb 10.
[Is] ISSN:1096-1208
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Ankylosing spondylitis (AS) is a chronic inflammatory arthritis of unknown origin. Its autoimmune origin has been suggested but never proven. Several reports have implicated K. pneumoniae as a triggering or perpetuating factor in AS; and the HLA-B27 antigen has also been found in association with AS. But there is no satisfactory explanation of why the presence of HLA-B27 predisposes to AS and the precise role played by K. pneumoniae in the disease has not yet been clarified. However, various studies have shown that the results of molecular, immunological, and microbiological studies could establish the link between K. pneumoniae infections and HLA-B27 in the aetiopathogenesis of AS. In this review, we have examined the evidence linking the interaction between K. pneumoniae infections and HLA-B27 in AS, and tried to exploit the possible mechanisms by which K. pneumoniae infections might induce pathologic processes to develop novel diagnostic criteria. Finally, we have also summarized some dietary regimens that could be helpful in the therapeutic management of AS patients.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 10863 MEDLINE  
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[PMID]: 29506567
[Au] Autor:Wang JL; Yang MY; Xiao S; Sun B; Li YM; Yang LY
[Ad] Address:Liver Cancer Laboratory, Department of Surgery, Xiangya Hospital, Central South University, Xiangya Road 87, Changsha, Hunan, 410008, China.
[Ti] Title:Downregulation of castor zinc finger 1 predicts poor prognosis and facilitates hepatocellular carcinoma progression via MAPK/ERK signaling.
[So] Source:J Exp Clin Cancer Res;37(1):45, 2018 Mar 05.
[Is] ISSN:1756-9966
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Castor zinc finger 1 (CASZ1) plays critical roles in various biological processes and pathologic conditions, including cancer. However, the prognostic importance and biologic functions of CASZ1 in hepatocellular carcinoma (HCC) are still unclear. METHODS: qRT-PCR, western blot and immunohistochemistry analyses were used to determine CASZ1 expression in HCC samples and cell lines. The clinical significance of CASZ1 was assessed in two independent study cohorts containing 232 patients with HCC. A series of in vitro and in vivo experiments were performed to explore the role and molecular mechanism of CASZ1 in HCC progression. RESULTS: Here we report that CASZ1 expression was downregulated in HCC tissues and cell lines. Low CASZ1 expression was closely correlated with aggressive clinicopathological features, poor clinical outcomes and early recurrence of HCC patients. Moreover, overexpression of CASZ1 in HCCLM3 cells significantly inhibited cell proliferation, migration, invasion in vitro and tumor growth and metastasis in vivo, whereas silencing CASZ1 significantly enhanced the above abilities of PLC/PRF/5 cells. Further mechanism study indicated that these phenotypic changes were mediated by MAPK/ERK signaling pathway and involved altered expression of MMP2, MMP9 and cyclinD1. Finally, we proved that CASZ1 exerted its tumor-suppressive effect by directly interacting with RAF1 and reducing the protein stability of RAF1. CONCLUSIONS: Our study for the first time demonstrated that CASZ1 is a tumor suppressor in HCC, which may serve as a novel prognostic predictor and therapeutic target for HCC patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1186/s13046-018-0720-8

  4 / 10863 MEDLINE  
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[PMID]: 29280227
[Au] Autor:Rudie JD; Rauschecker AM; Nabavizadeh SA; Mohan S
[Ad] Address:Department of Radiology, Division of Neuroradiology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA.
[Ti] Title:Neuroimaging of Dilated Perivascular Spaces: From Benign and Pathologic Causes to Mimics.
[So] Source:J Neuroimaging;28(2):139-149, 2018 Mar.
[Is] ISSN:1552-6569
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Perivascular spaces (PVSs), also known as Virchow-Robin spaces, are pial-lined, fluid-filled structures found in characteristic locations throughout the brain. They can become abnormally enlarged or dilated and in rare cases can cause hydrocephalus. Dilated PVSs can pose a diagnostic dilemma for radiologists because of their varied appearance, sometimes mimicking more serious entities such as cystic neoplasms, including dysembryoplastic neuroepithelial tumor and multinodular and vacuolating neuronal tumor, or cystic infections including toxoplasmosis and neurocysticercosis. In addition, various pathologic processes, including cryptococcosis and chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids, can spread into the brain via PVSs, resulting in characteristic magnetic resonance imaging appearances. This review aims to describe the key imaging characteristics of normal and dilated PVSs, as well as cystic mimics and pathologic processes that directly involve PVSs.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1712
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1111/jon.12493

