Cervical epidural abscess due to actinomycosis: demonstration by MRI.
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Actinomyces↗
Biomedical subjects
N de Tribolet
Publications and source records attributed to N de Tribolet.
Three-dimensional volume rendering for magnetic resonance angiography in the screening and preoperative workup of intracranial aneurysms.
This study was undertaken to evaluate the capacity of three-dimensional (3-D) time-of-flight (TOF) magnetic resonance (MR) angiography with VoxelView (VV) 3-D volume rendering to detect and characterize intracranial aneurysms and to compare this rendering technique with that of maximum intensity projection (MIP). Forty patients with a total of 53 intracranial aneurysms (10 giant and subgiant, 43 saccular) were consecutively admitted to University Hospital, Lausanne, Switzerland, and investigated with 3-D TOF MR angiography. Source images of the 43 saccular aneurysms were processed with both MIP and VV. The aneurysm detection rate of the two techniques and their ability to characterize features of an aneurysm, such as its neck and its relation to the parent vessel, were compared. Intraarterial digital subtraction angiography was used as the gold standard to which these techniques could be compared and evaluated. Four aneurysms, less than 3 mm in size, were missed using MIP compared to three missed using VV. The representation of aneurysmal morphology using VV was superior to that found using conventional angiography in nine cases, equal in 16 cases, and inferior in seven cases. The representation of the aneurysm neck using VV was superior to MIP in 21 cases, equal in 17 cases, and inferior in one case; it was superior to that shown using conventional angiography in 10 cases, equal in 18 cases, and inferior in four cases. Time-of-flight MR angiography in conjunction with both MIP and VV 3-D reconstruction was able to visualize all aneurysms that were larger than 3 mm. Compared to MIP, VV provides a better definition of the aneurysm neck and the morphology of saccular aneurysms, making VV valuable for use in a preoperative diagnostic workup.
Adult↗
Single cell monitoring of growth arrest and morphological changes induced by transfer of wild-type p53 alleles to glioblastoma cells.
Mutation of the p53 tumor suppressor gene is one of the earliest identified genetic lesions during malignant progression of human astrocytomas. To assess the functional significance of these mutations, wild-type (WT) p53 genes were introduced into glioblastoma cell lines having mutant, WT, or null endogenous p53 alleles. Populations of cells with mutant or null endogenous p53 alleles and exogenous WT p53 were spontaneously selected in culture for cells expressing only mutant p53 or no p53, which then displayed a growth and tumorigenic phenotype identical to the parental cells. To determine the phenotypic consequences of WT p53 expression before the occurrence of mutations, we developed a single cell assay to monitor WT p53-dependent transcription activity. Transfer and expression of exogenous WT p53 genes to cells with endogenous mutant or deleted, but not WT, p53 alleles caused growth arrest and morphological changes, including increased cell size and acquisition of multiple nuclei. This supports the hypothesis that genetic lesions of the p53 gene play an important role in the genesis of astrocytomas. Furthermore, the high sensitivity of the episomal single cell reporter strategy developed here has potential clinical applications in the rapid screening of patients for germ-line mutations of the p53 gene or any other gene with known targets for transcriptional transactivation.
Alleles↗
Differential expression of triiodothyronine receptors in schwannoma and neurofibroma: role of Schwann cell-axon interaction.
Regulation of gene expression in Schwann cells may be determined, at least in part, by the interaction of these cells with axons. Two peripheral nerve tumors, neurofibroma and schwannoma, represent good tools for studying Schwann cell activity in the presence or absence of axon action. In the present work we studied the expression of triiodothyronine receptors (T3R) by Schwann cells in these two tumors and also in adult normal sciatic nerve. Confirming the results of the histological examination, immunostaining of the neurofilaments showed the presence of fascicles or scattered axons in all neurofibroma sections studied. In these neurofibromas, Schwann cells did not express T3R immunoreactivity. Furthermore, in adult normal sciatic nerve, Schwann cells which ensheathed axons were devoid of any T3R expression. In contrast, in schwannoma, the complete absence of axons was demonstrated by the lack of neurofilament immunostaining. Here, Schwann cells deprived of axonal interaction displayed clear T3R immunoreactivity. In schwannoma cell cultures, Schwann cells continued to express T3R, even in cultures treated with medium that had been conditioned with rat sensory neurons. On the basis of these results, we suggest that, beside the possible regulatory mechanisms for T3R, the synthesis of T3R is regulated, at least in part, by Schwann cell-axon interaction.
