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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...

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Updated: Jun 19, 2026

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke
11:32

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Published on: January 3, 2025

The decrease in procarboxypeptidase U (TAFI) concentration in acute ischemic stroke correlates with stroke severity,

R Brouns1, E Heylen, J L Willemse

  • 1Department of Neurology and Memory Clinic, ZNA Middelheim Hospital, Antwerp, Belgium.

Journal of Thrombosis and Haemostasis : JTH
|October 31, 2009
PubMed
Summary
This summary is machine-generated.

Plasma procarboxypeptidase U (proCPU) levels decrease in the first 72 hours after ischemic stroke. This reduction correlates with stroke severity, progression, and poor long-term outcomes, highlighting proCPU

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A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
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Last Updated: Jun 19, 2026

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke
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A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
06:01

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

Published on: August 18, 2015

Area of Science:

  • Biochemistry
  • Neurology
  • Thrombosis Research

Background:

  • Plasma procarboxypeptidase U (proCPU, TAFI) concentration may indicate thrombotic tendency.
  • Elevated proCPU levels have been observed in ischemic stroke patients.
  • Understanding proCPU's role in acute ischemic stroke is crucial for developing targeted therapeutics, including carboxypeptidase inhibitors.

Purpose of the Study:

  • To investigate the relationship between plasma proCPU concentration and kinetic profile in acute ischemic stroke.
  • To assess the correlation with initial stroke severity, subacute stroke evolution, and long-term stroke outcome.

Main Methods:

  • Plasma proCPU concentration was measured in 136 stroke patients at multiple time points (admission, 24h, 72h, day 7).
  • Evaluated associations between proCPU changes and stroke severity (TIA vs. stroke, NIHSS), stroke evolution (progression, infarct volume), and long-term outcome (mRS).

Main Results:

  • ProCPU concentration showed a significant decrease within the first 72 hours post-stroke, followed by a return to baseline.
  • This biphasic pattern, with a nadir at 72 hours, was more pronounced in patients experiencing severe stroke.
  • The pattern was also more evident in those with unfavorable stroke evolution and poor long-term outcomes.

Conclusions:

  • A decrease in plasma proCPU concentration during the initial 72 hours after ischemic stroke onset is linked to increased stroke severity.
  • This proCPU reduction also correlates with unfavorable stroke evolution and poorer long-term outcomes.
  • Findings suggest proCPU dynamics are a potential biomarker for stroke prognosis.