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Biomedical subjects

F Fernandez

Publications and source records attributed to F Fernandez.

At least 109 records · Page 6Linked to original sources
PubMed1989

Psychostimulant response in AIDS-related complex patients.

Methylphenidate or dextroamphetamine was used to treat 17 of 32 patients with AIDS-related complex who were referred for neuropsychiatric evaluation of symptoms representative of cognitive and/or affective dysfunction. All 17 patients were found to have some degree of cognitive impairment. Psychiatric diagnoses included organic mental disorder (8), adjustment disorder (5), and major depression (4). The 17 patients were receiving no other psychoactive or neurotoxic medications nor were they receiving concomitant investigational antiviral or chemotherapeutic agents. Clinical response to psychostimulant therapy was rated using the Efficacy Index of the Clinical Global Impressions. Pharmacotherapy with either psychostimulant was clinically effective in improving affective parameters in 89.5% (15) of the 17 patients, with 79% (13) of the 17 achieving a moderate to marked response. No adverse side effects were encountered.

AIDS-Related Complex↗
PubMed1989

Anxiety and the neuropsychiatry of AIDS.

Acquired immune deficiency syndrome (AIDS) and human immunodeficiency virus (HIV)-related disorders are increasingly prevalent. They have psychopathologic and neuropsychiatric complications that warrant a systematic neurobehavioral assessment and a differential diagnosis of emotional disturbances in HIV-infected patients. This article provides an overview of HIV-spectrum disorders and discusses the management of anxiety in patients with HIV infection.

AIDS Dementia Complex↗
PubMed1988

Further studies on the mechanisms for the antithrombotic effects of sulfated polysaccharides in rabbits.

A recent study (Fernandez et al., Thromb. Haemostas. 1987; 57: 286-93) demonstrated that when rabbits were injected with the minimum weight of a variety of glycosaminoglycans required to inhibit tissue factor-induced thrombus formation by approximately 80%, exogenous thrombin was inactivated approximately twice as fast in the post-treatment plasmas as the pre-treatment plasmas. In this study, we investigated the relationship between inhibition of thrombus formation and the extent of thrombin inhibition ex vivo. We also investigated the relationship between inhibition of thrombus formation and inhibition of prothrombin activation ex vivo. Four sulfated polysaccharides (SPS) which influence coagulation in a variety of ways were used in this study. Unfractionated heparin and the fraction of heparin with high affinity to antithrombin III potentiate the antiproteinase activity of antithrombin III. Pentosan polysulfate potentiates the activity of heparin cofactor II. At less than 10 micrograms/ml of plasma, all three SPS also inhibit intrinsic prothrombin activation. The fourth agent, dermatan sulfate, potentiates the activity of heparin cofactor II but fails to inhibit intrinsic prothrombin activation even at concentrations which exceed 60 micrograms/ml of plasma. Inhibition of thrombus formation by each sulfated polysaccharides was linearly related to the extent of thrombin inhibition achieved ex vivo. These observations confirm the utility of catalysis of thrombin inhibition as an index for assessing antithrombotic potential of glycosaminoglycans and other sulfated polysaccharides in rabbits. With the exception of pentosan polysulfate, there was no clear relationship between inhibition of thrombus formation and inhibition of prothrombin activation ex vivo.

Animals↗
PubMed1988

Interferon-induced organic mental disorders associated with unsuspected pre-existing neurologic abnormalities.

Eleven patients ranging in age from 52 to 80 years, undergoing treatment for cancer with various preparations of interferon received neurobehavioral evaluations after experiencing unexpectedly severe organic mental disorders. The reactions ranged from delirium to extrapyramidal symptoms, mania, and neurasthenia with catatonic episodes. Computed tomographic (CT) scans of the brain disclosed unsuspected pre-existing neurologic abnormalities in all patients, including cerebral atrophy (6/11), brain metastases (4/11), and evidence of head injury incurred 40 years earlier (1/11). These findings suggest that cancer patients with pre-existing neurologic dysfunctions are at increased risk for severe interferon neurotoxicity.