Animals↗
Long-term results after ventriculo-atrial shunting in children.
A consecutive series of 120 patients with infantile hydrocephalus who were submitted to ventriculo-atrial shunting was studied. The average follow-up was 11 years. There was no operative mortality; 7 patients died during the follow-up period, but only in 1 case was the cause of death a consequence of the shunt procedure. The incidence rates of infection and slit ventricle syndrome were 4.2% and 1.8%, respectively. Shunt revision was performed on 253 occasions yielding a revision rate of 2.2 per patient. Of these 253 revisions 167 (66%) took the form of elective lengthening of the atrial catheter. The number of reoperations to adjust the length of the atrial catheter or to revise the distal end of the shunting system is a major disadvantage, which actually favors ventriculo-peritoneal shunting as the primary procedure for the treatment of pediatric hydrocephalus.
Cerebrospinal Fluid Shunts↗
Xenon CT measurement of cerebral blood flow in hydrocephalus.
Since the recognition of normal-pressure hydrocephalus as an entity (1965), ventriculo-atrial or peritoneal shunting has been proposed as a treatment for this disease. Unfortunately, selection of patients who would benefit from shunting has always been difficult, and no clinical or brain imaging criteria have been entirely satisfactory. Functional studies intended to measure the local cerebral blood flow (lCBF) seem more promising. Xenon CT CBF measurement has been chosen because of its ability to measure deep white matter lCBF with good spatial resolution. This preliminary study reports the results of lCBF measurement in four patients examined by this technique before and after shunting or cerebrospinal fluid subtraction by lumbar puncture. In this small collective the two patients who improved clinically after shunting or lumbar puncture also had a substantial improvement in deep white matter lCBF.
Administration, Inhalation↗
Expression of the CD44 adhesion molecule in tumours of the central and peripheral nervous system.
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Adult↗
Hypotensive effect of nimodipine during treatment for aneurysmal subarachnoid haemorrhage.
To determine the incidence of induced systemic hypotension in patients after aneurysmal subarachnoid haemorrhage (SAH) and nimodipine treatment 87 consecutive cases were reviewed. The patients were managed according to the same Nimodipine treatment protocol. After confirmation of SAH the nimodipine treatment was started as a continuous intravenous perfusion at a dosage of 0.5 mg/h and gradually increased every 6 hours if haemodynamically tolerated until the maintenance dose of 2 mg/h was reached. Median systemic pressure was continuously measured and tolerated until a lowest limit of 75 mmHg. In 31 patients (36%) hypotension with values below 75 mmHg during at least 30 minutes was noted and needed Nimodipine reduction. Intravenous Nimodipine administration was responsible for hypotension in 26 cases as compared to 5 cases due to oral administration. 38% of all patients required support by vaso-active agents (Dopamine or Nor-adrenaline). There was no statistically significant difference of incidence of delayed ischaemic deterioration comparing the Nimodipine-reduction group with the normal dose group. This study demonstrates that a considerable risk exists of Nimodipine induced hypotension in intravenous administration despite gradually increasing the doses. Correction of hypotension through further induced hypervolaemia accompanied by vasoactive agents can lead to critical haemodynamic situations. We therefore recommend oral Nimodipine administration.
Administration, Oral↗
Differential CD44 expression patterns in primary brain tumours and brain metastases.
Splicing variants of CD44 (CD44v) are increasingly recognised as metastasis-promoting factors in rodent and some human cancers. However, the frequency for CD44v expression in human cancers and their metastases and the status of CD44v expression in low or non-metastatic tumours is still uncertain. To address this issue, we investigated CD44 expression patterns in brain metastases (BMTs) spread from more than ten organs and five types of primary brain tumours (PBTs) by Northern blot, reverse transcription-polymerase chain reaction (RT-PCR) and immunocytochemical analysis. The results demonstrated that all of the 56 PBTs examined express standard form of CD44 (CD44s) but none of them express CD44v. In contrast, 22 of 26 BMTs studied were found with CD44v expression. Our data thus present direct evidence of a general distribution of CD44 in BMTs but suggest that such expression is an extremely rare event in PBTs. Therefore, the presence or absence of CD44v expression may be related to high or low metastatic potential of human malignancies.
Adult↗
Microsatellite instability in human brain tumors.
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Astrocytoma↗
Transplantation in humans of encapsulated xenogeneic cells without immunosuppression. A preliminary report.
