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Biomedical subjects

L Bodson

Publications and source records attributed to L Bodson.

17 recordsLinked to original sources
PubMed1989

[Direct transfer of obstetrical data by magnetic means in a randomized multicenter trial of the subjective count of fetal movements by the mother-to-be].

Ten Belgian maternity hospitals have collaborated in an international clinical multicenter trial: Multicenter Fetal Movement Trial. Nine maternity hospitals were already managing a computerized data bank before their participation in the trial. In seven of these centers the local team was able to write a program for direct transmission of data, using standard sequential ASCII files. This procedure presents many advantages: there is a gain in time and money, since it is no longer necessary to fill out data collecting forms, or coding at a central level. Transcription errors are avoided, adhesion to strict and standard definitions is guaranteed, the micro-systems are performing in a suitable fashion in each center, modifications of parameters (and corrections) are done very quickly and, automatically carried out, on the basis of clinical data as well as "research" data, transmission by telecommunication is immediately and easily feasible.

Belgium↗
PubMed1987

Thromboxane and prostacyclin release in adult respiratory distress syndrome.

Plasma thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured in 84 patients at risk of developing adult respiratory distress syndrome (ARDS) (44 patients following multiple trauma, 29 patients following abdominal surgery and 11 patients with acute pancreatitis). Forty-nine of these 84 patients developed an ARDS. High (greater than 140 pg/ml plasma) TXB2 values were found in 52/84 patients. The median values of TXB2 were: 360 pg/ml in multiple injured, 250 pg/ml in abdominal surgery and 410 pg/ml in acute pancreatitis patients. The median TXB2 value was 575 pg/ml in patients developing ARDS and 140 pg/ml in those without this complication: this difference was statistically significant (p less than 0.05). The median values of 6-keto-PGF1 alpha were 55 pg/ml in multiple injured, 25 pg/ml in abdominal surgery and 120 pg/ml in acute pancreatitis patients. The median 6-keto-PGF1 alpha value was 122 pg/ml in ARDS patients and 25 pg/ml in non-ARDS patients (statistically significant: p less than 0.05). High TXB2 and 6-keto-PGF1 alpha values were particularly related to sepsis in abdominal surgery patients (p less than 0.05) and in multiple injured patients (p less than 0.01). No relation could be established between abnormal TXB2 or 6-keto-PGF1 alpha values and death. High TXB2 values often persisted for several days and were observed particularly at the time ARDS diagnostic criteria were fulfilled.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Biochemical investigations after burning injury: complement system, protease-antiprotease balance and acute-phase reactants.

Seventeen burned patients were investigated--Group I (n=10) with a mean burned area expressed as unit burn standard (UBS) of 69 +/- 24 and Group II (n = 7) with a mean UBS of 23 +/- 8. Blood samples were collected immediately after admission, 6-12 h after injury, during the morning and evening of day 1, and then daily for 2 weeks. This prospective study demonstrated complement activation in vivo in all burned patients, measured by C3d/C3 ratio index which was not related to the extent of the burned surface. A significant protease-antiprotease imbalance, correlated to the severity of burns, was found, leukocyte elastase was increased throughout the observation period, alpha 2-macroglobulin drastically decreased in severely burned patients, and alpha 1-proteinase inhibitor promptly decreased below the normal level in patients with more than 40 UBS. Finally, there was a delayed but then persistent acute-phase reactant protein response involving C-reactive protein, haptoglobin and alpha 1-acid glycoprotein, the concentrations of which reached a plateau on days 6 or 7.

Acute-Phase Proteins↗
PubMed1986

Prostaglandin E2, prostacyclin, and thromboxane changes during nonpulsatile cardiopulmonary bypass in humans.

To study the effect of lung bypass on the production of prostaglandin E2, prostacyclin, and thromboxane A2, we measured simultaneously arterial and venous plasma concentrations of prostaglandin E2, 6-keto-prostaglandin F1 alpha (stable metabolite of prostacyclin), and thromboxane B2 (stable metabolite of thromboxane A2) before, during, and after cardiopulmonary bypass. Seventeen patients (age range 46 to 69 years) undergoing aorta-coronary bypass grafts were investigated. The prostaglandin E2 production rose sharply immediately after the onset of bypass (baseline: 9.7 +/- 2.9 pg/ml to 85 +/- 16.6 pg/ml in venous and 87 +/- 12 pg/ml in arterial plasma, p less than 0.03) and rapidly decreased after pulmonary reperfusion (53 +/- 6.4 and 57 +/- 20 pg/ml, respectively, in venous and arterial plasma at the end of bypass). The increase in prostaglandin E2 was influenced by the heart-lung machine itself (as demonstrated by a closed "bypass" circuit) and by lung bypass. Pulmonary metabolism of prostaglandin E2 was maintained after bypass. The prostacyclin production rose significantly at the beginning of bypass (154 +/- 26 pg/ml venous prebypass level to 361 +/- 94 pg/ml after aortic clamping, p less than 0.03). Prostacyclin decreased progressively during rewarming of the patient, pulmonary reperfusion, and discontinuation of bypass. When prostacyclin decreased, thromboxane B2 production rose significantly and reached peak arterial levels when the lungs were reperfused (112 +/- 33 pg/ml prebypass levels to 402 +/- 101 pg/ml, p less than 0.01). Except for prostaglandin E2, there were no significant differences between arterial and venous plasma levels of these substances. The same prostanoids were also measured in five patients undergoing major orthopedic operations, and no significant changes in prostanoids were observed. Our data demonstrate significant production of prostaglandin E2 in the systemic circulation during cardiopulmonary bypass in humans. They further indicate that lung bypass disturbs the plasma prostaglandin/thromboxane balance.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

[Results of hip arthroplasty using Gérard's coupled, non-cemented cups. Analysis of 92 cases reviewed].

