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Biomedical subjects

Nicolas de Tribolet

Publications and source records attributed to Nicolas de Tribolet.

27 records · Page 2Linked to original sources
PubMed2003

Cervical sympathetic block to reverse delayed ischemic neurological deficits after aneurysmal subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: The purpose of the present study was to evaluate the feasibility and safety of a locoregional cervical sympathetic block to improve cerebral perfusion in patients suffering from cerebral vasospasm after aneurysmal subarachnoid hemorrhage. METHODS: Nine consecutive patients with symptoms of delayed ischemic deficits, induced by angiographically confirmed cerebral vasospasm, were treated with the injection of locoregional anesthesia to block the ascending cervical sympathetic chain at the level of the superior cervical ganglion. Neurological status was recorded before and after the procedure, and cerebral angiography was performed before and after the procedure. RESULTS: No complications occurred in this short series. The procedure appeared to be simple and safe. Horner's signs appeared within 12+/-0.1 minutes and lasted for an average of 6.3+/-4 hours. In all patients, improved cerebral perfusion was detected at the confirmatory angiography but without change in vessel caliber. One patient died of the complications of the initial hemorrhage, and 2 died of the consequences of the severe vasospasm despite maximal medical treatment. In all the other cases, the neurological status promptly returned to normal within 48 hours after the locoregional treatment. CONCLUSIONS: Patients with mild to moderate symptoms seem to benefit greatly from transient ipsilateral cervical sympathetic block. This simple technique may be helpful when used as an adjunct to the standard therapy to improve cerebral perfusion.

Adult↗
PubMed2003

T-cell immune responses in the brain and their relevance for cerebral malignancies.

In order that cellular immune responses afford protection without risk to sensitive normal tissue, they must be adapted to individual tissues of the body. Nowhere is this more critical than for the brain, where various passive and active mechanisms maintain a state of immune privilege that can limit high magnitude immune responses. Nevertheless, it is now clear that immune responses are induced to antigens in the brain, including those expressed by cerebral malignancies. We discuss hypotheses of how this can occur, although details such as which antigen presenting cells are involved remain to be clarified. Antitumor responses induced spontaneously are insufficient to eradicate malignant astrocytomas; many studies suggest that this can be explained by a combination of low level immune response induction and tumor mediated immunosuppression. A clinical objective currently pursued is to use immunotherapy to ameliorate antitumour immunity. This will necessitate a high level immune response to ensure sufficient effector cells reach the tumor bed, focused cytotoxicity to eradicate malignant cells with little collateral damage to critical normal cells, and minimal inflammation. To achieve these aims, priority should be given to identifying more target antigens in astrocytoma and defining those cells present in the brain parenchyma that are essential to maintain antitumour effector function without exacerbating inflammation. If we are armed with better understanding of immune interactions with brain tumor cells, we can realistically envisage that immunotherapy will one day offer hope to patients with currently untreatable neoplastic diseases of the CNS.

Animals↗
PubMed2003

Third ventricle colloid cyst associated with subarachnoid haemorrhage.

Colloid cyst of the third ventricle is a rare, benign pathology of endothelial origin. Excellent prognosis is achieved when the cyst is diagnosed early and excised. Hydrocephalus can occur as an acute, fatal complication or can cause chronic symptoms such as headaches. A case of a patient with a third ventricle colloid cyst in association with prepontine subarachnoid haemorrhage is presented. This was a 29-year-old healthy male who was admitted because of a depressed consciousness. Neuro-radiological imaging revealed a mass in the third ventricle, a biventricular hydrocephalus and a prepontine subarachnoid haemorrhage without any evidence of a cerebral aneurysm. Perimesencephalic nonaneurysmal subarachnoid haemorrhage is well known but its cause is still a matter of debate. A description is given of the association of this type of subarachnoid haemorrhage with an acute hydrocephalus caused by a third ventricle colloid cyst. Because of the potential morbidity and mortality of third ventricle colloid cysts, this association is described and should be considered as a rare presentation of third ventricle colloid cyst.

Adult↗
PubMed2002

Preclinical Auger and gamma radiation dosimetry for fluorodeoxyuridine-enhanced tumour proliferation scintigraphy with [123I]iododeoxyuridine.

