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Biomedical subjects

L Picard

Publications and source records attributed to L Picard.

At least 73 records · Page 4Linked to original sources
PubMed1996

Arteriovenous malformations of the corpus callosum--radioanatomic study and effectiveness of intranidus embolization.

Forty-three patients with arteriovenous malformations (AVMs) of the corpus callosum treated by embolization were reviewed. The following clinical and radioanatomic characteristics were found: 84% (36 patients) presented with intracranial hemorrhage, 43% (20 nidi) of the lesions were located in the posterior half of the corpus callosum, multiple nidi were more frequent (21%) than expected, 27 nidi (59%) were fed by branches of both the anterior and posterior cerebral arteries, AVMs mainly drained into the internal cerebral vein and/or interhemispheric superficial veins, and 19 (41%) had both draining pathways, 10 patients (23%) had impaired drainage through the straight sinus due to dysplasia. Staged embolization was performed in 245 feeders. Curative occlusion (more than 95%) was obtained in 17 patients (40%) and considerable occlusion (more than 75%) in 33 patients (77%). Large and giant, diffuse-type, and multifocal AVMs were difficult to completely embolize. Complications associated with embolization occurred in six patients, mostly during the first 5 years. Only two patients had a permanent deficit related to a complication. Overall morbidity and mortality were 7% and 2%, respectively. Nine patients were referred for stereotactic radiosurgery, three of whom were completely cured and five patients have not been assessed. Most AVMs in the corpus callosum are supplied by multi-axial feeders, so multi-target intranidus embolization is very important to prevent the development of other feeders secondary to the hemodynamic shift. Combined therapy using maximum embolization and subsequent radiosurgery may be the most effective method to treat AVMs in the corpus callosum.

Adolescent↗
PubMed1995

Alpha-tocopherol attenuates lung edema and lipid peroxidation caused by acute zymosan-induced peritonitis.

BACKGROUND: Inflammation-induced disease as seen with trauma and infection can lead to increased lung oxidant activity resulting in cell membrane lipid peroxidation. Acute zymosan-induced peritonitis in rats produces lung inflammation, edema, and lipid peroxidation. We determined whether administered alpha-tocopherol (vitamin E), the key antioxidant protection against cell membrane lipid peroxidation, would improve this process. METHODS: Male Wistar rats were given 0.75 mg/kg of intraperitoneal zymosan, volume resuscitated, monitored, and killed at 4 or 24 hours. Lung histologic changes and levels of conjugated dienes, a marker of lipid peroxidation, were used to monitor injury. The levels of vitamin E, vitamin C, and catalase were used to monitor antioxidant defenses. The effect of administering alpha-tocopherol (50 mg/kg) by gavage immediately after zymosan on the degree of the lung injury was then determined. RESULTS: Twenty-four hours after zymosan was administered, the vitamin E levels in plasma were significantly decreased, but lung tissue vitamin E levels were maintained, whereas tissue catalase and vitamin E levels decreased. Lung tissue-conjugated diene levels, alveolar edema, and neutrophil count were significantly increased. alpha-Tocopherol treatment increased the postzymosan plasma vitamin E levels by 50%. Lung tissue vitamin E levels did not increase; however, the degree of lung injury and lipid peroxidation was significantly attenuated. Tissue catalase levels were also maintained. CONCLUSIONS: We conclude that alpha-tocopherol given at the onset of a progressing inflammatory injury can protect the lung from oxidant damage and attenuate the degree of lung injury.

Acute Disease↗
PubMed1995

Innocuity of agents for radiocontrast enhancement of urinary tract stones.

OBJECTIVES: Mineral kidney stones are frequently difficult to detect due to their radiotranslucency. We have recently developed a method that enhances the visibility of such stones by retrograde infusions of certain heavy metal salt solutions such as cesium or lanthanide gadolinium. This report describes toxicologic studies carried out on the use of those contrast agents to introduce this technique eventually into clinical trials. METHODS: Systemic absorption was assessed in dogs through infusion of radioactive contrast agent into the renal pelvis with or without ureteral obstruction. Radioactivity in urine and blood was monitored. Local toxicity was studied in animals infused with the contrast agent at intervals up to 4 weeks. RESULTS: Reabsorption studies under high intrapelvic pressures (70 cm H2O or higher), demonstrated reabsorption of cesium. However, at normal intrapelvic pressures, only a moderate reabsorption of cesium was observed. No gadolinium reabsorption was detected even at high intrapelvic pressures. Histopathologic studies showed no major urothelial lesions but only a transient inflammatory reaction that was undetectable 4 weeks following exposure to gadolinium salts. CONCLUSIONS: Gadolinium salt solutions are good positive radiocontrast agents for mineral kidney stones without having serious toxic effects or systemic reabsorption.

Absorption↗
PubMed1995

Narcolepsy associated with arteriovenous malformation of the diencephalon.