The authors have reviewed 92 cases of uncemented surface hip replacements with a minimum follow-up of 3 years. They were operated on using the Gérard technique which must be very precise to avoid devascularisation of the femoral head. 17 failures had to be operated on again. The main indications were necrosis of the femoral head and degenerative arthritis without excentration in patients aged between 50 and 60 years. In this type of patient, satisfactory results were obtained in more than 80%. It is concluded that this type of hip arthroplasty is valuable, provided there are good indications and a precise technique. It should be avoided in elderly, obese and porotic patients, in whom a total hip prosthesis is a better solution.

Adult↗
PubMed1984

Changes in cerebrospinal fluid enzyme activity after severe head injury. Diagnostic and prognostic values.

We studied CSF CK and LDH isoenzyme activities in 27 patients with severe head injury and in 10 patients with chronic hydrocephalus not related to trauma. CSF enzymes showed an increased activity immediately after trauma, contrasting with the low values measured in the patients with hydrocephalus. In severe head injury, we found a correlation between enzyme release and brain dysfunction assessed according to two methods: the Glasgow coma scale (GCS), and the Liège coma scale (LCS) which uses elements of the GCS and the study of 5 brain stem reflexes. The correlation between enzyme activity and the Liège coma scores is better than that observed with the Glasgow coma scores. High enzyme activity is associated with a bad outcome at six months. It has a prognostic value on so far as it reflects the severity of traumatic structural brain damage.

Adolescent↗
PubMed1982

[Gas embolism in the rat].

Gaseous carbon dioxide was used to produce experimental pulmonary embolism in anaesthetized rats, the vagal nerves of which were either intact or severed. 1. Within seconds following intravenous CO2 injection, pulmonary hypertension, moderate systemic hypotension and bradycardia occurred. After a short hyperventilation period, intact rats showed a brief and transient apnea. Vagotomy suppresses (1) apnea presumably by interruption of reflexes from J pulmonary receptors (Paintal, 1967) and (2) bradycardia by the same token or by suppression of a reflex from auricular origin (Thorén, 1976). 2. Following that initial phase, the events were totally dependent on the right ventricular ability to overcome the pulmonary vascular resistance. If it failed, left and right pressures fell and a secondary apnea followed systemic hypotension. Vagotomy had no effect at this stage. Only half of all animals showed these features. 3. Pulmonary hypertension and hyperventilation lasted twenty minutes at least in intact rats, while vagotomized ones showed an evolution toward acute pulmonary oedema and death. 4. With the same amount of CO2/kg, the dogs of Verstappen et al. (1977) showed only minimal cardio-vascular alterations. The mode of effective embolization in the two species was probably different, as a function of the respective circulation times. But this geometrical point of view is not the only one to be considered: in rats, the rise of pulmonary arterial blood pressure remains even when mechanical obstruction by bubbles has dissipated and a local prolonged vasospasm could be advocated. 5. Acute pulmonary oedema rapidly occurring in vagotomized rats seems to be related to the hyperinflation (very large tidal volume) as also seen in this species with other intensive respiratory drives.

Animals↗
PubMed1979

[Not Available].

Explore the source record for details and available documents.

Animal Population Groups↗
PubMedDate not supplied

[The value of mobile intensive care unit (MICU): does it remain to be proven?].

Recent international guidelines about emergency situations (ILCOR / ERC) pointed to the need of the whole "chain of survival". ALS, Advanced Life Support (the last and "medical" part of the chain ) is important and influences survival rate. If no doubt exists about "what" and "when" to do in such situations, there is no consensus in industrialized countries about "who" should be in charge of such out-of-hospital acute diagnosis and treatment: emergency physicians, emergency nurses, emergency medical technicians (EMT), other "new" professionals ? ... A description of the MICU system in Belgium is given.

Belgium↗
PubMedDate not supplied

Biochemical pathways of acute lung injury.

Complement fragments (C3, C3d, C5a), thromboxane B2 (TxB2), 6-keto-PGF1 alpha and immunoreactive trypsin (IRT) were measured in 98 patients at risk of developing the adult respiratory distress syndrome (ARDS): 53 multiple trauma, 28 abdominal surgery and 17 acute pancreatitis. Sixty-five of these patients developed ARDS: 30 multiple trauma, 19 abdominal surgery and 16 acute pancreatitis patients. Forty of the 65 ARDS patients and 9 out of the 33 non-ARDS patients died. Mean value of the C3d to C3 ratio was abnormal in both ARDS and non-ARDS patients. C5a-like activity was detected in 70 out of the 98 patients (49 ARDS and 22 non-ARDS patients). TxB2 abnormal values (greater than 100 pg . ml-1) were found in 70% of the patients, especially when sepsis occurred. No correlation could be made between abnormal 6-keto PGF1 alpha values and ARDS or sepsis. The mean peak IRT value was 675 micrograms . 1(-1) for ARDS patients and 274 micrograms . 1(-1) for non-ARDS patients (p less than 0.05). A firm correlation was also measured between IRT and sepsis (p less than 0.01). C5a-like activity was regularly detected soon after injury, while TxB2 and IRT tend to appear later in patients developing ARDS. Neither C3d/C3, nor C5a-like activity, nor TxB2, nor IRT are specific markers of ARDS, since they also appeared in severely ill patients who did not develop ARDS.

6-Ketoprostaglandin F1 alpha↗