Aged↗
PubMed1988

Ultrasound and spermatogenesis in the rat.

Using exposure conditions comparable to those which have been associated by others with positive results, we tested for effects of ultrasound on sperm production over a period of 12 weeks following treatment. Continuous wave exposure with spatial average intensities of 1, 2 and 4 W/cm2 and exposure times up to 10 minutes were used. In some experiments, the exposures were repeated after an elapsed time of 48 h. No significant changes in spermatogenesis were related to any of the exposure conditions in spite of the fact that some of the treatments caused thermal tissue damage near bone. No effects of exposure were found in weights of the testis, prostate, seminal vesicle, or whole body.

Animals↗
PubMed1988

Response of HIV-related depression to psychostimulants: case reports.

Four depressed and cognitively impaired patients with HIV-related disease had a marked therapeutic response to treatment with psychostimulants. Use of dextroamphetamine and methylphenidate brought a prompt remission of depressive and cognitive dysfunctions without adverse side effects. The results suggest the need for further evaluation of psychostimulants in the treatment of HIV patients whose depression proceeds from an affective disturbance (either primary or secondary) or from a specific organic mental disorder. The importance of neuropsychiatric assessment of depressed HIV patients is stressed, and diagnostic and treatment guidelines are given.

Acquired Immunodeficiency Syndrome↗
PubMed1988

[Hemodynamic effects on intravenous propafenone in hypertrophic myocardiopathy].

None of the medical treatments of hypertrophic cardiomyopathy is perfect. In the present study conducted on 11 patients with hypertrophic cardiomyopathy in whom the usual treatments were either ineffective or badly tolerated, the haemodynamic effects of propafenone administered intravenously were investigated. The drug was injected centrally in doses of 2 mg/kg over 10 minutes, then by continuous intravenous infusion of 1.5 mg/min during 30 minutes. Various parameters were recorded before and after propafenone treatment by right and left cardiac catheterization. This anti-arrhythmic drug, which has beta-blocking and amiodarone-like properties, reduced left intraventricular obstruction but had no beneficial effect on diastolic function. The baseline and induced left intraventricular gradients were reduced from 30.4 to 17.7 mmHg and from 74 to 43 mmHg respectively. Diastolic function values showed a fall in dp/dt min from 1470 to 1307 mm/sec and an increase in T value from 0.066 to 0.084. The use of propafenone in hypertrophic cardiomyopathy must be accurately determined by long-term oral studies.

Adolescent↗
PubMed1988

[Prognostic factors in dilated cardiomyopathies].

One hundred and sixteen patients (mean age 46 years) with dilated cardiomyopathy documented by haemodynamic investigations and angiography with normal coronary arteriography were followed up for a mean period of 29 +/- 19 months. During that period, 36% of the patients died after a follow-up of 30 +/- 20 months. The actuarial death rates were 15% at 2 years, 45% at 6 years and 60% at 10 years. The main factors predictive of survival at 10 years were the clinical and haemodynamic markers of left heart failure. The death rate was multiplied by 1.6 in patients in stages III or IV of the NYHA classification (83% vs 51%, p less than 0.01), by 2.6 in patients with left ventricular end-diastolic pressure above 15 mmHg (73% vs 29%, p less than 0.01), by 2.2 when the indexed end-diastolic volume rose above 200 ml/m2 (75% vs 35%, p less than 0.01), by 2.2 when the left ventricular ejection fraction was below 40% (75% vs 35%, p less than 0.05) and by 2.6 when angiographic mitral valve regurgitation was present (75% vs 34%, p less than 0.01). The death rate at 9 years was 2.3 times higher in patients with left bundle branch block (72% vs 36%, p less than 0.05). A cardiothoracic index over 0.60 proved to be of poor prognosis at one year (death rate: 19%). While alcoholism played no part in the prognosis, the death rate in smokers was consistently higher than in non smokers (56% vs 32% at 6 years, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1988

Treatment of severe, refractory agitation with a haloperidol drip.

