Neurosurgery
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Cell therapies represent a promising alternative treatment for neurodegenerative diseases of the spinal cord, and traumatic spinal cord injury. Cell survival, migration, proliferation and differentiation are intrinsic factors that greatly influence the therapeutic potential of cell therapies. Other factors like local inflammatory and immune response also play an important role. This study analyzed the migration patterns of fetal-derived neural precursors (NPCs) transplanted to the spinal cord of healthy Gottingen minipigs. ⋯ Understanding the migration patterns and other dynamics of different cell lines will allow neurosurgeons to ensure accurate delivery and maximize effectiveness of cell therapeutics in the spinal cord.
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To investigate the role of cigarette smoke exposure (CSE) in the regulation of cerebral smooth muscle cell (SMC) phenotypic modulation in a NAPDH (NOX)-dependent manner and its effect on cerebral aneurysm (CA) formation and rupture. ⋯ CSE initiates oxidative stress-induced phenotypic modulation of SMCs leading to CA formation and rupture. These molecular changes implicate oxidative stress in the pathogenesis of CAs and may provide a potential target for future therapeutic strategies.
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There is no monitoring from the injured spinal cord to define the optimal values of physiological parameters in ICU. We present a technique for continuously monitoring intraspinal pressure (ISP) and spinal cord perfusion pressure (SCPP). ⋯ ISP at the injury site can be measured safely after TSCI. The optimum SCPP varies among TSCI patients.
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Posttraumatic stress disorder (PTSD) is one of the hallmark conditions of soldiers returning from Operations Iraqi Freedom and Enduring Freedom, with as many as 20% of soldiers affected. Approximately 30% of patients do not respond to conventional treatment, resulting in a significant unmet treatment need. Amygdalar activity is increased in fear learning and PTSD, leading our group and others to hypothesize that amygdalar stimulation may attenuate PTSD-related symptoms. Prior studies showed decreased avoidance behavior with right amygdalar stimulation in a foot-shock paradigm. However, the underlying molecular mechanisms remain incompletely understood. Human and animal studies indicate an anxiolytic function for the neurotransmitter Neuropeptide Y (NPY) in PTSD patients and models of PTSD. We hypothesized that amygdalar stimulation would attenuate behavioral effects in the predator scent model of PTSD and that effects would be mediated by NPY. ⋯ Bilateral amygdalae stimulation attenuated anxiety-like behavior in the predator scent model of PTSD, and treatment was correlated with increased amygdalar NPY. Amygdalar stimulation may alleviate PTSD symptoms, and these data provide the first evidence of a possible underlying molecular mechanism.
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There is no proven effective therapy to prevent early brain injury (EBI) after subarachnoid hemorrhage (SAH) despite extensive research efforts. Sphingosine kinase (SphK) 1 has been reported as an important signaling node in antiapoptotic signaling. Heparin is a pleiotropic drug that antagonizes many pathophysiological mechanisms. In this study, we evaluated if heparin prevents EBI after SAH by antiapoptotic mechanisms including SphK1. ⋯ Low-dose heparin posttreatment may decrease the development of post-SAH EBI through anti-apoptotic mechanisms, including sphingosine-related pathway activation, implying its efficacy for early prevention of brain injury after acute aneurysm rupture in a clinical setting.