52 research outputs found
Determination of nutrient salts by automatic methods both in seawater and brackish water: the phosphate blank
9 páginas, 2 tablas, 2 figurasThe main inconvenience in determining nutrients in seawater by automatic methods is simply solved:
the preparation of a suitable blank which corrects the effect of the refractive index change on the recorded
signal. Two procedures are proposed, one physical (a simple equation to estimate the effect) and the other
chemical (removal of the dissolved phosphorus with ferric hydroxide).Support for this work came from CICYT (MAR88-0245 project) and
Conselleria de Pesca de la Xunta de GaliciaPeer reviewe
Mixed Cerebrovascular Disease and the Future of Stroke Prevention
Stroke prevention efforts typically focus on either ischemic or hemorrhagic stroke. This approach is overly simplistic due to the frequent coexistence of ischemic and hemorrhagic cerebrovascular disease. This coexistence, termed “mixed cerebrovascular disease”, offers a conceptual framework that appears useful for stroke prevention strategies. Mixed cerebrovascular disease incorporates clinical and subclinical syndromes, including ischemic stroke, subclinical infarct, white matter disease of aging (leukoaraiosis), intracerebral hemorrhage, and cerebral microbleeds. Reliance on mixed cerebrovascular disease as a diagnostic entity may assist in stratifying risk of hemorrhagic stroke associated with platelet therapy and anticoagulants. Animal models of hemorrhagic cerebrovascular disease, particularly models of cerebral amyloid angiopathy and hypertension, offer novel means for identifying underlying mechanisms and developing focused therapy. Phosphodiesterase (PDE) inhibitors represent a class of agents that, by targeting both platelets and vessel wall, provide the kind of dual actions necessary for stroke prevention, given the spectrum of disorders that characterizes mixed cerebrovascular disease
[Effect of cardiac embolism sources on origin of territorial cerebral infarcts].
BACKGROUND AND PURPOSE: To test the association of cardiac sources of embolism with territorial type brain infarcts.
METHODS: From a prospective cerebral ischemia data base the 106 consecutive patients with territorial type cerebral infarcts on computerized tomography were analyzed. The 85 consecutive patients with lacunar lesions served as a comparison group. The association of cardiac sources of embolism with territorial types infarcts was assessed using univariate Chi Square tests and logistic regression models. Cardiac sources of embolism were defined as:atrial fibrillation, left cardiac thrombi, valvular vegetations, wall motion and valvular abnormalities, left atrial enlargement, open foramen ovale, septal aneurysm, mitral valve prolaps, and aortic arch atherothrombosis (all findings--except for atrial fibrillation--assessed by echocardiography).
RESULTS: Atrial fibrillation was significantly associated with territorial type infarcts (odds ratio 2.2, 95% confidence interval 1.01-4.8). This effect was independent of additional cardiac diseases, other cardiac abnormalities, carotid artery stenosis, and patient age. Most likely due to the small sample size, left cardiac thrombi only showed a non-significant trend towards an association with territorial infarcts (odds ratio 3.0, 95% confidence interval 0.7-12.3). The rate of all other cardiac findings did not differ significantly between the comparison groups.
CONCLUSION: Atrial fibrillation and cardiac thrombi showed an association with territorial type infarcts. Other so-called cardiac sources of embolism--except for mechanical valves and bacterial endocarditis which were not represented in our sample--revealed no clinically relevant association with embolic brain infarct pattern
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Frequency and determinants of microembolic signals on transcranial Doppler in unselected patients with acute carotid territory ischemia. A prospective study
Few data exist regarding to the occurrence of microembolic high-intensity transient signals (HITS) on transcranial Doppler ultrasound (TCD) in unselected acute stroke patients. The aim of this study was to investigate prospectively the frequency and determinants of HITS in acute carotid territory ischemia. We hypothesized that carotid artery disease, cardiac abnormalities, and nonlacunar infarcts were independent predictors of HITS in acute stroke.
We investigated 145 consecutive patients with acute internal carotid artery territory ischemia. The median time interval between stroke and TCD examination was 2 days. TCD monitoring was performed for 30 min on each middle cerebral artery. The frequency of HITS was cross-classified with carotid artery status, potential cardiac sources of embolism, and nonlacunar infarct subtype. Multivariate logistic regression models determined the independent relationship of these variables to HITS.
Microembolic signals were detected in 35 patients (24.1%), Ipsilateral carotid artery disease was significantly and independently associated with HITS (odds ratio 3.3, 95% confidence interval 1.4-7.8, p = 0.007), whereas potential cardiac sources (OR 1.07, 95% CI 0.48-2.4, p = 0.84) and infarct subtype (OR 0.84, 95% CI 0.29-2.4, p = 0.75) were not.
High-intensity transient signals can be found in almost 25% of patients with acute anterior cerebral circulation ischemia and are significantly more prevalent among those with symptomatic carotid artery disease. Future clinical studies are required to determine whether HITS are a marker of increased stroke recurrence and can help to clarify stroke etiology in patients with competing stroke mechanisms
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Pilot study for cerebral balloon angioplasty: design considerations and case-control methods
Effect of beta-blocker therapy on the risk of infections and death after acute stroke--a historical cohort study.
BACKGROUND:Infections are a frequent cause for prolonged hospitalization and increased mortality after stroke. Recent studies revealed a stroke-induced depression of the peripheral immune system associated with an increased susceptibility for infections. In a mice model for stroke, this immunosuppressive effect was reversible after beta-blocker administration. The aim of our study was to investigate the effect of beta-blocker therapy on the risk of infections and death after stroke in humans. METHODS:625 consecutive patients with ischemic or hemorrhagic stroke, admitted to a university hospital stroke unit, were included in this historical cohort study. The effect of beta-blocker therapy on post-stroke pneumonia, urinary tract infections and death was investigated using multivariable Poisson and Cox regression models. RESULTS:553 (88.3%) patients were admitted with ischemic stroke, the remaining 72 (11.7%) had a hemorrhagic stroke. Median baseline NIHSS was 8 (IQR 5-16) points. 301 (48.2%) patients received beta-blocker therapy. There was no difference in the risk of post-stroke pneumonia between patients with and without beta-blocker therapy (Rate Ratio = 1.00, 95%CI 0.77-1.30, p = 0.995). Patients with beta-blocker therapy showed a decreased risk for urinary tract infections (RR = 0.65, 95%CI 0.43-0.98, p = 0.040). 7-days mortality did not differ between groups (Hazard Ratio = 1.36, 95%CI 0.65-2.77, p = 0.425), while patients with beta-blocker therapy showed a higher 30-days mortality (HR = 1.93, 95%CI 1.20-3.10, p = 0.006). CONCLUSIONS:Beta-blocker therapy did not reduce the risk for post-stroke pneumonia, but significantly reduced the risk for urinary tract infections. Different immune mechanisms underlying both diseases might explain these findings that need to be confirmed in future studies
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