Publications by authors named "G Sonti"

Context: Although osteopathic manipulative treatment (OMT) is used to manage myriad conditions, there has been some hesitation regarding the safety of applying OMT to patients with intracranial injuries or elevated intracranial pressure (ICP).

Objective: To assess the safety of two OMT techniques--pedal pump and thoracic pump--on ICP and cerebral perfusion pressure (CPP) in patients with traumatic brain injuries (Glasgow Coma Scale score < or =8).

Methods: We prospectively enrolled consecutive patients admitted to the intensive care unit (ICU) for traumatic brain injury.

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IL-1beta induces anorexia and adipsia. Here, we report that intracerebroventricular (ICV) pretreatment with an antisense (but not sense) phosphothio-oligodeoxynucleotide to the IL-1 receptor type I (IL-1RI, 1.28 microg or 239 pmol twice daily for 3.

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Pathophysiological and pharmacological concentrations of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) in the cerebrospinal fluid (CSF) induce anorexia in normal rats. Obesity in humans and rodents is associated with increased TNF-alpha messenger RNA and protein levels in various cell types. This suggests that obese individuals may have differential regulation of cytokine production and dissimilar responsiveness to cytokines.

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Interleukin-1 beta (IL-1 beta) is released during pathophysiological processes. IL-1 beta induces neurological manifestations when administered into the cerebrospinal fluid (CSF) at pathophysiological concentrations detected during central nervous system (CNS) infections and other neurological disorders. In the present study, we investigated the regulation of the IL-1 beta system in the CNS in response to the chronic intracerebroventricular (icv) microinfusion of IL-1 beta at estimated pathophysiological concentrations in the CSF.

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The creatine kinase-B (CKB) enzyme is proposed to have a pivotal role in the regeneration of ATP in the nervous system. In the present study, the steady-state levels of CKB mRNA were determined by RNase protection assay in seventeen separate brain regions obtained from rats during the initial interval of the light period or period of inactivity in rats. The antisense probe used specifically hybridizes to CKB mRNA and discriminates CKB from CKM mRNA.

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