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  1. Article ; Online: Variation in bony landmarks and predictors of success with sacral neuromodulation.

    Husk, Katherine E / Norris, Lauren D / Willis-Gray, Marcella G / Borawski, Kristy M / Geller, Elizabeth J

    International urogynecology journal

    2019  Volume 30, Issue 11, Page(s) 1973–1979

    Abstract: Introduction and hypothesis: We assessed variations in sacral anatomy and lead placement as predictors of sacral neuromodulation (SNM) success. Based solely on bony landmarks, we also assessed the accuracy of the 9 and 2 protocol for locating S3.: ... ...

    Abstract Introduction and hypothesis: We assessed variations in sacral anatomy and lead placement as predictors of sacral neuromodulation (SNM) success. Based solely on bony landmarks, we also assessed the accuracy of the 9 and 2 protocol for locating S3.
    Methods: This is a retrospective cohort study performed from October 2008 to December 2016 at the University of North Carolina at Chapel Hill. Fluoroscopic images were used to assess sacral anatomy and lead location. Success was defined as >50% symptom improvement after stage I and clinical response at most recent follow-up.
    Results: Of 249 procedures, 209 were primary implants and 40 were revisions among 187 (89.5%) women and 22 (10.5%) men. Success rate was 83.3% for primary implants and 89.4% for revisions. Success was associated with shorter implant duration (21.3 ± 22.2 vs 33.6 ± 25.8 months), higher body mass index (30.3 ± 7.8 vs 27.6 ± 6.1 kg/m
    Conclusions: Variations in sacral anatomy and lead placement did not predict SNM success. The 2-cm protocol was verified while the 9-cm protocol was not, although neither was predictive of success, which may obviate the need to mark bony landmarks prior to fluoroscopy.
    MeSH term(s) Adult ; Aged ; Anatomic Landmarks ; Cohort Studies ; Electric Stimulation Therapy/instrumentation ; Female ; Forecasting ; Humans ; Implantable Neurostimulators ; Male ; Middle Aged ; Retrospective Studies ; Sacrum/anatomy & histology ; Treatment Outcome ; Urinary Bladder, Overactive/therapy
    Language English
    Publishing date 2019-02-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 1050631-7
    ISSN 1433-3023 ; 0937-3462
    ISSN (online) 1433-3023
    ISSN 0937-3462
    DOI 10.1007/s00192-019-03883-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3070: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: A gut-restricted glutamate carboxypeptidase II inhibitor reduces monocytic inflammation and improves preclinical colitis.

    Peters, Diane E / Norris, Lauren D / Tenora, Lukáš / Šnajdr, Ivan / Ponti, András K / Zhu, Xiaolei / Sakamoto, Shinji / Veeravalli, Vijayabhaskar / Pradhan, Manisha / Alt, Jesse / Thomas, Ajit G / Majer, Pavel / Rais, Rana / McDonald, Christine / Slusher, Barbara S

    Science translational medicine

    2023  Volume 15, Issue 708, Page(s) eabn7491

    Abstract: There is an urgent need to develop therapeutics for inflammatory bowel disease (IBD) because up to 40% of patients with moderate-to-severe IBD are not adequately controlled with existing drugs. Glutamate carboxypeptidase II (GCPII) has emerged as a ... ...

    Abstract There is an urgent need to develop therapeutics for inflammatory bowel disease (IBD) because up to 40% of patients with moderate-to-severe IBD are not adequately controlled with existing drugs. Glutamate carboxypeptidase II (GCPII) has emerged as a promising therapeutic target. This enzyme is minimally expressed in normal ileum and colon, but it is markedly up-regulated in biopsies from patients with IBD and preclinical colitis models. Here, we generated a class of GCPII inhibitors designed to be gut-restricted for oral administration, and we interrogated efficacy and mechanism using in vitro and in vivo models. The lead inhibitor, (
    MeSH term(s) Animals ; Humans ; Mice ; Colitis/drug therapy ; Colitis/metabolism ; Colon/pathology ; Cytokines/metabolism ; Disease Models, Animal ; Glutamate Carboxypeptidase II/antagonists & inhibitors ; Inflammation/pathology ; Inflammatory Bowel Diseases/drug therapy ; Inflammatory Bowel Diseases/pathology ; Mice, Inbred C57BL
    Chemical Substances Cytokines ; Glutamate Carboxypeptidase II (EC 3.4.17.21)
    Language English
    Publishing date 2023-08-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.abn7491
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6941: 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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  3. Article ; Online: Partner-Drug Resistance and Population Substructuring of Artemisinin-Resistant Plasmodium falciparum in Cambodia.

