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Article ; Online: Immunochemistry Analysis Using Chromogenic Substrates on Tissue Sections.

Vijayaraj, Preethi

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2386, Page(s) 1–16

Abstract: Immunohistochemistry (IHC) is a highly sensitive protein detection technique developed using the principle of antigen-antibody binding reaction. With immunohistochemistry, it is possible to visualize the abundance, distribution, and localization of ... ...

Abstract	Immunohistochemistry (IHC) is a highly sensitive protein detection technique developed using the principle of antigen-antibody binding reaction. With immunohistochemistry, it is possible to visualize the abundance, distribution, and localization of proteins in situ. This chapter discusses the standard protocols involved in IHC detection using chromogenic substrates, including pre-treatment of tissues, types of chromogenic substrates, and troubleshooting at various stages of the protocol.
MeSH term(s)	Chromogenic Compounds ; Immunochemistry ; Immunohistochemistry
Chemical Substances	Chromogenic Compounds
Language	English
Publishing date	2021-09-29
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1771-7_1
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The aCCR(2)ual of M2 Macrophages Provides Some Breathing Room.

Vijayaraj, Preethi / Gomperts, Brigitte N

Cell stem cell

2017 Volume 21, Issue 1, Page(s) 1–3

Abstract: Lung tissue can robustly regenerate functional alveolar units after injury, but the mechanisms are unknown. Lechner et al. (2017) in this issue of Cell Stem Cell demonstrate that lung regeneration is facilitated by bone-marrow-derived myeloid cells that ... ...

Abstract	Lung tissue can robustly regenerate functional alveolar units after injury, but the mechanisms are unknown. Lechner et al. (2017) in this issue of Cell Stem Cell demonstrate that lung regeneration is facilitated by bone-marrow-derived myeloid cells that are recruited to the lung through a CCL2-CCR2 chemokine axis and by IL-13 expressing innate lymphoid cells.
MeSH term(s)	Animals ; Chemokine CCL2/immunology ; Humans ; Interleukin-13/immunology ; Lung/physiology ; Lung Injury/immunology ; Lung Injury/pathology ; Macrophages, Alveolar/immunology ; Macrophages, Alveolar/pathology ; Receptors, CCR2/immunology ; Regeneration/immunology
Chemical Substances	CCL2 protein, human ; CCR2 protein, human ; Chemokine CCL2 ; Interleukin-13 ; Receptors, CCR2
Language	English
Publishing date	2017--06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2017.06.006
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Zs.A 6589: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Book ; Thesis: Altered signaling, but no cell fragility in mice lacking all type II keratin genes

Vijayaraj, Preethi

2008

Author's details	vorgelegt von Preethi Vijayaraj
Language	English
Size	vii, 96 Bl., Ill., graph. Darst.
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Univ., Diss.. - Nicht für den Austausch--Bonn, 2008
Database	Special collection on veterinary medicine and general parasitology

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Book ; Online ; Thesis: Altered signaling, but no cell fragility in mice lacking all type II keratin genes

Vijayaraj, Preethi [Verfasser]

2007

Author's details	vorgelegt von Preethi Vijayaraj
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Language	English
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Targeting PEA3 transcription factors to mitigate small cell lung cancer progression.

Shia, David W / Choi, WooSuk / Vijayaraj, Preethi / Vuong, Valarie / Sandlin, Jenna M / Lu, Michelle M / Aziz, Adam / Marin, Caliope / Aros, Cody J / Sen, Chandani / Durra, Abdo / Lund, Andrew J / Purkayastha, Arunima / Rickabaugh, Tammy M / Graeber, Thomas G / Gomperts, Brigitte N

Oncogene

2022 Volume 42, Issue 6, Page(s) 434–448

Abstract: Small cell lung cancer (SCLC) remains a lethal disease with a dismal overall survival rate of 6% despite promising responses to upfront combination chemotherapy. The key drivers of such rapid mortality include early metastatic dissemination in the ... ...

