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Article ; Online: Micropuncture of the kidney: a primer on techniques.

Lorenz, John N

Comprehensive Physiology

2012 Volume 2, Issue 1, Page(s) 621–637

Abstract: Techniques to evaluate renal function at the single nephron level have been instrumental and indispensible in furthering our understanding of the mammalian kidney. Techniques that were first introduce in the 1920s, and later refined in the 1950s and ... ...

Abstract	Techniques to evaluate renal function at the single nephron level have been instrumental and indispensible in furthering our understanding of the mammalian kidney. Techniques that were first introduce in the 1920s, and later refined in the 1950s and 1960s, permit sophisticated interrogation of glomerular filtration and hemodynamics, and tubular epithelial transport activity. Much of what we know about the physiology and pathophysiology of the kidney has been produced or, to some degree, confirmed by renal micropuncture. While micropuncture is perhaps not as widely employed as before, it remains an essential tool for comprehensive evaluation of kidney function, particularly in this age of genetically pliable experimental models. This review aims to provide a introduction to common methodologies and approaches used to conduct micropuncture experiments. Topics covered include instrumentation and equipment, pipet fabrication techniques, animal preparation, and experimental procedures for evaluating single nephron hemodynamics and tubular function.
MeSH term(s)	Animals ; Electrochemical Techniques/methods ; Feedback, Physiological/physiology ; Glomerular Filtration Rate/physiology ; Hemodynamics ; Kidney/physiology ; Kidney Function Tests/methods ; Kidney Tubules/physiology ; Nephrons/blood supply ; Nephrons/physiology ; Punctures/instrumentation ; Punctures/methods ; Punctures/trends ; Specimen Handling/methods
Language	English
Publishing date	2012-01
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2040-4603
ISSN (online)	2040-4603
DOI	10.1002/cphy.c110035
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Chymase: the other ACE?

Lorenz, John N

American journal of physiology. Renal physiology

2009 Volume 298, Issue 1, Page(s) F35–6

MeSH term(s)	Angiotensin II/metabolism ; Animals ; Chymases/metabolism ; Diabetes Complications/metabolism ; Diabetic Nephropathies/etiology ; Diabetic Nephropathies/metabolism ; Disease Models, Animal ; Humans ; Hypertension/etiology ; Hypertension/metabolism ; Kidney/metabolism ; Mice ; Peptidyl-Dipeptidase A/metabolism ; Receptors, Leptin/genetics ; Receptors, Leptin/metabolism ; Signal Transduction/physiology
Chemical Substances	Receptors, Leptin ; Angiotensin II (11128-99-7) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; Chymases (EC 3.4.21.39)
Language	English
Publishing date	2009-11-18
Publishing country	United States
Document type	Comment ; Editorial ; 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.00641.2009
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Article: Unlocking the Role of sMyBP-C: A Key Player in Skeletal Muscle Development and Growth.

Song, Taejeong / McNamara, James W / Baby, Akhil / Ma, Weikang / Landim-Vieira, Maicon / Natesan, Sankar / Pinto, Jose Renato / Lorenz, John N / Irving, Thomas C / Sadayappan, Sakthivel

bioRxiv : the preprint server for biology

2023

Abstract: Skeletal muscle is the largest organ in the body, responsible for gross movement and metabolic regulation. Recently, variants in ... ...

Abstract	Skeletal muscle is the largest organ in the body, responsible for gross movement and metabolic regulation. Recently, variants in the
Language	English
Publishing date	2023-11-30
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.10.23.563591
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Article: HuR inhibition reduces post-ischemic cardiac remodeling by dampening acute inflammatory gene expression and the innate immune response.

Slone, Samuel / Anthony, Sarah R / Green, Lisa C / Nieman, Michelle L / Alam, Perwez / Wu, Xiaoqing / Roy, Sudeshna / Aube, Jeffrey / Xu, Liang / Lorenz, John N / Owens, A Phillip / Kanisicak, Onur / Tranter, Michael

bioRxiv : the preprint server for biology

2023

Abstract: Myocardial ischemia/reperfusion (I/R) injury and the resulting cardiac remodeling is a common cause of heart failure. The RNA binding protein Human Antigen R (HuR) has been previously shown to reduce cardiac remodeling following both I/R and cardiac ... ...

