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Biomedical subjects

J Marion

Publications and source records attributed to J Marion.

At least 19 recordsLinked to original sources
PubMed1992

Rhabdomyosarcoma of the head and neck in children.

Twenty-two children, 9 male and 13 female, with a non-orbital rhabdomyosarcoma of the head and neck, treated between 1970 and 1988, have been reviewed. Since 1972, treatment has consisted of combination chemotherapy, and where necessary radiotherapy and/or surgery. Complete clinical remission after initial chemotherapy was observed in 21 children. Six children were cured after primary treatment but 15 developed recurrent disease. Thirteen children had a parameningeal localized tumour, with eventual meningeal involvement in 5. Survival in this group was worse than in the non-meningeal group. Lymph node metastasis at first presentation (5 patients) had no influence on prognosis, whereas development of lymph node metastases during follow-up resulted in 100% mortality. All patients were retrospectively classified according to both the IRS-classification and TNM-descriptive system. No correlation with either system could be established. Fourteen of 15 children with recurrent disease were treated, 4 of whom were cured. Thus, 10 out of 22 (45%) children were long-term survivors.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1986

Naftidrofuryl in chronic arterial disease. Results of a six month controlled multicenter study using Naftidrofuryl tablets 200 mg.

The study was carried out on patients with intermittent claudication (Fontaine's stage II). The arterial and atheromatous origin of the disease was confirmed and localized by angiography or Doppler velocimetry examination. One hundred eighty-six patients were selected initially. Their pain-free walking distance on a treadmill (at a speed of 3 km/hour and an inclination of 10%) had to be 150-300 m. During the first month all patients received 3 placebo tablets daily. At the end of this run-in period (D-30; D 0) and after checking walking distance stability (allowed variation: +/- 20% between the two measurements) the patients were included in the study. One hundred fifty-four patients were selected and 118 remained during the whole study. The study was designed as a double-blind, using two parallel randomly selected groups. Sixty-four patients received for six months Naftidrofuryl (3 X 200 mg tablets daily with meals); 54 patients received placebo under the same conditions. During this period, clinical and paraclinical examinations were carried out every quarter (D 90 and D 180). After checking the initial homogeneity of the Naftidrofuryl and placebo-groups, the comparison between groups indicates a significant improvement in Naftidrofuryl group after 3 and 6 months of treatment. At the end of the study the observed differences in walking distance with Naftidrofuryl are approximately twice the difference in the reference group (D 90: p less than 0.05; D 180: p less than 0.02). The results of this study indicate that Naftidrofuryl is an efficient pharmacological tool for treatment of patients with chronic arterial disease (Fontaine's stage II).

Administration, Oral↗
PubMed1985

[Supraventricular tachycardia induced by effort and by catecholamines].

The role played by catecholamines in the initiation of certain forms of ventricular tachycardia is now recognised. On the other hand, a similar predominant or exclusive mechanism has not been demonstrated in supraventricular tachycardia. We observed a rate case of reproducible attacks of junctional tachycardia on effort in a 45 year old man. This patient had experienced attacks of tachycardia on effort for a number of years, stopping about 10 minutes after the end of effort. An exercise stress test performed for an anginal attack, induced a narrow complex tachycardia at 270/min at the first minute of the recovery period which terminated spontaneously 18 minutes later after a brief episode of atrial fibrillation. During a second exercise stress test, an episode of tachycardia at 250/min was recorded at the second minute of recovery, lasting 11 minutes. Investigations showed a retrograde concealed septal bundle of Kent activated retrogradely during reciprocating tachycardia. A similar form of tachycardia was induced by an injection of isoproterenol. The adrenergic mechanism of the arrhythmia led to the prescription of a beta-blocker (propranolol 120 mg/day), which effectively prevented clinical tachycardia and the forms of tachycardia induced by ergometric tests 15 days and 3 months after the initiation of treatment.

Cardiac Catheterization↗
PubMed1985

High-dose cytosine arabinoside and daunorubicin as consolidation therapy for acute nonlymphocytic leukemia in first remission: a pilot study.

