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[PMID]: 25865369
[Au] Autor:Kelly CJ; Zheng L; Campbell EL; Saeedi B; Scholz CC; Bayless AJ; Wilson KE; Glover LE; Kominsky DJ; Magnuson A; Weir TL; Ehrentraut SF; Pickel C; Kuhn KA; Lanis JM; Nguyen V; Taylor CT; Colgan SP
[Ad] Address:Mucosal Inflammation Program, University of Colorado, Aurora, CO 80045, USA; Department of Medicine, University of Colorado, Aurora, CO 80045, USA....
[Ti] Title:Crosstalk between Microbiota-Derived Short-Chain Fatty Acids and Intestinal Epithelial HIF Augments Tissue Barrier Function.
[So] Source:Cell Host Microbe;17(5):662-71, 2015 May 13.
[Is] ISSN:1934-6069
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Interactions between the microbiota and distal gut are fundamental determinants of human health. Such interactions are concentrated at the colonic mucosa and provide energy for the host epithelium through the production of the short-chain fatty acid butyrate. We sought to determine the role of epithelial butyrate metabolism in establishing the austere oxygenation profile of the distal gut. Bacteria-derived butyrate affects epithelial O2 consumption and results in stabilization of hypoxia-inducible factor (HIF), a transcription factor coordinating barrier protection. Antibiotic-mediated depletion of the microbiota reduces colonic butyrate and HIF expression, both of which are restored by butyrate supplementation. Additionally, germ-free mice exhibit diminished retention of O2-sensitive dyes and decreased stabilized HIF. Furthermore, the influences of butyrate are lost in cells lacking HIF, thus linking butyrate metabolism to stabilized HIF and barrier function. This work highlights a mechanism where host-microbe interactions augment barrier function in the distal gut.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1505
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[St] Status:In-Data-Review

  2 / 256255 MEDLINE  
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[PMID]: 25573176
[Au] Autor:Poindexter SV; Reddy VK; Mittal MK; Williams AM; Washington MK; Harris E; Mah A; Hiebert SW; Singh K; Chaturvedi R; Wilson KT; Lund PK; Williams CS
[Ad] Address:Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee; Vanderbilt Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee; and....
[Ti] Title:Transcriptional corepressor MTG16 regulates small intestinal crypt proliferation and crypt regeneration after radiation-induced injury.
[So] Source:Am J Physiol Gastrointest Liver Physiol;308(6):G562-71, 2015 Mar 15.
[Is] ISSN:1522-1547
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Myeloid translocation genes (MTGs) are transcriptional corepressors implicated in development, malignancy, differentiation, and stem cell function. While MTG16 loss renders mice sensitive to chemical colitis, the role of MTG16 in the small intestine is unknown. Histological examination revealed that Mtg16(-/-) mice have increased enterocyte proliferation and goblet cell deficiency. After exposure to radiation, Mtg16(-/-) mice exhibited increased crypt viability and decreased apoptosis compared with wild-type (WT) mice. Flow cytometric and immunofluorescence analysis of intestinal epithelial cells for phospho-histone H2A.X also indicated decreased DNA damage and apoptosis in Mtg16(-/-) intestines. To determine if Mtg16 deletion affected epithelial cells in a cell-autonomous fashion, intestinal crypts were isolated from Mtg16(-/-) mice. Mtg16(-/-) and WT intestinal crypts showed similar enterosphere forming efficiencies when cultured in the presence of EGF, Noggin, and R-spondin. However, when Mtg16(-/-) crypts were cultured in the presence of Wnt3a, they demonstrated higher enterosphere forming efficiencies and delayed progression to mature enteroids. Mtg16(-/-) intestinal crypts isolated from irradiated mice exhibited increased survival compared with WT intestinal crypts. Interestingly, Mtg16 expression was reduced in a stem cell-enriched population at the time of crypt regeneration. This is consistent with MTG16 negatively regulating regeneration in vivo. Taken together, our data demonstrate that MTG16 loss promotes radioresistance and impacts intestinal stem cell function, possibly due to shifting cellular response away from DNA damage-induced apoptosis and towards DNA repair after injury.
