2021
Sarecycline treatment for acne vulgaris: Rationale for weight‐based dosing and limited impact of food intake on clinical efficacy
Grada A, Del Rosso JQ, Graber E, Bunick CG, Gold L, Moore AY, Baldwin H, Obagi Z, Damiani G, Carrothers T, McNamee B, Hanze E. Sarecycline treatment for acne vulgaris: Rationale for weight‐based dosing and limited impact of food intake on clinical efficacy. Dermatologic Therapy 2021, 35: e15275. PMID: 34923732, PMCID: PMC9286649, DOI: 10.1111/dth.15275.Peer-Reviewed Original ResearchConceptsTetracycline-class antibioticsWeight-based dosingHigh-fat mealClinical efficacyAcne vulgarisFood intakeWeight-based dosing protocolAcne vulgaris patientsLow clinical efficacyExposure-response modelingPopulation pharmacokinetic modelingAcne vulgaris treatmentHigh-fat foodsDosing protocolDosing recommendationsInflammatory lesionsVulgaris patientsExtent of exposureClinical studiesImproved complianceGastrointestinal absorptionVulgaris treatmentDrug AdministrationPharmacokinetic modelingEfficacyGenetic Signatures From RNA Sequencing of Pediatric Localized Scleroderma Skin
Mirizio E, Liu C, Yan Q, Waltermire J, Mandel R, Schollaert KL, Konnikova L, Wang X, Chen W, Torok KS. Genetic Signatures From RNA Sequencing of Pediatric Localized Scleroderma Skin. Frontiers In Pediatrics 2021, 9: 669116. PMID: 34164359, PMCID: PMC8215272, DOI: 10.3389/fped.2021.669116.Peer-Reviewed Original ResearchLocalized sclerodermaLS patientsGene signatureClinical activity parametersPediatric localized sclerodermaSignificant functional disabilityInterferon-inducible chemokinesSkin transcriptional profileIFNγ signatureProgressive diseaseFunctional disabilityInflammatory lesionsLesion biopsyParaffinized tissuesDisease progressionHealthy controlsInflammatory diseasesFibrotic pathwaysScleroderma skinCellular expressionDiseaseL subjectsGene expression profilesSkinIFNγ
2020
Perniosis during the COVID‐19 pandemic: Negative anti‐SARS‐CoV‐2 immunohistochemistry in six patients and comparison to perniosis before the emergence of SARS‐CoV‐2
Ko CJ, Harigopal M, Damsky W, Gehlhausen JR, Bosenberg M, Patrignelli R, McNiff JM. Perniosis during the COVID‐19 pandemic: Negative anti‐SARS‐CoV‐2 immunohistochemistry in six patients and comparison to perniosis before the emergence of SARS‐CoV‐2. Journal Of Cutaneous Pathology 2020, 47: 997-1002. PMID: 32745281, PMCID: PMC7436569, DOI: 10.1111/cup.13830.Peer-Reviewed Original ResearchConceptsSARS-CoV-2 nucleocapsid proteinPerivascular lymphocytesImmunohistochemical stainingCOVID-19 pandemicSARS-CoV-2 immunohistochemistryNucleocapsid proteinSARS-CoV-2Inflammatory lesionsHistopathologic findingsIntravascular occlusionMicroscopic findingsPerniosisIntravascular materialLymphocytesLesionsPatientsStainingPandemicSuch casesCuffingHistopathologyCasesImmunohistochemistryFindingsProtein
2019
Multiplexed imaging of immune cells in staged multiple sclerosis lesions by mass cytometry
Ramaglia V, Sheikh-Mohamed S, Legg K, Park C, Rojas OL, Zandee S, Fu F, Ornatsky O, Swanson EC, Pitt D, Prat A, McKee TD, Gommerman JL. Multiplexed imaging of immune cells in staged multiple sclerosis lesions by mass cytometry. ELife 2019, 8: e48051. PMID: 31368890, PMCID: PMC6707785, DOI: 10.7554/elife.48051.Peer-Reviewed Original ResearchConceptsMultiple sclerosisMS disease activityT-cell phenotypeMass cytometryTypes of lymphocytesMultiple sclerosis lesionsNatalizumab cessationDisease activityMS patientsInflammatory lesionsImmune cellsSpinal cordLesion morphometryMS lesionsB cellsLesion typeSclerosis lesionsLesionsBlood vesselsCell phenotypeFunctional stateCytometryCellular contentCell-cell interactionsPhenotypeClinical approach to recurrent implantation failure: evidence-based evaluation of the endometrium
