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  1. Book ; Thesis: Aktiviertes Protein C kontrolliert epigenetisch p66shc

    Bock, Fabian

    ein neuer Schutzmechanismus im Rahmen der experimentellen diabetischen Nephropathie

    2015  

    Author's details vorgelegt von Fabian Maximilian Bock
    Language German
    Size 69 Blätter, Illustrationen, Diagramme
    Publishing place Heidelberg
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Dissertation, Ruprecht-Karls-Universität Heidelberg, 2016
    HBZ-ID HT019199594
    Database Catalogue ZB MED Medicine, Health

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  2. Article ; Online: Does it matter how we measure urinary creatinine in patients taking SGLT2 inhibitors?

    Bock, Fabian / Isermann, Berend

    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

    2023  Volume 39, Issue 5, Page(s) 739–741

    MeSH term(s) Humans ; Sodium-Glucose Transporter 2 Inhibitors/adverse effects ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use ; Creatinine/urine ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/urine ; Glomerular Filtration Rate ; Hypoglycemic Agents/therapeutic use ; Hypoglycemic Agents/adverse effects
    Chemical Substances Sodium-Glucose Transporter 2 Inhibitors ; Creatinine (AYI8EX34EU) ; Hypoglycemic Agents
    Language English
    Publishing date 2023-12-23
    Publishing country England
    Document type Editorial ; Journal Article
    ZDB-ID 90594-x
    ISSN 1460-2385 ; 0931-0509
    ISSN (online) 1460-2385
    ISSN 0931-0509
    DOI 10.1093/ndt/gfae007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: On-street parking availaibilty data in San Francisco, from stationary sensors and high-mileage probe vehicles.

    Bock, Fabian / Di Martino, Sergio

    Data in brief

    2019  Volume 25, Page(s) 104039

    Abstract: This dataset contains records of the measured on-street parking availability in San Francisco, obtained from the public API of ... ...

    Abstract This dataset contains records of the measured on-street parking availability in San Francisco, obtained from the public API of the
    Language English
    Publishing date 2019-06-04
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2786545-9
    ISSN 2352-3409 ; 2352-3409
    ISSN (online) 2352-3409
    ISSN 2352-3409
    DOI 10.1016/j.dib.2019.104039
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: High sodium intake does not worsen low potassium-induced kidney damage.

    Zhang, Yahua / Arroyo, Juan Pablo / Bock, Fabian / Zhang, Ming-Zhi / Harris, Raymond C / Terker, Andrew S

    Physiological reports

    2023  Volume 11, Issue 8, Page(s) e15671

    Abstract: High sodium and low potassium intake have both been linked to poor cardiovascular health outcomes and increased mortality rates. A combination of the two is thought to be particularly detrimental. While mechanisms are multiple, the kidney is an important ...

    Abstract High sodium and low potassium intake have both been linked to poor cardiovascular health outcomes and increased mortality rates. A combination of the two is thought to be particularly detrimental. While mechanisms are multiple, the kidney is an important target of harmful effects and low potassium influences on both proximal and distal nephron segments are especially potent. We recently reported that a combined high sodium/low potassium diet causes kidney injury and that low potassium in isolation can have similar effects. However, how sodium intake alters this process is not well-understood. Here we tested the hypothesis that a high sodium intake amplifies effects of low dietary potassium on kidney injury. We observed adding high sodium to low potassium caused an expected increase in blood pressure, but did not worsen markers of kidney injury, inflammation, and fibrosis. It also did not increase abundance or phosphorylation of the sodium chloride cotransporter or its regulatory kinases, SPAK and OxSR1, known renal targets of low potassium. Findings support the claim that dietary potassium deficiency, and not high sodium, is a dominant factor affecting kidney injury in animal models of high sodium/low potassium intake. This suggests further investigation is required to identify optimal ranges of sodium and potassium intake in both healthy populations and in those with kidney disease.
    MeSH term(s) Animals ; Kidney ; Sodium ; Kidney Diseases ; Potassium ; Sodium, Dietary/adverse effects
    Chemical Substances Sodium (9NEZ333N27) ; Potassium (RWP5GA015D) ; Sodium, Dietary
    Language English
    Publishing date 2023-04-20
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.15671
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Book: Lernkarten Biochemie

