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Biomedical subjects

S Daley

Publications and source records attributed to S Daley.

18 recordsLinked to original sources
PubMed2005

MRI-guided, open trial of abciximab for ischemic stroke within a 3- to 24-hour window.

The authors assessed the effect of IV abciximab on early neurologic improvement and ischemic lesion growth in 29 patients with supratentorial stroke and NIH stroke scale score (NIHSSS) > or = 4 (11.1 +/- 5.9), treated within 3 to 24 (13.6 +/- 5.5) hours of onset. The 48 to 72-hour NIHSSS improvement was 4.4 +/- 3.2 and the 24-hour lesion growth on DWI was +23% (-50%, +103%); 7/26 (27%) patients experienced lesion size decrease. Treatment of sub-24-hour stroke with abciximab improves early post-treatment neurologic status and often attenuates ischemic lesion growth.

Abciximab↗
PubMed1999

Initial clinical experience with IV tissue plasminogen activator for acute ischemic stroke: a multicenter survey. The t-PA Stroke Survey Group.

We assessed initial clinical experience with IV tissue plasminogen activator (t-PA) treatment of acute ischemic stroke in a standardized retrospective survey of hospitals with experienced acute stroke treatment systems. The incidence of symptomatic intracerebral hemorrhage (ICH) was 6% (11 of 189 patients; 95% CI 3 to 11%), similar to that in the National Institute of Neurological Disorders and Stroke (NINDS) t-PA Stroke Study. Deviations from the NINDS protocol guidelines were identified in 30% of patients (56 of 189). The incidence of symptomatic ICH was 11% among patients with protocol deviations as compared with 4% in patients who were treated according to the NINDS protocol guidelines, suggesting that strict adherence to protocol guidelines is prudent.

Aged↗
PubMed1998

Changes in protein turnover, IGF-I and IGF binding proteins in children with cancer.

Changes in insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding proteins (IGFBPs) were correlated with protein synthesis and breakdown using [1-13C]leucine before chemotherapy and during subsequent febrile neutropenia (FN) in eight children with cancer, aged 6.3-17.5 y. IGF-I levels were similar to age-matched controls before chemotherapy (mean +/- SEM: 250+/-28 and 228+/-22 microg l(-1), respectively). During FN, IGF-I fell to 156+/-22 microg l(-1) (p = 0.02), and rose to 276+/-27 microg l(-1) with recovery at 6 months (p = 0.004). Similarly, IGFBP-3 decreased from 4.0+/-0.2 mg l(-1) before chemotherapy to 3.0+/-0.3 mg l(-1) during FN (p = 0.01), and returned to 4.1+/-0.2 mg l(-1) at 6 months (p = 0.01). IGF-I correlated with IGFBP-3 (r = +0.7, p < 0.001). Scanning densitometry showed a decrease in IGFBP-3 from 94 to 54% during FN, when the presence of IGFBP-3 protease activity was observed. Compared with normal human serum, IGFBP-2 was elevated throughout the study. IGFBP-1 increased from 14.6+/-3.5 to 30.6+/-2.8 microg l(-1) (p = 0.004), whereas serum insulin decreased from 26.5+/-6.8 to 7.8+/-0.8 mU l(-1) (p = 0.03) before and during FN, respectively. Whilst IGF-I and IGFBP-3 fell, daytime growth hormone increased from 3.3+/-0.6 to 6.7+/-0.8 mU l(-1) (p=0.01), and cortisol from 197+/-48 to 594+/-98 nmol l(-1) (p = 0.005). Albumin decreased from 47+/-2 to 38+/-2 g l(-1) (p = 0.004) and improved to 47+/-2 g l(-1) with recovery (p = 0.003). Protein synthesis increased from 4.5+/-0.4 to 5.0+/-0.6 g kg(-1)d(-1) before chemotherapy and during FN, while protein breakdown rose from 5.4+/-0.4 to 6.3+/-0.4 kg(-1)d(-1). Increasing protein breakdown was related to falling IGF-I and IGFBP-3 levels. Modification of IGFBP-3 by circulating proteolytic activity may alter IGF bioavailability, allowing protein synthesis to increase during periods of severe catabolic stress.

Adolescent↗
PubMed1997

Pathophysiology and mechanisms of acute ischemic stroke. The NINDS rt-PA Stroke Study Group.

