Anesthetic Management for Pulmonary Resection: Current Concepts and Improving Safety of Anesthesia.

Increasingly complex procedures are routinely performed using minimally invasive approaches, allowing cancers to be resected with short hospital stays, minimal postsurgical discomfort, and improved odds of cancer-free survival. Along with these changes, the focus of anesthetic management for lung resection surgery has expanded from the provision of ideal surgical conditions and safe intraoperative patient care to include preoperative patient training and optimization and postoperative pain management techniques that can impact pulmonary outcomes as well as patient lengths of stay.

Decline in serum hemoglobin in the 7 days after cardiac catheterization.

Objectives: Bleeding is an established complication following cardiac catheterization and lower preoperative hemoglobin concentration is a potentially modifiable risk factor for adverse outcomes after cardiac surgery. However, typical changes in serum hemoglobin concentration after cardiac catheterization are poorly defined. The authors sought to identify the pattern of change in serum hemoglobin concentration within 7 days after cardiovascular catheterization, factors associated with this change and any association with adverse outcomes.

System x(c)(-) regulates microglia and macrophage glutamate excitotoxicity in vivo.

It is widely believed that microglia and monocyte-derived macrophages (collectively referred to as central nervous system (CNS) macrophages) cause excitotoxicity in the diseased or injured CNS. This view has evolved mostly from in vitro studies showing that neurotoxic concentrations of glutamate are released from CNS macrophages stimulated with lipopolysaccharide (LPS), a potent inflammogen. We hypothesized that excitotoxic killing by CNS macrophages is more rigorously controlled in vivo, requiring both the activation of the glutamate/cystine antiporter (system x(c)(-)) and an increase in extracellular cystine, the substrate that drives glutamate release.

The potential role of B cell-targeted therapies in multiple sclerosis.

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the CNS. Until recently, most therapeutic interventions have targeted T cells in the treatment of MS. Recent data show that B cells also have a role in the pathogenesis of MS.

A mouse model of ischemic spinal cord injury with delayed paralysis caused by aortic cross-clamping.

Background: Spinal cord ischemia and paralysis are devastating perioperative complications that can accompany open or endovascular repair surgery for aortic aneurysms. Here, we report on the development of a new mouse model of spinal cord ischemia with delayed paralysis induced by cross-clamping the descending aorta.

Methods: Transient aortic occlusion was produced in mice by cross-clamping the descending aorta through a lateral thoracotomy.

B cells and autoantibodies: complex roles in CNS injury.

Emerging data indicate that traumatic injury to the brain or spinal cord activates B lymphocytes, culminating in the production of antibodies specific for antigens found within and outside the central nervous system (CNS). Here, we summarize what is known about the effects of CNS injury on B cells. We outline the potential mechanisms for CNS trauma-induced B cell activation and discuss the potential consequences of these injury-induced B cell responses.

Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord.

Macrophages dominate sites of CNS injury in which they promote both injury and repair. These divergent effects may be caused by distinct macrophage subsets, i.e.

B cells produce pathogenic antibodies and impair recovery after spinal cord injury in mice.

Traumatic injury to the mammalian spinal cord activates B cells, which culminates in the synthesis of autoantibodies. The functional significance of this immune response is unclear. Here, we show that locomotor recovery was improved and lesion pathology was reduced after spinal cord injury (SCI) in mice lacking B cells.

An efficient and reproducible method for quantifying macrophages in different experimental models of central nervous system pathology.

Historically, microglia/macrophages are quantified in the pathological central nervous system (CNS) by counting cell profiles then expressing the data as cells/mm(2). However, because it is difficult to visualize individual cells in dense clusters and in most cases it is unimportant to know the absolute number of macrophages within lesioned tissue, alternative methods may be more efficient for quantifying the magnitude of the macrophage response in the context of different experimental variables (e.g.

Macrophages promote axon regeneration with concurrent neurotoxicity.

Activated macrophages can promote regeneration of CNS axons. However, macrophages also release factors that kill neurons. These opposing functions are likely induced simultaneously but are rarely considered together in the same experimental preparation.

Mechanisms and implications of adaptive immune responses after traumatic spinal cord injury.

Traumatic spinal cord injury (SCI) in mammals causes widespread glial activation and recruitment to the CNS of innate (e.g. neutrophils, monocytes) and adaptive (e.

Characterization and modeling of monocyte-derived macrophages after spinal cord injury.

Spinal cord injury (SCI) elicits a neuroinflammatory reaction dominated by microglia and monocyte-derived macrophages (MDM). Because MDM do not infiltrate the spinal cord until days after injury, it may be possible to control whether they differentiate into neuroprotective or neurotoxic effector cells. However, doing so will require better understanding of the factors controlling MDM differentiation and activation.

Central nervous system and non-central nervous system antigen vaccines exacerbate neuropathology caused by nerve injury.

Previously, we showed that autoimmune (central nervous system myelin-reactive) T cells exacerbate tissue damage and impair neurological recovery after spinal cord injury. Conversely, independent studies have shown T cell-mediated neuroprotection after spinal cord injury or facial nerve axotomy (FNAx). The antigen specificity of the neuroprotective T cells has not been investigated after FNAx.

Spinal cord injury triggers systemic autoimmunity: evidence for chronic B lymphocyte activation and lupus-like autoantibody synthesis.

Clinical and experimental data indicate that spinal cord injury (SCI) elicits pathological T-cell responses. Implicit in these data, but poorly understood, is that B lymphocytes (B cells) also contribute to the delayed pathophysiology of spinal trauma. Here, for the first time, we show that experimental spinal contusion injury elicits chronic systemic and intraspinal B cell activation with the emergence of a B cell-dependent organ-specific and systemic autoimmune response.

Bone marrow transplants provide tissue protection and directional guidance for axons after contusive spinal cord injury in rats.

Contusive spinal cord injury (SCI) produces large fluid-, debris- and inflammatory cell-filled cystic cavities that lack structure to support significant axonal regeneration. The recent discovery of stem cells capable of generating central nervous system (CNS) tissues, coupled with success in neurotransplantation strategies, has renewed hope that repair and recovery from CNS trauma is possible. Based on results from several studies using bone marrow stromal cells (MSCs) to promote CNS repair, we transplanted MSCs into the rat SCI lesion cavity to further investigate their effects on functional recovery, lesion morphology, and axonal growth.

Passive or active immunization with myelin basic protein impairs neurological function and exacerbates neuropathology after spinal cord injury in rats.

Myelin-reactive T-cells are activated by traumatic spinal cord injury (SCI) in rodents and humans. Despite the historical association of these cells with experimental and clinical neuropathology, recent data suggest a neuroprotective role for myelin-reactive T-cells. Because of the biological and therapeutic implications of these findings, we attempted to reproduce the original neuroprotective vaccine protocols in a model of rat SCI.

Pegylated brain-derived neurotrophic factor shows improved distribution into the spinal cord and stimulates locomotor activity and morphological changes after injury.

The neurotrophin brain-derived neurotrophic factor (BDNF) shows promise for the treatment of central nervous system (CNS) trauma and disease. Effective delivery methods are required, however, for BDNF to be useful as a therapeutic agent. To this end, we examined the penetration of intrathecally infused N-terminal pegylated BDNF (peg-BDNF) compared to similar infusion of native BDNF after spinal cord injury (SCI).