[Mh] MeSH terms primary: Cell Proliferation
Gamma Rays
Intestinal Mucosa/metabolism
Intestine, Small/metabolism
Nuclear Proteins/metabolism
Radiation Injuries, Experimental/metabolism
Regeneration
Transcription Factors/metabolism
[Mh] MeSH terms secundary: Animals
Apoptosis
Cell Proliferation/drug effects
Cell Survival
DNA Damage
Female
Gene Expression Regulation
Goblet Cells/metabolism
Goblet Cells/pathology
Histones/metabolism
Intestinal Mucosa/drug effects
Intestinal Mucosa/pathology
Intestine, Small/drug effects
Intestine, Small/pathology
Male
Mice, Inbred C57BL
Mice, Knockout
Nuclear Proteins/deficiency
Nuclear Proteins/genetics
Phenotype
Radiation Injuries, Experimental/etiology
Radiation Injuries, Experimental/pathology
Radiation Tolerance
Regeneration/drug effects
Signal Transduction
Stem Cells/metabolism
Stem Cells/pathology
Tissue Culture Techniques
Transcription Factors/deficiency
Transcription Factors/genetics
Wnt3A Protein/pharmacology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Name of substance:0 (Cbfa2t3 protein, mouse); 0 (H2AX protein, mouse); 0 (Histones); 0 (Nuclear Proteins); 0 (Transcription Factors); 0 (Wnt3A Protein)
[Em] Entry month:1505
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[Da] Date of entry for processing:150316
[St] Status:MEDLINE
[do] DOI:10.1152/ajpgi.00253.2014

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[PMID]: 25747723
[Au] Autor:Jia Y; Yu H; Fernandes SM; Wei Y; Gonzalez-Gil A; Motari MG; Vajn K; Stevens WW; Peters AT; Bochner BS; Kern RC; Schleimer RP; Schnaar RL
[Ad] Address:Department of Pharmacology, Third Military Medical University, Chongqing, China; Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Md....
[Ti] Title:Expression of ligands for Siglec-8 and Siglec-9 in human airways and airway cells.
[So] Source:J Allergy Clin Immunol;135(3):799-810.e7, 2015 Mar.
[Is] ISSN:1097-6825
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Balanced activation and inhibition of the immune system ensures pathogen clearance while avoiding hyperinflammation. Siglecs, sialic acid-binding proteins found on subsets of immune cells, often inhibit inflammation: Siglec-8 on eosinophils and Siglec-9 on neutrophils engage sialoglycan ligands on airways to diminish ongoing inflammation. The identities of human siglec ligands and their expression during inflammation are largely unknown. OBJECTIVE: The histologic distribution, expression, and molecular characteristics of siglec ligands were explored in healthy and inflamed human upper airways and in a cellular model of airway inflammation. METHODS: Normal and chronically inflamed upper airway tissues were stained for siglec ligands. The ligands were extracted from normal and inflamed tissues and from human Calu-3 cells for quantitative analysis by means of siglec blotting and isolation by means of siglec capture. RESULTS: Siglec-8 ligands were expressed on a subpopulation of submucosal gland cells of human inferior turbinate, whereas Siglec-9 ligands were expressed more broadly (submucosal glands, epithelium, and connective tissue); both were significantly upregulated in patients with chronic rhinosinusitis. Human airway (Calu-3) cells expressed Siglec-9 ligands on mucin 5B (MUC5B) under inflammatory control through the nuclear factor κB pathway, and MUC5B carried sialoglycan ligands of Siglec-9 on human upper airway tissue. CONCLUSION: Inflammation results in upregulation of immune-inhibitory Siglec-8 and Siglec-9 sialoglycan ligands on human airways. Siglec-9 ligands are upregulated through the nuclear factor κB pathway, resulting in their enhanced expression on MUC5B. Siglec sialoglycan ligand expression in inflamed cells and tissues may contribute to the control of airway inflammation.
