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  1. AU="Koba, Wade R"
  2. AU="Cui, Hongyan"
  3. AU="Ross, Nina E"
  4. AU="Atwa, Hanaa A"
  5. AU="Reid, Carly"

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  1. Article: Haematopoietic stem cell numbers are not solely determined by niche availability.

    Takeishi, Shoichiro / Marchand, Tony / Koba, Wade R / Borger, Daniel K / Xu, Chunliang / Guha, Chandan / Bergman, Aviv / Frenette, Paul S / Gritsman, Kira / Steidl, Ulrich

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Haematopoietic stem cells (HSCs) reside in specialized microenvironments, also referred to as niches, and it has been widely believed that HSC numbers are determined by the niche size ... ...

    Abstract Haematopoietic stem cells (HSCs) reside in specialized microenvironments, also referred to as niches, and it has been widely believed that HSC numbers are determined by the niche size alone
    Language English
    Publishing date 2023-10-29
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.10.28.564559
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Prenatal vitamin D deficiency alters immune cell proportions of young adult offspring through alteration of long-term stem cell fates.

    Ueda, Koki / Chin, Shu Shien / Sato, Noriko / Nishikawa, Miyu / Yasuda, Kaori / Miyasaka, Naoyuki / Bera, Betelehem Solomon / Chorro, Laurent / Doña-Termine, Reanna / Koba, Wade R / Reynolds, David / Steidl, Ulrich G / Lauvau, Gregoire / Greally, John M / Suzuki, Masako

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Vitamin D deficiency is a common deficiency worldwide, particularly among women of reproductive age. During pregnancy, it increases the risk of immune-related diseases in offspring later in life. However, exactly how the body remembers exposure to an ... ...

    Abstract Vitamin D deficiency is a common deficiency worldwide, particularly among women of reproductive age. During pregnancy, it increases the risk of immune-related diseases in offspring later in life. However, exactly how the body remembers exposure to an adverse environment during development is poorly understood. Herein, we explore the effects of prenatal vitamin D deficiency on immune cell proportions in offspring using vitamin D deficient mice established by dietary manipulation. We show that prenatal vitamin D deficiency alters immune cell proportions in offspring by changing the transcriptional properties of genes downstream of vitamin D receptor signaling in hematopoietic stem and progenitor cells of both the fetus and adults. Further investigations of the associations between maternal vitamin D levels and cord blood immune cell profiles from 75 healthy pregnant women and their term babies also confirm that maternal vitamin D levels significantly affect immune cell proportions in the babies. Thus, lack of prenatal vitamin D, particularly at the time of hematopoietic stem cell migration from the liver to the bone marrow, has long-lasting effects on immune cell proportions. This highlights the importance of providing vitamin D supplementation at specific stages of pregnancy.
    Language English
    Publishing date 2023-09-13
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.09.11.557255
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  3. Article: Non-Invasive Targeted Hepatic Irradiation and SPECT/CT Functional Imaging to Study Radiation-Induced Liver Damage in Small Animal Models.

    Kabarriti, Rafi / Brodin, N Patrik / Yaffe, Hillary / Barahman, Mark / Koba, Wade R / Liu, Laibin / Asp, Patrik / Tomé, Wolfgang A / Guha, Chandan

    Cancers

    2019  Volume 11, Issue 11

    Abstract: Radiation therapy (RT) has traditionally not been widely used in the management of hepatic malignancies for fear of toxicity in the form of radiation-induced liver disease (RILD). Pre-clinical hepatic irradiation models can provide clinicians with better ...

    Abstract Radiation therapy (RT) has traditionally not been widely used in the management of hepatic malignancies for fear of toxicity in the form of radiation-induced liver disease (RILD). Pre-clinical hepatic irradiation models can provide clinicians with better understanding of the radiation tolerance of the liver, which in turn may lead to the development of more effective cancer treatments. Previous models of hepatic irradiation are limited by either invasive laparotomy procedures, or the need to irradiate the whole or large parts of the liver using external skin markers. In the setting of modern-day radiation oncology, a truly translational animal model would require the ability to deliver RT to specific parts of the liver, through non-invasive image guidance methods. To this end, we developed a targeted hepatic irradiation model on the Small Animal Radiation Research Platform (SARRP) using contrast-enhanced cone-beam computed tomography image guidance. Using this model, we showed evidence of the early development of region-specific RILD through functional single photon emission computed tomography (SPECT) imaging.
    Language English
    Publishing date 2019-11-15
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers11111796
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Bisected, complex N-glycans and galectins in mouse mammary tumor progression and human breast cancer.