High-dose (HD) cytosine arabinoside (ARA-C) is more effective treatment than conventional-dose ARA-C regimens for patients with relapsed acute nonlymphocytic leukemia (ANLL). We report here that HD ARA-C given during the first remission of ANLL has resulted in long remission durations and a high proportion of patients who survive more than three years free of disease. From August 1979 to September 1983, 36 adult patients with ANLL in first remission received one to three courses of HD ARA-C (3 g/m2 by one-hour infusion every 12 hours for 12 doses on days 1 through 6) alone or with daunorubicin (30 mg/m2 for two or three doses on days 7 through 9). Three patients died of sepsis or hemorrhage during consolidation, and 14 patients have relapsed from five to 48 months after diagnosis. The remaining 19 patients are in continued complete remission (CCR) from 11 to 62 months. Denoting all deaths in remission as relapse, the actuarial probability of CCR is 42% at 62 months, with an apparent plateau in the survival curve. Of the first 22 patients treated, ten remain in CCR from 37 to 62 months with no therapy for at least three years. Due to its heightened anti-leukemic activity, HD ARA-C allows brief but effective consolidation of ANLL in first remission, with long-term disease-free survival comparable to other approaches.

Acute Disease↗
PubMed1983

HLA typing of cultured amniotic fluid cells.

HLA typing was performed on 18 cultures of human amniotic fluid cells using cytotoxicity and absorption technics. Confirmation of antigen assignments was obtained in nine of ten instances, where HLA typing also was performed on cord blood. Three major problems were encountered in performing these studies: (1) complement cytotoxicity, (2) false-positive reactions, and (3) false-negative reactions. False-positive and false-negative reactions occurred more frequently with sera defining HLA-B locus specificities than with sera defining HLA-A locus specificities. Absorption studies were helpful in making antigen assignments when false reactions occurred. Preliminary studies suggest that the frequency of false-positive reactions can be decreased by absorbing HLA typing sera with antigen-negative amniotic fluid cultured cells, buffy coat, or platelets. Accurate antigen assignment is difficult when parental HLA types are unavailable.

Absorption↗
PubMed1982

["Pericardial" friction rubs in pulmonary embolism (author's transl)].

In a series of sixty-five patients with pulmonary embolism, the main clinical feature was a systolic and diastolic friction rub in three cases. Such friction rubs are found in 1 to 5% of patients with pulmonary embolism. The characteristics of the rub are identical to those of pericardial friction rubs. According to some authors, a friction rub indicates massive pulmonary embolism. However, a friction rub may be found in less severe cases if embolization involves the paracardiac lobes or segments. The rub may be caused by one or the other of the following mechanisms. Severe pulmonary embolism or a free blood clot floating in the right atrium or ventricle may produce a sound resembling a friction rub. More often, a genuine pleuro-pericardial or pericardial friction rub originates in an inflammatory reaction to a contiguous pulmonary infarct. It is important to establish accurate diagnosis of pulmonary embolism in spite of a pericardial friction rub because of the therapeutic implications. Anticoagulant therapy in sufficient dosage must not be withheld in this situation.

Adult↗
PubMed1980

Role of metastatectomy without chemotherapy in the management of osteosarcoma in children.

In a series of 18 consecutive non metastatic osteosarcoma patients, metastases developed in 12 and successful metastatectomies could be performed in 6. No adjuvant chemotherapy was given. Four of these 6 patients survived. The importance of length of disease-free survival is described. Radiotherapy and chemotherapy as adjuvants to prevent or postpone the development of metastases are mentioned and an EORTC-SIOP trial on this subject is briefly discussed.

Adolescent↗
PubMed1979

Origin of the arachidonic acid released post-mortem in rat forebrain.

To determine the origins of the arachidonic acid released post-mortem in brain tissue, [3H]arachidonic acid was injected by the intracerebro-ventricular route and radioactivity monitored in complex lipids and free arachidonic acid at various times after decapitation. The specific activity of the released arachidonic acid was close to that in the total phospholipid fraction and much lower than that of the neutral lipids. The phospholipid with the closest specific activity to the free arachidonic acid recovered at the end of the post-mortem period was phosphatidylinositol. Phosphatidylcholine showed a small but significant decrease in radioactivity post-mortem and could contribute 37% of the arachidonic acid released to the free fatty acid fraction. Arachidonic acid released in rat forebrain after decapitation thus comes from a mixture of phospholipids with phosphatidylinositol and phosphatidylcholine being the major source. Phosphatidylserine and phosphatidic acid did not make important contributions to the free arachidonic acid. In the microsomal fraction, the specific activity of the free arachidonic acid was very close to that in phosphatidylinositol.