  5 / 10863 MEDLINE  
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[PMID]: 29203735
[Au] Autor:Shaprynskyi VO; Shaprinskiy YV; Karyi YV; Lysenko SA
[Ad] Address:Vinnitsa National Pirogov Memorial Medical University, Vinnitsa, Ukraine.
[Ti] Title:Histomorphologic changes of esophageal mucosa in experimental third degree stricture.
[So] Source:Wiad Lek;70(5):891-894, 2017.
[Is] ISSN:0043-5147
[Cp] Country of publication:Poland
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Nowadays the level of early and late complications after the operations for esophageal corrosive strictures such as esophago-organ anastomotic leak, development of infections, pneumonia, pleural empyema, mediastinitis, peritonitis, postoperative corrosive stricture development etc. remains rather high. Besides, postoperative mortality rate is high as well - 3.5-30 %. For that reason, an experimental model of esophageal stricture was suggested and ultrastructural mucosal changes in the stricture itself were studied to elaborate the unified pathogenic approach in treatment of esophageal stricture and improvement of its results. The aim of our work was to study the dynamics of ultrastructural changes both in normal esophageal walls and in third degree esophageal stricture Materials and Methods: The experiment was carried out on white male rats weighting 250-300 grams, to whom the third degree esophageal stricture model was created. After layer-by-layer incision of anterior abdominal wall abdominal portion of the esophagus was completely ligated (10 rats). In the control group (6 rats) anterior abdominal wall was opened with its subsequent layered closure. The animals were withdrawn from the experiment on the third day by ketamine overdose, and the samples were taken for ultrastructural study. RESULTS: Electron microscopic study of submicroscopic organization of basal, prickle, superficial epithelial cells in stratified non-squamous epithelium, smooth myocytes of muscle plate and contractile elements in esophageal muscular layer was carried out. Nuclear membrane, membranes of mitochondria, endoplasmic reticulum and cytoplasmic Golgi complex were found to be subjected to focal lysis. The third degree esophageal stricture caused destructive lesions in ultrastructural architectonics of stratified non-squamous epithelium cells, smooth myocytes of muscle plate and contractile elements in esophageal muscular layer of rats. CONCLUSION: Thus, catabolic processes leading to organelle disintegration develop in esophageal cells of rats with third degree stricture.
[Mh] MeSH terms primary: Esophageal Mucosa/ultrastructure
Esophageal Stenosis/pathology
Esophagus/ultrastructure
[Mh] MeSH terms secundary: Animals
Constriction, Pathologic/pathology
Disease Models, Animal
Esophageal Mucosa/pathology
Esophagus/pathology
Male
Microscopy, Electron
Rats
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:171206
[St] Status:MEDLINE

  6 / 10863 MEDLINE  
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[PMID]: 29513680
[Au] Autor:Wood PL; Tippireddy S; Feriante J; Woltjer RL
[Ad] Address:Metabolomics Unit, College of Veterinary Medicine, Lincoln Memorial University, Cumberland Gap Pkwy., Harrogate, TN, United States of America.
[Ti] Title:Augmented frontal cortex diacylglycerol levels in Parkinson's disease and Lewy Body Disease.
[So] Source:PLoS One;13(3):e0191815, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Research from our laboratory, and that of other investigators, has demonstrated augmented levels of diacylglycerols (DAG) in the frontal cortex and plasma of subjects with Alzheimer's disease (AD) and Mild Cognitive Impairment (MCI). We have extended these observations to investigate the frontal cortex of subjects with Parkinson's disease (PD) and Lewy Body Disease (LBD), with and without coexisting pathologic features of AD. METHODS/PRINCIPAL FINDINGS: Utilizing a high-resolution mass spectrometry analytical platform, we clearly demonstrate that DAG levels are significantly increased in the frontal cortex of subjects with PD, LBD with intermediate neocortical AD neuropathology, and in LBD with established neocortical AD neuropathology. In the case of the PD cohort, increases in cortical DAG levels were detected in cases with no neocortical pathology but were greater in subjects with neocortical pathology. These data suggest that DAG changes occur early in the disease processes and are amplified as cortical dysfunction becomes more established. CONCLUSIONS: These findings suggest that altered DAG synthesis/metabolism is a common feature of neurodegenerative diseases, characterized by proteinopathy, that ultimately result in cognitive deficits. With regard to the mechanism responsible for these biochemical alterations, selective decrements in cortical levels of phosphatidylcholines in LBD and PD suggest that augmented degradation and/or decreased synthesis of these structural glycerophospholipids may contribute to increases in the pool size of free DAGs. The observed augmentation of DAG levels may be phospholipase-driven since neuroinflammation is a consistent feature of all disease cohorts. If this conclusion can be validated it would support utilizing DAG levels as a biomarker of the early disease process and the investigation of early intervention with anti-inflammatory agents.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0191815