Abstract	Myocardial ischemia/reperfusion (I/R) injury and the resulting cardiac remodeling is a common cause of heart failure. The RNA binding protein Human Antigen R (HuR) has been previously shown to reduce cardiac remodeling following both I/R and cardiac pressure overload, but the full extent of the HuR-dependent mechanisms within cells of the myocardium have yet to be elucidated. In this study, we applied a novel small molecule inhibitor of HuR to define the functional role of HuR in the acute response to I/R injury and gain a better understanding of the HuR-dependent mechanisms during post-ischemic myocardial remodeling. Our results show an early (two hours post-I/R) increase in HuR activity that is necessary for early inflammatory gene expression by cardiomyocytes in response to I/R. Surprisingly, despite the reductions in early inflammatory gene expression at two hours post-I/R, HuR inhibition has no effect on initial infarct size at 24-hours post-I/R. However, in agreement with previously published work, we do see a reduction in pathological remodeling and preserved cardiac function at two weeks post-I/R upon HuR inhibition. RNA-sequencing analysis of neonatal rat ventricular myocytes (NRVMs) at two hours post-LPS treatment to model damage associated molecular pattern (DAMP)-mediated activation of toll like receptors (TLRs) demonstrates a broad HuR-dependent regulation of pro-inflammatory chemokine and cytokine gene expression in cardiomyocytes. We show that conditioned media from NRVMs pre-treated with HuR inhibitor loses the ability to induce inflammatory gene expression in bone marrow derived macrophages (BMDMs) compared to NRVMs treated with LPS alone. Functionally, HuR inhibition in NRVMs also reduces their ability to induce endocrine migration of peripheral blood monocytes
Language	English
Publishing date	2023-01-18
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.01.17.524420
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Article ; Online: Pharmacologic Inhibition of Pain Response to Incomplete Vascular Occlusion Blunts Cardiovascular Preconditioning Response.

Kirschner, Akiva / Koch, Sheryl E / Robbins, Nathan / Karthik, Felix / Mudigonda, Parvathi / Ramasubramanian, Ranjani / Nieman, Michelle L / Lorenz, John N / Rubinstein, Jack

Cardiovascular toxicology

2021 Volume 21, Issue 11, Page(s) 889–900

Abstract: Complete vascular occlusion to distant tissue prior to an ischemic cardiac event can provide significant cardioprotection via remote ischemic preconditioning (RIPC). Despite understanding its mechanistic basis, its translation to clinical practice has ... ...

Abstract	Complete vascular occlusion to distant tissue prior to an ischemic cardiac event can provide significant cardioprotection via remote ischemic preconditioning (RIPC). Despite understanding its mechanistic basis, its translation to clinical practice has been unsuccessful, likely secondary to the inherent impossibility of predicting (and therefore preconditioning) an ischemic event, as well as the discomfort that is associated with traditional, fully occlusive RIPC stimuli. Our laboratory has previously shown that non-occlusive banding (NOB) via wrapping of a leather band (similar to a traditional Jewish ritual) can elicit an RIPC response in healthy human subjects. This study sought to further the pain-mediated aspect of this observation in a mouse model of NOB with healthy mice that were exposed to treatment with and without lidocaine to inhibit pain sensation prior to ischemia/reperfusion injury. We demonstrated that NOB downregulates key inflammatory markers resulting in a preconditioning response that is partially mediated via pain sensation.
MeSH term(s)	Anesthetics, Local/pharmacology ; Animals ; Cytokines/blood ; Cytokines/genetics ; Disease Models, Animal ; Echocardiography ; Forelimb/blood supply ; Ischemic Preconditioning/methods ; Lidocaine/pharmacology ; Ligation ; Male ; Mice, Inbred C57BL ; Myocardial Infarction/blood ; Myocardial Infarction/diagnostic imaging ; Myocardial Infarction/physiopathology ; Myocardial Infarction/prevention & control ; Myocardial Reperfusion Injury/blood ; Myocardial Reperfusion Injury/diagnostic imaging ; Myocardial Reperfusion Injury/physiopathology ; Myocardial Reperfusion Injury/prevention & control ; Myocardium/metabolism ; Myocardium/pathology ; Pain Threshold/drug effects ; Radial Artery/diagnostic imaging ; Radial Artery/physiology ; Regional Blood Flow ; Time Factors ; Mice
Chemical Substances	Anesthetics, Local ; Cytokines ; Lidocaine (98PI200987)
Language	English
Publishing date	2021-07-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	2036765-X
ISSN	1559-0259 ; 1530-7905
ISSN (online)	1559-0259
ISSN	1530-7905
DOI	10.1007/s12012-021-09680-z
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Zs.A 5817: Show issues

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Article ; Online: V2a Neurons Constrain Extradiaphragmatic Respiratory Muscle Activity at Rest.