    Parobek, Christian M / Parr, Jonathan B / Brazeau, Nicholas F / Lon, Chanthap / Chaorattanakawee, Suwanna / Gosi, Panita / Barnett, Eric J / Norris, Lauren D / Meshnick, Steven R / Spring, Michele D / Lanteri, Charlotte A / Bailey, Jeffrey A / Saunders, David L / Lin, Jessica T / Juliano, Jonathan J

    Genome biology and evolution

    2017  Volume 9, Issue 6, Page(s) 1673–1686

    Abstract: Plasmodium falciparum in western Cambodia has developed resistance to artemisinin and its partner drugs, causing frequent treatment failure. Understanding this evolution can inform the deployment of new therapies. We investigated the genetic architecture ...

    Abstract Plasmodium falciparum in western Cambodia has developed resistance to artemisinin and its partner drugs, causing frequent treatment failure. Understanding this evolution can inform the deployment of new therapies. We investigated the genetic architecture of 78 falciparum isolates using whole-genome sequencing, correlating results to in vivo and ex vivo drug resistance and exploring the relationship between population structure, demographic history, and partner drug resistance. Principle component analysis, network analysis and demographic inference identified a diverse central population with three clusters of clonally expanding parasite populations, each associated with specific K13 artemisinin resistance alleles and partner drug resistance profiles which were consistent with the sequential deployment of artemisinin combination therapies in the region. One cluster displayed ex vivo piperaquine resistance and mefloquine sensitivity with a high rate of in vivo failure of dihydroartemisinin-piperaquine. Another cluster displayed ex vivo mefloquine resistance and piperaquine sensitivity with high in vivo efficacy of dihydroartemisinin-piperaquine. The final cluster was clonal and displayed intermediate sensitivity to both drugs. Variations in recently described piperaquine resistance markers did not explain the difference in mean IC90 or clinical failures between the high and intermediate piperaquine resistance groups, suggesting additional loci may be involved in resistance. The results highlight an important role for partner drug resistance in shaping the P. falciparum genetic landscape in Southeast Asia and suggest that further work is needed to evaluate for other mutations that drive piperaquine resistance.
    MeSH term(s) Adult ; Antipruritics/pharmacology ; Artemisinins/pharmacology ; Cambodia ; Drug Resistance ; Female ; Humans ; Malaria, Falciparum/drug therapy ; Malaria, Falciparum/parasitology ; Male ; Mefloquine/pharmacology ; Phylogeny ; Plasmodium falciparum/classification ; Plasmodium falciparum/drug effects ; Plasmodium falciparum/genetics ; Plasmodium falciparum/isolation & purification ; Protozoan Proteins/genetics ; Protozoan Proteins/metabolism ; Quinolines/pharmacology ; Treatment Failure
    Chemical Substances Antipruritics ; Artemisinins ; Protozoan Proteins ; Quinolines ; artemisinin (9RMU91N5K2) ; piperaquine (A0HV2Q956Y) ; Mefloquine (TML814419R)
    Language English
    Publishing date 2017-08-29
    Publishing country England
    Document type Journal Article
    ZDB-ID 2495328-3
    ISSN 1759-6653 ; 1759-6653
    ISSN (online) 1759-6653
    ISSN 1759-6653
    DOI 10.1093/gbe/evx126
    Database MEDical Literature Analysis and Retrieval System OnLINE

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