Kliman HJ, Frankfurter D. Clinical approach to recurrent implantation failure: evidence-based evaluation of the endometrium. Fertility And Sterility 2019, 111: 618-628. PMID: 30929719, DOI: 10.1016/j.fertnstert.2019.02.011.Peer-Reviewed Original ResearchConceptsRecurrent implantation failureImplantation failureHigh-quality embryosEvidence-based evaluationInflammatory markersRetained productsInflammatory lesionsHistologic evaluationQuality embryosClinical approachGrowth disordersActionable findingsEndometriumFunctional testsPatientsMolecular eraComplete assessmentTissueCycling tissueEndometrialFailureBest optionLesionsEvaluation
2012
Inflammatory Disorders of the Large Intestine
Jain D, Warren B, Riddell R. Inflammatory Disorders of the Large Intestine. 2012, 552-635. DOI: 10.1002/9781118399668.ch35.Peer-Reviewed Original ResearchChronic inflammatory bowel diseaseAcute infectious colitisLarge intestinal biopsiesInflammatory bowel diseaseInfection-related conditionsMain infectious agentsDiagnosis of dysplasiaDiagnosis of inflammationInfectious colitisTransplant recipientsVariety of virusesBowel diseaseIntestinal biopsiesInflammatory lesionsInflammatory disordersChronic conditionsDisease burdenEnteric infectionsDifferential diagnosisFrequent causeRare diseaseSpecific diagnosisInfectious agentsImmune systemLarge intestine
2008
Acute upregulation of an NKG2D ligand promotes rapid reorganization of a local immune compartment with pleiotropic effects on carcinogenesis
Strid J, Roberts SJ, Filler RB, Lewis JM, Kwong BY, Schpero W, Kaplan DH, Hayday AC, Girardi M. Acute upregulation of an NKG2D ligand promotes rapid reorganization of a local immune compartment with pleiotropic effects on carcinogenesis. Nature Immunology 2008, 9: 146-154. PMID: 18176566, DOI: 10.1038/ni1556.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Transformation, NeoplasticEpidermisHistocompatibility Antigens Class IImmunologic SurveillanceLangerhans CellsLigandsMiceMice, Inbred StrainsNK Cell Lectin-Like Receptor Subfamily KReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-deltaReceptors, ImmunologicReceptors, Natural Killer CellSkin NeoplasmsT-LymphocytesUp-RegulationConceptsNKG2D ligandsImmune compartmentLangerhans cellsT cellsRAE-1Local immune compartmentIntraepithelial T cellsΑβ T cellsEpithelial infiltrationTissue immunosurveillanceGraft rejectionInflammatory lesionsReceptor NKG2DAcute changesLigand MICACytotoxic lymphocytesAcute upregulationImmunosurveillanceEarly phaseCarcinogenesisUpregulationPleiotropic effectsCellsNKG2DCarcinoma
2003
Helicobacter-Induced Chronic Active Lymphoid Aggregates Have Characteristics of Tertiary Lymphoid Tissue
Shomer NH, Fox JG, Juedes AE, Ruddle NH. Helicobacter-Induced Chronic Active Lymphoid Aggregates Have Characteristics of Tertiary Lymphoid Tissue. Infection And Immunity 2003, 71: 3572-3577. PMID: 12761142, PMCID: PMC155770, DOI: 10.1128/iai.71.6.3572-3577.2003.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigen PresentationAntigens, SurfaceAutoimmunityCell Adhesion MoleculesCell AggregationChemokine CCL21Chemokine CXCL13Chemokines, CCChemokines, CXCHelicobacter InfectionsHepatitis, ChronicImmunoglobulinsLiverLymphoid TissueMembrane ProteinsMiceMucoproteinsVascular Cell Adhesion Molecule-1ConceptsChronic active hepatitisTertiary lymphoid organsLymphoid organsActive hepatitisInflammatory lesionsHepatic inflammatory lesionsMucosal addressin cell adhesion moleculeTertiary lymphoid tissuePeripheral node addressinLiver cell suspensionsLiver tissue sectionsB220-positive B cellsChemokines SLCHepatic inflammationInflammatory infiltrateChronic autoimmunityLymphoid aggregatesLymphoid tissueFluorescence-activated cell sortingT cellsCell adhesion moleculeB cellsStromal cellsSmall venulesAdhesion moleculesPathogenesis of mouse hepatitis virus infection in gamma interferon-deficient mice is modulated by co-infection with Helicobacter hepaticus.