Stroke is a leading cause of death and disability among Americans. The recent US Food and Drug Administration approval of recombinant tissue plasminogen activator (rt-PA, Activase) for the treatment of acute ischemic stroke offers the first proven therapy to reverse or ameliorate stroke symptoms. rt-PA is thought to restore circulation in the patient with acute ischemic stroke by dissolving an occluding thrombus or embolus. A basic understanding of cerebral circulation and the mechanism by which stroke compromises brain tissue is fundamental to appreciating this new therapy. The importance of prompt stroke diagnosis and treatment cannot be underestimated.

Acute Disease↗
PubMed1997

Code Stroke: rapid transport, triage and treatment using rt-PA therapy. The NINDS rt-PA Stroke Study Group.

With the approval of rt-PA therapy for ischemic stroke, stroke care has acutely transitioned from focusing on rehabilitative services to emergency services. This treatment, which must be initiated within the first three hours after the onset of stroke symptoms, requires reorganization of current management approaches. Developing a Code Stroke Team facilitates this process and helps to identify potential thrombolysis candidates. A pathway to deliver rapid care begins with 911 notification and transport, emergency department triage and procedures, and moves through the initiation of thrombolytic therapy. We call this pathway "Code Stroke".

Cerebrovascular Disorders↗
PubMed1997

Nursing management of acute complications following rt-PA in acute ischemic stroke. The NINDS rt-PA Stroke Study Group.

In the National Institutes of Neurologic Disorders and Stroke (NINDS) recombinant tissue plasminogen activator (rt-PA) stroke trial, the primary adverse events monitored were intracranial hemorrhage (ICH), systemic bleeding, death and new stroke. Nurses caring for the study patients noted these adverse events and other complications. In addition to what is known about acute ischemic stroke (AIS), the NINDS trial provides further information for optimal care of this specific group of patients. The complications found in this trial require expert nursing care to monitor, prevent and intervene, making clinical decisions relevant to the patients needs. The critical decision-making process must be grounded in knowledge of acute stroke physiology and thrombolysis.

Acute Disease↗
PubMed1997

Nursing care of acute stroke patients after receiving rt-PA therapy. The NINDS rt-PA Stroke Study Group.

Treatment with tissue plasminogen activator (rt-PA) for acute stroke requires intensive care of the patient. The risk of thrombolytic therapy and the need for rapid interventions make it clear that the nursing role during this time is crucial. Nurses should be familiar with safe dosage and administration of rt-PA for stroke, which is clearly different than administration of rt-PA for myocardial infarction. Furthermore, thrombolytic stroke treatment must be accompanied by intensive neurological monitoring to observe for complications. Intracerebral hemorrhage is usually accompanied by an acute change in neurological status and vital sign instability. Intensive monitoring of neurologic condition, vital signs, cardiac status and other standard critical care practices must be initiated immediately to optimize patient outcome.

Algorithms↗
PubMed1997

Using the NIH Stroke Scale to assess stroke patients. The NINDS rt-PA Stroke Study Group.

The stroke patient is acutely ill within minutes of symptom onset. Typically, he or she is awake and thus requires a focal neurologic exam to evaluate vision, movement, sensation and language. With the advent of acute stroke treatments that need to be rapidly implemented, it is critical that the nurse be able to assess patients and relay the information accurately and efficiently to other members of the health care team. Performing and documenting the awake stroke exam in the most efficient and useful manner is key to the nursing care of the stroke patient. The National Institutes of Health Stroke Scale (NIHSS) is a systematic assessment tool designed to measure the neurologic deficits most often seen with acute stroke patients. Originally designed as a research tool, it is a nonlinear ordinal scale, with possible scores ranging form 0-42. Exam performance has been timed to take 5-8 minutes. Use of the NIHSS includes documentation of neurologic status and outcome, data collection for planning safe nursing care and standardization of information exchanges between nurse caregivers and other health care professionals.

Cerebrovascular Disorders↗
PubMed1997

Education to improve stroke awareness and emergent response. The NINDS rt-PA Stroke Study Group.

