Embargoed for: 8 a.m. CT/9 a.m. ET, Wednesday, Feb. 1, 2012
NEW ORLEANS, Feb. 1, 2012 (GLOBE NEWSWIRE) — Regardless of presentation date and time, all four abstracts will have the same embargo release at 8 a.m. CT, Wednesday, Feb. 1, 2012. For more information Feb. 1-3, call the ASA News Media Staff Office at the New Orleans Convention Center at (504) 670-6010. Before or after these dates, call Communications in Dallas at (214) 706-1396. For public inquiries call (800) AHA-USA1 (242-8721).
Abstract 3962
Animal study shows endothelial progenitor cells enhance motor function after stroke
A new study found that rats, post-stroke, which were treated with endothelial progenitor cells had better functional outcomes than those left untreated.
Endothelial progenitor cells (EPC) are produced in the bone marrow. They are “starter” cells for forming blood vessels. Higher levels of EPCs in the blood stream are associated with fewer heart attacks.
In 34 male rats, researchers established baseline motor performance using a single pellet-reaching task. The animals were then divided into four groups: stroke alone, stroke plus EPC; sham plus EPC; and sham alone. Stroke was induced by delivering Endothelin-1 onto the middle cerebral artery contralateral to the preferred paw. One, three and five weeks later all animals were tested for accuracy on the skilled reaching task.
Testing with a single pellet-reaching task showed:
Rats given EPC immediately after stroke had 27 percent higher reaching accuracy at three weeks and 32 percent at five weeks compared to animals who did not receive EPCs. Control animals scored a reaching accuracy of 41 percent and 46 percent at weeks three and five. Stroke decreased this task to 12 percent and 18 percent respectively. Infarct sizes weren't significantly different between the animals.
The results show that EPCs did not reduce infarct size, but did help the animals regain limb movement, researchers said.
Note: Actual presentation is 5:55 p.m. CT, Wednesday, Feb. 1, 2012.
Abstract 3369
Intravenous bone marrow stem cell therapy is safe
In a new study, stroke patients were safely treated with injections of bone marrow-derived stem cells in an effort to regain function.
A total of 120 stroke patients, age 18 to 75 years, with moderate severity stroke participated in the study. Half of the participants were treated with stem cells taken from bone marrow in the iliac crest (hip), then harvested and infused into a vein. The remaining half served as controls. Participants were watched for any reaction after infusion and tumor formation for up to one year.
Participants' level of physical impairment was assessed with the National Institutes of Health Stroke Scale (NIHSS), functional status with a modified Rankin Scale (mRS), and ability to perform activities of daily living with Barthel index. Seventy-nine patients underwent whole body positron emission tomography (PET) at the end of one year.
They found:
43 patients (73 percent) of the stem cell group achieved assisted independence (Barthel index of 60 or above) at six months versus 36 (61 percent) in the control group. However, the difference did not achieve statistical significance (p=0.17). Trends were similar in mRS and NIHSS but none achieved statistical significance. No patient developed evidence of tumor in PET scan at one year.
The researchers said that stem cell therapy appeared safe. Detailed results on clinical outcomes, cerebral infarct volume, dose response analysis and PET scans will be presented.
Note: Actual presentation is 6:15 p.m. CT, Wednesday, Feb. 1, 2012.
Abstract 3337
Stem cell therapy is safe in stroke patients and may facilitate recovery
The use of stem cell therapy in stroke patients appeared safe and feasible and may actually aid in functional recovery after stroke, researchers said.
Stem cell therapy used in 20 patients appeared to be safe with no signs of clinical, laboratory or radiologically detected adverse events. When compared to controls, stroke patients receiving stem cell therapy had statistically significant improvements in daily living activities (using modified Barthel index) such as feeding, dressing, mobility, etc. There was also an increase in brain activity in areas of the brain that deal with movement planning and motor function when compared to controls.
Note: Actual presentation is 6:10 p.m. CT, Thursday, Feb. 2, 2012.
