• Refine Query
  • Source
  • Publication year
  • to
  • Language
  • 529
  • 393
  • 124
  • 37
  • 36
  • 35
  • 33
  • 19
  • 17
  • 12
  • 6
  • 6
  • 6
  • 4
  • 3
  • Tagged with
  • 1420
  • 504
  • 364
  • 248
  • 223
  • 188
  • 146
  • 141
  • 130
  • 129
  • 124
  • 91
  • 85
  • 83
  • 83
  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Neuronal and microglial changes within the salvaged ischaemic penumbra : a clinical imaging study

Morris, Rhiannon Sian January 2014 (has links)
No description available.
2

Simultaneous Imaging and Current Clamp Recordings from Hippocampal Slices during Simulated Ischemia

White, Sean 27 September 2008 (has links)
Following sudden failure of the Na+/K+ATPase pump, the acute neuronal swelling and dendritic damage that occurs within minutes of stroke onset are consequences of anoxic depolarization (AD). The AD front in our protocol is imaged as an increase in tissue light transmittance (LT) propagating across gray matter of the hippocampal slice preparation. Under current clamp in the single neuron, AD is recorded as a sharp depolarization within 6 min of O2/glucose deprivation (OGD). Simultaneous imaging and current clamp recordings show that the increased LT front and sudden depolarization are coincident. AD onset in CA1 hippocampal neurons is delayed in slices pretreated with 10 μM dibucaine (dib), a local anaesthetic understood to block voltage-gated sodium channels, and 10 to 100 µM carbetapentane (CP), a sigma1 receptor agonist. We examined if changes to single cell excitability could explain how dibucaine and CP work to inhibit AD. Pretreatment of slices with dibucaine for 30 min had no effect upon resting membrane potential, or whole cell input resistance (n=11). However dib pretreatment consistently raised spike threshold, decreased AP frequency and increased the fast afterhyperpolarization (fAHP). Orthodromic and antidromic APs were also eliminated within 15 min. Intracellular dibucaine application in addition to similar effects upon intrinsic electophysiological properties reduced the peak potential of the fast AD while extending the time until the persistent depolarization of AD reached zero. In contrast, 30 -100 μM CP had no effect upon orthodromic or antidromic responses, probably because unlike dibucaine it did not markedly raise spike threshold. Also unlike dibucaine, the fAHP was eliminated while the slow AHP was accentuated, resulting in a lowering of the AP frequency during steady depolarization. Both drugs appear to inhibit AD onset by reducing cortical excitability at the level of the single pyramidal neuron, but through strikingly different mechanisms. Our simultaneous imaging and single cell recording under current clamp allowed for further examination of potential cell recovery after AD in CA1 neurons and astrocytes, as well as confirmation of AD generation in the CA3 region. Indirect evidence for a more robust AD generation and propagation was evident in the transverse slices of dorsal hippocampal CA3 region compared to coronal slices. AD in astrocytes was lower in amplitude and more prolonged, as well as often displaying recovery to near resting potential. This supported our previous imaging experiments showing that astrocytes quickly recover their volume post-AD. / Thesis (Master, Neuroscience Studies) -- Queen's University, 2008-09-25 15:44:07.114
3

Acute Post-ischemic Seizures are Associated with Increased Mortality and Brain Damage Following Hypoxia-ischemia in Adult Mice

El-Hayek, Youssef Hanna 06 January 2012 (has links)
Post-stroke seizures are associated with worsened outcome following stroke, but the underlying pathophysiology is poorly understood. Here I combined behavioral, electrophysiological and histological assessments to examine acute seizures in adult mice following hypoxia-ischemia (HI). C57BL/6 mice aged 4-9 months received a permanent occlusion of the right common carotid artery and were then exposed to systemic hypoxia (8% O2, ~30 minutes). The HI episode resulted in decreases in cerebral blood flow, suppression of EEG activities and extensive brain injury in the hemisphere ipsilateral to the carotid artery occlusion. Generalized motor seizures were observed within 72 hours following HI. These seizures occurred nearly exclusively in animals with the extensive ipsilateral brain injury, but their generation was not associated with EEG discharges in bilateral hippocampal and cortical areas. Animals exhibiting these seizures had a high rate of mortality. Post-HI treatments with diazepam and phenytoin suppressed these motor seizures and improved post-HI animal survival. Based on these data, I conclude that these seizures are a consequence of HI brain injury, contribute to mortality following HI, and that they may originate from deep subcortical structures.
4

Acute Post-ischemic Seizures are Associated with Increased Mortality and Brain Damage Following Hypoxia-ischemia in Adult Mice

El-Hayek, Youssef Hanna 06 January 2012 (has links)
Post-stroke seizures are associated with worsened outcome following stroke, but the underlying pathophysiology is poorly understood. Here I combined behavioral, electrophysiological and histological assessments to examine acute seizures in adult mice following hypoxia-ischemia (HI). C57BL/6 mice aged 4-9 months received a permanent occlusion of the right common carotid artery and were then exposed to systemic hypoxia (8% O2, ~30 minutes). The HI episode resulted in decreases in cerebral blood flow, suppression of EEG activities and extensive brain injury in the hemisphere ipsilateral to the carotid artery occlusion. Generalized motor seizures were observed within 72 hours following HI. These seizures occurred nearly exclusively in animals with the extensive ipsilateral brain injury, but their generation was not associated with EEG discharges in bilateral hippocampal and cortical areas. Animals exhibiting these seizures had a high rate of mortality. Post-HI treatments with diazepam and phenytoin suppressed these motor seizures and improved post-HI animal survival. Based on these data, I conclude that these seizures are a consequence of HI brain injury, contribute to mortality following HI, and that they may originate from deep subcortical structures.
5

Regeneration in the adult brain after focal cerebral ischemia : exploration of neurogenesis and angiogenesis /

Jiang, Wei, January 2006 (has links)
Diss. (sammanfattning) Umeå : Umeå universitet, 2006. / Härtill 4 uppsatser.
6

The JAK2/Y343/STAT5 signaling axis is required for erythropoietin-mediated protection against ischemic injury in renal tubular epithelial cells /

Breggia, Anne C., January 2008 (has links)
Thesis (Ph.D.) in Biochemistry and Molecular Biology--University of Maine, 2008. / Includes vita. Includes bibliographical references (leaves 103-123).
7

Pain and distress during ischemia

Ebert, Robert Ralph. January 1979 (has links)
Thesis (M.S.)--University of Wisconsin--Madison. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 70-75).
8

Changes in heart muscle mitochondria during ischemia and reperfusion

Little, Stephen E. January 1981 (has links)
Thesis (Ph. D.)--University of Wisconsin--Madison, 1981. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 304-333).
9

The effect of high energy phosphate levels on contractile abnormalities in myocardial ischemia and reperfusion

Hafez, Hafez M. Sami. January 1984 (has links)
Thesis (Ph. D.)--University of Wisconsin--Madison, 1984. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 205-225).
10

The JAK2/Y343/STAT 5 Signaling Axis is Required for Erythropoietin - Mediated Protection against Ischemic Injury in Renal Tubular Epithelial Cells

Breggia, Anne C. January 2008 (has links) (PDF)
No description available.

Page generated in 0.0548 seconds