  7 / 10863 MEDLINE  
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[PMID]: 29411894
[Au] Autor:Xu Y; Lu X; Hu Y; Yang B; Tsui CK; Yu S; Lu L; Liang X
[Ad] Address:State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, Guangdong Province, China.
[Ti] Title:Melatonin attenuated retinal neovascularization and neuroglial dysfunction by inhibition of HIF-1α-VEGF pathway in oxygen-induced retinopathy mice.
[So] Source:J Pineal Res;, 2018 Feb 07.
[Is] ISSN:1600-079X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Retinopathy of prematurity (ROP) is a retinopathy characterized by retinal neovascularization (RNV) occurring in preterm infants treated with high concentrations of oxygen and may lead to blindness in severe cases. Currently, anti-VEGF therapy is a major treatment for ROP, but it is costly and may cause serious complications. The previous study has demonstrated that melatonin exerted neuroprotective effect against retinal ganglion cell death induced by hypoxia in neonatal rats. However, whether melatonin is anti-angiogenic and neuroglial protective in the progression of ROP remains unknown. Thus, this study was to investigate the effect of melatonin on RNV and neuroglia in the retina of oxygen-induced retinopathy (OIR) mice. The results showed a reduction in retinal vascular leakage in OIR mice after melatonin treatment. Besides, the size of retinal neovascular and avascular areas, the number of preretinal neovascular cell nuclei, and the number of proliferative vascular endothelial cells within the neovascular area were significantly decreased in mice treated with melatonin. After oxygen-induced injury, the density of astrocytes was decreased, accompanied by morphologic and functional changes of astrocytes. Besides, retinal microglia were also activated. Meanwhile, the levels of inflammatory factors were elevated. However, these pathologic processes were all hindered by melatonin treatment. Furthermore, HIF-1α-VEGF pathway was activated in the retina of OIR mice, yet was suppressed in melatonin-treated OIR mice retinas. In conclusion, melatonin prevented pathologic neovascularization, protected neuroglial cells, and exerts anti-inflammation effect via inhibition of HIF-1α-VEGF pathway in OIR retinas, suggesting that melatonin could be a promising therapeutic agent for ROP.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1111/jpi.12473

  8 / 10863 MEDLINE  
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[PMID]: 29431420
[Au] Autor:Xiao M; Man T; Zhu C; Pei H; Shi J; Li L; Qu X; Shen X; Li J
[Ad] Address:Department of Gastroenterology, Zhongshan Hospital , Fudan University , 180 Fenglin Rd. , Shanghai 200032 , China.
[Ti] Title:MoS Nanoprobe for MicroRNA Quantification Based on Duplex-Specific Nuclease Signal Amplification.
[So] Source:ACS Appl Mater Interfaces;10(9):7852-7858, 2018 Mar 07.
[Is] ISSN:1944-8252
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:MicroRNAs (miRNAs) play significant regulatory roles in physiologic and pathologic processes and are considered as important biomarkers for disease diagnostics and therapeutics. Simple, fast, sensitive, and selective detection of miRNAs, however, is challenged by their short length, low abundance, susceptibility to degradation, and homogenous sequence. Here, we report a novel design of nanoprobes for highly sensitive and selective detection of miRNAs based on MoS -loaded molecular beacons (MBs) and duplex-specific nuclease (DSN)-mediated signal amplification (DSNMSA). We show that MoS nanosheets not only exhibit high affinity toward MBs but also act as an efficient quencher for absorbed MBs. The strong fluorescence-quenching ability of MoS in combination with cyclic DSNMSA contributes to the superior sensitivity of our method, with a limit of detection 4 orders of magnitude lower than that of traditional hybridization methods. Moreover, the nanoprobes also show high selectivity for discriminating homogenous miRNA sequences with one-base differences because of the discrimination ability of MBs and DSN. Furthermore, we demonstrate that the MoS -loaded MB nanoprobes can be utilized for multiplexed detection of miRNAs. Given its high sensitivity and specificity, as well as the multiplexed function; this novel method as an effective tool shows a great promise for simultaneous quantitative analysis of multiple miRNAs in biomedical research and clinical diagnosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1021/acsami.7b18984