Abstract	Small cell lung cancer (SCLC) remains a lethal disease with a dismal overall survival rate of 6% despite promising responses to upfront combination chemotherapy. The key drivers of such rapid mortality include early metastatic dissemination in the natural course of the disease and the near guaranteed emergence of chemoresistant disease. Here, we found that we could model the regression and relapse seen in clinical SCLC in vitro. We utilized time-course resolved RNA-sequencing to globally profile transcriptome changes as SCLC cells responded to a combination of cisplatin and etoposide-the standard-of-care in SCLC. Comparisons across time points demonstrated a distinct transient transcriptional state resembling embryonic diapause. Differential gene expression analysis revealed that expression of the PEA3 transcription factors ETV4 and ETV5 were transiently upregulated in the surviving fraction of cells which we determined to be necessary for efficient clonogenic expansion following chemotherapy. The FGFR-PEA3 signaling axis guided the identification of a pan-FGFR inhibitor demonstrating in vitro and in vivo efficacy in delaying progression following combination chemotherapy, observed inhibition of phosphorylation of the FGFR adaptor FRS2 and corresponding downstream MAPK and PI3K-Akt signaling pathways. Taken together, these data nominate PEA3 transcription factors as key mediators of relapse progression in SCLC and identify a clinically actionable small molecule candidate for delaying relapse of SCLC.
MeSH term(s)	Humans ; Small Cell Lung Carcinoma/drug therapy ; Small Cell Lung Carcinoma/genetics ; Small Cell Lung Carcinoma/pathology ; Phosphatidylinositol 3-Kinases/genetics ; Neoplasm Recurrence, Local ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Cell Line, Tumor
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Transcription Factors
Language	English
Publishing date	2022-12-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-022-02558-6
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Article ; Online: Molecular mechanisms of endothelial differentiation.

Le Bras, Alex / Vijayaraj, Preethi / Oettgen, Peter

Vascular medicine (London, England)

2010 Volume 15, Issue 4, Page(s) 321–331

Abstract: The differentiation of embryonic stem cells along the endothelial cell lineage requires a tightly coordinated sequence of events that are regulated in both space and time. Although significant gaps remain in this process, major strides have been made ... ...

Abstract	The differentiation of embryonic stem cells along the endothelial cell lineage requires a tightly coordinated sequence of events that are regulated in both space and time. Although significant gaps remain in this process, major strides have been made over the past 10 years in identifying the growth factors, signal transduction pathways, and transcription factors that function together as critical mediators of this process. Examples of some of the signal transduction pathways include the hedgehog (HH), WNT, BMP, and Notch pathways. A complex interplay between growth factors, and activation of a variety of signal transduction pathways leads to the induction of transcriptional programs that promote the differentiation of embryonic stem cells along the endothelial lineage and ultimately into arterial, venous, and lymphatic endothelial cells. The purpose of this review is to summarize the recent advances in our understanding of the molecular mechanisms underlying endothelial differentiation.
MeSH term(s)	Animals ; Cell Differentiation/physiology ; Embryonic Stem Cells/cytology ; Embryonic Stem Cells/metabolism ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Humans ; Signal Transduction/physiology
Language	English
Publishing date	2010-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1311628-9
ISSN	1477-0377 ; 1358-863X
ISSN (online)	1477-0377
ISSN	1358-863X
DOI	10.1177/1358863X10371685
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Article: Direct exposure to SARS-CoV-2 and cigarette smoke increases infection severity and alters the stem cell-derived airway repair response.

Purkayastha, Arunima / Sen, Chandani / Garcia, Gustavo / Langerman, Justin / Vijayaraj, Preethi / Shia, David W / Meneses, Luisa K / Rickabaugh, Tammy M / Mulay, A / Konda, B / Sim, Myung S / Stripp, Barry R / Plath, Kathrin / Arumugaswami, Vaithilingaraja / Gomperts, Brigitte N

bioRxiv : the preprint server for biology

2020

Abstract: Most demographic studies are now associating current smoking status with increased risk of severe COVID-19 and mortality from the disease but there remain many questions about how direct cigarette smoke exposure affects SARS-CoV-2 airway cell infection. ... ...