    Bock, Fabian

    die komplette Biochemie in einem Set

    2013  

    Author's details Fabian Bock
    Keywords Physiologische Chemie ; Biochemie
    Language German
    Size 293 Lernkarten in Schuber, Ill
    Edition vollst. neu konzipierte Aufl., 1. Aufl
    Publisher Urban & Fischer in Elsevier
    Publishing place München
    Document type Book
    ISBN 3437435833 ; 9783437435836
    Database Former special subject collection: coastal and deep sea fishing

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  6. Article: On-street parking availaibilty data in San Francisco, from stationary sensors and high-mileage probe vehicles

    Bock, Fabian / Di Martino, Sergio

    Data in Brief. 2019 Aug., v. 25

    2019  

    Abstract: This dataset contains records of the measured on-street parking availability in San Francisco, obtained from the public API of the SFpark project.¹In 2011, the San Francisco Municipal Transportation Agency (SFMTA) started a project on smart parking, ... ...

    Abstract This dataset contains records of the measured on-street parking availability in San Francisco, obtained from the public API of the SFpark project.¹In 2011, the San Francisco Municipal Transportation Agency (SFMTA) started a project on smart parking, called SFpark, whose goal was the improvement of on-street parking management in San Francisco, mostly by means of demand-responsive price adjustments [1]. One of the key points of the project was the collection of information about on-street parking availability. To this aim, about 8,000 parking spaces were equipped with specific sensors in the asphalt, periodically broadcasting availability information. The SFpark project made available a public REST API, returning the number of free parking spaces and total number of provided parking spaces per road segment, for 5,314 parking spaces on 579 road segments in the pilot area. We collected parking availability data from 2013/06/13 until 2013/07/24, by querying this API at approximately 5-min intervals. As a result, we obtained in total about 7 million observations of parking availability on the road segments. These observations represent the first dataset we are providing.In addition, we simulated the achievable sensing coverage of on-street parking availability that could be achieved by a fleet of taxis, if they were equipped with sensors able to detect free parking spaces, like side-scanning ultrasonic sensors [3], or windshield-mounted cameras [4]. In particular, by exploiting real taxi trajectories in San Francisco from the Cabspotting project [5], we first computed the frequencies of taxi visits for each road segment covered by the SFpark sensors. Then, we downsampled the first dataset, in order to have a parking availability information for a road segment at a given time only in presence of a transit of a taxi on that segment at that time. This step was replicated for 5 different sizes of taxi fleets, namely 100, 200, 300, 400, and 486.Consequently, in total six datasets are available for further research in the field of on-street parking dynamics.All these datasets can be downloaded at: https://dataverse.harvard.edu/dataset.xhtml?persistentId=doi:10.7910/DVN/YLWCSU.
    Keywords bitumen ; data collection ; prices ; transportation ; ultrasonics
    Language English
    Dates of publication 2019-08
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 2786545-9
    ISSN 2352-3409
    ISSN 2352-3409
    DOI 10.1016/j.dib.2019.104039
    Database NAL-Catalogue (AGRICOLA)

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  7. Article ; Online: Rac1 promotes kidney collecting duct repair by mechanically coupling cell morphology to mitotic entry.

    Bock, Fabian / Dong, Xinyu / Li, Shensen / Viquez, Olga M / Sha, Eric / Tantengco, Matthew / Hennen, Elizabeth M / Plosa, Erin / Ramezani, Alireza / Brown, Kyle L / Whang, Young Mi / Terker, Andrew S / Arroyo, Juan Pablo / Harrison, David G / Fogo, Agnes / Brakebusch, Cord H / Pozzi, Ambra / Zent, Roy

    Science advances

    2024  Volume 10, Issue 6, Page(s) eadi7840

    Abstract: Prolonged obstruction of the ureter, which leads to injury of the kidney collecting ducts, results in permanent structural damage, while early reversal allows for repair. Cell structure is defined by the actin cytoskeleton, which is dynamically organized ...

