GLORIA

GEOMAR Library Ocean Research Information Access

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Effects of desflurane and isoflurane on intestinal tissue oxygen pressure during colorectal surgery (2002)
    Oxford, UK : Blackwell Science, Ltd
    Anaesthesia 57 (2002), S. 0 
    Details
    ISSN: 1365-2044
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary Volatile anaesthetics differ in the effects they have on splanchnic haemodynamics and oxygenation. The aim of this study was to evaluate the effects of desflurane and isoflurane as part of a balanced anaesthetic technique on intestinal tissue oxygenation during colorectal surgery. Data were analysed from 44 patients randomly assigned to receive either desflurane (desflurane group, n= 20), or isoflurane (isoflurane group, n= 24) for inhalational anaesthesia. Tissue oxygen pressure (Ptisso2)␣was measured on the serosal side of the large intestine prior to colonic resection (T1) and␣following the completion of the bowel anastomosis (T2). In addition, haemodynamic and oxygenation parameters were assessed. No difference in mean Ptisso2 was observed between the groups at T1 [desflurane group: 8.1 (2.9) kPa vs. isoflurane group: 7.7 (2.7) kPa]. Following completion of the anastomosis (T2) mean Ptisso2 was higher in the isoflurane group [9.6 (2.9) kPa] than the desflurane group [7.7 (2.4) kPa, p = 0.025]. During surgery no difference between the␣groups could be observed with regard to haemodynamics and global oxygenation parameters. The lack of a difference between the groups in Ptisso2 before resection of the colon suggests that,␣under normal conditions, desflurane and isoflurane have comparable effects on intestinal blood␣flow and oxygenation. However, following local ischaemia, the reactive hyperaemia seems␣to␣be better preserved during isoflurane anaesthesia indicated by a local increase in Ptisso2␣(p = 0.013) following completion of the bowel anastomosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.0003-2409.2001.02363.x
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Penetration of Endogenous Steroid Hormones Corticosterone, Cortisol, Aldosterone and Progesterone into the Brain is Enhanced in Mice Deficient for Both mdr1a and mdr1b P-Glycoproteins (2002)
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 14 (2002), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Numerous investigations have confirmed an important role for multidrug-resistance gene 1-type P-glycoproteins (MDR1-type P-gps) in the blood–brain barrier, protecting the brain against the accumulation of a wide range of toxic xenobiotics and drugs. Several studies have provided evidence in vitro that certain steroid hormones are transported by MDR1-type P-gps; however, the question of whether this might also apply to the situation in vivo still remained to be determined. We used mice deficient for both murine mdr1a and mdr1b P-gps [mdr1a/1b(−/−)] to determine the uptake of [3H]-cortisol, [3H]-corticosterone, [3H]-aldosterone and [3H]-progesterone into the plasma, brain, testes, liver, spleen, pituitary and adrenal glands. We provide evidence that the access of the endogenous steroid hormones corticosterone, cortisol and aldosterone is regulated by MDR1-type P-gps in vivo. As peripherally administered steroid hormones accumulate in the brain of mice deficient for MDR1-type P-gps, mdr1a/1b proteins are likely to transport these hormones out of the brain, providing a kinetic barrier to their entry. Intracerebral progesterone concentrations are influenced by MDR1-type P-gp function as well; however, the effects are only small. In addition, all four endogenous glucocorticoid hormones accumulated in the testes of mdr1a/1b(−/−) mice. Our findings underline the importance of MDR1-type P-gps as an endogenous barrier system controlling the access of endogenous steroid hormones at the blood–brain barrier to maintain homeostatic control and to protect central nervous system neurones.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2826.2002.00836.x
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    facet.materialart.