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Adrenal Medulla↗
Human astrocytomas and glioblastomas express monocyte chemoattractant protein-1 (MCP-1) in vivo and in vitro.
Expression of the monocyte chemoattractant protein-1 (MCP-1) was examined in human central nervous system tumours (glioblastomas and astrocytomas) and normal human brain. Northern blot analysis demonstrated constitutive expression of MCP-1 mRNA in 6 of 12 glioblastoma cell lines. Expression could be stimulated by interleukin (IL)-1 beta and tumour necrosis factor (TNF)-alpha in all cell lines tested. Immunoprecipitation demonstrated secretion of both isoforms, MCP-1 alpha and -beta, of the MCP-1 protein. Reverse-transcription polymerase chain reaction and Northern blot analysis on tissues demonstrated MCP-1 mRNA expression in 17 of 17 glioblastomas, 3 of 6 anaplastic astrocytomas and 6 of 6 low-grade astrocytomas, as well as in fetal brain but not in normal adult brain. In situ hybridization on 2 glioblastomas and 1 low-grade astrocytoma indicates that neoplastic astrocytes and endothelial cells express MCP-1 mRNA in vivo. Moreover, tumour cyst fluids of glioblastomas and astrocytomas were able to induce monocyte chemoattraction in an in vitro assay. This chemotactic activity was specifically neutralized by anti-MCP-1 antibodies in 9 of 10 samples, further demonstrating the production of bioactive MCP-1 in vivo and supporting an important role for this factor in the infiltration of monocytes/macrophages into tumour tissue.
Astrocytoma↗
Analysis of the p53 gene and its expression in human glioblastoma cells.
Chromosome 17p has been shown to be an early and frequent target for loss of heterozygosity through mitotic recombination in astrocytomas. These losses are frequently accompanied by point mutations in the p53 gene of the remaining allele, resulting in loss of wild type p53 function. However, a fraction of astrocytomas retain constitutional heterozygosity and do not have p53 mutations; some of these lose wild type p53 activity through binding to the protein product of amplified mdm2 genes. To test whether loss of wild type p53 biological function is a necessary step in astrocytoma progression we analyzed p53 expression and biological function in 13 glioma cell lines. All the cell lines expressed a 2.8-kilobase p53 transcript and showed various amounts of p53 protein by immunoprecipitation, except for cell line LN-Z308 which had only a small truncated p53 mRNA and no protein expression. To test whether the p53 expressed in these cell lines was functionally wild type or mutant we transfected them with a plasmid construct harboring a chloramphenicol acetyltransferase (CAT) reporter gene under the control of transcriptional elements that are induced by wild type but not mutant p53. Four lines were shown to retain wild type p53 function. Sequencing of the p53 gene in two of these cell lines confirmed the wild type genotype. These results show that inactivation of the p53 gene is not an obligatory step in glioblastoma genesis. This suggests either that two pathways (p53 inactivation dependent or independent) may lead to a tumor group classified histologically as glioblastoma or that in some cases p53 mutations are bypassed due to the presence of mutations in downstream effector genes.
Animals↗
IL-6 stimulates growth and inhibits constitutive, protein synthesis-independent apoptosis of murine B-cell hybridoma 7TD1.
Interleukin-6 (IL-6) is a well-known survival/growth factor for murine B-cell hybridoma 7TD1 cells. In this study, we analyzed the behavior of 7TD1 cells in the absence or presence of IL-6. After IL-6 deprivation, the cells became growth arrested and demonstrated signs considered to be hallmarks of apoptosis. To assess the underlying molecular mechanism of IL-6-regulated apoptosis, two chemical compounds, cycloheximide (CHX) and aurintricarboxylic acid (ATA), were used to treat the cells. ATA, a DNA endonuclease inhibitor, efficiently prevented DNA fragmentation and increased cell survival in the absence of IL-6. CHX, an inhibitor of protein synthesis, failed to prevent apoptosis and blocked cell survival signals induced by IL-6. These results suggest, first, that IL-6 promotes 7TD1 cell survival by inhibiting an endogenous constitutive cell death program and, second, that this inhibition requires de novo protein synthesis.
Animals↗
Sellar and parasellar extra-axial cavernous hemangiomas.
