ASK family kinases mediate cellular stress and redox signaling to circadian clock.

Daily rhythms of behaviors and physiologies are generated by the circadian clock, which is composed of clock genes and the encoded proteins forming transcriptional/translational feedback loops (TTFLs). The circadian clock is a self-sustained oscillator and flexibly responds to various time cues to synchronize with environmental 24-h cycles. However, the key molecule that transmits cellular stress to the circadian clockwork is unknown.

Matrix metalloproteinase inhibition attenuates brain edema after surgical brain injury.

Background: Neurosurgical operations can result in inevitable brain injury due to the procedure itself. This surgical brain injury (SBI) can cause post-operative complications such as brain edema following blood-brain barrier (BBB) disruption leading to neurological deficits.

Methods: We tested whether inhibition of matrix metalloproteinases (MMPs) 9 and 2 provided neuroprotection against SBI.

Matrix metalloproteinase inhibition attenuates brain edema in an in vivo model of surgically-induced brain injury.

Objective: Neurosurgical procedures can result in brain injury by various means, including direct trauma, hemorrhage, retractor stretch, and electrocautery. This surgically-induced brain injury (SBI) can cause postoperative complications such as brain edema after blood-brain barrier (BBB) disruption. The present study seeks to test a matrix metalloproteinase (MMP) inhibitor for preventing postoperative brain edema and BBB disruption in an in vivo model of surgically-induced brain injury.

One-stage anterior approach for four-vessel occlusion in rat.

Background And Purpose: We report a modified 4-vessel occlusion (4VO) rat model.

Method: We used a 1-stage anterior approach for making bilateral hemispheric ischemia.

Results: Modified 4VO method decreased cerebral blood flow to 12% to 14% of baseline levels.

Role of c-Jun N-terminal kinase in cerebral vasospasm after experimental subarachnoid hemorrhage.

Background And Purpose: Inflammation could play a role in cerebral vasospasm after subarachnoid hemorrhage (SAH). SP600125 a c-Jun N-terminal kinase (JNK) inhibitor reduces inflammation. The present study examined if SP600125 could reduce cerebral vasospasm.

Role of p53 and apoptosis in cerebral vasospasm after experimental subarachnoid hemorrhage.

Our previous studies indicate that apoptosis in endothelial cells of major cerebral arteries contributes to cerebral vasospasm after subarachnoid hemorrhage (SAH). This study examined the pathologic roles of tumor suppressor p-53 in cerebral vasospasm using an established dog double-hemorrhage model. Twenty mongrel dogs were divided into four groups: (1) control, (2) SAH, (3) SAH+DMSO (vehicle), and (4) SAH+pifithrin-alpha (PFT) (p53 inhibitor).

Nicotine exposure, mimicked smoking, directly and indirectly enhanced protein kinase C activity in isolated canine basilar artery, resulting in enhancement of arterial contraction.

Cigarette smoking is a significant risk factor in the incidence of cerebrovascular disorders. Among the many compounds in cigarette smoke, nicotine is considered to most significantly affect cerebral arterial tone. The purpose of this study is to investigate precise pharmacological effects of nicotine on the regulation of cerebral arterial tone.

Encephalocele in the ethmoid sinus presenting as a massive intracerebral hemorrhage after a "polypectomy": a case report.

The discovery of a congenital transethmoidal encephalocele in an adult patient is very rare and is sometimes misdiagnosed as a polyp of the ethmoid sinus. It is important to note that a congenital transethmoidal encephalocele presenting as a massive intracerebral hemorrhage in an adult patient has never been reported. This study's patient underwent endoscopic polypectomy and suffered from massive intracerebral hemorrhage because the encephalocele contained a frontobasal artery.

Gene transfer of extracellular superoxide dismutase failed to prevent cerebral vasospasm after experimental subarachnoid hemorrhage.

Background And Purpose: We examined the therapeutic effect of human extracellular superoxide dismutase (ECSOD) gene transfer in the prevention of delayed cerebral vasospasm after experimental subarachnoid hemorrhage (SAH) because it was reported ECSOD relieved early-stage vasospasm.

Methods: Twenty mongrel dogs were divided randomly into 4 groups to serve as control, SAH, SAH+adenovirus ECSOD (AdECSOD), and SAH+no transgene (AdBglII) groups, respectively. An established canine double-hemorrhage model of SAH was used by injecting autologous arterial blood into the cisterna magna on day 0 and day 2.

Differences in diffusion-weighted and T2-weighted magnetic resonance imaging findings in the acute and chronic stages of ischemic cerebrovascular disease--two case reports.

A 71-year-old man presented with sudden onset of vertigo and a 77-year-old man suffered consciousness disturbance. Diffusion-weighted magnetic resonance (MR) imaging on admission showed hyperintense areas in the left cerebellar hemisphere in the first patient and in the brainstem in the second patient. Both patients were treated with argatroban and edaravone, and the neurological deficits markedly improved one month after admission.

Ras protein contributes to cerebral vasospasm in a canine double-hemorrhage model.

Background And Purpose: Mitogen-activated protein kinase (MAPK) has been shown to be involved in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH). In the present study we examined the role of Ras protein, an upstream regulator of MAPK, and the effects of the inhibitors of Ras farnesyltransferase (FTase), FTI-277 and FTase inhibitor I, on angiographic vasospasm and clinical evaluations.

Methods: Twenty-five dogs were randomly divided into 5 groups: control, SAH, SAH+dimethyl sulfoxide, SAH+FTI-277, and SAH+FTase inhibitor I.

Caspase inhibitors prevent endothelial apoptosis and cerebral vasospasm in dog model of experimental subarachnoid hemorrhage.

Apoptosis in the endothelium of major cerebral arteries may play a role in the initiation and maintenance of cerebral vasospasm after subarachnoid hemorrhage (SAH). We tested the therapeutic effect of caspase inhibitors on endothelial apoptosis and on cerebral vasospasm in an established dog double-hemorrhage model. Thirty-one mongrel dogs were divided into five groups: control; SAH; SAH treated with vehicle [DMSO]; SAH treated with Ac-DEVD-CHO [a specific caspase-3 inhibitor]; and SAH treated with Z-VAD-FMK [a broad caspase inhibitor].

Interlaminar fixation using the atlantoaxial posterior fixation system (3XS system) for atlantoaxial instability: surgical results and biomechanical evaluation.

This study evaluated the surgical results for patients with atlantoaxial instability due to various lesions treated using the atlantoaxial posterior fixation system (3XS system; Kisco DIR, Paris, France), together with a biomechanical study of this system. The strength of the 3XS system during torsion was examined using a biomechanical simulation model. The 3XS system consists of a transverse unit, hooks, and rods.