Bilateral CSDH was an independent predictor for the recurrence of CSDH. Antiplatelet or anticoagulant drugs might facilitate the growth of CSDH. These results may help to identify patients at high risk for the recurrence of CSDH.

BACKGROUND AND PURPOSE:In the treatment of carotid atherosclerosis, the rate of stenosis and characteristics of plaque should be assessed to diagnose vulnerable plaques that increase the risk for cerebral infarction. We performed carotid black-blood (BB) MR imaging to diagnose plaque components and assess plaque hardness based on MR signals.

Symptomatic low-grade carotid stenosis with vulnerable plaque confirmed by MRI was associated with a high rate of stroke recurrence that was refractory to aggressive medical treatment. However, carotid endarterectomy was safe and effective for such patients. Plaque characterization by MRI has the potential for more accurate stroke risk stratification in the management of carotid low-grade stenosis.

Targeting viral vectors to appropriate cell types so that norexpressing tumor cell lines, while all cell lines were equally mal cells are not adversely affected is an important goal susceptible to a tissue nonspecific HSV recombinant, hrR3. for gene therapy. Previously, we described a novelIn vivo, G92A replicated well in subcutaneous xenografts approach to viral gene therapy using a conditional, repliof human hepatoma cells (Hep3B) in athymic mice, but not cation-competent herpes simplex virus (HSV), where repliin non-hepatoma subcutaneous tumors (PC3 and HeLa), cation and associated cytotoxicity are limited to a specific whereas, hrR3 replicated well in both tumor types. Intratucell-type by the regulated expression of an essential moral inoculation of G92A inhibited the growth of estabimmediate-early viral gene product. In this report we analished subcutaneous hepatoma tumors in nude mice, but lyze the hepatoma-specific replication, cytotoxicity and not prostate tumors. Replication-competent viral vectors anti-tumor effect of recombinant HSV G92A, regulated by controlled by cell-specific transcriptional regulatory the albumin enhancer/promoter. G92A efficiently replicated sequences provide a new therapeutic strategy for tumor in vitro in two human hepatoma cell lines expressing albutherapy. min, but not in four human non-hepatoma, albumin-non-

Transcription factors belonging to the basic helixloop-helix (bHLH) family are involved in various cell differentiation processes. We report the isolation and functional characterization of a novel bHLH factor, termed OUT. OUT, structurally related to capsulin/epicardin/Pod-1 and ABF-1/musculin/MyoR, is expressed mainly in the adult mouse reproductive organs, such as the ovary, uterus, and testis, and is barely detectable in tissues of developing embryos. Physical association of OUT with the E protein was predicted from the primary structure of OUT and confirmed by co-immunoprecipitation. However, unlike other bHLH factors, this novel protein failed to bind E-box or N-box DNA sequences and inhibited DNA binding of homo-and heterodimers consisting of E12 and MyoD in gel mobility shift assays. In luciferase assays, OUT inhibited the induction of E-boxdependent transactivation by MyoD-E12 heterodimers. Deletion studies identified the domain responsible for the inhibitory action of OUT in its bHLH and C-terminal regions. Moreover, terminal differentiation of C2C12 myoblasts was inhibited by exogenous introduction of OUT. These inhibitory functions of OUT closely resemble those of the helix-loop-helix inhibitor Id proteins. Based on these findings, we propose that this novel protein functions as a negative regulator of bHLH factors through the formation of a functionally inactive heterodimeric complex.