Abstract 2981
Alcohol may provide protection after stroke
Ethanol (pure alcohol) in comparable levels to the legally intoxicated range for humans appeared to provide a protective effect in rats after stroke. Ethanol reduced the amount of brain damage and behavioral dysfunction in the animals. The behavioral functions include limb movement and coordination ability.
Administration of 1.5 grams per kilogram of body weight of ethanol (near the legal limit for driving) most effectively reduced the amount of damaged brain tissue and behavioral dysfunction when administered two, three or four hours after stroke. Ethanol did not promote bleeding in the brain after stroke when used in combination with thombolytics such as recombinant tissue plasminogen activator or urokinase.
The researchers conclude that ethanol is a potential treatment for stroke.
Note: Actual presentation is 6:15 p.m. CT, Wednesday, Feb. 1, 2012.
Abstract 2686
A protein in plasma may indicate stroke severity
Blood plasma levels of a certain protein are tightly linked to the inflammatory response following stroke and are higher in patients with more severe stroke, researchers said.
The protein, called HMBG1, is released from dying cells as a “danger” signal, and contributes to inflammation. HMBG1 concentrations were analyzed in 114 patients with stroke at 1, 3, 30, 180 and 365 days after their stroke. A group of healthy volunteers served as controls. The size of the area damaged by stroke was determined with magnetic resonance imaging and stroke severity was measured by the National Institutes of Health Stroke Severity Score. The association between HMBG1 and inflammation was analyzed at each time point.
Researchers found:
HMBG1 was elevated up to 30 days after stroke with the highest value on day three. Patients with more severe strokes had higher plasma HMBG1 levels than patients with less severe stroke. There was a robust association between HMBG1 and the number of circulating white blood cells one day after stroke which persisted up to one year after stroke. Initial plasma HMBG1 was not predictive of long-term outcome.
Plasma HMBG1 is elevated after ischemic stroke and is higher in patients with more severe strokes, the researchers said. The robust and independent association of HMBG1 and white blood cell counts suggests that white blood cells may be the primary source of the plasma protein after stroke, researchers said.
Note: Actual presentation is 6:15 p.m. CT, Wednesday, Feb. 1, 2012.
Abstract 108
A cellular protein may protect blood vessels from aging
A protein that helps regulate how cells store fatty acids and use glucose may play a major role in protecting blood vessels from aging.
The nuclear protein called peroxisome proliferator activated receptor-gamma (PPARg) regulates fatty acid storage and glucose metabolism, and may decrease inflammation. To examine the role of this protein in blood vessels, researchers studied mice carrying a human genetic mutation that interferes with the function of PPARg within the endothelial cells of the vasculature. These transgenic mice were compared to control mice. Because disease of the carotid arteries greatly increases the risk for stroke as human's age, they assessed function of these arteries in young and old mice from both groups.
Blood vessels were studied using acetylcholine, an agent that acts on endothelial cells to cause blood vessels to dilate. Carotid arteries from older mice carrying the genetic mutation in PPARg had a substantially reduced vasodilator response, suggesting the endothelial cells were dysfunctional. Additional experiments suggested that elevated oxidative stress was responsible for the dysfunction.
Researchers said these findings provide the first evidence that age-related vascular dysfunction is accelerated following cell-specific interference with endothelial PPARg. Thus, PPARg may normally function to protect against vascular aging.
Note: Actual presentation is 7:54 a.m. CT, Thursday, Feb. 2, 2012.
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Author disclosures are available on the abstracts.
NR12-1006 (ISC 2012/New Frontiers in Basic Science Tip Sheet)
Statements and conclusions of study authors that are presented at American Stroke Association scientific meetings are solely those of the study authors and do not necessarily reflect association policy or position. The association makes no representation or warranty as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at www.heart.org/corporatefunding.
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CONTACT:
ASA News Media Office in Dallas: (214) 706-1396
ASA News Media Office in New Orleans (Feb. 1-3): (504) 670-6010
For Public Inquiries: (800) AHA-USA1 (242-8721)
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