Compton SR, Ball-Goodrich LJ, Zeiss CJ, Johnson LK, Johnson EA, Macy JD. Pathogenesis of mouse hepatitis virus infection in gamma interferon-deficient mice is modulated by co-infection with Helicobacter hepaticus. Journal Of The American Association For Laboratory Animal Science 2003, 53: 197-206. PMID: 12784855.Peer-Reviewed Original ResearchConceptsIFN-gamma KO miceGamma interferon-deficient miceMouse hepatitis virusInterferon-deficient miceDevelopment of peritonitisKO miceH. hepaticusMultisystemic infectionHelicobacter hepaticusMouse hepatitis virus infectionHepatitis virus infectionAberrant immune responseSelf-limiting infectionMinimal pathologic changesMultifocal hepatic necrosisLater time pointsAcute necrotizingAcute peritonitisAcute phaseInflammatory lesionsImmunocompetent miceChronic infectionHepatic necrosisMHV infectionPathologic changes
2002
PULMONARY TOXICITY OF SIMULATED LUNAR AND MARTIAN DUSTS IN MICE: I. HISTOPATHOLOGY 7 AND 90 DAYS AFTER INTRATRACHEAL INSTILLATION
Lam CW, James JT, McCluskey R, Cowper S, Balis J, Muro-Cacho C. PULMONARY TOXICITY OF SIMULATED LUNAR AND MARTIAN DUSTS IN MICE: I. HISTOPATHOLOGY 7 AND 90 DAYS AFTER INTRATRACHEAL INSTILLATION. Inhalation Toxicology 2002, 14: 901-916. PMID: 12396402, DOI: 10.1080/08958370290084683.Peer-Reviewed Original ResearchConceptsParticle-laden macrophagesPeribronchiolar inflammationLung lesionsPulmonary toxicityChronic pulmonary inflammationChronic inflammatory lesionsEvidence of inflammationAcute inflammatory responseNumber of macrophagesFocal alveolitisLung injurySeptal thickeningPulmonary inflammationInflammatory lesionsMild fibrosisExamination 7Chronic mildInflammatory responseAlveolitisFibrosisInflammationLungOverall severityMSS groupMice
2000
Glutamate excitotoxicity — a mechanism for axonal damage and oligodendrocyte death in Multiple Sclerosis?
Werner P, Pitt D, Raine CS. Glutamate excitotoxicity — a mechanism for axonal damage and oligodendrocyte death in Multiple Sclerosis? Journal Of Neural Transmission. Supplementa 2000, 375-385. PMID: 11205156, DOI: 10.1007/978-3-7091-6301-6_27.Peer-Reviewed Original ResearchConceptsCentral nervous systemAMPA/kainate antagonistMultiple sclerosisGlutamate excitotoxicityImmune cellsKainate antagonistAxonal damageAntigen-primed T cellsMyelin-producing cellsLack of effectSite of entryCNS inflammationInflammatory attacksExperimental autoimmunePerivascular cuffsAutoimmune demyelinationInflammatory lesionsClinical differencesOligodendrocyte survivalEffective therapyGlutamate receptorsOligodendrocyte deathT cellsExcitotoxicityLesion size
1992
The relationship between acute inflammatory lesions of the preterm placenta and amniotic fluid microbiology
Romero R, Salafia C, Athanassiadis A, Hanaoka S, Mazor M, Sepulveda W, Bracken M. The relationship between acute inflammatory lesions of the preterm placenta and amniotic fluid microbiology. American Journal Of Obstetrics And Gynecology 1992, 166: 1382-1388. PMID: 1595794, DOI: 10.1016/0002-9378(92)91609-e.Peer-Reviewed Original ResearchConceptsAcute inflammatory lesionsPositive amniotic fluid cultureAmniotic fluid cultureInflammatory lesionsFluid cultureAmniotic cavityChorionic plateMicrobial invasionAmniotic fluid microbiologySeverity of inflammationPattern of inflammationMixed patternUmbilical vasculitisPreterm laborConsecutive patientsPreterm placentasAcute inflammationMicrobiologic studiesUmbilical cordInflammationChorioamniotic membranesLesionsStrong associationIntact membranesPlacenta
1987
Contemporary Imaging of Renal Inflammatory Disease
Piccirillo M, Rigsby C, Rosenfield A. Contemporary Imaging of Renal Inflammatory Disease. Infectious Disease Clinics Of North America 1987, 1: 927-964. PMID: 3333666, DOI: 10.1016/s0891-5520(20)30157-4.Peer-Reviewed Original ResearchConceptsRenal inflammatory diseaseInflammatory diseasesConventional excretory urographyManagement of patientsUpper urinary tractRenal inflammatory lesionsAbscess collectionXanthogranulomatous pyelonephritisInflammatory lesionsExcretory urographyUrinary tractPlain filmsContemporary imagingComputed tomographyBacterial infectionsFungal infectionsInfectionDiseaseWide spectrumPyelonephritisPyonephrosisMalakoplakiaUrographyPatientsLesions
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