[Mh] MeSH terms primary: Antigens, CD/genetics
Antigens, Differentiation, B-Lymphocyte/genetics
Epithelial Cells/immunology
Lectins/genetics
Respiratory Mucosa/immunology
Rhinitis/genetics
Sialic Acid Binding Immunoglobulin-like Lectins/genetics
Sinusitis/genetics
[Mh] MeSH terms secundary: Adult
Antigens, CD/immunology
Antigens, Differentiation, B-Lymphocyte/immunology
Cell Line
Chronic Disease
Epithelial Cells/drug effects
Epithelial Cells/pathology
Female
Gene Expression Regulation
Humans
Lectins/immunology
Ligands
Lipopolysaccharides
Male
Middle Aged
Mucin-5B/antagonists & inhibitors
Mucin-5B/genetics
Mucin-5B/immunology
NF-kappa B/genetics
NF-kappa B/immunology
Primary Cell Culture
RNA, Small Interfering/genetics
RNA, Small Interfering/metabolism
Respiratory Mucosa/drug effects
Respiratory Mucosa/pathology
Rhinitis/immunology
Rhinitis/pathology
Sialic Acid Binding Immunoglobulin-like Lectins/immunology
Signal Transduction
Sinusitis/immunology
Sinusitis/pathology
Tumor Necrosis Factor-alpha
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Antigens, CD); 0 (Antigens, Differentiation, B-Lymphocyte); 0 (Lectins); 0 (Ligands); 0 (Lipopolysaccharides); 0 (MUC5B protein, human); 0 (Mucin-5B); 0 (NF-kappa B); 0 (RNA, Small Interfering); 0 (SIGLEC8 protein, human); 0 (SIGLEC9 protein, human); 0 (Sialic Acid Binding Immunoglobulin-like Lectins); 0 (Tumor Necrosis Factor-alpha)
[Em] Entry month:1504
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:150309
[St] Status:MEDLINE

  4 / 256255 MEDLINE  
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[PMID]: 25707055
[Au] Autor:Xu LT; Courtney RJ; Ehlers JP
[Ti] Title:Bevacizumab therapy and multimodal ultrawide-field imaging in immunogammopathy maculopathy secondary to Waldenström's macroglobulinemia.
[So] Source:Ophthalmic Surg Lasers Imaging Retina;46(2):262-5, 2015 Feb.
[Is] ISSN:2325-8179
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Waldenström's macroglobulinemia (WM) is associated with retinal findings of hyperviscosity, such as venous dilation, and findings of immunogammopathy maculopathy, such as serous macular detachment. This report describes a case of bilateral serous macular detachment with intraretinal schisis-like fluid in a patient with WM. Enhanced depth imaging optical coherence tomography revealed a thickened choroid with hyperreflective accumulations in the retinal pigment epithelium layer. Ultrawide-field fundus autofluorescence demonstrated a central area of hyperautofluorescence corresponding to the area of serous macular detachment. Ultrawide-field fluorescein angiography was characteristically silent. Intravitreal bevacizumab therapy resulted in significant reduction in intraretinal fluid but minimal change in subretinal fluid. Long-term follow-up demonstrated alterations in retinal architecture and improved serous detachments.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1502
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.3928/23258160-20150213-06

  5 / 256255 MEDLINE  
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[PMID]: 25525173
[Au] Autor:Ehlers JP; Itoh Y; Xu LT; Kaiser PK; Singh RP; Srivastava SK
[Ad] Address:Ophthalmic Imaging Center, Cole Eye Institute, Cleveland Clinic, Cleveland, Ohio, United States Cole Eye Institute, Cleveland Clinic, Cleveland, Ohio, United States....
[Ti] Title:Factors associated with persistent subfoveal fluid and complete macular hole closure in the PIONEER study.
[So] Source:Invest Ophthalmol Vis Sci;56(2):1141-6, 2015 Feb.
[Is] ISSN:1552-5783
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: To investigate preoperative and intraoperative factors associated with persistent subfoveal fluid in surgically closed macular holes (MHs). METHODS: This was a prospective consecutive case series of eyes undergoing surgical repair for full-thickness MH in the PIONEER study, a prospective intraoperative optical coherence tomography (OCT) multisurgeon single-center study. Thirty-seven eyes (36 patients) with surgically closed MH were studied. Quantitative OCT analysis was performed including intraoperative MH area, volume, ellipsoid zone to retinal pigment epithelium (EZ-RPE) height, extent of subretinal hyporeflectivity (SRHR), and the amount of postoperative subfoveal fluid. RESULTS: Persistent subfoveal fluid was identified in 58% of eyes at 2 weeks following surgery. The mean time to two-line improvement in visual acuity was greater in eyes with persistent subfoveal fluid (P = 0.03). Final visual acuity did not correlate with the initial presence of fluid. Two intraoperative factors following internal limiting membrane (ILM) peeling were associated with the formation of persistent subfoveal fluid: EZ-RPE height and SRHR width (P < 0.01). These were both negatively correlated with amount of postoperative subfoveal fluid (P = 0.028 and 0.04, respectively). CONCLUSIONS: Persistent subfoveal fluid following MH surgery is a common finding that appears to delay visual recovery but not effect final visual outcome. The incidence of persistent subfoveal fluid appears to be related to intraoperative alterations after ILM peeling in the outer retinal architecture (e.g., increased EZ-RPE height and SRHR width). This finding suggests a novel mechanism for facilitating MH closure through ILM peeling (e.g., altering photoreceptor/RPE adherence and increasing retinal mobility that allows for complete hole closure).
