Leveraging retained physical capabilities to improve quality of life as assessed by persons with severe motor impairments.

Purpose: The main objective of this article is to present an alternative method of interacting with a computer which empowers persons with very severe motor impairments to leverage retained capabilities in order to independently control parts of their daily lives. The input strategy is based on tiny intentional contractions of a single muscle of choice (requiring a minimum of physical contribution only) which are used as selection markers in the context of scanning.

Method: To demonstrate the usefulness of the idea, two applications (combined in a single software system) have been implemented (initially): a module turning the PC into a Universal Remote Control and a Text-To-Speech module.

Building a computer model of the Haemobear blood pump.

Further development of the Haemobear blood pump requires theoretical predictions of the dynamic behavior of the rotor. These predictions can be used to compare different rotor geometry at desired operating conditions before a prototype is built. The study focuses on a rotor-dynamic model of the rigid rotor with six degrees of freedom (6-DoF), which is implemented using the Matlab-Simulink software package.

Inactivation of cerebellar nitric oxide synthase by ethanol in vitro.

The N-methyl-D-aspartate receptor/nitric oxide synthase (NOS)/guanylate cyclase pathway, which plays a crucial role in synaptic plasticity in the brain, is modulated by ethanol. We studied the effect of ethanol in vitro on NOS in rat cerebellum and showed that ethanol (25-200 mM) inactivated NOS in a dose-dependent manner. This inactivation was prevented by the biopterin cofactor tetrahydrobiopterin (BH4) as well as by L-arginine, a NOS substrate, but not by NADPH.

Changes in some pro- and antioxidants in rat cerebellum after chronic alcohol intake.

Some pro- and antioxidants were measured in the cerebellum from ethanol-fed rats using ethanol administration in drinking water as a model of moderate alcohol intoxication. After 4 weeks of ethanol intake, a 30% increase in the nonheme iron content in the cerebellum occurred in ethanol-fed rats as compared to control animals. The low-molecular-weight-chelated iron (LMWC-Fe) content as well as the percentage of total nonheme iron represented by LMWC-Fe were increased in the cerebellar cytosol after chronic ethanol administration.

Effect of chronic ethanol feeding on lipid peroxidation and protein oxidation in relation to liver pathology.

Liver lipid peroxidation, nonheme iron, antioxidants, and protein oxidation were investigated in experimental alcohol-induced liver disease in the rat. Wistar male rats were intragastrically and continuously infused for 4 weeks with a high-fat diet plus an ethanol or an isocaloric amount of dextrose, maintaining a high blood alcohol level (200-300 mg%). This model induced fatty liver, spotty necrosis, and focal inflammation.

[Alcohol and free radicals: from basic research to clinical prospects].

An oxidative stress occurs in the liver of rats following various conditions of ethanol administration. The ethanol-inducible cytochrome P450 2E1 plays a key role in its generation, favoured itself by an increase in the "redox-active" fraction of intracellular non-heme iron. Administration of ethanol elicits the generation of the 1-hydroxyethyl radical, which has been identified in vivo.

[Alcohol and free radicals: from basic research to clinical prospects].

An oxidative stress occurs in the liver of rats following various conditions of ethanol administration. The ethanol-inducible cytochrome P450 2E1 plays a key role in its generation, favoured itself by an increase in the "redox-active " fraction of intracellular non-heme iron. Administration of ethanol elicits the generation of the 1-hydroxyethyl radical, which has been identified in vivo.

Inactivation of Cu,Zn-superoxide dismutase by free radicals derived from ethanol metabolism: a gamma radiolysis study.

The reactions of free radicals derived from ethanol metabolism with Cu,Zn SOD were studied. 1-Hydroxyethyl radicals were generated by gamma radiolysis of a N2O-saturated ethanolic solution (10(-2) M) in phosphate buffer (10(-3) M, pH 7.4).

Quantification of Mn-SOD mRNAs by using a competitive reverse-transcription polymerase chain reaction.

The manganese superoxide dismutase plays an important role in the cellular response to oxidative stress and appears to be highly regulated by many factors. The study of this gene's expression is difficult to achieve due to multiple rat Mn-SOD transcripts. In this report we described the quantification of the rat Mn-SOD transcripts by competitive reverse transcription-polymerase chain reaction.

Alcohol and antioxidant systems.

Following the pioneer report of Di Luzio (Physiologist 6, 169-173, 1963) concerning the prevention of the acute ethanol-induced fatty liver by antioxidants, many observations have shown that ethanol-induced liver injury may be linked, at least partly, to an oxidative stress resulting from increased free radical production and/or decreased antioxidant defence. The disturbances induced in the major hepatic enzymatic and non-enzymatic antioxidant systems following experimental acute and chronic ethanol administration are reviewed, emphasizing the important role of dietary alpha-tocopherol in modifying the induction of oxidative stress and its usual expression as increased lipid peroxidation. Adaptative increases in some elements of the hepatic antioxidant defence partly counteract the enhanced generation of prooxidant free radicals following chronic ethanol intake.