    Unknown
    Response to Letter Regarding Article, "Relation of Nailfold Capillaries and Autoantibodies to Mortality in Patients With Raynaud Phenomenon" [Correspondence] (2016)
    American Heart Association (AHA)
    Details
    Publication Date: 2016-06-01
    Electronic ISSN: 1524-4539
    Topics: Medicine
    Published by American Heart Association (AHA)
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Loss of AngiomiR-126 and 130a in Angiogenic Early Outgrowth Cells From Patients With Chronic Heart Failure: Role for Impaired In Vivo Neovascularization and Cardiac Repair Capacity [Heart Failure] (2012)
    American Heart Association (AHA)
    Details
    Publication Date: 2012-12-18
    Description: Background— MicroRNAs are key regulators of angiogenic processes. Administration of angiogenic early outgrowth cells (EOCs) or CD34 + cells has been suggested to improve cardiac function after ischemic injury, in particular by promoting neovascularization. The present study therefore examines regulation of angiomiRs, microRNAs involved in angiogenesis, in angiogenic EOCs and circulating CD34 + cells from patients with chronic heart failure (CHF) and the role for their cardiac repair capacity. Methods and Results— Angiogenic EOCs and CD34 + cells were isolated from patients with CHF caused by ischemic cardiomyopathy (n=45) and healthy subjects (n=35). In flow cytometry analyses, angiogenic EOCs were largely myeloid and positive for alternatively activated M2 macrophage markers. In vivo cardiac neovascularization and functional repair capacity were examined after transplantation into nude mice with myocardial infarction. Cardiac transplantation of angiogenic EOCs from healthy subjects markedly increased neovascularization and improved cardiac function, whereas no such effect was observed after transplantation of angiogenic EOCs from patients with CHF. Real-time polymerase chain reaction analysis of 14 candidate angiomiRs, expressed in angiogenic EOCs, revealed a pronounced loss of angiomiR-126 and -130a in angiogenic EOCs from patients with CHF that was also observed in circulating CD34 + cells. Anti–miR-126 transfection markedly impaired the capacity of angiogenic EOCs from healthy subjects to improve cardiac function. miR-126 mimic transfection increased the capacity of angiogenic EOCs from patients with CHF to improve cardiac neovascularization and function. Conclusions— The present study reveals a loss of angiomiR-126 and -130a in angiogenic EOCs and circulating CD34 + cells from patients with CHF. Reduced miR-126 expression was identified as a novel mechanism limiting their capacity to improve cardiac neovascularization and function that can be targeted by miR-126 mimic transfection.
    Keywords: Angiogenesis, Ischemic biology - basic studies
    Electronic ISSN: 1524-4539
    Topics: Medicine
    Published by American Heart Association (AHA)
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    {alpha}1-A680T Variant in GUCY1A3 as a Candidate Conferring Protection From Pulmonary Hypertension Among Kyrgyz Highlanders [Original Articles] (2014)
    American Heart Association (AHA)
    Details
    Publication Date: 2014-12-17
    Description: Background— Human variation in susceptibility to hypoxia-induced pulmonary hypertension is well recognized. High-altitude residents who do not develop pulmonary hypertension may host protective gene mutations. Methods and Results— Exome sequencing was conducted on 24 unrelated Kyrgyz highlanders living 2400 to 3800 m above sea level, 12 (10 men; mean age, 54 years) with an elevated mean pulmonary artery pressure (mean±SD, 38.7±2.7 mm Hg) and 12 (11 men; mean age, 52 years) with a normal mean pulmonary artery pressure (19.2±0.6 mm Hg) to identify candidate genes that may influence the pulmonary vascular response to hypoxia. A total of 140 789 exomic variants were identified and 26 116 (18.5%) were classified as novel or rare. Thirty-three novel or rare potential pathogenic variants (frameshift, essential splice-site, and nonsynonymous) were found exclusively in either ≥3 subjects with high-altitude pulmonary hypertension or ≥3 highlanders with a normal mean pulmonary artery pressure. A novel missense mutation in GUCY1A3 in 3 subjects with a normal mean pulmonary artery pressure encodes an α 1 -A680T soluble guanylate cyclase (sGC) variant. Expression of the α 1 -A680T sGC variant in reporter cells resulted in higher cyclic guanosine monophosphate production compared with the wild-type enzyme and the purified α 1 -A680T sGC exhibited enhanced sensitivity to nitric oxide in vitro. Conclusions— The α 1 -A680T sGC variant may contribute to protection against high-altitude pulmonary hypertension and supports sGC as a pharmacological target for reducing pulmonary artery pressure in humans at altitude.