[Mh] MeSH terms primary: Recovery of Function
Retinal Perforations/surgery
Retinal Pigment Epithelium/pathology
Tomography, Optical Coherence/methods
Visual Acuity/physiology
[Mh] MeSH terms secundary: Aged
Body Fluids
Female
Follow-Up Studies
Humans
Male
Monitoring, Intraoperative
Prospective Studies
Retinal Perforations/pathology
Retinal Perforations/physiopathology
Retinal Pigment Epithelium/physiopathology
Treatment Outcome
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1503
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[Da] Date of entry for processing:150214
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.14-15765

  6 / 256255 MEDLINE  
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[PMID]: 25326580
[Au] Autor:Finigan JH; Vasu VT; Thaikoottathil JV; Mishra R; Shatat MA; Mason RJ; Kern JA
[Ad] Address:Division of Pulmonary and Critical Care Medicine, National Jewish Health, Denver, Colorado; Division of Oncology, National Jewish Health, Denver, Colorado; Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado, Denver, Colorado FiniganJ@NJHealth.org....
[Ti] Title:HER2 activation results in ß-catenin-dependent changes in pulmonary epithelial permeability.
[So] Source:Am J Physiol Lung Cell Mol Physiol;308(2):L199-207, 2015 Jan 15.
[Is] ISSN:1522-1504
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The receptor tyrosine kinase human epidermal growth factor receptor-2 (HER2) is known to regulate pulmonary epithelial barrier function; however, the mechanisms behind this effect remain unidentified. We hypothesized that HER2 signaling alters the epithelial barrier through an interaction with the adherens junction (AJ) protein ß-catenin, leading to dissolution of the AJ. In quiescent pulmonary epithelial cells, HER2 and ß-catenin colocalized along the lateral intercellular junction. HER2 activation by the ligand neuregulin-1 was associated with tyrosine phosphorylation of ß-catenin, dissociation of ß-catenin from E-cadherin, and decreased E-cadherin-mediated cell adhesion. All effects were blocked with the HER2 inhibitor lapatinib. ß-Catenin knockdown using shRNA significantly attenuated neuregulin-1-induced decreases in pulmonary epithelial resistance in vitro. Our data indicate that HER2 interacts with ß-catenin, leading to dissolution of the AJ, decreased cell-cell adhesion, and disruption of the pulmonary epithelial barrier.
[Mh] MeSH terms primary: Adherens Junctions/metabolism
Cell Adhesion/physiology
Receptor, ErbB-2/metabolism
Respiratory Mucosa/metabolism
beta Catenin/metabolism
[Mh] MeSH terms secundary: Cell Line
Electric Impedance
Enzyme Activation
Humans
Lung/physiology
Neuregulin-1/metabolism
Permeability
Phosphorylation
Protein Kinase Inhibitors/pharmacology
Quinazolines/pharmacology
RNA Interference
RNA, Small Interfering
Receptor, ErbB-2/antagonists & inhibitors
Signal Transduction
Tight Junctions/metabolism
beta Catenin/genetics
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Neuregulin-1); 0 (Protein Kinase Inhibitors); 0 (Quinazolines); 0 (RNA, Small Interfering); 0 (beta Catenin); 0VUA21238F (lapatinib); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Entry month:1504
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[Da] Date of entry for processing:150116
[St] Status:MEDLINE
[do] DOI:10.1152/ajplung.00237.2014

  7 / 256255 MEDLINE  
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[PMID]: 25428587
[Au] Autor:Yuan G; Yang G; Zheng Y; Zhu X; Chen Z; Zhang Z; Chen Y
[Ad] Address:The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory for Oral Biomedicine of Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan 430079, China Department of Cell and Molecular Biology, Tulane University, New Orleans, LA 70118, USA...
[Ti] Title:The non-canonical BMP and Wnt/ß-catenin signaling pathways orchestrate early tooth development.
[So] Source:Development;142(1):128-39, 2015 Jan 1.