Narcolepsy associated with localized brain lesions is rare, and few reports of well-documented cases have been published. We describe the case of a 20-year-old male (HLA DQw1 negative) who fulfilled clinical and polygraphic criteria of symptomatic narcolepsy. Narcolepsy in this patient was associated with an arteriovenous malformation involving the structures around the third ventricle. Clinical symptoms improved after embolization and radiosurgery. These findings support the hypothesis that lesions in the vicinity of the third ventricle can cause symptomatic narcolepsy.

Adult↗
PubMed1995

Effect of graded increases in smoke inhalation injury on the early systemic response to a body burn.

OBJECTIVE: To study the early (first 24 hrs) effect of increasing lung exposure to smoke on the hemodynamic response to a modest body burn. DESIGN: A prospective randomized study. SETTING: Laboratory at a university medical center. SUBJECTS: Thirty-two adult yearling female sheep. INTERVENTIONS: Adult sheep (n = 32) were given an 18% of body surface burn; 24 sheep were then exposed to cotton toweling smoke using 12 breaths of a tidal volume of 5, 10, or 20 mL/kg. Animals were awakened, resuscitated to baseline oxygen delivery, and then killed at 24 hrs. MEASUREMENTS AND MAIN RESULTS: Vascular pressure, cardiac output, and oxygen consumption and delivery were measured, as well as blood gases, lung and soft tissue lymph flow, and fluid balance. We found that a 5-mL/kg tidal volume smoke exposure x 12 breaths did not produce significant airway inflammation or alter the cardiopulmonary response to a burn alone. Oxygen consumption (VO2) remained at baseline and the net 24-hr positive fluid balance of 1.5 L was comparable to a burn alone. Increasing the smoke exposure to 10 mL/kg tidal volume, which produced a moderate airway injury, resulted in a significant increase in early fluid requirements, a 40% early increase in VO2, a doubling of positive fluid balance, as well as a marked increase in burn edema. However, gas exchange was not impaired. The 20-mL/kg tidal volume exposure resulted in an early 100% increase in VO2, a three-fold increase in fluid requirements at 1 to 4 hrs, compared with burn alone, in addition to a severe airway inflammation with mucosal slough and resulting impaired gas exchange. CONCLUSIONS: The addition of a smoke exposure which produces airway inflammation and injury significantly increases early post burn systemic metabolic demands and fluid requirements, as well as the degree of burn edema and positive fluid balance compared with a burn alone. The magnitude of the accentuated response appears to correspond with the degree of airway inflammation and not with alveolar dysfunction.

Animals↗
PubMed1995

Increased early postburn fluid requirements and oxygen demands are predictive of the degree of airways injury by smoke inhalation.

The combination of burn and smoke inhalation was studied to determine if early hemodynamic and metabolic abnormalities would correspond with the degree of subsequent smoke-induced airways injury. Adult sheep (n = 45) given an 18% total body surface third-degree burn alone or with smoke exposures of 12 breaths of 5, 10, or 20 mL/kg tidal volume were continuously monitored with airways assessed at 4 or 24 hours. With increased smoke exposure (20 mL/kg tidal volume), oxygen consumption (VO2) in the first several hours and net positive fluid balance, especially in the first 6 hours, increased by 100% and 300%, respectively, over that seen with burn alone. The degree of increase in fluid requirement, net fluid retention, and VO2 with smoke, compared with burn alone, correlated best with the degree of airways damage quantitated at 24 hours, r = 0.83, 0.85, and 0.89, respectively. Airways damage at 4 hours did not predict the damage seen at 24 hours. Systemic changes were not caused by gas-phase toxins, such as carbon monoxide, because smoke filtered of particles had the same blood carbon monoxide control as whole smoke, but the systemic response was equal to burn alone, and there was no airways injury. The cause of the systemic changes is likely the result of the intense airways inflammation.

Animals↗
PubMed1995

Proteinase-resistant factors in human erythrocyte membranes mediate CD4-dependent fusion with cells expressing human immunodeficiency virus type 1 envelope glycoproteins.

Murine CD4+ cells are resistant to human immunodeficiency virus type 1 (HIV-1) entry and to fusion with cells expressing HIV-1 envelope glycoproteins (Env). The role of human-specific factors in Env/CD4-mediated fusion is shown by the ability of transient cell hybrids formed between CD4+ murine cells and human HeLa cells to fuse with Env+ cells. Fusion events were observed when other human cells, including erythrocytes, were substituted for HeLa cells in the hybrids. Experiments with erythrocyte ghosts showed that the factors allowing Env/CD4-mediated fusion are located in the plasma membrane. These factors were fully active after extensive digestion of erythrocytes with proteinase K or pronase. Nonprotein components of human plasma membranes, possibly glycolipids, could therefore be required for Env/CD4-mediated fusion and virus entry.