Patients delay in responding to stroke as an emergency in part because they have deficient information about the disease and treatment. Healthcare providers may also have a lack of information about stroke assessment and management, which could attribute to delays in patient care. In order to provide early, rapid stroke treatment in eligible persons, the public and the healthcare community must be informed. Information on stroke risk, symptoms and treatment should be provided to those likely to experience stroke, the general public and the emergency and medical communities who may witness and intervene when stroke occurs. Programs developed at the eight centers of the National Institute of Neurological Disorders and Stroke (NINDS) rt-PA stroke trial provide a sampling of approaches that increase awareness in these groups. Lessons learned include: 1. Program planning should start with a community needs assessment. 2. A variety of strategies can be applied to meet the community needs and resources. 3. Educational principles and models should be utilized in planning effective programs. 4. The message must be simple: "Stroke is an emergency. Time is brain".

Cerebrovascular Disorders↗
PubMed1993

The distribution of fibro-fatty atherosclerotic lesions in the aortae of casein- and cholesterol-fed rabbits.

Atherosclerotic lesions were induced in the aortas of 50 rabbits by feeding a semi-purified cholesterol-free casein diet or normal rabbit chow with a low level of added cholesterol for 6 or 10 months. Following perfusion fixation, the aortae from these animals were opened along their length, stained with oil red O and photographed en face. Orifice associated lesions were mapped by measuring radial lesion length at 10 degrees intervals circumferentially around ostia. Histology of these lesions revealed abundant smooth muscle cells surrounded by collagen and elastin in the extracellular matrix, typical of fibrous plaques, as well as oil red O staining lipid and some macrophage derived foam cells. These fibro-fatty lesions were found distal and lateral to ostia, at the same locations as fatty streaks seen in rabbits fed a 2% cholesterol diet for 1 week to 2 months in previous studies. The results of this study show that in moderately hypercholesterolemic rabbits fed an atherogenic diet for 6 to 10 months, advanced atherosclerotic plaques develop in the same location as the fatty streaks seen in short term experiments.

Animals↗
PubMedDate not supplied

Cocaine blunts human CD4+ cell activation.

Cocaine is reported to be immunotoxic. The biochemical mechanisms responsible for the immunopharmacological outcomes of cocaine in vivo and in vitro remain, however, to be fully elucidated. Our experimental data confirm that exposure of normal human T cells to micromolar concentrations of cocaine modulates T-cell responses to stimulation by a variety of stimuli, and indicate that cocaine impairs early activation events during CD4+ but not CD4- T-cell stimulation. Pre-incubation of enriched CD4+ T-cell subpopulations that express the homing receptor CD62L with nanomolar concentrations of the endogenous opioid peptide beta-endorphin leads to a more severe impairment of activation than that noted following pre-incubation with micromolar concentrations of cocaine alone. These findings begin to elucidate the molecular and cellular mechanisms of the immunopathology of cocaine. Our data support the proposition that cocaine abuse may place cocaine-abuser HIV-seropositive individuals at increased risk of opportunistic infections.

Antigens, CD↗
PubMedDate not supplied

Increased salivary cortisol reliably induced by a protein-rich midday meal.

OBJECTIVE: This study was conducted to determine whether an increase in salivary free cortisol would be reliably elicited by a midday meal, thus providing a convenient physiological challenge to the hypothalamic-pituitary-adrenal (HPA) axis, and whether this cortisol release depended on the protein content of the meal. METHOD: In healthy men, free cortisol was measured in saliva samples taken before and after two identical protein-rich midday meals (39% energy as protein) and compared with a day on which no meal was eaten. Next, in healthy women in a nonclinical setting, salivary cortisol was measured before and after a protein-rich meal (32% energy as protein) on one day and a low-protein meal (5% energy as protein) on another day. Measures of mood, appetite, and psychological well-being were also taken. RESULTS: An acute meal-dependent increase in salivary cortisol occurred, which was reliable over 2 test days. This increase in cortisol depended on the proportion of protein in the meal, increasing after the high-protein but not the low-protein meal. The extent of this increase in cortisol correlated significantly with poor psychological well-being in women. Some postmeal improvement of mood (positive affect) was associated with the high- but not the low-protein meal. CONCLUSIONS: The cortisol response to meals may have implications for the effects of meal composition on mood, cognitive function, and food choice. The measurement of free cortisol in saliva provides a psychologically stress-free and reliable technique to assess the cortisol response to a standard protein-rich meal, ie, a physiological challenge to the HPA axis in men and women that could be investigated in naturalistic settings outside the laboratory.

Adolescent↗