[Is] ISSN:1477-9129
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BMP and Wnt signaling pathways play a crucial role in organogenesis, including tooth development. Despite extensive studies, the exact functions, as well as if and how these two pathways act coordinately in regulating early tooth development, remain elusive. In this study, we dissected regulatory functions of BMP and Wnt pathways in early tooth development using a transgenic noggin (Nog) overexpression model (K14Cre;pNog). It exhibits early arrested tooth development, accompanied by reduced cell proliferation and loss of odontogenic fate marker Pitx2 expression in the dental epithelium. We demonstrated that overexpression of Nog disrupted BMP non-canonical activity, which led to a dramatic reduction of cell proliferation rate but did not affect Pitx2 expression. We further identified a novel function of Nog by inhibiting Wnt/ß-catenin signaling, causing loss of Pitx2 expression. Co-immunoprecipitation and TOPflash assays revealed direct binding of Nog to Wnts to functionally prevent Wnt/ß-catenin signaling. In situ PLA and immunohistochemistry on Nog mutants confirmed in vivo interaction between endogenous Nog and Wnts and modulation of Wnt signaling by Nog in tooth germs. Genetic rescue experiments presented evidence that both BMP and Wnt signaling pathways contribute to cell proliferation regulation in the dental epithelium, with Wnt signaling also controlling the odontogenic fate. Reactivation of both BMP and Wnt signaling pathways, but not of only one of them, rescued tooth developmental defects in K14Cre;pNog mice, in which Wnt signaling can be substituted by transgenic activation of Pitx2. Our results reveal the orchestration of non-canonical BMP and Wnt/ß-catenin signaling pathways in the regulation of early tooth development.
[Mh] MeSH terms primary: Bone Morphogenetic Proteins/metabolism
Tooth/embryology
Tooth/metabolism
Wnt Signaling Pathway
[Mh] MeSH terms secundary: Animals
Carrier Proteins/metabolism
Cell Lineage/drug effects
Cell Proliferation/drug effects
Down-Regulation/drug effects
Epithelium/drug effects
Epithelium/metabolism
HEK293 Cells
Homeodomain Proteins/metabolism
Humans
Integrases/metabolism
MSX1 Transcription Factor/metabolism
Mesoderm/embryology
Mice, Transgenic
Models, Biological
Odontogenesis/drug effects
Protein Binding/drug effects
Protein Kinase Inhibitors/pharmacology
Smad Proteins/metabolism
Tooth/cytology
Tooth Germ/cytology
Tooth Germ/drug effects
Tooth Germ/embryology
Tooth Germ/metabolism
Transcription Factors/metabolism
Transforming Growth Factor beta/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Bone Morphogenetic Proteins); 0 (Carrier Proteins); 0 (Homeodomain Proteins); 0 (MSX1 Transcription Factor); 0 (Msx1 protein, mouse); 0 (Protein Kinase Inhibitors); 0 (Smad Proteins); 0 (Transcription Factors); 0 (Transforming Growth Factor beta); 148294-77-3 (noggin protein); 184787-43-7 (homeobox protein PITX2); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases)
[Em] Entry month:1502
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[Da] Date of entry for processing:141217
[St] Status:MEDLINE
[do] DOI:10.1242/dev.117887

  8 / 256255 MEDLINE  
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[PMID]: 18661080
[Au] Autor:Pei J; Zhuo XY; Jia YX
[Ad] Address:Department of Pathology, Affiliated Stomatological Hospital, Nanchang University. Nanchang 330006, Jiangxi Province, China. peijingzi@163.com
[Ti] Title:[Clinical and pathological analysis of 8 patients with oral candidiasis].
[So] Source:Shanghai Kou Qiang Yi Xue;17(3):322-4, 2008 Jun.
[Is] ISSN:1006-7248
[Cp] Country of publication:China
[La] Language:chi
[Ab] Abstract:PURPOSE: To investigate the clinical and pathological diagnosis of oral candidiasis and reduce misdiagnosis. METHODS: The medical records of 8 patients with oral candidiasis were reviewed retrospectively, HE and PAS staining of histopathology were applied to study the specimens. RESULTS: It was found that oral candidiasis were identified by pathological diagnosis, but weren't considered clinically. Minor abscesses were all detected in the epithelium of conventional histopathologic sections, the hyphae were shown by PAS staining invading the epithelium. CONCLUSIONS: The results suggest that candidal infections should be considered, if there are hyperplastic or ulcerative lesions which last for long time; when minor abscesses are detected in the epithelium by histopathologic examination, oral candidiasis should be highly suspected, and be confirmed by PAS staining.