    Abstract Prolonged obstruction of the ureter, which leads to injury of the kidney collecting ducts, results in permanent structural damage, while early reversal allows for repair. Cell structure is defined by the actin cytoskeleton, which is dynamically organized by small Rho guanosine triphosphatases (GTPases). In this study, we identified the Rho GTPase, Rac1, as a driver of postobstructive kidney collecting duct repair. After the relief of ureteric obstruction, Rac1 promoted actin cytoskeletal reconstitution, which was required to maintain normal mitotic morphology allowing for successful cell division. Mechanistically, Rac1 restricted excessive actomyosin activity that stabilized the negative mitotic entry kinase Wee1. This mechanism ensured mechanical G
    MeSH term(s) Kidney Tubules, Collecting/metabolism ; rac1 GTP-Binding Protein/metabolism ; Cytoskeleton/metabolism ; Actins/metabolism ; Actin Cytoskeleton/metabolism
    Chemical Substances rac1 GTP-Binding Protein (EC 3.6.5.2) ; Actins
    Language English
    Publishing date 2024-02-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.adi7840
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Insulin-regulated aminopeptidase is required for water excretion in response to acute hypotonic stress.

    Zuchowski, Yvonne / Carty, Joshua / Terker, Andrew S / Bock, Fabian / Trapani, Jonathan B / Bhave, Gautam / Watts, Jason A / Keller, Susanna / Zhang, Mingzhi / Zent, Roy / Harris, Raymond C / Arroyo, Juan Pablo

    American journal of physiology. Renal physiology

    2023  Volume 324, Issue 6, Page(s) F521–F531

    Abstract: The objective of this study was to understand the response of mice lacking insulin-regulated aminopeptidase (IRAP) to an acute water load. For mammals to respond appropriately to acute water loading, vasopressin activity needs to decrease. IRAP degrades ... ...

    Abstract The objective of this study was to understand the response of mice lacking insulin-regulated aminopeptidase (IRAP) to an acute water load. For mammals to respond appropriately to acute water loading, vasopressin activity needs to decrease. IRAP degrades vasopressin in vivo. Therefore, we hypothesized that mice lacking IRAP have an impaired ability to degrade vasopressin and, thus, have persistent urinary concentration. Age-matched 8- to 12-wk-old IRAP wild-type (WT) and knockout (KO) male mice were used for all experiments. Blood electrolytes and urine osmolality were measured before and 1 h after water load (∼2 mL sterile water via intraperitoneal injection). Urine was collected from IRAP WT and KO mice for urine osmolality measurements at baseline and after 1 h administration of the vasopressin type 2 receptor antagonist OPC-31260 (10 mg/kg ip). Immunofluorescence and immunoblot analysis were performed on kidneys at baseline and after 1 h acute water load. IRAP was expressed in the glomerulus, thick ascending loop of Henle, distal tubule, connecting duct, and collecting duct. IRAP KO mice had elevated urine osmolality compared with WT mice due to higher membrane expression of aquaporin 2 (AQP2), which was restored to that of controls after administration of OPC-31260. IRAP KO mice developed hyponatremia after an acute water load because they were unable to increase free water excretion due to increased surface expression of AQP2. In conclusion, IRAP is required to increase water excretion in response to an acute water load due to persistent vasopressin stimulation of AQP2.
    MeSH term(s) Animals ; Male ; Mice ; Aminopeptidases/genetics ; Aminopeptidases/metabolism ; Aquaporin 2/genetics ; Aquaporin 2/metabolism ; Insulin/metabolism ; Mammals/metabolism ; Osmotic Pressure ; Vasopressins/pharmacology ; Vasopressins/metabolism ; Water/metabolism
    Chemical Substances Aminopeptidases (EC 3.4.11.-) ; Aquaporin 2 ; Insulin ; Vasopressins (11000-17-2) ; Water (059QF0KO0R) ; leucyl-cystinyl aminopeptidase (EC 3.4.11.3)
    Language English
    Publishing date 2023-03-30
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00318.2022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Angiotensin II acts through Rac1 to upregulate pendrin: role of NADPH oxidase.

    Pham, Truyen D / Verlander, Jill W / Chen, Chao / Pech, Vladimir / Kim, Hailey I / Kim, Young Hee / Weiner, I David / Milne, Ginger L / Zent, Roy / Bock, Fabian / Brown, Dennis / Eaton, Amity / Wall, Susan M

    American journal of physiology. Renal physiology

    2023  Volume 326, Issue 2, Page(s) F202–F218

    Abstract: Angiotensin II increases apical plasma membrane pendrin abundance and function. This study explored the role of the small GTPase Rac1 in the regulation of pendrin by angiotensin II. To do this, we generated intercalated cell (IC) Rac1 knockout mice and ... ...

