Preconditioning effect on cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage.

Background: Recent experimental evidence indicates that endogenous mechanisms against cerebral vasospasm can be induced via preconditioning.

Objective: To determine whether these vascular protective mechanisms are also present in vivo in humans with aneurysmal subarachnoid hemorrhage.

Methods: A multicenter retrospective cohort of patients with aneurysmal subarachnoid hemorrhage was examined for ischemic preconditioning stimulus: preexisting steno-occlusive cerebrovascular disease (CVD) and/or previous cerebral infarct.

Successful repair of a gunshot wound to the head with retained bullet in the torcular herophili.

Background: Nonlethal missile injuries to the dural venous sinus system are rare. To date successful repair of isolated penetrating injury to the torcular herophili has not been reported without significant associated morbidity. We report the case of a gunshot wound injury to the occipital region with retained bullet fragment in the confluence of the sinuses causing traumatic sinus venous thrombosis.

Langerhans cell histiocytosis in a 5-month-old presenting with biparietal masses.

Langerhans cell histiocytosis (LCH) is a rare proliferative disorder that occurs most commonly in the pediatric population as a result of pathological clonal proliferation of Langerhans cells with subsequent damage and destruction to surrounding tissue. Clinically, LCH presents in a variety of ways, which often results in prolonged time to diagnosis and subsequently poorer outcomes. In this case report, the authors describe an unusually early presentation of multisystem LCH in a patient at birth, which resulted in a 5-month delay to diagnosis and treatment.

Stealth surgery: subcutaneous endoscopic excision of benign lesions of the trunk and lower extremity.

Background: Benign subcutaneous lesions of the trunk are typically excised through overlying skin incisions, which can result in permanent, potentially disfiguring scars. We previously reported our experience with transaxillary subcutaneous endoscopic approach for removal of benign lesions of the neck. Here we report a similar approach for removing benign lesions of the trunk and lower extremity.

Interleukin-6 maintains bone marrow-derived mesenchymal stem cell stemness by an ERK1/2-dependent mechanism.

Adult human mesenchymal stem cells (MSCs) hold promise for an increasing list of therapeutic uses due to their ease of isolation, expansion, and multi-lineage differentiation potential. To maximize the clinical potential of MSCs, the underlying mechanisms by which MSC functionality is controlled must be understood. We have taken a deconstructive approach to understand the individual components in vitro, namely the role of candidate "stemness" genes.

PDCD10, the gene mutated in cerebral cavernous malformation 3, is expressed in the neurovascular unit.

Objective: Mutations in the programmed cell death 10 gene, PDCD10, cause the autosomal-dominant familial cerebral cavernous malformation 3 (CCM3). Little is known about the function of this gene in disease pathogenesis.

Methods: As a first step, we analyzed the messenger ribonucleic acid (mRNA) expression of CCM3 in the embryonic and postnatal mouse brain by in situ hybridization.

Reactivation of gammaHV68 induces neointimal lesions in pulmonary arteries of S100A4/Mts1-overexpressing mice in association with degradation of elastin.

S100A4/Mts-overexpressing mice have thick elastic laminae and mild pulmonary arterial hypertension (PAH), and the occasional older mouse develops occlusive neointimal lesions and perivascular inflammation. We hypothesized that a vasculotropic virus could induce neointimal lesions in the S100A4/Mts1 mouse by facilitating breakdown of elastin and migration and proliferation of smooth muscle cells. To test this hypothesis, we infected S100A4/Mts1 mice with gammaherpesvirus 68 (gammaHV68).

CCM2 expression parallels that of CCM1.

Background And Purpose: Mutations in CCM2 (MGC4607 or malcavernin) cause familial cerebral cavernous malformation (CCM), an autosomal dominant neurovascular disease. Both the function of this molecule and the pathogenesis of the disease remain elusive.

Methods: We analyzed the mRNA expression of Ccm1 and Ccm2 in the embryonic and postnatal mouse brain by in situ hybridization.

Mutations in apoptosis-related gene, PDCD10, cause cerebral cavernous malformation 3.

Objective: To identify the CCM3 gene in a population of 61 families with a positive family history of cerebral cavernous malformations (CCM), 8 of which had suggestive linkage to the CCM3 locus.

Methods: We searched for mutations within the CCM3 interval using a high-throughput screening technique, temperature-gradient capillary electrophoresis. Mutations detected by this device were subsequently sequenced, and the results were analyzed.

Cerebral venous malformations have distinct genetic origin from cerebral cavernous malformations.

Background And Purpose: Pathogenesis of cerebral venous malformation (CVM) is unknown. Because of coexistence of CVM and cerebral cavernous malformations (CCM), some studies have suggested that these 2 entities share a common origin and pathogenetic mechanism.

Methods: We have identified and ascertained over 200 families with CCM.