The Mini Supra-orbital Approach for Cerebral Aneurysm of the Anterior Portion of the Circle of Willis.

OBJECTIVES: Various mini-invasive approaches have been developed over the last decade to expose the suprasellar area. The supraorbital approach takes a predominant place in exposing the suprasellar area and the Sylvian fissure. OPERATIVE TECHNIQUE: Based on our surgical experience, the technique of supraorbital subfrontal approach is described in detail in this article. After an eyebrow incision, a small frontal craniotomy was performed. Indications, advantages and limitations: This mini-invasive approach was indicated for patients with unruptured aneurysm, in patients with aneurysmal SAH without intracranial hypertension, and especially in elderly patients. This minicraniotomy (1) gave quick and direct access to the aneurysm; (2) provided less trauma of the temporal muscle and improved the cosmetic resuilts; and (3) reduced the risk of postoperative epidural hematoma thanks to the small detachment of the dura mater from the vault. CONCLUSION: We concluded that this limited supraorbital approach gave adequate visualization and allows surgical manipulation within eloquent structures and can be specifically applied in absence of intracranial hypertension.

A kinetic study of SDF-1, VEGF and MCP-1 blood and tissue levels after aortic transplantation in mice.

Vascular rejection is characterized by intimal proliferation and perivascular inflammation. We hypothesize that recipient stem cell therapy could prevent or ameliorate the development of the obliterative lesion. We studied the kinetic expression of three cytokines (SDF-1, MCP-1, VEGF) implicated in mobilization, homing and differentiation of progenitor cells during vascular aggression. An aortic allograft mouse model was used (BALBc donor-C57BL6/j recipient). Ten mice were sacrificed at Day 0, D1, D3, D6, D9, D12, and D20. Cytokine rates were measured in blood and in graft tissue by an ELISA technique. Results showed that in the allograft, SDF-1 and VEGF tissue levels were significantly increased at D12 as compared to the isograft (SDF-1: 22.16 ng/mg vs. 5.69 ng/mg, t=3.38; VEGF: 28.3 pg/mg vs. 9.3 pg/mg, t=3.06). In allografted and isografted groups, MCP-1 tissue levels were higher at D0 as compared to the other time points, without any difference between the two groups. These results prompt us to consider cell therapy at D0 and D12 in this mouse model of aortic graft.

Quality of life and brain damage after microsurgical clip occlusion or endovascular coil embolization for ruptured anterior communicating artery aneurysms: neuropsychological assessment.

OBJECT: For anterior communicating artery (ACoA) aneurysms, endovascular coil embolization constitutes a safe alternative therapeutic procedure to microsurgical clip occlusion. The authors' aim in this study was to evaluate the quality of life (QOL), cognitive function, and brain structure damage after the treatment of ruptured ACoA aneurysms in a group of patients who underwent microsurgical clipping (36 patients) compared with a reference group who underwent endovascular coiling (14 patients). METHODS: At 14 months posttreatment all patients underwent evaluations by independent observers. These observers evaluated global efficacy, executive functions using a frontal assessment battery of tests (Trail making test, Stroop tasks, dual task of Baddeley, verbal fluency, and Wisconsin Card Sorting test), behavior dysexecutive syndrome (the Inventaire du Syndrome Dysexécutif Comportemental questionnaire [ISDC]), and QOL by using the Reintegration To Normal Living Index. Brain damage was analyzed using MR imaging. RESULTS: In the microsurgical clipping and endovascular coiling groups, the distribution on the modified Rankin Scale (p = 0.19) and mean QOL score (85.4 vs 83.4, respectively) were similar. Moreover, the proportion of executive dysfunctions (19.4 vs 28.6%, respectively) and the mean score on the ISDC questionnaire (8.9 vs 8.5, respectively) were not significant, but verbal memory was more altered in the microsurgical clipping group (p = 0.055). Magnetic resonance imaging revealed that the incidence of local encephalomalacia and the median number of lesions per patient increased significantly in the microsurgical clipping group (p = 0.003). CONCLUSIONS: In the 2 groups, no significant difference was observed regarding QOL, executive functions, and behavior. Despite the significant decrease in verbal memory after microsurgical clipping, the interdisciplinary approach remains a safe and useful strategy.

