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benzene/emorragia

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ArticoliTest cliniciBrevetti
Pagina 1 a partire dal 46 risultati

Bilateral subinternal limiting membrane hemorrhage in benzene toxicity.

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OBJECTIVE To report the clinical and spectral domain optical coherence tomography findings in a patient with bilateral central vision loss and a history of exposure to polyamides. METHODS The clinical presentation of the patient was documented with color fundus photographs and spectral domain
Acute myeloid leukemia (AML), also known as acute myelogenous leukemia, is associated with severe hemorrhagic coagulopathy, which is induced by the drop in red blood cells, platelets, and normal leukocyte and the increase of leukemic cells. The case described in this report was of a 32-year-old
OBJECTIVE It has been proposed that the novel spin trap agent disodium-[(tert-butylimino)methyl]benzene-1,3-disulfonate N-oxide (NXY-059) may be useful in the treatment of ischemia and stroke. To date, there is little information concerning the safety of NXY-059 when administered in combination with
Because free radical mechanisms may contribute to brain injury in hemorrhagic stroke, the effect of the free radical trapping agent disodium 4-[(tert-butylimino)methyl]benzene-1,3-disulfonate N-oxide (NXY-059) was investigated on outcome following intracerebral hemorrhage (ICH) in rat. ICH was

[On the mechanism of development of the hemorrhagic syndrome in chronic benzene poisoning].

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The mechanisms of refilling of xylem conduits and bleeding of tall birch during spring.

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Seasonal variations in osmolality and components of xylem sap in tall birch trees were determined using several techniques. Xylem sap was extracted from branch and trunk sections of 58 trees using the very rapid gas bubble-based jet-discharge method. The 5-cm long wood pieces were taken at short

In vitro effect of dextran-benzene-tetra-carboxylate hemoglobin on human blood rheological properties.

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While conducting pharmacological investigations into oxygen carriers, it is important to study the in vitro and in vivo rheological behavior of blood cells in the presence of such preparations. With regard to the original nature of human hemoglobin bound to benzene tetracarboxylate substituted
Circulating volume expansion for intentional hemodilution and/or resuscitation of hemorrhagic shock can be performed with hemoglobin-based oxygen carriers (HBOC) which, in addition to oxygen transport, have vasoactive effects through poorly documented mechanisms. Among these, the effects of HBOC on
Brominated benzenes appear in the environment and human tissues. Their detection in the environment may be as a result of their usage, e.g. hexabromobenzene (HBB), and as products of HBB degradation or metabolism. The aim of this study was to compare liver impairment in acute intoxication of mice
Our aim was to determine whether the newly described P2X1 antagonist NF449 [4,4',4'',4'''-(carbonylbis(imino-5,1,3-benzenetriylbis(carbonylimino)))tetrakis-benzene-1,3-disulfonic acid octasodium salt] could selectively antagonize the platelet P2X1 receptor and how it affected platelet function.

Central effects of mu, delta, and kappa receptor agonists in hemorrhagic shock.

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We have recently shown that selective mu-opiate receptor agonists increase blood pressure and heart rate when injected into the anteroventral hypothalamus (AV3V) of the conscious rat, and that lesions of this area may worsen the effects of hypovolemia. These experiments suggested the possibility

[Aplastic anemia: a model for its induction by oral and subcutaneous benzene in rats].

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OBJECTIVE To set up the experimental conditions to induce aplastic anaemia in rats by oral and subcutaneous administration of benzene. METHODS 6 groups with 6 male Wistar rats weighting 150 g each were formed. Each group with different conditions; 3 of them as experimental groups: 1) ES group

Modeling marrow damage from response data: evolution from radiation biology to benzene toxicity.

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Consensus principles from radiation biology were used to describe a generic set of nonlinear, first-order differential equations for modeling toxicity-induced compensatory cell kinetics in terms of sublethal injury, repair, direct killing, killing of cells with unrepaired sublethal injury, and
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