Abstract.It is well known that tumor necrosis factor (TNF) can have both contrary and pleiotropic effects in anti-tumor immune response. In the present study, we prepared two different tumor cell-based immunotherapy models: MCA38 adenocarcinoma and GL261 glioma intracranial interleukin-2 (IL-2)-based. Each tumor was transfected to express IL-2 with or without expression of the soluble form of tumor necrosis factor receptor type II (sTNFRII). Although mice in which TNF is blocked survive longer than IL-2 alone (35.2 versus 26 days), the reverse was observed for GL261 glioma. The differential effect on tumor growth implies enhanced TNF sensitivity of GL261 compared to MCA38. This notion is supported by the observation that TNF induces apoptosis in GL261 but not MCA38 tumors. We further examined tumor infiltrating CD11b + F4/80 + macrophages (or tumor-associated macrophages: TAM) for TNF production in vivo and found that TAM express cell surface TNF implying a role in eliminating glioma cells mediated by the cell surface form of TNF.

Background:Diffuse cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) refractory to medical management can be treated with intra-arterial administration of vasodilators, but valid bedside monitoring for the diagnosis and therapeutic assessment is poorly available. We demonstrate the successful application of regional cerebral oxygen saturation (rSO2) monitoring with multichannel near-infrared spectroscopy (NIRS) in assisting intra-arterial infusions of fasudil hydrochloride to a patient suffering from post-SAH vasospasm in the distal vascular territories.Case Description:A 63-year-old man presented with SAH and intracerebral hematoma due to ruptured right middle cerebral artery aneurysm developed aphasia and right-sided weakness on day 9 after SAH onset. Delayed cerebral ischemia attributable to diffuse vasospasm in the distal territories of the left anterior and middle cerebral arteries was suspected. Since the symptoms persisted despite maximal hyperdynamic therapy with dobutamine, intra-arterial fasudil treatment in the setting of rSO2 monitoring including the spasm-affected vascular territory with four-channel flexible NIRS sensors was subsequently performed. Decreased and fluctuating rSO2 in angiographically documented vasospastic territories increased immediately after intra-arterial fasudil infusion in accordance with relief of vasospasm that correlated with neurological improvement. The procedure was repeated on day 11 since the effect was transient and neurological deterioration and reduction of rSO2 recurred. The deficits resolved accompanied by uptake and maintenance of rSO 2 following the intra-arterial fasudil, resulting in favorable functional outcome.Conclusion:Continuous rSO2 monitoring with multichannel NIRS is a feasible strategy to assist intraarterial fasudil therapy for detecting and treating the focal ischemic area exposed to diffuse vasospasm.

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Currently carotid artery stenting (CAS) as well as carotid endoarterectomy (CEA) have become widely accepted forms of treatment for carotid artery stenosis, although complications associated with distal embolism remain problematic. Therefore it is important to have an accurate understanding of the properties of carotid plaque before undertaking CAS in order to ensure the safety of such a therapeutic treatment. This study was undertaken to determine the efficacy of using IVUS Virtual Histology TM (VH-IVUS) to evaluate the pathological properties of plaque contained within carotid artery stenosis. VH-IVUS was performed for six cases undergoing CAS during the period of July to December, 2005. VH-IVUS displays plaque composition under four color mappings of fibrous, fibro-fatty, calcification and necrotic core, being able to offer detailed tissue characterization of soft to hard plaque components. Plaque evaluation by VH-IVUS is both reproducible and objective, and is considered to be an effective method for evaluating the risk complications associated with CAS.