Jensen, Victoria N / Seedle, Kari / Turner, Sarah M / Lorenz, John N / Crone, Steven A

eNeuro

2019 Volume 6, Issue 4

Abstract: Breathing requires precise control of respiratory muscles to ensure adequate ventilation. Neurons within discrete regions of the brainstem produce oscillatory activity to control the frequency of breathing. Less is understood about how spinal and ... ...

Abstract	Breathing requires precise control of respiratory muscles to ensure adequate ventilation. Neurons within discrete regions of the brainstem produce oscillatory activity to control the frequency of breathing. Less is understood about how spinal and pontomedullary networks modulate the activity of respiratory motor neurons to produce different patterns of activity during different behaviors (i.e., during exercise, coughing, swallowing, vocalizing, or at rest) or following disease or injury. Here, we use a chemogenetic approach to inhibit the activity of glutamatergic V2a neurons in the brainstem and spinal cord of neonatal and adult mice to assess their potential roles in respiratory rhythm generation and patterning respiratory muscle activity. Using whole-body plethysmography (WBP), we show that V2a neuron function is required in neonatal mice to maintain the frequency and regularity of respiratory rhythm. However, silencing V2a neurons in adult mice increases respiratory frequency and ventilation, without affecting regularity. Thus, the excitatory drive provided by V2a neurons is less critical for respiratory rhythm generation in adult compared to neonatal mice. In addition, we used simultaneous EMG recordings of the diaphragm and extradiaphragmatic respiratory muscles in conscious adult mice to examine the role of V2a neurons in patterning respiratory muscle activity. We find that silencing V2a neurons activates extradiaphragmatic respiratory muscles at rest, when they are normally inactive, with little impact on diaphragm activity. Thus, our results indicate that V2a neurons participate in a circuit that serves to constrain the activity of extradiaphragmatic respiratory muscles so that they are active only when needed.
MeSH term(s)	Animals ; Male ; Medulla Oblongata/physiology ; Mice, Transgenic ; Neurons/physiology ; Respiration ; Respiratory Muscles/innervation ; Respiratory Muscles/physiology ; Spinal Cord/physiology
Language	English
Publishing date	2019-08-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2800598-3
ISSN	2373-2822 ; 2373-2822
ISSN (online)	2373-2822
ISSN	2373-2822
DOI	10.1523/ENEURO.0492-18.2019
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Article: A practical guide to evaluating cardiovascular, renal, and pulmonary function in mice.

Lorenz, John N

American journal of physiology. Regulatory, integrative and comparative physiology

2002 Volume 282, Issue 6, Page(s) R1565–82

Abstract: The development and widespread use of genetically altered mice to study the role of various proteins in biological control systems have led to a renewed interest in methodologies and approaches for evaluating physiological phenotypes. As a result, cross- ... ...

Abstract	The development and widespread use of genetically altered mice to study the role of various proteins in biological control systems have led to a renewed interest in methodologies and approaches for evaluating physiological phenotypes. As a result, cross-disciplinary approaches have become essential for fully realizing the potential of these new and powerful animal models. The combination of classical physiological approaches and modern innovative technology has given rise to an impressive arsenal for evaluating the functional results of genetic manipulation in the mouse. This review attempts to summarize some of the techniques currently being used for measuring cardiovascular, renal, and pulmonary variables in the intact mouse, with specific attention to practical considerations useful for their successful implementation.
MeSH term(s)	Animals ; Cardiovascular Physiological Phenomena ; Heart Function Tests/methods ; Kidney/physiology ; Kidney Function Tests/methods ; Lung/physiology ; Mice ; Models, Animal ; Respiratory Function Tests/methods
Language	English
Publishing date	2002-03-19
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00759.2001
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Article ; Online: Autonomic dysfunction following traumatic brain injury: translational insights.

Khalid, Fatima / Yang, George L / McGuire, Jennifer L / Robson, Matthew J / Foreman, Brandon / Ngwenya, Laura B / Lorenz, John N

Neurosurgical focus

2019 Volume 47, Issue 5, Page(s) E8

Abstract: Although there is a substantial amount of research on the neurological consequences of traumatic brain injury (TBI), there is a knowledge gap regarding the relationship between TBI and the pathophysiology of organ system dysfunction and autonomic ... ...

