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Primary Involvement (primary + involvement)

Distribution by Scientific Domains

Medical Sciences	50%

Selected Abstracts

Primary cancer of the sphenoid sinus,A GETTEC study,

HEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 3 2009
Pierre Olivier Vedrine MD
Abstract Background. Primary involvement of the sphenoid sinus occurs in 2% of all paranasal sinus tumors and is associated with dismal prognosis. Optimal management remains debatable. Methods. A total of 23 patients were treated for a primary cancer of the sphenoid sinus from 1988 to 2004. Charts were reviewed for patient-, tumor-, and treatment-related parameters. Univariate and multivariate analyses were conducted to identify prognostic factors for locoregional control and survival. Results. Cranial neuropathies were present in 12 patients. Pathologic findings included adenoid cystic carcinoma, adenocarcinoma, lymphoma, squamous cell carcinoma, sarcoma, neuroendocrine carcinoma, melanoma, and malignant hemangiopericytoma. All but 2 patients had stages III to IV cancer. Radiotherapy was performed in 18 patients and chemotherapy in 12. Of 10 patients undergoing surgery, total excision with grossly negative margins was achieved in 4 patients and subtotal resection in 6. Median locoregional control and overall survival were 12 and 41 months, respectively. On multivariate analysis, cranial neuropathy was associated with worse locoregional control and survival. Surgery was rarely complete because of advanced stages at presentation, but it yielded better outcomes than other treatments without surgery in non lymphoma-cases. Conclusion. Early CT and MRI should be performed when facing aspecific, rhinological, or neuro-ophtalmological symptoms. Cranial neuropathies indicate a worse prognosis. Surgery, including debulking surgery, may be preferred to combined modality treatments without surgery. Its apparently favorable impact on prognosis would need to be tested in homogenous histological groups of patients, which is impossible because of the rarity of the disease. Highly conformal radiotherapy (adjuvant or definitive) should be encouraged and optimized with concurrent chemotherapy in advanced stages. Aggressive multidisciplinary management including surgery, chemotherapy, and radiotherapy should be encouraged and adapted on histology and tumor extensions. Progress is still warranted to improve outcomes. © 2008 Wiley Periodicals, Inc. Head Neck, 2009 [source]

Muscarine activates the sodium,calcium exchanger via M3 receptors in basal forebrain neurons

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2006
Changqing Xu
Abstract Neurons of the medial septum/diagonal band of Broca (MSDB) project to the hippocampus. Muscarinic cholinergic mechanisms within the MSDB are potent modulators of hippocampal functions; intraseptal scopolamine disrupts and intraseptal carbachol facilitates hippocampus-dependent learning and memory tasks, and the associated hippocampal theta rhythm. In earlier work, we demonstrated that, within the MSDB, the septohippocampal GABAergic but not cholinergic neurons are the primary target of muscarinic manipulations and that muscarinic activation of septohippocampal GABAergic neurons is mediated directly via M3 receptors. In the present study, we examined the ionic mechanism(s) underlying the excitatory actions of muscarine in these neurons. Using whole-cell patch-clamp recording techniques in rat brain slices, we demonstrated that M3 receptor-mediated muscarinic activation of MSDB neurons is dependent on external Na+ and is also reduced by bath-applied Ni2+ and KB-R7943 as well as by replacing external Na+ with Li+, suggesting a primary involvement of the Na+,Ca2+ exchanger. We conclude that the M3 receptor-mediated muscarinic activation of MSDB septohippocampal GABA-type neurons, that is important for cognitive functioning, is mediated via activation of the Na+,Ca2+ exchanger. [source]

4-Hydroxynonenal: A membrane lipid oxidation product of medicinal interest

MEDICINAL RESEARCH REVIEWS, Issue 4 2008
G. Poli
Abstract A comprehensive focus on 4-hydroxynonenal (HNE) as candidate molecule in a variety of pathophysiological conditions occurring in humans is here provided. Despite an active, now well characterized, metabolism in most cells and tissues, HNE can be easily detected and quantified by means of several methods, although with different sensitivity. Measurements of HNE and/or stable metabolites in biological fluids are already applied as lipid peroxidation/oxidative stress markers in a huge number of human disease processes, often sustained by inflammatory reactions. A primary involvement of this aldehydic product of membrane lipid oxidation in inflammation-related events, as well as in regulation of cell proliferation and growth, in necrotic or apoptotic cell death, appears supported by its marked ability to modulate several major pathways of cell signaling and, consequently, gene expression. The actual knowledge of HNE reactivity, metabolism, signaling and modulatory effect in the various human organs should provide a solid background to the investigation of the aldehyde's contribution to the pathogenesis of human major chronic diseases and would likely promote advanced and oriented applications not only in diagnosis and prevention but also in molecular treatment of human diseases. © 2007 Wiley Periodicals, Inc. Med Res Rev, 28, No. 4, 569,631, 2008 [source]

"Cloud-like enhancement" is a magnetic resonance imaging abnormality specific to neuromyelitis optica,

ANNALS OF NEUROLOGY, Issue 3 2009
Shoichi Ito MD
Neuromyelitis optica (NMO) is presumably mediated by an autoantibody against aquaporin-4 densely expressed at the blood-brain barrier. In 18 patients with NMO, brain magnetic resonance imaging (MRI) findings were systematically reviewed. Brain MRI abnormalities were found for 89% of the patients, and the most prominent feature was "cloud-like enhancement," multiple patchy enhancing lesions with blurred margin, found in 90% of the patients with positive contrast enhancement. In NMO, brain MRI abnormalities are frequent, and cloud-like enhancement appears to be an MRI finding specific to NMO, possibly caused by primary involvement of the blood-brain barrier by the autoantibodies. Ann Neurol 2009;66:425,428 [source]