ASB2 targets filamins A and B to proteasomal degradation.

The ordered series of proliferation and differentiation from hematopoietic progenitor cells is disrupted in leukemia, resulting in arrest of differentiation at immature proliferative stages. Characterizing the molecular basis of hematopoietic differentiation is therefore important for understanding and treating disease. Retinoic acid induces expression of ankyrin repeat-containing protein with a suppressor of cytokine signaling box 2 (ASB2) in acute promyelocytic leukemia cells, and ASB2 expression inhibits growth and promotes commitment, recapitulating an early step critical for differentiation. ASB2 is the specificity subunit of an E3 ubiquitin ligase complex and is proposed to exert its effects by regulating the turnover of specific proteins; however, no ASB2 substrates had been identified. Here, we report that ASB2 targets the actin-binding proteins filamin A and B for proteasomal degradation. Knockdown of endogenous ASB2 in leukemia cells delays retinoic acid-induced differentiation and filamin degradation; conversely, ASB2 expression in leukemia cells induces filamin degradation. ASB2 expression inhibits cell spreading, and this effect is recapitulated by knocking down both filamin A and filamin B. Thus, we suggest that ASB2 may regulate hematopoietic cell differentiation by modulating cell spreading and actin remodeling through targeting of filamins for degradation.

[Treatment of aneurysmal subarachnoid hemorrhage]. / Traitement de l'hémorragie méningée anévrismale.

The incidence of subarachnoid hemorrhages is about 10.5/100,000 persons/year. Early obliteration of the aneurysmal sac is necessary to avoid rebleeding. The neurovascular staff meeting must decide the appropriate obliteration procedure for each patient. Intraoperative morbidity is 8% after endovascular coiling and 10% after microsurgical clipping. Endovascular coiling leads to complete obliteration of the aneurysm in 60% of patients and microsurgical clipping in 95%. Delayed ischemic deficits may be prevented by volemic expansion and calcium channel blockers. Hospitalization and general prophylaxis against deep venous thrombosis, pain and seizures are essential. Curative treatment is required against common complications such as intraparenchymatous hematoma, hydrocephalus, and delayed ischemic deficit.

Role of FAN in tumor necrosis factor-alpha and lipopolysaccharide-induced interleukin-6 secretion and lethality in D-galactosamine-sensitized mice.

Tumor necrosis factor (TNF) alpha-induced neutral sphingomyelinase-mediated generation of ceramide, a bioactive lipid molecule, is transduced by the adaptor protein FAN, which binds to the intracellular region of the CD120a TNFalpha receptor. FAN-deficient mice do not exhibit any gross abnormality. To further explore the functions of FAN in vivo and because CD120a-deficient mice are resistant to endotoxin-induced liver failure and lethality, we investigated the susceptibility of FAN-deficient animals to lipopolysaccharide (LPS). We show that after d-galactosamine sensitization, FAN-deficient mice were partially resistant to LPS- and TNFalpha-induced lethality. Although LPS challenge resulted in a hepatic ceramide content lower in mutant mice than in control animals, it triggered similar histological alterations, caspase activation, and DNA fragmentation in the liver. Interestingly, LPS-induced elevation of IL-6 (but not TNFalpha) serum concentrations was attenuated in FAN-deficient mice. A less pronounced secretion of IL-6 was also observed after LPS or TNFalpha treatment of cultured peritoneal macrophages and embryonic fibroblasts isolated from FAN-deficient mice, as well as in human fibroblasts expressing a mutated FAN. Finally, we show that d-galactosamine-sensitized IL-6-deficient mice were partially resistant to endotoxin-induced liver apoptosis and lethality. These findings highlight the role of FAN and IL-6 in the inflammatory response initiated by endotoxin, implicating TNFalpha.