3T3 Cells↗
PubMed1995

[Venous angiography: importance in the diagnosis of brain death. 125 cases].

According to many ethical and humanitarian arguments, the diagnosis of "brain death" is more and more an emergency. The forensic criteria include abolition of consciousness, abolition of brain stem reflexes, abolition of spontaneous breathing joined to electrocerebral silence. However using EEG criteria of electrical silence may be unreliable because of technical artefacts or depressed electrical activity due to drug intoxication and hypothermia. Venous angiography was used in 125 cases: our experience proves reliability and efficiency of angiographic criteria for diagnosis of brain death. For organ transplant, it is better to be as fast as possible: transplanted organ will be better and it reduces the cost of a long useless intensive care. When it is necessary, we suggest to allow the choice between EEG and angiography.

Brain Death↗
PubMed1995

[The anatomy and the MRI anatomy of the interhemispheric cerebral commissures].

Correlation of myelin-stained or cryotomic sections of human brain with inversion-recovery MR images can display the cerebral commissures as white-matter tracts (in hypersignal on MRI), crossing the mid-line. MRI shows routinely in three orthogonal planes a) the corpus callosum stretched above the supra-tentorial ventricles, it's four portions (rostrum, genu, body and splenium) and connections with the Deep Grey Nuclei b) the fornix, intralimbic commissure joining anteriorly the mammillary bodies (through it's columns) to the alveus posteriorly and inferiorly (via it's two crura), arcing around the thalamus and lying over the hippocampus and the dentate gyrus as shown on the frontal sections c) the anterior commissure, white-matter tract connecting the two temporal lobes. In axial view, the anterior commissure has the shape of bicycle handlebars, coursing posteriorly, inferiorly and laterally behind the head of the caudate nucleus and passes into the lateral nucleus of the globus pallidus into the inferior and middle temporal gyri. Because the anterior commissure is easily recognisable in all planes, it's appears to be a important landmark for identification of the lateral and medial nuclei of the globus pallidus on axial and sagittal planes d) at least, the posterior commissure, anterior margin of the pineal region, closely related to the superior colliculi, acquire a major importance in the AC-PC line delineation becoming a reference landmark for stereotatical procedures.

Brain↗
PubMed1994

Administration of large doses of vitamin C does not decrease oxidant-induced lung lipid peroxidation caused by bacterial-independent acute peritonitis.

Acute zymosan-induced peritonitis in rats produces lung inflammation and lipid peroxidation. The effect of this process on plasma and lung tissue ascorbic acid was determined, as was the effect of infusing 150 mg/kg of ascorbic acid immediately after zymosan on the degree of lung insult. Ascorbic acid levels were significantly decreased in plasma and lung tissue at 24 h after zymosan, and lung tissue conjugated diene and neutrophil content was also significantly increased. Vitamin C infusion increased postzymosan plasma levels by 50% over normal control levels. However, lung tissue ascorbic acid was still decreased, and no decrease in the lung injury process was noted. Added ascorbic acid also did not prevent a decrease in plasma vitamin E with the peritonitis. We conclude that the amount of ascorbic acid given in this study did not diminish the lung oxidant inflammatory changes. An insufficient dose or inadequate time for plasma ascorbic acid to equilibrate with the lung cytosol are possible explanations for the lack of attenuation of lung oxidant stress.

Acute Disease↗
PubMed1994

Changes in lung and systemic oxidant and antioxidant activity after smoke inhalation.

We determined the oxidant activity in lung airways, parenchyma, and systemic tissues in response to smoke inhalation, comparing lipid peroxidation with physiologic and histologic change. Adult sheep were given a controlled amount of cooled smoke from burned cotton toweling, containing a uniform particle diameter of 3-4 microns. The mean peak carboxyhemoglobin was 45 +/- 4%. Animals were monitored unanesthetized for 24 h and killed. Severe respiratory failure was noted, as a result of airways mucosal ulceration, submucosal edema, and atelectasis, along with increased airways fluid, but minimal alveolar edema. Airway fluid malondialdehyde (MDA) content was threefold greater than plasma. However, airways mucosa and lung parenchymal tissue, lipid peroxidation, and oxidized glutathione were not increased, suggesting the only direct oxidant activity was present only at the airways surface. Other factors besides oxidants are likely to be involved in the lung injury. However, a marked systemic oxidant stress was noted as evidenced by a significant increase in liver tissue MDA and decrease in reduced glutathione and catalase activity. The tissue oxidant stress also corresponded with a 75% increase in systemic oxygen consumption and an increase in soft tissue vascular permeability. We conclude that: 1) the only direct lung oxidant stress after smoke was noted in airways fluid, while lung tissue lipid peroxidation was not seen despite severe airways injury and atelectasis, and 2) major systemic physiologic changes, as evidenced by increased systemic oxygen demands and systemic microvascular permeability are seen with smoke exposure in addition to evidence of systemic tissue oxidant stress. The likely source of the oxidant activity was a smoke-induced systemic inflammation.