  9 / 10863 MEDLINE  
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[PMID]: 29471141
[Au] Autor:Wesseling M; Sakkers TR; de Jager SCA; Pasterkamp G; Goumans MJ
[Ad] Address:Laboratory of Experimental Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands; Laboratory of Clinical Chemistry and Histology, University Medical Center Utrecht, Utrecht, The Netherlands.
[Ti] Title:The morphological and molecular mechanisms of epithelial/endothelial-to-mesenchymal transition and its involvement in atherosclerosis.
[So] Source:Vascul Pharmacol;, 2018 Feb 20.
[Is] ISSN:1879-3649
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cell transdifferentiation occurs during cardiovascular development or remodeling either as a pathologic feature in the progression of disease or as a response to injury. Endothelial-to-Mesenchymal Transition (EndMT) is a process that is classified as a specialized form of Epithelial-to-Mesenchymal Transition (EMT), in which epithelial cells lose their epithelial characteristics and gain a mesenchymal phenotype. During transdifferentiation, cells lose both cell-cell contacts and their attachment to the basement membrane. Subsequently, the shape of the cells changes from a cuboidal to an elongated shape. A rearrangement of actin filaments facilitates the cells to become motile and prime their migration into the underlying tissue. EMT is a key process during embryonic development, wound healing and tissue regeneration, but has also been implicated in pathophysiological processes, such organ fibrosis and tumor metastases. EndMT has been associated with additional pathophysiological processes in cardiovascular related diseases, including atherosclerosis. Recent studies prove a significant role for EndMT in the progression and destabilization of atherosclerotic plaques, as a consequence of EndMT-derived fibroblast infiltration and the increased secretion of matrix metalloproteinase respectively. In this review we will discuss the essential molecular and morphological mechanisms of EMT and EndMT, along with their common denominators and key differences. Finally, we will discuss the role of EMT/EndMT in developmental and pathophysiological processes, focusing on the potential role of EndMT in atherosclerosis in more depth.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher

  10 / 10863 MEDLINE  
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[PMID]: 29454752
[Au] Autor:Löfdahl A; Wenglén C; Rydell-Törmänen K; Westergren-Thorsson G; Larsson-Callerfelt AK
[Ad] Address:Lung Biology, Department of Experimental Medical Science, Lund University, Lund, Sweden. Electronic address: anna.lofdahl@med.lu.se.
[Ti] Title:Effects of 5-Hydroxytryptamine Class 2 Receptor Antagonists on Bronchoconstriction and Pulmonary Remodeling Processes.
[So] Source:Am J Pathol;, 2018 Feb 16.
[Is] ISSN:1525-2191
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Serotonin [5-hydroxytryptamine (5-HT)] is associated with several chronic pulmonary diseases, recognizing 5-HT receptor antagonists as potential inhibitors of tissue remodeling. However, the effects of 5-HT receptors, especially 5-HT receptors on airway function and remodeling, are unclear. We investigated the role of 5-HT receptors on airway smooth muscle contractility and remodeling processes. Murine precision-cut lung slices were pretreated with 5-HT receptor antagonists (EXT5, EXT9, RS 127445, and PRX 08066), as well as ketanserin (5-HT receptor antagonist) (1, 10 µmol/L), before addition of cumulative concentrations of 5-HT to induce bronchoconstriction. Remodeling effects after treatment with 10 µmol/L 5-HT and 5-HT receptor antagonists were further studied in distal lung tissue by examining release of profibrotic transforming growth factor (TGF)-ß1 and proliferation of human bronchial smooth muscle cells (HBSMCs). 5-HT-induced bronchoconstriction was significantly reduced by EXT5, EXT9, and ketanserin, but not by RS 127445 or PRX 08066. The 5-HT receptor antagonists significantly reduced TGF-ß1 release. 5-HT, in combination with TGF-ß1, increased proliferation of HBSMCs, a process reduced by EXT5 and EXT9. Our results indicate that EXT5 and EXT9 may relieve bronchoconstriction in murine airways and serve as an add-on effect in attenuating pulmonary remodeling by improving airway function. The antiproliferative effect on HBSMCs and the inhibition of TGF-ß1 release further support a role of 5-HT receptors in pathologic remodeling processes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:Publisher


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