[Mh] MeSH terms primary: Candidiasis, Oral/diagnosis
[Mh] MeSH terms secundary: Candidiasis, Oral/complications
Humans
Hyperplasia/etiology
Oral Ulcer/etiology
Retrospective Studies
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1505
[Js] Journal subset:D; IM
[Da] Date of entry for processing:080728
[St] Status:MEDLINE

  9 / 256255 MEDLINE  
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[PMID]: 24343710
[Au] Autor:Nicol MR; Fedoriw Y; Mathews M; Prince HM; Patterson KB; Geller E; Mollan K; Mathews S; Kroetz DL; Kashuba AD
[Ad] Address:Eshelman School of Pharmacy, University of North Carolina, Chapel Hill, NC, USA....
[Ti] Title:Expression of six drug transporters in vaginal, cervical, and colorectal tissues: Implications for drug disposition in HIV prevention.
[So] Source:J Clin Pharmacol;54(5):574-83, 2014 May.
[Is] ISSN:1552-4604
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Effective antiretroviral (ARV)-based HIV prevention strategies require optimizing drug exposure in mucosal tissues; yet factors influencing mucosal tissue disposition remain unknown. We hypothesized drug transporter expression in vaginal, cervical, and colorectal tissues is a contributing factor and selected 3 efflux (ABCB1/MDR1, ABCC2/MRP2, ABCC4/MRP4) and 3 uptake (SLC22A6/OAT1, SLC22A8/OAT3, SLCO1B1/OATP1B1) transporters to further investigate based on their affinity for 2 ARVs central to prevention (tenofovir, maraviroc). Tissue was collected from 98 donors. mRNA and protein expression were quantified using qPCR and immunohistochemistry (IHC). Hundred percent of tissues expressed efflux transporter mRNA. IHC localized them to the epithelium and/or submucosa. Multivariable analysis adjusted for age, smoking, and co-medications revealed significant (P < 0.05) differences in efflux transporter mRNA between tissue types (vaginal ABCB1 3.9-fold > colorectal; vaginal ABCC2 2.9-fold > colorectal; colorectal ABCC4 2.0-fold > cervical). In contrast, uptake transporter mRNA was expressed in <25% of tissues. OAT1 protein was detected in 0% of female genital tissues and in 100% of colorectal tissues, but only in rare epithelial cells. These data support clinical findings of higher maraviroc and tenofovir concentrations in rectal tissue compared to vaginal or cervical tissue after oral dosing. Quantifying mucosal transporter expression and localization can facilitate ARV selection to target these tissues.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1505
[Cu] Class update date: 150515
[Lr] Last revision date:150515
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1002/jcph.248

  10 / 256255 MEDLINE  
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[PMID]: 25835502
[Au] Autor:Carulli AJ; Keeley TM; Demitrack ES; Chung J; Maillard I; Samuelson LC
[Ad] Address:Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA....
[Ti] Title:Notch receptor regulation of intestinal stem cell homeostasis and crypt regeneration.
[So] Source:Dev Biol;402(1):98-108, 2015 Jun 1.
[Is] ISSN:1095-564X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The Notch signaling pathway regulates intestinal epithelial cell homeostasis, including stem cell maintenance, progenitor cell proliferation and differentiation. Notch1 and Notch2 receptors are expressed in the epithelium, but individual contributions to these functions are unclear. We used genetic deletion to define receptor roles on stem cell function, cell proliferation/differentiation, and repair after injury. Loss of Notch1 induced a transient secretory cell hyperplasia that spontaneously resolved over time. In contrast, deletion of Notch2 had no secretory cell effect. Compound deletions of Notch1 and Notch2 resulted in a more severe secretory cell hyperplasia than deletion of Notch1 alone. Furthermore, only double deletion of Notch1 and Notch2 decreased cell proliferation, suggesting a low threshold for maintenance of proliferation compared to differentiation. Stem cells were affected by deletion of Notch1, with reduced expression of Olfm4 and fewer LGR5(+) stem cells. Deletion of Notch2 had no apparent affect on stem cell homeostasis. However, we observed impaired crypt regeneration after radiation in both Notch1- and Notch2-deleted intestine, suggesting that higher Notch activity is required post-injury. These findings suggest that Notch1 is the primary receptor regulating intestinal stem cell function and that Notch1 and Notch2 together regulate epithelial cell proliferation, cell fate determination, and post-injury regeneration.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1505
[Cu] Class update date: 150515
[Lr] Last revision date:150515
[Js] Journal subset:IM
[St] Status:In-Data-Review


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