Animal experiments have shown that short blocking of thymidine (dThd) synthesis with fluorodeoxyuridine (FdUrd) results in significantly increased DNA incorporation of [(125)I]iododeoxyuridine ([(125)I]IdUrd) in tumour and rapidly cycling tissues. Based on these results, we give an Auger and gamma radiation dosimetry estimate for a scintigraphy study in glioblastoma patients using [(123)I]IdUrd. The Auger radiation dosimetry calculated for patients is based on measurement of DNA-incorporated [(125)I]IdUrd in rapidly dividing tissues in nude mice xenografted with human glioblastoma. Further data obtained 0.5, 6 and 24 h after injection of [(125)I]IdUrd allowed calculation of the additional gamma radiation exposure using MIRDOSE3.1. High gradients of radioactivity concentration between dividing and non-dividing tissues were observed 6 and 24 h after injection of [(125)I]IdUrd combined with FdUrd pretreatment. While the estimated Auger radiation absorbed doses of [(123)I]IdUrd in six rapidly cycling normal tissues in patients are low, the equivalent doses become significant with application of the recommended preliminary radiation weighting factor (W(R)) of 20 for stochastic effects of DNA-associated Auger radiation. Using the latter W(R), extrapolation of the animal results to the proposed patient injection with 300 MBq [(123)I]IdUrd combined with FdUrd pretreatment indicates that the effective dose will be 5.42 mSv, including 1.67 mSv from Auger and 3.75 mSv from gamma radiation. The predicted Auger radiation effective dose for patients undergoing [(123)I]IdUrd scintigraphy will be significant if the enhancement of DNA incorporation that is achieved by means of FdUrd pretreatment is similar to that obtained in animals.

Animals↗
PubMed2002

Anoxia induces macrophage inhibitory cytokine-1 (MIC-1) in glioblastoma cells independently of p53 and HIF-1.

Human astrocytic brain tumors select for mutations in the p53 tumor suppressor gene early in malignant progression. p53 is activated upon various kinds of cellular stress leading to apoptosis or cell cycle arrest, but is also implicated in complex biological processes such as inhibition of angiogenesis and metastasis. In an effort to shed light on consequences mediated by p53 inactivation in gliomas, we established the Tet-On system for p53 in the LN-Z308 glioblastoma cell line. The macrophage inhibitory cytokine-1 (MIC-1) gene was identified as a most prominent p53 target gene upon gene expression profiling. Oxygen deprivation, an important cellular stress, revealed MIC-1 as an anoxia responsive gene in glioblastoma cell lines. MIC-1 up-regulation by anoxia is mediated through an alternative, p53 and hypoxia inducible factor 1 (HIF-1) independent pathway. Furthermore, ectopic expression of MIC-1 in LN-Z308 cell line completely abolished its inherent tumorigenicity in nude mice, while proliferation in vitro was not affected. In the present experimental model MIC-1 may exert its anti-tumorigenic properties via a paracrine mechanism mediated by host cells in vivo. Taken together, these data suggest that MIC-1 is an important downstream mediator of p53 function, while acting itself as an intercessor of cellular stress signaling and exerting anti-tumorigenic activities.

Animals↗
PubMed2002

Promising survival for patients with newly diagnosed glioblastoma multiforme treated with concomitant radiation plus temozolomide followed by adjuvant temozolomide.

PURPOSE: Temozolomide is a novel oral alkylating agent with demonstrated efficacy as second-line therapy for patients with recurrent anaplastic astrocytoma and glioblastoma multiforme (GBM). This phase II study was performed to determine the safety, tolerability, and efficacy of concomitant radiation plus temozolomide therapy followed by adjuvant temozolomide therapy in patients with newly diagnosed GBM. PATIENTS AND METHODS: Sixty-four patients were enrolled onto this open-label, phase II trial. Temozolomide (75 mg/m(2)/d x 7 d/wk for 6 weeks) was administered orally concomitant with fractionated radiotherapy (60 Gy total dose: 2 Gy x 5 d/wk for 6 weeks) followed by temozolomide monotherapy (200 mg/m(2)/d x 5 days, every 28 days for six cycles). The primary end points were safety and tolerability, and the secondary end point was overall survival. RESULTS: Concomitant radiation plus temozolomide therapy was safe and well tolerated. Nonhematologic toxicities were rare and mild to moderate in severity. During the concomitant treatment phase, grade 3 or 4 neutropenia, thrombocytopenia, or both were observed in 6% of patients, including two severe infections with Pneumocystis carinii. During adjuvant temozolomide, 2% and 6% of cycles were associated with grade 3 and 4 neutropenia or thrombocytopenia, respectively. Median survival was 16 months, and the 1- and 2-year survival rates were 58% and 31%, respectively. Patients younger than 50 years old and patients who underwent debulking surgery had the best survival outcome. CONCLUSION: Continuous daily temozolomide and concomitant radiation is safe. This regimen of concomitant chemoradiotherapy followed by adjuvant chemotherapy may prolong the survival of patients with glioblastoma. Further investigation is warranted, and a randomized trial is ongoing.

Adult↗
PubMedDate not supplied

Survivin in brain tumors: an attractive target for immunotherapy.

Survivin, a member of the inhibitor of apoptosis proteins gene family, was recently shown to be expressed by tumors originating from different cell lineages. There are also cumulative evidences that spontaneous immune response against survivin derived epitopes may occur. Here, using RT-PCR, Western-blot analysis and immunohistochemistry, we show that survivin is widely expressed by gliomas, meningiomas and schwannomas, both in vitro and in vivo. These data indicate that survivin may serve as an attractive target for immunotherapies designed for brain tumors.

Adolescent↗