A case of agitated delirium secondary to bilateral occipital cerebral infarctions in a cancer patient was refractory to trials of large doses of intravenous psychotropic agents, but continuous intravenous infusion of haloperidol controlled agitation rapidly and safely. A total haloperidol dose of 600 mg/day was used without complications. Haloperidol by continuous infusion should be considered in the management of severe, refractory agitation in patients who are medically ill.

Acute Disease↗
PubMed1987

The inhibition of thrombin-dependent positive-feedback reactions is critical to the expression of the anticoagulant effect of heparin.

Heparin catalyses the inhibition of two key enzymes of blood coagulation, namely Factor Xa and thrombin, by enhancing the antiproteinase activities of plasma antithrombin III and heparin cofactor II. In addition, heparin can directly inhibit the activation of Factor X and prothrombin. The contributions of each of these effects to the anticoagulant activity of heparin have not been delineated. We therefore performed experiments to assess how each of these effects of heparin contributes to its anticoagulant activity by comparing the effects of heparin, pentosan polysulphate and D-Phe-Pro-Arg-CH2Cl on the intrinsic pathway of coagulation. Unlike heparin, pentosan polysulphate catalyses only the inhibition of thrombin by plasma. D-Phe-Pro-Arg-CH2Cl is rapid enough an inhibitor of thrombin so that when added to plasma no complexes of thrombin with its inhibitors are formed, whether or not the plasma also contains heparin. Heparin (0.66 microgram/ml) and pentosan polysulphate (6.6 micrograms/ml) completely inhibited the intrinsic-pathway activation of 125I-prothrombin to 125I-prothrombin fragment 1 + 2 and 125I-thrombin. On the addition of thrombin, a good Factor V activator, to the plasma before each sulphated polysaccharide, the inhibition of prothrombin activation was demonstrable only in the presence of higher concentrations of the sulphated polysaccharide. D-Phe-Pro-Arg-CH2Cl also completely inhibited the intrinsic-pathway activation of prothrombin in normal plasma. The inhibitory effect of D-Phe-Pro-Arg-CH2Cl was reversed if thrombin was added to the plasma before D-Phe-Pro-Arg-CH2Cl. The inhibition of the activation of prothrombin by the three agents was also abolished with longer times with re-added Ca2+. Reversal of the inhibitory effects of heparin and pentosan polysulphate was associated with the accelerated formation of 125I-thrombin-antithrombin III and 125I-thrombin-heparin cofactor complexes respectively. These results suggest that the anticoagulant effects of heparin and pentosan polysulphate are mediated primarily by their ability to inhibit the thrombin-dependent activation of Factor V, thereby inhibiting the formation of prothrombinase complex, the physiological activator of prothrombin.

Calcium↗
PubMed1987

The role of the hematocrit in bleeding.

Low hematocrit is an often neglected cause in the pathogenesis of a prolonged bleeding time in an anemic patient. There has been ample evidence in the literature, indicating a relationship between hematocrit and the bleeding time; and that the transfusion of RBCs may correct the prolonged bleeding time often observed in anemic patients. It is unclear how a low hematocrit causes a prolongation in the bleeding time; however, two hypotheses have been put forward. First, in small blood vessels, blood flow is such that the RBCs cause the physical dispersion of platelets towards the subendothelial surface, thus promoting interaction with the blood vessel wall. Secondly, following injury to a small blood vessel, RBCs activate platelets by releasing small amounts of adenosine diphosphate (ADP) into the microvasculature following the hemolysis that often occurs during hemostasis. The fact that the hematocrit influences the bleeding time may be of clinical importance in the treatment of anemic patients, particularly those presenting a bleeding tendency.

Adenosine Diphosphate↗