Animals↗
PubMed1979

Evidence for the use of a pool of the free arachidonic acid in rat cerebral cortex tissue for prostaglandin F2alpha synthesis in vitro.

To determine if the arachidonic acid which is released post-mortem in rat cerebral cortex is directly available for the in vitro synthesis of prostaglandin F2 alpha, cerebral cortex slices or homogenates were incubated in the presence of [2H8]arachidonic acid. The deuterium to protium ratios in the prostaglandin F2 alpha were compared to those in the free arachidonic acid and other lipids of the tissue after 5 and 60 min of incubation. In the slice, the prostaglandin F2 alpha reached maximum labelling before any of the lipids examined except for a pool of rapidly labelled free arachidonic acid located at the damaged surfaces of the tissue. The prostaglandin F2 alpha recovered in the medium after 60 min of incubation had a deuterium to protium ratio twice that of the prostaglandin F2 alpha found in the tissue. Norepinephrine doubled the labelling of the prostaglandin produced by the slice. The labelling of the prostaglandin F2 alpha in homogenates was 10 times higher than in tissue slices and the deuterium to protium ratio of the total free arachidonic acid was similar to that of prostaglandin F2 alpha. The results indicate that exogenous and endogenous arachidonic acid do not mix appreciably in the intact slice and that the prostaglandin synthetase is present on the damaged surface as well as the intact interior of the slice.

Animals↗
PubMed1979

Isoproterenol and aminophylline reduce lung capillary filtration during high permeability.

Pseudomonas bacteremia in sheep causes a prolonged increase in lung vascular permeability to protein. Isoproterenol and aminophylline could effect lung fluid balance after Pseudomonas by reducing vascular pressures or by blocking release of permeability mediators. We measured vascular pressures, lung lymph flow, and lymph and plasma protein concentrations in unanesthetized sheep under baseline conditions and during steady-state increased permeability after Pseudomonas. Pseudomonas caused pulmonary vascular pressures to rise and lung lymph flow to increase fivefold, but lymph/plasma protein concentration did not change. Pulmonary vascular pressures and lung lymph flow decreased during intravenous infusion of isoproterenol and aminophylline. The decrease in lymph flow after isoproterenol and isoproterenol plus aminophylline was linearly related to the decrease in microvascular pressure (r = 0.71). Lymph/plasma total protein concentration ratios and lymph clearance of proteins with molecular radii 36--96 A remained high during isoproterenol and aminophylline. These drugs can substantially reduce transvascular filtration primarily because they reduce lung vascular pressures.

Aminophylline↗
PubMed1978

Increase in vivo of unesterified fatty acids, prostaglandin F2 alpha but not thromboxane B2 in rat brain during drug induced convulsions.

The amount of free arachidonic acid and prostaglandin F2 alpha in rat cerebral hemispheres was increased following convulsions induced by carbachol and metrazol. The level of thromboxane B2 was not affected and prostaglandin endoperoxides could only be "trapped" after a very short convulsive period. Unesterified fatty acid levels at 2 minutes post-mortem were decreased by 50% in the cerebral hemispheres of phenytoin treated rats. Under the same conditions, phenobarbital and diazepam had little effect on the levels of free fatty acids in rat brain.

Animals↗
PubMed1976

The biosynthesis of prostaglandins by brain tissue in vitro.

Brain tissue slices in vitro synthesize both PGF2alpha and PGE2 from endogenous precursors at almost linear rates over the first hour. PGF2alpha biosynthesis predominates except for the cat cerebellum. Catecholamines and adrenochrome greatly activate the formation of PGF2alpha in slices and homogenates. The mechanism appears related to endoperoxide reduction rather than increased availability of precursor. The arachidonic acid for prostaglandin biosynthesis in slices is derived from an intracellular pool that forms immediately after animal death and is sufficient to saturate by cyclooxygenase completely and account for the linear kinetics. Biosynthesis of prostaglandins in vivo must be orders of magnitude less than that found in vitro, unless there is local tissue damaged. PGF2 alpha catabolism by cerebral cortex is very small; however, PGE2 is converted to PGF2alpha by brain slices by a 9-keto reductase activity in significant amounts when added in pharmacological amounts.

5,8,11,14-Eicosatetraynoic Acid↗