Animals↗
PubMed1994

Comparison of plasma reduced glutathione and oxidized glutathione with lung and liver tissue oxidant and antioxidant activity during acute inflammation.

We determined whether plasma levels of reduced glutathione (GSH) and oxidized glutathione (GSSG) accurately reflect the tissue GSH and GSSG levels in lung and liver during a progressive acute inflammation-induced increased oxidant activity. We also determined whether plasma GSH also reflected other antioxidant defenses. Male Wistar rats (n = 38) were given intraperitoneal zymosan (.75 mg/g body weight) producing an acute progressive peritonitis and generalized inflammation. Animals were resuscitated then killed at 4 or 24 h. Plasma and tissue levels of GSH, GSSG, vitamin C, alpha-tocopherol, and catalase were measured. Conjugated dienes and malondialdehyde were used as tissue markers of lipid peroxidation. We found lung and liver tissue GSH to be decreased significantly at 4 h while GSSG was increased. Lipid peroxidation was also present in the lung. At 24 h, GSH remained decreased in liver and GSSG remained increased in lung along with the lipid peroxides conjugated dienes and malondialdehyde. In addition, overall antioxidant defenses were decreased in both lung and liver. Plasma GSH remained decreased at 24 h corresponding with the decrease in liver GSH as well as the decrease in other plasma and tissue antioxidants. However, plasma GSSG levels were not significantly increased, at any time point, indicating plasma GSSG does not accurately reflect tissue oxidant activity.

Acute Disease↗
PubMed1994

Human cytomegalovirus infection induces transcription and secretion of transforming growth factor beta 1.

Human cytomegalovirus (CMV) infection can elicit a transitory, but profound, immunodepression in immunocompetent individuals. Cytopathogenic destruction of CMV-infected leukocytes alone does not seem sufficient to explain this phenomenon, which suggests that immune system mediators (cytokines) may play a role in amplifying local modifications wrought by CMV infection. We reported previously that transforming growth factor beta 1 (TGF-beta 1) stimulates CMV replication (J. Alcami, C. V. Paya, J. L. Virelizier, and S. Michelson, J. Gen. Virol. 74:269-274, 1993). Since TGF-beta 1 can have profound negative effects on cell growth and immune responses, we investigated the induction of TGF-beta 1 following CMV infection of permissive fibroblasts. TGF-beta 1 promoter was activated by immediate-early (IE) proteins in the absence of infection and transactivated at 5 and 9 h after infection. TGF-beta 1 mRNA increased during the early phase of infection, suggesting that this phenomenon is due to enhanced transcription of the TGF-beta 1 gene. A comparative study of the influence of CMV infection and IE protein expression on TGF-beta 1 promoter function in permissive cells pointed to a possible cooperative role between IE proteins and protein(s) expressed during the early phase of viral infection. Induction of TGF-beta 1 by CMV infection could modify infected cells individually, surrounding tissues, and systemic immune reactions to the advantage of virus replication by both upregulating CMV replication and downregulating host immune responses.

Cytomegalovirus Infections↗
PubMed1994

Effect of increasing the tidal volume of smoke breaths on smoke-induced lung dysfunction.

We determined the effect of a graded increase in lung exposure to a toxic smoke by increasing smoke tidal volume (VT) or the number of smoke breaths. Sheep were anesthetized and then insufflated with cooled cotton toweling smoke; VT was 5, 10, or 20 ml/kg, and smoke breaths were varied from 12 to 48. The smoke had a uniform particle size (3 +/- 0.4 microns diam). Peak carboxyhemoglobin levels varied from 8 +/- 2 to 45 +/- 4% in the lowest to highest exposure groups, respectively. Animals were monitored unanesthetized for 24 h, and then they were killed. Oxygenation (ratio of arterial PO2 to fraction of inspire O2) decreased from 480 +/- 21 to 200 Torr, and compliance decreased by approximately 50% in the highest smoke exposure groups, whereas only a modest decrease in oxygenation and no compliance changes were seen with lesser exposures. A moderate tracheobronchitis, some atelectasis, and no alveolar edema were noted in the lower smoke exposure groups, whereas severe tracheobronchitis, airway edema, and alveolar atelectasis were observed in the highest exposure group. Only modest alveolar flooding was noted. Impaired oxygenation and anatomic injury correlated best with the total smoke delivered (r = 0.59). Increasing VT from 5 to 20 ml/kg did not increase airway or alveolar injury if the total smoke mass delivered was maintained constant. The degree of impaired oxygenation did not correlate with measured lung water (r = 0.27) or lung lymph flow (r = 0.31).

Aerosols↗