Cavernous hemangiomas can grow extra-axially within dural sinuses, particularly the cavernous sinus and present like tumours. Five cases of cavernous hemangiomas arising within or from the wall of the cavernous sinus are reported. Three of them had an "endophytic" growth within the cavernous sinus with a lateral extension into the middle cranial fossa, a medial extension into the sella and an anterior extension into the superior orbital fissure. Two cases presented with an "exophytic" extension from the sinus wall at the point of entry of the third and fourth cranial nerves respectively. These patterns of growths are best appreciated by MRI. Keeping in mind that these lesions are contained within a pseudocapsule will help in planing surgical strategy. Characteristic MRI findings of cavernous hemangiomas in this location include hypo-intensity on T 1-weighted images, marked hyperintensity on T2-weighted images and Gadolinium enhancement.
Adult↗
Extreme lateral lumbar disc herniation: clinical presentation in 178 patients.
A retrospective analysis of clinical characteristics of 178 consecutive patients with extreme lateral lumbar disk herniation, amongst 3047 patients operated on for herniated lumbar disc, is presented. The level specific incidence of extreme lateral disc herniation (ELLDH) ranged from a low of 4.5% at L4-5 to peak of 17.4% at L3-4 although the largest number of ELLDH occurred at L4-5 and L5-S1 for a total number of 139 cases (78.1%). 43.6% of all L3 radiculopathies were caused by an L3-4 ELLDH, whereas only 4.4% of all L5 radiculopathies were caused by an L5-S1 ELLDH. Leg pain, either of the sciatic or the femoral type, was the first and dominant clinical symptom of radiculopathy, but pain radiation occurred not always in the appropriate dermatomal segment. ELLDH at upper levels (L2-3 and L3-4) caused usually none or only minor low back signs (76.2%), whereas ELLDH at lower levels more often caused moderate or major lumbar symptoms and signs (59.6%). Positive femoral nerve traction test with upper ELLDH showed a high frequency (84.4%) and reliability and is therefore an important clinical parameter in this situation. Motor deficits occurred more often (78.8%) than sensory deficits (46.6%), were usually of the monoradicular type and were therefore a more reliable clinical sign than sensory disturbances.
Adolescent↗
Growth of small saccular aneurysms to giant aneurysms: presentation of three cases.
We report on three patients with a documented small saccular aneurysm growing to a giant size over several years. In the first patient, a small dilation of the left carotid bifurcation grew to an asymptomatic giant aneurysm of 2 cm in diameter over 11 years. In the second patient, a ruptured aneurysm of the proximal middle cerebral artery (MCA) was erroneously treated by partial ligature of the MCA. Twenty-three years later, the aneurysm had grown to a giant polylobed calcified mass compressing the neighboring brain. In the third patient, a ruptured aneurysm of the dorsal part of the carotid syphon grew over 17 years to a giant calcified mass of 5 cm in diameter despite Hunterian ligation of the common carotid artery in the neck. The three reported cases illustrate the continuous growth and the long-term risks of not treating or of insufficiently treating aneurysms.
Adult↗
Production of interleukin-1 receptor antagonist by human glioblastoma cells in vitro and in vivo.
We investigated the expression and production of the interleukin-1 receptor antagonist (IL-1ra) in three human glioblastoma cell lines (LN443, LN444, LN859). Reverse transcription-polymerase chain reaction (RT-PCR) demonstrated the expression of IL-1ra mRNA transcripts in the three cell lines. These three cell lines also expressed mRNA for IL-1 alpha, IL-1 beta, as well as IL-1 receptor type I and type II, suggesting the presence of an IL-1 autocrine loop in these cell lines. Northern blot analysis demonstrated that the IL-1ra mRNA expression increased with IL-1 beta or tumor necrosis factor (TNF)-alpha but not with GM-CSF stimulation in both LN443 and LN444 cell lines. PMA stimulation increased the mRNA expression in LN444 but not in LN443 cells. Immunocytochemical staining showed IL-1ra immunoreactivity in these three cell lines. ELISA on culture supernatants demonstrated that the IL-1ra was secreted from the cell lines in agreement with the mRNA expression. RT-PCR with isoform-specific primers showed that both intracellular and secreted forms of IL-1ra were expressed by the three cell lines, with a predominance of the intracellular form. In vivo study with RT-PCR and Northern blot analysis demonstrated IL-1ra mRNA in six out of 12 human glioblastoma and two out of five anaplastic astrocytoma tissues, although the expression level was not high in some cases. Immunohistochemistry demonstrated the presence of IL-1ra within the cytoplasm of tumor cells in six out of 10 glioblastomas in vivo. These results suggest a potential role of IL-1ra in regulation of the IL-1 autocrine loop in glioblastomas.
Base Sequence↗