    Miwa, Hazuki E / Koba, Wade R / Fine, Eugene J / Giricz, Orsi / Kenny, Paraic A / Stanley, Pamela

    Glycobiology

    2013  Volume 23, Issue 12, Page(s) 1477–1490

    Abstract: Bisected, complex N-glycans on glycoproteins are generated by the glycosyltransferase MGAT3 and cause reduced cell surface binding of galectins. Previously, we showed that MGAT3 reduces growth factor signaling and retards mammary tumor progression driven ...

    Abstract Bisected, complex N-glycans on glycoproteins are generated by the glycosyltransferase MGAT3 and cause reduced cell surface binding of galectins. Previously, we showed that MGAT3 reduces growth factor signaling and retards mammary tumor progression driven by the Polyoma middle T antigen (PyMT) expressed in mammary epithelium under the mouse mammary tumor virus (MMTV) promoter. However, the penetrance of the tumor phenotype became variable in mixed FVB/N and C57BL/6 female mice and we therefore investigated a congenic C57BL/6 Mgat3(-/-)/MMTV-PyMT model. In the absence of MGAT3, C57BL/6 Mgat3(-/-)/MMTV-PyMT females exhibited accelerated tumor appearance and increased tumor burden, glucose uptake in tumors and lung metastasis. Nevertheless, activation of extracellular signal-regulated kinase (ERK)1/2 or protein kinase B (AKT) was reduced in ∼20-week C57BL/6 MMTV-PyMT tumors lacking MGAT3. Activation of focal adhesion kinase (FAK), protein tyrosine kinase Src, and p38 mitogen-activated protein kinase were similar to that of controls. All the eight mouse galectin genes were expressed in mammary tumors and tumor epithelial cells (TECs), but galectin-2 and -12 were not detected by western analysis in tumors, and galectin-7 was not detected in 60% of the TEC lines. From microarray data reported for human breast cancers, at least 10 galectin and 7 N-glycan N-acetylglucosaminyl (GlcNAc)-transferase (MGAT) genes are expressed in tumor tissue, and expression often varies significantly between different breast cancer subtypes. Thus, in summary, while MGAT3 and bisected complex N-glycans retard mouse mammary tumor progression, genetic background may modify this effect; identification of key galectins that promote mammary tumor progression in mice is not straightforward because all the eight galectin genes are expressed; and high levels of MGAT3, galectin-4, -8, -10, -13 and -14 transcripts correlate with better relapse-free survival in human breast cancer.
    MeSH term(s) Animals ; Antigens, Polyomavirus Transforming/metabolism ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Disease Models, Animal ; Disease Progression ; Female ; Galectins/metabolism ; Humans ; Mammary Neoplasms, Experimental/genetics ; Mammary Neoplasms, Experimental/metabolism ; Mammary Neoplasms, Experimental/pathology ; Mammary Tumor Virus, Mouse/metabolism ; Mice ; Mice, Inbred Strains ; N-Acetylglucosaminyltransferases/deficiency ; N-Acetylglucosaminyltransferases/genetics ; N-Acetylglucosaminyltransferases/metabolism ; Polysaccharides/metabolism
    Chemical Substances Antigens, Polyomavirus Transforming ; Galectins ; Polysaccharides ; N-Acetylglucosaminyltransferases (EC 2.4.1.-) ; beta-1,4-mannosyl-glycoprotein beta-1,4-N-acetylglucosaminyltransferase (EC 2.4.1.144)
    Language English
    Publishing date 2013-09-13
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1067689-2
    ISSN 1460-2423 ; 0959-6658
    ISSN (online) 1460-2423
    ISSN 0959-6658
    DOI 10.1093/glycob/cwt075
    Database MEDical Literature Analysis and Retrieval System OnLINE

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