    Abstract Angiotensin II increases apical plasma membrane pendrin abundance and function. This study explored the role of the small GTPase Rac1 in the regulation of pendrin by angiotensin II. To do this, we generated intercalated cell (IC) Rac1 knockout mice and observed that IC Rac1 gene ablation reduced the relative abundance of pendrin in the apical region of intercalated cells in angiotensin II-treated mice but not vehicle-treated mice. Similarly, the Rac1 inhibitor EHT 1864 reduced apical pendrin abundance in angiotensin II-treated mice, through a mechanism that does not require aldosterone. This IC angiotensin II-Rac1 signaling cascade modulates pendrin subcellular distribution without significantly changing actin organization. However, NADPH oxidase inhibition with APX 115 reduced apical pendrin abundance in vivo in angiotensin II-treated mice. Moreover, superoxide dismutase mimetics reduced Cl
    MeSH term(s) Animals ; Mice ; Aldosterone/pharmacology ; Aldosterone/metabolism ; Angiotensin II/pharmacology ; Angiotensin II/metabolism ; Mice, Knockout ; NADPH Oxidases/metabolism ; Sulfate Transporters/genetics ; Superoxides/metabolism ; rac1 GTP-Binding Protein/metabolism
    Chemical Substances Aldosterone (4964P6T9RB) ; Angiotensin II (11128-99-7) ; NADPH Oxidases (EC 1.6.3.-) ; Sulfate Transporters ; Superoxides (11062-77-4) ; Rac1 protein, mouse ; rac1 GTP-Binding Protein (EC 3.6.5.2) ; Slc26a4 protein, mouse
    Language English
    Publishing date 2023-12-07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00139.2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Alveolar repair following LPS-induced injury requires cell-ECM interactions.

    Sucre, Jennifer Ms / Bock, Fabian / Negretti, Nicholas M / Benjamin, John T / Gulleman, Peter M / Dong, Xinyu / Ferguson, Kimberly T / Jetter, Christopher S / Han, Wei / Liu, Yang / Kook, Seunghyi / Gokey, Jason J / Guttentag, Susan H / Kropski, Jonathan A / Blackwell, Timothy S / Zent, Roy / Plosa, Erin J

    JCI insight

    2023  Volume 8, Issue 14

    Abstract: During alveolar repair, alveolar type 2 (AT2) epithelial cell progenitors rapidly proliferate and differentiate into flat AT1 epithelial cells. Failure of normal alveolar repair mechanisms can lead to loss of alveolar structure (emphysema) or development ...

    Abstract During alveolar repair, alveolar type 2 (AT2) epithelial cell progenitors rapidly proliferate and differentiate into flat AT1 epithelial cells. Failure of normal alveolar repair mechanisms can lead to loss of alveolar structure (emphysema) or development of fibrosis, depending on the type and severity of injury. To test if β1-containing integrins are required during repair following acute injury, we administered E. coli lipopolysaccharide (LPS) by intratracheal injection to mice with a postdevelopmental deletion of β1 integrin in AT2 cells. While control mice recovered from LPS injury without structural abnormalities, β1-deficient mice had more severe inflammation and developed emphysema. In addition, recovering alveoli were repopulated with an abundance of rounded epithelial cells coexpressing AT2 epithelial, AT1 epithelial, and mixed intermediate cell state markers, with few mature type 1 cells. AT2 cells deficient in β1 showed persistently increased proliferation after injury, which was blocked by inhibiting NF-κB activation in these cells. Lineage tracing experiments revealed that β1-deficient AT2 cells failed to differentiate into mature AT1 epithelial cells. Together, these findings demonstrate that functional alveolar repair after injury with terminal alveolar epithelial differentiation requires β1-containing integrins.
    MeSH term(s) Mice ; Animals ; Lipopolysaccharides/toxicity ; Escherichia coli ; Lung ; Emphysema ; Integrins
    Chemical Substances Lipopolysaccharides ; Integrins
    Language English
    Publishing date 2023-07-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.167211
    Database MEDical Literature Analysis and Retrieval System OnLINE

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