Abstract	Most demographic studies are now associating current smoking status with increased risk of severe COVID-19 and mortality from the disease but there remain many questions about how direct cigarette smoke exposure affects SARS-CoV-2 airway cell infection. We directly exposed mucociliary air-liquid interface (ALI) cultures derived from primary human nonsmoker airway basal stem cells (ABSCs) to short term cigarette smoke and infected them with live SARS-CoV-2. We found an increase in the number of infected airway cells after cigarette smoke exposure as well as an increased number of apoptotic cells. Cigarette smoke exposure alone caused airway injury that resulted in an increased number of ABSCs, which proliferate to repair the airway. But we found that acute SARS-CoV-2 infection or the combination of exposure to cigarette smoke and SARS-CoV-2 did not induce ABSC proliferation. We set out to examine the underlying mechanism governing the increased susceptibility of cigarette smoke exposed ALI to SARS-CoV-2 infection. Single cell profiling of the cultures showed that infected airway cells displayed a global reduction in gene expression across all airway cell types. Interestingly, interferon response genes were induced in SARS-CoV-2 infected airway epithelial cells in the ALI cultures but smoking exposure together with SARS-CoV-2 infection reduced the interferon response. Treatment of cigarette smoke-exposed ALI cultures with Interferon β-1 abrogated the viral infection, suggesting that the lack of interferon response in the cigarette smoke-exposed ALI cultures allows for more severe viral infection and cell death. In summary, our data show that acute smoke exposure allows for more severe proximal airway epithelial disease from SARS-CoV-2 by reducing the mucosal innate immune response and ABSC proliferation and has implications for disease spread and severity in people exposed to cigarette smoke.
Keywords	covid19
Language	English
Publishing date	2020-07-29
Publishing country	United States
Document type	Preprint
DOI	10.1101/2020.07.28.226092
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Article ; Online: High-Throughput Drug Screening Identifies a Potent Wnt Inhibitor that Promotes Airway Basal Stem Cell Homeostasis.

Aros, Cody J / Paul, Manash K / Pantoja, Carla J / Bisht, Bharti / Meneses, Luisa K / Vijayaraj, Preethi / Sandlin, Jenna M / France, Bryan / Tse, Jonathan A / Chen, Michelle W / Shia, David W / Rickabaugh, Tammy M / Damoiseaux, Robert / Gomperts, Brigitte N

Cell reports

2020 Volume 30, Issue 7, Page(s) 2055–2064.e5

Abstract: Mechanisms underpinning airway epithelial homeostatic maintenance and ways to prevent its dysregulation remain elusive. Herein, we identify that β-catenin phosphorylated at Y489 (p-β- ... ...

Abstract	Mechanisms underpinning airway epithelial homeostatic maintenance and ways to prevent its dysregulation remain elusive. Herein, we identify that β-catenin phosphorylated at Y489 (p-β-catenin
MeSH term(s)	Animals ; Bronchi/cytology ; Bronchi/drug effects ; Bronchi/metabolism ; Bronchi/pathology ; Cell Differentiation/drug effects ; Drug Evaluation, Preclinical/methods ; Female ; High-Throughput Screening Assays/methods ; Homeostasis/drug effects ; Humans ; Lung/cytology ; Lung/drug effects ; Lung/metabolism ; Lung/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Precancerous Conditions/metabolism ; Precancerous Conditions/pathology ; Small Molecule Libraries/pharmacology ; Stem Cells/cytology ; Stem Cells/drug effects ; Stem Cells/metabolism ; Stem Cells/pathology ; Transfection ; Wnt Proteins/antagonists & inhibitors ; Wnt Proteins/metabolism ; Wnt Signaling Pathway/drug effects ; beta Catenin/antagonists & inhibitors ; beta Catenin/metabolism
Chemical Substances	Small Molecule Libraries ; Wnt Proteins ; beta Catenin
Language	English
Publishing date	2020-02-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2020.01.059
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Article ; Online: Distinct Spatiotemporally Dynamic Wnt-Secreting Niches Regulate Proximal Airway Regeneration and Aging.