Effects of acute ethanol administration on the uptake of 59Fe-labeled transferrin by rat liver and cerebellum.

The uptake of iron by the liver and cerebellum was measured in rats using [59Fe]transferrin. An acute ethanol load (50 mmol/kg body wt., i.

Mitochondrial respiratory activity and superoxide radical generation in the liver, brain and heart after chronic ethanol intake.

Functional characteristics of mitochondria isolated from liver, brain and heart were studied in ethanol-fed rats using ethanol administration in drinking water as a model of moderate alcohol intoxication. Our results show a slight decrease in liver cytochrome aa3 content, the mitochondrial alteration which is most consistently observed during chronic ethanol feeding. In liver and heart mitochondria, ethanol consumption led to an increase in state 3 respiration with NAD(+)-linked substrates, whereas no changes were apparent in respiration rates with succinate as substrate.

Restoration of taxol sensitivity of multidrug-resistant cells by the cyclosporine SDZ PSC 833 and the cyclopeptolide SDZ 280-446.

Background: Taxol, a promising agent for the treatment of cancer, has entered phase II clinical trials. Nevertheless, it belongs to the class of compounds that show impaired retention in multidrug-resistant cells expressing P-glycoprotein (Pgp), a drug efflux pump. Chemosensitizers like verapamil modulate multidrug resistance by interfering with the efflux action of Pgp and thus can decrease drug resistance or can restore drug sensitivity by restoring normal drug accumulation and distribution within the multidrug-resistant tumor cell.

[Free radicals, oxidative stress and antioxidant vitamins].

Free radicals having oxidizing properties are produced in vivo. The monoelectronic reduction of dioxygen generates the superoxide radical (.O2-) which, according to the experimental conditions, behaves as a reducing or an oxidizing agent.

The effect of interleukin-1 on cytokine gene expression in cultured human articular chondrocytes analyzed by messenger RNA phenotyping.

Objective: To investigate the pattern of cytokine gene expression in human articular chondrocytes in culture in response to interleukin-1 beta (IL-1 beta). The effect of serum and variations in culture conditions was also studied.

Methods: Messenger RNA was extracted from cells, reverse-transcribed to complementary DNA, and amplified by the polymerase chain reaction (PCR), using specific oligonucleotide primers.

Effects of chronic ethanol administration on free radical defence in rat myocardium.

Cellular protection against free radical reactions was measured in myocardium from ethanol-fed rats using ethanol administration in drinking water as a model of moderate alcohol intoxication. The activities of Cu,Zn-superoxide dismutase (SOD) and glutathione-S-transferase were higher in ethanol-fed rats than in controls, whereas Mn-SOD, catalase and glutathione peroxidase activities were not altered by ethanol treatment. Myocardial zinc was higher and selenium concentration lower in ethanol-fed rats than in controls.

Implication of free radical mechanisms in ethanol-induced cellular injury.

Numerous experimental data reviewed in the present article indicate that free radical mechanisms contribute to ethanol-induced liver injury. Increased generation of oxygen- and ethanol-derived free radicals has been observed at the microsomal level, especially through the intervention of the ethanol-inducible cytochrome P450 isoform (CYP2E1). Furthermore, an ethanol-linked enhancement in free radical generation can occur through the cytosolic xanthine and/or aldehyde oxidases, as well as through the mitochondrial respiratory chain.

Effect of allopurinol on the hepatic and cerebellar iron, selenium, zinc and copper status following acute ethanol administration to rats.

An acute ethanol load (50 mmol/kg, i.p.) induces an increase in the total non-heme iron and in the low-molecular-weight non-heme iron complexes (LMW-Fe) content both in liver and cerebellum.

Disturbances in myocardial creatine kinase following ethanol administration to rats--trials of prevention by allopurinol, desferrioxamine and propranolol.

A significant decrease in myocardial creatine kinase (CK) activity is apparent 2 hr after an acute ethanol load (2.3 g/kg, i.p.

Iron chelation by deferoxamine inhibits lipid peroxidation during cardiopulmonary bypass in humans.

Iron catalysis is involved in oxygen-derived free radical generation and subsequent lipid peroxidation, which have been reported to occur during cardiopulmonary bypass in humans. We assessed the effects of the iron chelator deferoxamine on the susceptibility of circulating low density lipoproteins (LDLs) to induced peroxidation in 20 adult patients (10 controls and 10 treated) undergoing cardiopulmonary bypass for coronary or valve procedures. Deferoxamine was given both intravenously (30 mg/kg body wt, starting 30 minutes before bypass and extending for the next 4 hours) and as an additive to the cardioplegic solution (250 mg/l).

Effect of acute ethanol administration on the subcellular distribution of iron in rat liver and cerebellum.

An acute ethanol load (50 mmol/kg, i.p.) produced altogether a decrease in the non-heme iron content of the serum and an increase in the iron content in liver and cerebellum.