The function of melatonin as a protective agent against newborn hypoxic-ischemic (H-I) brain injury is not yet well studied, and the mechanisms by which melatonin causes neuroprotection in neurological diseases are still evolving. This study was designed to investigate whether expression of MT1 receptors is reduced in newborn H-I brain injury and whether the protective action of melatonin is by alterations of the MT1 receptors.We demonstrated that there was significant reduction in MT1 receptors in ischemic brain of mouse pups in vivo following H-I brain injury and that melatonin offers neuroprotection through upregulation of MT1 receptors. The role of MT1 receptors was further supported by observation of increased mortality in MT1 knockout mice following H-I brain injury and the reversal of the inhibitory role of melatonin on mitochondrial cell death pathways by the melatonin receptor antagonist, luzindole. These data demonstrate that melatonin mediates its neuroprotective effect in mouse models of newborn H-I brain injury, at least in part, by the restoration of MT1 receptors, the inhibition of mitochondrial cell death pathways and the suppression of astrocytic and microglial activation. K E Y W O R D Shypoxic-ischemic brain injury, melatonin, MT1, newborn

In experienced hands, central nervous system tumors can be embolized with NBCA liquid adhesive with a high degree of safety and efficacy. We think that adroit embolization technique with NBCA and other embolisates should be part of the contemporary neuroendovascular armamentarium.

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Ischemic stroke (IS) is a leading disease with high mortality and disability, as well as with limited therapeutic window. Biomarkers for earlier diagnosis of IS have long been pursued. Family and twin studies confirm that genetic variations play an important role in IS pathogenesis. Besides DNA mutations found previously by genetic linkage analysis for monogenic IS (Mendelian inheritance), recent studies using genome-wide associated study (GWAS) and microRNA expression profiling have resulted in a large number of DNA and microRNA biomarkers in polygenic IS (sporadic IS), especially in different IS subtypes and imaging phenotypes. The present review summarizes genetic markers discovered by clinical studies and discusses their pathogenic molecular mechanisms involved in developmental or regenerative anomalies of blood vessel walls, neuronal apoptosis, excitotoxic death, inflammation, neurogenesis, and angiogenesis. The possible impact of environment on genetics is addressed as well. We also include a perspective on further studies and clinical application of these IS biomarkers.

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Arterial venous malformations (AVMs) are rare conditions that are difficult to manage. Therapeutic options include selective embolization with or without surgical excision. Recurrence, however, is high despite correction of the primary abnormality. Cosmetic concern is among the indications for treatment, particularly if the AVM occurs on the face or scalp. Historically, AVM excision and the residual defect correction have been performed separately. We present the first case reported of a successful embolization and interval excision with immediate reconstruction using a dermal fat graft, as a novel approach to correct soft tissue defect following the resection of an AVM. A 35-year-old man presented with a 20-year history of a nonpulsating mass posterior to the hairline in the right frontoparietal region, measuring 4.0 cm on its longest axis. Embolization of the AVM was achieved by injecting N-butyl cyanoacrylic acid and ethiodol. One month after embolization, surgical excision of the mass was performed. The resulting disfiguring contour defect was immediately corrected using a dermal fat graft harvested from the groin. At 4 months' follow-up, the graft was viable with no evidence of resorption or epidermal cyst formation. In addition, there was no recurrence of the AVM and no complications at the donor site. This case demonstrates the utility of a dermal fat grafts in correcting the impending defect in 1 stage avoiding a second-stage procedure and significant period of cosmetic disfigurement. This method should be considered as a treatment option for patients requiring moderately sized AVM excisions in cosmetically sensitive areas.

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