Abstract	Although there is a substantial amount of research on the neurological consequences of traumatic brain injury (TBI), there is a knowledge gap regarding the relationship between TBI and the pathophysiology of organ system dysfunction and autonomic dysregulation. In particular, the mechanisms or incidences of renal or cardiac complications after TBI are mostly unknown. Autonomic dysfunction following TBI exacerbates secondary injury and may contribute to nonneurologial complications that prolong hospital length of stay. Gaining insights into the mechanisms of autonomic dysfunction can guide advancements in monitoring and treatment paradigms to improve acute survival and long-term prognosis of TBI patients. In this paper, the authors will review the literature on autonomic dysfunction after TBI and possible mechanisms of paroxysmal sympathetic hyperactivity. Specifically, they will discuss the link among the brain, heart, and kidneys and review data to direct future research on and interventions for TBI-induced autonomic dysfunction.
MeSH term(s)	Autonomic Nervous System Diseases/etiology ; Autonomic Nervous System Diseases/physiopathology ; Brain/physiopathology ; Brain Injuries, Traumatic/complications ; Brain Injuries, Traumatic/physiopathology ; Heart/physiopathology ; Humans ; Kidney/physiopathology
Language	English
Publishing date	2019-11-01
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2026589-X
ISSN	1092-0684 ; 1092-0684
ISSN (online)	1092-0684
ISSN	1092-0684
DOI	10.3171/2019.8.FOCUS19517
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Article ; Online: RNA SEQ Analysis Indicates that the AE3 Cl

Vairamani, Kanimozhi / Wang, Hong-Sheng / Medvedovic, Mario / Lorenz, John N / Shull, Gary E

Scientific reports

2017 Volume 7, Issue 1, Page(s) 7264

Abstract: Loss of the AE3 ... ...

Abstract	Loss of the AE3 Cl
MeSH term(s)	Adenosine Triphosphate/metabolism ; Animals ; Antiporters/genetics ; Antiporters/metabolism ; Biological Transport, Active ; Carbon Dioxide/metabolism ; Computational Biology/methods ; Energy Metabolism/genetics ; Fatty Acids/metabolism ; Gene Expression ; Gene Ontology ; Glucose/metabolism ; Hydrogen-Ion Concentration ; Hypoxia/metabolism ; Male ; Mice ; Myocardium/metabolism ; Neovascularization, Pathologic/genetics ; Neovascularization, Pathologic/metabolism ; Sequence Analysis, RNA ; Sodium/metabolism ; Vasodilation
Chemical Substances	Antiporters ; Fatty Acids ; Slc4a3 protein, mouse ; Carbon Dioxide (142M471B3J) ; Adenosine Triphosphate (8L70Q75FXE) ; Sodium (9NEZ333N27) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2017-08-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-07585-y
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Article ; Online: Fast skeletal myosin-binding protein-C regulates fast skeletal muscle contraction.

Song, Taejeong / McNamara, James W / Ma, Weikang / Landim-Vieira, Maicon / Lee, Kyoung Hwan / Martin, Lisa A / Heiny, Judith A / Lorenz, John N / Craig, Roger / Pinto, Jose Renato / Irving, Thomas / Sadayappan, Sakthivel

Proceedings of the National Academy of Sciences of the United States of America

2021 Volume 118, Issue 17

Abstract: Fast skeletal myosin-binding protein-C (fMyBP-C) is one of three MyBP-C paralogs and is predominantly expressed in fast skeletal muscle. Mutations in the gene that encodes fMyBP-C, ...

Abstract	Fast skeletal myosin-binding protein-C (fMyBP-C) is one of three MyBP-C paralogs and is predominantly expressed in fast skeletal muscle. Mutations in the gene that encodes fMyBP-C,
MeSH term(s)	Actin Cytoskeleton/metabolism ; Actins/metabolism ; Animals ; Calcium/metabolism ; Carrier Proteins/metabolism ; Isometric Contraction/physiology ; Mice ; Muscle Contraction/physiology ; Muscle Fibers, Fast-Twitch/metabolism ; Muscle Strength ; Muscle, Skeletal/metabolism ; Myofibrils/metabolism ; Myosins/metabolism ; Sarcomeres/metabolism
Chemical Substances	Actins ; Carrier Proteins ; myosin-binding protein C ; Myosins (EC 3.6.4.1) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-02-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2003596118
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