    Keywords: Pulmonary circulation and disease
    Print ISSN: 1942-325X
    Electronic ISSN: 1942-3268
    Topics: Medicine
    Published by American Heart Association (AHA)
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    Relation of Nailfold Capillaries and Autoantibodies to Mortality in Patients With Raynaud Phenomenon [Vascular Medicine] (2016)
    American Heart Association (AHA)
    Details
    Publication Date: 2016-02-02
    Description: Background— In incipient Raynaud phenomenon, nailfold capillaroscopy and autoantibody tests are obtained to screen for an emerging connective tissue disease. Whether the presence of abnormal nailfold capillaries and autoantibodies are related to mortality in patients with incipient Raynaud phenomenon is not known. Methods and Results— In 2958 consecutive patients (78% women, median age 45 years) with incipient Raynaud phenomenon without previously known connective tissue disease, nailfold capillaroscopy and laboratory tests for antinuclear antibodies (ANA) and ANA subsets were obtained at initial presentation. During a median follow-up period of 9.3 years, 227 women (9.9% of female patients) and 129 men (20% of male patients) with Raynaud phenomenon died. In comparison with a demographically matched standard population, survival was poorer in patients with Raynaud phenomenon (log-rank test P 〈0.0001). In patients with Raynaud phenomenon, mortality was higher in men than in women ( P 〈0.0001, Cox proportional hazards model). In women, the presence of abnormal nailfold capillaries, ANA, and anti–Scl-70 antibodies were related to an increase in all-cause mortality. The conjoint presence of abnormal nailfold capillaries and autoantibodies was associated with the highest mortality rates. In men, abnormal nailfold capillaries, and ANA and ANA subsets, as well, were not related to survival. In both sexes, patients’ age and serum creatinine were associated with mortality. Conclusions— In Raynaud phenomenon, male sex, age, and serum creatinine are related to mortality. Abnormal nailfold capillaries and autoantibodies are associated with an increase in all-cause mortality in female patients, but not in male patients with Raynaud phenomenon.
    Keywords: Epidemiology, Diagnostic Testing, Vascular Disease
    Electronic ISSN: 1524-4539
    Topics: Medicine
    Published by American Heart Association (AHA)
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    Altered Activation of Endothelial Anti- and Proapoptotic Pathways by High-Density Lipoprotein from Patients with Coronary Artery Disease: Role of High-Density Lipoprotein-Proteome Remodeling [Coronary Heart Disease] (2013)
    American Heart Association (AHA)
    Details
    Publication Date: 2013-02-26
    Description: Background— Endothelial dysfunction and injury are thought to play an important role in the progression of coronary artery disease (CAD). High-density lipoprotein from healthy subjects (HDL Healthy ) has been proposed to exert endothelial antiapoptotic effects that may represent an important antiatherogenic property of the lipoprotein. The present study therefore aimed to compare effects of HDL CAD and HDL Healthy on the activation of endothelial anti- and proapoptotic pathways and to determine which changes of the lipoprotein are relevant for these processes. Methods and Results— HDL was isolated from patients with stable CAD (HDL sCAD ), an acute coronary syndrome (HDL ACS ), and healthy subjects. HDL Healthy induced expression of the endothelial antiapoptotic Bcl-2 protein Bcl-xL and reduced endothelial cell apoptosis in vitro and in apolipoprotein E–deficient mice in vivo. In contrast, HDL sCAD and HDL ACS did not inhibit endothelial apoptosis, failed to activate endothelial Bcl-xL, and stimulated endothelial proapoptotic pathways, in particular, p38-mitogen-activated protein kinase–mediated activation of the proapoptotic Bcl-2 protein tBid. Endothelial antiapoptotic effects of HDL Healthy were observed after inhibition of endothelial nitric oxide synthase and after delipidation, but not completely mimicked by apolipoprotein A-I or reconstituted HDL, suggesting an important role of the HDL proteome. HDL proteomics analyses and subsequent validations and functional characterizations suggested a reduced clusterin and increased apolipoprotein C-III content of HDL sCAD and HDL ACS as mechanisms leading to altered effects on endothelial apoptosis. Conclusions— The present study demonstrates for the first time that HDL CAD does not activate endothelial antiapoptotic pathways, but rather stimulates potential endothelial proapoptotic pathways. HDL-proteome remodeling plays an important role for these altered functional properties of HDL. These findings provide novel insights into mechanisms leading to altered vascular effects of HDL in coronary disease.
    Electronic ISSN: 1524-4539
    Topics: Medicine
    Published by American Heart Association (AHA)
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...