Aros, Cody J / Vijayaraj, Preethi / Pantoja, Carla J / Bisht, Bharti / Meneses, Luisa K / Sandlin, Jenna M / Tse, Jonathan A / Chen, Michelle W / Purkayastha, Arunima / Shia, David W / Sucre, Jennifer M S / Rickabaugh, Tammy M / Vladar, Eszter K / Paul, Manash K / Gomperts, Brigitte N

Cell stem cell

2020 Volume 27, Issue 3, Page(s) 413–429.e4

Abstract: Our understanding of dynamic interactions between airway basal stem cells (ABSCs) and their signaling niches in homeostasis, injury, and aging remains elusive. Using transgenic mice and pharmacologic studies, we found that Wnt/β-catenin within ABSCs was ... ...

Abstract	Our understanding of dynamic interactions between airway basal stem cells (ABSCs) and their signaling niches in homeostasis, injury, and aging remains elusive. Using transgenic mice and pharmacologic studies, we found that Wnt/β-catenin within ABSCs was essential for proliferation post-injury in vivo. ABSC-derived Wnt ligand production was dispensable for epithelial proliferation. Instead, the PDGFRα
MeSH term(s)	Aging ; Animals ; Cell Differentiation ; Cell Proliferation ; Mice ; Mice, Transgenic ; Stem Cells/metabolism ; Wnt Signaling Pathway ; beta Catenin/metabolism
Chemical Substances	beta Catenin
Language	English
Publishing date	2020-07-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2020.06.019
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Zs.A 6589: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: A three-dimensional human model of the fibroblast activation that accompanies bronchopulmonary dysplasia identifies Notch-mediated pathophysiology.

Sucre, Jennifer M S / Wilkinson, Dan / Vijayaraj, Preethi / Paul, Manash / Dunn, Bruce / Alva-Ornelas, Jackelyn A / Gomperts, Brigitte N

American journal of physiology. Lung cellular and molecular physiology

2016 Volume 310, Issue 10, Page(s) L889–98

Abstract: Bronchopulmonary dysplasia (BPD) is a leading complication of premature birth and occurs primarily in infants delivered during the saccular stage of lung development. Histopathology shows decreased alveolarization and a pattern of fibroblast ... ...

Abstract	Bronchopulmonary dysplasia (BPD) is a leading complication of premature birth and occurs primarily in infants delivered during the saccular stage of lung development. Histopathology shows decreased alveolarization and a pattern of fibroblast proliferation and differentiation to the myofibroblast phenotype. Little is known about the molecular pathways and cellular mechanisms that define BPD pathophysiology and progression. We have developed a novel three-dimensional human model of the fibroblast activation associated with BPD, and using this model we have identified the Notch pathway as a key driver of fibroblast activation and proliferation in response to changes in oxygen. Fetal lung fibroblasts were cultured on sodium alginate beads to generate lung organoids. After exposure to alternating hypoxia and hyperoxia, the organoids developed a phenotypic response characterized by increased α-smooth muscle actin (α-SMA) expression and other genes known to be upregulated in BPD and also demonstrated increased expression of downstream effectors of the Notch pathway. Inhibition of Notch with a γ-secretase inhibitor prevented the development of the pattern of cellular proliferation and α-SMA expression in our model. Analysis of human autopsy tissue from the lungs of infants who expired with BPD demonstrated evidence of Notch activation within fibrotic areas of the alveolar septae, suggesting that Notch may be a key driver of BPD pathophysiology.
MeSH term(s)	Alginates/chemistry ; Bronchopulmonary Dysplasia/metabolism ; Bronchopulmonary Dysplasia/pathology ; Cell Culture Techniques ; Cell Hypoxia ; Cells, Cultured ; Culture Media/chemistry ; Glucuronic Acid/chemistry ; Hexuronic Acids/chemistry ; Humans ; Receptors, Notch/metabolism ; Signal Transduction
Chemical Substances	Alginates ; Culture Media ; Hexuronic Acids ; Receptors, Notch ; Glucuronic Acid (8A5D83Q4RW)
Language	English
Publishing date	2016-03-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00446.2015
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